(No emergencies or surgery- these must go to nearest polyclinic or hospital ER). . . Holistic integrative chronic natural medicine practice (HRT, pain relief, infection eg HIV AIDS, TB, /cancer/obesity screening & prevention;
Category Archives: Womens’ Health Initiative WHI
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,
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, 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.
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.
update 8 August 2013 the OregonUniversity Linus Pauling Institute website still promotes the numerous benefits of fishoil.
update 2 August 2013 the Topol- Rowen- Peskin rejection of need for fish oil EPA+DHA was not supported by the recently NEJM-published R&P 5 year trial in Italy, which compared modified ie patented ethylester marine essential fatty acids with olive oil.
This R&P trial was thus not a trial of fish oil (concentrate or otherwise), nor placebo-controlled, since olive oil is hardly a placebo- in the 13.4year Spanish EPIC trial published last year , olive oil dramatically reduced all-cause mortality by 1/4 and CVD mortality by 44%. The full 2013 NEJM R&P paper is inexcusably silent in omitting this cardinal fact that it was no ways placebo-controlled- placebo means an inert comparator.
the 2010 Nordic study ( Dyerberg ea Copenhagen University- who first reported in 1978 the association between marine omega3 PUFA and health in Eskimos) http://www.nordicnaturals.com/images/pdfs/tgstudy.pdf details the better bio-availability of natural ie triglyceride- bound fish oil- EPA+DHA compared to that in processed ethylester low-triglyceride omega3 products- as used in the R&P and GISSI trials of patented commercial designer products. .
2 June 2013 Its some 4 years since this healthsite started promoting marine oil for optimal development and health.
what say you to the latest hype about the predictable negative result of the Italian N-3 Cardiovascular Risk and Prevention trial R&P from the NEJM? ie that omega3 oil was no better than olive oil.
the major problem is that the R&P trial didnt use natural clean FISH OIL, nor in primary prevention.
Nowhere does it say it used fish oil- it says N-3 ie omega3, and in patients with multiple vascular disease. Nor does the original 2010 R&P plannng paper state that in fact it used a patent formula of chemically changed ethyl esters in tertiary prevention,
like the GISSI trial used apparently patent branded altered Om3 after heart attacks – it wasnt natural clean fish oil..
the GISSI abstracts 1999 and 2008 also dont mention fish oil.So it wasnt natural fish oil like I use and promote- clean codliver oil or clean om3 concentrate from clean factories in northern Europe and now even from Cape Town.. The R&P abstract paper cleverly doesnt mention the brand Omega3 name- but Pfizer funded the trial…Its the “top” journals likely up to their old tricks, publishing probable infomercials paid for in this case by Pfizer and mates, without making that clear.I cant see if these Italian trials used Lovza/Omacor or whatever Big Pharma chemically altered snakeoils.But looking at the extensive debate already around Dr Topol’s condemnation of real fishoil supplement, many commentators fell into the same trap- they didnt notice that R&P didnt use fish oil, but about 850mg/day ethyl esters of omega3.
Synthetic patent designer drugs dont do what the natural food/supplement/human biophysiologic product does.
Ethyl esters eg ethinylestradiol, and xenohormones eg Premarin, are dangerously different from estradiol. Look at the controversy, the danger in using altered natural products eg:
slowrelease niacin instead of natural niacin.
or neurontin/lyrica or benzos instead of natural GABA to bind to the GABA receptors. or anabolic steroids eg methyltestost instead of testosterone. or methylprogesterone Provera instead of progesterone. or margarine instead of butter !. or methanol – dangerously different from ethanol; or synthetic substitutes for natural digoxin…
or the Women’s Health Initiative- which through gross misrepresentation stopped many women from using beneficial physiological human HRT for 10 years, despite the bad design of the WHI that used long-proven risky xenohormones (premarin, provera) at dangerous older age, while in the first 6 years it enormously benefitted women in the first decade after menopause.. .It’s dis-ingenouos of Messrs Rowen, Topol and Peskin not to state this, that the R&P TRIAL DIDNT USE FISH OIL..
Dr Rowen and Mr Peskin are heavily promoting their own PEO Parent Essential Oil Brand of Omega6 plant oils. The evidence is that such combination is excellent benefit- but I see no science, no reason not to balance it with clean fish oil since this is now so deficient in general diet.But surely Prof Topol is doing patients a huge disservice in backing the R&P trial in dumping fish oil -when that trial didnt use fish oil, and makes no conclusion about fish ol?
I await the full copy of the R&P study – which the NEJM mysteriously doesnt make available on line as they usually do with any seriously important new study.. .No-one doubts that good plant oils , good mixed diet have benefit.there is no doubt that a few gms of fish oil a day have huge benefit.
Its the balance that matters- and the avoidance of smoking, sloth, adiposity, refined sugars and cooked animal fats that matters.so I see no reason to change from taking/ recommending daily a tsp (or 4) of codliver oil (ie about 800 – 3000mg EPA+DHA) ,
and olives/ mixed nut/plant/olive oils on salads/pasta etc ,
what say you?…
NATIONAL MAMMOGRAPHY DAY 21 OCT 2011: WORLD BREASTCANCER AWARENESS MONTH National_Breast_Cancer_Awareness_Month : THE DEBATE AGAINST XRAY SCREENING MAMMOGRAPHY OF LOWRISK WELL BREASTS. MOTIVATION FOR NON-XRAY SCREENING MAMMOGRAPHY:
A medical scheme recently asked for a motivation letter for a member wanting them to fund a non-xray mammogram.
Thinking women cannot do like a postmenopausal professor in genetics – a senior health lecturer and counsellor no less- shrug off the issue of their blind obedience to medical diktat as “not my field”, when unquestioningly undergoing invasive let alone known hazardous tests like screening xray mammography, and major therapy for asymptomatic hidden lumps, on the say-so of their doctors/ their medical scheme advisors, however great their eminence.
Safety in numbers of eminent opinions is no assurance that the collective conventional wisdom and Guidelines are correct, when such conventional wisdom is as likely as not turned on its head in a few years.
Blind obeisance without careful personal study of the evidence for and against is as foolish as taking the advice of the glib salesman self-promoter in any costly and therefore risky investment, be it in health as in finances, property, a motor car, costly other assetts, a job or a glib new lover.
This week Dr Joe Mercola highlights the latest reports from USA, the double disaster of xray mammography increasing the risk of breast cancer in women with a familial risk; and more than half of women xray- screened regularly over 10 years receive at leat one false-positive recall- with all the extra breast procedures, and upset, that that entails.
Look at what happened to USA and UK-Europe when they blindly followed the advice of the snakeoil vendors the Bush-Blair Gang in invading Iraq in 2003, and listened to the advice of their self-enriching financial gurus and bankers that led to the demise of balanced national budgets and the western capitalist system in 2008. The USA has achieved the unthinkable, being downgraded to the most bankrupt country, worse than many southern European nations now are, because Bush for the benefit of his cronies abandoned the common-sense balanced budgets reducing national debt insisted on by Clinton, and plunged USA into multitrillion dollar debt that future generations of taxpayers have to pay. .
In women without breast symptoms or familial risk of breast cancer, regular analysis of evidence to April 2011 on the pros and cons of SCREENING xray mammography ie breast imaging, showed increasingly the risk but no benefit of such xray screening.
The anonymous Wikipedia review outlines the violently opposing views of the screening mammography issue – from sceptical independent analysts, and from the zealous majority, the lucrative vested-interest screening xray mammography – breast surgery industry, who claim shortterm benefit from emotive early diagnosis and treatment. .
It is a sign of the paradigm shift in medical thinking and dogma when a leading medical school eg Tygerberg Hospital no longer accepts women with a palpable breast mass referred for diagnosticxray mammography, but instead first sees them for careful history, examination and fine needle aspiration biopsy.
Last months’ leading Radiology journal features a debate between the two opposing viewpoints; ; as does a recent medscape debate; http://www.medscape.com/viewarticle/734977 with Heaod of Radiology Daniel Kopans at Harvard spearheading the xray mammographers and breast surgeons argument – Just the facts: mammography saves lives with little if any radiation risk to the mature breast.
and Dr Cornelia Baines from Toronto University joins the European and USA critics of routine screening in exhaustively analysing why so many studies convincingly confirm the original Canadian Breast Cancer Screening Study Miller, Baines ea 2004 evidence against routine xray screening – xray screening did not reduce breast cancer mortality after 13years when compared to routine clinical breast examination;
– and the 2009 recommendation of the US Preventitive Task Force to limit recommendation for xray screening mammography to well women only from age 50 years onwards, and every 2 years not annually. Since April 2011 at least nine more authoritative independent scientific papers listed below detail why routine screening xray mammography of well breasts (in women not at known increased risk) gives no longterm meaningful reduction in either invasive breast cancer or mortality. In fact, there is evidence that such repeated breast trauma- crushing, irradiation, surgery and therapy – actually increases risks of mastectomy, breast cancer and mortality after 10 years, just as oral xeno-hormone replacement therapy may.
The Dec 2010 UK NHS recommendation brochure by contrast limits screening mammography to women over 50yrs up to 70yrs, and only every 3 yrs. Thus the UK recommends only about 7 screening mammograms over her lifetime for well lowrisk women. This contrasts with the pressure on USA women to have screening from age 40 years annually ie four times as many as in UK- about 30 screening mmmograms over her lifetime. …
The latest published study, from the University of California no less – confirms their earlier 2007 study that the more costly computer-aided detection was not associated with higher breast cancer detection rates or more favorable stage, size, or lymph node status of invasive breast cancer. CAD use during xray screening mammography in the USA is associated with decreased specificity but not with improvement in the detection rate or prognostic characteristics of invasive breast cancer. When previously well women are followed up over decades with xray screening mammography, objective studies of at least thirteen first-world countries – Australia, U.S.A, Norway, Denmark, Sweden, Italy, France, Switzerland, Netherlands, Belgium, U.K, Scotland, Northern Ireland, and Ireland – show no patient benefit from such screening xray in reducing breast surgery, advanced breast cancer, mastectomy, or mortality,.
Such evidence and argument against screening of the asymptomatic male without familial risk has been widely accepted for prostate cancer screening. Why are women with no known increased risk perversely all irradiated about 15 to 30 times from their 40s?
And a new study from Minneapolis finds that lowrisk women ie without dense breasts, symptoms or family history need not have screening xray mammography more than every 3 -4 years. The Mayo Clinic lists simply the obvious risks of xray mammography.
There is yet another obvious reason – conveniently not mentioned by researchers and xray mammographers – why screening xray mammography may miss cancers ie give false negative results: because adult female bosoms are obviously threedimensional, not flat like health mens’.. But xray mammography (unlike CAT or MRI scans) is done in only two – the vertical and lateral planes.
Unlike eg the limbs, spine, chest and head, globular female breasts cannot be xrayed meaningfully in the anterior-posterior plane superimposed on the chest, and thus small breast cancers close to the lateral chest wall or the armpits cannot be xray imaged. By contrast, examination with the hands, with thermography, with ultrasound, MRI and now with (eg SureTouch) mechanical pressure transducers check for suspicious lumps in three dimensions ie also in the anterior-posterior plane.
3D breast xray imaging is becoming a reality . But it still relies on xray irradiation.
Research PhD Geneticist Dr Natalie Bjorklund-Gordon pleads for altenatives to xray screening mammography, she explains exquisitely why she will not have xray screening mammography (let alone screening colonoscopy) . She pleads for nonxray safe and sure technology for screening.
But review shows that proven alternatives are available here and worldwide. Thermomammography is now highly evolved over the past 40 years; and mechanical tactile breast mapping over the past decade.
As these on-line reviews detail, is it ethical let alone cost-beneficial to promote routine screening mammography on women at any age who do not have probable breast cancer?
But for those well women who desire screening mammography for peace of mind, infrared thermomammography is the physiological gold standard that may pick up precancerous increased bloodflow years before a cancer mass is detectable by other ie anatomical mammography methods so as to allow non-interventional preventative steps;
while mechanical tactile mammography (eg SureTouch) as recommended by the Cancer Association of RSA is the safe non-invasive anatomical screening tool of choice.
Yet Curves Tokai is still promoting the pernicious offer of free membership of curves upon production of a recent mammogram – without bothering to warn of the major potential hazards of screening xray mammography. . So long as the Curves empire is openminded ie accepts the alternatives to xray mammography eg MRI, thermography and Digital Tactile Mammography
For anxious women, third party funders should pay for these safe and at least as specific and sensitive non-invasive investigations (rather than for invasive xray screening mammography at two to four times the cost).
In conclusion: all thinking women hold the primary responsibility for their own and their families’ health. It therefore behoves every woman let alone man to take responsibility for prevention when young for their future health. Like Dr Bjorklund-Gordon, they have to make informed decisions about the risk:benefit of having invasive screening like xray mammography and biopsies – just as they have to about their education, careers, financial management and relationships- about their health choices including screening.
- Oct 2011 Utzon-Frank N, Lynge E ea Cancer Epidemiol.Balancing sensitivity and specificity: Sixteen year’s of experience from mammography in Copenhagen, show that after 14 -16 years of xray mammography every 2 years, the incidence of new breast cancers detected at 14-16years actually rose by 50% compared to in the first 12 years.
- Sept 2011 Junod Zahl ea in Investigation of the Apparent Breast Cancer Epidemic in France show 8-fold increase between 1980 and 2000 in the number of xray mammography machines in France. Opportunistic and organised screening increased over time. In comparison to age-matched cohorts born 15 years earlier, recent cohorts had adjusted incidence proportion over 11 years that were 50 (23-76)% higher for women aged 50 to 79 years. Given that mortality did not change correspondingly, this increase in adjusted incidence was considered an estimate of overdiagnosis. Breast cancer may be overdiagnosed because screening increases diagnosis of slowly progressing non-life threatening cancer and increases misdiagnosis among women without progressive cancer. We suggest these effects could largely explain the reported “epidemic” of breast cancer.
- Sept 2011 Jorgensen Keen & Gotzsche at the authoritative Cochrane Centre ask Is xray mammographic screening justifiable considering its substantial overdiagnosis rate and minor effect on mortality? They point out that the original Swedish Two-County Trial was the most optimistic and pivotal for the introduction of screening, but subsequent trials of higher quality found smaller effects...
- Sept 2011 Suhrke P, Gøtzsche PC, Zahl P ea BMJ note in Effect of mammography screening on surgical treatment for breast cancer in Norway: that the aim of screening xray mammography is to reduce surgery and deaths. But in 35 408 women aged 40-79 with invasive breast cancer or ductal carcinoma in situ treated surgically from 1993 to 2008, xray mammography screening in Norway was associated with a noticeable- 70%- increase in breast cancer surgery in women aged 50-69 (the age group invited to screening) and also an increase in mastectomy rates. Although over-diagnosis is likely to have caused the initial increase in mastectomy rates and the overall increase in surgery rates in those screened, the more recent decline in mastectomy rates has affected all age groups and is likely to have resulted from changes in surgical policy.
5. Sept 2011 Haukka J, Autier P ea. University of Finland examine Trends in Breast Cancer Mortality in Sweden before and after Implementation of Mammography Screening. : Incidence-based mortality modelling comparing the risk of breast cancer death in screened and unscreened women in nine Swedish counties suggested a 39% risk reduction in women 40 to 69 years old after introduction of mammography screening in the 1980s and 1990s. Without individual data it is impossible to completely separate the effects of improved treatment and health service organisation from that of screening, which would bias our results in favour of screening. However, our estimates from publicly available data suggest considerably lower benefits than estimates based on comparison of screened versus non-screened women.
6. Aug 2011 Int J Cancer. Hofvind S, Graff-Iversen S. ea at the Cancer Registry of Norway- dissect Breast cancer incidence trends in Norway-explained by hormone therapy or mammographic screening? A decline in breast cancer incidence has been observed in several countries after 2002. Reduced use of menopausal hormonal therapy (HT), as a consequence of the publication of results from the Women’s Health Initiative, has been argued to be the main reason. the interpretation of breast cancer incidence trends in Norway from 1987 to 2009 is complicated because the xray breast screening program was introduced during a period with increasing HT use. Both factors likely contributed to the observed trends, and the role of each may vary across age
7. August 2011 Professor of Surgery Michael Baum from University London has argued for years that Breast xray screening should be scrapped.
8. August 2011 Fenton JJ, Barlow W E ea; J Natl Cancer Inst.Breast Cancer Surveillance Consortium. University of California,examined the Effectiveness of computer-aided detection CAD in community mammography, concludingCAD use during film-screen screening mammography in the United States is associated with decreased specificity but not with improvement in the detection rate or prognostic characteristics of invasive breast cancer. http://www.ncbi.nlm.nih.gov/pubmed/21795668
9. August 2011 Autier P, Gavin A. ea studied Advanced breast cancer incidence following population-based mammographic screening : Breast cancer mortality is declining in many Western countries. If mammography screening contributed to decreases in mortality, then decreases in advanced breast cancer incidence should also be noticeable. They assessed incidence trends of advanced breast cancer in areas where mammography screening has been practiced for at least 7 years ie Australia, Italy, Norway, Switzerland, Netherlands, U.K, U.S.A, Scotland, Northern Ireland, Age-adjusted annual percent changes were stable or increasing in ten areas (APCs of -0.5% to 1.7%). Thus in areas with widespread sustained mammographic screening, trends in advanced breast cancer incidence do not support a substantial role for screening in the decrease in mortality. http://www.ncbi.nlm.nih.gov/pubmed/21252058
10. July 2011 Autier, Vatten ea in BMJ in Breast cancer mortality in neighbouring European countries 1986-2000 with different levels of screening but similar access to treatment compare Norway with Sweden, Belgium with Netherlands and Eire with Ulster, The contrast between the time differences in implementation of xray mammography screening and the similarity in reductions in mortality between the country pairs suggest that screening did not play a direct part in the reductions in breast cancer mortality. http://www.ncbi.nlm.nih.gov/pubmed/21798968
11. June 2011: PhD research clinical scientist geneticist Dr Natalie Bjorklund-Gordon details exquisitely “why I am not having screening mammography” (or screening colonoscopy). http://www.science20.com/selective_genetics/why_i_am_not_having_screening_mammogram-79776
Update on institutionalized modern medicines fraud: REBUTTAL & COUNTERREBUTTAL: IMPACT OF ADVERSE NEWS MEDIA ON PRESCRIPTIONS FOR OSTEOPOROSIS: EFFECT ON FRACTURES AND MORTALITY
REBUTTAL OF: IMPACT OF ADVERSE NEWS MEDIA ON PRESCRIPTIONS FOR OSTEOPOROSIS: EFFECT ON FRACTURES AND MORTALITY
18 months ago a warning was published about the risk of Negligence Damages for Prescribing Bisphosphonates- Fosomaxes- for common osteoporosis.
A year later an updated review of the evidence rebutted the attempt by an Australian group (Phillip Sambrook MD, BS, LLB, FRACP ea ) to promote routine use of bisphosphonates, blame the news media for wrongly sensationalizing these largely unnecessary drugs’ rare but lethal adverse effects.
Now three other eminent Australian professors, of Oral and Maxillofacial Surgery and Endocrinology (Paul Sambrook, Chris Nordin and Alastair Goss) publish a further rebuttal of Phillip Sambrook ea for serious errors in underestimating by at least twentyfold both the incidence and the seriousness of bisphosphonate risks.
In a USA case for damages against Merck, for irreversible osteonecrosis- resulting in jaw amputation- following Fosamax, a patient was last year awarded $1.5million . This American class action is about over 1500 Fosamax cases against Merck. So far two related case against Merck have been dismissed. But all such cases are on appeal. The robust American tort system may yet hammer Merck. .
As recently as october 2010 Merck staunchly defends Fosamax’s safety for osteoporosis.
The FDA has recently added a warning about Fosamax-related thigh fractures.
But no evidence has ever been published that the catastrophic risk of bisphosphonates- however rare- is justified for routine osteoporosis when
1.In common osteoporosis, Bisphosphonates have no multisystemic benefits except for halving fracture risk, and
2.Appropriate combination of natural supplements- as this column has repeatedly revewed -approximately halve all risks ie of both osteoporosis fractures and all other common major diseases of aging, and thus chronic disability and deaths, without any significant risks.
Curent Authority statements eg from the Mayo Clinic simply fail to say this- why risk bisphosphonates? New reports in November-December of dozens of osteonecrosis cases on bisphosphonates have just appeared on Pubmed from Italy, Germany, Romania and Spain.
In fact a major international study has just beeen published showing the obvious, that survival in the elderly is strongly linked to gait speed and mobility. It is common cause that such integrated function is dependent on optimal joint, neuromuscular and cardiovascular integration- to which (- unlike the score of natural human micronutrient supplements that deplete with age-) bisphosphonates and strontium contribute nothing except bone density.
Fosamax lobbyists studiously avoid the plain truth that it is not osteoporosis; but frailty – falls – that is the chief cause of major elderly fractures- and that bisphosphonates and strontium may make bones appear denser.
Its too early to judge strontium ranelate (which also has rare but catastrophic risk- the DRESS syndrome); but fosamaxes in some cases make bones more brittle; without in the slightest combating senescence frailty ie muscle, mobility, vascular, cancerous, arthritic, immune, mood, cognitive and neurological deterioration (unlike the multinutrient microsupplements – vitamins, minerals and biologicals like fish oil, chondroglucosamine, sex hormones which together halve all chronic major degenerative diseases and premature mortality) ..
August 15, 2010 Regulators like the FDA and WHO the world health organization and their worldwide equivalents are notorious for bowing to their chief funders- Big Pharma- in registering new designer drugs on the flimsiest evidence, often despite vociferous objection from some honest assessor at the Regulator; then waiting till there is an uproar of complaints over the drug before they belatedly demand more evidence of cost-benefit from the manufacturer, and admit that key adverse data were suppressed from the outset- as happenened and is still happening most notoriously in the case of aspartamate Canderal.
And what was obvious from the word go, that in the case of last year’s swine flu vaccines and the spurious pandemic declaration, the Regulators/WHO expert committees were heavily loaded with biased specialists paid by vaccine manufacturers.
But why are the fosamaxes and other bisphosphonates still allowed to be prescribed for osteoporosis? When the first report of long bone fracture associated with them first appeared on Pubmed 16 years ago (Guanabens 1994) and they are unnecessary -indeed contra-indicated – for osteoporosis. Not for nothing does a recent ABC Good Morning America broadcast ask: “Fosamax: Is Long Term Use of Bone Strengthening Drug Linked to Fractures”?
This review is in fact an update on The Fraud of Modern Medicines.
A recent review from Oxford lists the myriad adverse effects of bisphosphonates. They say “All four currently approved nitrogen-containing bisphosphonates have a favorable tolerability and safety profile.” But why don’t they discuss the reality which is that although all these adverse effects may be infrequent, why risk such serious complications such as 30% incidence of oesophagogastric symptoms?; oesophageal stenosis and cancer?, toxiderma, atrial fibrillation, eye, muscle bone joint pain?; or incapacity from jaw and teeth loss or longbone fracture related to bisphosphonates for osteopororis?, when bisphosphonates are clinically unnecessary and unjustified for osteoporosis.
Why dont they state the truth, that there are no head to head trials against the basket of proven natural supplements, comparing fracture and global benefits versus risks of bisphosphonates ? Most reviews eg Wikipedia say bisphosphonates are “ the leading prescription for osteoporosis”; but this is simply for the same reasons that statins are for lipidemia, angiotensin blockers for hypertension and sulphonylureas/ glitazones are for type 2 diabetes, and aspartame is for artificial sweetening- because drug companies market such hoped-for $billion rainchecks overwhelmingly, and fund no comparative trials against the gold standard old supplement basket that makes most hazardous modern drugs like statins, glitazones and bisphosphonates mostly redundant.
Filleul ea from Univ Mona, Belgium have just reviewed the world literature from 2003-2009, finding 2400 cases of BIOJ bisphosphonate induced osteonecrosis of the jaw. of these about 215 were not cancer cases. Such cases very rarely occur without cancer. So why risk them?
So why does an Australian team bewail decreased use of the fosamaxes? Impact of adverse news media on prescriptions for osteoporosis:effect on fractures and mortality. Their statistical modelling is perhaps no more than promotion of bisphosphonates since it ignores the high number of adverse effects that bisphosphonates cause long term; and the major reduction in allcause disability and premature mortality that balanced appropriate supplements ( instead of bisphosphonates ) produce. Why would the lead author of so many papers- Professor Phillip Sambrook – promote bisphosphonate as the prime pharmacological prevention, and only calcium and vitamin D as the supplementary prevention of osteoporosis fractures? when the evidence so strongly favours safe multisupplements including appropriate lowdose hormone balance as preventative against all major chronic diseases? Can a new-drug proponent who sits on the medical advisory boards of and has received speaker fees from Amgen, Merck Sharp & Dohme, Novartis, Sanofi-Aventis and Servier. be considered objective ? Their critique of the media for publicizing the potential disaster from bisphosphonates is hollow when they fail to mention the numerous potential risks, and the numerous benefits instead from supplements.
Geusens, Sambrook ea in 2008 published a major review on Drug Insight: choosing a drug treatment strategy for women with osteoporosis-an evidence–based clinical perspective.. ‘The most important clinical determinant in the clinical choice of drug therapy for fracture prevention is a woman’s fracture risk; second is the evidence for fracture prevention in terms of spectrum, size and speed of effect. Other determinants include the potential extraskeletal benefits and safety concerns of the drugs.” But they again studiously avoid considering supplements (vitamins plus minerals plus appropriate hormone combination) as one of the drug regimes, especially as osteoporosis is simply one of the co-morbidities of aging, and far less of a risk for premature death and disability than stroke, cardiovascular, cancer, diabetes, frailty, dementia, arthritic disease and premature death – all of which can along with fractures be avoided and mitigated by the basket of supplements. So their review is surely biased in excluding all but new designer patent drugs while excluding the best and safe anabolics. .
It is well proven from observational studies that longterm use of appropriate natural supplements reduce all-cause mortality by at least a third: In the Womens’ Health Initiative WHI, appropriate hormone replacement HRT reduced all-cause mortality i.e. deaths from vascular disease, cancer and fractures by 1/3 as well. In the UKPDS the plant extract metformin reduced all-cause mortality also by 1/3. Understandably, metformin halves the incidence of new diabetes by reducing insulin resistance, hence it also reduces fracture risk let alone cancer and vascular disease risk .
Incontestable data shows that epidemic deficiency of vitamin D , vitamin C, magnesium, vitamin B especially B6, vitamin K, fish oil, and prime hormone dysregulation (thyroid, insulin, cortisol vs androgens and estrogens) in first-world aging populations are associated with increased mortality from all degenerative diseases especially fracturing, cardiovascular and cancer. It also showed that vigorous supplements of balanced vitamins, minerals (especially B,C,D,K, and Ca, Mg, Zn, Bo, Mn, Se, Cr), fish oil, and human sex (co)hormones (testosterone, progesterone, estradiol, metformin) drastically reduce all morbidity and especially fractures even (perhaps especially ) in the well-off over nourished..
In contrast to bisphosphonates- which are aimed solely at reducing fracture in the at-risk elderly and thus reduce all-cause mortality by perhaps 10%- these supplements in appropriate doses and balanced combination reduce all-cause aging disease and preventable premature mortality by at least 50%, without any adverse risks. .
Neville-Webbe ea (2010) note that bisphosphonates have anti-cancer potential. So use it for terminal cancer fracture pain. Why use it for anticancer potential in those with just osteoporosis when the basket of supplements (including approriate HRT, vigorous dose vitamin D and if approriate metformin) gives safe global protection against all the major aging diseases?
Just the reduction in excess diet omega6 oils will mean that only 10% of the current necessary omega3 daily allowance (3.5gm) will be essential.
In 2007 a leading team from the International menopause Society Genazzani ea warned that “Recent controversies with hormone replacement therapy (HRT) have caused much concern in women and their health-care providers. As a result, the number of HRT users in USA has fallen dramatically. Consequently, the potential HRT-induced reduction in fracture risk is lost so that, in the next few years, we can expect an excess of 43,008 fractures per year in women aged 65 – 69 years. In addition, the recent evidence on the merits of early initiation of HRT on cardiovascular disease risk and neurocognitive function and the effect of type and combination of hormones on breast cancer risk now require an urgent review by the regulatory authorities of their recommendations about HRT.”
Now – 8 years after the debacle the WHI caused – the Endocrine Society has at last come out with a Position Statement admitting the grave consequences from the hysterical misinterpretation of the early release of the Womens Health initiative results in 2002-2004, especially in rising fracture and colon cancer rates from avoidance of appropriate HRT in menopausal women across midlife. . Let alone, as Genazzani ea said above and we discussed at international, UK and European menopause meetings in 2003-2006, the potential loss of benefit against breast cancer, heart, stroke, depressive, diabetic and neurocognitive problems.
In conclusion: A major intervention is required from governments, world authorities to reduce all-cause morbidity and mortality : by drastically curtailing the marketing and prescription of rarely essential prescription designer drugs like bisphosphonates, and strontium ranelate for osteoporosis; by insisting on increasing universal intake of proven natural multisupplements that are increasingly deficient in the food chain for the poor, for infants, youngsters and the multiplying aging- in the latter, including appropiate HRT; and by forcing the processed food industry to stop stuffing foods and drinks with not just salt and aspartame but also fructose, sucrose, various growh hormones, and omega6 oils.
But neither Big Pharma manufacturers, governments, so-called independent regulators, nor university and private practice leaders or retail pharmacists will do so, promote evidence-based supplements over risky new drugs- there is too much money at stake from lost taxes. research funding, lower under-patent snake-oil sales and far less major disease and hospital admissions.
So it is up to patients and honest healthcare providers to insist that evidence-based supplements – not trading practice based on huge marketting and snakeoil preaching for profiteering – be prescribed for prevention/ managing the major diseases of aging including osteoporosis.