Category Archives: prevention

SPECIALIST NATURAL MEDICINE CLINIC 2014

SPECIALIST NON-XRAY PAIN, BONE, BREAST, BRAIN,  HEART, CHEST, GENITOURINARY, HORMONE RISK SCREENING  @ NATURAL MEDICINE CLINIC

BREAST CANCER  MONTH  DISCOUNT

for appointments for consultations,   or non-xray procedures by registered practitioners :  Sure Touch breast prescreening on  Saturday mornings  (1 Nov then 29 Nov then 6 Dec)  by Sister Zeneath Ismail – cash R650 (then R450 if followup scan desired within 3 months);   – bone density  cash R450 -tariff item 3612-  anytime;  Unlike radiologists’  and thermography reports (which describe only  the imaging finding), the rates quoted include relevant breast or bone consultation and management planning  by a specialist physician.

IF BOOKED TOGETHER, (not necessarily the same morning) then combined breast and bone screening is R1000.

OTHER SERIOUS health problems ARE DEALT WITH BY CONSULTATION DURING THE WEEK (OR ON A DIFFERENT SATURDAY MORN) : heart- ECG,  fatigue, HRT, sexual health, hypertension, depression, memory/dementia, lung & lungfunction, anaemia-haematology; kidney/bladder/pelvic, hormone-endocrine, depression, osteoporosis, sleep, diabetes, thyroid, adrenal; cramp; skin,  infection including STDs & HIV/AIDs, stroke, epilepsy-neurology, dizziness, heartburn/digestive/liver,  neuropathy,  sexual health, menopause, HRT, genotourinary; immune problems, or arthritis relief;

Thermography no-touch infrared screening  for suspicious  cancer /inflammatory  changes:  by Radiographer Melinda-next in March 2015.   R900 breasts; R1100  head and  upper;  or lower body & pelvis;  R1300 whole body.

Bookings/queries contact Evelyn/ Reyhana / Val at  the Natural Medicine Clinic, 1st Floor no 15, Grove Medical Bldg, opp ABSA (ABSA Parkade parking)  near Warwick/Cavendish  Square Claremont Cape Town RSA, ph +27216831465 or a/h +2783 4385248 or reyhanadaya@yahoo.com  .

For the disabled – by arrangement  drive  up the ramp  to the Clinic door on the Grove Bldg 1st floor  parking deck.

Under CMS Council for Med Schemes Reg 10(6), open Medical schemes eg hospital plans  have to pay from their own funds (not members’ savings) for appropriate outpatient consultation (tariff item 0191) for  PMBs ie major conditions eg  cancer,   depression, neck/spinal problems, serious heart, lung, other disease., etc. Breast and osteoporosis concerns are generally part of menopause consultations N95.9   (if not already eg breast cancer code C50) and thus are often billable  med scheme benefits. The menopause billable item only applies if you are 45yrs upwards, unless you have had total hysterectomy.

On patients’ requests, appropriate invoice can be prepared and submitted to your scheme for refund of your due benefits. Some schemes eg hospital plans  falsely deny due benefits until reported to their regulator  CMS. For medical plans where the billable tariff benefit rate is higher than the breast screening fee paid, the med plan rate 0191  will be charged eg R747.50 by the contracted  specialist,  and refundable by Discovery to the member. some basic schemes eg Keycare, Bonitas require preauthorization, or referral by their contracted GP  .

 

VALUE OF STROKE CLOTBUSTERS QUESTIONED

Thrombolysis review controversy

Sarah Colyer  in the Australian Jnl of Medicine MJA  Monday, 13 October, 2014 reviews the raging argument:   “LEADING neurologists have condemned an Australasian College for Emergency Medicine decision to fund its own analysis of thrombolysis for acute stroke, which the college claims would be free of the conflicts of interest that plague existing guidance on the treatment.The Australasian College for Emergency Medicine (ACEM) is inviting proposals for consultants to analyse the published literature on thrombolysis in acute ischaemic stroke, which it has refused to endorse as a standard of care. (1)

Professor Yusuf Nagree, chair of the ACEM Scientific Committee, said unlike reviews published to date, its analysis would be “uniquely independent”.

“We are trying to find researchers who have no preconceived views or biases”, he told MJA InSight. An expert advisory panel would also be established to support the project, including an emergency physician, neurologist, GP, public health expert and lay person.

A Cochrane review published earlier this year found thrombolytic therapy significantly reduced death and dependency rates at 3‒6 months after stroke, and that this overall benefit was apparent despite an increase in symptomatic intracranial haemorrhage and deaths at 7‒10 days.(2)

While we await sight of the full Cochrane  paper, it is noteworthy that the abstract fails to give the absolute numbers.

Cochrane Database Syst Rev. 2014 Jul 29;7:CD000213. doi: 10.1002/14651858.CD000213.pub3.

Thrombolysis for acute ischaemic stroke.  Wardlaw JM1, Murray V, Berge E, del Zoppo GJ.:

“Most strokes are due to blockage of an artery in the brain by a blood clot. Prompt treatment with thrombolytic drugs can restore blood flow before major brain damage has occurred and improve recovery after stroke in some people. Thrombolytic drugs, however, can also cause serious bleeding in the brain, which can be fatal. One drug, recombinant tissue plasminogen activator (rt-PA), is licensed for use in selected patients within 4.5 hours of stroke in Europe and within three hours in the USA. There is an upper age limit of 80 years in some countries, and a limitation to mainly non-severe stroke in others. Forty per cent more data are available since this review was last updated in 2009.

OBJECTIVES:

To determine whether, and in what circumstances, thrombolytic therapy might be an effective and safe treatment for acute ischaemicstroke.

SEARCH METHODS:

We searched the Cochrane Stroke Group Trials Register (last searched November 2013), MEDLINE (1966 to November 2013) and EMBASE (1980 to November 2013). We also handsearched conference proceedings and journals, searched reference lists and contacted pharmaceutical companies and trialists.

SELECTION CRITERIA:

Randomised trials of any thrombolytic agent compared with control in people with definite ischaemic stroke.

DATA COLLECTION AND ANALYSIS:

Two review authors applied the inclusion criteria, extracted data and assessed trial quality. We verified the extracted data with investigators of all major trials, obtaining additional unpublished data if available.

MAIN RESULTS:

We included 27 trials, involving 10,187 participants, testing urokinase, streptokinase, rt-PA, recombinant pro-urokinase or desmoteplase. Four trials used intra-arterial administration, while the rest used the intravenous route. Most data come from trials that started treatment up to six hours after stroke. About 44% of the trials (about 70% of the participants) were testing intravenous rt-PA. In earlier studies very few of the participants (0.5%) were aged over 80 years; in this update, 16% of participants are over 80 years of age due to the inclusion of IST-3 (53% of participants in this trial were aged over 80 years). Trials published more recently utilised computerised randomisation, so there are less likely to be baseline imbalances than in previous versions of the review. More than 50% of trials fulfilled criteria for high-grade concealment; there were few losses to follow-up for the main outcomes.Thrombolytic therapy, mostly administered up to six hours after ischaemic stroke, significantly reduced the proportion of participants who were dead or dependent (modified Rankin 3 to 6) at three to six months after stroke (odds ratio (OR) 0.85, 95% confidence interval (CI) 0.78 to 0.93). Thrombolytic therapy increased the risk of symptomatic intracranial haemorrhage (OR 3.75, 95% CI 3.11 to 4.51), early death (OR 1.69, 95% CI 1.44 to 1.98; 13 trials, 7458 participants) and death by three to six months after stroke (OR 1.18, 95% CI 1.06 to 1.30). Early death after thrombolysis was mostly attributable to intracranial haemorrhage. Treatment within three hours of stroke was more effective in reducing death or dependency (OR 0.66, 95% CI 0.56 to 0.79) without any increase in death (OR 0.99, 95% CI 0.82 to 1.21; 11 trials, 2187 participants). There was heterogeneity between the trials. Contemporaneous antithrombotic drugs increased the risk of death. Trials testing rt-PA showed a significant reduction in death or dependency with treatment up to six hours (OR 0.84, 95% CI 0.77 to 0.93, P = 0.0006; 8 trials, 6729 participants) with significant heterogeneity; treatment within three hours was more beneficial (OR 0.65, 95% CI 0.54 to 0.80, P < 0.0001; 6 trials, 1779 participants) without heterogeneity. Participants aged over 80 years benefited equally to those aged under 80 years, particularly if treated within three hours of stroke.

AUTHORS’ CONCLUSIONS:

Thrombolytic therapy given up to six hours after stroke reduces the proportion of dead or dependent people. Those treated within the first three hours derive substantially more benefit than with later treatment. This overall benefit was apparent despite an increase in symptomatic intracranial haemorrhage, deaths at seven to 10 days, and deaths at final follow-up (except for trials testing rt-PA, which had no effect on death at final follow-up). Further trials are needed to identify the latest time window, whether people with mild stroke benefit from thrombolysis, to find ways of reducing symptomatic intracranial haemorrhage and deaths, and to identify the environment in which thrombolysis may best be given in routine practice.”

Post-publication commentary:   Ryan Radecki2014 Aug 04 09:38 a.m.    “The tPA Cochrane Review Takes Us For Fools”   It’s been 5 years since the last Cochrane Review synthesizing the evidence regarding tPA in acute ischemic stroke. Clearly, given such a time span, in an area of active clinical controversy, a great deal of new, important, randomized evidence has been generated!                   Or, sadly, the only new evidence available to inform practice is IST-3 – a study failing to demonstrate benefit, despite its pro-tPA flaws and biases. So, it ought not be a very exciting update, considering the 2009 version included 26 trials, and the 2014 update now includes only 27 trials. Their summary conclusion, with only additional evidence of regression to the mean, ought remain essentially the same, or even less optimistic, right?

Interv Neurol. 2014 May;2(3):97-104. doi: 10.1159/000356087.

Future directions for intra-arterial therapy for acute ischaemic stroke: is there life after three negative randomized controlled studies?

Maingard J1, Yan B2.   Royal Melbourne Hospital, Melbourne, Vic., Australia.

The three randomised controlled trials, Interventional Management of Stroke III (IMS3), Mechanical Retrieval and Revascularization of Stroke Clots Using Embolectomy (MR RESCUE) and Synthesis Expanasion: A Randomized Controlled Trial on Intra-Arterial Versus Intravenous Thrombolysis in Acute Ischaemic Stroke (SYNTHESIS EXP) showed no significant difference in clinical outcomes comparing intra-arterial (IA) therapy with intravenous thrombolysis. This article will explore the reasons for failure to show superiority of IA therapy.:

There are many reasons for the disappointing results of the three randomised controlled trials. Opposing views on IA therapy exist. Critics argue that only a small percentage of patients will be eligible for IA therapy and that it will never be cost-effective. Additionally, current trials have failed to address superior recanalization rates of new generation devices and lack of patient selection by advanced imaging. Time-to-treatment is longer in these randomised controlled trials and stroke outcomes were worse than anticipated. The current randomised controlled trials also took long periods to complete. There is emerging evidence that general anesthetic negatively influences outcome. Next generation trials will attempt to address these issues. Key Messages: There are disparate explanations for the disappointing results from the three IA therapy randomized controlled studies. Poor recanalisation rates with first generation endovascular devices, lack of advanced neuroimaging to aid in patient selection, lack of data surrounding the use of general anaesthesia, and prolonged time-to-treatment are potential contributors to negative results. The new generation of trials has the potential of addressing these pressing issues.

22 OCTOBER 2014 HEALTH ADVISORY: MERS SARRS , POLIO; EBOLA; CHIKUNGUNYA. OPTIMIZE VITS C AND D3 DOSES. DIARY JOURNAL: DEATH BY VITAMINS/MINERALS DEFICIENCY?: THE EASILY AVOIDABLE FLARE? AND EASY CURE? 2012-2014- MIDDLE-EAST CORONAVIRUS OUTBREAK: its not primarily the virus, but a deficiency syndrome?.

neil.burman@gmail.com Cape Town, South Africa

CONSPIRACY OF SILENCE, DENIALISM?  THE FLARE AND CURE OF MERS?- MIDDLE-EAST SEVERE ACUTE RESPIRATORY- RENAL SYNDROME SARRS  CORONAVIRUS  OUTBREAK; AND EBOLA?  : An Inconvenient truth?  human (sunshine-) vitamins C+D DEFICIENCY  syndrome facilitating  a benign virus spread from eg  camels  (or mosquitos) to middlemen eg camelmen  to human vit C/D deficient  contacts- in whom the infection becomes lethal ?.   Copyright reserved.  A narrative  diary journal since August 2013

ALWAYS READ IN CONCERT WITH avoiding-the-semmelweis-reflex-vitamins-c-d3-avoiding-vitamin-denialism

and  diet-nutritional– vitamin risks-and-benefitS 

and THE CRUCIAL ROLE OF PROHORMONES (SOLTRIOL-VITAMIN D3 -NOT  VIT D2  – AND VITAMIN C ) AS HRT IN REDUCING ALL MAJOR DISEASE. Salute Dr Walter Stumpf.

22 Oct  2014:       HEALTH ADVISORY FOR VISITORS TO OR FROM MIDDLE & FAR EAST,  EUROPE,  AFRICA, the AMERICAS:  The MERS infection outbreak worsens:  – > a case a day past week; 17 cases (one of whom returned home to Qatar) – and deathrate (9 deaths) this month in KSA  has doubled past month,  awesome for such a rich and sophisticated country,\

though well below that of the ebola epidemic – some 8000 cases with up to 70% deathrate  so far-  that is ravishing central  west Africans impoverished by genocidal warlords; not to mention flu, cholera, HIV, TB, polio-and dengue-like illnesses.  Liberian workers  who flew to USA  and Germany  with Ebola died; but now two  Dallas  nurses who treated him have ebola. .  The nurse who treated an ebola visitor to Spain  is again critical. But West Africans are reportedly trying to flee to South Africa to escape the epidemic. and 9 out of 16 Medicine sans Frontiers staff who contracted ebola have died. .

SO  OPTIMIZE YOUR DIET, VITAMINS D3   &  C DOSES, SUNSHINE, AND  AVOID  SELFSABOTAGE- SMOKING, SUGARS, ALCOHOLISM, AND RASH HYGIENE.

13 Cases Under Treatment

432 Cases Recovered
774 Cases
* Total

As of 12 pm  October 24, 2014

* Since 2012.
329

22 Oct 2014:  now the KSA declares  12 Cases Under Treatment, 431 Cases Recovered, 772 Cases, 329 deaths; ie 9 more cases in KSA past week  ie  1.3/day. So thats 18 cases in 22days ie the case rate up to >0.8/day, with 10 deaths  – all with previous chronic illhealth –  this month ie mortality lately 55% (8 Saudi males age 51-69, a Saudi woman age 55 and an expat male age 40)….

14  Oct 2014  The first MERS case outside KSA was reported yesterday in Qatar, in a returnee from KSA, ie thats 5 cases this week contracted in KSA, reportedly bringing world total to 892 cases and 356 deaths.  Crof says Over the past 30 days Saudi Arabia has reported 17 MERS infections, 9 of which were from the Taif region; which concurs with the HSA stats excluding the backlog of old cases reported last month…  Four  Saudi males this week  with MERS in Jubail, Taif and now Riyadh , and  deaths each in Riyadh and Taif..  so Saudi MERS  cases there  now 10 Cases Under Treatment, 429 Cases Recovered, 763 Total; and 324 deaths ie 43% death rate . In 14 days this month that’s 9 new cases in KSA, 5 deaths, 3 cases recovered; compared to September’s  net   ?12  new cases. The stats for September (incl  19  deaths)  are blurred by the adjustments announced on 19 Sept (with previously unreported cases up to 3 June, with net 16 new cases after other corrections); so the new cases and deaths reported in August may be correct-4 new pts,  4 deaths; and July 9 new  cases, 6 deaths; and June 28  new cases? .. .

So the MERS  case rate in KSA so far this  month has mushroomed from the  0.3/day  in July, the  nadir of 0.13/d in August, ? 0.4  in Sept,  to 0.64/d this month; and the deathrate from 0.2/d  in July to the nadir of 0.13/d in Aug to >0.6/d this month.

BUT 6/9 OF THE NEW CASES THIS MONTH HAVE BEEN IN THE GARDEN RESORT CITY OF TAIF 100 KM SOUTH OF MAKKAH- mostly in Saudi men with camel contact.  perhaps this may be because of a resevoire of MERS in camels there. The climate may be favourable for humans BUT ALSO FOR MERS- October temps of 15 to 30c, humidity of 40%, 11 mm rainfall.’

 

     MORE ON OPTIMAL VITAMIN D3  DOSE, AND THE DIFFICULTY OF ACHIEVING CLINICAL  OVERDOSE:      Four  new reports highlight  how  difficult, and important  it is to achieve adequate optimal bloodlevels of vitamin D with vigorous vitamin D3 supplements, let alone overdose with any significant adversity: note three   used the  recommended vitamin D3,   not the long-condemned mislabeled Lennons/Aspen vitamin D2 (which is misleadingly labelled  “caciferol” without disclosing that it is D2 not D3). Even a single  2 million iu overdose of vit D3 in nonagenarians had no adverse effect-since the bloodlevel was back to zero by 3 weeks, thats above 100 000iu/day on average….

 with serum 25-hydroxy vitamin D (25(OH)D) < 30 ng/mL  on  placebo or vitD3 (n = 35)   60,000 units/week for 6 weeks.   mean baseline level of 25(OH)D was 9.6+-9.6 ng/mL, and after 6 weeks doubled to 19.5 ± 4.3 ng/mL,  (P < 0.0001). After discontinuing supplement at 6 weeks, serum 25(OH)D level dropped moderately  by  12 weeks (16.1 ± 8.3 ng/mL) as compared with the baseline.  The change in serum 25(OH)D level from baseline to 6 weeks in the intervention group was inversely related to baseline 25(OH)D levels and patient’s weight. In the control group, change in 25(OH)D was not significant.  Thus  vit D3 about
10 0000iu/day in these small and often malnourished people raises bloodlevel by only about 10ng/mL.
        Kearns ,Tangpricha ea, Emory University Georgia USA   in Eur J Clin Nutr. 2014 Oct 1 describe    The effect of  single  250 000iu bolus of vitamin D3  in healthy adults over the winter and following year: a randomized, double-blind, placebo-controlled trial.   At baseline, young healthy participants had a mean plasma 25(OH)D concentration of 17.5±6.1 ng/ml. Only two subjects exhibited plasma 25(OH)D concentrations >30 ng/ml. At 5 days, subjects on  vitamin D3 had  only doubled mean plasma 25(OH)D (39 vs 19 ng/ml, P<0.001). Plasma 25(OH)D concentrations returned to baseline by  90 and 365 days in the vitamin D3 group,  remained unchanged in the placebo group. PTH and calcium concentrations were unrelated to changes in 25(OH)D levels and similar between groups over time.

   van den Ouweland ,  Vollaard ea  Nijmegen, The Netherlands in    BMC Pharmacol Toxicol. 2014 Sep 30   describe  Pharmacokinetics and safety issues of an accidental overdose of 2,000,000 IU of vitamin D3 in two nursing home patients: a case report.      intermittent high doses  vitamin D3 is increasingly used as  strategy for rapid normalization of low 25-hydroxyvitamin D (25(OH)D) blood concentrations in patients with vitamin D deficiency. Oral overdose of 2,000,000 IU of vitamin D3 in two nonnagenarian  nursing home patients was monitored from 1 hr up to 3 months . Peak blood 25(OH)D3 concentrations were observed 8 days after intake (210  and 162ng/mL, respectively (ref: 20-80 ng/mL),   followed by a rapid decrease to undetectable levels after day 14.  Remarkably, plasma calcium levels increased only slightly up to 2.68 and 2.73 mmol/L, respectively (ref: 2.20-2.65 mmol/L) between 1 and 14 days after intake,; phosphate and creatinine levels remained within reference range. No adverse clinical symptoms were noted.   CONCLUSION:A single massive oral dose of 2,000,000 IU of vitamin D3 does not cause clinical toxicity requiring hospitalization. Toxicity in the long term cannot be excluded as annual doses of 500,000 IU of vitamin D3 for several years have shown an increase in the risk of fractures. This means that plasma calcium levels may not be a sensitive measure of vitamin D toxicity in the long term in the case of a single high overdose. 

 

            As previously reported, to avoid dehydration stones and vascular calcification – especially in hot dry climates – , the precautions with vigorous vit D3   are to add some vit K2 and magnesium to the supplement, and maintain good water intake .
           The fourth current paper, from Morocco, reports inexplicable use of dangerous massive dose of vit D2 in neonates- amounting to about 120 000iu/kg ie about 12 times the maximum adult dose reported :   Hmami , Bouharrou  ea Morocco University,  Arch Pediatr. 2014 Oct;21:1115-9.        [Overdose or hypersensitivity to vitamin D   Vitamin D intoxication with severe hypercalcemia is rare in the neonatal and infancy period. nine cases of babies were admitted between the ages of 25 and 105 days for treatment of severe dehydration  8 to 15% with  hypercalcemia, with preserved diuresis and loss weight between 100 and 1100 gm secondary to taking 600,000 units of vitamin D (Sterogyl(®). The pregnancies & deliveries  were normal. Clinical signs were dominated by weight loss, vomiting, and fever. The vitamin D values in nine patients were toxic (139 – 300 ng/mL, ; normal >20ng/mL; toxicity if >100ng/mL). Nephrocalcinosis was shown  in seven patients. DNA study  in eight patients, did not reveal a mutation of the vitamin D 24-hydroxylase gene (CYP24A1). Treatment consisted of intravenous rehydration with diuretics and corticosteroids. Serum calcium returned to  normal range within 4-50 days, with weight gain progressively over the following weeks. The follow-up (2 years for the oldest case) showed persistence of nephrocalcinosis. Genetic susceptibility and metabolic differences appear to modulate the threshold of vitamin D toxicity. However, respect for recommended doses, recognized as safe in a large study population, reduces the risk of toxicity.
and as in adults,    Yao ,  Huang  ea  Prediction of Allergies in Taiwanese Children (PATCH) Study Group in  J Pediatr. 2014 Oct 1 demonstrate a significant relationship between insufficient serum vitamin D levels and worse lung function in children in the community with a suggested dose-response effect.

            8 Oct 2014  1st Ebola case diagnosed in Dallas USA in  a Liberian visitor, who died today (one of > 4000 deaths  in W Africa estimated so far); and a new case in Spain, the first infection outside Africa. Ebola anxiety spreads..                                                                                                                                                  It is alarming that the MERS deathrate is not falling but rising  there-5  new MERS  cases already this month,  vs 12 in Sept,  5 cases  in August; and  now 8 deaths  in past 38 days..

VITAMIN D3 DOSE: We get excellent results in outpatient adults with loading oral dose of  vit D3 of about 200 000 to 400 000iu depending on illness severity and body mass; then pro rata about 50 000iu  per week till better, tapering to fortnightly when well; pro rata in kids. We monitor calcium and 25OH vitamin D3 levels occasionally  if affordable – but with the tapering regime, and published data, do not see or expect hypercalcemic problems from a mean conservative weekly maintenance dose of about 3500iu/d longterm, with predicted bloodlevel of 25OHvitD of about 35-40ng/ml.  As a senior with average chronic dis-ease load, I take 50 000iu vit D3 weekly, but double it occasionally if I do get a bad cold; so I never miss a day’s work;   recent stress-related shingles (2nd attack in 30 years)  was just a nuisance, settled in 3 weeks with this regime plus multigrams of buffered vit C a day; oral lysine and alphalipoic acid each about 1/2 gm/day; and for a few days some weak steroid and humic acid cream topically for the neuritis and blistering, which has already healed to almost invisible.  This week at a family practice clinic I saw two successive women with shingles – now a frequent occurrence, even  without HIV…

Khan in Toronto in OHDM  this September  describes a ~60yr old man with tongue cancer who was treated inter alia with Vit D3 10 000iu a day; after a year his 25oH vitD level was ~106ng/ml; when his dose was halved; his dose response  bore out the general experience that at average adult mass, vit D level rises by about 10ng/ml for every 1000iu vit D3 per day or pro rata dose weekly etc  eg 50 000iu/wk or 100 000iu fortnightly may give average vit D level of ~70ng/ml.  .

Singh & Bonham 2014 at Kansas University describe  A Predictive Equation to Guide Vitamin D Replacement Dose in Patients. The recommended daily allowance for vitamin D is grossly inadequate for correcting low serum concentrations of 25-hydroxyvitamin D in many adult patients.  In their population (average BMI 31.5) ,about 5000 IU vitamin D3/day is usually needed to correct deficiency, and the maintenance dose should be ≥2000 IU/day. The required dose may be calculated from the predictive equations specific for ambulatory and nursing home patients”   A BMI of 31.5kg at a mean height of about 1.7m gives a mean weight of 91kg, which at the consensus daily  vit D3 dose of 80iu/kg/d totals ~7100iu/d or 50 000iu/wk- perhaps a reasonable maintenance dose for winter, half  that in summer if reasonable weekly sun exposure. .

​​​​​​30 Sept 2014 another new Mers case in KSA, a 70yr old Saudi man in AlMadinah. 

AND   From: David Ponsonby  September 29, 2014   http://healthimpactnews.com/2014/flu-vaccine-is-the-most-dangerous-vaccine-in-the-united-states-based-on-settled-cases-for-injuries/ 

       “The last report issued  December 2013 for the previous 3 months  by the USA Department of Justice (Vaccine Court), for compensation made by the USA Services for people injured or killed by vaccines – available as a Power Point presentation –   139 claims settled , with 70 of them being compensated. So, just over 50% of the claims filed for vaccine damages were compensated during this period.     Once again, the greatest percentage of damages compensated were for the influenza vaccine, and most of those were for Guillain-Barré Syndrome (GBS).           Yet these facts, in a Department of Health website, are never reported in the mainstream media. Read the report yourself in the Power Point file here.   Of the 70 cases compensated, 42 ie 60% were for the flu vaccine. The combined total of the other 40% of cases settled included the following vaccines: Hep B, Tetanus, HPV, DTaP, MMR, IPV, PCV, Hib, Meningococcal, Varicella, TD.”

         As detailed elsewhere n this column, there is at least 70 years of strong experience worldwide that  all microorganism infections are greatly diminished by natural  prevention (not synthetic vaccines loaded with toxic heavy metals and allergenics eg egg) , and  easily treated ie  thrown off, with vigorous immune-boosting supplements:  (mega)grams a day of vitamin C or as kgs/day of fresh produce;        vitamin D3 80+ iu/kg/d to  >10 000iu/d ie 300 000  to 600 000iu loading dose; then    +-50 000iu/wk,  plus  plenty of skin exposure to sunshine; iodine; zinc; selenium; silver; the other vitamins; Ecchinacea etc.  This applies both to acute and chronic infections and degenerative conditions.

to be used in highrisk cases eg MERS, AIDS, ebola etc: The  landmark trial  Effect of High-Dose Vitamin D3 on Hospital Length of Stay in Critically Ill Patients With Vitamin D Deficiency- The VITdAL-ICU Randomized Clinical Trial  by Amrein, Dobnig ea ,   published   today in JAMA  from Austrian hospitals  is most encouraging about the immense value of vigorous dose and bloodlevels of vitamin D3 against all types of severe disease.  The dose used in this trial (loading dose 540 000iu  =~18000iu/d 1st month, but averaging only ~8000iu/d in the first 3mo) did not achieve vigorous vit D bloodlevel, presumably because the loading dose of vit D3 in oil (540 000iu) was given by tube into the stomachs of critically ill patients; it would have better been given by transdermal injection, or else a much higher loading gastric dose given so as to speedily achieve a bloodlevel of around 70 (60 to 80) instead of half of this that was achieved in the crucial first few weeks .                                      from May 2010 through September 2012 at 5 ICUs the trial recruited  492 medical (60%) and surgical (40%)  critically ill adult white patients , 35% women, BMI mean 27, mean age  64.6 years (SD, 14.7) with vitamin D deficiency (≤20 ng/mL) assigned to receive either vitamin D3 540 000 IU, or  placebo    given orally or via nasogastric tube; ;  followed by monthly maintenance doses of 90 000 IU for 5 months- ie= about 18000iu/day for the first mo, then 90 000iu   mthly ie only 3000iu/d.           .     RESULT: on placebo the 25hydroxyvit D3 level doubled  from 13 at baseline to 17 at a month to 26ng/ml at 6mo.. By contrast, on vit D3 supplement it doubled to 34 at days 3 and 7 and day 28, but up to 46 at 6 months ie only 80% higher than the control group – thus 1/3 to 1/2 of the optimal target; with this, where 100% of patients were below 25OHvitD at baseline ie on admission to ICU, by 7 days, 87% were still in this bracket and none above 60ng/ml on placebo vs 25%  below 20  and 13% above 60 on vit D3; and by 6mo 35% were still that low on placebo, vs 5%  at that low, but 22% above 60 on vit D3. So it is not surprising that Median hospital stay 20 days was not significantly different between groups  Hospital mortality and 6-month mortality were also not significantly different (hospital mortality: 28% for vitamin D3 vs 35% for placebo; hazard ratio [HR], 0.81  P = .18; 6-month mortality: 35.0%  for vitamin D3 vs 42.9%  for placebo; HR 0.78  P  = .09). For the severe vitamin D deficiency subgroup analysis (n = 200), length of hospital stay was not significantly different between the 2 study groups: 19.5 days. Hospital mortality was significantly 40% lower with 28 deaths among 98 patients (28.6% ) for vitamin D3 compared with 47 deaths among 102 patients (46.1% ) for placebo (HR, 0.56 P for interaction = .04), but not 6-month mortality (34.7%] for vitamin D3 vs 50.0%  for placebo- ie 31% lower; HR, 0.60, P for interaction = .12). No serious adverse events were observed. The highest 25-hydroxyvitamin D levels measured were 107 ng/mL on day 7 and 106 ng/mL at month 6- well below the theoretical minimum toxic threshold of 150 or 250ng/ml..”

BUT  compared to the Austrian trial in overweight 27+kg BMI elderly whites given 540 000iu to start  by tube,              in   Salahudfin ea’s  randomized controlled trial in young emaciated   Pakistani men BMI 17.2kg, Vitamin D3 600 000iu  injection (which achieved twice the blood 25OH vit D3 level of the Austrian patients), had  accelerated clinical recovery from tuberculosis with  “impressive clinical (weight gain, chest xray and sputum clearing)  improvement  over 3 months on outpatient TB therapy (Directly Observed Therapy (DOTS) with 2 months of  4 antituberculous drugs followed by 6 months Isoniazid and Ethambutol)  with two doses 600 000iu vit D3 imi (vs placebo inj)  a month apart-  ie = ~20 000iu/d for the first 2 months, but equivalent to about 7 000iu/day over the 3 months treatment period . This dose  of vitamin D is as recommended for vitamin D supplement by the Pakistan Endocrine Society.  Trough  25OH vit D levels increased from about 20 to 90ng/ml.    After 12 weeks, the vitamin D supplemented pts (mean 28 yrs, BMI 17.2kg, 85% moderate to far advanced lung disease)  had  significantly greater mean weight gain (kg) + 3.75,  versus + 2.61, p 0.009; lesser residual disease by chest xray-  30% fewer zones involved 1.35 v/s 1.82 p 0.004,   and 50% or greater reduction in cavity size 106 (89.8%) v/s 111 (94.8%), p 0.035. Vitamin D supplementation led to significant increase in MTBs-induced IFN-g secretion in patients with baseline ‘Deficient’ vitamin D serum levels (p 0.021). Patients in the vitamin D arm and serum < 30 ng/mL (‘Insufficient’ and ‘Deficient’ groups) at enrollment had significantly greater improvements in TB severity scores compared to patients with normal baseline vitamin D levels; p 0.014.”

         “This corresponds with the earliest reports of the benefits of vitamin D in TB patients published in 1848 [21] that describes disease arrest, weight gain and reduction in mortality in patients with TB treated with cod liver oil compared to standard therapy alone. More recently, Martineau et al  [7]  demonstrated that a single oral dose of 2.5 mg (100,000 IU) of vit D2 significantly reduced growth of mycobacteria . A randomized, placebo controlled study on 67 Indonesian patients, by Nursyam et al , Jakarta  [22] reported that pulmonary TB patients given 420,000 IU of vitamin D over 6 weeks  ie 10 000iu/day had significantly higher sputum conversion rates as compared to placebo (p 0.002). Martineau et al. [8] showed that 100,000 IUs of 25-hydroxyvitamin D3 supplementation significantly improved sputum conversion rates in patients with the Taq1 25-hydroxyvitamin D receptor polymorphism of the tt genotype. ”                                                                    .

As Salahuddin ea note, the good results in Pakistan in only 3 months with vigorous  INITIAL dose vit D3  contrasts with Two recently published large randomised, controlled trials of conservative vitamin D3 over months  that achieved far lower blood vitamin D levels found no difference in clinical outcomes or mortality after 400,000 IU of 25-hydroxyvitamin D3 or placebo were given by   Martineau ea  in London, UK to 146 pulmonary TB patients – where mean (trough  or midpoint)  vit D level  (after 100 000iu vitamin D(3) or placebo at baseline and 14, 28, and 42 days after starting standard tuberculosis treatment) – was surprisingly only  40ng/ml at 56days – ie after a mean of 7000iu/d by  56 days,  vs 10ng/ml  on placebo)- less than half of the bloodlevel  achieved on vit D3  in the Pakistan trial.

So the Austrian ICU patients would undoubtedly have done much better if given more effective  (ie in critically ill pts intramuscularly imi or subcutaneously) loading dose like the Salhuddin trial did.

 

29 Sept 2014  MAJOR  SAUDI  UPDATE:   FRESH MERS FLAREUP WORSENS:  There have lately been 3 new cases, (2 Saudis and an expat), near Mecca; 2 in Riyadh- and now   death of  a  38yr old previously well  Saudi woman in Riyadh.

Thats  3 MERS deaths; and 4 new cases – Saudis- in central KSA  the past  10days, 11 this month; contradicting  the puzzlingly optimistic comment this week from KSA  health ministry’s Fakeih that  “MERS is not an issue in Saudi anymore. We are  doing all we can to have a safe Hajj for all our guests.”  If MERS is not an issue, why is the new caserate  there picking up, and the deathrate not falling?

the KSA Ministry‘s recent audit found  some 19 previously unlisted MERS cases in the 10 week April -May 2014 surge – all but three of the cases were in Jeddah- plus some false positives , and  changes of status..

The totals there now are 8 Cases Under Treatment, 426 Cases Recovered,753 Total; and 319 deaths ie 42% death rate .

But outside KSA there have been no further MERS cases or deaths reported for months, so thats apparently worldwide 885 cases , deaths 353 = 40%. But the deathrate outside KSA remains only 26%. and outside Arabia the deathrate remains 10/30 ie 33%.
     Despite the surge in KSA in the ~10 weeks mid-March till early June, before  the peak summer season in the Northern Hemisphere,   the ongoing outbreak in KSA (14 cases there since the month’s lull till mid-August)  contrasts with the last MERS cases reported outside KSA  in early-mid-July   about 10 weeks ago - 2 cases in Abu Dhabi ie the UAE,  & 5  in Iran. .

So thats a total in KSA of 20 more new cases  and 13 more deaths  than was reported before the audit on 12 Sept.  Of the  KSA 749 total,   27% were  healthcare workers; 65% were Saudis-  the vast majority this season in Jeddah and Riyadh;  ​​​​61% male; 4% under 16yrs, 45% between 16-45, 27% 45-60. and 24% 60+ years. ie approx  15% of all cases in  every 15year age bracket from 16yrs up, but only 4% in the first 15 years. Deathrate was “only” ~18% in  EACH OF the three  15year agebrackets up to 45 years, but 45% in the 46-60yr olds; and quadrupled to 80% over age 60years.Thus unlike eg flu, only in the KSA elderly is  MERS par excellence a highly risky infection    .

MERS IN KIDS:   the likely number in KSA extrapolated from 4% of 749 cases is about 30  kids under 16yrs;  but the new KSA  bargraphs show ~18% deaths in kids ie about 5-6 died. so the child deathrate has doubled from  9% 1/11.    In Dr Memish’s April paper there were only    11 pediatric cases  positive by screening and confirmatory PCR for MERS-CoV reported from Saudi Arabia. Two patients were symptomatic and the other 9 cases were asymptomatic. The median age of patients was 13 (range 2-16) years. There were eight females and three males (2.7:1 ratio). One symptomatic patient died  (1/11 = 9%) and the other symptomatic patient recovered. The diagnosis of patients was based on positive nasopharyngeal swabs on the majority of the patients.  Most cases of childhood MERS-CoV infection was asymptomatic and tested positive during contact investigation of older patients. Severe disease can occur in children with underlying conditions.

So in KSA  with a mean population age close to 20 years, the age distribution of MERS is roughly spread across adult lifespan, sparing  (with both low incidence and low mortality) children who make up almost half the population. This is the opposite of the claimed swine flu severity in kids in the “pandemic” of 2009.  Perhaps in KSA this is as expected since generally schoolchildren take more dairy products, get more exercise, sunlight, fresh produce  and supplements, and wear less sun-exclusive clothing- supporting  vit D+C deficiency evidence as the proximate  cause of MERS-CoV susceptibility in KSA adults..

So despite repeated published warning from the top KSA scientists that their conservative (ie covered) dress and diet  code puts Saudis at very high risk of known vitamins C & D & Zinc deficiency, the blackout on acknowledging this and promoting vigorous vits C and D3 & Zinc supplements continues, with 80% death risk for the elderly and 20% for every  child who contracts MERS in KSA. Until proved otherwise by simple trial of vigorous supplements, this  denial, omission    in fact may be culpable homicide on the part of KSA authorities- especially as the KSA, with a mean annual income per head similar to UK and western Europe and with similar Caucasian origin population, notoriously has life expectancy 5 years lower than that of UK and much of the North Atlantic  lands. .

16 Sept 2014  one new case today 31yr old expat male, prev chronic, in ICU Riyadh; yesterday  76yr Saudi male  in the far south, prev chronic, in ICU. total thus 730, 29 active,…  already 5 in 2wks this month.. as the Hajj picks up…

12 Sept 2014 Bad news strikes KSA with the Hajj in full swing- after 3 clear days, 2 new MERS cases but not in the eastern provinces like the last cluster, this time one each in Riyadh and the Mekkah region, both Saudis, both in ICU;  but not the usual seniors- a 38yr old male with previous health issues;  and 28yr old female, neither of them healthcare workers.                                                                    So now the KSA numbers are 28 under care;  399 recovered; 729 total; 302 died.

8 SEPT 2014 after 9 case-free days, the 727th  new case, 60y old male expat, in Jubail, in ICU…

31 August 2014 THE KSA MERS CASE RATE PICKS UP: 42% death- rate: another new case 29 Aug, a 34 yr old expat health worker in Jubail, ie 3 cases in past 7 days. another MERS-related death- a 69yr old Saudi man in Dammam- as usual, with preexisting disease. .  So KSA has  now  25 Cases Under Treatment;    399 Cases Recovered ; 302 cases died;  total  726 Cases ie 42% died.  45% dead or impaired.    5 new cases past month.  and apparently 4 deaths. KSA reporting does not allow analysis of duration of illness to assess the current mortality rate.

Yet  Drosten, Memish ea from the international  Corona Virus Study Group write in the NEJM this week:  “Transmission of MERS-coronavirus in household contacts is only 5% in 26 MERS index patients and their 280 household contacts. Strategies to contain the MERS-CoV depend on knowledge of the rate of human-to-human transmission, including subclinical infections.   The median time from the onset of symptoms in index patients to the latest blood sampling in contacts was 17.5 days (range, 5 to 216; mean 34.4d“.

This again confirms  the obvious, that the virus, like the common cold, is low virulence and transmissibility EXCEPT in the frail  and elderly – who (perhaps like many overworked hospital workers)  in KSA who as reported there  apparently get little sunshine, little vitamin D3, and likely little vitamin C. The rate of MERS in students, kids, farm workers, labourers  remains very low, presumably because they get plenty of sunshine. And no article/report on MERS from KSA – where all adults are forced to cover up their skin outdoors- says that anyone is encouraged to vigorously top up their vits C and D3 levels.
​​​

OUTCOMES: triangulating cases  scantily reported on the KSA MERS website   with 30 new cases since mid-June,  5F (28-55yrs, 4 Saudis)  and 25 men; there have been 8 deaths all in men between 38 and 80yrs old. The high deathrate in the men may be because their average age was about 59yr vs 41yr in the women.

August:   5 new cases  (1 Saudi  female; 1 male  an expat HCW; 2 of the men- 69 and 72yrs, Saudis, chronics,   died within 3 and 6 days respectively ),

July:  10  cases;  2 Saudi female; of the 8 men, 2 are HCW , 2  expats- one of whom died the same day aet 73yrs.

June: 24 cases.  Reporting was upgraded 1 June, so stats before July- with the ~100 case undated backlog reported- are problematic. from mid June there were 15 cases reported, 3 females; 5 deaths (2 expats aet 38 & 42)  in the 12 men; the Saudi deaths were aet 45-80yrs.

27 August 2014  2 new cases past 3 days, Saudi man and woman in Dammam.(one subsequently proven false +ve)   25 Cases Under Treatment, 399 Cases Recovered ;   725 Cases   Total;   301 cases passed away .
​​​​​​​​​

 24 August 2014: 12 days free of new MERS cases in KSA.      but on 22 Aug the death of another male, a 66yr old expat, was reported in Riyadh,  this  totals  23 Cases Under Treatment, 399 Cases Recovered; 301 cases passed away, (May Allah have mercy upon them). * Total  723 Cases.  44.8% dead or impaired.

​​​​But Alghamdi ea from the KSA Govt &  Universities, and Lincoln University UK have this week  published  The pattern of Middle East respiratory syndrome coronavirus in Saudi Arabia: from June 2013-May 2014  ie some 425 cases (before the recent June “discovery” of another 100+ cases there). This study deduces that the outbreak thrived especially in Riyadh and Jeddah  with high temperature and low humidity ie summer desert conditions;   older men being at much higher risk than their kinswomen. . But once again, the paper  studiously avoids the obvious reasons why KSA is at the hub of the MERS storm. The authors   like the KSA authorities totally ignore the repeatedly published studies by their own academics the past decade, and even by USA authorities like Prof Mike Holick, that Saudis have markedly low vitamin C and D and even zinc levels. And their increasingly orthodox overdress as they age and have more leisure time drastically increases their vitamin D deficiency.

This comes back to usual Media and Governmental  Semmelweis denialism , persisting  with the myth that good diet  and prescription medicines are  enough.  In fact balanced nutrition with fresh natural produce is becoming a rarity even in stable progressive urban cities, and  the resultant epidemics of infections let alone degenerative diseases are in most cases due, (apart from deliberate pollution especially with plastics, estrogenics , pesticides, endocrine disruptors eg phthalates,  heavy metals including fluorides, bromates;   dioxin etc,  radioactivity,  and high refined carbs,  and inadequate fish oil and medium chain triglycerides  and water intake),  to micronutrient deficiencies especially of vitamins C, D3, K2,  and crucial minerals like magnesium, zinc, iodine, selenium, chromium  etc.

Modern infectious outbreaks like the resurgence of influenza, polio, TB, HIV  and MERS, and hemorrhagic fevers like Ebola and Marburg, are arguably as others have proposed deficency diseases – eg scurvy, since all the severe infections listed, never mind acute bacterial infections, have been shown for almost a century to respond dramatically to highdose vit C, vit D3 and some zinc, and multivite (A,B), without antibiotics or much benefit from eg ARVs or tuberculostatics. .

     As of 12 pm  August 20, 2014:  “now only 25 Cases Under Treatment; 398 Cases Recovered Total  723 Cases;  300 cases passed away”

​​​​    19 August 2014 : KSA  updated figures  no new MERS cases past  7 days.  BUT  another death- a 72yr old Saudi man  with previous chronic disease,  in Riyadh on 17 Aug. so  “As of 12 pm  Aug 19, 2014:  723 Cases,  26 Cases Under Treatment; 397 Cases Recovered; 300 cases passed away   (May Allah have mercy upon them).”. ie the death + impaired rate  326/723 has risen to 46.4%, deathrate 41.6%. ?? 855 cases, 334 deaths  worldwide?

So thats 326 patients in KSA who died or are still impaired by MERS, who might have been spared by simple highdose vits (D3 +  C) supplement-at trivial cost,  no major adverse effects, but massive evidence of protection and cure against all serious diseases; in a population at long-known high vits C+D3 deficiency risks. .

The Zeitgeist occupation analysis of MERS cases to 4 June shows unchanged pattern: 164 Health workers,    150 retired persons,  23 children,  11 pilgrims, 3 tourists,  2 construction labourers, 1 butcher, 1 camelbreeder, 1 shepherd… (out of 838 cases reported till then- ie occupation was disclosed in only 44% ie 380 pts) . The reason for the majority nondisclosure is not given.

The question remains: why are (inter)national authorities ignoring all the published evidence linked below, that vigorous dose vitamin D3 supplement eg 5000iu/kg  loading dose then 1500iu/kg/fortnight eg 100 000iu every two weeks , plus a few grams of buffered vitamin C a day, drastically reduces all diseases including virus infections?

12 August 2012 KSA  reports (after a month free of new cases)  despite peak summer there, two new  previously chronically ill   Saudi cases  in two days:  a 72year Riyadh man; a 59 year old  man far south of Riyadh; and death of a previously reported apparently formerly  well 74 year Riyadh Saudi man. But they dont say when these recent elderly Saudis took ill or died.  Total in KSA now 723 cases, 41% deaths. 28 cases under treatment  ie 45.2% dead or impaired. ..

To put MERS in perspective, Ebola in Central Africa this year has  infected  over 2000 cases, 50% deaths, probably worsening the >100 000 malaria deathrate per year in the region, globally >200 million cases a year with a million ie 0.5% deaths.. ..  Mosquito-spread Chikungunya virus spreads from Africa/Asia   to over 570 000 people  across  the central Americas .. …   .

9 Aug 2014  still not over:  NOT THE END OF THE ARABIAN MERS CoV OUT- BREAK-  STILL MORE QUESTIONS THAN ANSWERS, :  its now  30 days since the last reported MERS case –  BUT  the  fact  is that the KSA Bulletin chillingly reports  “As of 12 pm  9  Aug, 2014:    1.” still 27 Cases Under Treatment     2. 396 Cases Recovered.  3. 298 cases passed away (May Allah have mercy upon them).  total 721 case.   so 30 days after the last recorded new case,   27 patients there are still suffering from MERS sequelae – for at least four weeks duration now, likely now permanent?. .

27 cases out of 721 total reported in KSA is only about 4%. But since these 27 cases remain under care a month  after the last reported new case, they must now  be at best approaching chronically impaired, if not on renal  or respiratory assistance.  ie the total of dead and impaired rises to 325/721 = about 45%. More important, KSA has apparently not yet released an analysis of the demography and primary and secondary causes of death of these cases- presumably by MERS definition, respiratory and renal . This analysis is urgently needed. All we know for certain is that there was a MERS outbreak apparently in one of their Dialysis units; and that the outbreak was especially bad in health workers especially hospital staff.

COMBINED SEVERE ACUTE RENAL AND RESPIRATORY FAILURE: Forty years ago we (Burman ND, Austin M, Thatcher GN ea) delivered a review of Groote Schuur Hospital experience at a local South  African renal congress on the high mortality of combined  acute renal and respiratory failure in the age of hemodialysis and ventilators, respiratory intensive care, antibiotics and immunosuppression. . Apart from the common major sepsis,  trauma and allergic eg antibiotic  causes, the obvious “primary” cause – which any virus eg MERS-CoV  may mimic- , is the “autoimmune” hypersensitivity Goodpastures Syndrome GPS – which untreated has a mortality of ~80% but with modern treatment perhaps 20%. This is half the deathrate reported in KSA from MERS. There is no shortage of respiratory and renal ICU and dialysis, advanced medical specialists  in KSA centres. So from GPS perspective, much better salvage might be expected.

GPS is rare affecting about 1ppm (0.5-1.8 per million people) per year in Europe and Asia.[5] The peak age ranges for the onset of the disease are 20-30 and 60-70 years.[5]  It is also unusual among autoimmune diseases in that it is more common in males , less common in blacks than whites. This may partly explain why the inhabitants of the dromedary-exporting Horn of Africa have been spared MERS outbreaks.

A recent review from Germany gives the mean time from onset of MERS to acute renal failure of only 11 +-2 days (c0mpared to 20 days in SARS). It is well reported that those contracting acute MERS are already sufferers from major chronic illnesses eg diabetic- cardiorenal-respiratory ie heavily predisposed to  immune failure if not already in renal failure.

Humans have some four  primary excretory/detox  systems: hepato-gastrointestinal; skin; renal; and  lung. In Arabia, water is scarce, the desert climate is hot and dry, and the obligatory dress for the observant almost total body cover by robes. So MERS SARRS is high risk especially as it knocks out the two main excretory systems- renal, respiratory, and in  very high ambient temperatures  also the skin;  except for the affluent minority  who have aircooled spacious private homes and offices;  with  often a reported  element of viral gastroenteritis, akin to influenza. .

The mystery remains: why is the  UAE reporting 73 cases/9.2million ie 8 per million,  but only 12% mortality, compared to the adjoining KSA 721 cases/30 million ie 24 per million?  with 93% of world MERS cases recorded from KSA and UAE, and all cases anywhere traceable back to the Arabian Peninsula. The KSA and UAE urgently need to publish an analysis of the demography and pathophysiology of their MERS cases. Is it mostly indigenous Arabs who are contracting and especially dying from MERS in these countries, or also many foreign workers, mainly malnourished labourers?

A major factor is likely demographic: Wiki says In KSAThere are 20 million Saudi citizens and 5 million foreigners living in Saudi Arabia.[14] Most Saudis are Sunni Muslims, approximately 23 percent are Wahhabis, With the world’s second largest oil reserves , the Kingdom is categorized as a high income economy with the 19th highest GDP in the world.   Saudi Arabia is an absolute monarchy.[70] However, according to the Basic Law of Saudi Arabia adopted by royal decree in 1992, the king must comply with Sharia (Islamic law) and the Quran, while the Quran and the Sunnah (the traditions of Muhammad) are declared to be the country’s constitution.[71] According to The Economist‘s 2010 Democracy Index, the Saudi government is the seventh most authoritarian from among the 167 countries rated.[72]. The ethnic composition of Saudi citizens is 90% Arab and 10% Afro-Asian.[212] Saudi Arabian dress strictly follows the principles of hijab (the Islamic principle of modesty, especially in dress).

In the UAE ie Emirates, Wiki says in 2013  UAE’s total population was 9.2 million; 1.4 million Emirati citizens and 7.8 million expatriate ie  16.6% Emirati (citizenry), 23% other Arabs,  54.4% Asians,  and 6.0% other expatriates. Thus the relatively democratic  & liberal  UAE has only 40% Arab ie (majority also Wahhabi) Muslim  population, compared to  some 90% in the KSA. .    in 2005, 76% of the total UAE population was Muslim, 9% Christian, and 15% other (mainly Hindu). Census figures do not take into account the many “temporary” visitors and workers while also counting Baha’is and Druze as Muslim.[65] Among Emirati citizens, 85% are Sunni Muslim, while Shi’a Muslims are 15%.

The comparable life expectancy in the  bigger but relatively poor mostly caucasian countries of Europe is 80 yrs (Portugal), 81 (UK) to 83yrs , and 84.6 in Japan. Why the richer   KSA has so much lower life expectancy can only be due to combination of culture (overdress?) and perhaps genetics-  but Israel, also a predominantly eastern mediterranean semitic people, like Europe  has life expectancy of  82.1 years. on that tabulation, UAE expectancy is 79.2yrs, USA 79.8, but KSA  only 74.3.

Comparison of Gross domestic product and per capita income for 2014 fail to explain the differences in life expectancy ie survival between the highest earning countries, with KSA, UAE, Israel and much of the middle east countries falling in the $30 to $40 000 per capita income bracket.

NO NEW CASES WORLDWIDE: 4 suspected  MERS cases  investigated in Hong Kong after arriving there  via Dubai have proved negative for MERS.

while Ebola, AIDS, cholera, polio  and bubonic plague spread despite major efforts at containment… with at least USA and UK preparing for ebola outbreak, and China for the  bubonic plague.

8 August 2014  Ebola virus disease EVD update – West Africa  Disease outbreak news     Between 5 and 6 August 2014, a total of 68 new cases of Ebola virus disease (laboratory-confirmed, probable, and suspect cases) as well as 29 deaths were reported from Guinea, Liberia, Nigeria, and Sierra Leone.     On Wednesday, 6 August and Thursday, 7 August, an Emergency Committee  determined  that   the current outbreak constitutes a Public Health Emergency of International Concern. and advised that:                 it constitutes an ‘extraordinary event’ and a public health risk to other States; the possible consequences of further international spread are particularly serious in view of the virulence of the virus, the intensive community and health facility transmission patterns, and the weak health systems in the currently affected and most at-risk countries.

It was the unanimous view of the Committee that the conditions for a Public Health Emergency of International Concern (PHEIC) have been met.   New cases and deaths attributable to EVD continue to be reported by the Ministries of Health in Guinea, Liberia, Nigeria, and Sierra Leone. Between 5 and 6 August 2014, 68 new cases (laboratory-confirmed, probable, and suspect cases) of EVD and 29 deaths were reported from the four countries as follows: Guinea, 0 new cases and 4 deaths; Liberia, 38 new cases and 12 deaths; Nigeria, 4 new cases and 1 death; and Sierra Leone, 26 new cases and 12 deaths.

As of 6 August 2014, the cumulative number of cases attributed to EVD in the four countries stands at 1 779, including 961 deaths. The distribution and classification of the cases are as follows: Guinea, 495 cases (355 confirmed, 133 probable, and 7 suspected), including 367 deaths; Liberia, 554 cases (148 confirmed, 274 probable, and 132 suspected), including 294 deaths; Nigeria, 13 cases (0 confirmed, 7 probable, and 6 suspected), including 2 deaths; and Sierra Leone, 717 cases (631 confirmed, 38 probable, and 48 suspected), including 298 deaths.- mortality rate so far 55%.

For a viral hemorrhagic illness, as for acute MERS and flu,  Ebola treatment and prevention  remains supportive, including plenty of fluids and salts, multivites incl K1,   highdose vitamin C eg a few grams hourly to tolerance,  vitamin D3 perhaps 300 000iu orally to start then 100 000iu weekly, iodine, zinc, selenium, garlic, ginger, ecchinacea and colloidal silver till out of the woods.. . 

29 July 2014  the first Wiki update in weeks  indeed shows no reported increase in KSA cases with 41% fatalities; but total Arabian Peninsula cases up to 825 with 321deaths  ie 39% fatalities, and  96.3% of global – 855 cases and 331 deaths ie 39%.

 28 July 2014 THE END OF THE ARABIAN MERS CoV OUTBREAK? its now apparently 18 days without new MERS cases reported from KSA , compared to 6 cases in the previous week… .              so the Wiki figure of WHO-reported cases  in the Arabian Peninsula (plus the 2 recent cases in UAE)  totals 814/(835 globally  ie 97.5%  of reported world cases),  with 315 Peninsula  deaths ie 38.7% fatality rate- but only 13% in the  far less coverup- restrictive UAE with its huge foreign worker population. . . supporting the studies of KSA scientists  of more severe vit D deficiency in the most covered-up observant people, citizens of Saudi Arabia and its fellow ultra-observant Wahhabi bordering neighbour states (except the UAE)  to the south and east. .

and now Ebola epidemic outbreaks kill hundreds in central Africa.  The nocturnal fruit bat (that locals eat)  is apparently the vector. There is strong reasoning that these could be prevented, successfully treated (humans if not bats) with safe highdose vits C and D3.  Like humans, all tested families of bats, including major insect- and fruit-eating bat families, cannot synthesize vitamin C,.    and have very low vit D levels,  make vitamin D only if they roost in sunlight.

and Central Africans are very darkskinned, and the masses malnourished from rampant  genocidal wars, so they will have the lowest levels of vitamins C and  D3. 

20 July 2014  MAYBE..  JUST LACK OF REPORTING?          ‘s A Time’s Memory   to 17 July shows  17  more reported MERS cases (all outside the KSA -still 721  cases, 297 deaths): globally 852 with 329 deaths;   Arabia 829 with 319 deaths; ie rest of world 23 cases and 10 deaths-  similar mortality 41% in Arabia compared to 43% in the 23 infected cases who returned to  their own countries  (middle east, north Africa, Europe, USA, Malaysia, Philippines) not on  the Arabian peninsula- from  their visit/working  there or,  rarely, contact with returnees. .  So has the outbreak  stopped in the past 10 day

ps the USAEBN radio website reports startlingly different case numbers in far fewer  nations, especially tenfold more cases  in Qatar and half the number in UAE.  Time will tell. . this high occurrence in Qatar is not reported anywhere else? on 24 July it reports for KSA alone  834 Cases (897 in the Arabian Peninsula); 288 Fatalities. globally 873 cases with death rate only 35%.      still the massive discrepancies with startlingly far more cases in Qatar and Philippines and far less in the UAE. This website claims, perhaps not implausibly,  that “Government Organizations Do not want to publish total numbers of cases for fear of panic, USAEBN will be trying to track it.”

Virologist Dr Ian MacKay IN MID JULY  puts the world total of cases at 846 in his informative analysis of age and gender demography.

But with neighbouring Iraq in civil war breakdown and even polio flareup, who knows how many there are suffering and dying from unmonitored  MERS CoV.

14 July 2014  The UAE reports 2 new cases of MERS CoV – the first in a long time-, bringing their total to about 73 cases, 9 deaths ie 12% fatality. . KSA reported one new case 10 July ie  4  past week, and 5 in each of the  the  previous few weeks; with no deaths, tally now 721 cases, 295 deaths ie 41%.                       The UK Gov travel warning is about terrorism in the region, not MERS.

The vexed question of the method of spread of MERS CoV between animals- dromedary camels- and humans  continues to be hotly debated between expert virologists and camelmen. The KSA has still not issued [ any restriction on camel imports from the suspected source of the MERSCoV- the Horn of Africa.

But the argument is irrelevant for practical purposes.  Tradition, belief  dies hard, like the strictly enforced hijab overdress, and camelkeeping: Riyadh’s camel market stretches several miles along a highway out of the city. It’s not true. Camels occupy a special place in Saudi society,  We live,  sleep,  eat and spend our whole lives with camels, we drink their milk, its a medicine.. There’s no disease,” said a trader at the market”.       Its the story of 160 years ago, the cholera-spreading London’s  Broad St water pump until Dr John Snow recognized and stopped the source of the cholera diarrhoea epidemic.   This  far more lethal KSA  lung-kidney epidemic is simpler- encourage people worldwide to get plenty of free natural sunshine , or if living at far north darker  latitude or  practicing hijab and unable to sunbathe- especially over Ramadan- take at negligible cost  vigorous supplement of vitamin  D3 to a high safe  bloodlevel .

8 July 2014  Spread of MERS CoV- Down but not out: from 15 cases a day in early May,  now KSA has reported  8 new cases past 7 days;   ie 720 total, 294 deaths- 4 new cases past 3 days, with 1 new death. 18 new cases in 24 days since 13 June. So the rate of new cases is not dropping there the past month – or simply more cases being tested and reported. Only sick cases who see doctors, and their contacts, and city  health workers,  are likely being screened.

The death rate in KSA  since the outbreak 2 years ago remains 40%.      why should this be? other than that Saudis do not benefit from the midsummer as do other populations-  they remain shrouded in overdress and thus severely vitamine D deficient? and the virus seems to spread not airborne  but by direct contact – human to human, or camel-(milk?)-human?  and the KSA has not yet been reported to have stopped mass camel importation from the Horn of Africa for butchers to supply meat.

MERS CASES BY OCCUPATION:     Shane Granger has tabulated more recent reported MERS  cases by occupation where data is available  –  >375 cases:Health Care Workers (HCW) the  largest group – 161:  includes all types of unidentified Health workers (i.e. Nurses,  Doctors, hospital and clinic staff).                             Retired: also  161 (incl Pilgrims 11).                                             Schoolkids 18 -third. Farmers 12 – fourth.  .  tourist 3; construction 2;  Camelbreeder, butcher , shepherd one each.

The retirees are the elderly, generally frailer, probably more at leisure, more orthodox ie more ritually overdressed?  and circulating /concentrated more through/in  the cities especially Mekkah, Riyadh,  Jeddah, and visiting the more frail and sick worldwide; thus more susceptible.

Healthworkers are obviously the most stressed and hardworking,  exposed to concentration of symptomatic MERS cases and thus ingestion and surface (if not droplet) contamination .

The major surprise is the low occurrence in schoolkids, pilgrims, and non-health industry workers, teachers, clergy, armed forces,  shop  and office staff, non-healthcare  govt workers,    etc.

This also favours nutritional ( sunlight/vit D/C/zinc) deficiency as a significant factor in susceptibility of retirees and healthworkers to MERS. The general population (unless seriously ill with other disease)  is largely immune to MERS, like flu and common colds, in them  the MERS CoVirus seemingly causes nothing more.

4 July 2014  frail pilgrims  should postpone the Hajj this year.  the  European Centre reports     KSA 716 cases, 293 deaths;    worldwide 843 cases (817 in Arabia incl now 4 in Iran), 322 deaths. in 21 countries, ie 21 cases outside the Middle East (ie outside the camel contagion area  south-east across the Arab states that have had 791 cases so far)  .  So thats about 10 new cases over the mid summer  in KSA the past 15 days so far. Only 1 new  death.  Case reporting from the rest of the world lags behind.

So the Philippines has advised its citizens to postpone Hajj to Mecca this year.

Certainly  frail pilgrims – especially with diabetic and cardiorenal/respiratory diseases -all over the world will be wise to  postpone. And the KSA is at last considering stopping import of camels (4.7 million a year mostly for human consumption,  – mostly from Somalia, which has never reported a MERS case) –  from the Horn of Africa- their main meat supply. This appears to be the source of the outbreak- simply camel colds that kill only sickly humans who unlike camels avoid sunshine by edict… .    Up to April 2014, it was predominantly a disease of older men; (it appears that camels are men’s work);  but by midMay the male dominance in human MERS cases was fading.

But is the core problem the well-camel MERS-Covirus carriers? It is in fact more likely that the prime cause is that the entire KSA population is at extreme risk – both because those who can afford it overdress by religious edict, especially upperclass Muslim women in total coverup and thus badly vitamin D deficient;  and  because the KSA imports vast numbers of mostly poor unskilled foreigners to do mostly manual work. Such poor labourers are usually undernourished, living in poor conditions, and with poor access to medicines and medical care until they collapse; and unless outdoor labourers, living and working long hours indoors, and hence also badly vitamin-D and C deficient. .   The Wiki review  Saudi Arabia  “Foreign workers estimated them to number 1/3 of KSA residents recently.  Saudi Arabia has become increasingly dependent on foreign labour, and although foreign workers remain present in technical positions, most are now employed in the agriculture, cleaning and domestic service industries. The hierarchy of foreign workers is often dependent on their country of origin; workers from Arab and Western countries generally hold the highest positions not held by Saudis, and the lower positions are occupied by persons from Africa, the Indian subcontinent, and Southeast Asia.  the situation has persisted because of a reluctance by Saudis to take on menial work and a shortage of Saudi candidates for skilled jobs.[.. The Saudi economy has, therefore, remained dependent on importees for expertise in specialized industries, and on the Asian workforce for the construction industry, menial and unskilled tasks.[8]  Saudization is generally considered to have been a failure.[10]

THE MERS-CoV CAMELTRAIN FROM AFRICA:   This again begs the huge question:  if camels carrying asymptomatic airways MERS CoV are indeed the virus vector from Africa –  almost 5000 a year from Somalia alone- imported into KSA  through Jeddah port,  WHY ARE THE  EXPORTING  CAMEL- TRADERS and camel- breeders IN NORTH AFRICA NOT  SUFFERING vastly from MERS  respiratory-renal syndrome?  They are likely Muslim if not black Africans;  oil-rich Arabia employs vast numbers of overseas expats as labourers, and outside the KSA, Arabia especially the UAE  hosts hundreds of thousands of non-Muslim professionals. But unlike say Indians and other Asians, Pinoys and Malaysians are mostly Muslim, so are more likely to observe cover-up dress code,  and thus be more vulnerable to MERS. . This again supports the evidence that   the current symptomatic serious MERS-CoV   SARRS – Severe Acute Respiratory Renal Syndrome –  that occurs in and kills almost exclusively vit D deficient frail observant Muslims  – is due to conditioned  sunlight deficiency.          The north African camel breeders and traders, and  the camel herders and camel men in Arabia  ( like cowboys on the prairies and herders worldwide in hot  climates), are unlikely  devout well -berobed  Bedouin  of Arabia.  Camelmen like cowboys get  plenty of sunshine vit D, if only via bare faces and arms; and thus can with probable impunity,  immunity against MERS, drink raw camel milk and travel with vast camel herds.

27 June 2014 update: (compared to  13 June 2014 KSA  702 cases, 292 death, worldwide 826 cases, 326 deaths): there are now reported in KSA 710 or 718 cases ie 8 -16 in 2  weeks, no more deaths; and globally  833 cases & 322 deaths. . Australian virologist Dr Ian Mckay postulates why vast camel imports (from Africa, via Jeddah  port)  for eating  is likely the source of MERS in Saudi Arabia.                 He omits the obvious link in the chain, that the deathrate from MERS CoV is far  lower outside Saudi Arabia because  this sunny  country is the strictest in the world for enforcing Wahhabi hijab total overdress code   and thus profound acquired vitamin D deficiency even in men,  and worse in  females who  in public  – unlike men- must have even their  heads and faces veiled by a niqab- and in pilgrims from other lands who as part of  their holy pilgrimage undertake to follow permanently  the strict hijab dresscode. Their simple option is  to take effective permanent  vitamin D3 orally  eg 50 000 iu weekly.

IT IS COMMON CAUSE THAT ONE DOESNT, CANNOT   PREVENT OR TREAT INFECTION BY POOR NUTRITION OR LOWDOSE ANTI- MICROBIALS- such policy is futile if not dangerous for breeding resistance as well as disease extension.   The studies below confirm the obvious, (as Klenner, Pauling,  Cameron ea showed the past 50 years with highdose vit C injection), that  vitamin D3 orally also works as a multiantimicrobial agent if given as early as possible in safe very high dose and bloodlevel eg 600 000iu monthly (in the first month, – in Salhuddin’s  Pakistan PTB patients (presumably also Sunni muslim) initially mean wt 45kg, thats vit D3 ~440iu/kg/d) for two doses ie a mean of 300iu/kg/day over 90days;   not the current preventative recommendation of 80iu/kg /day to a safe blood level of around 50-60ng/ml. As Holick has said, with adequate water intake  even 50 000iu vit D3 a day ie 1.5million iu/month for months causes no toxicity. Given the 40% mortality rate in the frail Saudi MERS patients, and in acute severe influenza and other serious viral infections, it can be expected that such  highdose immediate vitamin D3 therapy orally with eg 600 000iu, combined with highdose vitamin C, zinc and some multivite,  (never mind appropriate antibiotics in acute bacterial infection) will similarly virtually eliminate mortality.

But no KSA Govt website mentions this- except the Saudi Gazette a year ago which strongly urged vitamin D supplement in the KSA as even daily sun exposure does not bring most Saudi women above the vitamin D deficiency threshold. It says Since Muslim women can only reveal the hands and face, they may need to be out in the sun for longer than 30 minutes. But the review conspicuously  fails to mention that in public outdoors in KSA, women must have even the head and face covered. It also  propagates surprising  dangerous  nonsense that “severe deficiency needs monthly vitamin D injectionMom, have you taken your vitamin D injection this month?, when all it requires is an oral daily, weekly  or fortnightly  dose vitamin D3  at trivial cost.” It does stress  “One of the main reasons why vitamin D deficiency is so common in the Kingdom is because there are very few food sources of vitamin D. Foods which have fairly good amounts of vitamin D are fish liver oil, sweet potatoes, egg yolks, vegetable oils, butter, and fatty fish such as salmon, sardines, and tuna,” said Dr. Rasha Jameel, a consultant in family medicine at a local hospitalIn the United States, all milk and dairy products are fortified with vitamins A and D, but no such measures are in place in the Kingdom“.

This correlates with a new metaanalysis (in the  BMJ this month) of observational studies from Europe and USA, that all-mortality hazard ratio over a mean of 10 years  increases by 57% as vit D level falls from the highest to the lowest level. The KSA apparently chooses to ignore that, as this column reported recently from WHO data, despite  apparently being the wealthiest country per capita  of bigger populations  in the world,  KSA’s population life expectation is about 5 years lower than eg far less sunny Britain’s; ie KSA  all-cause mortality rate is avoidably materially higher. Despite KSA medical professors  having reported in studies  that most of the KSA population is deficient in vits D and C, the  KSA Govt website  chooses to ignore this on official websites;  unlike other even Middle-Eastern governments promoting vit D fortification or meaningful safe supplements costing trivial amounts.

Even a new study last year from KSA universities confirmed that ” Most commonly consumed food products by Saudi population which are supposed to be fortified by vitamin D are either not fortified or contain an amount less than  (apparently  from their table 2 ~ half of)  recommended by guidelines set for US marketplace”. Even a UAE authority recently stressed “Can fortified milk fight Vitamin D deficiency? Shockingly low levels of D3 among UAE population cannot be rectified by milk alone.” As Holick ea, including  a Turkish University 2010  trial report,  oral vitamin D3 is far more  effective , and safer than,   either vitamin D2, or vitamin D injection -never mind much cheaper. This current ostrich-head-in-the-sand denialism by the KSA government is like that of the RSA govt under Presidents Mbeki and Zuma 10-15 years ago about preventing and treating HIV-AIDS  – considering that the safe and beneficial daily intake of vitamin D3 is now universally recognized as 4000 if not 10 000iu/day (ie about 80iu/kg/day or pro rata up to perhaps fortnightly) , to a mean blood vit D  level of about 60 to 80ng/ml. .

As Prof Mike Holick pointed out a few years ago, “Even in Saudi Arabia, Qatar and South Africa, more than 50% of the population is deficient in vitamin D, all because of their avoidance of sun. Based on some of the literature, it seems that we could probably decrease health care costs across the board by 25% if everybody had optimal vitamin D status.” As Al Faraj ea reported in Riyadh in 2003,   Prof Zahid Naeem from a KSA university wrote in 2010,Vitamin D deficiency is an ignored epidemic in KSA  and globally“; confirmed by a KSA study by Ali ea in 2012:Even in a sunny country like Saudi Arabia the prevalence of vitamin D deficiency in young female is high“..  One does not need to  speculate why the KSA and all governments globally choose to ignore this inconvenient truth,  downplay effective vigorous  vitamin C and D3 (sunshine) supplements-  such widespread vitamin D and C deficiencies, like cigarette smoking and alcohol abuse,   suit governments and Big Pharma-  the Disease Industry- in reducing populations growths and creating jobs for the highly profitable Disease Industry and it’s shareholders-   for whom Only Disease Pays. Cheap safe natural  Prevention Does not Pay since it at least halves sickness never mind disease industry jobs, taxes  and profiteering in the global $multitrillion Disease and Diet and Vaccine and Invasive Screening Industry scams.

And Karen Hansen ea at Univ Wisconsin 2014 have  just shown  that  giving vitamin D2  (not D3)  50 000iu fortnightly for a year is actually adverse – as Holick and others have  show – IT DEPRESSES – perhaps halves – THE BIOLOGICALLY ACTIVE blood 25OHVIT D3 while boosting perhaps 5 fold the far less active blood 25OHvit D2 levels , and actually worsens  rheumatoid arthritis clinically and serologically . One can speculate whether vit D2 actually blocks optimal function of VDRs vitamin D receptors. Trials published 2012 from Japan and Netherlands showed that vitamin D3 – blood 1,25(OH)2D3 (but not TNFalpha blockers) blocked  inflammation (ie TNF tumour necrosis factor alpha activation of vascular calcification).                                                 

Salahudfin ea’s new randomized controlled trial  from Pakistan Vitamin D3 injection accelerates clinical recovery from tuberculosis  shows “impressive clinical (weight gain, chest xray and sputum clearing)  improvement  over 3 months on outpatient TB therapy (Directly Observed Therapy (DOTS) with 2 months of 4 antituberculous drugs [Isoniazid, Rifampicin, Ethambutol and Pyrazinamide] followed by 6 months Isoniazid and Ethambutol)  with two doses 600 000iu vit D3 imi  (vs placebo inj)  a month apart-  ie equivalent to about 7 000iu/day over the 3 months treatment period . This dose  of vitamin D is as recommended for vitamin D supplement by the Pakistan Endocrine Society.  Trough  25OH vit D levels increased from about 20 to 90ng/ml.    After 12 weeks, the vitamin D supplemented pts (mean 28 yrs, BMI 17.2kg, 85% moderate to far advanced lung disease)  had  significantly greater mean weight gain (kg) + 3.75, (3.16 – 4.34) versus + 2.61, p 0.009; lesser residual disease by chest xxray-  30% fewer zones involved 1.35 v/s 1.82 p 0.004,   and 50% or greater reduction in cavity size 106 (89.8%) v/s 111 (94.8%), p 0.035. Vitamin D supplementation led to significant increase in MTBs-induced IFN-g secretion in patients with baseline ‘Deficient’ vitamin D serum levels (p 0.021). Patients in the vitamin D arm and serum < 30 ng/mL (‘Insufficient’ and ‘Deficient’ groups) at enrollment had significantly greater improvements in TB severity scores compared to patients with normal baseline vitamin D levels; p 0.014. This corresponds with the earliest reports of the benefits of vitamin D in TB patients published in 1848 [21] that describes disease arrest, weight gain and reduction in mortality in patients with TB treated with cod liver oil compared to standard therapy alone. More recently, Martineau et al  [7]  demonstrated that a single oral dose of 2.5 mg (100,000 IU) of vit D2 significantly reduced growth of mycobacteria . A randomized, placebo controlled study on 67 Indonesian patients, by Nursyam et al , Jakarta  [22] reported that pulmonary TB patients given 420,000 IU of vitamin D over 6 weeks  ie 10 000iu/day had significantly higher sputum conversion rates as compared to placebo (p 0.002). Martineau et al. [8] showed that 100,000 IUs of 25-hydroxyvitamin D3 supplementation significantly improved sputum conversion rates in patients with the Taq1 25-hydroxyvitamin D receptor polymorphism of the tt genotype.                                                                     .        

            As Salahuddin ea note, the good results in Pakistan in only 3 months with vigorous  INITIAL dose vit D3  contrasts with Two recently published large randomised, controlled trials of conservative vitamin D3 over months  that achieved far lower blood vitamin D levels found no difference in clinical outcomes or mortality:           after 400,000iu of 25-hydroxyvitamin D3 or placebo were given by   Martineau ea  in London, UK to 146 pulmonary TB patients – where mean (trough  or midpoint)  vit D level  (after 100 000iu vitamin D(3) or placebo at baseline and 14, 28, and 42 days after starting standard tuberculosis treatment) – was surprisingly only  40ng/ml at 56days – ie after a mean of 7000iu/d by  56 days,  vs 10ng/ml  on placebo)- less than half of the bloodlevel  achieved on vit D3  in the Pakistan trial ;      

        and  by Wejse et al  2009  in  Guinea-Bissau to 365 TB patients  – who received  300,000 IUs of vit D3   ie only 100,000 IU or placebo at inclusion and again 5 and 8 months after the start of treatment,  ie below 1000iu vit D3 per day over the 12 month trial period “. The Guinea-Bisseau pts thus might have achieved a mean blood vit D level boost of only  10ng/ml.. and now Havers ea (Baltimore)   show Low 25(OH)D is common in diverse HIV-infected populations and is an independent risk factor for clinical and virologic failure; Low 25(OH)D was associated with high body mass index (BMI), winter/spring season, country-race group, and lower viral load. Baseline low 25(OH)D was associated with increased risk of human immunodeficiency virus (HIV) progression and death (adjusted hazard ratio (aHR) 2.13; 95% confidence interval [CI], 1.09–4.18) and virologic failure (aHR 2.42; 95% CI, 1.33–4.41). and Shepherd ea (Eurocoord) Low Vitamin D predicts short term mortality in HIV-positive persons Odds of death decreased by 46.0%( P = .04) for a 2-fold increase in latest 25(OH)D level.. In patients with current 25(OH)D <10 ng/mL, hsIL-6 concentration increased by 4.7%(95% CI, .2,9.4, P = .04) annually after adjustment for immunological/inflammatory markers, and no change in hsCRP rate was observed (P = .76)

19 June 2014 update  no new cases reported from anywhere the past few days, may be because the KSA is not reporting regularly.   so the great news is that more than 2 years after the onset of the MERS CoV outbreak in Arabia, no ongoing transmission has been reported from any of the 22 countries so far affected.

THE POLIO  SPREADING GLOBAL EPIDEMIC This decline of the MERS outbreak with the heat of summer contrasts sadly with the now-declared  global epidemic of wild natural  poliomyelitis- which was hoped to be extinct by now, with Hindu- run India being declared polio-free; but now  spreading out with mass refugees from wherever war and chaos are successfully ignited by profiteers and fanatics  to neighbouring countries. Eg   an expanding militant  Islamic Wahhabi  arc – ie ultraorthodox overdress code – predisposing to vitamin D deficiency?  from Asia- Pakistan, Afghanistan, to middle east – Syria, Palestine, Iraq, Israel;        to East/West Central Africa eg Somalia, Cameroon, Ethiopia,  Kenya, Nigeria, Guinea-Bissau, –  with 365 cases reported in 2013. Perhaps more important is zero natural virus cases in Niger and Chad but cases caused by the circulating vaccine derived virus.  The wartorn  DRCongo  and Sudan are likely next polio outbreaks, while Angola has banned Islam because of its perceived militancy. …

And in February,   never mind an outbreak of polio-like paralysis in northern California, a new case was  reported  in a  South African neighbour-  in Botswana – for the first time there  in 20 years -; “Polio virus is endemic in five countries besides Nigeria: Afghanistan, Egypt, India, Niger and PakistanScientists confirmed that the virus isolated from the boy in Botswana came from Nigeria by laboratory tests that showed it was genetically similar to the strain that has been infecting children in Nigeria . In the past 18 months, polio viruses genetically linked to northern Nigeria have caused new cases of polio in nine previously polio-free countries. Besides Botswana, they are Benin, Burkina Faso, Cameroon, the Central African Republic, Chad, Ghana, Ivory Coast and Togo.” So polio is likely to break out in RSA  not because of Islamic overdress but because of the masses of war refugees absorbed by democratic dispensation  from the polio-afflicted African states to the north, and poor water supplies, sanitation and nutrition,   in so many areas in the northern provinces, despite mass polio vaccination. . In Cape Town’s poorer  areas’  clinics, we see almost as many foreign pan-African refugees as we do local black Africans.

VITAMIN C & D AGAINST POLIO: but as with flu, HIV, TB and likely all infections, the rescue remedy that the Disease Industry  firmly ignores  is freely available also against polio (and all other infections –  as shown so successfully by Dr Fred Klenner after WW2 with highdose vitamin C);  and at least two  published studies  in modern times ie on Pubmed (FDA- Ivanov 2006 USA)  shows the predictable enhancement by vitamin D3 as an adjuvant  of immune response to vaccine against  poliovirus- presaged by a 1949 paper from Foster ea Univ Pennsylvania . .

15 June 2014 new case reported in the 23nd country – Bangladesh, arrived from USA via Abu Dhabi airport. But now disproven. CRUCIAL EFFECTIVE VITAMIN D3 DOSING: TRIALS USING SUBOPTIMAL VIT D DOSES AND LEVELS ARE MISLEADING:            A major new  metaanalysis of the benefit of Vitamin D and Respiratory Tract Infections VIDARIS in PLOS 2013  by Sweden’s Karolinska  Institute Bergman ea showed that in the 11 relevant trials (published between 2007 and 2012 ie done through the first decade of this century) using vit D3, “Overall, vitamin D showed a protective effect against RTI (OR, 0.64; 95% CI, 0.49 to 0.84). And the average vit D level at baseline was only 24ng/ml, but with the mediocre  vit D3 doses used then  of average 2000iu/d (300 – 4000iu/day) given for between 7wks and 3 yrs, the average bloodlevel achieved on replacement was only 50% higher at 36ng/ml”.      This confirms more direct experience  with higher doses that blood level increment, and benefit,  is proportionate to vit D3 dose, at least up to the proven speculative  safe upper dose of at least 10 000iu/day (whereas the proven safe longterm daily dose is> 50 000iu/day). “More important, the protective effect was larger in studies using once-daily dosing compared to eg monthly  bolus doses (OR = 0.51 vs OR=0.86, p = 0.01)”. This concurs with our experience of major benefit  against respiratory infection that is  based on published studies giving a loading month’s dose of about 80-100 iu/kg/day  ie ~3000iu/kg; then that monthly dose split conservatively eg 50 000iu every week or two depending on mass, and severity of ill-health; to a more successful blood-level of 60 to 100ng/ml. Similarly, the  2014 VIDA trial   across USA-    Effect of Vitamin D3 on Asthma Treatment Failures in Adults With Symptomatic Asthma and Lower Vitamin D Level, Castro ea,  showed “Vitamin D3 for 28 weeks did not reduce the rate of first treatment failure or exacerbation in adults with persistent asthma and vitamin D insufficiency. These findings do not support a strategy of therapeutic vitamin D3 supplementation in patients with symptomatic asthmaBut this trial had the same severe limitation as the Swedish metanalysis of vit D3 benefit- it also used only 4000iu/d. “While all were vitamin D insufficient ie below 30 ng/ ml  before the trial and half were deficient with levels below 20 ng/mL, supplementation brought levels above the 30 ng/mL threshold for 82% in that group – mean levels were 41.8 ng/mL at week 28 in the supplement group, while the mean stayed in the deficient range for those who got placebo. ”  So 4000iu/day merely doubled the bloodlevel to only about 40ng/ml – only about half of the putative optimal dose.  These recent studies force us to conclude that bad weather, and  bad prevalent respiratory viruses,  and especially with major acute, or chronic illness as in those with or at risk of serious infections eg major trauma or sepsis,   MERS-CoV, Ebola, malaria, cholera, cancer, diabetics, smokers, asthmatics, bronchitics,   AIDS-TB., pneumonia and old age  sufferers, and especially hospital, laboratory  and clinic- health workers-  we should for an average 70kg adult give a loading dose of about 4000iu/kg, ie 300 000iu, then 10 000 iu/d,  or 50 000iu every 5 days, or more simply 75 000iu (about 1.5ml of 100cws vit D3 powder) weekly; or at a stretch, 300000 if not 400 000iu monthly. . As  the common  imported vit D3 powder concentrate  is 100 oooiu / Gm ie per 2 ml, it is simple to take the slightly sweetish powder up to  2 or more 4 ml teaspoons ie 200 000  -400 000 iu on the tongue.    The majority of residents of developed countries now live urbanised with mechanized transport, and – especially in Muslim or cold countries-  dont  live and work / walk  all day stripped in the sun. The poor malnourished  peasants  live crowded in ghettoes , and  the poorest are generally the darker skinned and therefore make the least vitamin D3. So with rare exceptions, everyone needs the vigorous vitamin D 3 doses discussed above. But at the prevalent bulk vit D3  powder price of  at most about  US$0,o2 per 100 ooo iu, at a mean population age of around 20 to 25 yrs -outside  Europe- it would cost a country of eg 50 million people perhaps $o.5 per head per  year ie conservatively $25 million a year to prevent > 90% of common illnesses including drugging and violence consequences.  Of course no government can tolerate  such massive loss of jobs and taxes  in a decimated disease industry that now turns over $ trillions annually – up to 18 % of national budgets.     So it’s up to individual adults, especially householders, educators and employees ,  to see that the cheapest cure-all  after clean water – vitamin D3 – at $2/citizen per year-  is recommended and freely available.

13 June 2014 KSA now has apparently reported 702 cases, 292 deaths ie 14 more cases, 12 more deaths in past 11 days.. worldwide 826 cases, 326 deaths. And a new multinational vitamin D study  confirms why vitamin D3 not D2 must be given. TIME TO SWOP FROM MISNAMED  “STRONG CALCIFEROL” VIT D2 TO THE REAL VIT  D3. 6 June 2014   on the 10th anniversary of the SARS epidemic , a new 2013 review (by Japanese epidemiologists) Remembering SARS-CoV: A Deadly Puzzle and the Efforts to Solve It brings home the lessons, the similarities between the two recent killer coronavirus outbreaks, in both outbreaks affecting only residents of closed communities (Arabia and China respectively), with carriage of the virus by travelers into their closed kin communities elsewhere. .  Especially the problems of hospital confinement, and superspreaders.          Sun-blocking culture among the Chinese whereever they live in their ethnic communities is also stressed in modern literature. Lu et al 2012 show very high levels of vitamin D deficiency in Shanghai. The  obvious lesson of the past decades was not noted then or now- prevention is better than cure, as in AIDS and pneumonia and all other infections, simply by superboosting the immune boosters within sensible limits –  sunshine/vitamin D3 and C, zinc, iodine, selenium; and for the likely deficient, appropriate iron .. 4 June 2014. Saudi Arabia reports confirm they have indeed  uncovered many more cases, as tabulated by the Wiki report yesterday- 689 cases, 283 deaths. Shane Granger in his Random Analytics concurs. The graph by the KSA authorities shows that most of the unreported cases reputedly occurred from March through to the first week of May, and that that outbreak is almost over, down from a peak of over 100 cases a week ie at the end of their winter- when vitamin D levels are at their lowest-  to about 25 cases a week. .They do not say when the excess MERS-related deaths occurred. Who knows how many more cases and deaths are underreported from the KSA, when the annual Hajj is imminent, and religious tourism is a vast industry for the KSA. This  MERS outbreak is in contrast to  the 8200 recorded case SARS (coronavirus) outbreak of 2002/3 in China, S.E.Asia, (Canada and USA)  and sparsely across Europe – but only 1/4 of the MERS’ ie  9.6% mortality . Just one case was recorded in the middle east and Africa- in Kuwait. Although the SARS and MERS  viruses were traced through mammals to bats, the affected populations were genetically  different-  Chinese  versus Arabic ie Caucasian. But a decade after the SARS outbreak, Chinese in Shanghai also had 85% below the vit D insufficiency threshold (30ng/ml) at the end of winter.  An International Osteoporosis Foundation study of 2009 showed very high prevalence of vit D insufficiency throughout Asia including China- but worse in Malays. Thus the susceptibility to and mortality from SARS and MERS  in the respective races- like Swine flu susceptibility in the frail in USA and Mexico in 2009 and anywhere since-   is likely due like any disease to the combination of both socioeconomic  burden, genes and sunshine vitamin deficiency. But whereas socioeconomics;  genes; and ethnic taboo on sun exposure as in strict Muslims,  are not easily correctable,  traditional micronutrient deficiency is- especially vigorous vitamin and mineral  supplements, without offending cultural taboos.                                                                  

3 June 2014 update :   In the past 5 days, Google websites  reported 2 new  cases/d in KSA.  BUT Wikipedia this evening reports the latest collation: in KSA, 688 cases with 282 deaths ie 41% mortality; this is far higher than in its close 7 Arab neighbours  including Iran, with a total of only  89 cases but only 26% mortality. If these figures are accurate, there have apparently been 125 cases in KSA since 29 May ie 25 new cases/day there; but 96 deaths ie 19 per day. But this gross epidemic has not been reported on Google, so hopefully the Wiki MERS tabulation will be corrected- unless it because the KSA was not announcing cases. .  Apart from the 8 Middle East nations counted above, the Wiki  figures for the outside 16 countries in the rest of the world  – 25 cases,  7 deaths ie 28% mortality, are more consistent with reports to date outside KSA, and moderately lower than  the fatality rate reported in KSA . All MERS- confirmed cases were contracted in the Arabian peninsula (or from travelers from there). All adults  in the KSA including visitors  would by edict be  almost totally robed  when  outdoors, the women also with hijab. On the other hand,   observant pilgrims from non Arab countries are more likely both older-  having chronic degenerative diseases ie more vulnerable- , but  likely  get more sunshine skin exposure at home,   and taking protective supplements before and after; thus possibly explaining  the lower mortality and low  prevalence of carriage of MERS outside Arabia.  The average  Saudi Arabian is aged around 20years, but  the young there presumably  face the same policy   against skin sun exposure,  and apparently against protective micronutrient supplements. 31 May 2014  Mers update   the past 2 days just one new case in Saudi Arabia, but 2 cases in Algeria back from KSA  - the 21st country ; and now a total of 6 cases in Iran with 1 death.

29 May 2014: The 26 May Cape Town suspect’s  deep nasopharyngeal swab screens  have proved negative for Influenza A eg swine flu, and MERSCoV, and she is recovering. . The NICD says they have perhaps  5 requests for screening in returnees from KSA, all negative for MERS CoV. KSA reports 3 new cases past 48hrs ,  while of recent screened cases there, 4 more  have recovered and gone negative. ie  565 cases , but 6 more deaths ie 186 died -  33%;                Worldwide  thus at least 680 cases / 215 died. But apart from KSA and Jordan (5/10 died= 55%) the fatality rate in the other 19 countries reported is thus  also 22.6%, as low as 13% mortality in UAE if their figures are to be believed.  The problem is we dont know how many subjects were screened in each country to get the perspective.. Perhaps UAE simply screened many more ‘well’ people with “flu’. of recent cases reported from countries outside Arabia, virtually all presented clinically with serious URTI.  Only 2 MERS-COV cases have been finally confirmed in USA, both travelers back from KSA. Thus it is apparent from all the screening patchily reported  the past 2 years that:                                                                                                                                                          1. air/physical contact  crossinfection between humans (as between camels and humans)  is common; 2. but resultant  actual colonization (ie the asymptomatic MERS CoV carrier- akin to say the common staph nasal carrier)  is reassuringly low- likely in mildly immunocompetent people with suboptimal   vigorous eg vit D3 levels and intake of vits C, zinc etc; and  cleared naturally within days; 3. BUT of those colonized with  invasive MERS CoV  who actually present sick enough-ie with MERS-  (generally those with  comorbidities) to consult doctors, mortality may be > 50% (as eg in KSA,  Jordan, Qatar, UK) – likely because they have poorly controlled diabetes, HIV, heart/lung/kidney disease;  or very low vit D3 levels and very low intake of vit C, zinc etc. 4. So far survivors of MERS  apparently do not stay carriers of the virus. These observations will be simple to affirm/ refute by storing, or immediately testing, all carriers’ and cases’ blood  for 25OH vit D3 (albeit expensive)  as well as the other obvious markers  . But it is harmless and virtually cost-free to treat all such people anyway with vigorous vits D3, C and zinc against all latent/patent  diseases. Parallel experience with seasonal flu/ common colds  is that while the URTI  may have been protracted till the patients consult, virtually all cases quickly resolve with vigorous supplements (vits C, D3, iodine, multivite,  appropriate iron, and appropriate decongestants/ “vix” steaming. And of course it is simple and appropriate to deep-sniff pure vit C + D3 powder- as easy as using a nasal sprayer. .                                                                                                                         27 May 2014  Jordan reports  a  fresh (10th) case;      KSA  now 562 cases -no new cases, but one  more death;   national  school exams start there irrespective.. so global total now may be 650..now   2 in Iran. – – the 21st country?. Its not to say that >650 people have caught the illness,  since apart from 30% who died of MERS , at least 20% were well, found only on viral swabs of contacts, ie by definition did not have the MERSyndrome that has killed 30%.. The  global  authorities have not revealed how many of the balance of 50% of those who screened positive actually developed any flu-like symptoms, as opposed to those who survived pneumonia & renal failure. Vigilance is necessary everywhere since both seasonal (H1N1) flu is spreading in the southern hemisphere, and MERS from Arabia with the recent peak there, and business, social and umrah travelers pouring through the Middle East  hubs- especially to and from the worldwide Muslim diaspora , and trade hubs, . . “If you get sick within 14 days of being in the Arabian Peninsula, call a doctor and tell the doctor where you traveled.” said an NBC report earlier this month. 26 May 2041 Our  first ‘ground zero’ MERS suspect returnee from Riyadh  today screened in Cape Town?:  after a weekend with  my own flu attending a 3day medical congress here, and bad family news last night, I was caught flatfooted this morning at a  walk-in local family practice clinic full of people with sudden flu/gastro gripes: the first lady  in (robust, no chronic illness)   with usual sudden  overnight flu   had after two weeks visiting her family in KSA, jetted back from there   just two weeks ago, having sat  behind a man coughing and spluttering.               Before starting highdose  supplements etc, she was  deep nasopharyngeal swabbed for flu and MERS  exam  by our South African National Institute for Communicable  Disease.  Then we will,  if she/her family prove positive,  contact the airline to start tracing all passengers and contacts here. She is hardly in the  risk category that has rocked the KSA. We dont know yet about her flight fellows..

25 May 2014:  HOPEFULLY THE MERS SURGE IN KSA IS OVER?      latest  cumulative Saudi reports are of  ~558 MERS cases in KSA,   179 deaths ie ~7 new cases detected a day (none elsewhere) . Thus in the 3 weeks since 3 May, unverified reports mainly from middle east websites  are of about 101 new cases ie about 5 new cases a day, and 42 deaths in KSA   ie 2/day- ~40% mortality. The rate of new cases presenting and being detected is down, but with the incubation time-lag (5 to 14 days till illness if any),  assuming that all sick citizens are  promptly tested, the mortality rate will fall next week from its peak a week ago.  Tightening protective measures in the KSA  and no doubt  in all global air-hubs outside KSA are hopefully working- there has apparently not been another reported cases outside KSA the past week. 96% of all cases detected have been in KSA & UAE, with 90% of deaths from MERS being  in detected cases there. The lack of new cases reported elsewhere suggests that the global figures are now about 641 cases and 208 deaths ie about 32% mortality. .

22 May 2014 update:    in KSA   544 cases, 176 deaths  ie  so far 18 cases/million, 32% mortality;    UAE 7/million;    worldwide 661 cases,  207 deaths  ie 32% globally. But excluding KSA and UAE, the occurrence of MERS  in the rest of the world – including most of the >billion Muslims-  has been 50 cases ie <1 / 100million; and all of these cases have apparently  been direct human returnees from the middle  east, or their immediate contacts.  Has one non-Muslim died or been seriously ill from the virus? This information is not available on the internet. But there is No pandemic in sight.  At least, as Australian observer  Ian Mackay points out, the trend in new cases in KSA is downwards the past month. The common denominator in KSA appears to be  that especially city Muslim women there must be virtually totally  covered when outdoors in public view.. But as noted earlier in this column, repeated university studies there by their own specialists have shown that their people are especially vulnerable to vitamins D and C deficiency, so easily correctable , a testable hypothesis at trivial cost? This perhaps easily controllable plague  is surely an unintended consequence for  one of the most highly learned and religiously devout peoples in the world? Is the  epidemic growing solely  in the KSA because by strict custom, Saudi Arabian residents (and their pilgrim   visitors-who also are likely  ultraobservant)   have  to  cover up maximally, Dress to Kill? In the rest of the Arabian peninsula the MERS incidence rate is only a fraction? although the deathrate is similar.

19 May 2014 update:  KSA toll now  537 cases / 173 deaths  ie 31% mortality. The total there was inflated by 19 patients in the Jeddah  dialysis unit contracting MERS some time recently. It remains to be disclosed  how many of these cases were diabetic, were on vigorous vits C/D supplements, and died? The global figures are now 620 cases tested positive and 202 deaths.

17 May  2014 including a 3rd case (by direct contagion from a newly arrived traveler) in USA, there are  now  about 650 MERS cases reported  worldwide, 200 deaths ie 32%  fatalities;   14 new cases daily globally  the past 3 days;   KSA  529  cases   168 deaths (ie 11 new cases  a day; and 16  deaths the past 3 days). But 96% of all cases worldwide  to date  presented in the Arabian peninsula’s  80 million Arab population, and apparently   all 27 outside cases were exports from KSA or their immediate contacts. .. The Wiki entry  Tourism in KSA  states plainly :  “In December 2013, Saudi Arabia announced its intention to begin issuing tourist visas for the first time in its history.  Restrictions and security : Visas are only issued for business, relatives of Saudis, transit to a third country, and Muslim pilgrims; general tourism is not allowed.”   So effectively  in KSA cities  there are in public  only heavily-garbed  Muslims.  Apparently nownon-muslim tourists can visit the KSA in a group organized by an accredited agency”, obviously provided they conform to local religious norms. But “A limited tourist visa programme was cancelled in March 2014.[5]       Saudi Arabia does not currently issue a visa for tourist travel. Hence apparently the KSA population especially in the cities is  overwhelmingly  Muslims conforming to orthodox Wahhabi  Sunni outdoor   attire- although there are apparently  some 1 million christians (ie 1:30 of the population -presumably mostly professional/technician experts- in the big cities) in the KSA. Apparently there are over a million camels in the KSA,  (apparently nearly 25million worldwide) with a lifespan akin to humans. “Camels  come from neighboring Middle Eastern countries, in part, but also from countries in eastern Africa, including such already beleaguered places as Sudan and Somalia, Nigeria, Tunisia, Ethiopia.     Just now online, not scheduled for formal publishing until this summer, is a brand-new CDC report  finding widespread evidence of MERS-CoV in African dromedary camels too.” With the dromedary  numbers (at least 1 per 30 Saudi  citizens), camels’ huge stamina ie resistance to disease, including apparently the MERS virus they carry,  their cherished role including as pets, meat, transport, racingstock,  and supply of fresh warm milk  in KSA society; and  the reported low human vitamin D (and perhaps C) levels in the heavily-garbed city  citizens,  no wonder camels  are an ongoing source  of the hitherto unknown MERS coronavirus illness for immunodepleted citizens in KSA? whereas the camels themselves apparently suffer no more than a mild cold. A  respiratory virus infection in a temperate climate is usually easily thrown off with symptomatic Rx, supplements and plenty of fluids; but on the other hand, in  middle east desert  temperatures and in all-over robes, hyperthermia and dehydration from MERS  may more obvious cause of pneumonia and  (pre)renal failure- especially in a population with high rate of sickle cell, diabetic, overweight, cardiovascular and hypertensive disease. Average temperature  are about 29-330C ie mean peaks of 40C; with humidity  17% in Riyadh & Medina, but much higher in Jeddah;  intermediate in Mecca..

And “Middle Eastern countries import tens of thousands of camels from eastern Africa annually. Many Saudi camels are imported. Scientists don’t yet know where the MERS virus originated or how camels got it, but it has been found in African countries and as far away as Spain’s Canary Islands, where a tiny population of camels lives for the past 400 years .        ” Camels in the kingdom are like dairy cows, beef cows, racehorses, pulling horses, beloved Labradors, and living daily reminders of holy scripture, all in one. (Camels appear, honorably, in the Quran.)” As the latest report from Pulitzer Centre Prof Cynthia Gorney’s Nat Geographic account of MERS ends, “Fresh warm camels milk straight from the udder is “Very heavy, very sweet, very therapeutic” Ameer said, after I stopped shouting at him over the phone.  If I were still in Saudi Arabia at this moment, I told him, I would be smacking him upside the head.”  What likely gave Ameer his claimed  immunity? that he had been years in USA?, and like Arabian desert camel-keepers probably  lightly clothed and much in the sun- thus with good vitamin D levels?

A new report today from WHO chillingly details a party of at least 9  Umrah pilgrims since April 2014 who  from Jeddah visited Mecca and Medina  and then back via Jeddah to Amsterdam, Greece and USA with developing MERS – from the Jeddah sub-clade which has been identified in at least 30 cases there.. These linkages do not explain why the MERS outbreak has mushroomed solely in KSA residents – not in Muslim communities outside Arabia into which travelers flying home via Jeddah  have imported the virus. The co-factor may be that, having inhaled/ingested  the virus from human carriers in the KSA, these foreign travelers, often with co-morbidities, were also more vulnerable to the MERS virus because of their adherence to the same  all-over dress orthodoxy, and dietary vitamins D & C and perhaps zinc depletion  (with or without sickle cell trait) as has been reported prevalent in the KSA; and detailed with references below. A study is awaited of comparative skin shade,  diet and skin sunshine exposure (ie degree of conformance to strict Sharia covering) between Saudi Arabians of longterm Arab descent, and their relatives and  similarly conforming co-religionists in the distant diaspora Muslim overseas communities  that send Umrah and Hajj  pilgrims through Jeddah to Mecca and the other shrines. A current  wiki-islam website stresses the serious health hazards (both skeletal- rickets and osteoporosis – and across all system diseases including immune-infection- protection) of full-cover Islamic ie hijab dress through sunlight vitamin D deficiency, unless vigorous vitamin D supplement is taken.  It is no surprise that this is as much of a danger for hijab Muslims  in high-sunshine desert latitudes as in bleak low-sunshine cities far north.. This might explain why the latest WHO population statistics (perhaps 2011 ie before the MERS outbreak) show that – despite being perhaps  the richest  per-capita nation (from oil reserves)  in the world,- the KSA has expected survival age 5 years below that of UK, especially from combined (hypertension-diabetes-coronary heart- kidney ) disease rate of 375 in KSA vs eg 80 in UK. But even then, a different WHO website showed flu and pneumonia deathrate (before the MERS outbreak)  37 in hot, dry KSA ie 50% higher vs 23.7 in UK. and in about 2011, KSA had a mean population age of 20 years, with annual (agri-and seafood)  imports  ie dependence of US$17billion, due to its desert-limited agripotential; with predicted rapidly increasing urbanization .  It will cost pennies, and a few weeks’ followup of supplement dispensing to KSA citydwellers, (and incoming pilgrims before they leave their diaspora homes for the KSA),  of vigorous dose vitamins D3 +  C and a multisupplement including the other vitamins , magnesium, zinc,  iodine; and  fish oil and virgin coconut oil (ie a blanket antioxidant, antiinfection, antihypertensive  insulin-sensitizing umbrella supplement)  to confirm if the emerging epidemic of  MERS (let alone hypertension-heart-diabetes-kidney  disease)  in KSA  is significantly slowed, as  common infective and degenerative diseases  are here  in Cape Town, by such supplements. This simple prospective clinical monitoring of those receiving or not receiving  the swine flu vaccine in 2009 was universally recommended, but Authorities refused to enforce such simple monitoring, so there is  no clinical  evidence that the swine flu vaccine significantly reduced morbidity from the outbreak, which was globally statistically trivial except in the Mexican source outbreak. Similarly, there is no evidence that the spread of MERS-CoV  in KSA is epidemic considering that even in the four most densely populated cities – in the three abutting  midwest  provinces  – containing almost half the national population,  – the detected spread of MERS illness is still so low (except in the incubator hospitals). Even though camels are so widespread. it is intuitive that rural/desert citizens may take  both more fresh  (desert)  crops (ie vit C) and more  vit D- from both camel milk  and more sun exposure from  outdoor work with more skin exposure in such labourers. Some  pictures of camel attendants apparently in the KSA  on the internet  show bareheaded men in vests.  16 May 2014   the latest  KSA  stats reported are 515 cases, 160 deaths ie 30% mortality. Globally 621, deaths 189 14 May 2014  now ~592 cases reported in 20 countries – the latest in the Netherlands, and a 3rd case in USA;  with ~31% mortality (KSA 495 cases, 152 deaths ie 31%; with 20% asymptomatic). 12 May 2014:  USA reports a 2nd case arrives there. a 5th death with MERS has been reported in Jordan.  Saudi Arabia reports 8 new cases since yesterday, and 2 more deaths.   But  as expected, in the KSA eye of the storm , it appears that only contacts of  patients are being screened- at least 20% of patients who screen positive for the virus have remained well. So the morbidity and mortality% are in fact very skewed, they are apparently not screening the local population for carriers. The ~28% death rate refers only to deaths in the cohort that were afflicted  with MERS and their contacts.

11 May 2014  A new Reuters report today highlights the widespread intimate contact with camels in KSA. “Does the KSA want to control the uncontrollable?                                So far, the reported cases have all originated in Saudi Arabia or in the southeastern part of the Empty Quarter, in the UAE. There are no reports of those outside Saudi Arabia having transmitted the disease to others. the past week has seen another ~116cases  ~15 cases a day- reported in the Middle East, and another 34 deaths  there ie the total has reached ~578 cases (483 in KSA- Kingdom of Saudi Arabia) and ~163 deaths (142 in KSA). So  the death rate has fallen  to  <28% overall.  Lebanon and USA  become the 18th/19th countries to report a case of  a returning traveler.  But virtually all  identified cases originated in the KSA neighbourhood. The latest figures show that MERS originated and breeds exclusively in the Middle East- (cases per million ppm the past 2 years) in 16 ppm in KSA(483 cases total), 6ppm in UAE (53 total),    3.5 ppm in Qatar(7  total)  and  1ppm or less  in Jordan (9 total- the first reported cases, in April 2012)) or elsewhere. Apart from the frequency of camels, and the high prevalence of deficiency of vitamin D and possibly vitamin C reported below, ethnic culture may play a major role:  In KSA, Qatar and UAE the great majority of citizens are Wahhabi Sunni muslims. By contrast, Yemen is only 65% Sunni, but  Oman is distinctly different Sharia culture. Iraq and Iran are predominantly Shia culture.

Jordan on the other hand is a unique  Hashemite culture although also  70% Sunni;  so contrary to the Wahhabi countries,  “ Jordan is one of the most liberal countries in the Middle East, with a secular government“. So the increasing prevalence of MERS in the Wahhabi Arabian peninsula peoples relates perhaps  to the likely cluster of predisposing factors:   well-covered male and especially female orthodox attire, if not also higher prevalence of sickle cell trait, and diet,  which is associated with deficiency of vits D, C, A and E as referenced below. Feminist Muslim websites may correctly argue that Hijab does not cause vitamin D deficiency;  but it likely contributes significantly to it’s spread via lowered vitamin D production in skin – with orthodox Muslim women arguing that such women can arrange private sunlight skin exposure. This trend to vitamin D deficiency from low oral   and sunlight-mediated  vitamin D is incidentally mirrored in  new studies:. :                                                            from  USA – The Vitamin D status of Prison Inmates- which confirmed that, on a ‘sufficient’  diet including vitamin D intake,  the higher the security isolation of inmates (and therefore least sun-exposed), the lower the vitamin D status- especially in the darkest-skinned inmates; from Israel   Effect of different dress style on vitamin D level in healthy young Orthodox and ultra-Orthodox students in Israel; and in southern Italian nuns.

So vit D deficiency in MERS  may be like  in AIDS:  Vitamin D Deficiency in HIV: A Shadow on Long-Term Management)? (2014, London UK).  But vigorous vitamin D charge – by sunshine and especially vit D3 supplement- as an immune and anabolic booster is one of the safest and cheapest preventions of all disease that there is. With the Ramadan Hajj to the KSA this year only 6 weeks  away, intended pilgrims need to top up their vitamin D3 levels and multivites vigorously now, to boost both their infection resistance and improve control of all major diseases they have;  and take plenty of vitamin C with them.  So should  their communities, contacts  here as pilgrims return from the Hajj. SUNSHINE AND ORANGES: ANTIBIOTICs VITAMINS C AND  D like vitamin CVitamin D is hardly a new anti-infective agent as an Israeli study (Borella ea 2014) now confirms, since sunshine sanatoria were  the only effective treatment of tuberculosis in the pre-antibiotic era even after WW2; and ” An association has been established between low levels of vitamin D and upper respiratory and enteric infections, pneumonia, otitis media, Clostridium infections, vaginosis, urinary tract infections, sepsis, influenza, dengue, hepatitis B, hepatitis C, and HIV infections“. Especially in this post-antibiotic age of rampant antibiotic resistance. Sunshine and Oranges - Empty Cradles-  is  ironically,  the account of Britain’s infamous ruthless  export- banishment to the Colonies -from the early to post WW2  20th C   of thousands of surplus children of poor or orphaned families. Shades of the forced transport of ‘felons’ to Devil’s Island and the British outposts of previous centuries.  Usually clad in scanty rags, in Australia  they certainly   had plenty of sunshine ie vitamin D , and  the abundant local oranges (vitamin C);  but like their surviving mothers, much grief and poverty – while from lack of these same nutrients, their kith and kin back in UK  were ailing with infections and rickets . .

3  May 2014  four months later:  MERS RESURGENCE: NOT A PANDEMIC BUT A DEFICIENCY SYNDROME? more precautions needed:  With the recent flareup of MERS Middle Eastern Respiratory Syndrome in the Gulf States, the number of reported cases since New year has more than doubled to 457 ie to >24 cases a week there, but still only in residents/ travelers from/through the Middle East hub, and their contacts;   in 17 countries including Europe, Egypt, Malaysia,  Philippines and now a traveler from Riyadh to USA.  The death toll has reached 133/457    ie the death rate  has  fallen steeply   from 42% last December to 29% overall, understandably as more cases are detected by screening in the source, the Kingdom of Saudi Arabia KSA.   Wiki   and Reuters seem to give  the most update  (if not WHO-confirmed) stats. So the evidence so far is that, while camels are endemic carriers there,  most  recent sick cases have apparently been been traceable  human to human transmission – apparently all among Muslims, and in the malnourished or chronically ill older, and  health workers as in the case just reported in USA.      So there is no apparent spread by other vectors eg bird and farmyard swine as in the case of influenza. Since the reports available indicate that the MERS virus is dangerous only in those already malnourished or with serious other systemic disease, it is like flu-  pretty harmless in the well adequately nourished and housed. While frequent flyers are generally well off and well nourished, the same cannot be said for those in virtual ghetto  slavery all over the world, eg migrant labourers  working on contract  in the Gulf States, who have apparently been among the latest victims . So as with the overblown Swine Flu non-pandemic of 2009, there is no good evidence to label MERS  a deadly epidemic, it in fact seems to have low cross-infectivity compared to say influenza which spreads like wildfire- but with no more morbidity (except in Muslims?) than the common cold corona viruses.

WHY IS MERS  LIMITED OVERWHELMINGLY TO AND SPREADING ONLY IN THE KSA and UAE?  is it a unique genetic trait of Saudis?  or is it micromalnutrition unique to this  ultra-orthodox Muslim nation with unique almost total skin coverup outdoors? why was there no outbreak of MERS in the millions of pilgrims who did the Hadj to the KSA last year?   the KSA is 100% muslim, whereas the UAE only 76%, with far more foreigners working and living there. It is common cause that peoples who keep well covered during daylight hours – as ultraobservant Muslim (and ultra-orthodox Jewish)  women and  men do, have much lower vitamin D levels. Those on restricted diets are also more prone to malnutrition including vit D deficiency, especially if low in dairy products. Common sense perhaps explains  why Saudis – in the heart of Islam (Mecca, Riyadh, Jeddah, Tobuk) have low vitamin D and likely also low vitamin C and zinc levels, and thus more infections. Moderate to severe vitamin D deficiency was reported prevalent  last year in Saudis by Al-Daghri,  Sabico  ea  from King Saud University Riyadh- where Hasanato in 2006 reported low vitamins A, C and E and zinc levels in severe sickle cell disease. El-Hazmi ea  from the Saudi College of Medicine also in 2011 reported that Saudi Arabia and Bahrain have the highest prevalence of sickle cell genes in the Middle East,  at up to 18%. Bahrain has just opened a sickle cell hospital, but Bahrain has the tiniest population (1.3million) of the Gulf States although the highest population density, compared to the 38million of the KSA plus the UAE which have had over 90% of MERS cases. Most if not all the camels in Bahrain are in a zoo; whereas in the KSA camels are a favourite if not sacred possession and listed first as the  domestic animal. So the absence of MERS in Bahrain is unsurprising.

The UAE on the other hand also has many camels as entertainment if not also for travel – with 5000 camels entered in a beauty contest there alone.. So, despite long days ie much sunshine exposure in Arabia, low  fresh water availability likely reduces hygiene  (washing and oral hydration) capacity for the masses let alone camels.  And the well-covered dress code, and low availability of private sun-exposed balconies and courtyards  (unlike apparently more liberal Muslim countries) mean that the Saudi masses do not have the opportunity to get much-needed sun exposure to even the face, neck and limbs let alone the torso.

        Hence Saudis have as obvious  major risk factors for MERS  -not just the teeming MERS reservoir in their valued  camels (also a staple   milk supply), but more importantly endemic deficiency of vitamins C, D (and perhaps E, zinc) and water compared to relatively less clothed populations in other  hot but also better water-supplied  countries that also do not carry much sickle cell disease.

Camel meat is apparently no longer a staple in the KSA where staples now include Bread, hummus, rice, and  Tabbouleh- a “salad” generally made of parsley, bulgur, tomatoes, garlic, and lemon; Kapsa: the national dish is chicken and rice with vegetables; and Kebab:  a base of roasted lamb or chicken and vegetables in pita bread. There seems  little vitamin D in that varied diet, especially not pita bread or rice.

      The only good unfortified and unprocessed food sources of vitamin D are apparently oily fish,  liver, mushrooms, and (if fortified),  egg yolk and dairy products ; or else vitamin D3 supplements. ..

Finally, it is common cause from published studies and our local experience that infections eg HI, TB,  influenza,  herpes  and the common (Corona virus) cold are easily treated and prevented by vigorous safe intake of vits C & D combined with the other multivites, zinc, iodine, iron and selenium. In advanced infection cases of eg HIV and TB (in trials  from Central Africa and Canada), combining even modest doses of just 2 or 3 of these supplements with appropriate antivirals and antibiotics reduced dreadful morbidity and mortality by two-thirds. NATURAL PREVENTION/TREATMENT: with the theoretical double peril of influenza and MERS-   (ie as with the looming  Influenza A gastro-/respiratory season in the southern hemisphere),  with no proven  vaccines or antivirals reported or likely, those in contact with Middle East travelers- or any infection eg flu  outbreak- are again reminded to boost their immunity  and global health with safe effective lowcost NUTRITIONAL ANTIINFECTIVE supplements: 1.VITAMIN D3 CHOLECALCIFEROL 2500-4000iu/kg/month  (not the weak  vit D2 ergocalciferol  falsely labelled  “Strong” Calciferol tabs) most simply taken as a few scoops ie 50 000 to 250 000iu of vit D3 powder/MONTH at all ages (AND IDEALLY target BLOOD- LEVEL 80-100ng/ml depending on overall illhealth state. IT IS VIT D3 THAT IS STRONG CALCIFEROL, NOT VIT D2, since experts report that vit D3 is apparently four times more potent than D2. 2. MULTIVITES with zinc selenium and iodine (and iron for likely deficient eg kids, young women), but  especially 3.  buffered VITAMIN C ASCORBATE  at least 3gm/d orally ( if not with bad infection symptoms – 10 or >30gms / day if not ivi)  at trivial cost as powder;  to tolerance; 4. with eg  ecchinacea, melatonin, garlic, colloidal silver, sutherlandia and whatever other antiviral available locally. Since flu and colds disrupt both sleep and outdoor activity, nothing makes as much sense as co-supplementing both of the day and night hormones melatonin and vitamin D; as well as the other sunshine vitamin- ascorbic acid (solar-produced in abundance in  eg fruit) – to improve both sleep, rest and immunity. For small kids/infants the vitamins and minerals can simply be taken as powder in liquid ie in feeding bottle or a  glass. It is increasingly notorious how depleted modern breastfeeding mothers (on the industrial polluted fructose-sucrose-  aspartame PUFA-antibiotic-hormone-glyophos- GMO laden  food chain now prevalent)  and baby formulae  (unlike colostrum from pasture-fed eg New Zealand dairies) are in such lifesaving  immune and anabolic anticancer  boosters.

Ironically,  recently  Prof Zahid Naeem ea from the KSA Qassim University publicised in their university International Jnl of Health Science   Vitamin D Deficiency- An Ignored Epidemic in 2010  and 2012  , with prevalence there of up to 80% in the KSA despite the abundant sunshine, thus urging vitamin D supplementation. . But such simple prevention – of all disease but especially wished-for megaprofit  pandemics like flu and HIV-  is anathema to the multinational Big Pharma and their lobbyists in the global Disease Industry, which employs millions worldwide and generates trillions in income for government and corporates. Prevention does not pay. Simple prevention suits no-one working in the disease  and drug and hospital industry since it makes most health workers especially doctors and administrators and hospital  largely redundant. It seems that public health officials choose to go on ignoring the deficiency epidemic even in the KSA- unlike Dubai, there is no website of the KSA Govt promoting vitamin D supplementation.  The solution is too cheap – and embarrassingly simple.  An anonymous blogger details the numerous reasons for endemic vitamin D deficiency in especially the Gulf States.. at least the Dubai Govt publicises the deficiency, and supplementation. Is it irony, or an indictment of the prevailing world-wide largely male-dominated -subservient female culture,   that already back in 2001, there were strong warnings about Niqabs and Burqas as Impediments to Health? already in 2012, dairies in the UAE were fortifying milk with vitamin D; and in 2001 academics published a study showing the many reasons for prevalent vitamin D deficiency in the KSA. and Prof Mike Holick  in 2010 published an authoritative review  The Vitamin D Deficiency Pandemic: a Forgotten Hormone Important for Health urging vigorous vitamin D supplementation universally. As detailed elsewhere in this column last year,  the prophet of vitamin D and melatonin  the late Prof Walter Stumpf must be shaking his head repeatedly along with  the late Prof Linus Pauling, about the neglect of authorities  to promote and distribute vigorous supplements of vitamin C and D3 to the afflicted Arabian peoples let alone worldwide. But then we need to be reminded of the infamous Vitamin Murders, how Prof Sir Jack Drummond was mysteriously murdered with his family on holiday in France in 1952, when he and Linus Pauling were  the  leading vitamin discoverers and promoters  of the 20th century (as Walter Stumpf was of melatonin and vitamin D). The Big Pharma Disease Industry combined with the might of the FBI  and the FD  could never shut Pauling up;  but by whom and why the Drummonds were murdered remains unsolved, thus fertile conspiracy theory. Reading Drummond’s papers on the internet, one can understand why the burgeoning patent drug industry then as now hated natural lowcost unpatentable remedies, unbeatable natural safe  antiinfective agents like vits C and D and iodine – each almost universal panaceas. . .

This universal truth about industry suppressing  natural remedies  is the Semmelweis Paradox, that had the leading obstetrician of his day murdered in his prime by his jealous rivals.

27 Dec 2013  the outbreak not over:  9 new cases;   ie overall deathrate 42%, but past 2 weeks  4.5 cases a week just from the KSA..  :  Since April 2012, the European Centre reports  175 laboratory-confirmed cases, including 73 deaths, of acute respiratory disease caused by Middle East respiratory syndrome coronavirus (MERS-CoV), have been reported by national health authorities.  27 December,  Saudi Arabia confirmed nine cases (five asymptomatic healthcare workers and four patients suffering from chronic disease, two of whom had died).  24 Dec 2013 the score now stands at 166  (163 at 16 Dec)  cases and 71 fatalities- 42% –   in 18  months since the first identified case in June 2012; ie per week – 2  new cases and 1 fatality .  No pandemic. No outbreak. Considering the duration of the awareness  of the new virus in humans- apparently from bats/camels/swine,  even after 18 months of millions of pilgrims visiting the Middle East, and far more foreign travelers flying through those hubs, and intensive surveillance on those routes east and west,   the morbidity and mortality have been negligible with only a handful of perhaps related deaths in frail patients. Whether as with seasonal avian  ie H1N1 flu from China to the West and south there will be a flareup of MERS-CoV cases  in the pending winter from now on  in the Middle East, remains to be seen..

12 November 2013   Considering that the Hajj has just ended with millions of pilgrims returning home,  and vast numbers of multinational passengers transit through the Middle East hubs, its reassuring  that (depending on which reports are duplicates and delayed) only 3 or 5  tested positive cases and 1 or 2  deaths have been reported the past week:    especially since only serious flu-like cases are likely to be tested- but more so in the affluent who can afford to fly.   So far no reports of MERS-CoV case are apparent in South Africa, although flu-like illness remains  common here. Perhaps more people are heeding warnings to take multivites plus zinc plus vigorous vits C and D. The ECDC    and  OSAP  and NowNews  and GlobalAlert report   As of  11 November 2013, there have been  at least 154 laboratory confirmed cases of MERS  CoV worldwide, including 65 deaths ie 42% in TESTED cases. All cases have either occurred in the Middle East or have had direct links to a primary case infected in the Middle East.        Saudi Arabia has reported  at least 125 symptomatic and asymptomatic cases including 53 deaths  Jordan two cases both of whom died   United Arab Emirates five cases, including one fatality Qatar five cases, including two deaths  and  Oman one case who has  just died.       Thirteen cases have been reported from outside the Middle East: inthe UK (4), France (2), Tunisia (3), Germany(2), Italy (1) and Spain (1). 31 Oct 2013 with the Hajj over, the latest score is 149 cases and 63 deaths ie 42%. http://www.who.int/csr/don/2013_10_31/en/index.html ie 5 new cases a week from the region, 30% deaths. http://gmggranger.wordpress.com/2013/10/29/quikstats-mers-cov-in-the-arabian-peninsula-nov-2013/ 17 Oct 2013 with the Hajj in full swing, the latest tally is apparently 139 cases and 60 deaths.  So thats only 1 case  reported a week the past 4 weeks, and no deaths in that time.  Promising news, although we continue to see bad viral-like  respiratory-gastro infections in adults locally with the volatile weather.

20 Sept 2013 with below a month to go to the Hajj, the latest Quickstats are 135 cases confirmed, and 60 deaths ie 44% mortality- all new cases and deaths apparently in  KSA and the Gulf States. Thus in the past 7 weeks,  41 new cases have been reported ie 6  a week, all in the Gulf  States; with unaltered  mortality  (44%) apparently restricted to the chronically frail. This as the drastically variable  Cape Town weather alternates sunshine joy and freezing wet  snow or hail, with high prevalence of both respiratory and gastroenteritis attacks, sometimes with protracted debilitating bronchitis; how much of this is local seasonal colds- coronavirus– or  flu, orMERS-CoV,  or  the explosive Norwalk virus, is speculative and academic. Basically So What since management is symptomatic, and vigilant prevention  crucially effective with hygiene, home rest and multivites but especially highdose vits D3 up to 10 000 (100iu/kg)  iu/day or weekly equivalent plus  buffered vit C up to tolerance >100mg/kg/day, zinc, selenium and for the malnourished, iron; perhaps safe plant  immune boosters like sutherlandia, garlic etc; and avoidance of smoking, sugar and the likes-  boozing and sweetened soft drinks (fructose, aspartame,sucralose).

11 August 2013  OUT OF AFRICA?  no new cases of MERS-CoV have been reported the past week; but while camels (in Oman) are now also suspect hosts/ transmitters in the M E,  there is some evidence that the MERS virus has the closest virus match yet found to bat CoV  in South Africa. As a precaution, with upgrading of shrines in Mecca, KSA is actively reducing  overcrowding by Hajj visitors by 20%, and warning the frail  and elderly not to go this year. With the prevalent bad winter respiratory and gastroenteritis  infections at least around densely populated and polluted Gauteng and  KZ-Natal,  and especially the floral mountain kingdom of greater Cape Town-   all are encouraged to take vigorous doses of vitamins D3 and Superenhanced vitamin C with a broad multimineral-multivite –  extra vits A, E, B &   coQ10;  the minerals zinc,  selenium, iodine, colloidal  silver, (and iron in the young commonly at risk of deficiency);  probiotics ;  rooibos or buchu or green honey and lemon tea,  sutherlandia;  licorice, St John’s wort, garlic,  echinacea, olive leaf  etc;   including sniffing vitamin C ; and  if snotty rhinitis/sinus/bronchitis symptoms,  steaming with eucalyptus etc.. And during acute attacks especially of respiratory and gastro attacks,  avoid sugar,  fat,  dairy and wheat intake.

2 August 2013  The Hajj to Mecca this year is  in the third week of October.  While over 15 million (of the world’s ~1.5billion) Muslims visit Mecca – Umrah- annually, some 3 million pilgrims worldwide make the seasonal Hajj visit trip, with pro rata from South Africa  only 2000 (of our ~2.5million) apparently the quota of pilgrims allowed this year   by Saudi Arabia . But increasing numbers of frequent flyers of all nationalities and races to and from South Africa – Europe fly via the Gulf States  Emirates airline, if not commuting to work and visit family there – including professional sports teams for tournaments… So this week’s flood of warning bulletins  on the Gulf State respiratory infection outbreak are cause for urgent caution and prevention, perhaps grim news for those who fly that ME route, and their families and close associates and neighbourhoods. The 49% deathrate reported in the now 94 cases- 3 more reported  1 August  from KSA- so far from the MERS-CoV Corona Virus MiddleEast Respiratory Syndrome outbreak is alarming, that has spread the past 10 months  from the Kingdom of Saudi Arabia KSA  and  the Gulf States  to Tunisia, Europe – France, Germany, Italy-  and UK . It is now being recognized as distinct not just from the common cold coronavirus but also from the Chinese Severe Acute SARS-CoV virus outbreak since 2003, of which over 8000 cases have been recognized , but the latter virus having a fatality rate of only <10%; and the current violent but selflimited Norwalk virus  gastroenteritis (explosive vomiting and diarrhoea for 1 -3days;  (fatality rate <0.1%) raging in UK,  it recently is the commonest cause of foodborne infection in USA  .

No clinically effective vaccine or synthetic drug treatment has yet been found for these coronaviruses . The same lack of specific antiviral therapy applies against gastroenteritis viruses and influenza, but the mythical 2009 swine flu ‘pandemic’ was even milder (than some seasonal flu outbreaks) with a proven mortality rate far below 1% considering how rapidly far and widely it spread. The reservoir if any of MERS-CoV may  be cave bats, (and, ominously, perhaps swine – c/f the 2009 swine flu ‘pandemic’ that wasnt; shades of the deadly Nipah virus outbreak of 1999 – from bats to pigs to man).. But the fact that MERS-Co is spread human to human, and mainly men ,  has been attributed perhaps to women in strict sharia society being well veiled and thus shielded from inhaling (and transmitting) the air-born virus, never mind womens’ generally stronger immune systems and hygiene, self-care. So beware   all those in close contact with recent air-travelers through the ME states and surrounding subcontinent airports – never mind the S-E-Asia airhubs of Hong Kong and Singapore: it maybe  only a matter of weeks before cases occur on the other continents especially in city dwellers, public transport commuters, factory and office workers; and who knows, perhaps where bats and swine cohabit close to cities, as around South Africa.. .. Its cold comfort that the latest report  yesterday and today,  note that this stage is perhaps like SARS in 2002 and swine flu in 2009, the ‘bottom of the iceberg’, with only severe cases being admitted, tested, reported, in already chronically ill frail patients; especially diabetics and renal failure – to which older Muslims are particularly prone; while the virus spreads silently, mildly if not harmlessly  in the well majority, as in two young well  women health workers in contact with a chronically ill elderly female case in Riyadh, KSA … ANTI-INFECTIVE PROTECTANTS and advice are available from the Natural Remedies Centre, 15 Grove Bldg, Grove Ave, Claremont, Cape Town ph 002721-6831465 or -6717415: Fortunately  all Health Shops  are well stocked with the many  almost 100% protectants against serious infections including fungi bacteria and viruses – colds (ie corona-) and flu’-virus (let alone against all others) afforded by the basket of locally available (although mostly imported)  natural lowcost evidence-based  nutritionals – supplements  the past decades: safe  hefty combinations of a number of immune-boosting  vitamins, minerals and foods, herbs. This septuagenarian author has, touch wood, on this combination- increased at occasional  times of suspected colds-fever- , despite great stress, and flu ‘pandemics’, and avoiding vaccinations,     not had a bad infection lasting a day in the past 5 years despite working in the highest risk  poor townships and acute hospital clinics with rampant HIV – multiresistant TB cases .

BREAST SCREENING and BAD DIET ARE OBSESSIVE-COMPULSIVE DISORDERS. ASSAULT UPDATE 2014: FLOOD OF PROGRESS AGAINST BREAST CANCER/ DISEASE.

neil.burman@gmail.com  Cape Town.                   read this  in concert with:                       combatting rising-occurrence-of-breast-cancer-in-younger-women;  and
update 21 Oct 2014 Dr Garry Gordon writes :
        “Hello ,  What are you doing to detox your patients on a daily basis? We live in a crazy world where  nutritional supplements with little or no clear risks to consumers are seized/ restricted, but Authorities drag feet  on stopping the use of a proven toxin like BP-A found as a coating inside of most canned goods.  Please understand that Randy Jirtle at Duke has shown that BP-A made healthy brown Agouti mice become obese, yellow and diabetic!  That effect led to an epigenetic change, which will persist for generations and was shown to be an epigenetic change in methylation.Plan to protect yourself with lots of methylation support. I take my Beyond B12 sublingual product that provides Methyl Folate and Methyl B12. Please know virtually everyone tests positive for BP-A in urine much of the time, as we have great difficulty in avoiding this poison in our daily living. Yet authorities  ignores the dangers although they finally are doing something to protect babies a little.

How can anyone practice effective medicine today and ignore the toxin burden we all carry. Remember when I got out of training in 1958 normal sperm count was 140 million; today few have 40 million. I detox daily with my “Power Drink” and PEMF and I definitely show real benefits even at age 79.

“BPA has been linked to possible health problems of the brain, breast and prostate. In 2008, the environmental group Natural Resources Defense Council asked the FDA to ban use of the chemical because of what it termed “serious adverse health effects.”

In 2011, the American Medical Association deemed BPA an “endocrine-disrupting agent” and urged that “BPA-containing products with the potential for human exposure be clearly identified.” The FDA said it continues to evaluate the safety of BPA-containing products.”

http://online.wsj.com/article/SB10001424127887323740804578600113164806902.html?mod=djemHL_t

Wassertheil-Smoller S ea .   Albert Einstein College of Medicine, NY, write in Breast Cancer Res Treat. 2013 Oct;141(3):495-505.  Multivitamin and mineral use and breast cancer mortality in older women with invasive breast cancer in the women’s health initiative..  “Multivitamin use is common in the United States. It is not known whether multivitamins with minerals supplements (MVM) used by women already diagnosed with invasive breast cancer would affect their breast cancer mortality risk.   a prospective cohort study  of 7,728 women aged 50-79 at enrollment in the women’s health initiative (WHI) in 40 clinical sites across the United States diagnosed with incident invasive breast cancer during WHI and followed for a mean of 7.1 years after breast cancer diagnosis, showed :” At baseline, 37.8 % of women reported MVM use. After mean post-diagnosis follow-up of 7.1 ± 4.1 (SD) years, there were 518 (6.7 %) deaths from breast cancer. In adjusted analyses, breast cancer mortality was 30 % lower in MVM users as compared to non-users (HR = 0.70; 95 % CI 0.55, 0.91). This association was highly robust and persisted after multiple adjustments for potential confounding variables and in propensity score matched analysis (HR = 0.76; 95 % CI 0.60-0.96). Postmenopausal women with invasive breast cancer using MVM had lower breast cancer mortality than non-users. The results suggest a possible role for daily MVM use in attenuating breast cancer mortality in women with invasive breast cancer but the findings require confirmation.

Tying up Garry Gordon’s two themes above  is obviously the fact that , as in eg the USA ARED (Centrum) trial, the Lemon-Rollo McMaster supermouse trials and the Scottish Highlands,  and China supplement trials, multisupplements are longterm (especially with vigorous levels of vitamins C and D and magnesium) both antioxidant, insulin sensitizing, methylating, Nitric-oxide promoting and (heavy metal) detoxicants- ie promote healthspan and suppress degenerative diseases and infection. . .

 UPDATE 18 OCT 2014: more arguments against screening mammography from UK and Canada:Curr Oncol. Oct 2014; 21(5): 210–214.  Reflections on screening mammography and the early detection of breast cancer.  A Countercurrents Seriesa    S.A. Narod, MD  *Women’s College Research Institute, Women’s College Hospital, Toronto, ON.A little learning is a dangerous thing.— Alexander Pope, An Essay on CriticismIn the stormy aftermath of the recent publication of results from the 25-year Canadian National Breast Screening Study (nbss)1, various opinions questioning the validity of the study’s results have been expressed27. I was a latecomer to the study. In 2005, I was charged with oversight of the final record linkage and the statistical analysis and interpretation of the final data set. Dr. Anthony Miller has been my mentor since 1987. Our first joint paper, on screening for cervical cancer, was published in 19918. I chose not to respond to individual criticisms, but instead to collect my thoughts and to try to explain why the study authors saw no benefit from screening.Most of the criticism from the radiology community focuses on issues of study design (which they claim was inadequate) and on the quality of the mammography (which they also claim was inadequate). Cancer survivors bolster those criticisms with testimonials and appeals to common sense. Supporters of the study are drawn from the public health community, and they tend to focus on overdiagnosis and health economics.

The report at issue is not the first emerging from the nbss. Earlier reports9,10 were criticized for not having allowed adequate follow-up time. But the 25-year results resemble the early results, and the authors are no longer criticized for premature disclosure. None of the first-generation critics have acknowledged the consistency; instead, they look elsewhere and point out other weaknesses. They claim that high-risk women were assigned to the mammography arm in violation of the principle of randomization. In his bestseller The Emperor of All Maladies, Siddhartha Mukherjee says, as a matter of fact, that high-risk women were assigned surreptitiously to the mammography arm, which explains the lack of observed benefit11.

The most recent nbss report1 tallied the breast cancers that occurred in each of the two study arms after the screening period ended (that is, between years 6 and 25), counting 2584 cancers in the screening arm and 2609 cancers in the control arm. If the screening arm had been enriched for women at “high risk,” that enrichment must have been performed in a peculiar fashion, using only risk factors that have a transient effect. Perhaps Dr. Mukherjee would care to explain what those factors were. It follows that the excess of cancers seen in the screening period (years 1–5: 666 vs. 524) was a result of early diagnosis and not from stacking the deck.

In any case, compelling evidence against the criticism of assignment of high-risk women to the screening arm is provided in the most recent analysis1, and that criticism is no longer raised (although no one has retracted or apologized). Instead, critics now insist that many women with palpable lesions were sent directly to the screening arm by duplicitous research assistants. There is no reason to believe that such actions (which would involve a national conspiracy of dozens of coordinators who spoke two official languages) were taken, but even if they had been, the study and its conclusions would not necessarily be invalidated. Even if all the women with prevalent cancers had been shunted to the screening arm, the situation could still be remedied by ignoring all cancers found at the first screening round (prevalent cancers) and focusing instead on the incident cancers. Such a strategy is not uncommon in screening studies. In the nbss, no woman had the opportunity to “cross the floor” from one study arm to the other after initial assignment. Therefore, if we exclude all prevalent cases from the analysis and focus on women with no cancer at study entry, we can re-evaluate the benefit of mammography thereafter. The hazard ratio for death from breast cancers detected in screening rounds 2–5 was 0.90 (95% confidence interval: 0.69 to 1.16;p = 0.40).

But what about crossover? It is claimed that a certain proportion of the women in the control arm—perhaps as high as 20%—opted for screening off-study, in particular after the screening period was over. That crossover will, some say, eclipse a benefit of screening that might otherwise have ensued. That is, the benefit of mammography (which might well have been substantial) was nullified by a subcohort of independently-minded women who went for mammography at the end of the 5 years. That speculation is fanciful, but if true, should be welcomed, because it can now be said to a patient who, at age 40, requests a mammogram, that there is no hurry; she can come back in 5 years for a mammogram and achieve the same net benefit. And when she comes back at age 45, she can be reprieved again until age 50.

Crossover is a form of contamination that results in misclassification of the exposed and unexposed groups. In a trial, it will tend to bias the result toward the null. The best way to avoid misclassification is to randomize the patients after they agree to participate—as the nbss did. In contrast, in the Swedish two-county trial (discussed in more detail a little later in this article), the subjects were randomized by intention-to-treat—that is, by whether they received or did not receive an invitation to mammography1215. Of the 78,085 women in Sweden who were offered screening, 69,645 accepted and 8440 declined. In effect, then, 8440 women in the Swedish study were de facto misclassified (versus an undisclosed number of hypothetical crossers-over in the Canadian study). The proponents of the Swedish study do not see that misclassification as a shortcoming, but instead use it to buoy their argument in favour of screening. They say that if everybody invited for screening came for screening, then the protective effect would have been more profound. In the Swedish study, all women in the control group were offered a screening test after the screening period ended (a reasonable thing to do); but those authors were not criticized for “contaminating” their study.

The second issue raised concerns the quality of the mammography. After all, the nbss tests were completed 30 years ago using 30-year-old technology. I still wonder how things might have been done differently. Mammography screening identified 212 women with breast cancer who would otherwise have been missed. They had cancers that were, on average, 1.4 cm in size, with 67% being node-negative. The survival of those women was very good. At the end of the study period, 170 women with a nonpalpable mammography-detected breast cancer were alive or had died of other causes. How many of those lives did screening save? Fifty? Twenty-five? Ten? Unfortunately, all we can say is that the number was too few to be noticed. If a significant number of those 170 lives had, in fact, been saved, surely the difference between study arms would have been noticeable. Breast cancer deaths numbered 180 in the mammography group and 171 in the control group. Perhaps some of the survivors believe that their lives were saved. They might perhaps have written a letter to the editor of their local newspaper extolling the virtues of mammography. But 42 women with a nonpalpable mammography-detected cancer died (none of whom has written a letter to the editor).

I am also among the authors of several publications on the benefits of screening by magnetic resonance imaging (mri) in high-risk women1618. Those studies were greeted as successes, given that they demonstrated how, with the use of mri, breast cancers could be downstaged. Those studies were accepted by the radiology community as being supportive of screening. Whether mri reduces mortality has not yet been shown. I cannot predict whether  mri screening will be effective in reducing mortality 10 years down the line, but I fully expect that if a mortality benefit fails to materialize, the studies will be criticized for using 30-year-old equipment and a poor study design.

Much of the criticism of the nbss has come from Drs. Daniel Kopans and László Tabár, and fellow travellers such as Siddhartha Mukherjee and Patrick Borgen27,11. They use the Swedish two-county trial as evidence of a good study that supports the use of mammography and quote a 30% reduction in mortality. Naturally, they do not criticize their canonical study, but it is time to take a closer look.

In the nbss, women were randomized on an individual basis after they had attended the study centre. The result was two groups of equal size and 100% compliance with the first screen. In Sweden, the two counties were divided into 19 geographic strata that were then divided into either 2 blocks (Östergötland) or 3 blocks (Kopparberg). The resulting 45 blocks were randomized, and women in more than half the blocks were sent a letter of invitation to screening. Of the 59% of women who received an invitation, 89% came for the first screen and 83% came for the second screen14.

The Canadian women were offered 5 mammograms 1 year apart. The Swedish women were offered mammograms every 2 years (ages 40–49) or every 3 years (ages 50–74) for up to 8 years. They underwent fewer screens (Table i). The cancers detected by mammography in Canada were similar in size to those detected in Sweden (Table i), but the size of the cancers occurring in the control group were very different. Those comparisons suggest that physical examinations or breast cancer awareness (or both) were important contributors to the size of cancers detected in Canada. A diminution of cancer mortality would not be expected to be associated with a 0.2 cm mean difference in tumour size, but might be expected with a net reduction of 0.7 cm in size19. Of the cancers detected in the screening arm of the Canadian trial, 68% were palpable. That fact has been a source of criticism. But a physical examination was not conducted as part of the screening protocol in Sweden, and the comparable number of palpable tumours was not given. Therefore, given the much longer mean time between screening visits in Sweden, and the high proportion of women in the screening arm that were never screened, I estimate that between 70% and 80% of the cancers in the mammography arm in Sweden would have been palpable and could have been detected by physical examination—had it been done. The fact that the relevant number is not given is a critical lapse. Suppose, for the sake of argument, that 100% of the cancers detected in the screening arm in Sweden were in fact palpable (not a gross exaggeration). What then would be the point of mammographic screening? And if that number (the palpable fraction) is not available, how can the results be judged? Neither the Swedish nor the Canadian trial can exclude the possibility that the benefit from invitation to mammography might have been restricted to women with palpable cancers.

A comparison of key parameters in the Canadian National Breast Screening Study (nbss) and the Swedish two-county trial

The Canadian study reports the number of cancers detected in the follow-up period after the end of the screening period and the number of subsequent deaths from breast cancer. From year 6 to year 25, 2584 incident cancers occurred in the screening group, resulting in 298 deaths (11.5%), and 2609 incident cancers occurred in the control group, resulting in 321 deaths (12.3%). Those data are important because they confirm that, in the absence of screening, the cancer incidence and mortality are equal in the study groups. Where are the comparable numbers for the Swedish study? Again, they are not given. But in looking at the extraordinary Figure 1 from the most recent report of the Swedish study12, the mortality curves are seen to continue to separate at 25 to 29 years after the initiation of screening, and long since screening had stopped.

Tabár and colleagues ask readers to believe that the benefits of mammography are everlasting (or at least for 20 years beyond the end of screening). They make that claim despite having no surety about whether the deaths from breast cancer in years 25–29 were the result of cancers diagnosed during the screening period or diagnosed after screening had stopped. They claim that most of the deaths from breast cancers diagnosed in the control arm occurred more than 10 years after diagnosis. Thus, the reader is asked to accept that a mean of 2.3 mammograms obtained in year 1–7 are more likely than a baseline imbalance in breast cancer risk to lead to a reduction in breast cancer mortality of 30% in years 25–29!

The incidence and mortality rates corresponding to cancers that were diagnosed after the screening trial was stopped are unavailable. Seeing the survival curves corresponding to cases detected in the screened and unscreened cohorts would be interesting. In the nbss, most cancer deaths occurred, as expected, within 10 years from diagnosis1. When the nbss was challenged as to having achieved an even balance in the study groups, the authors provided the relevant data. The Swedish authors should do the same. Patrick Borgen has stated that the  nbss is the “worst clinical trial ever done”5—an extraordinary statement. Either he has devoted his life to poring over medical tracts with the zeal of a Talmudic scholar, or he is speaking nonsense. But refuting his claim is easy: it takes merely the time required to read the Swedish papers.

Once the facts are accepted (that screening mammography fails to do what it was intended to do, and that overdiagnosis is real and substantial), then the most interesting questions can begin to be addressed. Did the nbss  fail because mammography is not a sufficiently sensitive imaging technique? Or has the screening community been working under false premises?

Consider sensitivity. Proponents of mammography say that the technique is currently better than it was in the 1980s, largely because it is more sensitive. (Specificity is also important, but is not at issue here.) They argue that “the more sensitive, the better.” The earlier a cancer can be identified and managed, the better. The smaller, the better. But those contentions generate an interesting paradox. Consider a woman with a small early-stage breast cancer. The recommendation is that this woman be followed with annual bilateral mammography for 5 or more years to identify recurrences and contralateral cancers20. That recommendation is based on the knowledge that the risk of contralateral cancer is between 0.5% and 0.8% annually21 and that a diagnosis of contralateral cancer is associated with an increase in mortality from breast cancer22. (It has not been shown that screening for contralateral cancer reduces mortality.) But mri is a much more sensitive screening tool than mammography, and by using mri in that setting, a small contralateral breast cancer can be identified in 4% of women with newly-diagnosed breast cancer23. And yet routine mri of the contralateral breast is not recommended, because it has not been shown to improve survival. Instead, the recommendation for follow-up with annual mammography continues. The paradox is this: If 8 years’ worth of incident breast cancers can be identified in one shot, why bother to pick them up in dribs and drabs? The mri-detected occult lesions are understood not to be clinically meaningful because they do not adversely affect mortality (overdiagnosis); however, if a similar lesion were to be found as a primary cancer in the ipsilateral breast, the radiologists insist that it is clinically meaningful. Once the paradigm that an increase in sensitivity increases overdiagnosis is accepted (that is, not all lesions are clinically meaningful), then it is the responsibility of clinicians to try to determine the ideal level of sensitivity.

The nbss has been berated for working with 30-year-old machinery, but I think that the greater problem is that clinicians are still working under 30-year-old assumptions. How much is really known about the relationship between size and survival? How confident is our community about early detection? It is universally accepted that tumour size and survival are inversely related for women diagnosed with palpable breast cancer24. That understanding is the rationale for early detection by mammography or other means. But it does not logically follow that a decrease in tumour size will necessarily lead to a decrease in mortality.

Consider two analogous situations. First, among women with breast cancer who experience a local recurrence, the strongest predictor of death is a short time from diagnosis to local recurrence25. However, that finding does not imply that a further shortening of the time from diagnosis to recurrence through intensive imaging would worsen survival. Second, studies of children with neuroblastoma noted that the children diagnosed in the first year of life experienced much better survival than those diagnosed thereafter26. That observation encouraged physicians to consider that screening for neuroblastoma by measuring urinary metabolites would increase the proportion of children diagnosed in the first year and thereby reduce mortality. The resulting clinical trial unfortunately found no benefit27. Neuroblastoma with a favorable prognosis is detectable by screening, but those cases are associated with a very high rate of spontaneous regression or maturation of the neuroblastoma into benign ganglioneuroma. Very few cases of neuroblastoma detected by screening have unfavourable biologic features such as N-Myc amplification28.

The relationship between breast cancer size and survival is not fixed, and the slope of the curve that defines the relationship varies according to the stage and pathologic features of the breast cancer24. The strongest relationship is seen with large cancers and node-positive cancers29. The relationship is attenuated among women with triple-negative cancers, with her2 (human epidermal growth factor receptor 2)–positive cancers, and with BRCA1-positive cancers19,30. Size does not predict mortality well for women with nonpalpable cancers29. Is it possible that there are additional categories wherein the size–survival relationship does not hold, and that eventually every woman with breast cancer will be able to be assigned to one of those categories? If more specific categorization were to be possible, then there would be no expectation of benefit from early detection—through mammography or any other means. In statistical terms, the question is “Are there variables n1, n2, n3, … nx, such that, after adjusting for n1, n2, n3, … nx in a follow-up study, size is no longer predictive of survival?” For example, in a study of 5423 women with cancers of less than 2.0 cm, tumour size was not predictive of survival after adjustment for grade, hormone receptor status, and her2 expression30. Those data suggest that, as the mean size of breast cancers in a population diminishes, further reductions in size can achieve only marginally less benefit. The lesson of mammography should be used to rethink the fundamentals of breast cancer and its natural history so that planning can commence for the experiments and clinical studies that will lead to better outcomes in the future.

 

Curr Oncol. Oct 2014; 21(5): 215–216.  re: Reflections on screening mammography and the early detection of breast cancer   Baum, MD ChM* *Professor Emeritus of Surgery &  Medical Humanities, University College, London, U.K.

I welcome this opportunity to comment on the piece by Dr. Steven Narod in this issue of Current Oncology. His commentary systematically responds to, and rebuts, the near-hysterical reactions to the recent publication of the 25-year follow-up results of the Canadian National Breast Cancer Screening Study1. I admire his restraint in the face of criticisms that go way beyond the boundaries of polite scientific disputation.

Much of the criticism the authors of the trial have faced goes so far as to accuse them of being guilty of scientific misconduct and fraud. Those charges are libellous, but I’m sure that Narod et al. are wise enough not to resolve their differences in a court of law, but simply to open their books to scientific scrutiny, in a way that fair-minded clinicians can judge who are the real culprits. Narod has achieved precisely that end in his timely and measured response. My only criticism is minor … in that he doesn’t go far enough. For example, it could easily be pointed out that the results of the National Breast Cancer Screening Study sit comfortably within the confidence intervals of a Cochrane Collaboration overview of the screening trials, with no hint of heterogeneity2. If anything, the trial in that overview that is closest to being an outlier is the Swedish two-county trial, whose authors are the shrillest of all the critics3.

The debate is so polarized that, leaving aside possible conflicts of interest, the only assumption that can be made is that the clash is one of ideology rather than scientific discourse. In other words, the true believers in the screening dogma will never be persuaded of the error of their ways by data alone, and so when facts don’t fit their prejudice, they resort to ad hominem attacks.

I was one of those who established the first screening centre in London and South East England in 1988, but as an open-minded clinical scientist, I allowed the emerging new data to change my mind. With all due modesty, that is what is called an expression of scientific integrity. Of course, as Narod points out, the prolonged and futile debate merely inhibits real progress on the subject. The importance of breast screening programs lies not in their success, but in their failure. As Huxley put it, “The tragedy of science is the slaying of a beautiful hypothesis by an ugly fact.”

The national breast screening programs around the world have provided us with a natural experiment of the greatest historical importance, not because of their success in reducing breast cancer mortality, but because of the observations that have emerged concerning overdiagnosis of the disease4,5. About two hundred years ago, cancer was defined by its microscopic appearance. With the discovery and use of the modern microscope, the nineteenth century saw the birth of scientific oncology. Rudolf Virchow, often called the founder of cellular pathology, provided the scientific basis for the modern pathologic study of cancer6. As earlier generations had correlated autopsy findings observed with the unaided eye with the clinical course of cancer one hundred years earlier7, so Virchow correlated the microscopic pathology of the disease. However, the material he was studying came from the autopsies of patients dying from cancer. In the mid-nineteenth century, pathology correlations were performed either on cadavers or on living subjects presenting with locally advanced or metastatic disease who were almost always predetermined to die in the absence of effective therapy. Since then, and without pause for thought, the microscopic identification of cancer according to those classical criteria has been associated with the assumed prognosis of fatal disease in the absence of treatment.

A syllogism at the heart of the diagnosis of cancer therefore runs like this: People frequently die from malignant disease. Under the microscope, this malignant disease has many histologic features that we will call “cancer.” Ergo, anything that looks like “cancer” under the microscope will kill you. The screening debacle therefore suggests that some of the earliest stages of “cancer,” if left unperturbed, will not progress to a disease with lethal potential. Those pathologic entities might have microscopic similarity to true cancers, but their appearances alone are insufficient to predict a life-threatening disease.

Conventional mathematical models of cancer growth are linear or logarithmic—in other words, completely predictable at the outset. They predict transition from in situ phases to early invasive, and from early invasive to late invasive over time. Most natural biologic mechanisms are nonlinear or are better described by chaos theory8. Prolonged latency followed by catastrophe should not be all that surprising. We accept the case for prostate cancer, because we know that most elderly men will die with prostate cancer in situ and not of prostate cancer. In fact, the United Kingdom’s national prostate-specific antigen screening trial (protect) is predicated on that fact, with two a priori outcome measures defined: deaths from prostate cancer, and the number of cancers over-detected and treated unnecessarily9.

Next, it is worth noting that, contrary to all common-sense predictions, the increased detection rate of ductal carcinoma in situ has led to an increase in the mastectomy rate for the screened population4,5. Up to 45% of women with a screen-detected case of ductal carcinoma in situ end up undergoing mastectomy because of the multicentricity of the disease10. And yet the paradox is that clinically detected multicentric invasive breast cancer is relatively uncommon11. Surely that is proof enough that at least half the foci of ductal carcinoma in situ will regress if left alone; of course, determining which half remains the problem.

In conclusion, then, it can be stated with a great deal of conviction that a large proportion (on the order of 50%) of screen-detected (preclinical) foci of breast cancer are not programmed to progress if left unperturbed. That observation is of seismic importance and could set the agenda for breast cancer research into the next decade. The choice to ignore those observations, either because they do not support personal prejudice or because of some sleazy political agenda, will result in our community missing an opportunity of a life-time—and that would be unforgivable.

Narod is to be congratulated for his systematic and robust rebuttal of the unjustified attempts to destroy the credibility of the Canadian trial by a small group of vociferous critics who provide a background noise so loud that it nearly drowns out the true signal of the 25-year experiment of population screening for breast cancer.

“There’s non so blind as those that will not see.”— Jonathan Swift, Polite Conversation

Curr Oncol. Oct 2014; 21: 205–207. Screening mammography: the turning of the tide?  W.D. Foulkes, MBBS PhD McGill University, Montreal, Quebec     This issue of Current Oncology features a Counter-currents article by Dr. Steven Narod, “Reflections on screening mammography and the early detection of breast cancer”1, that is accompanied by a commentary from Professor Michael Baum2 supporting Narod’s thesis. Indeed, in Baum’s view, Narod’s only error was not to push home the point that the Canadian National Breast Cancer Screening Study (nbss) is not an outlier among mammography screening studies. He commends Narod for a measured response to the widespread criticism that followed publication of the 25-year follow-up results of the by now notorious nbss.

It seems as if almost everyone has an opinion on screening mammography. Everyone is entitled to an opinion, of course; but discussions about mammographic screening tend to take on a special, almost unique, quality—which perhaps speaks to the investments (financial, psychological, and career) made by many of the protagonists, which Professor Baum fleetingly mentions as potential conflicts of interest in his editorial. Baum prefers to see the ongoing debate—if that is what it is—as a clash of ideologies. But what are these ideologies that are so opposed?

Essentially, Baum’s argument is that the proponents of screening are not really scientists, in the sense that they do not accept refutation of data by data. He could be right, but I think the more parsimonious and psychologically more plausible explanation is that the aforementioned investments are simply too great: the stakes are too high. That the stakes are high is, in my view, very clear. Breast cancer is a common disease, and if population-based screening mammography is shown to have failed and is therefore no longer offered, billions of dollars would be saved every year in the United States alone3.

Narod contrasts the results of two large trials of mammography (one carried out in Sweden, the two-county study) with the nbss data. Having read these carefully laid out arguments, I think that most disinterested, but informed, readers will accept that many of the legion of criticisms that have been placed at the door of the nbss simply do not hold up to scrutiny. But mud sticks, and so many observers who do not like the results of the nbss point again and again to the same “flaws.”

One of Narod’s most telling points is that the survival curves for the two arms of the Swedish trial continue to remain separate up to 29 years after the trial was started. That observation is not consistent with any known effect of mammographic screening. It is much more likely that the populations were simply different to start with.

Further discussion of the pros and cons of these two trials is now fairly pointless. There are not much new data to be had, and I can’t see Drs. Kopans and Tabár, on reading Narod’s article, deciding that perhaps the benefits of mammography have, after all, been overestimated. Without new data, we can’t resolve this critical issue. So perhaps we need to stop the current process and actually do some new research to gather the required data.

A recent Perspective article in the New England Journal of Medicine4 noted the presence of a deep chasm separating women’s views of the likely benefit of mammographic screening and the actual data available. The nongovernmental Swiss Medical Board subsequently determined that women could not make informed decisions about screening without access to more nuanced information. Moreover, the Board felt that the benefits of mammographic screening were likely to be so small that no new screening programs should be introduced and existing programs should be allowed to run down. Their decision caused the expected uproar, but it is interesting to note that the results of a reader poll after a Clinical Decisions article 2 years earlier in the New England Journal of Medicine5 showed that a clear majority did not think that screening mammography should be started at age 40. Those results are contrary to the recommendation of many breast cancer organizations. But on the basis of these newer findings, it seems to me that the tide has turned, insofar as there are now enough interested parties prepared to question the benefits of mammography.

One of the points that Narod makes bears some discussion: He sees the problem not in terms of 30-year-old mammography machines in nbss study, but in 30-year-old thinking about the biology of breast cancer on the part of those who support screening. Logically, it can be seen that, as breast cancers enlarge, the number of cancer cells within them increases, which can provide opportunities for more malignant clones to emerge. Earlier detection will thus prevent those emerging clones from worsening outcomes. This quasi-Halstedian view, that a breast cancer makes a stately progression through biologically distinct and distinguishable stages and that the grade worsens as the tumour enlarges (assumptions that are at the heart of the original explanation of how mammography “works”6), are no longer part of mainstream thinking about breast cancer biology. Even ductal carcinoma in situ seems to possess many of the molecular changes found in invasive breast cancers, albeit at lower frequencies7,8. It seems as if the “die is cast” fairly early in the life of a breast cancer9. Intrinsic subtypes hold true as cancers grow and metastasize10, and the sojourn time varies from subtype to subtype11. Some breast cancers regress12. Others grow very rapidly13. These are not ideal biologic circumstances for the success of an “across the board” screening program. That conclusion is even borne out by a careful examination of the two-county study data14. The one group for whom screening mammography would be hoped to work—women between 40 and 49 years of age with a grade iii breast cancer (a group likely to contribute disproportionately to the observed mortality from breast cancer)—does not seem to achieve any mortality savings (see Figure 20 in Tabár et al.14). Survival at 16 years from randomization was identical in the invited and screened groups (relative risk: 0.95; 95% confidence interval: 0.55 to 1.64). One wonders if, in fact, the shoe is on the other foot. What has been learned about interpreting screening data from the current understanding of the natural history of breast cancer?

On the other side of the ledger, overdiagnosis has emerged in the past several years as a major issue in breast cancer screening. Quantifying the benefits and harms of mammography make for sobering reading by disinterested parties. If one starts with a sample of 1000 U.S. women 50 years of age, and if those women are screened annually for a decade, fewer than 4 women will avoid a breast cancer death; 3–14 women will suffer the consequences of over-diagnosis; and many hundreds will have at least 1 false alarm15. Work by Welch and Frankel suggests that women would think differently about mammographic screening for breast cancer if they were made aware of those figures at time of invitation for screening. Using best estimates, only 1 woman in 4 who develop a screen-detected breast cancer will avoid a breast cancer death16. The other 3 will do just as well, or just as poorly, without screening—or, of more concern, will have been diagnosed with a cancer that was not destined to ever present clinically. In the observational Norwegian study, only one third of the reduction in deaths from breast cancer could be attributed to mammographic screening per se17. Most women with a screen-detected breast cancer are therefore either diagnosed early (but with no effect on outcome) or are overdiagnosed.

We have been here before. Maureen Roberts, director of the Edinburgh breast screening project, died of breast cancer in 1989. While hopeful that mammographic screening would benefit women, she concluded from an analysis of the Edinburgh trial results that it did not. Before she died, she wrote “Breast screening: time for a rethink?” for the British Medical Journal18, concluding, “I feel sad to be writing this; sad because naturally after so many years I am sorry that breast screening may not be of benefit. I am also sad to seem to be critical of the many dear and valued colleagues I’ve worked with over the years, particularly those who have made such a magnificent contribution to the care and welfare of women with breast cancer. But they will recognise that I am telling the truth.”

It is time to work toward a trial of screening mammography that will incorporate variable thresholds, molecular markers, genetic testing, and psychological and physical measures of the effect of overdiagnosis. One of the two authors of the New England Journal of Medicine Perspective article discussed earlier, an ethics representative on the Swiss Medical Board, has argued that there is a moral requirement for a randomized controlled trial of mammography19 based on Welch’s idea of differing detection thresholds. I believe that women will be interested in such a study. But because almost every major U.S. medical organization focusing on breast cancer prevention, diagnosis, or treatment has stated that women should begin undergoing mammography annually from the age of 40 years, will any agency have the courage to fund it?

 
October 07, 2014  Dr. Joe Mercola DC  does a nice review of recent critiques  in   Why So Many Mixed Messages on Mammogram Benefits?
                       Earlier this year, one of the largest and longest studies of mammography to date — involving 90,000 women followed for 25 years — found that mammograms have no impact on breast cancer mortality. The Canadian Breast Screening Trial ll Miller ea 
Over the course of the study, the death rate from breast cancer was virtually identical between those who received an annual mammogram and those who did not, while 22 percent of screen-detected invasive breast cancers were over-diagnosed, leading to unnecessary treatment. The researchers concluded “the data suggest that the value of mammography screening should be reassessed.”2
A Cochrane Collaboration review also found no evidence that mammography screening has an effect on overall mortality, which, taken together, seriously calls into question whether mammography screening really benefits women.3
Public health agencies, however, have been slow to update their recommendations. The American Cancer Society recommends annual mammograms for average-risk women starting at the age of 40, while the US Preventive Services Task Force recommends mammograms every other year starting at age 50
The conflicting recommendations send women mixed messages on whether screening is helpful or harmful, yet, earlier this year the Swiss Medical Board made a clear-cut recommendation: no more systematic mammography.  
Why Did the Swiss Medical Board Do Away with Routine Mammograms? 
After a year of reviewing the available evidence and its implications, the Swiss Medical Board, an independent health technology assessment initiative, noted they became “increasingly concerned” about what they were finding. The “evidence” simply did not back up the global consensus of other experts in the field suggesting that mammograms were safe and capable of saving lives.
        On the contrary, mammography appeared to be preventing only one death for every 1,000 women screened, while causing harm to many more. Their thorough review left them no choice but to recommend that no new systematic mammography screening programs be introduced, and that a time limit should be placed on existing programs.  
In their report, made public in February 2014,4 the Swiss Medical Board also advised that the quality of mammography screening should be evaluated and women should be informed, in a “clear and balanced” way, about the benefits and harms of screening.  
Unfortunately, many women are still unaware that the science backing the health benefits of mammograms is sorely lacking. Instead of being told the truth, women are guilt-tripped into thinking that skipping their yearly mammogram is the height of medical irresponsibility. It can be hard to stand your ground against such tactics.  
      When it comes to cancer prevention, however, many doctors are just as confused and manipulated as the average person on the street because of the relentless industry and media propaganda that downplays or ignores research that dramatically contradicts their profit-based agenda.
Five Facts About Mammograms That Every Woman Should Know
Before your next (or first) mammogram, you may be interested to know the following:

1. Mammograms May Offer Less Benefit Than You Think:

In one survey, most women said they believed mammography reduced the risk of breast cancer deaths by at least half and prevented at least 80 deaths per 1,000 women screened.5 In reality, mammography may, at best, offer a relative risk reduction of 20 percent and prevent in absolute terms only onebreast-cancer death per 10,000 women.

2. Mammography May Increase the Risk of Breast Cancer in Women with a BRCA 1/2 Mutation:

Results published in the British Medical Journal (BMJ) show that women carrying a specific gene mutation called BRCA1/2 (which is linked to breast cancer) are particularly vulnerable to radiation-induced cancer.6

Women carrying this mutation who were exposed to diagnostic radiation (which includes mammograms) before the age of 30 were twice as likely to develop breast cancer, compared to those who did not have the mutated gene. They also found that the radiation-induced cancer was dose-responsive, meaning the greater the dose, the higher the risk of cancer developing.

3. False Positives are Common (and Dangerous)

In the US, the risk of having a false-positive test over 10 mammograms is a concerning 58 percent to 77 percent!78 When a woman is told she may have breast cancer, it causes considerable anxiety and psychological distress. Meanwhile, you will be subjected to more testing, such as biopsy or surgery, which carry their own set of risks, unnecessarily.

4. Mammograms May Not Work if You Have Dense Breasts

Up to 50 percent of women have dense breast tissue, which makes mammograms very difficult to decipher. Dense breast tissue and cancer both appear white on an X-ray, making it nearly impossible for a radiologist to detect cancer in these women. It’s like trying to find a snowflake in a blizzard.

Breast density laws have been passed in California, Connecticut, New York, Virginia, and Texas, making it mandatory for radiologists to inform their patients who have dense breast tissue that mammograms are basically useless for them. A law is now being considered at a federal level as well.

5. There are Other Screening Options

There are other screening options, each with their own strengths and weaknesses, and you have a right to utilize those options.  Remember, only a biopsy can confirm cancer.  Screening tools only aid in the process of showing concern.  

Your Waist Size Is Linked to Your Breast Cancer Risk It’s important to remember that getting a mammogram, if you choose to, is not the same as prevention. In order to truly avoid breast cancer, you need to focus your attention on actual prevention and not just early detection, and one way to do this is by maintaining a healthy weight, and, particularly, a healthy waist size.

Researchers analyzed data from 93,000 mostly overweight post-menopausal women. This included data such as their general health, cancer status, and skirt size (which was used as a gauge of waist size). The latter – skirt size – was strongly linked to breast cancer risk.9 As TIME reported:10

An increase in skirt size was the single most predictive measure of breast cancer risk, the study concluded. When women went up a single skirt size over a 10-year span between their mid-20s and mid-60s, they were shown to have a 33% greater risk of developing breast cancer after menopause. Buying two skirt sizes up during that same period was linked to a 77% increased risk.”

Clothing sizes can be quite ambiguous, of course, with a size 8 in one brand equal to another’s size 10. Yet, the premise that increasing waist size might increase cancer risk is sound. Breast cancer is the most common cancer in women, and obese women are thought to be up to 60 percent more likely to develop cancer than those of normal weight.

The reason for this increased risk is because many breast cancers are fueled by estrogen, a hormone produced in your fat tissue. So the more body fat you have, the more estrogen you’re likely to produce. However, excess fat around your mid-section may be particularly dangerous.

Why Your Waist-to-Hip Ratio Matters     If you have a high waist-to-hip ratio, i.e. you carry more fat around your waist than on your hips, you may be at an increased risk for certain chronic conditions. Certain body compositions do tend to increase your risk of chronic disease, and carrying extra inches around your midsection has been repeatedly shown to increase cardiovascular health risks. Your waist size is also a powerful indicator of insulin sensitivity, as studies clearly show that measuring your waist size is one of the most powerful ways to predict your risk for diabetes, and this could also play a role in cancer as well.

To calculate your waist-to-hip ratio, measure the circumference of your hips at the widest part, across your buttocks, and your waist at the smallest circumference of your natural waist, just above your belly button. Then divide your waist measurement by your hip measurement to get the ratio. (The University of Maryland offers an online waist-to-hip ratio calculator11 you can use.) To determine your waist-to-hip ratio, get a tape measure and record your waist and hip circumference. Then divide your waist circumference by your hip circumference. For a more thorough demonstration, please review the video below.

Waist to Hip Ratio Men Women
Ideal 0.8 0.7
Low Risk <0.95 <0.8
Moderate Risk 0.96-0.99 >0.81 – 0.84
High Risk >1.0 >0.85

  The Sugar Connection  Obesity, including abdominal obesity, is driving up rates of breast cancer in many developed countries. And what is driving up rates of obesity? Many factors, actually, but sugar certainly plays a primary role. There is no shortage of research linking excessive sugar consumption with obesity, and the intake of sugar-sweetened beverages appears to have a particularly strong link. It was more than five years ago when UCLA researchers found that adults who drank at least one sugar-sweetened beverage a day are 27 percent more likely to be overweight or obese.12 Even those who only drank soda occasionally had a 15 percent greater risk.

This is far more than simply an issue of consuming “empty calories,” as sugary drinks, soda, and even fresh-squeezed fruit juice contain fructose, which has been identified as one of the primary culprits in the meteoric rise of obesity and related health problems—in large part due to its ability to turn on your “fat switch.” Alarmingly, research presented at the American Heart Association’s Epidemiology and Prevention/Nutrition, Physical Activity and Metabolism 2013 Scientific Sessions suggested sugary beverages are to blame for about 183,000 deaths worldwide each year, including 133,000 diabetes deaths, 44,000 heart disease deaths, and 6,000 cancer deaths.

About 77 percent of food items in US grocery stores contain added sugar. So it’s no wonder that, while the American Heart Association recommends a daily sugar limit of six teaspoons for women and nine for men, the average American consumes more like 22. If health agencies really wanted to make a dent in breast cancer, they would focus on sharing the truth about sugar (and grains), and their role in obesity and cancer. Unfortunately, breast cancer is big business, and mammography is one of its primary profit centers. This is why the industry is fighting tooth and nail to keep it, even if it means ignoring (or downplaying) the truth.

Avoiding Sugar and Other Top Breast Cancer Prevention Tips   I believe the vast majority of all cancers, including breast cancer, could be prevented by strictly applying basic, commonsense healthy lifestyle strategies, such as the ones below. No available screening method, whether mammography or otherwise, is going to lower your risk of breast cancer… but the tips that follow will:

    • Avoid sugar, especially fructose, and processed foods. All forms of sugar are detrimental to your health in general and tend to promote cancer. Refined fructose, however, is clearly one of the most harmful and should be avoided as much as possible. This automatically means avoiding processed foods, as most are loaded with fructose.
    • Optimize your vitamin D levelsVitamin D influences virtually every cell in your body and is one of nature’s most potent cancer fighters. Vitamin D is actually able to enter cancer cells and trigger apoptosis (programmed cell death). If you have cancer, your vitamin D level should probably be between 70 and 100 ng/ml. Vitamin D works synergistically with every cancer treatment I’m aware of, with no adverse effects. Ideally, your levels should reach this point by exposure to the sun or a tanning bed, with oral vitamin D used as a last resort and balanced by other nutrients like vitamin K2 and magnesium.
    • Limit your protein. Newer research has emphasized the importance of the mTOR pathways. When these are active cancer growth is accelerated. One way to quiet this pathway is by limiting your protein to one gram of protein per kilogram of lean body mass, or roughly a bit less than half a gram of protein per every pound of lean body weight. For most people, this ranges between 40 and 70 grams of protein a day, which is typically about 2/3 to half of what they are currently eating. You can eat 25% more if you are exercising or pregnant.
    • Avoid unfermented soy productsUnfermented soy is high in plant estrogens, or phytoestrogens, also known as isoflavones. In some studies, soy appears to work in concert with human estrogen to increase breast cell proliferation, which increases the chances for mutations and drives the phenotype associated with cancer.
    • Improve your insulin and leptin receptor sensitivity. The best way to do this is by avoiding sugar and grains and restricting carbs to mostly fiber vegetables. Also make sure you are exercising, especially with Peak Fitness.
    • Exercise regularly. One of the primary reasons exercise works to lower your cancer risk is because it drives your insulin levels down, and controlling your insulin levels is one of the most powerful ways to reduce your cancer risks. It’s also been suggested that apoptosis (programmed cell death) is triggered by exercise, causing cancer cells to die in the way nature intended. Studies have also found that the number of tumors decrease along with body fat, which may be an additional factor. This is because exercise helps lower your estrogen levels, which explains why exercise appears to be particularly potent against breast cancer.

In addition to exercise, try to limit your sitting time to three hours a day while taking 10,000 daily steps during your non-exercise hours.

  • Maintain a healthy body weight. This will come naturally when you begin eating right and exercising. It’s important to lose excess body fat because fat produces estrogen, creating a vicious self-perpetuating cycle.
  • Drink a pint to a quart of organic green vegetable juice daily. This is a simple way to get more cancer-fighting nutrients into your diet. Please review my juicing instructions for more detailed information.
  • Get plenty of high-quality, animal-based omega-3 fats, such as krill oil. Omega-3 deficiency is a common underlying factor for cancer.
  • Curcumin. This is the main active ingredient in turmeric and in high concentrations can be very useful adjunct in the treatment of cancer. It actually has the most evidence-based literature supporting its use against cancer of any nutrient, including vitamin D.13 For example, it has demonstrated major therapeutic potential in preventing breast cancer metastasis.14 It’s important to know that curcumin is generally not absorbed that well, so I’ve provided several absorption tips here. Newer preparations have also started to emerge, offering better absorption. For best results, you’ll want to use a sustained-release preparation.
  • Avoid drinking alcohol, or at least limit your alcoholic drinks to one per day.
  • Avoid electromagnetic fields as much as possible. Even electric blankets may increase your cancer risk.
  • Avoid synthetic hormone replacement therapy, especially if you have risk factors for breast cancer. Many forms of breast cancer are estrogen-fueled, and according to a study published in the Journal of the National Cancer Institute, breast cancer rates for women dropped in tandem with decreased use of hormone replacement therapy. (There are similar risks for younger women who use oral contraceptives. Birth control pills, which are also comprised of synthetic hormones, have been linked to cervical and breast cancers.) If you are experiencing excessive menopausal symptoms, you may want to consider bioidentical hormone replacement therapy instead, which uses hormones that are molecularly identical to the ones your body produces and do not wreak havoc on your system. This is a much safer alternative.
  • Avoid BPA, phthalates, and other xenoestrogens. These are estrogen-like compounds that have been linked to increased breast cancer risk.
  • Make sure you’re not iodine deficient, as there’s compelling evidence linking iodine deficiency with certain forms of cancer. Dr. David Brownstein, author of the book Iodine: Why You Need It, Why You Can’t Live Without It, is a proponent of iodine for breast cancer. It actually has potent anticancer properties and has been shown to cause cell death in breast and thyroid cancer cells. For more information, I recommend reading Dr. Brownstein’s book. I have been researching iodine for some time ever since I interviewed Dr. Brownstein, as I do believe that the bulk of what he states is spot on. However, I am not at all convinced that his dosage recommendations are correct. I believe they are far too high.
  • Avoid charring your meats. Charcoal or flame-broiled meat is linked with increased breast cancer risk. Acrylamide—a carcinogen created when starchy foods are baked, roasted, or fried—has been found to increase cancer risk as well.
 
 27 Sept 2014   Three  thoughtful  new reviews, from Universities in Australia (Robin Bell),  Kuwait (Yusuf Luqmani) and Cape Town (Tim Noakes),  highlight the deadly ethical  problem of the myth-based zealous profiteering  Disease Industry promotion in the well of cancer screening,  and the high carbs low fat-low cholesterol  diet, and “statin deficiency” – iatrogenic  “OBSESSIVE-COMPULSIVE DISORDERS ” that profiteers cultivate in the guileless.
       It is not coincidence that the Food and Disease Industry insist that the dangerous high carbs low fat diet they have promoted for the past 40 years, and mass cancer screening for the past >20years , are correct- for the simple perverse reason that such lies pay ie Only Disease Pays. This brings us via  Lupton’s question of Ethics vs Science  in the fraught  narrow parenting domain,  to our everywhere dilemma:  Can Health Science , Human,  Animal and plant  Rights Survive the Onslaught of ruthless commerce and politics?

           Breast screening: an obsessive compulsive disorder.  in Cancer Causes Control. 2014 Jul 11.  Prof Yunus Luqmani  a British oncology biochemist,  Kuwait University writes   “Mammographic screening was  founded on the premises that “it  saves lives”, early is better than late,’  which prevails  in several countries but  controversial since its inception. Findings and interpretation of clinical trials data vary considerably, with disagreement on the outcome and value of such  procedure, not just about the benefits but about the potential harms of mass screening. Many are being screened for the benefit of the few. Even this might be acceptable  but  for concern for many  women with screen detected cancers that will potentially not cause them harm, and who are very likely receiving unnecessary treatment. Many  call for complete cessation of indiscriminate screening if not re-assessment of  age  and periodicity . Of great concern is that screening is being vigorously advocated by many healthcare workers, the media, and lay persons alike without proper awareness or appreciation of the consequences. Although some National leaflets  now present a truer picture, there is   distinct lack of transparency to allow women to distinguish perception from reality and to make informed choices. How many would elect to be screened if they knew that for every one woman who is notionally saved by early detection, anywhere from 2 to 10 otherwise healthy women are being turned into breast cancer patients?  

          Screening mammography – early detection or over-diagnosis     Climacteric. 2014 Sep 16:1-7. Epidemiologist  Prof Robin Bell  Monash University,  Australia examines  benefits and harms of organized screening mammography. Most  recent reduction in breast cancer-specific mortality is explained by use of adjuvant therapy rather than screening mammography. Impact of screening mammography in countries where women present with early disease and have access to adjuvant treatment is modest. There is a wide range of estimates for the magnitude of over-diagnosis. All-cause mortality (rather than breast cancer-specific mortality) should be used when assessing impact of screening as otherwise the harm of cancer treatment in those  over-diagnosed will be missed. Conclusions The benefits and harms of screening mammography are finely balanced. The impact of screening mammography is at best neutral but may result in overall harm. Women should be informed of the issue of over-diagnosis. It is time to review whether organized mammographic screening programs should continue.  
        AND ON DIET:             It is common cause that humans consume their energy requirements from what they can get- and since animal protein is the most costly,  and excess harmful, this means from carbs or fat, of which natural  animal/ dairy/ nut  fat is the most satisfying. So while keeping energy output and adequate animal protein intake  stable, needed energy intake comes from balance of fat and carbs.
       A  major bone of contention locally is the merits of the Banting diet –  in his words,  ‘four meals per day, consisting of meat, greens, fruits, and dry wine’- before the age of mass refined and chemically-and genetically-polluted food and maize-fed livestock.
        Cereals-carbohydrates in his time 160 years ago were thus largely replaced by fresh meat fats and fresh produce. Considering he was born in 1796, his life of  82 years was   almost double the then average lifespan despite his having been severely obese until he found his optimal diet advised by Dr William Harvey based on Professor Claude Bernard’s work on diabetes.
        But Banting was a businessman  of the pre-automobile  era:  unlike labourers, you walked, or you saddled up- without tarmac, coaches were slow. With modern understanding of the importance of avoiding the sedentary lifestyle and overload of both alcohol, salt, refined carbohydrates, protein, and synthetic ie transfats (margarine) , the Banting diet has adapted in modern times  to be optimal for many people for both energizing and keeping slim and well – with its accent on minimal refined/ processed carbs including concentrated cereals,  pure starches, cooked fatty pastries, and commercial fruit juice;
        with high natural fat 50+% as the  ideal brain-muscle-metabolic energy source- from unprocessed meat,  fish, eggs, cream, coconut, butter, cheese;  and modest mixed nuts; matched with copious  greens and other lowstarch rainbow vegetables.
     The futility of low fat (ie high carbs) diet was borne out in the biggest and costliest   -$billion – trial ever- the Women’s Health Initiative  WHI, published in 2006 (Rossouw ea)  and for cancer,  this week (Thomson ea)“Randomized controlled trial of 48,835 postmenopausal women aged 50 to 79 years,  who participated in the WHI Dietary Modification Trial;  randomly assigned to  intervention [40%]) or comparison group  [60%]) in a free-living setting,  enrollment between 1993 and 1998 in 40 US clinical centers; mean follow-up in this analysis was 8.1 years.  Intensive behavior modification in group and individual sessions designed to reduce total fat intake to 20% of calories and increase intakes of vegetables/fruits to 5 servings/d and grains to at least 6 servings/d. The comparison group received diet-related education materials.    “Dietary advice to reduce fat for cancer and cardiovascular disease, stroke or coronary heart disease   prevention after menopause  was not supported in the  WHI.   The diet had no effects on incidence of CHD , stroke ,  or CVD.  In fact  Women with higher baseline fat intake (quartile) had breast cancer risk only  HR-0.76; 0.62, 0.92 during intervention). Thus the highest  fat intake lowered breast cancer risk by 24%There were no intervention effects   ie no benefits of low fat diet on invasive breast 1.08  or colorectal cancer, other cancers, cancer-specific or overall mortality.
 
        and  the WHI (Shikany ea 2006 and 2011further showed direct association of  higher Dietary carbs (glycemic load GL  glycemic index)   and risk of breast cancer and cardiovascular disease risk factors .There was a trend toward significance for the positive association between GL and in situ cancers (1.40, 0.94-2.13; P = 0.07).   GL inversely associated with high-density lipoprotein HDL  cholesterol (P for trend = 0.004) and positively with triglycerides,  total cholesterol (P = 0.018) and low-density lipoprotein cholesterol.
             Professor Tim Noakes  Cape Town keeps on pointing out the lack of science in the perverse western (Ancell Keys)   paradigm of high carbs low fat processed diet (as in the WHI) , with  futile overreliance on  synthetic drugs eg statins,  and appliances, surgery  to reverse the consequent epidemic degenerative diseases- and keep the medical disease industry profitable. .

This brings us to the cutting edge of modernity: Can  Ethics Survive the Onslaught of Science ? (Prof Michael Lupton, Bond University, Australia  2013)?  Can health science  survive the onslaught of perverse incentives, profiteering- the Semmelweis Reflex that denies what is cheap, natural and best?
24 Sept 2014  update after the Angela Jolie hype: This month’s JAMA say it all: the less breast  surgery the better:
                              Use of and Mortality After Bilateral Mastectomy Compared With Other Surgical Treatments for Breast Cancer in California, 1998-2011. Kurian &  Gomez    Stanford Univ.  JAMA. 2014;312:902-914.                Bilateral mastectomy is increasingly used to treat unilateral breast cancer. Because it may have medical and psychosocial complications, a better understanding of its use and outcomes is essential to optimizing cancer care. Conclusions and Relevance  Use of bilateral mastectomy increased significantly throughout California from 1998 through 2011 and with median follow-up of 89 months  was not associated with lower mortality than that achieved with breast-conserving surgery plus radiation. Unilateral mastectomy was associated with higher mortality than were the other 2 surgical options.
Contralateral Prophylactic Mastectomy   Is It a Reasonable Option?         Editorial|Sept 3, 2014     Lisa Newman, Univ Michigan,   JAMA. 2014;312:895-897 The professional oncology community has worked diligently to generate data that facilitate surgical planning and the decision-making process for patients with newly diagnosed breast cancer. Several lines of evidence support the importance of prioritizing treatment of the known cancer over and above consideration of a risk-reducing mastectomy for the unaffected breast (contralateral prophylactic mastectomy [CPM]). For example, the equivalent overall survival for breast-conserving surgery (BCS) and mastectomy makes CPM an unnecessary option for women who are eligible for lumpectomy and desire breast preservation. Incidence of metachronous contralateral breast cancer (ie, contralateral cancer detected several months after initial breast cancer diagnosis) is relatively low, at 0.25% to 1% per year,1,2 and these cancers are usually detected at early, highly curable stages. Synchronous occult contralateral breast cancer is uncommon, as documented by studies revealing incidental cancer in only 1% to 3% of CPM specimens.3,4 Survival is comparable for patients with unilateral vs metachronous bilateral breast cancer5,6 and typically is associated with the stage of first cancer, consistent with the concept that the initially presenting tumor has a lead-time advantage in establishing distant organ micrometastases.
The corollary is obvious:    Less Informed Women With High Anxiety Are More Likely to Choose Bilateral Mastectomy for Breast Cancer  San Francisco Cancer Symposium  PracticeUpdate Editorial Team, 2014 Sept   Women with higher anxiety levels and less knowledge about breast cancer recurrence and survival are more likely to choose bilateral mastectomy ,    Katharine Yao, MD, of  University of Chicago  stated, “There is so much information about breast cancer that it’s easy for patients to get overwhelmed. As doctors, we have to be aware of each patient’s knowledge level and the concerns and worries he or she has. We need to do a better job of educating patients that the risk of developing contralateral breast cancer is actually low and that breast cancer can come back in other parts of the body no matter what type of surgery they have.”    Overall, 59% of patients chose lumpectomy, 32% unilateral mastectomy, and 9% CPM. Eighty-three (58%) considered CPM, and 12 (21%) of this latter group chose CPM contralateral prophylactic mastectomy.
 
11 August 2014  The current SA Menopause Society newsletter says:

Benefits of mammography

“the benefits of screening mammography are modest at best” (Elmore & Harris BMJ 2014;348:g3824). This is the conclusion after the latest research to come out of Norway where the introduction of screening has been gradually introduced over the last 2 decades (Weedon-Fekjaer et al BMJ 2014;348:g3701).The Norwegian authorities invited women between 50 and 70 years old to attend for screening every second year and looked at before and after death rates from breast cancer. They found RELATIVE risk reduction of 28% in those invited compared with those not invited to be screened. Without knowing the ACTUAL risk reduction or the harms of screening this sounds like a “good deal”. However it is an observational study not a randomised trial and therefore susceptible to various biases.For women to make up their own minds about screening, actual figures of benefits and harms need to be given because without accuracy perceived dangers and benefits are very far from reality. For example in the US or UK asking women about their estimates of breast cancer deaths – taking 1000 women aged 50 and following them for 20 years – gave the following results:

Of 1000, number
alive after 20 years
Deaths from
breast cancer
Deaths from
other causes
Women’s estimates
without screening
801 160 39
with screening 881 80 39
In reality
without screening
956 5 39
with screening 956-7 4 39-40

Women believe that breast cancer is a far greater threat than it really is. They also believe that screening halves such risk.

If actual death reductions from breast cancer are taken into account, screening benefits are modest at best and if all cause deaths are taken into account the benefits all but disappear.

20 July 2014 Two new papers from Scandinavia highlight the harms of screening mammography.:

Clin Adv Hematol Oncol. 2014 June;12:407-11    Screening mammography:   do the benefits always outweigh the harms?  Brodersen J, Jørgensen KJ, Brawley OW.

APMIS. 2014 May 26. doi: 10.1111/apm.12278.
Overdiagnosis: How cancer screening can turn indolent pathology into illness.    Brodersen J1, Schwartz LM, Woloshin S. The shift from illness to disease has had a profound impact on modern medicine – particularly in the realm of cancer screening. In screening, it is not patients with illness who seek help from the healthcare system; it is asymptomatic healthy individuals who are invited into the healthcare system to be examined for pathology. The underlying assumption of screening is that abnormalities and pathology always progress. If this were true, it would always make sense to look for disease even when people feel well. The million (or more accurately multi-billion) dollar question is whether the fundamental assumption that disease invariably leads to illness is valid. This is the question that the present paper will try to explore and answer.
The current Wiki article on Cancer Screening    firmly denies benefit for screening for silent prostate cancer;  and for xray screening mammography it  firmly questions  the benefit in lives saved versus the harms of screening.  The balance for screening mammogram is summed up by Wiki : “The phenomenon of finding pre-invasive malignancy or nonmalignant benign disease is commonplace in all forms of cancer screening, including pap smears for cervical cancer, fecal occult blood testing for colon cancer, and prostate-specific antigen testing for prostate cancer. All of these tests have the potential to detect asymptomatic cancers, and all of them have a high rate of false positives and lead to invasive procedures that are unlikely to benefit the patient.”
                Reality  remains that, in average  lean  well adults ie without obvious risks , the only screening justified is regular noninvasive SELF- EXAMINATION of breast, skin, testes, electronic bloodpressure; and professional optometric, dental,  skin and bloodpressure screening and, if suspicious, urine multistix exam.  By contrast, regular xray (chest or  mammogram- cumulative radiation risk) and pelvic  internal exams are highly invasive, thus indicated only for symptomatic or familial-risk cases. .
PEER (perverse) PRESSURE, Beliefs, perceptions, indoctrination –  by peer bodies, Corporates like Hospitals and Big Pharma, Regulators,  Accredition Bodies and dangled incentives – which obviously have commercial group vested self-interests  –  die hard:                                     Prev Med. 2014 Jul 16.Miller JW1,  Goff BA ea .  CDC & Washington State University, USA,   studied Physicians’ Beliefs about Effectiveness of Cancer Screening Tests: National Survey of Family Physicians, General Internists, and Obstetrician-Gynecologists(excluding breast radiologists, pathologists,  and oncologist/surgeons). RESULTS: of   1574 respondents-   62% response rate- the majority agreed with the effectiveness of: mammography aged 50-69 years, Pap tests  aged 21-65 years, and colonoscopy for aged ≥50 years.  Physicians typically listed their respective specialty organizations as a top influence for screening  recommendations.  CONCLUSIONS: There were several substantial inconsistencies between physician beliefs in the effectiveness of cancer screening tests and the actual evidence of these tests’ effectiveness which can lead both to underuse and overuse of cancer screening tests.
    This outcome obviously damns professional bodies in respect at least of the evidence discouraging  screening mammography of well breasts.
   Its as Soren Kierkegaard wrote 150 years ago about religious conviction- the difficulty of following ethical theistic belief against the majority tide of convenience and venality;
  and Steven Jay Gould’s Non-Overlapping Magisteria of Science and Religion- for some (but not all), the difficulty of reconciling apparent scientific medical evidence (is it ever immutable? ) with belief, dogma- whether from mythical (is it always?)  religious belief, or simply vested interest.
       As we were taught 50 years ago, if new medical discoveries stand the test of time – they often dont-  it takes a generation for  the majority to accept, apply them. Almost two generations of women have now been martyred by repetitive screening xray mammography. Must it take yet another generation before such barbaric screening is abandoned? As Winwood Reade  and AC Grayling philosophized, countless millions have suffered genocide, holocaust in the post-Greko-Roman “enlightened”  two  millennia for vested interests in the guise of religious let alone medical dogma  .
14 July 2014:  BASTILLE DAY CLARION CALL FOR TRUTH TO PROTECT WOMEN:      Screening mammography & Bambi  This column reported these issues a few months ago (see Dr Gerd Gigerenzer PhD  below in May, and April 16, 2014  from the Swiss Medical Board: Abolishing Mammography Screening Programs? ), but they are worth repeating from Groote Schuur Hospital.  A professor of Obstets and Gyne there writes in the current South African Menopause Matters  news email (“an  editorial opinion that does not necessarily represent the views of  SAMS”) :
(the answer to his question: Whatever happened to Evidence-Based medicine? is quite simple: if  it doesnt pay, then evade, deny and mock the evidence, or better, shoot the messenger who dares blow the whistle on  inconvenient truth. )

The Professor writes: “Screening mammography is an emotive subject. Correctly so, because if it did clearly have more benefits than harms then it should be advocated, promoted and sold as an intervention in every woman’s interest.

      Regrettably screening mammography does not clearly have more benefits than harms and given that it is an unpleasant and costly process it should not be promoted. Both the protagonists and the antagonists claim ample facts supporting their arguments while finding fault with the others’ data. One of the latest trial outcomes from Canada (Miller et al BMJ 2014;348:g366) reports on a large group of women (nearly 90 000) who were randomised to mammography annually for 5 years or annual physical breast examination. This took place in the 1980s and the women were in their 50s and were followed up for 25 years.

Diagnoses of breast cancer and deaths from the disease were collected from national databases, as were all-cause mortality figures. The researchers showed that during the 5 years of mammography (or not) more women were diagnosed with breast cancer in the mammography arm (and treated) but the deaths were not significantly different in the two groups. Similarly over the entire study period there were more cancers diagnosed in the mammography arm but the number of deaths were similar, with the conclusion that mammography was not superior to annual examinations and resulted in overdiagnoses.

This is essentially a negative outcome if “deaths avoided” or “lives saved” are taken as the end points. Maybe modern screening techniques work better but also maybe better treatments have reduced mortality rates. The most recent Cochrane Review suggests that if 1000 women aged 50 were screened for 10 years then 4 women would die from breast cancer. Without screening 5 would die.

If the group’s deaths from any cancer are counted then the results are 21 per 1000 with or without mammography. So does mammography screening save lives? The supposed benefit?

If the harms are tallied for the same 1000 women then 100 in the mammography arm would have a false positive-evaluation and 5 would have an unnecessary partial or complete breast removal (Gøtzche et al Cochrane Reviews 2013;6:CD001877). The financial and convenience costs are not commented on.

Yet screening mammography is treated like a religion. Any suggestion to curtail its promotion is seen as “unfair to women” or not doing “the right thing”. A bit like Bambi bashing. How can something so obviously right be challenged?

Nowhere are the facts more disguised than in breast cancer screening pamphlets (Gigerenzer BMJ 2014;348:g2636). The data are presented without numbers ”Most doctors feel that early detection tests for breast cancer save thousands of lives each year” or as relative risk reduction with the difference between 4 and 5 deaths per 1000 being a “20% reduction in deaths”. A final fallacy of the leaflets is extrapolating ahead where 1 life saved over a decade means 2.5 lives over 25 years which is not supported by the data.

No wonder 98% of women in France, Germany and the Netherlands overestimate the benefit of screening by a factor of 10, 100 or more, or do not know. They get much of their information from leaflets – put out by people whose likelihoods depend on screening – which are blatantly misleading. Advertising of medicines is not allowed to make claims that cannot be backed up by evidence, so why can screening pamphlets?

These semi-facts promote beliefs that screening prevents or reduces the risk of breast cancer and saves many lives through the early detection of aggressive tumours. These beliefs are not valid according to an independent Swiss group reporting in a lead article in NEJM (Biller-Andorno & Jüni 2014;370:1965-7) which states that public health programmes that do not produce more benefits than harms are hard to justify ethically – like mammography screening.

Their report caused an uproar because it challenges a tightly held myth – like the existence of Bambi.    What has happened to evidence-based medicine?

Menopause Matters is a monthly review of matters menopausal that have recently appeared in the journals. It is produced for the South African Menopause Society by Athol Kent and the summaries concentrate on clinical issues although some underlying patho-physiology will be included to ensure a scientific basis for the work. It does not necessarily reflect the views of SAMS or its managementf
15 June 2014 this month:  SMALL BENEFITS, SUBSTANTIAL HARMS WITH MAMMOGRAPHY SCREENING  is a trenchant review by Prof Cornelia Baines breast clinician from Canada on why xray screening mammography does well breasts and women far more harm than good.                Prof Stephen  Duffy statistician at UCL argues the reverse.

DIET RISKS FOR BREAST CANCER:

already 30 years ago Seely and Horrobin in Diet and breast cancer: possible connection with sugar consumption hypothesized: younger and older women (possibly pre- and post-menopausal women) differ with respect to such correlations. In older women a strong correlation was found between breast cancer mortality and sugar consumption (correlation coefficient = 0.9).. In younger women the correlation with diet is weak. A possible connecting link between sugar consumption and breast cancer is insulin. This is an absolute requirement for the proliferation of normal mammary tissue and experimental mammary tumours may regress in its absence. Insulin secretion occurs in response to blood glucose level and could be excessive if the regulatory mechanism is overtaxed by large sugar intake. The same mechanism might account for the increased risk of mammary cancer in diabetics.
  A  major Nurses’ Health decades-long Study  review from Harvard shows no relationship between fat intake and breast cancer.
By contrast, studies from  Mexican  2004,  Canada 2005, Italy 2006 , and New York  2009 confirm direct association between sugar intake and breast cancer. . Only a study from Denmark 2005  shows no relationship.
Hence the HighFat LowCarbs (William Banting 1863) diet is now established by the rigorous scientific references of the past 150 years  assembled by science writer Gary Taubes in The Diet Delusion ,  and advised to all  for prevention and management of obesity and all other common major diseases including breast and all cancers.
      As investigative journalists write recently, like Taubes and rational scientists the past 50years,  the major cause of all common chronic degenerative disease including cancer and immunoincompetence is not fat but refined carbs – the root cause of the SACCHARINE DISEASES  that Cleave, Campbell, Burkitt reported occurring in pastoral tribes converting to the western commercialized diet of sugar, refined cereals and rice .                   They note that in the Mouse Cancer Study in cancer-prone mice, 2011,  which claimed that high (fat)cholesterol intake promotes breast cancer, the control mice  (not major carnivores but omnivores) were fed a balanced natural chow with 4.5% fat, 23% protein, and 50% carbohydrate, whereas the test mice were fed a totally synthetic chow meant to represent a western human  cholesterolemic  diet: 20% fat, 17% protein, and 48% carbohydrate. So in fact the high risk factor for cancer and all disease was not the higher fat intake (20%  as dairy fat) vs 4.5%- from fish meal and soy/cereals) but the 48% carbs (2/3  sucrose, 15% (malto)dextrins -which absorb as rapidly as glucose) intake and 19% casein (a major health problem)   in the test chow. They failed to include a control group on what is natural mouse diet ie free of refined carbs and milk :  “RSPCA 2014:   Wild mice – opportunistic omnivores- will eat a wide variety of seeds, grains, and other plant material as well as invertebrates, small vertebrates and carrion”. Thus plenty of natural seed/grain fats and mixed protein and plant carbs,  zero sugar or refined carbs- ie the Banting diet. ..
A new 18year observational  followup  study from Sweden last year in 62000 people assessed total energy intake – carbohydrate  from median 61 to 39% , protein 11 to 19% , and  fat 27 to 42% . LCHP scores were positively related to intake of animal protein, but negatively related to plant protein. For carbohydrate and fat, associations were consistent in sucrose and whole grain and saturated and unsaturated fat, respectively. Across the range of macronutrients, there was no clear significant trend for particular cancers. This is not surprising as the intake of carbs range d from 40 to 60% and fat from 27 to 42%. Thus no cohort was on a highfat low carbs ketogenic diet as Banting, Noakes  et al find successful. . the lowest % carbs group at best had similar fat % intake ie there was no low-carbs cohort taking below 30% carbs..There is a vast difference in calorie intake  between their “optimal’  LCHP 42:40 fat:carbs ie 1:1  , versus the  true ketogenic HifatLowcarbs diet of eg 50:<30 fat:carbs ie >1.66:1.
       Allowing up to 20% protein in total energy intake, fat may need to  be  close to 50% energy and carbs below 30%, thus ensuring ketogenesis to shed excess fat and avoid depositing more glycogen and adiposity ; so eg for a 2000kcal/day  diet, thats  up to 100gms protein 400kcal mostly from flesh and nuts; carbs below 150gms 600kcal (in nuts and  rainbow vegs) , and fat up to 1000 kcal ie 110gms from cream (not milk), nuts, avo, eggs, butter, cheese and fatty flesh. .

It is no wonder the public is confused.

The truth of more than four decades worth of research is now very clear: the potential benefit of mammography screening is small and the harms are substantial at all ages, but especially so for women in their 40s.

The bottom line is that mammography screening, implemented to reduce breast cancer deaths due to earlier detection of breast cancer, has been eclipsed by therapy and increased awareness.

- See more at: http://umanitoba.ca/outreach/evidencenetwork/archives/4490#sthash.rf9YcMYp.dpuf

It is no wonder the public is confused.

The truth of more than four decades worth of research is now very clear: the potential benefit of mammography screening is small and the harms are substantial at all ages, but especially so for women in their 40s.

The bottom line is that mammography screening, implemented to reduce breast cancer deaths due to earlier detection of breast cancer, has been eclipsed by therapy and increased awareness.

- See more at: http://umanitoba.ca/outreach/evidencenetwork/archives/4490#sthash.rf9YcMYp.dp

VITAMIN INTAKE AND BREAST CANCER:

VITAMIN C  each 100mg/day increment reduces allcause mortality by 27%, and breast cancer mortality by 22%:   a metaanalysis by the Karolinska- Harris ea   last month found 10 trials of vitamin C use and intake  in breast cancer, included 17,696 breast cancer cases, 2791 total deaths, and 1558 breast cancer-specific deaths. The summary RR (95% CI) for post-diagnosis vitamin C supplement use was 0.81 (95% CI 0.72-0.91) for total mortality and 0.85 (95% CI 0.74-0.99) for breast cancer-specific mortality. The summary RR for a 100mg per day increase in dietary vitamin C intake was 0.73 (95% CI 0.59-0.89) for total mortality and 0.78 (95% CI 0.64-0.94) for breast cancer-specific mortality- ie 25% lower mortality for every 100mg higher daily vit C intake..

VITAMIN D AND BREAST CANCER:
20 years  ago Newmark from Sloan Kettering NY wrote :  High dietary fat increases mammary epithelial cell proliferation, particularly the “hormonally driven” hyperproliferation during breast growth and development in young animals. Increased dietary calcium (and probably vitamin D) lessens the increase of proliferation induced by high fat. These data, although limited, suggest that the maximum effect of diet (high fat increase, as well as calcium and vitamin D modulation) on eventual breast cancer may be during puberty, and adolescence, when the mammary gland is actively growing and developing. (3) An inverse epidemiological correlation exists between sunlight availability as a source of vitamin D and the risk of breast cancer in the U.S. and Canada. (4) Current vitamin D and calcium dietary intake in the U.S. is far below the RDA in all female age groups, particularly for the elderly. (5) Reduction of breast cancer risk, and simultaneously osteoporosis, might be achieved by increasing dietary intake of calcium and vitamin D to RDA levels. This may be particularly applicable to females during puberty and adolescence.
                    20 years later we now still find:                 Vitamin D and Cancer: The promise not yet fulfilled(California) ; and is there a link (France)?

BUT The Vitamin D Council    sums up the study evidence eg in a major Brit J Cancer metaanalysis last month of 30 prospective studies in 32000 BRCA  patients, and a Chinese study a year ago,   show  that  those with highest  vitamin D levels have 50-90% lower risk of  breast cancer risk, and mortality, and the chance of breast cancer spreading.  so far all they can recommend is that  vitamin D dose should for a robust adult not exceed        10 000iu/day, or pro rata at longer intervals eg 150 000iu a fortnight.  Compared to those with the lowest quartile of plasma 25(OH)D level, women with highest quartile 25(OH)D level showed a significant decreased breast cancer risk (Q4 vs.Q1: OR = 0.10, 95% CI = 0.06–0.15) and every 1 ng/ml increment of plasma 25(OH)D level led to a 16% lower odds of breast cancer.

         It is likely that- given the limits on vitamin C intake due to diarrhoea, and cost, and bloating-  increments in vit D3 intake above the current mediocre 400iu/d norm- up to the generally well-tolerated 10 000iu/day, with supplement of vitamin K2-  will give even better benefit against breast cancer than vitamin C.     
                                                                                                                               
20 May 2014 BREASTS TO KILL: KILLER BRAS
          For the past 4 years, Sure Touch examiners  have observed that many women who wear underwired bras have a string of pearl – fibrous lumps- where the bra wire cuts into them inferiorly; and sometimes radially under the ‘ spokes’ of the bra cups.  We have not yet detected a cancer in such symmetrical  lumpiness, which we find diminishes with change to a soft bra and healing massage with Lugols iodine, coconut oil and DMSO.
          This bra risk   was postulated  in  the book  Dressed To Kill: The Link Between Breast Cancer and Bras(1995, 2005), (NaturalNews).     
Dr Joe Mercola muses: ” Would you believe that two of the nation’s most prominent cancer organizations are completely disinterested in a common wardrobe practice that studies suggest could be a leading cause of breast cancer in women? Wearing bras, says the book  ,appears to be a common trigger of this harrowing disease, yet the American Cancer Society (ACS) and the Susan G. Komen Foundation continue to deny any link between the two.
            ” Authors Sydney Ross Singer and Soma Grismaijer, husband and wife medical anthropologists, have conducted extensive research into the link between bras and breast cancer. They are convinced that the lymphatic constriction imposed by wearing bras prevents women’s bodies from effectively clearing out toxins and other waste, leading to an accumulation of these cancer-causing substances. Bras can also cut off circulatory flow within the body, leading to other health problems.
              “[B]ecause lymphatic vessels are very thin, they are extremely sensitive to pressure and are easily compressed,” the Singers are quoted as saying, noting that the perpetual use of bras over the course of several decades can eventually lead to cancer. “Less oxygen and fewer nutrients are delivered to the cells, while waste products are not flushed away.”
             These are powerful claims, and science seems to back them. Based on an analysis comparing women who wear bras to those who don’t, breast cancer risk was found to be significantly higher among women in the former group. At the same time, women who do not wear bras have about the same risk of developing breast cancer as the average man does, which is not very high.
               Beginning in 1991, the Singers initiated a 30-month “Bra and Breast Cancer” study that evaluated roughly 4,000 women from five major U.S. cities. All the women were Caucasian and came from mostly middle-income homes, ranging in age from 30 to 79. About half of them had previously been diagnosed with breast cancer.After determining the bra-wearing habits of all the women, the Singers determined that wearing a bra increases a woman’s risk of developing breast cancer by double. Shockingly, wearing a bra to sleep at night is even worse, with three out of four, or 75 percent, of women who engage in this practice regularly developing the condition.
                 “Women who want to avoid breast cancer should wear a bra for the shortest period of time possible — certainly for less than 12 hours daily,” said Sydney Singer, as quoted by HealingCancerNaturally.com.     One would think that such information would be pertinent to Komen and other cancer organizations, which are purportedly raising money to find a cure. But the Singers and others have never been able to get their attention, with both Komen and the ACS denying any link between bras and breast cancer.So the Singers are calling on women everywhere to not only boycott supporting these organizations, but also to send over their bras whenever they are asked for money. Awareness about the potential dangers of wearing bras should at least be acknowledged by these groups that claim to support cancer awareness, and yet the response of ACS and Komen on the issue has been less than acceptable.
           “Because of this unscientific stonewalling of this information,” Singer wrote, “over the past 20 years 2,000,000 women in the US alone have gotten breast cancer who may have prevented it by simply loosening their bra and wearing it less time each day.”
             To learn more about Dressed To Kill, visit:
http://www.killerculture.com.
19  May 2014 update:  Dr Gerd Gigerenzer PhD, professor at a number of top USA and German institutions and expert in uncertainty, heuristic problem-solving, writes: This One Graphic Will Change the Way You Look at Breast Cancer Screening:  The most trenchant reasoning against screening xray mammography this year is in  Time Magazine 1 May 2014;  which he argues definitely applies to screening mammography: he details four tricks used by zealous proponents of screening mammography to infamously  persuade gullible women why ““If you haven’t had a mammogram, you need more than your breasts examined.”  These tricks are as follows, but are debunked  by the absolute facts in his Fact Box below. He says:

“First, look at the benefit. Out of every thousand women aged 50 and older, five without screening died from breast cancer, compared to four in the screening group. This is an absolute reduction of 1 in 1,000. In fact, it might even be an optimistic estimate because the Canadian follow-up study of women for 25 years after these trials found no reduction at all. But the exact number is not my point here. What I want to explain is how women are being misled.

Trick #1: State that screening reduces breast cancer mortality by 20% or more, because it sounds more impressive than explaining that the absolute risk reduction is 1 in 1,000.   This trick has been used for years in pamphlets. You might think, well, it’s not much, but at least one life is saved. But even that is not true. The number of deaths from all cancers, breast cancer included, is the same in both groups, as seen in line two of the fact box.            And that leads us to                                                                                                                             trick #2: Don’t mention that mammography screening doesn’t reduce the chance of dying from cancer. Talk only about the reduction in dying from breast cancer.      Often, and particularly if a person had multiple cancers, the exact cause of death is unclear. For this reason, total cancer mortality is the more reliable information when you look at it in terms of the larger goal: saving lives. In plain words, there is no evidence to date that routine mammography screening saves lives.             Now let’s look at the harms.

Trick #3: Don’t tell women about unnecessary surgery, biopsies and other harms from overtreatment. If you are asked, play these down.            The first way a mammogram can harm women is if it comes back with a false positive, leading to invasive and unnecessary biopsies. This isn’t the rare fluke most people seem to think it is. This happens to about a hundred out of every thousand women who participated in screening. Legions of women have suffered from this procedure and the related anxieties. After false alarms, many worried for months, developing sleeping problems and affecting relationships with family and friends.

Second, not all breast cancers are life-threatening. Women who have a nonprogressive or slowly growing form that they would never have noticed during their lifetime often undergo lumpectomy, mastectomy, toxic chemotherapy or other interventions that have no benefit for them and that are often accompanied with damaging side-effects. This happened to about five women out of a thousand who participated in screening.

The final trick #4    Tell women about increased survival. For instance, “If you participate in screening and breast cancer is detected, your survival rate is 98%.” Don’t mention mortality.

1 May 2014 update:  Dr Iona Heath FRCP, past president of the New Zealand Royal College of GPs ,  says in March that  Breast cancer mammography screening causes more harm than good.  Dr Kurt Kroenke from Univ Indiana two weeks ago  wrote That most screening test results will be normal or negative is commonplace, but the reality that abnormal results are frequently false-positive is not always well appreciated, nor is it fully conveyed to patients. How does a patient feel after a false-positive test result? Tosteson and colleagues1 concluded from their longitudinal study that “false-positive mammograms are associated with a measurable, small, and transient effect on personal anxiety.” However, a closer look at all the outcomes assessed in this well-done study reveal some adverse consequences that, although not serious, may nonetheless be meaningful.
          Given the harms of  screening, the Spanish consortium sum it up nicely last February:  Optimal (mammography)  screening is characterized by quinquennial or triennial periodicities for the low or moderate risk-groups and annual periodicity for the high-risk group.   This last group  is in reality tiny.                                                                                                                                                                    
        As this ongoing Woman’s Care column  stresses, very few well women at any age justify screening mammography, or any screening beyond thorough annual review and bloodpressure  and breast exam check. Only if the annual checkup, with  the examining clinician’s concern about clinical breast feel, or the woman’s  breast symptoms (which in fact rarely originate in the breast and are mostly easily resolved) raise suspicions, may some sort of  no-xray breast imaging be justified- soft SureTouch or ultrasound, or no-touch thermography .  No woman without an obvious  growing solitary breast lump or nipple bleeding/ discharge warrants the harms of initial xray screening mammogram.
                                                                                                                                                                        Unlike Bone Density  Screening available on request,  Sure Touch Breast screening is not charged for since it is part of a proper professional clinical consultation- which can be booked for any regular workday. It is the expert clinical consultation, and any necessary advised evidence-based   natural breast supplements and other changes for prevention, that are billed- obviously at viable market rates, but reduced on justified request based on usual means test.
Breast imaging on its own, without expert clinical assessment and advice , is hazardous because it may cause unwarranted concern and lead to the fearsome  and costly invasive cascade; and because breast imaging without thorough risk factor assessment including expert clinical exam may miss disease that justifies further steps if not immediate resolution.
                                                                                                                                                                HOW TO AVOID UNSETTLING, HARMING WOMEN?  As applies to unjustified mass prostate screening of well men, two new relevant publications below this month highlight the widening gap around MASS BREAST MAMMOGRAPHY SCREENING, between realist  holists- independent  Swiss reviewers  looking at the welfare of women and the real cost-benefits  of  breast screening till now – versus the burn & cut-at-any-cost  screening-industry Dutch career  radiologists’ and cancer experts’  vested-interest view looking solely at breast cancer deaths 2004-5, like most for-profit breast -career specialists   targeting every last well breast from 40years upwards.
The latest Cochrane metanalysis  2013   “found that breast cancer mortality was an unreliable outcome that was biased in favour of screening, mainly because of differential misclassification of cause of death.”
                                                                                                                                                                       Boston San Francisco- Illinois and Spanish- Catalonia-  universities’  reviewers recently make a less in-your-face case  against universal mass mammography screening,  rather selective screening frequency based on individualized risk factors and  potential harms.. But they dont refer to equally effective non-xray imaging techniques; or the fact that no imaging techniques except tissue histology can confirm or exclude cancer. .
                                                                                                                                                                against: DO NO HARM:  April 16, 2014 / NEJM  Perspective   from the Swiss Medical Board: Abolishing Mammography Screening Programs?          Nikola Biller-Andorno, and Peter Jüni, http://www.nejm.org/doi/full/10.1056/NEJMp1401875?query=TOC      In January 2013, the Health Ministers of the Swiss Cantons, the Swiss Medical Association, and the Swiss Academy of Medical Sciences mandated the Swiss Medical Board (a medical ethicist,  a clinical epidemiologist, a clinical pharmacologist, an oncologic surgeon, a nurse scientist, a lawyer, and a health economist), an independent health technology assessment initiative,  to prepare a review of mammography screening.We were aware of the controversies that have surrounded mammography screening for the past 10 to 15 years. When we reviewed the available evidence and contemplated its implications in detail, however, we became increasingly concerned.
          First, we noticed that the ongoing debate was based on a series of reanalyses of the same, predominantly outdated trials. The first trial started 50 years ago in New York City and the last  in 1991 in the United Kingdom.1 None of these trials were initiated in the era of modern breast-cancer treatment, which has dramatically improved the prognosis of women with breast cancer. Could the modest benefit of mammography screening in terms of breast-cancer mortality that was shown in trials initiated between 1963 and 1991 still be detected in a trial conducted today?
                                                                                                                                                                      
             Second, we were struck by how nonobvious it was that the benefits of mammography screening outweighed the harms. The relative risk reduction of approximately 20% in breast-cancer mortality associated with mammography that is currently described by most expert panels2 came at the price of a considerable diagnostic cascade, with repeat mammography, subsequent biopsies, and overdiagnosis of breast cancers — cancers that would never have become clinically apparent. The recently published extended follow-up of the Canadian National Breast Screening Study is likely to provide reliable estimates of the extent of overdiagnosis. After 25 years of follow-up, it found that 106 of 484 screen-detected cancers (21.9%) were overdiagnosed.3 This means that 106 of the 44,925 healthy women in the screening group were diagnosed with and treated for breast cancer unnecessarily, which resulted in needless surgical interventions, radiotherapy, chemotherapy, or some combination of these therapies.
      In addition, a Cochrane review of 10 trials involving more than 600,000 women showed no evidence of mammography screening benefit  on overall mortality.1 In the best case, the small reduction in breast-cancer deaths was attenuated by deaths from other causes. In the worst case, the reduction was canceled out by deaths caused by coexisting conditions or by the harms of screening and associated overtreatment. Did the available evidence, taken together, indicate that mammography screening indeed benefits women?
                                                                                                                                                                        
      Third, we were disconcerted by the discrepancy between women’s perceptions of the benefits of mammography screening and the benefits to be expected in reality. The figure  Women’s Perceptions of the Effects of Mammography Screening on Breast-Cancer Mortality as Compared with the Actual Effects. shows the numbers of 50-year-old women in the United States expected to be alive, to die from breast cancer, or to die from other causes if they are invited to undergo regular mammography every 2 years over a 10-year period, as compared with women who do not undergo mammography. The numbers in Panel A are derived from a survey about U.S. women’s perceptions,4 in which 717 of 1003 women (71.5%) said they believed that mammography reduced the risk of breast-cancer deaths by at least half, and 723 women (72.1%) thought that at least 80 deaths would be prevented per 1000 women who were invited for screening. The numbers in Panel B reflect the most likely scenarios according to available trials1-3: a relative risk reduction of 20% and prevention of 1 breast-cancer death. The data for Switzerland, reported in the same study, show similarly overly optimistic expectations. How can women make an informed decision if they overestimate the benefit of mammography so grossly?
                                                                                                                                                                        
      The Swiss Medical Board’s report was made public on February 2, 2014 . It acknowledged that systematic mammography screening might prevent about one death attributed to breast cancer for every 1000 women screened, even though there was no evidence to suggest that overall mortality was affected. At the same time, it emphasized the harm — in particular, false positive test results and the risk of overdiagnosis. For every breast-cancer death prevented in U.S. women over a 10-year course of annual screening beginning at 50 years of age, 490 to 670 women are likely to have a false positive mammogram with repeat examination; 70 to 100, an unnecessary biopsy; and 3 to 14, an overdiagnosed breast cancer that would never have become clinically apparent.5 The board therefore recommended that no new systematic mammography screening programs be introduced and that a time limit be placed on existing programs. In addition, it stipulated that the quality of all forms of mammography screening should be evaluated and that clear and balanced information should be provided to women regarding the benefits and harms of screening.
The report caused uproar and was emphatically rejected by a number of Swiss cancer experts and organizations, some of which called the conclusions “unethical.” One of the main arguments used against it was that it contradicted the global consensus of leading experts in the field — a criticism that made us appreciate our unprejudiced perspective resulting from our lack of exposure to past consensus-building efforts by specialists in breast-cancer screening. Another argument was that the report unsettled women, but we wonder how to avoid unsettling women, given the available evidence.
The Swiss Medical Board is nongovernmental, and its recommendations are not legally binding. Therefore, it is unclear whether the report will have any effect on the policies in our country. Although Switzerland is a small country, there are notable differences among regions, with the French- and Italian-speaking cantons being much more in favor of screening programs than the German-speaking cantons — a finding suggesting that cultural factors need to be taken into account. Eleven of the 26 Swiss cantons have systematic mammography screening programs for women 50 years of age or older; two of these programs were introduced only last year. One German-speaking canton, Uri, is reconsidering its decision to start a mammography screening program in light of the board’s recommendations. Participation in existing programs ranges from 30 to 60% — variation that can be partially explained by the coexistence of opportunistic screening offered by physicians in private practice. At least three quarters of all Swiss women 50 years of age or older have had a mammogram at least once in their life. Health insurers are required to cover mammography as part of systematic screening programs or within the framework of diagnostic workups of potential breast disease.
                                                                                                                                                                              

     It is easy to promote mammography screening if the majority of women believe that it prevents or reduces the risk of getting breast cancer and saves many lives through early detection of aggressive tumors.4 We would be in favor of mammography screening if these beliefs were valid. Unfortunately, they are not, and we believe that women need to be told so. From an ethical perspective, a public health program that does not clearly produce more benefits than harms is hard to justify. Providing clear, unbiased information, promoting appropriate care, and preventing overdiagnosis and overtreatment would be a better choice.

from the  Universities of Zurich &  Bern,  Switzerland; and   Harvard Medical School, Boston . Dr. Biller-Andorno is a member of the expert panel of the Swiss Medical Board; Dr. Jüni was a member of the panel until August 30, 2013

                                                                                                                                                                      FOR-SCREENING- FOR CAREER/PROFIT :  do the maximum: 
Breast. 2014 Apr 5.  Breast cancer screening halves the risk of breast cancer death: A case-referent study. Paap E, Verbeek AL,Broeders MJ ea.  Netherlands Breast Screening Centres.   Large-scale epidemiologic studies have consistently demonstrated the effectiveness of mammographic screening programs, however the benefits are still subject to debate. We estimated the effect of the Dutch screening program on breast cancer mortality. In a large multi-region case-referent study, we identified all breast cancer deaths in 2004 and 2005 in women aged 50-75 who had been invited for screening (cases). Cases were individually matched to referents from the population invited to screening. A total of 1233 cases and 2090 referents were included in this study. We found a 58% reduction in breast cancer mortality in screened versus unscreened women (adjusted OR = 0.42, 95% CI 0.33-0.53). Screening, i.e. early detection and treatment, has resulted in a substantial reduction in breast cancer mortality, indicating that the Dutch breast cancer screening program is highly effective.
                                                                                                                                                                 update  23 March 2014: Caroline Huang at the  Ethox Centre at Oxford writes in   Screening mammography: benefits, harms, and evidence-based guidelines in the US and UK:   The Ethox Centre is a multidisciplinary bioethics research centre in the University of Oxford’s Nuffield Department of Population Health.“Authors Bleyer and Welch claim there has been only an 8% reduction in late-stage breast cancer diagnoses (an absolute reduction of 8 cases per 100,000 women), and while mortality has decreased, it appears that most of the benefit has come from better treatment rather than better screening. (For cancer screening to be considered effective, the US National Cancer Institute says that cancer deaths and late-stage cancer diagnoses should decrease, while early-stage cancer diagnoses should increase.[2])
Contrast these findings to another mammography study published the same week in The Lancet, conducted by an independent panel in the UK as a meta-analysis of 11 randomized trials.[3] The panel estimated overdiagnosis of early-stage breast cancers in the UK to be between 11 and 19%. Crucially, though, there appeared to be a 20% mortality benefit from screening alone.What might account for these significantly different estimations of breast cancer screening effectiveness? The most obvious factor is the frequency and age at which average-risk women are offered mammography. In the UK, women ages 50-70 are offered screening every three years through the NHS Breast Cancer Screening Programme. In the US, women ages 40-70 are typically offered screening every one or two years.      
                      Though a 2009 US Preventive Services Task Force (USPSTF) report recommended that average-risk women should receive screening from ages 50-74 every two years,[4] this recommendation has been not been adopted by professional organizations such as the American Cancer Society, the American College of Radiologists, and the National Cancer Institute. In fact, a study published in November in Preventive Medicine showed that there has been no difference in mammograms provided across any age groups in the US since the 2009 USPSTF report was published.[5]These two studies (and many others preceding them) raise plenty of practical questions about diagnostic thresholds, benefits of population screening, limitations of current radiology technologies, and understanding of which cancers do and do not become invasive. But I want to raise a broader question: should there be an ethical imperative compelling different US professional groups that address the same disease or disorder to adopt a common set of evidence-based guidelines?                                                                                                                                                       
          And if there isn’t, then what is the value of having a group like the USPSTF to issue recommendations that may ultimately be ignored by its target audiences?A few reasons for adopting a common set of evidence-based guidelines might be reducing patient and provider confusion, enhancing low-cost access to care, and potentially redistributing funds to further the reach of proven services or improve research. While the National Breast Cancer Screening Programme requires only the NHS to adopt and implement new recommendations, the more fragmented US system means that screening is not organized by a single body and thus involves competing recommendations that could confuse patients trying to make informed choices and providers trying to assist them in doing so. Additionally, because US insurers are increasingly moving towards funding only evidence-based services, having a common set of guidelines would help ensure that providers’ recommended services are covered under patients’ insurance rather than falling into a category of services with questionable benefit that might not be covered. This is perhaps not the optimal ethical consideration to have to make, but it is a necessary component of realistic preventive care. Finally, at the health system level, providing mammograms only to women ages 50-74 might mean that resources currently allocated to mammograms for women ages 40-49 could be put towards more mammograms for women ages 50-74 or other related preventive health services or research.Despite these reasons, however, it would be equally problematic to remove clinical groups’ ability to disagree with recommendations that they believe result from poor statistics or faulty logic. It also does not seem like there is intrinsic opposition to adopting recommendations produced by independent panels or other clinical groups.   
                                                                                                                                                                        The same Preventive Medicine study discussed above references two cases in which recommendations resulted in immediate changes to screening patterns: (1) the National Cancer Institute and American Cancer Society’s 1997 recommendation that mammography be expanded to women ages 40-49 resulted in increased screening, and (2) the USPSTF’s 2008 recommendation against prostate cancer screening in men ages 75 and older resulted in fewer early-stage prostate cancer diagnoses. So the USPSTF has not always been unsuccessful in having its recommendations taken seriously, even in a case where less screening is recommended, and at least one breast cancer screening recommendation has previously had a quick adoption in practice.These cases – as well as the USPSTF 2002 recommendation that originally suggested offering mammography to women ages 40-49 once every 1-2 years, which is reflected in current clinician groups’ guidelines – suggest that the USPSTF’s target audiences aren’t willfully ignoring meta-analyses of available data. Rather, clinicians, advocacy groups, and patients have questioned the methodology behind the 2009 USPSTF recommendation, in a similar fashion to the critiques being raised over the NEJM study.                                                                                
                                                                                                                                                                        
               For example, the American College of Radiology suggested that Bleyer and Welch failed to properly account for an increasing incidence of invasive late-stage breast cancers unrelated to screening uptake.[6] In light of this information, we might reframe the second question to ‘How do we ensure that groups like the USPSTF incorporate the right kind of data into their analyses and recommendations?’ That answer might have to do with rethinking how consultation with relevant clinical and patient advocacy groups is carried out, as well as examining a broader range of data sources. To circle back to the contrast between the NEJM and Lancet findings, it is important to think about how and why the UK’s National Breast Cancer Screening Programme seems to have lower rates of overdiagnosis and greater mortality benefit from screening relative to the US screening system.                                                                                                                                                                                                                                                                             At the very least, these kinds of contradictory non-US outcomes should prompt a re-evaluation of which kinds of evidence we have chosen to evaluate.We might also point to the discourse around prostate-specific antigen (PSA) testing – which has been linked to overdiagnosis of early-stage, non-invasive prostate cancer – as one model for where breast cancer screening recommendations may go. Importantly, while clinical organizations have not reached consensus in whether PSA testing should be recommended as a yearly exam for men over 50,[7] they do agree that a careful discussion of PSA testing’s potential harms and benefits is always appropriate.Indeed, the authors of both the Lancet and NEJM articles conclude with similar thoughts: physicians must initiate conversations about the pros and cons of mammography so that patients can make informed choices. That assertion seems uncontroversial enough to be accepted by the various professional groups involved – so perhaps any common set of guidelines we should expect groups to adopt should relate to the communication of evidence rather than potentially controversial or insufficient evidence itself.”
                                                                                                                                                                      15/3/ 2014 update: Great Mammography Debate :  Dr. Patrick Borgen, Chairman of Surgery at Maimonides Medical Center in Brooklyn, New York, talks about the role of screening mammography, a topic bracketed by strong opinions. It has been a particular focus of discussion at the 31st Annual Miami Breast Cancer Conference, held March 6 through March 9, 2014, in Miami, Florida.

               Commentary  The mammography debate is one of the facets of the Miami Breast Cancer Conference this year.   It seems as though the field of breast cancer has always been controversial, going back half a century, and breast cancer is a disease that, more than most others, is very polarizing. This disease engenders great passion—and great debate, which has been ongoing about the role of screening mammography.

            A few weeks ago, The New York Times covered an article that was published in the British Medical Journal 1 about the Canadian National Breast Screening Study. On the surface, this study failed to show any benefit from mammography. That was the story that the writer, Gina Kolata, picked up and ran with. Ms. Kolata had written about her own experience with breast cancer a number of years ago; her breast cancer had not been picked up on a mammogram, and so she is somewhat biased.

               In short, the Canadian study evaluated mammograms from more than 90,000 women who had very primitive mammograms between 1980 and 1984, and that is really the first problem with this study: the technology and the equipment then was incredibly limited, such that the mammograms only showed 30% of breast cancers; whereas, today, mammography detects 70% to 80% of breast cancers. Thus, taking results generated by technology from 34 years ago and making a conclusion about them in today’s world is a stretch.

One of the fundamental flaws of the Canadian study, besides the dated technology on which the conclusions were based, was that it was not randomized. Nurses, and, in some provinces in Canada, doctors, did a clinical breast exam, and, if they felt a mass or a lump, they preferentially put the patient into the mammography arm. That is what I would have done in their place; if I felt a lump, I would not be willing to send someone home.

By the end of the study, there were more than 100 extra breast cancers in the mammography arm and more breast cancers that had spread to lymph nodes in the mammography arm. And, in fact, the chance of dying of breast cancer was higher in the mammography arm.

All of the authorities with whom I have ever spoken or read who have reviewed this study dismiss it as very flawed. A number of the doctors who were involved with the study resigned their positions in protest. Despite all of that, The New York Times ran an article headlined, “Vast Study Casts Doubts on Value of Mammograms” (February 11, 2014).

Well, it is a vastly flawed study, and, in fact, there are six other, much larger and much better controlled studies, all of which showed a reduction in breast cancer mortality from 20% up to 40% in women who have mammograms—and that is certainly what we observe clinically.

We felt that it was important to really highlight this at the Miami Breast Cancer Conference this year. My guess is that our audience already knows this; but, what we would like to give them is the science about why the Canadian study was flawed so that they can talk to their patients and talk to their colleagues who may not be in the breast cancer field. That is really what I think our mission is for part of this year’s conference.

We think that this is dangerous information. We think that women will unnecessarily lose their lives to breast cancer if they forego mammography, which this study frankly says one should. I have a busy practice in Brooklyn, New York, and, at least once or twice a week, I see someone, without any question, whose life was saved by a mammogram.

I think that we all agree we need something better than mammography. We all agree that mammography can lead to over-diagnosis of breast cancers, and over-diagnosis happens, of course, when we screen for diseases in other areas of the body. We all accept this limitation.

But, for a major media outlet to take a single study that was deeply flawed and not even mention the existence of other studies, even as a point–counterpoint, I think was a bit outrageous!

12 March 2014 this publication on the Huffington Post website  today under screening mammography is as appropriate as when it was published in 2010:

The NBCAM has assured women that “early (mammography) detection results in a cure nearly 100 percent of the time.” More specifically, the NBCAM is directed to claims for reducing the incidence and mortality of breast cancer through early detection by annual mammography starting at age 40. Moreover, mammograms can miss cancers in premenopausal women due to the density of their breasts, and also fail to detect cancers smaller than half an inch.

Still denied by the ACS is clear evidence that premenopausal mammography poses significant risks of breast cancer. The routine practice of taking two films annually for each breast results in approximately 0.5 rad (radiation absorbed dose) exposure. This is about 500 times the dose from a single chest X-ray and is broadly focused on the entire chest rather than narrowly on the breast. This is also 25 times higher than is allowed by the Environmental Protection Agency for whole-body radiation from local nuclear industries (0.02 rad). Moreover, the breast is the most sensitive organ to ionizing radiation.

As warned by the prestigious National Academy of Sciences in 1972 but still ignored by the ACS, the premenopausal breast is highly sensitive to the risks of cancer from mammography, as each rad exposure increases the risks of breast cancer by 1 percent. This results in a cumulative 10 percent increased risk for each breast following a decade of routine screening. This can also accounts for the 19-percent increased incidence of breast cancer since 1975. Not surprisingly, the prestigious U.S. Preventive Task Force, supported by the National Breast Cancer Coalition, warned last year against routine premenopausal mammography. Also, not surprisingly, routine premenopausal mammography is practiced by no nation other than the U.S.

Risks of premenopausal mammography are some four-fold greater for the 2 percent of women who are carriers of the A-T gene (ataxia telangiectasia) and are highly sensitive to the carcinogenic effects of radiation. By some estimates, this accounts for up to 20 percent of all breast cancers diagnosed annually. Compounding these problems, missed cancers are common in premenopausal women due to the density of their breasts.

That most breast cancers are first recognized by women was admitted by the ACS in 1985. “We must keep in mind that at least 90 percent of the women who develop breast cancer discover the tumors themselves.” Furthermore, an analysis of several 1993 studies showed that women who regularly performed breast self-examination (BSE) detected their cancers much earlier than women failing to examine themselves. The effectiveness of BSE, however, depends on training by skilled professionals, enhanced by an annual clinical breast examination. Nevertheless, in spite of such evidence, the ACS dismisses BSE, and claims that “no studies have clearly shown [its] benefit.”

As reported in our 1999 publication in the International Journal of Health Services, an article in a leading Massachusetts newspaper featured a photograph of two women in their twenties. The article promised that early detection by mammography results in a cure “nearly 100 percent of the time.” Questioned by journalist Kate Dempsey, an ACS communications director responded: “The ad isn’t based on a study. When you make an advertisement, you just say what you can to get women in the door. You exaggerate a point — Mammography today is a lucrative [and] highly competitive business.”

If all 20 million U.S. premenopausal women submitted to annual mammograms, the minimal annual costs would be $2.5 billion. Such costs would be increased some fourfold if the industry, supported by radiologists, succeeds in its efforts to replace film machines, costing about $100,000, with high-tech digital machines, costing over $400,000, even in the absence of any evidence for their improved effectiveness.

With this background, it is hardly surprising that the National Breast Cancer Awareness Month neglects to inform women how they can reduce their risks of breast cancer. In fact, we know a great deal about its avoidable causes which remain ignored by the ACS. These include:

    • Prolonged use of the Pill, and estrogen replacement therapy.
    • Prolonged consumption of milk from cows injected with a genetically engineered growth hormone to increase milk production. This milk is contaminated with high levels of a natural growth factor, which increases risks of breast cancer by up to seven-fold.
    • High consumption of meat, as it is contaminated with potent natural or synthetic estrogens. These are routinely implanted in cattle before entry into feedlots, about 100 days prior to slaughter, to increase muscle mass and profits for the meat industry.
    • Prolonged exposure to a wide range of hormonal ingredients in conventional cosmetics and personal care products.
  • Living near hazardous waste sites, petrochemical plants, power lines, and nuclear plants.

The enthusiastic and continuing support of premenopausal mammography by the ACS is hardly surprising in view of its major conflicts of interest that still remain unrecognized. Five radiologists have served as ACS presidents. In its every move, the ACS promotes the interests of the major manufacturers of mammogram machines and films, including Siemens, DuPont, General Electric, Eastman Kodak and Piker. The mammography industry also conducts research for the ACS, serves on its advisory boards, and donates considerable funds. DuPont is also a substantial backer of the ACS Breast Health Awareness Program. It sponsors television shows touting mammography; produces advertising, promotional materials and literature for hospitals and doctor; and lobbies Congress for legislation promoting the availability of mammography. The ACS has been and remains strongly linked with the mammography industry, while ignoring or criticizing the value of breast self-examination, even following training by a qualified nurse or clinician.

The ACS conflicts of interest extend well beyond the mammography industry. The ACS has received contributions in excess of $100,000 from a wide range of “Excalibur (industry) Donors,” who manufacture carcinogenic products. These include petrochemical companies (DuPont, BP and Pennzoil), Big Pharma (AstraZenceca, Bristol Myers Squibb, GlaxoSmithKline, Merck & Company and Novartis), and cosmetic companies (Christian Dior, Avon, Revlon and Elizabeth Arden).

Samuel S. Epstein, M.D. is professor emeritus of Environmental and Occupational Medicine at the University of Illinois at Chicago School of Public Health; Chairman of the Cancer Prevention Coalition; and a former President of the Rachel Carson Trust. His awards include the 1998 Right Livelihood Award and the 2005 Albert Schweitzer Golden Grand Medal for International Contributions to Cancer Prevention. Dr. Epstein has authored 270 scientific articles and 20 books on cancer prevention, including the groundbreaking “The Politics of Cancer” (1979), and most recently “Toxic Beauty” (2009, Benbella Books: http://www.benbellabooks.com) about carcinogens, besides other toxic ingredients, in cosmetics and personal care products. Email: epstein@uic.edu. Web: http://www.preventcancer.com.

update 6 March 2014    Switzerland debates dismantling its breast cancer screening programme   BMJ 2014;348:g1625   “A row has erupted in Switzerland after the Swiss Medical Board  recommended that the country’s mammography screening programme for breast cancer be suspended because it leads to too many unnecessary interventions.
              In a report made public on 2 February, the board said that while systematic mammography screening for breast cancer saved 1-2 women’s lives for every 1000 screened, it led to unnecessary investigations and treatment for around 100 women in every 1000.1 “The desirable effect is offset by the undesirable effects,” said the report, which was based on study data from 1963 to 1991   comparing 1000 women who were screened with 1000 women who were not. The report also concluded that screening was not cost effective.…”

update 1 Mar 2014   Supporting informed decision making when clinical evidence and conventional wisdom, clash.   The nub of the screening mammography war – and all hard-sell marketing hype-  is elegantly analyzed by a USA multiUniversity Communications team in Against conventional wisdom: when the public, the media, and medical practice collide.       Jakob Jensen ea argue that “the screening mammography  controversy was driven by the systematic removal of uncertainty from science communication. To increase comprehension and adherence, health information communicators remove caveats, limitations, and hedging so science appears simple and more certain. This streamlining process is, in many instances, initiated by researchers as they engage in dissemination of their findings, and  is facilitated by public relations professionals, journalists, public health practitioners, and others whose tasks involve using the results from research for specific purposes.   Uncertainty is removed from public communication because many communicators believe that it is difficult for people to process and/or that it is something the audience wants to avoid. Uncertainty management theory posits that people can find meaning and value in uncertainty.                  CONCLUSIONS: Science is routinely simplified as it is prepared for public consumption.     In line with the model of information overload, this practice may increase short-term adherence to recommendations at the expense  of long-term message consistency and trust in science”. 

          The Mammography Saves Lives  screening campaign  was and is to recruit all older women to regular screening; it  was progressively oversold   by removing, ignoring the science uncertainty. “Science is routinely simplified as it is prepared for public consumption. In line with the model of information overload, this practice may increase short-term adherence to recommendations at the expense of long-term message consistency and trust in science”.


We see the same collusion between corporate marketeers and government regulators in so many high-profit industries:
  on Pubmed,  screening mammography features for 50 years, and continued to expand exponentially without hindrance until enough epidemiologists – led by the Cochrane Group- collectively  rang enough alarm bells the past decade. The zealous huge-profit USA  radiology-oncology industry simply shouted down the negative result of the massive Canadian Screening Mammography trial outcome   30 years ago in 90 000 women, and continue to do so with the 25year results now reported. The huge Breast Industry retaliates by threatening whistle blowers.

*at the same time around 50years ago, as many of us were starting medical studies, Keys and Stamler  et al in USA did bad epidemiological studies that subverted the facts of  healthy indigenous diets around Europe, Africa and Asia, and the healthy traditional English-speaking (USA and the British Empire) working population’s mainly fresh meat/fish  fat and farm produce diet,
      to claim that the reverse be promoted-  factory-produced low fat low cholesterol high carbohydrate (cereals, potato, white flour and white rice) –  and worse, quadrupling of fructose and sucrose intake, with increasing obesity;   and then noxious statins- for-all for the resultant carbs-inducedlipidemia “epidemic”;  and the  dangerous hypoglycemic drugs for mushrooming type 2 diabetes, and NSAIDs for arthritis; and numerous wannabe antiobesity drugs; and finally the new industry of bariatric surgery!.
        see the classic expose books: John Gofman’s  Preventing Breast Cancer 1996; James le Fanu ‘s  The Rise and Fall of Modern Medicine 1999 ; Gary Taubes’ The Diet Delusion (2007);  Ben Goldacre’s Bad Pharma 2012 and Peter Gotzsche’s Mammography Screening: Truth, Lies and Controversy 2013

*and as a result,  the past 30years,- against all rational food  science and biology – Montsanto’s Government- approved  rape  of healthy food agriculture by genetically modified crops laced with toxic environmentally persistent glyphosate C3H8NO5P- Roundup.

It is no irony that one of the leading medical scientists of the 20th century Dr John Gofman took part in  the Manhattan  nuclear Project, was a pioneer of VLDL lipidology, and then an activist for protecting women against the accumulating harm of mammography – “there is no safe dose of radiation”.

 at Exam. Resulting Risk of Mammogram-Induced Breast Cancer. 1998
Any age in 1 exam: 1 chance in about 1,100.
30-34 range. 5 exams: 5 chances/1100, or 1 chance in 220.
Any age in 1 exam: 1 chance in about 1,900.
35-49 range. 10 exams: 10 chances/1900, or 1 chance in 190.
Any age in 1 exam: 1 chance in about 2,000.
50-64 range. 15 exams: 15 chances/2,000, or 1 chance in 133.

Dr Emily Transue MD eloquently describes her personal disillusionment with screening mammography.

                                                                                                                                                                                     update 23 Feb 2014     Like Wikipedia on breast screening, Karen Kaplan in the L.A.Times this week challenges mammography radiologists: stop lying to patients about the benefits of screening mammography. As Dr David Katz in the Huffington Post muses, can we unmuddle mammography?                                                                            The USA National Cancer Association promotion conspicuously avoids mentioning the equal balance between benefits and risks of screening mammography, 
and Dr Charles Wright in the Toronto Globe and Mail  says   “It’s time for a new approach to mammograms  
     The New York Times review this week turns the report of the Canadian trial to focus on the importance of breast self-examination; their other review  agrees that  Vast Study Casts Doubts on Value of Mammograms.
It is damning that Cochrane studies   (which date from about 1994) -for mammography published only since year 2000 – have consistently found that screening mammography imaging has no material longterm survival benefit for women with apparently normal breasts, with numerous potential harms.
      The question remains, should people  without suspicious cancer  symptoms or bad family history  have any invasive screening (of breast and prostate) beyond regular appropriate physical examination? when all of us should follow  sensible lifestyle, diet and appropriate supplements to minimize both acute and chronic diseases, and thus die well in old age.
                If women without apparent high risk  will not be satisfied by clinical reassurance, prescreening  image recording without compression irradiation will depend on what is locally available.
The USA National Cancer Institute at the NIH , while dutifully promoting regular screening mammography, negates their promotion by listing  precisely  7 lines,  one benefit : Early detection of breast cancer with screening mammography means that treatment can be started earlier in the course of the disease, possibly before it has spread. Results from randomized clinical trials and other studies show that screening mammography may  reduce the number of deaths from breast cancer among women ages 40 to 70, especially for those over age 50..
            But it lists 46 lines of potential harms:” What are some of the potential harms of screening mammograms?      
1. “Finding cancer early doesnt  reduce a woman’s chance of dying from breast cancer or any cause. Even though mammograms can detect malignant tumors that cannot be felt, treating a small tumor does not always mean that the woman will not die from the cancer. A fast-growing or aggressive cancer may have already spread to other parts of the body before it is detected.                                                              
2. Fear: “Women with such detected  early tumors live a longer period of time fearing that they likely have a fatal disease… screening mammograms dont help prolong the life of a woman who is suffering from other, more life-threatening health conditions. Depression anxiety let alone suicide are increased .
3. “False-negative results occur when mammograms appear normal even though breast cancer is present. Overall, screening mammos miss about 20% of breast cancers that are present at the time of screening.. from  high breast density i.e., glandular tissue and connective tissue, together known as fibroglandular tissue) and fatty tissue.  Because fibroglandular tissue and tumors have similar density, tumors can be harder to detect in women with denser breasts more often among younger women than among older women because younger women are more likely to have dense breasts. As a woman ages, her breasts usually become more fatty, and false-negative results become less likely. False-negative results can lead to delays in treatment and a false sense of security for affected women.                              
4. “False-positive results occur when radiologists decide mammograms are abnormal but no cancer is actually present. All abnormal mammograms should be followed up with additional testing (diagnostic mammograms, ultrasound, and/or biopsy) to determine whether cancer is present… more common for younger women, women who have had previous breast biopsies, women with a family history of breast cancer, and women who are taking estrogen (for example, menopausal hormone therapy).        False-positive mammogram results can lead to anxiety and other forms of psychological distress in affected women. The additional testing required to rule out cancer can also be costly and time consuming and can cause physical discomfort. .                                                                                                            
5. “Overdiagnosis and overtreatment. Screening mammograms can find cancers and cases of ductal carcinoma in situ (DCIS, noninvasive tumor  cells that may become cancerous build up in the lining of breast ducts) that need to be treated. However, they can also find cancers and cases of DCIS that will never cause symptoms or threaten a woman’s life, leading to “overdiagnosis” of breast cancer. Treatment of these latter cancers and cases of DCIS is not needed leads to “overtreatment.” Overtreatment exposes women unnecessarily to the adverse effects associated with cancer therapy.      Because doctors often cannot distinguish cancers and cases of DCIS that need to be treated from those that do not, they overtreat .                                                                                                                              
6. “Radiation exposure. Mammograms require very small doses of radiation. The risk of harm from this radiation exposure is extremely low, but repeated x-rays have the potential to cause cancer. 

They fail to list other adverse effects:                                                                                       7. Pain and bruising of crush mammography- sometimes prolonged;                     8. spreading early and likely dormant cancer.                                                                   9. Increased incidence of breast cancer and thus more irradiation, mastectomy and all-cause mortality, and                                                                                                              10. complications of surgery, radiotherapy and chemotherapy.                                                 ………………………..

           the Rapid Responses to the 25year  Breast cancer incidence and mortality of the Canadian National Breast Screening Study show again the Great Divide between objective  epidemiological evidence,  and vested-interest belief by those whose careers and incomes depend on zealous pursuit of early (pre)cancers.
                 Prof Michael Baum as a former UK Screening Mammography leader again trenchantly quotes reality to protect women from terrorism by screening mammography and mastectomy, in particular urging the same policy of watchful waiting to see the natural course of early  cancer-   that has saved so many men from harmful diagnostic and therapeutic invasion of asymptomatic prostate cancer.
                  We must stress that, if the patient refuses or is denied conventional oncotherapy, Watchful Waiting should always be supported including by all possible improvements in multibeneficial diet, lifestyle and supplements, and avoidance of cancer-promoting estrogenics .
…………………………………….
     Women who choose not to have mammography and oncotherapy for highly suspicious lumps or even advancing cancers, or have been classified by cancer clinics  as too advanced for oncotherapy- told they have very short life expectancy- illustrate the lesson of watchful waiting with active intervention. We  see surprising regression in breast lumps, breast cancer and quality life extension in those who refuse to accept the oncologists’  death predictions  and who apply strong faith and  some of the many evidence-based changes and preventative natural supplement remedies we have  collated,    before or  even after the gamut /  gauntlet  of crush mammography, biopsy, surgery and radio-chemotherapy.
                                                                                                                                                           update 21 Feb 2014 The Oncologist publishes epidemiologist Archie Bleyer’s   “Were Our Estimates of Overdiagnosis With Mammography Screening in the United States Based on Faulty Science”?   rebuttal of radiologist Prof Daniel Kopans’  denial of the overdiagnosis of breast cancer.
        The point Bleyer again makes is that women have the choice provided they are fully informed of the pros and cons, and the options to screening mammography  and biopsy.
                 16 Feb 2014 update:   a slew of new papers reinforces the futility and hazards of mammography screening for early breast cancer- and the divide between the vested interests of mammographers/ oncologists – those who make their living from finding every possible cancer-  and the welfare of women:
                    Natural News today reviews criticisms of mammography from USA.
   in  NEJM 13 Feb , 2014,       Lisa Rosenbaum MD , Univ Pensylvania:  sums up the dilemma of real but unprofitable evidence vs profiteering, culture  and feeling  : Misfearing” — Culture, Identity, and Our Perceptions of Health Risks  Despite knowing that heart disease kills more women each year than all cancers combined, most women fear breast cancer far more — and their health-related behavior reflects this difference. If our sense of risk is less about fact than about feeling, how do we adjust it?
                
BMJ Feb 11,  2014: 25year  Breast cancer incidence and mortality of the Canadian National Breast Screening Study: randomised screening trial   Anthony  Miller, Cornelia  Baines, Steven  Nar ea,  compared breast cancer incidence and mortality up to 25 years later  in 89 835 volunteer women aged 40-59 randomly assigned to mammography (five annual mammography screens) or control (no mammography) in 15 screening centres in six Canadian provinces, 1980-85 . .  Women aged 40-49 in the mammography arm and all women aged 50-59 in both arms received annual physical breast examinations. Women aged 40-49 in the control arm received a single examination followed by usual care in the community.  Main outcome measure Deaths from breast cancer.  Results During the five year screening period, 666 invasive breast cancers were diagnosed in the mammography arm (n=44 925 participants) and 524 in the controls (n=44 910), and of these, 180 women in the mammography arm and 171 women in the control arm died of breast cancer during the 25 year follow-up period. The overall hazard ratio for death from breast cancer diagnosed during the screening period associated with mammography was 1.05 (95% confidence interval 0.85 to 1.30). in those aged 40-49 and 50-59 . During the entire study period, 3250 women in the mammography arm and 3133 in the control arm had a diagnosis of breast cancer, and 500 and 505, respectively, died of breast cancer. Thus the cumulative mortality from breast cancer was similar between women in the mammography arm and in the control arm (hazard ratio 0.99, 95% confidence interval 0.88 to 1.12). After 15 years of follow-up a residual excess of 106 cancers was observed in the mammography arm, attributable to over-diagnosis.   Conclusion Annual mammography in women aged 40-59 does not reduce mortality from breast cancer beyond that of physical examination or usual care when adjuvant therapy for breast cancer is freely available. Overall, 22% (106/484) of screen detected invasive breast cancers were over-diagnosed, representing one over-diagnosed breast cancer for every 424 women who received mammography screening in the trial.
                        Editorial Too much mammography  11 February 2014   BMJ 2014;348:g1403 http://dx.doi.org/10.1136/bmj.g1403  Mette Kalager,Hans-Olov Adami, Michael Bretthauer, Norway.                                     Long term follow-up does not support screening women under 60.   Before being widely implemented, mammography screening was tested in randomised controlled trials in the 1960s to 80s. Meta-analyses of these trials showed a relative reduction in deaths from breast cancer of between 15% and 25% among women aged 50 to 69.1 2 3 Only the Canadian National Breast Screening Study showed no reduction in breast cancer mortality.1 2 3 This large randomised controlled trial compared physical breast examination with combined physical breast examination and annual mammography in women aged 40 to 59.1 2 3    In a linked paper (doi:10.1136/bmj.g366), Miller and colleagues present the results for up to 25 years of follow-up in the Canadian study.4 No difference in breast cancer mortality was observed between the mammography and control arms, whereas a significant excess incidence of invasive breast cancer was observed in the mammography arm, resulting in 22% overdiagnosis. This means that 22% of screen detected invasive cancers would not have reduced a woman’s life expectancy if left undetected. The major strengths of this study include its randomised design, intense intervention with five annual mammography screenings, high compliance, and complete, long term follow-up. The lack of mortality benefit is also biologically plausible because the mean tumour size was 19 mm in the screening group and 21 mm in the control group. This 2 mm difference—which might be even smaller if overdiagnosed cancers could be excluded from the screening group—represents a minimal proportion of the entire clinical course for breast tumours.  But the trial also has some potential limitations. No quantitative data are available on the degree of contamination in the control arm or possible confounding by screening mammography after the trial. It seems unlikely, however, that such potential limitations would conceal a clinically important benefit. The rate of overdiagnosis did not include ductal carcinoma in situ, and the trial provides no data for women older than 60.

               The Canadian study, launched in 1980, is the only trial to enroll participants in the modern era of routine adjuvant systemic treatment for breast cancer, and the women were educated in physical breast examination as advocated today.4 These important features may make this study more informative for a modern setting, compared with other randomised trials. The results of the study are strikingly similar—for both lack of efficacy and extent of overdiagnosis—to recent studies evaluating today’s screening programmes.5 6 7 The real amount of overdiagnosis in current screening programmes might be even higher than that reported in the Canadian study,4 because ductal carcinoma in situ, which accounts for one in four breast cancers detected in screening programmes,8 was not included in the analyses.

                Other studies also indicate that improved treatment rather than screening is the reason for the decline in breast cancer mortality during the past four or five years.5 7 Even though different studies arrive at different reductions in breast cancer mortality (from 10% to 25%), these benefits translate to only marginal differences in absolute effects. Much larger variation is seen in the estimates of overdiagnosis.6 In studies based on statistical modelling, overdiagnosis was less than 5%.6 By contrast, most observational studies report higher estimates of overdiagnosis, ranging from 22% to 54%,6 depending on denominator used.9 When the number of breast cancers detected at screening is used as the denominator (as in the Canadian study), the amount of overdiagnosis observed in the previous randomised controlled trials is strikingly similar (22-24%).4 10

How do the data on mammography screening compare with data on prostate cancer screening by prostate specific antigen, which is currently not encouraged in the United Kingdom and other countries owing to its small effect on mortality and large risk of overdiagnosis (www.screening.nhs.uk/prostatecancer)? The figure on bmj.com shows that the absolute harms (overdiagnosis) and benefits (mortality reduction) are not very different between the screening types. The 20 year risk of breast cancer for a 50 year old woman is 6.1% with screening (including 22% overdiagnosis 4),11 and 5.0% without screening; and the corresponding numbers for prostate cancer in a 50 year old man are 3.9% with screening (including 45% overdiagnosis 12) and 2.7% without screening.11 The 20 year risk of death from cancer for a 55 year old woman is 1.5% with screening (assuming a 20% reduction in mortality2)11 and 1.9% without screening; and the corresponding numbers for prostate cancer in a 55 year old man are 1.0% with (assuming a 20% reduction in mortality12) and 1.3% without screening.11

           Nevertheless, the UK National Screening Committee does recommend mammography screening for breast cancer but not prostate specific antigen screening for prostate cancer, stating that the “aim is to only implement programs that do more good than harm and that the informed choice is a guided principle of screening” (www.screening.nhs.uk/screening). Because the scientific rationale to recommend screening or not does not differ noticeably between breast and prostate cancer, political pressure and beliefs might have a role.

             We agree with Miller and colleagues that “the rationale for screening by mammography be urgently reassessed by policy makers.” As time goes by we do indeed need more efficient mechanisms to reconsider priorities and recommendations for mammography screening and other medical interventions. This is not an easy task, because governments, research funders, scientists, and medical practitioners may have vested interests in continuing activities that are well established.

                RESPONSES:  12 February 2014  BMJ 2014;348:g366 :                     1. rebuttal by USA  radiologists : Daniel B. Kopans, Professor of Radiology Harvard Medical School.  Having been one of the experts called on in 1990 to review the quality of their mammograms I can personally attest to the fact that the quality was poor (1). To save money they used second hand mammography machines. The images were compromised by scatter since they did not employ grids for much of the trial. They failed to fully position the breasts in the machines so that cancers were missed because the technologists were not taught proper positioning, and their radiologists had no specific training in mammographic interpretation.   

The CNBSS’s own reference physicist wrote:“..in my work as reference physicist to the NBSS, [I] identified many concerns regarding the quality of mammography carried out in some of the NBSS screening centers. That quality [in the NBSS] was far below state of the art, even for that time (early 1980’s). ” (2)

In this latest paper (3) the authors gloss over the fact that only 32% of the cancers were detected by mammography alone. This extremely low number is consistent with the poor quality of the mammography. At least two thirds of the cancers should be detected by mammography alone (4). In their accompanying editorial (5) Kalager and Adami admit that ” The lack of mortality benefit is also biologically plausible because the mean tumour size was 19 mm in the screening group and 21 mm in the control group….a 2 mm difference.” Poor quality mammography does not find breast cancers at a smaller size and earlier stage and would not be expected to reduce deaths.

The documented poor quality of the CNBSS mammography is sufficient to explain their results and all of the above disqualifies the CNBSS as a scientific study of mammography screening, but it was even worse than that. In order to be valid, randomized, controlled trials (RCT) require that assignment of the women to the screening group or the unscreened control group is totally random. A fundamental rule for an RCT is that nothing can be known about the participants until they have been randomly assigned so that there is no risk of compromising the random allocation. Furthermore, a system needs to be employed so that the assignment is truly random and cannot be compromised. The CNBSS violated these fundamental rules (6). Every woman first had a clinical breast examination by a trained nurse (or doctor) so that they knew the women who had breast lumps, many of which were cancers, and they knew the women who had large lymph nodes in their axillae indicating advanced cancer. Before assigning the women to be in the group offered screening or the control women they knew who had large incurable cancers. This was a major violation, but it went beyond that. Instead of a random system of assigning the women they used open lists. The study coordinators who were supposed to randomly assign the volunteers, probably with good, but misguided, intentions, could simply skip a line to be certain that the women with lumps and even advanced cancers got assigned to the screening arm to be sure they would get a mammogram. It is indisputable that this happened since there was a statistically significant excess of women with advanced breast cancers who were assigned to the screening arm compared to those assigned to the control arm (7). This guaranteed that there would be more early deaths among the screened women than the control women and this is what occurred in the NBSS. Shifting women from the control arm to the screening arm would increase the cancers in the screening arm and reduce the cancers in the control arm which would also account for what they claim is “overdiagnosis”.                                                                                                                                          The analysis of the results from the CNBSS have been suspect from the beginning. The principle investigator ignored the allocation failure in his trial and blamed the early excess of cancer deaths among screened women on his, completely unsupportable, theory that cancer cells were being squeezed into the blood leading to early deaths. This had no scientific basis and was just another example of irresponsibility in the analysis of the data from this compromised trial and he finally retracted the nonsense after making front page headlines (6).

      The compromise of the CNBSS trial is indisputable. The 5 year survival from breast cancer among women ages 40-49 in Canada in the 1980’s was only 75%, yet the control women in the CNBSS, who were supposed to represent the Canadian population at the time, had a greater than 90% five year survival. This could only happen if cancers were shifted from the control arm to the screening arm. The CNBSS is an excellent example of how to corrupt a randomized, controlled trial. Coupling the fundamental compromise of the allocation process with the documented poor quality of the mammography should, long ago, have disqualified the CNBSS as a legitimate trial of screening mammography. Anyone who suggests that it was properly done and its results are valid and should be used to reduce access to screening either does not understand the fundamentals, or has other motives for using its corrupted results.

        2.  confirmation:   http://www.bmj.com/content/348/bmj.g366?tab=responses  Per-Henrik Zahl, MD & statistician   Norwegian Institute of Public Health.   In this 30-year old study, the authors report no mortality reduction when screening with mammography and 22% overdiagnosis (1). The sensitivity of the mammography technique has improved tremendously in the last three decades. Ten years ago we got digital mammography and recently we have got tomosynthesis (2). The detection rate at mammography in the Canadian study was about 3 per 1000 in the second and later screening rounds (3). In digital mammography, the corresponding detection rate is 6 per 1000 screened woman and in tomosynthesis, the detection rate is 8 per 1000 (2). It could even have been higher if the pathologists had time to perform more biopsies (personal communications). In tomosynthesis a large number of stellate lesions appear, many more than in traditional mammography, and they are probably representing a reservoir of overdiagnosed breast cancers. In the last 15 years, the rate of interval cancer has been constant and is at the same level as in Canada 30 years ago (4). Thus, the level of overdiagnosis is far much bigger today than in Canada 30 years ago.

             update 6 Feb 2014 This column has noted  that in the 2012 report of the the giant ATLAS (and aTTom) trials in 37  countries the past decade (discussed in detail below), despite the claimed 80% cure rate of early silent  breast cancer (diagnosed by mammography screening at around 55yrs),   by 15 years after repeated screening mammography- surgery-radiotherapy,  tamoxifen for 5 or 10 years and annual screening mammography followup,   of the women who had died by age 70yrs and had autopsy,   some 43% had (silent) recurrence of breast cancer- although this had been detected in far fewer living women. The 15 year ATLAS results overall were depressing- in those originally early silent estrogen-receptor positive breast cancers, although only about 20% had clinical recurrence by a mean age of 70yrs, of the 22% who had died by then,  almost half ie 43% had recurrence of breast cancer at autopsy.
How successful was tamoxifen versus placebo?
Why was  the Atlas trial  felt not to justify a no-tamoxifen control group?
               Sir Richard Peto’s earlier Oxford review (Horm Res 1989;32:165) Effects of Adjuvant Tamoxifen and of Cytotoxic Therapy on Mortality in Early Breast Cancer. An Overview of 61 Randomised Trials Among 28,896 Women  sought information worldwide on mortality according to assigned treatment in all randomised trials that began before 1985 of adjuvant tamoxifen or cytotoxic therapy for early breast cancer (with or without regional lymph node involvement). Coverage was reasonably complete for most countries. In 28 trials of tamoxifen nearly 4,000 of 16,513 women had died,  reductions in mortality due to treatment  were significant when tamoxifen was compared with no tamoxifen (p < 0.0001), any chemotherapy with no chemotherapy (p=0.003), and polychemotherapy with single-agent chemotherapy (p=0.001). In tamoxifen trials, there was a clear reduction in mortality only among women aged 50 or older, for whom assignment to tamoxifen reduced the annual odds of death during the first 5 years by about one fifth. In chemotherapy trials there was a clear reduction only among women under 50, for whom assignment to polychemotherapy reduced the annual odds of death during the first 5 years by about one quarter. Direct comparisons showed that combination chemotherapy was significantly more effective than single-agent therapy. Because it involved several thousand women, this overview was able to demonstrate particularly clearly that both tamoxifen and cytotoxic therapy can reduce five-year mortality.
         A decade later  the 1998 Tamoxifen for early breast cancer: overview of the randomised trials:  Oxford Early Breast Cancer Trialists’ Collaborative GroupCorresponding Author (The Lancet, 1998: 351,: 1451 – 1467) confirmed Peto’s review:  In 1995, information was sought on each woman in any randomised trial that began before 1990 of adjuvant tamoxifen versus no tamoxifen before recurrence on 37 000 women in 55 such trials, comprising about 87% of the worldwide evidence. Compared with the previous such overview, this approximately doubles the amount of evidence from trials of about 5 years of tamoxifen and, taking all trials together, on events occurring more than 5 years after randomisation.
                Nearly 8000 of the women had a low, or zero, level of the oestrogen-receptor protein (ER) measured in their primary tumour. Among them, the overall effects of tamoxifen appeared to be small, and subsequent analyses of recurrence and total mortality are restricted to the remaining women (18 000 with ER-positive tumours, plus nearly 12 000 more with untested tumours, of which an estimated 8000 would have been ER-positive). For trials of 1 year, 2 years, and about 5 years of adjuvant tamoxifen, the proportional recurrence reductions produced among these 30 000 women during about 10 years of follow-up were 21% (SD 3), 29% (SD 2), and 47% (SD 3), respectively, with a highly significant trend towards greater effect with longer treatment (χ21=52·0, 2p<0·00001). The corresponding proportional mortality reductions were 12% (SD 3), 17% (SD 3), and 26% (SD 4), respectively, and again the test for trend was significant (χ21= 8·8, 2p=0·003). The absolute improvement in recurrence was greater during the first 5 years, whereas the improvement in survival grew steadily larger throughout the first 10 years. The proportional mortality reductions were similar for women with node-positive and node-negative disease, but the absolute mortality reductions were greater in node-positive women. In the trials of about 5 years of adjuvant tamoxifen the absolute improvements in 10-year survival were 10·9% (SD 2·5) for node-positive (61·4% vs 50·5% survival, 2p<0·00001) and 5·6% (SD 1·3) for node-negative (78·9% vs 73·3% survival, 2p<0·00001). These benefits appeared to be largely irrespective of age, menopausal status, daily tamoxifen dose (which was generally 20 mg), and of whether chemotherapy had been given to both groups. In terms of other outcomes among all women studied (ie, including those with “ER-poor” tumours), the proportional reductions in contralateral breast cancer were 13% (SD 13), 26% (SD 9), and 47% (SD 9) in the trials of 1, 2, or about 5 years of adjuvant tamoxifen. The incidence of endometrial cancer was approximately doubled in trials of 1 or 2 years of tamoxifen and approximately quadrupled in trials of 5 years of tamoxifen (although the number of cases was small and these ratios were not significantly different from each other). The absolute decrease in contralateral breast cancer was about twice as large as the absolute increase in the incidence of endometrial cancer. Tamoxifen had no apparent effect on the incidence of colorectal cancer or, after exclusion of deaths from breast or endometrial cancer, on any of the other main categories of cause of death (total nearly 2000 such deaths; overall relative risk 0·99 [SD 0·05]).
            So, for corroboration we need the autopsy results of the women in the earlier tamoxifen vs placebo studies; and the 20 year results of the Atlas study. The ATLAS study reports clearly that silent breast cancer was more than twice as high in autopsied cases as in screening mammography during life. The conundrum remains whether  early cancer detection by regular repeated screening mammography, and early treatment by biopsy, surgery, radiotherapy and tamoxifen, is more beneficial or more harmful to women long term?
24 Jan 2014   Overdiagnosis    Overtreatment of Breast Cancer   .Am Soc Clin Oncol Educ Book. 2012;32:e40-e45. doi:  Alvarado M, Ozanne E, Esserman L. meetinglibrary.asco.org/sites/meetinglibrary.asco.org/files/Educational Book/PDF Files/2012/zds00112000e40.pdf  Dept Surgery Univ Calif San Francisco. write:   “Breast cancer is the most common cancer in women. Through greater awareness, mammographic screening, and aggressive biopsy of calcifications, the proportion of low-grade, early stage cancers and in situ lesions among all breast cancers has risen substantially. The introduction of molecular testing has increased the recognition of lower risk subtypes, and less aggressive treatments are more commonly recommended for these subtypes. Mammographically detected breast cancers are much more likely to have low-risk biology than symptomatic tumors found between screenings (interval cancers) or that present as clinical masses.                                                                                                                                
        Recognizing the lower risk associated with these lesions and the ability to confirm the risk with molecular tests should safely enable the use of less aggressive treatments. Importantly, ductal carcinoma in situ (DCIS) lesions, or what have been called stage I cancers, in and of themselves are not life-threatening. In situ lesions have been treated in a manner similar to that of invasive cancer, but there is little evidence to support that this practice has improved mortality. It is also being recognized that DCIS lesions are heterogeneous, and a substantial proportion of them may in fact be precursors of more indolent invasive cancers. Increasing evidence suggests that these lesions are being overtreated. The introduction of molecular tests should be able to help usher in a change in approach to these lesions. Reclassifying these lesions as part of the spectrum of high-risk lesions enables the use of a prevention approach. Learning from the experience with active surveillance in prostate cancer should empower the introduction of new approaches, with a focus on preventing invasive cancer, especially given that there are effective, United States Food and Drug Administration (FDA)-approved breast cancer preventive interventions.”                                                                                                                                                                                             5 January 2014:      Quantifying the Benefits and Harms of Screening Mammography.  H Gilbert Welch & Honor Passow  , Dartmouth Geisel school of medicine, NewHampshire  write:  JAMA Intern Med. 2013 Dec 30.                   Like all early detection strategies, screening mammography involves trade-offs. If women are to truly participate in the decision of whether or not to be screened, they need quantification of its benefits and harms. Providing such information is challenging, however, given the uncertainty-and underlying professional disagreement-about the data. In this article, we attempt to bound this uncertainty by providing a range of estimates-optimistic and pessimistic-on the absolute frequency of 3 outcomes important to the mammography decision: breast cancer deaths avoided, false alarms, and overdiagnosis. Among 1000 US women aged 50 years who are screened annually for a decade,                                                                        0.3 to 3.2  ie ~0.17%  will avoid a breast cancer death                                                490 to 670  ie ~58% will have at least 1 false alarm recall, and                               3 to 14 ie         0.85%  will be overdiagnosed and treated needlessly.                                            We hope that these ranges help women to make a decision: either to feel comfortable about their decision to pursue screening or to feel equally comfortable about their decision not to pursue screening. For the remainder, we hope it helps start a conversation about where additional precision is most needed
                                                                                                                                                                     A recent review of a new book by journalist Rolf Hefti- The Mammogram Myth-  consolidating the controversy for and against screening mammography is reviewed by Cape Ray. The book relies heavily on Dr John Gofman (1919-2007), a distinguished medical scientist,  a key member of the Manhattan Project that developed the first atomic bomb used on Nagasaki. In 1996 Gofman published a book entitled Preventing Breast Cancer: The Story of a Major, Proven, Preventable Cause of This Disease, in which he made the astonishing claim that 75% of all breast cancers were caused by women being exposed to ionising radiation from X-rays. As highlighted in a review in JAMA, Gofman’s claim — based on an extensive literature review and certain critical assumptions — was at variance with every other authority, including the National Academy of Sciences and the National Council on Radiation Protection.  Martin Yaffe of Toronto has recently shown that the risk of radiation-induced breast cancer from mammographic screening is not negligible, but this risk is small when compared to the expected reduction in mortality achieved through screening.
                                                                                                                                                                   So the dilemma for health professionals, and for  the target of the zealous Cancer Screening Industry-  healthy women in their prime-of-life middle years- remains:  why have xray mammography screening when the independent evidence from expert epidemiologists is that screening mammograpy  to find preclinical ie precancer does not in fact  meaningfully save lives, entend health or reduce breast surgery and cancer therapy, it actually increases all these risks compared to waiting till cancer presents clinically.                                                                                                                                             Zahl Jorgensen and Gotzsche  in their latest review show that Overestimated lead times in cancer screening has led to substantial underestimation of overdiagnosis.
and Gotzsche’s new book is an expose  of  Deadly Medicines and Organised Crime.  
                                                                                                                          20 July 2013   HUMAN PROGESTERONE  BREASTCANCER RISK  REVISITED: Its 3 years since this column last reviewed progesterone, in the context of osteoporosis,  bone building.   While the first Pubmed report on progesterone implants  is apparently sixty years ago (probably in veterinary reproductive use), Drs John Lee and Kathy Dalton promoted use of solo human progesterone P4 for (post)menopausal protection,  also  against cancer including breast cancer; which l’Hermite 2013 from France, and eg David Sturdee from UK, have recently favourably  summarized in respect of balanced transdermal estrogen and oral micronized progesterone P4. The evidence for P4 as  almost global protection as HRT   has largely been confirmed provided progesterone is used in moderation – ideally transdermally/ transvaginally  like estrogen (Genazzani ea);  some believe in the basal physiological bloodlevel of about 1 to 2 nmol/L,  in balance with basal levels of human estrogen and androgens.                                                                                                                                Vanadin Seiffert-Klauss ea in Munich have recently (2012) confirmed that “women in the (~10year) menopause transition lose trabecular bone at a rapid rate despite intermittently high and usually normal estrogen levels –  especially the lean women (BMI<20kg), and those with family fracture history”.  And in their PEKNO study, “Decreasing rates of ovulation, hormonal changes, and increasing bone loss pre-date menopause by several years.;  in addition to estradiol, progesterone may play a significant role in the interrelationship between the ovaries and the skeleton in women.  differentiation of human osteoblasts from perimenopausal women has been shown to be dose-dependent on progesterone at physiological concentrations.  Higher progesterone levels, as seen in the luteal phase of ovulatory cycles, may be associated with more bone formation and with slightly less bone resorption than anovulatory cycles in which progesterone levels are low (< 5.8 ng/ml)”.                 These data led to the initiation  in perimenopausal women of a large, prospective, 2-year observational PEKNO study – from which interim data indicate that a decrease in ovulation correlated with an increase in the loss of bone mineral density (BMD). A meta-analysis in women *with normal ovulation estimated a BMD increase of 0.5% per year, vs *with ovulatory disturbances (anovulation or short luteal phase) a BMD decrease of 0.7% per year in young women ; but * in postmenopausal women a 1.3% increase per year in BMD when receiving hormone replacement therapy with unopposed estrogens, and a further 0.4% increase in BMD in women receiving estrogens plus progestogens. The role of progesterone in bone metabolism in perimenopausal women who are estrogen-replete requires further study.”  
                                   Thus they show that postmenopausally, addition of progestin may boost BMD by 31% more than ERT alone. But currently some experts eg Kuhl and Schneider and David Zava   feel that evidence warrants caution, that oral human progesterone P4  may have a  role in breast cancer promotion;  although it has protective benefit against estrogen dominance in most circumstances eg against endometrial cancer. As this column has previously reviewed, longterm experience of experts like Greenblatt & Gambrell, Gelfand,  Lee Vliet  in N America;   Schleyer-Saunders, Whitehead & Studd (London) , Burger & Davis (Australia) ; and Davies ea (Cape Town) showed no increase but reduction in all postmenopausal morbidity including cancer with  non-oral eg implants of BIDHRT (estradiol balanced  with human antiestrogen eg testosterone and/or progesterone).
                                                                                                                                                              Now Stephenson ea  at the Tyler Women’s Wellness Center, Texas publish a 3  year study showing multiple benefits and no adverse effects of balanced   compounded bioidentical transdermal hormone therapy BIDHRT on hemostatic, inflammatory, immune factors; cardiovascular biomarkers; quality-of-life measures in peri- and postmenopausal women. Conventional  nonhuman hormone therapy HT eg CEE and medroxyprogesterone results in increased thrombotic events, and an increased risk of breast cancer and dementia  in large prospective clinical trials including the HERS and the Women’s Health Initiative studies.  Physiologic human sex steroid therapy with transdermal delivery for peri/postmenopausal women may offer a different risk/benefit profile, yet long-term studies of this treatment model are lacking.  In a  prospective, approved closed-label study, 75  women who met strict inclusion/exclusion criteria were enrolled; following baseline hormone evaluation,  women received compounded transdermal bioidentical hormone therapy of BiEst (80%Estriol/20%Estradiol), and/or Progesterone to meet established physiologic reference ranges for the luteal phase.          Subjects receiving  BIDHRT in doses targeted to physiologic reference ranges administered in a daily dose showed significant favorable changes in  menopausal symptoms, cardiovascular biomarkers, inflammatory factors, immune signaling factors, and health outcomes, despite very high life stress, and home and work strain in study subjects. There were no associated adverse events. This model of care warrants consideration as an effective and safe clinical therapy for peri/postmenopausal women especially in populations with high perceived stress and a history of stressful life events prior to, or during the menopausal transition.
                                                                                                                                                              This Texas   study supports the 2009 metanalysis by Holtorf: The bioidentical hormone debate: are bioidentical hormones (estradiol, estriol, and progesterone) safer or more efficacious than commonly used synthetic versions in hormone replacement therapy?   Patients report greater satisfaction with HRTs that contain progesterone compared with those that contain a synthetic progestin. Bioidentical hormones have some distinctly different, potentially opposite, physiological effects compared with their synthetic counterparts, which have different chemical structures. Both physiological and clinical data have indicated that progesterone is associated with a diminished risk for breast cancer, compared with the increased risk associated with synthetic progestins. Estriol has some unique physiological effects, which differentiate it from estradiol, estrone, and CEE. Estriol would be expected to carry less risk for breast cancer, although no randomized controlled trials have been documented. Synthetic progestins have a variety of negative cardiovascular effects, which may be avoided with progesterone.  Physiological data and clinical outcomes demonstrate that bioidentical hormones are associated with lower risks, including the risk of breast cancer and cardiovascular disease, and are more efficacious than their synthetic and animal-derived counterparts. Until evidence is found to the contrary, bioidentical hormones remain the preferred method of HRT. 
                                                                                                                                                                          And of course the recent 4year Kronos KEEPS study by Harman ea 2012 confirms that in early postmenopausal woemen, parenteral physiological-dose  estradiol has subtle benefits over oral premarin, with or without  parenteral progesterone, with no significant adverse effect..                                                                                                                                                                                                                                                                                                                                                                                                                  17 June 2013  SHOULD WE EVER TELL A PATIENT WITH A BREAST LUMP THAT IT’S CANCER?  or THAT IT MAYBE PRECANCER?  This was and is a  major dilemma in medicine. One of the big  lessons arising out of the high technology in living memory ie the past >century-our grandparents’ time-  is that before modern laboratory, imaging and surgical diagnostics, all we could do was wait and see, the trial of observation and therapy, prayer, meditation. Now we have gone to the other extreme in the aging,  bullying them to have risky invasive screening on the crass assumption that screening and early radical – invasive ie potentially  harmful-  treatment of silent ie precancer saves lives- when the evidence has become progressively clearer that unselective invasive screening of asymptomatic prostates and breasts simply creates worried well,  overdiagnoses silent disease which may never cause illness or death ,  and may hasten misery; whereas combining natural preventative remedies may benefit all systems  including regress cancer.
                                                                                                                                                             Silent hypertension and unrealised overweight/ metabolic syndrome  are radically different from cancer. With simple measurement  of asymptomatic arterial hypertension, visceral obesity and eg glycosuria, the earlier that risk factors are defined and addressed, and the earlier the adiposity/glycosuria/ hypertension corrected with lifestyle, abolishing smoking and boozing,  and diet improvements, supplements and if necessary the safest prescription drugs-  initially fish oil,  lowdose amiloretic and reserpine, metformin, and the basket of vitamins and minerals especially magnesium, zinc,  vits C and D3 –  the sooner is the progressive  risk  reversed to the heart, brain, mind, vision, lungs, digestive and excretory system, joints and legs, let alone to fertility, carcinogenesis and other immunoendocrine  functions                                                                                                                                                           So instead of driving well aging women witless with disease-mongering-  forced regular invasive xray screening mammography-  we should  instead respect the power of the mind over disease, and use simple careful history, and physiological  biometrics including behaviometrics to persuade and condition those at risk to take sensible precautions including if necessary supplements, exercise and corrective diet/psycho/hypnotherapy. The lesson of screening breasts and prostates for silent cancer  the past 20 years is that so many cases of silent dormant cancer regress spontaneously if left well alone, especially if they are left undiagnosed and instead just the score of common risk factors for  all common diseases addressed as this column keeps exploring. So when asymptomatic changes and lumps in breasts are detected by noninvasive means eg clinical or Sure Touch or thermal exam, there is no need to alarm the woman by labelling her a patient with breast disease – it is more than healing for her to show her that within a month, these changes can be reversed with  all the appropriate natural  steps as described in Combatting Breast Cancer , including the Magic Oils. If there were indeed (pre)malignant changes present, they too regress as normally happens in so many – so  leave well alone. As reviewed below,  up to  45% of apparently well adults who are killed  have silent cancers;    and in the giant ATLAS and aTTom trials in 37  countries the past decade (discussed in detail below), despite the claimed 80% cure rate of early silent  breast cancer (diagnosed at around 55yrs)  by 5 and 15 years after repeated screening mammography- surgery- and radiochemotherapy,  and annual screening mammography followup,   of the women who had died by age 70yrs and had autopsy, the similar 43% had (silent) recurrence of breast cancer. So  like men,  asymptomatic women should be discouraged from invasive screening; but the higher their risk score, the more readily they should be offered simple noninvasive breast screening, and thereby encouraged to optimize diet, habits, lifestyle, body build-fitness,  including with the battery of multibenefit preventative supplements . Like millions of partisans have sung in bitter wars and holocausts, Hirsh  Glik’s “Never Say that You Are Trodding the Final Path“- remains the hope-givimg mantra that all patients and caregivers  must hold to – the power of positive thought and action  if not prayer. Both mistakes and miracles happen.                                                                                                                                                                                                                                                                                 upate June 14 2013: a new review from Oxford University  Breast cancer mortality trends in England (1979-2009) and the assessment of the effectiveness of mammography screening concludes: In the Oxford region,  For all ages combined, mortality rates peaked for both underlying cause and mentions in 1985 and then started to decline, prior to the introduction of the NHSBSP in 1988.  There was no evidence that declines in mortality rates were consistently greater in women in age groups and cohorts that had been screened at all, or screened several times, than in other (unscreened) women, in the same time periods. Conclusions Mortality statistics do not show an effect of mammographic screening on population-based breast cancer mortality in England. update June 10 2013  a  review published today  by Coldman and Phillips on   Incidence of breast cancer and estimates of overdiagnosis after the initiation of a population-based mammography screening program   in Canada over 40years showed that ” the extent  of overdiagnosis of invasive cancer  was modest and primarily occurred among women  over the age of 60 years. However, overdiagnosis of ductal carcinoma in situ was elevated  for all age groups.”                                                                                                                                                                                                                                                                                                                    update 9 June 2013:    THE HARMFUL COERSIVE PRESSURE APPLIED ON WOMEN,  AND ON THEIR BREASTS, WITH SCREENING  XRAY  MAMMOGRAPHY:      Womens’ wishes must be respected when they  prefer no-xray no-squeeze prescreening, choose not to have xray mammography. Breast discomfort and breast trauma from xray mammography -breast sandwiching –   vary greatly between women and especially in young more hormonally-driven  breasts.. The pressure is manyfold:  not just in crushing the breasts, but in PTSD- post-traumatic stress disorder: Oxana Palesh & Cheryl Koopman report this month Breast cancer: PTSD—prevalent and persistent:  Receiving a diagnosis of breast cancer is likely to have aconsiderable impact on the psychological wellbeing of the patient. In a recent observational study, Vin-Raviv et al.1 reported that 23% of 1,139 women with newly diagnosed localized breast cancer experienced post-traumatic stress disorder (PTSD) symptoms. This is not to deny that many women experience post-traumatic character growth, as a recent Greek study discusses.   Posttraumatic stress disorder and posttraumatic growth in breast cancer patients.  But Elklit and Blum and O’Connor ea in Denmark a year earlier highlight  PTSD   as being highly relevant in oncology settings after early breast cancer.. This awareness has been reviewed on Pubmed from before 1997. A recent report says the physical crushing force applied in such breast compression  – snackwiching –  is briefly up to about  130 Newtons, ie 13 kg or  25 pounds force.    This compares to the gentle 1.5 to 2kg force applied briefly when having a mechanical tactile Sure Touch surface breast anatomical mapping, or professional clinical breast exam; or zero force with a no-touch infrared thermomammogram. Hence some  women report breast pain, bruising and discomfort for weeks after a compression xray mammogram. And because oncologists insist on followup regular xray mammography after cancer therapy with breast-conserving surgery & radiochemotherapy, women increasingly ignore breast lumps let alone any screening breast exams at all. It is common cause that stress, anxiety  increase cortisol, insulin  and thus estrogenic stimulation, and thus cancer risk to  breasts.  It is still unknown how much the longterm risk of breast problems and cancer is increased from rupturing breast cells (let alone spreading cancer cells) with repeated successive compression xray mammography and the cumulative xray dose used – especially when perhaps 1 in 10 women screened is recalled  by radiologists for more compression views, to find (by biopsy of perhaps 10 to 20 women per 1000) the 2 to 4 clinically undetected tiny breast (pre)cancers in each 1000 women so screened preventatively… And it is obvious that with denser more active breasts in young women- monthly high-turnover glandular cells (especially in those on cyclic synthetic estrogen-progestin contraception) –  both breast fragility and sensitivity are higher the earlier that xray mammography is commenced as radiologists insist.

              Hence Regulators in most countries have reduced recommendations for routine screening mammography to starting at age >50yrs and stopping by 70-75years (ie 10-12 times on average through midlife); whereas Radiology Associations ignore the risks and still advise screening annually from age 40 years,  for life  –   ie at least THREE times as many times from age 40years. So women are doubly exposed to harmful pressure both in being bullied that they need screening xray mammography – the lie that  ” screening mammography saves lives”  when the benefit of this is unproven, and in being forced to undergo breast crushing repeatedly. A woman who recently attended for Sure Touch in Port Elizabeth   objected to having her breasts snackwiched again by compression mammography. The flippant analogy is eerie when one considers how such women are expected to attend annually to have their breasts both flattened and irradiated – and more so with cumulative frying after therapeutic radiotherapy. No wonder some end up with a hard breast. . So while the young at heart may   love nudging breasts-,  and massage  heals, (and Bissell and Fletcher at the Berkley lab show that gentle nudging with about 50 gm pressure knocks errant breast ductal cells back into healthy behaviour) –   crushing force and coersion do women harm, not good; in contrast to men where forceful digital massage may (also with putative risk) relieve the infected painful prostate.. .

And Gøtzsche   and Jørgensen in  .Cochrane Database Syst Rev. have Jun 4 published update stats against Screening for breast cancer with mammographyfrom  PubMed and the WHO ‘s International Clinical Trials Registry  (to November 2012).  Eight eligible trials  included 600,000 women  in the age range 39 to 74 years. Three trials with adequate randomisation did not show a statistically significant reduction in breast cancer mortality at 13 years (relative risk (RR) 0.90); four trials with suboptimal randomisation showed a significant reduction in breast cancer mortality with an RR of 0.75 (95% CI 0.67 to 0.83). The RR for all seven trials combined was 0.81 (95% CI 0.74 to 0.87). We found that breast cancer mortality was an unreliable outcome that was biased in favour of screening, mainly from differential misclassification of cause of death. The trials with adequate randomisation did not find an effect of screening on total cancer mortality, including breast cancer, after 10 years (RR 1.02, 95% CI 0.95 to 1.10) or on all-cause mortality after 13 years (RR 0.99, 95% CI 0.95 to 1.03).  Surgeries – Lumpectomies and mastectomies (RR 1.20-1.31, 95% CI 1.08 to 1.42) were significantly more in the screened groups . The use of radiotherapy was similarly increased whereas there was no difference in the use of chemotherapy.              AUTHORS’ CONCLUSIONS: If we assume that screening reduces breast cancer mortality by 15% and that overdiagnosis and overtreatment is at 30%, it means that for every 2000 women invited for screening through 10 years, one will avoid dying of breast cancer and 10 healthy women, who would not have been diagnosed if there had not been screening, will be treated unnecessarily. Furthermore, more than 10%  will experience important psychological distress including anxiety and uncertainty for years because of false positive findings.        To help ensure that the women are fully informed before they decide whether or not to attend screening, we have an evidence-based lay  leaflet http://www.cochrane.dk. Because of substantial advances in treatment and greater breast cancer awareness since the trials, it is likely that the absolute effect of screening today is smaller than in the trials. Recent observational studies show more overdiagnosis than in the trials and very little or no reduction in the incidence of advanced cancers with screening”.                                                                                                              

update 26 May 2013  Apart from the strident promotion of preventative mastectomy by a film star,  reports the past week prompt review of :  why and whether  aggressive breast cancer may have doubled  in young women 25-39years old; and  it’s prevention by natural steps.

update 22 May 2013:   WHY DO SO MANY  WOMEN HAVE  RELAPSE OF BREAST CANCER BY 25 YEARS AFTER  DIAGNOSIS AND APPARENTLY CURATIVE TREATMENT OF EARLY SILENT BREAST CANCER?: three landmark new papers shine more light on why 43% of women who died by 15 years after aggressive treatment of  initial silent preclinical breast cancer had relapse/recurrence  of breast cancer at autopsy  – the  depressing result of the monumental 180 000 women-year  ATLAS trial:

Lisa Willis, Karen Page, Trevor Graham, Tomás Alarcón, Malcolm  Alison    & Ian  Tomlinson  from Universities of London, Oxford, Cambridge, and Barcelona  this month dissect  “What Can Be Learnt about Disease Progression in Breast Cancer Dormancy from Relapse Data?   why Breast cancer patients have an anomalously high rate of relapse up to 25 years  after apparently curative surgery removed the primary tumour. Disease progression during the intervening years between resection and relapse is poorly understood. There is evidence that the disease persists as dangerous, tiny metastases that remain at a growth restricted, clinically undetectable size until a transforming event restarts growth. This suggests a natural question and  a surprising answer: why are interesting trends in long-term relapse data not more commonly observed?”       But they are observed: another recent  15 year followup study, from Denmark (Grantzau ea), furthermore shows that DXRT after early breast cancer almost doubles the risk of radiotherapy-associated second cancer to 1:200 of women so treated..

       Thus at least dangerous dormant micrometastases, and the enormous cumulative  radiation exposure from both screening mammography over decades, and DXRT itself, will explain much of the 43% recurrence rate of breast cancer by 15 years (at autopsy in those who had died by then, at a  mean of only 70 years) seen in the ATLAS trial.

  These reports raise yet further doubts about the wisdom  of  regular mass xrayscreening of well breasts from age 50 years let alone 40years, and worse-  zealous major surgery and DXRT for preclinical disease, and then even worse, ongoing xray mammographic surveillance into old age.

      They point in the opposite direction:  that xray screening of well breasts should be avoided;  DXRT avoided in localized early breast cancer; and surveillance for breast cancer limited to the many available non-xray methods;

     and that women must be encouraged instead to maintain prevention with combination of safe natural (and multisystem-protecting)  means as discussed repeatedly in this column – lifestyle, diet, exercise, and massage and oral use of safe natural preventative supplements. Anticancer antiangiogenesis factors from our diet  are legion, include  cannabis, mushrooms, resveratrol, green tea, black rasberry  and Royal jelly. One would not recommend soya against breast cancr because of its phytoestrogen potential.

               Xradiation has been known for decades eg 1978   1990 to be both an angiogenic and an antiangiogenic factor in tumour growth angiogenesis (Judah Folkman 1971) . so it is  obviously a double-edged sword that should certainly not be used in the witchhunt for silent and usually irrelevant precancer in well breasts.

                   So we have the ludicrous situation reported today in JAMA  that despite all the evidence for 20 years now to stop or at least halve  mass xray screening and thus (over)treatment of silent early breast cancer, Physicians, Patients Not Following Advice From USPSTF on Mammography Screening: In 2009, the US Preventive Services Task Force (USPSTF) recommended against routine screening mammography for women under 50 years and advised biennial rather than annual screening for women aged over 49yrs. But women and physicians ignored these recommendations.  A new study from Harvard  found that in 2005 to 2011, the percentage of women aged 40 to 49 years reporting that they had undergone mammography screening in the previous year was the same, about 47%. As for women aged 50 to 74 years, the percentage reporting mammography screening in the previous 12 months for each year analyzed also remained essentially the same, in the upper 50% range.”

        Update 21 April 2013FIFTEEN YEAR FOLLOWUP STUDIES OF BREAST CANCER AND ALLCAUSE  MORTALITY FROM MENOPAUSE ONWARDS:                                                                           Overall, long-term studies do not favour invasive breast screening or adjuvant therapy of early breast cancer,  but actually argue  against  early diagnosis and treatment of both silent breast and prostate  cancer.  Rather, the focus must be on safe natural prevention to reduce the occurrence of all common degenerative diseases of aging.

       It is instructive to juxtapose  the diverse 15 year followup studies in 14 countries (Nordic Cochrane- Gotzsche, Jorgensen ea) of women routinely xray- mammography screened or not, with the 15 year ATLAS study  (that ended in 2010)  reviewed below in 36 countries,  of women zealously xray- screened for early breast cancer, prompt  biopsies and surgical/  radiotherapy treatment- the majority mastectomy-  and then randomized to tamoxifen for up to  10 years. and it is reported by the ATLAS authors that there was a major breach of protocol - The protocol stated that 20 000 patients would need to be randomised in ATLAS and the other trials of tamoxifen duration to detect reliably an absolute difference of 2–3% in mortality. Entry to ATLAS was halted in 2005 (with 12 894 patients, including 6846 with ER-positive disease) because the MA.17 trial  showed benefit from continued endocrine treatment after 5 years of tamoxifen..   Yet the MA17 trial was with a different drug- letrozole;  and bizarely, the trial conclusion was that “the results from the analyses based on the Cox model with time-dependent covariates  were similar for letrozole and placebo.”  ie that letrozole was no better than placebo.. Thus, like the Womens’ Health Initiative misguided early termination,  it is unclear why MA17 was used as reason to terminate the ATLAS trial.
             The 15 year ATLAS results overall were depressing- in those originally early silent estrogen-receptor positive breast cancers, although only about 20% had clinical recurrence by a mean age of 70yrs, of the 22% who had died by then,  almost half ie 43% had recurrence of breast cancer at autopsy.              Many new such trials are under way.
             The aTTom trial  the UK arm of the ATLAS trial similarly “followed women with early breast cancer after initial treatment  for about 15 years:  it  randomly assigned 6934 women (39% ER-positive, 61% ER-untested) at the completion of 4 or more years of tamoxifen therapy to either 5 additional years of tamoxifen or cessation of tamoxifen therapy. With a median follow-up of 4.2 years, there was a slight, non-significant advantage for the 10-year tamoxifen arm (RR, 0.94; 95% CI, 0.81–1.09; P = .4). Thus, the optimal duration of therapy is not known, but it is at least 5 years”. For undisclosed reasons this trial has apparently  never been published in full although it was first reported in 2008- this raises the usual question by eg Booth and Tannock 2008  of bias against negative results, whether there was suppression by sponsors…  And the aTTom trial design was heavily criticised at the outset in 1996.
                The meta-analysis published the past week by Heidi Nelson ea for the USPSTF  confirms the ATLAS study, showed that tamoxifen/ raloxifen for 5 years reduced absolute mortality from breast cancer by about 0.16% per year. Neither reduced breast cancer-specific or all-cause mortality rates. Both reduced the incidence of fractures, but tamoxifen increased the incidence of thromboembolic events more than raloxifene by 4 cases in 1000 women. Tamoxifen increased the incidence of endometrial cancer and cataracts compared with placebo and raloxifene. Trials provided limited and heterogeneous data on medication adherence and persistence. Many women do not take tamoxifen because of associated harms.
         It then becomes apparent  that  having early breast cancer detected – without the adverse risk factors of xray mammography of repeated breast crushing, radiation,  biopsies and overtreatement,                             but with better application of safe preventative measures including vitamin D3, melatonin, metformin, iodine, DMSO, coconut oil,  fish oil, sutherlandia, I3C/DIM, vitamins and minerals                  – while women will live healthy longer,  few women  (perhaps <5% of all deaths) will die of breast cancer.  The common risk factors (for all common premature disease and deaths) are  m   anaged with the same basket of safe natural effective preventatives including supplements like appropriate balanced hormone replacement -that this column addresses.                                                                                                                                                                                                                                                    
Dr.  Northrup says “[Gilbert Welch] pointed to a study [from] way back, of women who died in car accidents in their 40s. They sectioned their breast tissues and found that 40 percent of them – this is normal healthy women dying in car accidents – had evidence of ductal carcinoma in situ that was never going to go anywhere. This is the big dilemma,” .   Welch and Black 1997 reported Among seven autopsy series of women not known to have had breast cancer during life, the median prevalence of invasive breast cancer was 1.3% (range, 0% to 1.8%) and the median prevalence of DCIS was 8.9% (range, 0% to 14.7%). Prevalences were higher among women likely to have been screened (that is, women 40 to 70 years of age).

     Erbas ea at Univ Melbourne studied all sources for the prevalence of ductal carcinoma in situ. “The reported prevalence of undiagnosed DCIS in autopsy studies, of approximately 9%, has been used to suggest a larger reservoir of DCIS may exist in the population”.

      Update 18 April 2013:  a  new study from  Italy   graphically illustrates the lower sensitivity of xray screening – U/S ie  ultrasound picked up ‘significantly’ more tiny asymptomatic breast cancers  missed in 22,131  women with negative mammography.  “The overall U/S detection was 0.185%, but 0.55% with previous cancer vs 0.145% in women without cancer history (p = 0.0004),  0.22% in dense breasts (p = 0.17) vs .156% in fatty breasts. The U/S- generated invasive assessment was 0.19%  The benign to malignant open surgical biopsy ratio was  thus 0.17.”  This is likely more overdiagnosis unless the women simply apply the preventative measures recommended below.

             But while no screening method can diagnose cancer (only invasive biopsy can), and none can guarantee there arnt cancer cells busy germinating especially if stirred up by severe anxiety,  radiation, crushing, biopsy etc, Sure Touch mapping is more accurate than even U/S for  reassuring while reducing referral rate for U/S.

UPDATE 14 APRIL 2013: Because of the evidence the past score years set out below  that xray screening actually does more harm than good, integrative  medical clinics world wide do not promote xray screening mammography. But such clinics including in Cape Town generally offer regular safe and lower-cost  anatomical eg Sure Touch mechanical tactile if not ultrasound or MRI, and physiological no-touch eg thermography ie bloodflow studies,  –  for those who need peace of mind. Some women choose to alternate Sure Touch and thermomammography.

     While only 1 in 200 women have the familial gene risk,  the majority of older women have  the common multiple risk factors eg longevity, estrogenic and heavy metal pollution, stress, overweight density, smoking, alcohol; and  there are many simple remedies described in these  columns that can reverse most of the risk factors – not just of even genetic breast cancer and increasing overweight,  but of all the major diseases of aging.

The problem remains the stubbornness of third party payers including governments to listen to both the evidence and to womens’ wishes, and pay for such safe, cheaper and arguably more accurate prscreening than crush xray mammography, if any is desired or desirable .

Dr Johnnie Ham MD MSc MBA Californian ObGyn discusses why xray screening mammography and aggressive medical assault on  well breasts- the witchhunt for the pot of hidden gold,  silent preclinical breast cancer –  is a giant  con by the  for-profit high-tech medical goliath  industry   terrorizing and mutilating  naive women.

Governments -WHO  silence on harms of screening mammography : What is tragicomedy is that worldwide, government Regulators seem to be standing silently firm, not saying a word about the harm likely exceeding the medical benefit- the screening and cancer  industry is far too profitable in jobs, taxes and votes. Search on the internet for Government warnings on harms of screening mammography does not yield a word of warning. Regulators and Medical Schemes piously promote quality screening, but say nothing about the harms versus benefits. The FDA still promotes annual screening mammography  on line without a word about the risks and harms of mammography; others like the UK NHS promote it every 2 to 3 years.    Yet the US Senate is actually considering a Republican Act to promote more xray breast imaging.

UPDATE 12 April 2013  The Wiki entry on breast cancer prognosis says now: “One result of media hype- breast cancer’s high visibility -(compared to other cancers in eg men, and other common major diseases) is that statistics may be misinterpreted, such as the claim that breast cancer will be diagnosed in one in eight women during their lives—a claim that depends on the unrealistic assumption that no woman will die of any other disease before the age of 95.[132] This obscures reality that about ten more women will die from heart disease or stroke than from breast cancer.[133]The emphasis on breast cancer screening may be harming women by subjecting them to unnecessary radiation, biopsies, and surgery. One-third of diagnosed breast cancers might recede on their own.[134] Screening mammography efficiently finds non-life-threatening, asymptomatic breast cancers and pre-cancers, even while overlooking serious cancers. According to Prof Gilbert Welch of  Dartmouth Institute, research on screening mammography has taken the “brain-dead approach that says the best test is the one that finds the most cancers” rather than the one that finds dangerous cancers.[134]

The latest  report  Lancet 2011) on the Relevance of breast cancer hormone receptors and other factors to efficacy of Tamoxifen protection after breast cancer looked at 20 trials (n=21,457) in early breast cancer . In oestrogen receptor (ER)-positive disease, about 5 years of tamoxifen halved recurrence rates throughout the first 10 years but  no further gain or loss after year 10; risk was approximately independent of progesterone receptor status (or level), age, nodal status, or use of chemotherapy. Breast cancer mortality was reduced by about a third throughout the first 15 years. Overall non-breast-cancer mortality was little affected, despite small absolute increases in thromboembolic and uterine cancer mortality (both only in women older than 55 years), so all-cause mortality was substantially reduced. In ER-negative disease, tamoxifen had little or no effect on breast cancer recurrence or mortality.

       This is not surprising as tamoxifen like  all synthetic  sex hormones  /blockers has  a long list of adverse effects on bone, brain, cardiovascular, bladder, mood, immunity, body weight and metabolism,  womb etc.

But the Oxford UK-led (Davies ea)  landmark monumental  ATLAS trial (2012)  from 1996 -2010 in 36 countries and 180 000 women-years (mean presentation  age mid 50s, ER+ breast cancer about 1 cm size,   2/3 had mastectomy – which is now known to increase mortality) showed that after 6846 women taking tamoxifen  for up to 10 years, at about 15 years from diagnosis, tamoxifen in absolute terms  was only marginal benefit- marginally reduced the risk for breast cancer recurrence, compared with stopping tamoxifen (617 vs 711; P = .002), reduced breast cancer mortality  relatively by 8% (331 vs 397 deaths; P = .01) but that’s only about 1% in absolute terms, and reduced overall mortality by 10% (639 vs 722 deaths; P = .01). Over all, approximately 1/5 clinically relapsed,  1/7 deaths were from breast  cancer; but of those who died, webfigures 4a and 4b of  the supplementary appendix   of the main ATLAS  report showed that at autopsy almost half  (43%) indeed had recurrent breast cancer. This gives the lie to early screening and treatment-  15 years later, even with tamoxifen for  10 years, early xray mammography detection and conventional surgical-radio-chemotherapy treatment does not cure much more than half of women with preclinical ER+  breast cancer that screening detects.The risk for recurrence by year 15 was 21.4% in the continuers group and 25.1% in the control group. ie only 3.7% absolute reduction. In addition, breast cancer mortality by year 15 was significantly reduced by nearly 3%; it was 12.2% in the continuers group and 15.0% in the control group. ie only 2.8% absolute reduction. Thus even in these women with early breast cancer, the cure rate even with tamoxifen was poor- slight reduction in the 25% recurrence  and 15% breast cancer mortality rates. But almost  half of the women who died had recurrence.  Once again, the actual results published 4 months ago in the final Lancet report were much less impressive than the media release published 5 days later. Of these >6000 women allocated after initial surgery/ radio/chemotherapy to the tamoxifen or placebo  trial, 85% did not die of breast cancer. But the cure rate was at best still only about 75%, and only  half of those who died -by a mean of age 70 years – of any  causes were free of breast cancer.

11 April 2013  the SA Menopause Society Menopause Matters today  also features The Great Mammography Debate- concluding “The point being that the treatments of breast cancer are not benign and need to be drawn into the calculations when assessing the harms of screening mammography. If these treatments are carried out on a significant number of people who are not in danger of being harmed by their breast cancer in the first place (those over-diagnosed) then the scales of benefit versus harm from routine mammography may well tip in favour of harm. If so it may be unwise or even unethical to recommend screening by mammography.”

9 April 2013  Robert Stern at University of Arizona writes that “xray mammography alone is not a very good screening modality and has strikingly variable false positive, false negative, specificity, and efficacy rates, depending on what you read and who you believe.

   Worldwide, the days of simple repetitive yearly/ biannual mammograms for every living woman over some arbitrary age may be over soon.. breast cancer screening is about to evolve into a personalized, patient-centered program. It means you can’t just  order a mammogram when a  flag pops up saying it’s time.  It means understanding fairly complex risk stratification, the indications for these new technologies, and the clinical context for various imaging strategies”, mostly still based on irradiation;  as detailed in the American Medical Journal by Drukteinis ea at the Florida Mofitt Cancer Centre ..

8 April 2013: UPDATE:  see  vitamin D3 and Breast Cancer.

JAMA publishes on line from University Basel  Switzerland,   Shaw and Elger’s viewpoint on Evidence-Based Persuasionoften  an ethical imperative to  forcefully guide a hesitant patient into what seems to be the best decision, using arguments from Removal of Bias to Recommending Options and occasionally even Creating New Biases.      The eternal problem remains, what is truly right? Is mass flu vaccine right? Is screening xray  mammography truly lifesaving? especially if one quotes impressive but misleading relative risk reduction rather than in fact the crucial trivial absolute reduction?  Is Directive Counselling however well-meant exercising undue influence? They conclude that it  is an essential part of modern medical practice, without which it may be impossible to respect patients’ autonomy. Such necessary persuasion needs to meet 6 criteria.

A month ago BCAction held a webinar reported by Manie Clark

updating the risks and futility of screening xray mammography.

24 Mar 2013. THE COVERUP OF HARMS AND FUTILITY OF XRAY BREAST SCREENING CONTINUES IN USA Many opinions from around the world in recent NEJMs say it all about screening mammography:  most are subjective, emotive. There is no impartial objective evidence to support the gold standard xray mammography at all (except arguably  in cases of obvious cancer- when biopsy, and MRI scan is better and safer).   When there are acceptable prescreenings that do no harm and when combined,  give good sensitivity and specificity eg any two of  mechanical tactile imaging, thermomammography, breast ultrasound and (if affordable) MRI.
         Karla Kerlikowske ea  co-author already four peer-reviewed Pubmed-listed studies on xray  mammography this year..  the latest on screening well women from the  Breast Cancer Surveillance Consortium asks: Screening Outcomes in Older US Women Undergoing Multiple Mammograms in Community Practice: Does Interval, Age, or Comorbidity Score Affect Tumor Characteristics or False Positive Rates?Uncertainty exists about appropriate use of screening mammography among older women because comorbid illnesses may diminish the benefit of screening. We examined the risks from 1999 to  2006 on 140000  women aged 66 to 89 years at study entry undergoing mammo     . About 7% had  breast cancer,  in a data linkage between the Breast Cancer Surveillance Consortium and Medicare claims.  Cumulative probability of a false-positive mammo result was higher among annual screeners than biennial screeners irrespective of comorbidity: 48% of annual screeners aged 66 to 74 years had a false-positive result compared with 29% of biennial screeners. These women  who undergo biennial screening mammo had similar risk of advanced-stage disease and lower cumulative risk of a false-positive recommendation than annual screeners, regardless of comorbidity.
But their abstract abysmally fails to ask and answer the obviously far more important question:  – did screening mammo  give any  significantly lower mortality, surgery   or  radiotherapy at 15 or 20year followup compared to a matched  randomly selected cohort not screened over the same period, or compared to women who were screened only once at the outset??
   All independent studies show that women regularly screened by xray mammogram  do no better and sustain far more harms, in fact may die sooner than those not screened. Why did they not say this in their abstract, that xray mammo screening is unethical abusive harmful exploitation of women?
    The BCSC website registers over 8million screening mammograms done there 1996-2009 – 24% of women had 5 or more xray screens- ` yet similarly  fails to mention the crucial harms and mortality data in screened versus unscreened women.  The reason is obvious:  admitting the truth, that xray screening mammo is not only futile but harmful, would kill what must now be a $10billion a year   industry in USA for xray manufacturers, radiologists, breast surgeons, hospitals, medical schemes, oncologists and Big Pharma in the Find a Hidden  Breast Cancer Conspiracy against older women. . Indeed, the endgame would be that lawyers will swarm to call on women to sue the Breast Cancer Industry for wrongful assault.
23 Mar 2013  Dr Enza Ferreri is a London-based  Italian journalist philosopher of science, christian human and animal  rights activist, including saving  Britain from an Islamist President Charles Windsor.. She yesterday wrote a devastating critique of screening xray mammography, its profiteering  oversell by  Scandinavian and English-speaking governments’ propaganda that omit  to explain all the risks and lack of benefits. “On one side you have the stories about women whose ” life  was saved” by breast screening, on the other  women whose life was made hell by discovery of a possibly benign DCIS, and those who endure a nightmare of false positives believing that she has breast cancer when she hasn’t. “
22 Mar 2013 Even this month’s  European Radiology Congress, and the South African Menopause Society  SAMS newsletter Menopause Matters, and the Annals of Family Medicine - a new Copenhagen study- now question  screening xray mammography, including cumulative radiation damage to heart and lungs; and chronic psychological trauma from false positive reports.
False-positive findings on screening mammography causes long-term psychosocial harm: 3 years after a false-positive finding, women experience psychosocial consequences that range between those experienced by women  with a normal mammogram and those with a diagnosis of breast cancer. Not even a “positive” breast biopsy is a guarantee that it is cancer that needs treatment -apparently 4% of breast biopsies may be misread. so 2nd opinions are advised.
     the  SAMS author says: ”   the fundamental question  is “Does screening for cancer improve length or quality of life?”  The latest arguments from the UK ask if screening saves lives, if you take all causes of death into account (Baum BMJ 2013;346:f385).  Firstly, the author accepts that screening saves lives. If 10 000 women are screened for a decade then 4 deaths will be avoided. As treatments improve as they are doing all the time, then deaths avoided become lower, maybe 2 per 10 000 in the near future and thus screening becomes less valuable… current data about survival need to be used when making calculations about prolonging life.
     Secondly, overdiagnosis is important because if some women who do not have life-threatening disease are treated, they may die from the treatment. Mastectomy, radiation, chemo- or endocrine therapy are not trivial treatments. Surgery carries anaesthetic and sepsis possibilities, especially in obese patients.   Radiation is not without its risks, raising the incidence of ischaemic heart disease 27%  and of lung cancer 78%. These risks would be worth taking if there were no cases of overdiagnosis – but there are – somewhere between 10% and 50% -so any lives saved may be cancelled out by deaths caused.     So with all-cause mortality no longer showing benefit, it devolves to other factors such as the positive peace of mind screening provides or the negative over-investigation of false positives to sway decisions for or against screening. No wonder the editor of the BMJ (26th January 2013) asks “At what stage must we seriously consider whether this screening is a good use of £96m of  NHS budget?”  So how should we advise our patients? The statistics show the “lives saved” argument is neutralized. The cost of screening, time involved and morbidity from false positive tests are all non-fatal harms so these have to be weighed against  peace of mind of a negative result and these calculations are in the mind of the beholder.     The parallels with prostate specific antigen screening are uncanny and PSA testing is rapidly falling into disfavour or even disrepute. It seems those with vested interests are those promoting mammography screening. The moral position of doctors is becoming increasingly complex – can it be correct to say mammography screening in low-risk women is “the right thing to do”?
16 Mar 2013   Recently Bateman in Cape Town suggests  “PinkDrive intervention ‘over-rated’ : Breast health professionals are questioning the life-saving impact of the high profile non-profit breast cancer organisation PinkDrive.
      The Pink Drive website opens with some  fallacies eg  that:                                         xray mammo 23kg breast compression causes no pain or damage – wrong; that     It is a tool to diagnose breast cancer“-      wrong-only  histology does; and that diagnostic breast irradiation is no risk after age 40years ;  wrong- this column has quoted authoritative opinion and research eg Lemay,  Sherbrooke Univ 2011  to the contrary, the linear no-threshold model, although Mina Bissell’s  Berkley Lab 2011 research paper perhaps contradicts this – the jury is still out . .
          It is significant that of the seven Platinum Pink Drive sponsors, two are private Hospital chains with  major vested interest in the Breast Cancer Surgery and Reconstruction  Industry.
Contrary to the Pink Drive website stating  that mammograms diagnose breast cancer, a major new  study from Japan on xray mammography of almost 120000 women found histological cancer in 0.22% of those  who underwent mammography alone, 0.37% of those who underwent ultrasonography alone, and 0.5% of the 974 participants who underwent both mammography and ultrasonography. Recall rate due to mammographic abnormalities was 4.9% for women screened only with mammography and 2.6% for those screened with both modalities. The cancer detection rate was 0.22% for women screened only with mammography  and 0.31% for those screened with both modalities. Their conclusion that It is possible to reduce the recall rate in screening mammography by combining mammography and ultrasonography for breast screening is precisely the point, that  hazardous xray mammography screening with its immediate and  longterm risks is not needed when any two of the three well-tested lowcost zero-risk portable facilities are available eg Sure Touch Mechanical Tactile imaging, thermomammgraphy, and ultrasound, and two  combined give high sensitivity and specificity.
Neither of the above new abstracts raised the issue of overdiagnosis or longterm hazards.. In fact the NCI Nat Cancer Institute Journal itself published a study this month  from San Fran  University California showing that  in 140 000  women from 66years upward screened  between 1999 and 2006, Cumulative probability of a false-positive mammography result was higher among annual screeners than biennial screeners irrespective of comorbidity: 48%  of annual screeners aged 66 to 74 years had a false-positive result compared with 29%  of biennial screeners. Women aged 66 to 89 years who undergo biennial screening mammography have similar risk of advanced-stage disease and lower cumulative risk of a false-positive recommendation than annual screeners, regardless of comorbidity. Thus  even cancer comes and go. Reducing xray screening  in USA   to every second year reduced the frequency of false positive recall – overdiagnosis – from almost half – 48% – by above one third, without increase in advanced cancer.
A Comparative Table shows the many methods, procedures  for objective breast imaging (mammography) available.  Of the established procedures  it lacks only comparison with the gold standard- the oldest ie  manual clinical examination-  and with forty year old Infrared Thermography. As this column has stressed previously, mammography is not a patented word for xray breast imaging, it is simply a generic description of breast (mammo-) and image (-gram) . Any image of the breast is thus a mammo-gram, and the process is mammo-graphy.SCREENING METHODS COMPARATIVE TABLE:                   this table shows the relative merits of some different methods of breast imaging. Mechanical Tactile Sure Touch Imaging leads the field  for combined sensitivity and specificity, portability, all-age utility without problems of breast density interference, cost, risks and reproducible mapping. Like a photograph, a  plaster or other cast of the bust would thus also be a mammogram image- and unlike plastic surgeons,  dermatologists and thermographers, other health professionals and patients alike too often forget to record a photograph to compare changes in the skin and breast serially. .
NEJM 28 Feb from Harvard, Adler and Colbert’s  “Mammography Screening Poll Results”  is a sobering commentary  on the health professionals’ wrong perceptions about routine X-ray mammography screening of all well breasts from midlife. What do readers say about the indisputable overwhelming independent evidence against routine X-ray screening mammography?
One has to question  the rationality of most NEJM readers – surprisingly few in total – who responded to the poll after Bleyer and Welch’s  , Mette Kalager’s  , Baum, Jorgensen and Gotzsche’s publications last year, that the majority of NEJM readers polled still  promote X-ray screening despite the hard evidence, the absence of benefit from screening irradiation of well breasts- significant reduction in mortality in such women – in the face of multiple hazards of such screening.
The risks, the  list of hazards – in five broad categories – is so great that as pointed out below last month, not even the NCI National Cancer Institute itself any longer clearly  promotes routine  X-ray mammography screening. As Colbert and Adler and the 2nd Canadian mammography trial 20 yrs ago noted (Miller and Baines) , the evidence for presymptomatic screening X-ray mammo is no better than clinical digital exam. Early diagnosis of silent  breast precancer by xray screening and biopsy does not save lives, it is a vast waste of money except for the career Breast Industry, that has been characterized as  terrorizing and damaging gullible submissive women (Winifred Cutler, Athena Inst).

There are certainly many safe natural ways we  reviewed recently of  reversing the  risks of breast  proliferation and cancer, thus justifying periodic safe low cost breast screening  – mammo-imaging – by independent  eg digital, mechanical tactile  ” Sure Touch ” , ultrasound and/ or thermo- means.26 Feb 2013. There is a flood of new progress against breast disease , breast cancer and  xray screening mammography: Contrary to  the for-profit Breast industry,  like all independent authorities including the Cancer Association of South Africa CANSA , the National Cancer Institute of America in 2013 no longer recommends routine xray mammography   screening-          it rates  the EVIDENCE on X-ray screening mammography          as FAIR evidence for its sole and arguable benefit –  Decrease in total and breast cancer mortality –        -*Consistency of studies is only Fair. External Validity: Good.  Internal Validity: Variable,.           But as GOOD evidence for the FIVE major  HARMS of  xray  screening    -* both  consistency, internal & external validity -are good -

  • Discomfort if not cellular rupture and bruising from violent 23 kg 50 lb crushing,
  • Overdiagnosis and Resulting Treatment – including mastectomy or radiochemotherapy- of Insignificant Cancers:
  • False-Positives with Additional Testing and Anxiety.
  • False-Negatives with False senseof Security and Potential Delay in Cancer Diagnosis.
  • Radiation-Induced Breast Cancer.

Winifred Cutler’s Athena Institute  team warns again that screening X-ray mammography on well women is dangerous , inflicts terror,  it does not reduce but may worsen the occurrence of invasive breast cancer. The  Berkeley  Institute’s  Dr Venugopalan  under profs Mina Bissell and Daniel Fletcher  show that simply gentle massage  helps – Compressing Breast Cancer Cells Can Stop Out-of-Control Growth  Shelley Hwang ea show that in California simple lumpectomy for early breast cancer reduced deaths (up to 2009) by 28% compared to mastectomy. Belinski & Boyages at the  Westmead Centre in Australia show again that common very low vitamin D levels more than double the risk of breast cancer let alone colon and all other cancers. A  Harvard team (Liu ea) has just shown that the carnage of legalized poisoning (smoking  – lungcancer, vascular;  alcohol -liver disease, violence;  adulteration with refined sugar/fructose - diabetes, vascular disease, cancer)  aside,  breast cancer far outstrips the other common cancers (colon, prostate cancer) in  preventible  life years lost. Willaims ea show again the major benefit of metformin against lethal breast cancer. Amadou ea in France confirm again the strong  link between abdominal obesity and breast cancer from childhood throughout life. This again highlights the criminal stupidity of delaying metformin use till obesity let alone infertility or diabetes are established. Metformin can safely be introduced at any stage of life provided it is started at very low dose eg below 250mg/day and cautiously titrated to the maximum well-tolerated dose to avoid nausea and diarrhoea- and temporarily halved or stopped in case of intercurrent gastrointestinal upset. . Grani et al from Rome, Italy    and many others remind us that both thyroid and breast malfunction are common by middle age and need to be sought and managed together.    We know that in most aging populations, deleterious deficiency of especially  magnesium, iodine, selenium, sulphur, and  vits B, C, D and K , and melatonin and sex hormones is very common along with crippling multitoxic carcinogenic overload. So it is logical to use multisupplements, and massage anti- inflammatory anti-cancer antioxidant  chelating antiestrogenic deep – penetrating iodine, coconut oil and DMSO – into the breasts as multidisease prevention and part of treatment. Oz ea in Turkey show that DMSO is  more effective against breast cancer than thalidomide.  But more importantly, DMSO enhances transport of any anticancer  agents into cancer cells. Already in 2008 Frederick ea showed that Lugol’s Iodine is an important antiestrogen adjuvant against breast cancer. Hence we advise  the harmless combination of natural multisystem micronutrients- especially  fish oil, coconut oil, DMSO,   vitamin C, D, K, melatonin, metformin, selenium, Lugol’s iodine and appropriate progesterone/ testosterone/ DHEA  – as nutrient supplements against all chronic aging diseases especially in women at risk of breast cancer.  . At Univ  Newcastle on Tyne,   Dr Dorota Overbeck-Zubrzycka’s  landmark  PhD  thesis just published on    FOXP3 regulates metastatic spread of breast cancer via control of expression of CXCR4 chemokine receptor promises new gene therapy in future. and her parallel study with Harvey,  A. Griffiths & C. Griffith,  Randomised control trial of Breast Tactile Imaging as an assessment tool for diagnosis of breast lumps in 2009/10 is now being published in full in a leading UK journal, validating this ( Sure Touch) bedside and outpatient clinic procedure as an established no-risk screening procedure, objective breast mapping  record for anxious women as shown in USA, Indian and Chinese studies. Thus increasingly Authorities are accepting that screening X-ray mammography harms far outweigh trivial if any improvement in survival. But screening – by eg regular clinical exam and mechanical tactile mapping –  for early signs of breast degeneration allows gentle safe self – treatment of all multisystem diseases that reverses both the breast degeneration and multisystem risk factors.

4 Feb 2013 UPDATE: BREAST SCREENING: Time lag to benefit after screening for common internal problems:   routine high-tech mass screening is inappropriate insurance.
a lot of the prestigious British Medical Journal last issue of 23 January 2013 is dedicated to the Breast Screening controversy; with a number of critics questioning the November 2012 Government  (Marmot) whitewash of the gigantically costly- and risky- NHS  screening mammography program. Professor Michael Baum of London University in particular has argued against this process for the past decade, after being the lead UK breast surgeon to set up this program in the 1990s and realizing it’s folly and risks.

Editorial: Breast cancer screening: what does the future hold?

BMJ 2013; 346 doi: http://dx.doi.org/10.1136/bmj.f87  Cite this as: BMJ 2013;346:f8    Cliona C Kirwan, National Institute for Health Research clinician scientist in surgical oncology          :  “Overdiagnosis remains a problem; quantifying its effects and minimising its impact are priorities.
The role of national breast screening programs and the quality and transparency of information given to participating women are increasingly the subject of heated debate. In the past 12 months alone, the BMJ, the Lancet, and the New England Journal of Medicine have published 24 articles debating the value of breast cancer screening. After calls for an impartial review of the value of breast screening in the United Kingdom, the findings of an independent panel of experts, led by Professor Marmot, were published in November 2012.1 Currently in the UK, women aged 50-70 years are invited for screening every three years; 2.3 million women were invited during 2010-11. The rate of uptake currently stands at 73.4%, having steadily increased in the past decade.2 The primary aim of screening is to reduce mortality from breast cancer. Reduced breast cancer related mortality is balanced against the cost of screening in terms of physical and psychological harm to women and the financial impact on health services. Much recent debate has concerned overdiagnosis—that is, diagnosis of a condition that would never cause symptoms or death during a patient’s lifetime. Although over-investigation can cause harm (pain and anxiety from mammography and biopsies), this is usually …”

Personal View     Harms from breast cancer screening outweigh benefits if death caused by treatment is included : Prof Michael Baum

BMJ 2013; 346 doi: http://dx.doi.org/10.1136/bmj.f385 (Published 23 January 2013)      Cite this as: BMJ 2013;346:f385

13 Jan  2013   As this column has long noted, routine high-tech mass screening is inappropriate insurance/prevention. Contrary to the gospel of the American Radiology, Breast and endoscopy costly screening industry,  and Curves International,  no human  survives   for  > 10 000 years to benefit from routine hightech screening  to avoid premature disease and death ie ‘save a life’ . . There is still grave doubt about the risk:benefit of routine prostate screening in the well.
A new January 2013 BMJ paper by a California University team Lee et al    looks at  ‘noninvasive’ cancer  screening of  breast (xray mammography) and colon (testing stool for occult blood)   in Europe and USA.  It found that  at least 1000 patients must be screened for at least 10 years – ie >10 000 patient-years of screening- before screening for either cancer could be claimed to save  a life. The corollary is that such screening of the well has a very low  chance – below 1:10 000 in any year, ie  0.01%  –  of finding a silent killer cancer that will save/  extend a life.

Thus they advise against screening people with an expected lifespan of below about 10 years.   But who would undergo such bothersome risky screening even over 10  years for a proposed benefit  (in death risk reduction)  of 0.1% a decade ? They found the reasons against routine screening of those not at high risk ( ie no suspicious personal symptoms or familial history) are as usual   those of the ensuing anxiety, the  procedures – radiation and colonoscopy and biopsies – and overdiagnosis. The worst is of course the cumulative risk of breast irradiation, and perforation death from colonoscopy:        “For cancer screening,  about one in 10 patients who are screened (with xray mammography , or with fecal occult blood testing) will have a false positive result,  leading to recall worry and likely biopsy/  colonoscopy.  Serious complications (such as perforation, major bleeding, and death) occur in 3.1 colonoscopies per 1000 screened.  One in 100 routinely mammography-screened  women will be  biopsied, and one in 1000 will be subject to overdiagnosis (that is, diagnosed with a breast cancer that was unlikely to have been clinically evident during their lifetime) and possibly unnecessary treatment.”

The same arguments apply strongly against routine screening of men for prostate cancer, or smokers for lung cancer,  in the absence of symptoms. . It should be noted that even the Wikipedia Mammography review now strongly highlights the arguments against mass screening mammography. The introduction sums it up bluntly: “task force reports point out that in addition to unnecessary surgery and anxiety, the risks of more frequent mammograms include a small but significant increase in breast cancer induced by radiation.[3][4] The Cochrane Collaboration (2011) concluded that mammograms reduce mortality from breast cancer by an absolute amount of 0.05% or a relative amount of 15%, but also result in unnecessary surgery and anxiety, resulting in their view that it is not clear whether mammography screening does more good or harm.[5] They thus state that universal screening may not be reasonable.[6]     Mammography has a false-negative (missed cancer) rate of at least 10 percent. This is partly due to dense tissues obscuring the cancer and the fact that the appearance of cancer on mammograms has a large overlap with the appearance of normal tissues. A meta-analysis review of programs in countries with organized screening found 52% over-diagnosis.[6]

It can be argued that noninvasive screeing that finds suspicious premalignant signs can then motivate prevention by natural means- lifestyle diet and appropriate supplements. But since these preventative steps (including blood-pressure and waist/breast  girth measurements and monthly self-exam for breast changes)    hugely  reduce the risks of all serious  acute and  chronic diseases, accidents and premature disability and death, routine mass screening for common ‘silent’  internal cancers eg breast, prostate  colon lung womb and ovary , is irrelevant, risky and huge waste of resources for no benefit. Not applying sensible diet,  lifestyle, blood-pressure checks   and supplements is like failing to maintain  your car, house, computers and electrical appliances etc , until  these  crucial assets  break  down. The evidence against hightech screening of the well of course does not  stop the anxious well  from worrying. As a heavy cigarette-smoking prof  of lung medicine  said 30 years ago, if an anxious patient demands a scope despite reassurance that the risk:benefit doesnt justify it, it is wise to do it.  Or someone else will. At least in the context of the younger adult who will thereby be more motivated to apply prevention, non-xray non-invasive screening by eg Sure Touch breast mapping- from onset of menopause, or younger  in eg diabetics   and others more prone to cancer eg in AIDS,  – and ultrasound quantitative bone-density risk measurement  from toddlers upwards , in exercising ie sportspeople,  and in any serious chronic disease especially with hormone overtones  eg thyroid,  diabetes, COPD/ asthma, cancer, arthritis, paralysis, AIDS,TB, cardiacs, renal, liver disease –  are relatively low cost  and safe compared to the traditional  xray screening procedures. The brilliant new French movie The Intouchables is all about choices  of lifestyle and the risks entailed.  Thats what screening, and voluntary prevention, are about.  No  adult  should be pressurized – by vested interests –  into having hightech eg xray (breast, bone)  or more invasive (eg scope, biopsy) screening without understandable explanation of the possible  although  infrequent immediate and distant risks,  and remote if any  benefits. Only the frequent  incidental unexpected screening discovery of hypertension,  increased breast lumpiness/density,  and low bone density, and initiation of simple lifestyle diet changes  and safe supplement  therapy- the below- listed scores of supplements against all common degenerative diseases  (and if needed the best primary antihypertensive  – lowdose reserpine and co-amilozide – costs perhaps  $1  a month to control  most; and simple (breasts, arthritis, wound   or elsewhere)  antiinflammatory  self massage if indicated with Lugol’s iodine, and analgesic antioxidant coconut oil and DMSO),  gives huge early and permanent preventative  pain and inflammatory benefits without risks.  There are also  promising studies on Pubmed between 1989 and 2011 of the benefits of DMSO in management of prostate problems in rats, and humans for transrectal procedures  and intravenously as cancer adjuvant palliation. DMSO-MSM is cheaply and safely available . It comes back to basics that are anathema to politicians,  Government, profiteers, Big Business Pharma and the Disease Industry.  Motivating and enforcing better lifestyle and natural diet (minimizing sugar , aspartame, alcohol, processed food especially cornstarch) , and healthgiving realistic doses of supplements – vits (all –  especially B, C,  D3 and K), minerals  (especially Mg, Zn, I2, Se, P, Bo,) and biological (plant  and sealife – not land animal) extracts,  (including fish oil, metformin, bioidentical human hormones, tryptophan, MSM, DMSO, chondroglucosamine,  coconut oil, cinnamon, pepper, curcumin, arginine, carnitine, carnosine, ribose, coQ10, proline, rauwolfia) – reduces the occurrence of serious disease drastically with decades of health extension. This vastly reduces  profit to the Disease Hospital-Drug  and processed food- alcohol – tobacco industry in delayed disease till very old age, and thus loss of  skilled workers’  jobs – that need to be taken up  elsewhere. That’s called reinvention, recycling…

29 SEPT 2014 OVARIAN CANCER UPDATE: PROGESTERONE REPLACEMENT IS IDEAL; WHY USE ORAL HT? WHEN ESPECIALLY LONG TERM PROGESTINS GREATLY INCREASE RISK OF OVARIAN AS WELL AS BREAST CANCER.

: ABSTRACT:  since last review in  this column 5 years ago, what progress has there been with ovarian cancer OvCa? On Pubmed there are 81000 references,  45500 reviews on OvCa

5 Oct 2014:  Ovarian Cancer Often Arises from Precursor Endometriosis    Frontline Medical News, 2014 Sep 29, B Jancin

   29 Sept 2014  The good news is that if ovariectomy is not done at hysterectomy, then at least salpingectomy should be done- it does not cause earlier menopause.  And the modern fashion for progesterone cream as baseline hormone balancing in this age of estrogen dominance, the feminization of nature,  also adds major protection for heart, bone, memory, mood,  and against cancer, without the risks of estrogen.

Before this month’s update,  the latest, an Australian cancer review  Mette ea 2013, shows that cigarette smoking increases the risk of OvCa by 30% to 60%.

The latest   review 2013 Modugno ea at Univ Pittsburgh/Mayo Clinic  Hormone response in ovarian cancer: time to reconsider as a clinical target?   said “Ovarian cancer is the sixth most common cancer worldwide among women in developed countries and the most lethal of all gynecologic malignancies. There is a critical need for the introduction of targeted therapies to improve outcome. Epidemiological evidence suggests a critical role for steroid hormones in ovarian tumorigenesis. There is also increasing evidence from in vitro studies that estrogen, progestin, and androgen regulate proliferation and invasion of epithelial ovarian cancer cells. Limited clinical trials have shown modest response rates; however, they have consistently identified a small subset of patients that respond very well to endocrine therapy with few side effects. We propose that it is timely to perform additional well-designed trials that should include biomarkers of response.The most consistently reported reproductive and hormonally related factors found to protect against EOC are use of oral contraceptives (OCs), increasing parity, and having a tubal ligation. In contrast, increasing age and nulliparity have been consistently shown to increase EOC risk. 

    Recent studies, including the prospective Women’s Health Initiative (WHI) (Anderson et al. 2003) and the Million Women Study (Beral et al. 2007), report an increase in risk for both estrogen-only (ET) and estrogen–progestin (EPT) formulations, although the risk associated with EPT was lower than that of ET. A recent meta-analysis of 14 published studies found risk increases 22% per 5 years of ET use compared with only 10% per 5 years of EPT use, suggesting that risk differs by regimen (Pearce et al. 2009).               Exogenous androgens may be associated with EOC. One case–control study found that use of Danazol, a synthetic androgen commonly used in the treatment of endometriosis, significantly increased EOC risk (Cottreau et al. 2003), although this finding has not been replicated (Olsen et al. 2008). Ever use of testosterone (tablets, patches, troches, or cream) has been associated with a threefold increase in EOC (Olsen et al. 2008).             

     Reproductive disorders and other reproductive factors :  Factors affecting childbearing have also been shown to be associated with EOC. In most studies, infertility has been associated with an increased risk, which may be greatest among women who fail to conceive (Vlahos et al. 2010). In general, infertility treatment does not appear to increase EOC risk, although the subset of treated women who remain nulliparous may be at an increased risk (Vlahos et al. 2010).

         Endometriosis, defined as the presence and growth of endometrial tissue outside the uterine cavity, has also been associated with EOC. A recent pooled analysis of 13 case–control studies showed a threefold increase in the incidence of clear cell EOC and a twofold increase in endometrioid EOC among women with a self-reported history of endometriosis (Pearce et al. 2012).

    An increased risk of EOC was reported by one case–control study (Schildkraut et al. 1996) among women with polycystic ovary syndrome (PCOS), a condition associated with menstrual dysfunction, infertility, obesity, the metabolic syndrome, hyperandrogenism, and insulin resistance. However, the finding was based on a small number of cases (n=7) and the association was limited to nonusers of OCs and thin women. Further case–control and prospective studies have failed to confirm this relationship (Pierpoint et al. 1998, Olsen et al. 2008, Brinton et al. 2010).

   Tubal ligation has been consistently shown to be associated with reduction in EOC risk (Cibula et al. 2011). This protection appears similar in magnitude to OC use and child bearing (about 30%) and is protective in high-risk women (i.e. BRCA1/2 carriers) as well. Hysterectomy has also been shown to reduce EOC risk, although the magnitude of the association is not as great nor as consistent as that reported for tubal ligation (Riman et al. 2004). Finally, reproductive factors associated with other hormonally linked cancers, such as age at first menarche, age at menopause, and length of reproductive years, have not been consistently associated with EOC (Riman et al. 2004).

    Estrogens and androgens –  The evidence linking these  to EOC are mixed. The majority of women who develop ovarian cancer are postmenopausal at the time of diagnosis. In postmenopausal women, the major source of circulating estrogen is from the peripheral conversion (in skin and adipose tissue) of androstenedione by the enzyme aromatase.

    Progesterone and progestins- Epidemiological data suggest that progestins and progesterone may have a protective role against EOC. Importantly, there is some evidence that progesterone might synergize with chemotherapeutic drugs to induce apoptosis.

Now this month  comes exciting news about  a  Paradigm Shift: Prophylactic Salpingectomy for Ovarian Cancer Risk Reduction   Frontline Medical News, 2014 Sep 24, B Jancin     :   Removing the fallopian tubes at the time of pelvic surgeries as a potential means of reducing ovarian cancer risk appears to be a movement that’s picking up steam in clinical practice.
       A recent survey of 234 U.S. gynecologists showed prophylactic bilateral salpingectomy is catching on when performed in conjunction with hysterectomy, but far less so for tubal sterilization, Dr. Austin Findley observed at the annual Minimally Invasive Surgery Week.                                                                       A total of 54% of respondents indicated they routinely perform salpingectomy at the time of hysterectomy in an effort to reduce the risk of ovarian cancer as well as to avoid the need for reoperations. However, only 7% of the gynecologic surgeons said they perform salpingectomy for tubal sterilization, even though 58% of respondents stated they believe the procedure is the most effective form of tubal sterilization (J. Minim. Invasive Gynecol. 2013;20:517-21).
  “In my experience at various hospitals, I think these numbers are a pretty accurate reflection of what folks are doing,” commented Dr. Findley of Wright State University in Dayton, Ohio.
     The prophylactic salpingectomy movement is an outgrowth of the tubal hypothesis of ovarian cancer.
    “There is now increasing and dramatic evidence to suggest that most ovarian cancers actually originate in the distal fallopian tubes. I think this is a concept most people are unaware of or are just becoming accustomed to. The tubal hypothesis represents a major paradigm shift in the way we think about ovarian cancers. The previous belief that excessive ovulation is a cause of ovarian cancer is no longer regarded as accurate,” he explained at the meeting presented by the Society of Laparoscopic Surgeons and affiliated societies.
      Ovarian cancer is the No. 1 cause of mortality from gynecologic malignancy, accounting for more than 14,000 deaths per year, according to National Cancer Institute data. The lifetime risk of the malignancy is 1.3%, with the average age at diagnosis being 63 years.
       Only 10%-15% of ovarian cancers occur in women at high risk for the malignancy because they carry a BRCA mutation or other predisposing gene. The vast majority of ovarian cancer deaths are caused by high-grade serous tumors that have been shown to be strongly associated with precursor lesions in the distal fallopian tubes of women at low risk for the malignancy.
            There is no proven-effective screening program or risk-reduction method for these low-risk women. However, with 600,000 hysterectomies and 700,000 tubal sterilizations being performed annually in the United States, prophylactic salpingectomy has been advocated as an attractive opportunity to potentially reduce ovarian cancer risk. Other common pelvic surgeries in which it might be used for this purpose include excision of endometriosis and laparoscopy for pelvic pain. It also has recently been shown to be feasible and safe post partum at cesarean or vaginal delivery (Obstet. Gynecol. 2014 [doi: 10.1097/01.AOG.0000447427.80479.ae]).
   But the key word here is “potentially.” It must be emphasized that at present the ovarian cancer prevention benefit of prophylactic salpingectomy remains hypothetical; in theory, the procedure should reduce ovarian cancer risk, but there is not yet persuasive evidence that it actually does, Dr. Findley emphasized at the meeting, presented by the Society of Laparoendoscopic Surgeons and affiliated societies.
            In contrast, one well-established ancillary benefit of prophylactic salpingectomy is that it eliminates the need for future reoperation for salpingectomy. This was demonstrated in a large Danish cohort study including close to 10,000 women undergoing hysterectomy and a similar number undergoing sterilization procedures. Among the nearly two-thirds of hysterectomy patients who had both fallopian tubes retained, there was a 2.13-fold increased likelihood of subsequent salpingectomy, compared with nonhysterectomized women.
        Similarly, Danish women who underwent a sterilization procedure with retention of the fallopian tubes – typically tubal ligation with clips – were 2.42 times more likely to undergo subsequent salpingectomy, most often because of the development of hydrosalpinx, infection, ectopic pregnancy, or other complications (BMJ Open 2013;3 [doi:10.1136/bmjopen-2013-002845]).
     The most commonly cited potential risk of prophylactic salpingectomy – decreased ovarian function – now appears to be a nonissue. This was demonstrated in a recent retrospective Italian study (Gynecol. Oncol. 2013;129:448-51) as well as in a pilot randomized controlled trial conducted by Dr. Findley and his coworkers (Fertil. Steril. 2013;100:1704-8), which appears to have answered many skeptics’ concerns. Indeed, Dr. Findley’s coinvestigator Dr. Matthew Siedhoff said he has recently been approached by researchers interested in collaborating in a larger confirmatory randomized trial, but all parties eventually agreed it was a no-go.
    “It’s a little hard to demonstrate equipoise for a larger randomized controlled trial. We’re beyond that now, given that prophylactic salpingectomy really doesn’t seem to make a difference as far as ovarian function,” according to Dr. Siedhoff, director of the division of advanced laparoscopy and pelvic pain at the University of North Carolina, Chapel Hill.
         Another oft-expressed reservation about salpingectomy as a means of reducing ovarian cancer risk in women seeking sterilization is that salpingectomy’s irreversibility may lead to “tubal regret” on the part of patients who later change their mind about further pregnancies. However, Dr. Findley cited a recent editorial whose authors criticized colleagues who made that claim. The editorialists argued that the tubal regret concern indicates surgeons weren’t really listening to their patients’ true desires during the informed consent conversation.
     “We should not have started thinking about salpingectomy for female sterilization only once a decrease in ovarian cancer risk became part of the equation,” they declared (Obstet. Gynecol. 2014;124:596-9).
           Dr. Findley noted that Canadian gynecologists are leading the way forward regarding prophylactic salpingectomy as a potential method of ovarian cancer prevention. The Society of Gynecologic Oncology of Canada in a 2011 policy statement recommended patient/physician discussion of the risks and benefits of bilateral salpingectomy for patients undergoing hysterectomy or requesting permanent sterilization. The Society of Gynecologic Oncology followed suit with a similar clinical practice statement in late 2013.
        Additionally, the Canadian group declared that a national ovarian cancer prevention study focused on fallopian tube removal should be a top priority.
    Gynecologic oncologists in British Columbia recently reported the eye-catching results of a province-wide educational initiative targeting gynecologists and their patients. In 2010, all British Columbia gynecologists had to attend a course on the role of the fallopian tubes in the development of ovarian cancer, during which they were advised to consider performing bilateral salpingectomy for ovarian cancer risk reduction.
              Surgical practice changed dramatically in British Columbia in response. In 2009 – the year prior to the physician education initiative – salpingectomy was utilized in just 0.3% of permanent sterilization procedures. In 2010, it was 11.4%. By 2011, it was 33.3%.
           Similarly, only 7% of hysterectomies performed in British Columbia in 2009 were accompanied by bilateral salpingectomy. This figure climbed to 23% in 2010 and jumped further to 35% in 2011. Meanwhile the rate of hysterectomy with bilateral salpingo-oophorectomy remained steady over time at 44% (Am. J. Obstet. Gynecol. 2014;210:471.e1-11).
     This project was conducted in collaboration with the B.C. Cancer Agency, which maintains comprehensive province-wide registries. Over time, it will be possible to demonstrate whether prophylactic salpingectomy is indeed associated with a reduction in the incidence of ovarian cancer. “I think this study demonstrated that there’s a lack of awareness on this issue, but also [that there’s] potential effectiveness of introducing an educational initiative like this in changing our practice patterns. As we start talking more about this issue amongst our colleagues and our patients, we’re more likely to see a practice pattern shift in the United States as well,” Dr. Findley commented.

17 July 2009     A new cancer study of  over 7 million women years is another major coffin for unopposed estrogen ET, for progestin Pg, and for oral  sex hormone therapy SHT.

Danish  Universities prospectively document  the incidence of ovarian cancer OvCa in a million postmenopausal women PMW  from 1995 through 2005.  Compared to non-users, use of HT increased OvCa (mean age 62yrs) by about 40%   for up to 2 years after stopping Ht, ie increased the absolute incidence  of clinically diagnosed OvCa from ~ 0.04 to ~0.052% ie per 100 patient yrs.

Transdermal TD ET alone  increased risk by 13%; vaginal ET by 23%;                                            Oral ET alone increased  risk by  34%; oral E+ progestin Pg by  48%;          TDE+Pg by 67%.

Thus the relative incidence of OvCa rose about 33% by 7 years on HT, to 48% if HT continued beyond 7years.

In 2004 Glud ea reported an increase risk of 31% for OvCa in Danish women on OHT use – total ET dose of ~5gm ie for about  for 15yrs – at a time when the standard premarin  dose was 0.625mg/d (equivalent to l mg E2)  if not double that .

For perspective,  the relative incidence of cancers in similar mostly 1st world European women from the  the USA SEER data for 2006 age over 50  years  are: BrCa 0.33%,  uterus 0.07%, ovary o.03%(ie very similar to the baseline Danish figure of 0.04% above), colon 0.15%,and cervix 0.01%. The new (Norwegian)  analysis in the latest BMJ suggests that screening mammography may result in overdiagnosis of BrCa by up to 50% (the other 50% may arguably never have been clinically significant-diagnosed- during life) , so the provocative could argue that the relative incidence of clinically significant BrCa to OvCa is more like eg BrCa 0.2 to ovary 0.03 ie just below 10:1. But OvCa is notoriously about 70% fatal within a few years, so  the absolute  mortality rate – at age 60-64yrs-  from  the same SEER  source and period are as relevant: BrCa 0.063%, uterus 0.011%, ovary 0.033%, colon 0.03% & cervix 0.005%. ie new OvCa may be only 1/10th as common as newBrCa, but BrCa  kills only twice  as many PMW as OvCa.

And finally the 2007  survey by  Rossing ea of  Menopausal Hormone Therapy and Risk of Epithelial Ovarian Cancer in women in Washington State 2002-2005 showed that  ET -mostly premarin (but not ET + progestin- MPA medroxyprogesterone provera) – especially in  low-parity  younger slim women increased OvCa compared to non-users, and that this risk  was highest- up to 90%-  in  users of OET  for more than 6 years.

By comparison – BREAST CANCER BrCa and HT: Hoover ea  1976  are the first on Pubmed to report doubling in  risk of breast cancer  BrCA after 15yrs on premarin in USA ie at least 5gm cumulative dose.

In Denmark by 1994 Ravn ea reported that if there was a risk of BrCa from OHT, it was small, and only after prolonged use of estrogen (15-20 years).  But by 2004 -2005 Tjønneland ea , Stahlberg ea  and Ewertz ea  found increased risk for BrCa  of 61 to 112%  associated with current use of HT.  Stahlberg ea already in 2003 concluded from recent studies from both the USA and Europe that the combined treatment regimens with estrogen and progestin increase the risk of BrCa  beyond the risk of unopposed estrogen.

In Norway, a recent Tromso study suggested that the dominant HT therapy used in Norway was oral estradiol E2 plus the progestin norethisterone acetate. . An earlier Tromso study in only 35000 PMW was too small- it showed that use of such OHT for >5yrs trebled the incidence of breast cancer BRCa, but did not influence that of OvCa.

Apart from smokers’ lung cancer, the commonest cancer in older women- BrCa- clinically affects perhaps 5% of PMW  lifelong – but  with prompt therapy after clinical presentation kills as few as 5% of sufferers- and with appropriate OHT (premarin +- provera)  for up to 8years in the Women’s Health Initiative both the incidence of and mortality from BrCa, and all-cause mortality,  were reduced by about one-third. Hence appropriate HT saves many from both BrCa and from premature death and disability from the commonest degenerative diseases- vascular, dementing and fracturing. 75% of women who develop BrCa  die with it –  not from it but from far more prevalent degenerative diseases after an  otherwise normal lifespan. But the Danish evidence is that combined OHT will increase OvCa by >50%.

Ovarian Ca kills 70% of victims, and is it so rare compared to BrCa? .

Hence with the perhaps 2/3  lower incidence of OvCa, it is a relatively trivial problem for women overall- except for the 4  in  10 000 women  who develop it, who have <50% 5year survival, ie 3 out of 4  of whom it will kill within a few years- compared to <25% of breast cancer victims who will be killed by the BrCa.

However, it becomes clear that these hormone-dependent cancers are both  duration-  and total-dose HT related; but even more important, that unopposed OET is a risk if persisted more than about 12 yrs; and even if used in far lower dose parenterally, the risk of OvCa is far higher if combined with the European fashion of androgenic synthetic progestins Pg – even parenterally; whereas the American MPA for up to 8years at least apparently if anything mitigates the OvCa risk of ET..

By contrast this column has repeatedly reviewed evidence that balancing physiological ERT with physiological testosterone replacement TRT eliminates the risk  for BRCA and endometrial cancer of unopposed ERT +- PRT in PMW.  Intuitively this should also apply to ovarian cancer.

Hence the message strengthens that PMW should not be exposed for  any length of time at any stage to the much higher oro-hepatic HT doses (needed for symptom control) or OET+- Pg; but as in all other endocrine replacement for permanent  multisystem prevention – let alone sexual function-  patients with gonadal deficiency should have physiological sexhormone balance restored  ie with balanced parenteral  human androgen, estrogen and progesterone replacement.

It is common cause that (reproductive cycles and pregnancy aside) all the physiological  prime sex hormones-DHEAdehydroepiandrosterone, P4, T, E2, E3 – are as important as all other human hormones, essential life long  for optimal health; and that estrogen dominance (due to inadequate  androgen and progesterone levels) is deleterious. Hence most PMW require both physiological progesterone and androgen replacement- sometimes to balance excessively high endogenous estrogens, usually to accompany necessary ERT for full balance.

ndb

HRT UPDATE 2014 : NEUROPROTECTION: KEEPSTUDY RESULT with ESTRADIOL and PROGESTERONE: THE MOST IMPORTANT RCT IN HALF A CENTURY ON APPROPRIATE USE OF HRT IN WOMEN: Oral Versus Transdermal HRT

28 Sept  2014  AFFIRMNG THE PRIMACY OF PROGESTERONE REPLACEMENT AT ALL AGES FOR HORMONER IMBALANCE why we use progesterone cream  as the basic HRT- to protect all systems, brain, bones, heart, muscle, immune etc:                                                                

   Progesterone and neuroprotection. Singh M1, Su C.      Dept  Pharmacology and Neuroscience, Institute for Aging and Alzheimer’s Disease Research, University of Texas   Horm Behav. 2013 .
           
Numerous studies of the role of estrogen on brain  used the ovariectomized rodent as the  model. But while estrogen intervention in these animals  at least partially, restored cholinergic, neurotrophin and cognitive deficits in the ovariectomized animal,  removal of the ovaries results in the loss of not only circulating estrogen but of circulating progesterone as well. As such, deficits associated with ovariectomy may be attributed to the loss of progesterone as well. Similarly,  human menopause results in  precipitous decline of not just circulating estrogens, but in  progesterone as well and as such, increased risk for diseases such as Alzheimer’s disease during the postmenopausal period could also be contributed by this loss of progesterone. In fact, progesterone has been shown to exert neuroprotective effects, both in cell models, animal models and in humans. Here, we review the evidence that supports the neuroprotective effects of progesterone and discuss the various mechanisms that are thought to mediate these protective effects. We also discuss the receptor pharmacology of progesterone’s neuroprotective effects and present a conceptual model of progesterone action that supports the complementary effects of membrane-associated and classical intracellular progesterone receptors. In addition, we discuss fundamental differences in the neurobiology of progesterone and the clinically used, synthetic progestin, medroxyprogesterone acetate that may explain  negative findings of the combined estrogen/progestin arm of the Women’s Health Initiative-Memory Study (WHIMS) and suggest that the type of progestin used may dictate the outcome of either pre-clinical or clinical studies that addresses brain function.

 

1/1/2014:    Testosterone and progesterone, but not estradiol, stimulate muscle protein synthesis in postmenopausal women. JCEM  2014 Jan:   Smith ea ..  Remember, this is one of many reasons why women should never use unopposed estrogen- it melts collagen in muscle, except in the womb; and promotes  fattening,  breast growth; cancer (except in the colon);  inner hostility;  fluid retention;  thrombosis; and gallstones;  and perhaps prolapse, and fatness frailty, falls and thus fractures and death. …

it doesnt mean women mustnt be gven  estrogen alone . eg they may have obvious testosterone dominance post menopause, in which case if their estrogen balance is too low, with poor memory,  bad hot flushes and dryness, a little BiEst or estriol cream may be added to balance the testo dominance, as opposed to causing estrogen dominance – always with  some balancing P4  transdermal progesterone – not a patent synthetic ie commercial xenoprogestin.

as the 2013 consensus statement of the International Menopause Society says, estrogen replacemnt ERT should be started appropriately as soon as possible after menopause; but not a progestin (ie synthetic) since these have risks which human P4 progesterone does not have. As the KEEPS trial, and Genazzani ea 2008 confirmed, physiological transdermal human ERT and P4 even  in the short term (ie 5 years)  have the benefits of conservative doses of oral HRT but without the risks of oral ie hepatic first pass estrogens and progestins.

It is inappropriate, shortsighted to say- as many doctors and patients still unwisely do,  that taking HRT orally up to age 60years is safe convenience, when the cumulative risks  (especially of breast cancer) are lifelong .   So  it is common sense and good practice  to avoid the risks of oral HRT, use them permanently transdermally in balance for vital permanent protection with  avoidance of all risks.  But doctors and patients often refuse to think physiologically,  since that doesnt pay for  Big Pharma  and the  corporate Disease Industry, for whom Only Disease Pays. In fact it is negligence not to use balanced appropriate transdermal HRT permanently to retain the health of youth till a good peaceful death.

ndburman@gmail.com        Oct 6th , 2012 UPDATE:  THE KRONOS EARLY ESTROGEN STUDY KEEPS TRIAL PRELIMINARY  RESULT  just announced (3 Oct) by Mitch Harman ea at the current Florida North American Society Florida Congress.

It supercedes as the most important RCT in 50 years and  confirms in early postmenopausal women the results we summed up below in 2009 in pubertal Turner’s Syndrome girls in  the Indiana University study, which used the same dose of premarin but almost half the dose of estradiol patch- but found  better results with the E2 patch than premarin orally.

   see  global KEEPS results  at http://www.heraldonline.com/2012/10/03/4311575/hormone-therapy-has-many-favorable.html

 As we expected from the double blind randomized controlled KEEPStudy,  with no alerts of problems in any arm during the  5yr trial,

- with lower ie 0.45mg/d   premarin (than in the WHI)  vs E2  50mcg /d patch,  +-progesterone orally-
-both estrogens showed   no harm, uniform trend to better outcomes, with slight differences favouring one or the other estrogen route, but increase in both HDL and triglycerides on premarin.
Hence KEEPS does not change the evidence that the best regime  for both all-system benefits and zero risks  remains lowdose  parenteral estrogen eg  BiEst (estriol ~80%, estradiol ~20%) TD cream (eg 0.1%), balanced with progesterone TD  cream (eg  1%) for all-system protection and symptom relief; plus if needed testosterone  cream (eg ~0.5%) for low energy/mood/sexuality/breast protection. .
These preliminary KEEPS results further  refute the widespread  mythical wrong deductions that prophets of doom especially in North America and UK  drew  from the WHI trial and the Million Women Study  that so harmed womankind, which unjustified condemnation of all  and appropriate balanced HRT  it has taken 10 years to only partly correct. (Syd Shapiro, Richard Farmer, John Stevenson ea:  DOES HRT CAUSE BREAST CANCER? An application of causal principles to three studies parts 1 to 4: J Fam Plann Reprod Health Care.    2011-2012)  .
.

April  10, 2009:  THE MOST IMPORTANT HRT STUDY IN HALF A CENTURY:  Nabhan ea at Indiana University have just published perhaps the most important randomized controlled trial RCT in half a century on physiological benefits and pitfalls of Estrogen replacement ERT in women.

Pubmed search under menopause or HRT trials yields reports only from 1975, simply because that is when Medline was established.

But in fact William Masters  ea in 1953 in St Louis published the first traceable- and most important ever-  sex hormone SHRT  RCT,  giving balanced testosterone plus estradiol (in a ratio that they found was optimally 20:1) or placebo parenterally for 13 months apparently blind to already institutionalized old women at a mean age of 73years;  showing that while 1/3 were not unsurprisingly too far gone to benefit, 2/3 of them recovered sufficiently over 6 weeks that the nursing care on the ward could be halved for the next year of followup- without any significant reported adverse effects, and with uniform atrophy of the endometrium at 6months on curettage. This trial may not have been double blind, but Masters and Grody detailed  the randomization to hormone or control injection.

Albeit using perhaps half  the dose of hormones as far longer- acting esters (than Masters used),  Gelfand  in Montreal (1987-2004) confirmed the long-term safety and benefits of combined depot injection. As Gelfand wrote in 1999,  “The objectives for the management of a menopausal patient are ( I ) to increase longevity, (2) to prevent age-related deterioration, (3) to maintain a quality of life, (4) to prevent induced risks, and (5) to maintain a physiologic hormone balance.”   We  should  regard longevity as the lowest  priority,  Gelfand’s other four objectives are equally paramount- and the bedrock of medicine especially endocrinology is to mintain physiological balance. Why should   women be treated otherwise?

As this column has regularly described, most women  find that the  dose of about 0.5 to 1 mg testosterone and 25  to 50mcg of estradiol daily as a pro rata +- fortnightly tiny subcutaneous  depot (self) injection) via a 25g needle is optimal, providing reasonably physiological mean  blood levels, and once dose titration has found the right recipe,  some (like most men) prefer it to the bother of patches or creams.

And many groups world wide  have  for decades done so with  human E+T hormone combination long term as implants, albeit in a much lower ratio. Now this combination has become the physiological gold standard as creams and patches, which allows the patient more promptly and safely to determine her optimal dose and route of each sex hormone. Three monthly depot injection of Nebido testosterone undecanoate has become the gold standard in men, as it  will in due course in women at 5%  to 10% of the male dose.

For over 30 years scientific studies have broadcast the many adverse effects of oral CEE with progestins, especially on the risk of breast cancer long term. But, led by drug companies and their well-paid researchers and lobbyists promoting patented equine and other designer hormones so as to suppress the sale of cheap human sex hormones, women and gynecologists duped themselves into following Wyeth’s saturation marketing and, especially in the English-speaking countries, continued to use mostly oral conjugated equine estrogen and synthetic progestins.

Barbara Seamen, who died last year, was a prophet of sex hormone benefits and risks as Margaret Sanger was of proven safe barrier contraception. But  the climate against advocacy for women was still so hostile in USA  that even in 1978 Barbara and her psychiatrist husband Gideon Seamen published their book Women and the Crisis in Sex Hormones in UK (as Sanger had had to do with her book My Fight for Birth Control in 1934). A decade before the Seamens’ book,  Dr Robert Wilson’s hysterical  Feminine Forever had been  published in 1966 in USA – marketing  premarin CEE 1.25mg a day – leading up to the flood of endometrial cancer by the mid-1970s, and increasing breast cancer (Henderson ea 1980)..

But many doctors and patients were convinced about the dangers of progestin when the first badly analyzed results of the WHI- with oral OCEE premarin + MPA provera- were published in 2002; although the CEE- only arm of the WHI was allowed to continue another 2 years until it too was wrongly stopped because of overestimated accruing adverse events in all-age EXCEPT when started well under 60yrs.

But the hardest skeptics had to concede that oral CEE at the then-standard dose of 0.625mg/d (equivalent to estradiol 1mg/d) in women post hysterectomy reduces all common major aging events (fractures, breast & colon cancer, cardiovascular, memory problems and all-cause mortality) when started appropriately soon after menopause and used for up to 9 years- with the only adverse effects being increase in adiposity, urinary incontinence, venous thromboses and gallstones. .

The Womens’ Health Initiative WHI 2007 showed plainly that OHT started (as is conventional practice) soon after menopause ie near age 50yrs with OCEE alone (ie after hysterectomy) or with CEE+MPA,  for up to 8 years,  reduced all-cause mortality by 30%; BUT whereas CEE alone in this young cohort reduced both (breast cancer and CVD and fracture) events AND (breast cancer and CVD and fracture ) mortality by about 30% , CEE+MPA increased CHD and stroke events by 49%.

Thus in the young WHI cohort, given that all-cause mortality also fell by 30%, CEE +MPA must have reduced breast cancer mortality by even more to offset increased mortality from CVD in the young CEE+MPA cohort. . This improvement in survival after breast cancer with “appropriate” early and long term OHT has been long recognized.

Earlier studies eg the open prospective StaTur ( Soriano-Gullen ea 2005) in France  in girls with Turner Syndrome had already suggested  ” that growth hormone and estrogen (from about age 12yrs)   attain optimal adult height; and the use of percutaneous vs. oral estrogens was associated with greater height (_2.1 cm; 95% confidence interval, 1.00–3.25).”

Now the 12month Indiana trial highlights the physiological benefit for teenagers of human transdermal TD E2 (HERT 25 then 37.5mcg/day) versus  +- 20 times the estradiol equivalent dose as conjugated equine oral xenoestrogen (0.3mg then 0.46mg CEE/day) in obese short  prepubertal girls age +- 14 (range 11-17) yrs with Turner Syndrome TS (half 45XO karyotype; mean height 1.427m , weight 49.6kg, BMI 25.3kg/sqm).   At a CEE dose per kg body weight similar to that used in PMW postmenopausal women (mean weight +- 73kg, BMI 28.5kg in the WHI), the TDHRT dose had far superior effect over oral hormone therapy OCEE in promoting  better height,  bone density, and uterine and breast growth catch-up .

According to CDC tables 2000, the average height of USA 14yr old girls was 1.6m and BMI  19.3kg/sqm; but girls at 1.45m height had  mean BMI 17.7kg/sqm; thus the TS girls in the Indiana study at baseline  were 17cm shorter than average normal 46XX girls, but (like postmenopausal women) 43% over average weight for height. They report that there was no difference between the estrogen routes in change in body composition.

Although the Indiana study for economic reasons  omits blood sex hormone levels, the results highlight some stark facts about unopposed parenteral HERT versus OCEE in women without functioning ovaries:

* lowdose TD ERT had far more effect than OCEE in promoting progressive height and bone density accrual; but

*TD ERT is far more potent than the perceived “equivalent” dose of OCEE in promoting both myometrium, and glandular proliferation (breast and and endometrial) .

This observation obviously cannot simply be extrapolated from sex-hormone-naive girls to PMW; but it reinforces that

*in PMW,  human estrogen  (rather than breast-cancer-promoting OCEE) should be given parenterally in small enough dose  to replicate low average monthly physiological (free) estrogen levels in young women, and

*should never be given without ensuring that physiological androgen (and progesterone) levels as (in healthy young women) are available (naturally or by parenteral androgen replacement ART and parenteral progesterone replacement PRT) to offset the proliferative effect of even lowdose estrogen on both breast and uterus, let alone on dissolution of muscle collagen as witnessed by the doubling of postmenopausal stress incontinence on OET.

The Karolinska institute showed in 2007 that lowdose testosterone patch reversed the increase in breast proliferation caused by OE+P; and in 2008 that endogenous free TT levels have antiproliferative effect on breast tissue, perhaps mediated via the progesterone receptor; this confirms the observations of Masters, Greenblatt, Schleyer-Saunders, Gelfand, Gambrell, Vliet, Buster, Clarkson, Whitehead, Studd, Burger, Davis, Dimitrikakis Zhou and Bondi, and Davies’  Cape Town group, that the preservation of youthful female testosterone balance protects both breast and womb of primates from the proliferative effect of estrogen and progestin.

And in 2006 the Karolinska also reported in a retrospective observational study that previous HT (mostly OHT)  use was associated with a 70% increase in meningioma.

Last year l’hermite, Genazzani ea reviewed the sixty-year -known benefits of parenteral over  oral estrogen and progestins.

Shufelt and Braunstein last month  sum up the accumulating safety data on female  testosterone replacement TRT the past sixty years: that “replacement of serum plasma testosterone levels to or slightly above the reference range for young women does not increase the risk of hepatotoxicity, endometrial hyperplasia, behavioral, cardiovascular, cancer or haematolological adversity. Models of superphysiologic testosterone levels, such as polycystic ovarian disease, have not shown an increased risk of breast cancer. As with all hormone therapy, testosterone therapy should be individualized to optimize benefits without risks”.

ie   all SHT-  ERT,  TRT and PRT-  should be parenteral and titrated to physiological SH balance so as to give maximal well-being without causing significant proliferation in acne, hirsutism, adiposity, breast or uterus.

Hence it is unwise  to give  even TD estrogen unopposed even  after hysterectomy.

Even unopposed progesterone- as is now so popular as “natural” over-the-counter cream- has proliferative effects on the uterus and breast, so should not be used post menopause  without monitoring these organs and ensuring adequate blood levels of balancing androgen. While  progesterone itself  has many physiological benefits, both natural progesterone  and synthetic progestins  may activate dormant breast cancer (Horwitz 2008),  accelerate aging hearing loss (Sellars 1971; Dubno 2008; Horner 2008; Price 2009); and overall,  RCTs do not show that they reduce fracture risk.  And of course liberal use of progesterone will suppress what endogenous estrogen and testosterone remains  post menopause, as oral and depot synthetic hormones do in contraceptive use.

As always in human physiology, it is unpredictable to what extent progesterone may convert to testosterone and estradiol. Despite Dr John Lee’s enthusiastic advocacy (backed by no RCTs), the absence  of proven benefit of progesterone on bone density and fracture risk long term discredits progesterone as a significant source of estrogen and testosterone- but does not negate it’s indisputable role in longterm balanced HRT as an immunomodulating neuropsychoprotective.

The comprehensive recent review of HRT by Santiago Palacios points out that progesterone has a different function profile from all synthetics, being anti-aldosteronergic ie not fluid-retaining, and weakly anti-androgenic. He  stresses the target of ultralowdose estrogen to maximize the benefit:risk ratio, with consensus that appropriate HT started soon after menopause almost halve both CHD and fracture risk.

The KEEPS RCT now well under way (Harman, Naftolin ea – with roughly similar CEE  and TDERT dose to the Indiana trial, and oral micronized  progesterone) will no doubt again confirm the better safety profile of TD ERT over premarin, with no risk from the cyclical  progesterone- but that trial is only to run for 5 years ie to finish in 2012, so it will not negate Henderson’s strong 30year-old data that  oral CEE +- progestin taken for  more than about a dozen years  increases the incidence of breast cancer, although it lowers  mortality. So far KEEPS is running smoothly without concerns arising (Mitch Harman personal communication).

Prescribing appropriate OHT extends healthspan and lifespan. But should it ever be preferred if it increases the risk of thrombosis, and  from the 2nd decade of use breast cancer?  whereas this risk is minimized with addition of appropriate testosterone, especially if  all SHRT is parenteral.

In contrast to Victorian times when only a minority of women survived to menopause, the average age of menopause is now around woman’s  midlife, and there is never contra-indication to the healthspan-lengthening benefits of  balanced SHRT for the second half-century of life.

CONCLUSION:

The Indiana study in hormone-deficient teens is a signpost that both young and old need the youthful balance of physiological levels estradiol, testosterone and progesterone – for far more than reproduction, sexuality and femininity- but, crucially, at physiological parenteral dose that will not expose her to breast cancer activation, ie avoiding oral HT.

Crucial as  all three prime hormones  are in the young, sexuality and femininity   are sadly not essential for reproduction-  but once experienced, cherished  while the heart and eyelashes  still flutter… For obvious reasons well known to sexually active adults, like PMW at all ages, girls with Turner’s syndrome should also be  entitled to the benefits of appropriate triple hormone replacement from mid-teens so they too can experience appropriate mature adult sensuality and bonding.

The estrogen-progestin treatment of Turner’s Syndrome and PMW   is also a paradigm of the increasingly common problem of flattened sexuality in young women-  from birth-control  xeno-hormones;  cortisone and psychotrope use; AIDs and ARV use; metabolic syndrome and diabetes; and after pelvic cancer therapy or sterilization. All these women should be considered for appropriate  parenteral sex hormone therapy  (if necessary with all three hormones) based on both their clinical picture and full hormone profile.

ndb

METFORMIN REDUCES ALL CHRONIC DISEASES, INCLUDING IMPROVING THYROID FUNCTION.

this new report Metformin and low levels of thyroid-stimulating hormone in patients with type 2 diabetes mellitus from  McGill University; Montréal, Quebec. says nothing that is seriously clinically significant, it is merely common sense.

It does not show that metformin causes any heart or thyroid dysfunction ie change in thyroid hormone levels,  merely that it reduces TSH  in those on thyroid replacement.- indicating that  thyroid dose may be able to be tapered.    

A parallel new study from Italy  Metformin-induced thyrotropin suppression is not associated with cardiac effects  confirms there is no heart risk- quite the contrary.

People tend to fatten and slow down as they age, and these people tend to  metabolic syndrome ie obesity, cholesterolemia, hypertension, vascular disease and thus diabetes- same as patients with hypothyroidism. So type 2 diabetes, hypothyroidism (sometimes preceded by hyperthyroidism) and aging go together- usually without demonstrable direct cause and effect.

This new McGill University metformin study does not claim any cause and effect.  The link may be simply  that metformin (which is simply a carbon-hydrogen -nitrogen molecule)  improves all metabolic functions- antioxidant, nitric oxidant- including iodine/TRH/ TSH / thyroid/insulin   hormone responses. .

So as with all nutritional supplements and exercise  that improve metabolism, metformin may improve treated hypothyroidism by improving peripheral thyrooxine receptors , and thus lower need for thyroid replacement.
Metformin or the parent galega a medicinal plant extract used for many centuries reduces new diabetes and all diseases and deaths by 1/3 to 2/3.

it is among other things a prohormone regulator, improving common insulin resistance.

the definition of low TSH is arbitrary. If much below 1, it is suspicious of thyroid overactivity, excess thyroid hormones-
but rarely may reflect central ie pituitary failure to produce enough TRH/TSH and thus cause central hypothyroidism.

so TSH unless way outside the ‘normal’ range of 1 to 2 is a poor guide to health and disease, which is based on clinical  state and the thyroid hormone and antibody levels.

Most aging people develop some degrees of thyroid underactivity, which generally responds to replacement of deficient selenium, iodine and sex hormones without addition of risky thyroid hormones- for which conventional blood levels are a poor guide.

so as in all patients whatever their state and treatment, thyroid function should like all other functions be considered periodically.

ndb.


  Metformin and low levels of thyroid-stimulating hormone in patients with type 2 diabetes mellitus  McGill University; Montréal, Quebec.

Background: Small cross-sectional studies have suggested that metformin, a first-line oral hypoglycemic agent, may lower thyroid-stimulating hormone (TSH) levels. Our objective was to determine whether the use of metformin monotherapy, when compared with sulfonylurea monotherapy, is associated with an increased risk of low TSH levels (< 0.4 mIU/L) in patients with type 2 diabetes mellitus.

Methods: Using the Clinical Practice Research Datalink, we identified patients who began receiving metformin or sulfonylurea monotherapy between Jan. 1, 1988, and Dec. 31, 2012. We assembled 2 subcohorts of patients with treated hypothyroidism or euthyroidism, and followed them until Mar. 31, 2013. We used Cox proportional hazards models to evaluate the association of low TSH levels with metformin monotherapy, compared with sulfonylurea monotherapy, in each subcohort.

Results: A total of 5689 patients with treated hypothyroidism and 59 937 euthyroid patients were included in the subcohorts. Among patients with treated hypothyroidism, 495 events of low TSH levels were observed during follow-up (incidence rate 119.7/1000 person-years). In the euthyroid group, 322 events of low TSH levels were observed (incidence rate 4.5/1000 person-years). Compared with sulfonylurea monotherapy, metformin monotherapy was associated with a 55% increased risk of low TSH levels in patients with treated hypothyroidism (incidence rate 79.5/1000 person-years v.125.2/1000 person-years, adjusted hazard ratio [HR] 1.55, 95% confidence interval [CI] 1.09–2.20), with the highest risk in the 90–180 days after initiation (adjusted HR 2.30, 95% CI 1.00–5.29). No association was observed in euthyroid patients (adjusted HR 0.97, 95% CI 0.69–1.36).

Interpretation: In this longitudinal population-based study, metformin use was associated with an increased incidence of low TSH levels in patients with treated hypothyroidism, but not in euthyroid patients. The clinical consequences of this need further investigation.

HORMONES 2014, 13(2):252-258
Carlo Cappelli,1 Mario Rotondi,2 Ilenia Pirola,1 Barbara Agosti,3 Ana Maria Formenti,1 Pasquale De Cata,2 Massimo Salvetti,1 Luca Chiovato,2 Maurizio Castellano1

1Department of Medical and Surgical Sciences, Endocrine and Metabolic Unit, University of Brescia; 2Unit of Internal Medicine and Endocrinology, Fondazione Salvatore Maugeri Istituto di Ricovero e Cura a Carattere Scientifico, Istituto Superiore Prevenzione e Sicurezza Lavoro Laboratory for Endocrine Disruptors, University of Pavia; 3Diabetic Unit, Spedali Civili di Brescia; Italy  http://www.ncbi.nlm.nih.gov/pubmed/24776625

Abstract

OBJECTIVE: Metformin treatment may induce a decrease/suppression in serum TSH levels, mimicking sub-clinical hyperthyroidism (SHT). The aim of the present study was to retrospectively evaluate changes in several electrocardiographic indices in euthyroid subjects with diabetes who, after starting metformin treatment, developed a low serum TSH as compared to patients with SHT resulting from an underlying thyroid disease or TSH suppressive treatment with L-thyroxine.
DESIGN: Heart rate, P wave duration, P wave dispersion, QTmax, QTmin and QT-dispersion were assessed in 23 patients with diabetes treated with metformin before and after 6 months of TSH-suppression and in 31 control patients with SHT.
RESULTS: No significant changes in electrocardiographic parameters were observed from baseline to the TSH-suppression measurement. A significant difference in P wave duration (102.9±7.4 vs. 92.1±5.8 ms, p<0.001), P wave dispersion (13.1±3.4 vs. 7.1±3.5 ms, p<0.001), QTmax (399±18 vs. 388±16 ms, p=0.024), QTmin (341±14 vs. 350±17 ms, p=0.038) and QT dispersion (49.9±9.6 vs. 30.9±9.2 ms, p<0.001) were observed between the control group with SHT and the group of diabetic patients with low serum levels of TSH.
CONCLUSIONS: Our results show that the TSH-suppressive effect observed in patients taking metformin is not associated with peripheral markers of thyroid hormone excess, at least at the cardiac level.