Tag Archives: CURE FOR MERS

26 August 2015 VITAMIN D DEFICIENCY VIRUS EPIDEMIC: HEALTH ADVISORY: MERS,BATS; SARRS , POLIO; EBOLA; CHIKUNGUNYA. OPTIMIZE VITS C AND D3 DOSES. DIARY JOURNAL: DEATH BY VITAMINS/MINERALS DEFICIENCY?: THE EASILY AVOIDABLE FLARE? AND EASY CURE? 2012-2015- MIDDLE-EAST CORONAVIRUS OUTBREAK: its not primarily the virus, but a deficiency syndrome in eg Arabia?.

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 the-semmelweis-reflex-vitamins-c-d3-avoid vitamin-denialism

and  diet-nutritional– vitamin risks-and-benefitS 

and VITAMIN D UPDATE:  https://healthspanlife.wordpress.com/2015/06/16/vitamin-d-for-indoor-types-how-much-is-enough-toxic-especially-for-infants-acute-illness-icu-infections/

and THE CRUCIAL ROLE OF (PRO)HORMONES (MELATONIN, SOLTRIOL-VITAMIN D3 -NOT  VIT D2  – AND VITAMIN C ) AS HRT IN REDUCING ALL MAJOR DISEASE. Salute Dr Walter Stumpf the prophet of the day-night hormone twins  melatonin and soltriol.

What is the greater regional risk, when both Ebola and MERS have at least 40% fatality rate in the susceptible? although the desperately poverty-stricken in west Africa are far more vulnerable to ebola (from bat and common human transmission) than Saudis to MERS (from camel,  and seldom human transmission).
INCREASING RISK FROM GLOBAL VITAMIN D INSUFFICIENCY and THE COMING HAJJ  PILGRIMAGE:

5 September 2015: with the Hajj only a fortnight away, the fresh MERS outbreak in KSA continues its upsurge, with the past week 34 cases  and 11 deaths ie still rising weekly rates. Compared to 16 cases and 7 deaths there in July, August had eight times more– 127 cases;  and 42 deaths ie 33% mortality. Worse, the human outbreak has spread from Riyadh all over the country except on the coast. .

What is even more puzzling is that the KSA now plans to pay out over a $billion ie  $133 300 compensation for  each of the >1200 people who have died there of  MERS . This is despite the fact that, as reported repeatedly on links below, their own scientists keep publicizing that residents there have severe vitamin D deficiency owing to the KSA culturally enforced sun exclusion ie coverup code especially for older adults. And that it costs no more than ~$5 a year for vitamin D3  for each person to take a harmless multidisease protective dose eg adults 50 000 iu every fortnight if not weekly ( as with any microbial after a loading therapeutic dose of eg 200 000  to 500 000iu  if indicated ), with which we get excellent protection  everywhere. Unlike their excellent doctors, KSA authorities dont publish a word of warning and prevention on their English websites  about the deficiency of vits C & D well shown in their urban population.

          26 August 2015 : while the MERS  outbreak in S Korea terminated weeks ago at 184 cases and 29 deaths- ie  16% mortality, with no cases reported anywhere else outside Saudi Arabia in the world, where there were only 129 cases and 32deaths; the latest score from Riyadh KSA is 1171 cases and 502 deaths ie 43 cases and 15 deaths the past week.

Yet a new statement from the KSA MOH this week makes no mention of the apparent chief risk factor for MERS in KSA – their observant  citizens’ profound deficiency of the sunshine vitamin D3  that their sharia sun-excluding apparel  promotes, and that their health professionals have stressed for years, and that is so easily corrected by lifesaving vitamin D3 supplement at negligible cost.  Only prisoners denied any sunshine and supplements have as bad vitamin D deficiency.

25 Aug 2015just a month before the 2015 Hajj, Saudi Arabia has announced  a fresh MERS epidemic this month – based exclusively in Riyadh: in July there were only 16 new cases  with 7deaths  (compared to June‘s 27/14) ie the rate fell to about 4 cases a week. But this August the rate has mushroomed  twelve-fold since July, from 4 to 22/wk,  to now ~48 cases alone the past week @ ~7/day – 72% men;  ie already this month  105 cases, 31 deaths;  ie the recent death-rate has strayed to 29%. .  One of today’s 6 deaths  was among the 8 new  cases   reported today.   Almost all the cases lately have apparently been reported from one Riyadh hospital  the King AbdulAziz center. so the reported totals from KSA  are  now 1165 cases and 498 deaths ie 43% deathrate; with critical cases/ deaths  mostly in the elderly. .

So is   more incidental MERS contamination  being detected by wider surveillance of well contacts? One can speculate whether the recent spurt, and  deathrate, in KSA are because of wider MERS surveillance of asymptomatic people; and the very old dying of usual causes? when  finding of the virus may be coincidental, not pathogenic? Does symptomatic stable indicate anything more than a common febrile URTI? The figures on the KSA Govt website are radically different from those on the FluTrackers.com site.

And VITAMIN D DEFICIENCY THERE?  a new paper in Med Hypotheses. 2015 Aug from KSA again highlights the Saudi scientific community plea not to ignore the disaster of  epidemic and so easily and cheaply remediable vitamin  deficiency there- at least 63% are moderate to severely vitamin D deficientNabi, Hobani ea Jazan University, KSA   ask:  Can we hypothesize a link? High prevalence of vitamin D deficiency and cancer in KSA  populations:      In spite of so much sunshine, about 83.6% of Saudis are deficient in the ‘sunshine vitamin’  D –  31.9% have severe, 32% have moderate and 19.7% have mild vitamin D deficiency (VDD).  Females are more severely vitamin D deficient. Apart from the genetic anti-vitamin D factor- darker skin color – various  manmade factors contributing to skin sunlight deficiency  and thus likely to epidemic viruses (and also  significantly shorter adult life expectancy compared to other opulent countries) include  housing designs, religious practices, lifestyle choices- which in ultra-conservative-run KSA  seem to be uniquely sun-exclusive, and rigorously enforced.

            27 June Update  while the outbreak has leveled off in KSA at 1039 cases with 460 deaths ie 44%,  – only 8 cases but 7  deaths the past fortnight-  the total in S Korea has mushroomed to 182 with 31 deaths ie mortality up to 17%.                                                                                                                                                                                                                                                                                                                                                                                                                                                                         19 June 2015  South Korea reported  ‘its 24th death from the MERS virus and one new case, bringing to 166 the total number of confirmed cases since the first one was diagnosed on May 20′; with mortality  now up to 13% . ‘The number of people in quarantine has fallen 12 percent from the previous day to 5,930. Currently, 112 patients are in hospital for treatment and 30 others have been cured and released.   Thailand became the 27 th country (following S Korea and China)  to be infected with the respiratory virus, took 4 Days To Confirm first MERS Case- a 75-year-old businessman from Oman, Leading To Worries About Deadly Disease’s Spread.         India and Muslim countries gird themselves as risk escalates with Ramadan pilgrimage to the source- KSA Saudi Arabia- now in full swing.

As  especially in Muslim countries, and China, and South Africa, and all darkskinned people who shun the sun- as do all who use sunblockers,  prefer avoiding tanned wrinkled or darker skin or skin cancer- or those who work and live mostly indoors and with covered bodies, limbs and often faces-  Low vitamin D in yet another sunny country- Thailand  ; Jnl Clin  Translat Endocr March 2015 Siwamogsatham ea. Vitamin D deficiency and insufficiency is also common in Thailand ( latitude between 5°30′ N and 20°30′ N) where adequate UVB exposure is available all year round. Chailurkit et al. [12] conducted the largest-scale examination of vitamin D status in Thai population,reported a 50% prevalence rate of vitamin D insufficiency & deficiency , defined as serum 25(OH)D level < 30 ng/mL  .  Life style and environmental factors are the major factors that determine vitamin D status.. Thai women are at risk likely due to sunscreen usage and sun avoidant behavior  to maintain a fair complexion. Living in urban areas  and with less leisure time  in the sunlight., ncreases the risk of vitamin D insufficiency due to increased pollution, which decreases the amount of UVB available for cutaneous vitamin D synthesis.  Furthermore, in Thailand dairy products are not fortified with vitamin D and very few vitamin D-rich foods are part of the Thai diet. Thus, dietary intake of vitamin D in Thai people is generally low.

 

     17June 2015 update: while a German who contracted MERS in the Middle East in February has now died of lung complications in Germany,    KSA Saudi Arabia reported 17 cases and 8 deaths in the past two weeks, similar to the rates in May; totals now 1035 with 458 deaths. Wiki puts the world totals  (26 countries including the Korean who visited China) at 1340 cases with ~530  ie 39%  deaths .

But originating from a single visitor to KSA,  South Korea has now recorded 162MERS cases- 6 cases a day since 20 May-    and 20deaths ie 12%. There a survey- Hong ea in Int J Tuberc Lung Dis 2014  – reported Association between vitamin D deficiency and tuberculosis  in S Korea, with healthy  controls having frank vit D deficiency ( mean 25OHvitD level 16 ng/ml) but 60% higher than in TB patients (mean 9.86ng/ml). The prevalence of severe vitamin D deficiency was higher in patients with TB (51.1%) than in controls ( P = 0.001). The median 25(OH)D level increased from 11.40 ng/ml (IQR 7.85-15.73) to 13.18 ng/ml  after treatment completion (P = 0.037). Presence of TB and history of TB were independently associated with severe vitamin D deficiency.”

Yet as is not available  in local  South African RSA   TB-HIV clinics with prevalent vitamin D deficiency,  there is still no reported policy of vitamin D supplementation apparently reported from S Korea (or KSA, or RSA) , despite (as in KSA and RSA) a study there 2 years ago  (from Jeong of Dept Paediatrics at CHA University, Seongnam SKorea 2013)  “Factors affecting the vitamin D status in South Korean children”  finding  ” prevalence of vitamin D deficiency (
(15-20 ng/mL) was 19.5%. Overall, the mean serum 25(OH)D levels was 22.9±9.9 ng/mL. They were the highest in them preschoolers (2-5 years, 24.4 ng/mL) and the lowest in the adolescents (11-16 years,15.9 ng/mL). In addition, they were significantly higher in summer as compared with winter. The prevalence of vitamin D insufficiency and deficiency was relatively higher in our series of children. It is imperative that the public policies be established to provide vitamin D supplementation for South Korean children.” 

 ONGOING GLOBAL DENIAL OF NEED FOR MICRONUTRIENT SUPPLEMENTS:   It seems that national authorities from the Americas  to Europe to Africa to the middle east to Asia,  including the medical industry,  continue to refuse to heed overwhelming evidence that vigorous micronutrient supplements are needed, available, lowcost, highly effective and safe  to prevent and treat epidemics like HIV-TB, flu, MERS and Ebola – especially when vaccines and antiviral drugs are without benefit, and when vitamin D deficiency is universal in clothed indoor-studying- and -working  peoples, especially the poor who cannot buy supplements by choice. . .

            6 June 2015 update: After a quiet April, KSA is now suffering  fresh jeopardy from  acute  midsummer flareup of MERS. But so is  the world with outbreak  of MERS in Korea and China, while thousands of refugees from tribal wars in  the middle east and North and even South  Africa cause more concern for spread of such plagues.

As the Middle East  girds itself against mounting Islamic warfare in the region, after only a handful of MERS cases in April- 8 cases and 6 deaths- KSA has in May  seen 33 cases with  >50% fatality – 18 deaths; and already in June the case rate has doubled from April’s  1 a day  to May – June’s 2 cases a day, giving cumulative totals there  to 6 June of 1026 MERS cases and 450 deaths..

By contrast, in   South Korea   only  5 deaths (8% mortality) have been reported in 84 cases so far the past 16 days – including a Korean who got to China. That chillingly brings the outbreak firmly onto the Asian mainland.  South Korea now passes the UAE as the second biggest outbreak country after the KSA- but like the UAE and elsewhere, a far lower deathrate, perhaps simply because of initial contact tracking, since the outbreak has been totally in hospitals.

It seems that  Vitamin D deficiency may be as much the cause of MERS susceptibility in South Korea as in KSA?  A 2008 Korean University survey shows that despite its temperate latitude of  ~35degrees, and humidity, South Korea had widespread vitamin D deficiency even in its young people: Serum 25-hydroxyvitamin D [25(OH)D] levels and the prevalence of vitamin D insufficiency defined as serum 25(OH)D level of less than 20 ng/ml. Vitamin D insufficiency was found in 47.3% of males and 64.5% of females, whereas only 13.2% of male and 6.7% of female population had a serum 25(OH)D level of greater than 30 ng/ml. Vitamin D insufficiency was most prevalent in the age of 20-29, with a rate of 65.0% in males and 79.9% in females, and least prevalent in the age of 60-69 in males and 50-59 in females. Those who work usually indoors were more predisposed to vitamin D insufficiency. In the adult population, predictors for vitamin D insufficiency included young age groups, spring and winter seasons, living in an urban area, and indoor occupations.  CONCLUSIONS:Vitamin D insufficiency is very common, and it is now a greater threat to the younger generation in Korea. Current recommendations for vitamin D intakes for Koreans are inadequate, especially for the youth. In 2012 they reported “We found that vitamin D insufficiency or deficiency is a very common health problem in Korean adolescents, particularly in girls, and that serum 25(OH)D levels are inversely associated with insulin resistance and lipid profiles. These results suggest that more time spent in outdoor activity for sunlight exposure and higher vitamin D intake may be needed in younger adolescents in South Korea”

In a recent university study by  Han Seok Choi  on vit D deficiency in S Korea- perhaps the worst measured vit D deficient country  in the world? – he refers to  Autier ea in Lyon France in JCEM 2012 – “The average increase in (in adult) serum25(OH)D   was 0.78 ng/ml per microgram of vitamin D3  supplement (40IU ) per day”. ie the average ~20ng/ml vit D level in so many deficient adults  will increase by only ~8ng/ml for every 400iu vit D in an average daily “RDA” multi-supplement; to raise their level to a more efficient 60ng/ml requires at least ~2000iu/day or 60 000iu per month; and if diseased, to raise to a more vigorous 90ng/ml requires at least ~3000iu/d . But as others have reported, higher dose oral vitamin D3 gives a less vigorous response eg 10ng/ml rise per 1000iu/day; eg  my 25OHvit D level is about 90ng/ml on about 9000iu vit D3 supplement a day (half-life estimated 2 weeks to 2 months  in Modulation of the Immune Response to Respiratory Viruses by Vitamin D) and plenty of fat eg an average egg, cheese and doublecream yoghurt etc  daily ; with no rise in my corrected serum calcium, and no visible calcification on my xray chest or echocardiogram  . .Autier ea wrote “76 trials published from 1984 to  2011 included 6207 subjects  tested supplement doses ranging from 5 to 250 μg/d  ie 200 to 10 000iu/d(median, 20 μg/d).  In the absence of concomitant use of calcium supplements,  average increase in serum 25-hydroxyvitamin D concentrations was 0.78 ng/ml (1.95 nmol/liter) per microgram ie 40iu of vitamin D3 supplement per day. Compared to the vitamin D3, the vitamin D2 was associated with significantly lower increases (P = 0.03). Concomitant use of calcium supplementation and high 25-hydroxyvitamin D concentration at baseline was nonsignificantly associated with lower increases in 25-hydroxyvitamin D concentrations.

         “Vitamin D Deficiency Around the World   2015   Even the Indian Medical Association recently organized continuing medical education to address the rise of vitamin D deficiency in their sun-soaked nation. Endocrinologist Dr. Sanjay Badada told Times of India:1   Vitamin D deficiency is rapidly gaining epidemic proportions yet it is the most under-diagnosed and under-treated nutritional deficiency in the world.         In our experience, 40 percent to 50 percent patients get diagnosed with Vitamin D deficiency as a part of their normal routine tests with no apparent symptoms.    On the other hand, 80 percent to 90 percent of patients who come in with musculoskeletal complaints such as back pains, unexplained muscle pains, or general fatigue suffer from Vitamin D deficiency.     Vitamin D was also discussed at the 2015 European Congress of Endocrinology. One talk2 addressed the “Mediterranean paradox,” as researchers have tried to understand why as many as 90 percent of pregnant mothers (and their newborns) in the sunny Mediterranean region are deficient in vitamin D.      A systematic review looking at 15 studies concluded that predictors of low maternal vitamin D concentration included dark skin and sartorial habits—meaning the manner in which they dress, or in this case, being too covered up, preventing sun exposure on bare skin.     Moreover, vitamin D supplementation was very low, and few pregnant women met the recommended daily intake (RDI) of calcium and vitamin D.”

12 April 2015 update: KSA has now reported 977 cases with 426 deaths ie 43% deathrate. Ignoring the past 12 days (2 cases, 4 deaths),  the March rate was 1.9 cases per day with  49% deathrate; in Feb it was 3/day with only 42% deathrate. so while the reported caserate is down by a third, the fatality ie deathrate is up almost 20%. The Wiki  MERS report is now a month  out of date, with climbing deathrate.

Perhaps the lull in new MERS case detection/reporting  is merely a result of that region (like the war-torn Central Africa – never mind the ebola epidemic-)  being in the middle of an ethnic Muslim religious  war – genocide-  by fanatical  jihadists on both more “liberal” Islamists and other religions. This  increasingly threatens to overthrow the 20thC-European-created hereditary tribal governments of the desert/camel/oilfield region- KSA, Yemen,   Jordan, the Gulf States etc, as happened in Egypt; not to speak of the power vacuum instability  created in Iraq and Libya by more recent Western elimination of virtual dictators  without ability to ensure democratic succession there any more than in Egypt, Afghanistan or Pakistan; and the oppressive dictatorships that prevail  in Iran and Syria..

24 March 2015    KSA reports 964 cases   and    419 deaths ie  only 6cases and 3 deaths the past week. The Ebola outbreak meanwhile simmers down in W Africa in its anniversary week. . New reports from North America again highlight the importance of optimizing vigorous vitamin D3 dose and blood levels.

15 March 2015  MERS   so far this March, in KSA already  37 cases  , ie 17 a week,   21 deaths.  This brings the reported case  KSA total to 957 cases, 416 deaths; but deathrate the past 4 weeks to ~57% (the KSA website) . With the timelag in KSA reporting to international registries, Wiki reports that to 12 Mar there were  only 402deaths /938 cases in KSA ie 43% deaths; but 1082 cases worldwide with 439 ie 37% deathrate in 24 countries-  118  cases with 28 deaths  in the 8 middle east nations surrounding the KSA, giving a deathrate around but not in KSA of only 24%, and 3 deaths in 7 cases in their 3 African neighbouring countries;  and 8 deaths in 22 cases in 12 distant countries ie 36% deathrate.

so while there have apparently been no new MERS cases outside KSA in their summer for months, the ongoing reported caserate in KSA is alarming with the deathrate having climbed to 55%. Obviously, to explain the apparent rising deathrate,  detection and reporting of new MERS cases in KSA will likely be increasingly of only serious respiratory cases and their immediate contacts; and otherwise unexplained deaths; but the fact is that 10 MERS- associated deaths were  again detected there   the past week..

So while camels rather than bats are teeming with MERS virus and believed to be the main vactor to their human compatriots, it is instructive to to see a number of recent studies  (1, 2, 3) in north African camels showing that they have vitamin D levels 10 to 40 times higher than Arabian citizens who import them en masse, farm, nuture, milk  and eat them. MERS is if at all a trivial coronavirus corrhyza in such camels, like the common cold coronaviruses cause  in humans. This contrasts with the scarcity of MERS cases reported from N Africa- where camel farmers presumably do not cover up as religious law makes the Saudi citizens do.

And it  correlates with the epidemic of Ebola in central West Africa- Guinea, Sierra Leone and Liberia  , where the chief vector of Ebola seems to be ebola-resistant fruit bats, who live in the dark and have very low vitamin D levels- presumably like their very dark-skinned human compatriots, who presumably also still live largely in the forests or in cities and thus have equally low vitamin D levels; and thus far reported about 25000  suspected cases and 10000 deaths ie 40%; with no antiviral cure in sight; with ?4 deaths in ?18 cases so far reported outside  Africa.

These are more reasons to pour safe lowcost effective antivirals vits C and D3 (with balancing vits A,   Zinc etc) into such patients and their compatriots at risk. (vit K2 supplement matters only long term against arterial calcification, osteoporosis and cancer in longevity.)

7 March 2015.   EPIDEMIC BY power-crazy RELIGIOUS  & ECONOMIC EDICT?: MERS:  globally  ~1040 cases of MERS have been reported. But apparently none outside Saudi Arabia in recent  months: So March  opens in KSA  with 7 day MERS caseload  19  new cases (mean age ~56yrs), and 8  deaths ie total now 939 and deaths 403. . Thats ~20 cases reported the past 7 days there, with 10  deaths ie 50%… in a country in which  18 months  and more ago endemic vitamin D deficiency was reported in the Saudi Gazette by their scientistswidely attributed to the obvious cause, that in a land of such abundant sunshine, more so than in any other country in the world, women  are obliged by draconian religious law   to cover up almost totally outside their houses,   and  elderly observant men almost as much.

European Journal of Clinical Nutrition , (18 February 2015) Determinants of vitamin D deficiency among undergraduate medical students in Saudi Arabian BinSaeed, Al-Drees ea        A cross-sectional study was performed among 255 first- to fifth-year male undergraduate medical students of a major universities in Saudi Arabia.  Results:   Majority of Saudi medical students (75.2%) had 25(OH)D levels <30nmol/l = <12ng/ml,. Multivariate analysis showed that the odds of having 25(OH)D serum levels of greater than or equal to30nmol/l were seven times higher both in students who took vitamin D (odds ratio (OR)=7.2, 95% confidence interval (CI)=1.8–29.9, P=0.006) or multivitamin supplements (OR=6.9, 95% CI=1.7–27.3, P=0.006) within 1 year..   There was no significant association between 25(OH)D serum levels and average time spent outdoors per day (P=0.369) and type of clothing (long-sleeved vs short-sleeved; P=0.800).     Conclusions:   Vitamin D deficiency was highly prevalent in Saudi medical students. Modifiable factors such as vitamin D intake and PA could be targeted for intervention.

Wiki says (and Medscape echoes) that “Immune system: “While it is known that melatonin interacts with the immune system,[53][54] the details of those interactions are unclear. Antiinflammatory effect seems to be the most relevant and most documented in the literature.[55] There have been few trials designed to judge the effectiveness of melatonin in disease treatment. Most existing data are based on small, incomplete clinical trials. Any positive immunological effect is thought to be the result of melatonin acting on high-affinity receptors (MT1 and MT2) expressed in immunocompetent cells. In preclinical studies, melatonin may enhance cytokine production,[56] and by doing this counteract acquired immunodeficiences. Some studies also suggest that melatonin might be useful fighting infectious disease[57] including viral  and bacterial infections, and potentially in the treatment of cancer.”

on Pubmed melatonin as an immunomodulator goes back to 1980.

As Wiebke Arlt and Hewison wrote in 2004, “Aging is associated with a decline in immunity described as immunosenescence; paralleled by a decline in the production of several hormones, as typically illustrated by the menopausal loss of ovarian oestrogen production. However, other hormonal changes that occur with aging and that potentially impact on immune function include the release of the pineal gland hormone melatonin and pituitary growth hormone, adrenal production of dehydroepiandrosterone and tissue-specific availability of active vitamin D. It remains to be established whether hormonal changes with aging actually contribute to immunosenescence and this area is at the interface of fact and fiction, clearly inviting systematic research efforts. “

But Observant- aging-  Muslims are forbidden  the prime cicardian rhythm of outdoor sunshine stimulation of their skin,  and in women   even their retinae with total veiling. Thus although women are the tougher gender, observant  Islam condemns them to be increasingly   more compromised goods and chattels than even camels…

There is still no word that the KSA has recently bothered to promote vigorous dose vitamins D3 and C, ( with vit A, zinc, selenium and iodine), as simple safe potential antidotes to their heavily enforced overdressing blockading sunshine-vitamin D3 , that their own medical scientists have repeatedly warned about..

A new report saysEbola virus is among the most deadly pathogens, with case fatality rates of up to 90%.1 Ebola virus is categorized as a tier 1 pathogen by the US government because of its potential for deliberate misuse with significant potential for mass casualties. The current outbreak of Ebola virus in West Africa with more than 23 000 cases and 9000 deaths2 also demonstrates the long-underestimated public health threat that Ebola virus poses as a natural human pathogen. There are no licensed vaccines or postexposure treatments for combating Ebola virus.

But as with pollution, insecticides, road carnage, influenza, TB,  HIV-AIDS, malaria, cholera,  smoking, sugar, aspartame, alcoholism, it doesnt suit the Big Pharma  & Disease Corporates, their paid marketing professors/researchers at universities, and  government and hospital/ health industry, to promote avoidance, prevention, cure,  natural cheap available remedies like vitamins, minerals and other natural remedies, when disease requiring hospital admission, a patented synthetic vaccine or other drug is far more profitable. . Only Disease Pays.

28 Feb 2015   after a quiet KSA  2014/15 year-end with declining   MERS case reports- 11 in December,  20 in January, the past week has seen  18  new cases but 9 deaths in  KSA, the KSA totals SINCE 2012 UP  to  920 CASES AND 395 DEATHS (43%) ie  for  February  75cases and 31 deaths. . As always, until the KSA MOH Command clarifies, how many of these are current, versus catchup reports from previous weeks/months, remains to be seen. But as the winter recedes there, the death rate this month remains 41%%…. 

And in UAE  one new (expat) case died this month; and a new case in a nurse returning to the Philippines from KSA is the first case in that country, .. combining KSA with Wiki stats, bringing apparent world totals to perhaps about 1029 cases and 420 deaths.. The deathrate from MERS has widened starkly from 42% in to  30% outside   KSA.

8 Dec  2014:       HEALTH ADVISORY FOR VISITORS TO OR FROM MIDDLE & FAR EAST,  EUROPE,  AFRICA, the AMERICAS:  The MERS infection outbreak slacks off:  – down from the recent 2 cases a day to 25 cases in November with 12 deaths; 4 cases so far this month with 3 deaths- ie the deathrate is picking up.  .  No more exports reported from KSA since one  returned home to Qatar last month. the quadrupled case rate  since October has fallen back from 39 cases & 15 deaths a month  ; – and deathrate (9 deaths) in October in KSA  that  doubled to 0.6/day is back to the 55% rate,  still awesome for such a rich and sophisticated country.

though MERS is well below that of the ebola epidemic – some 5000 ie almost 40% deaths  among  15000 cases  so far-  that is ravishing central  west Africans impoverished by genocidal warlords; not to mention flu, cholera, HIV, TB, polio-and dengue-like illnesses . Two  ebola- infected people from  W Africa have died in USA, but 8 have recovered in USA from Ebola .

Latest evidence is that the current ebola epidemic is due to bats-   human overpopulation causing massive deforestation, displacing ecologically vital  bats (never mind vital bees,  birds and butterflies)  from their natural habitat.   Liberian workers  who flew to USA  and Germany  with Ebola died; but 8 of 9 infected cases have recovered there; as have infected European health workers. .. . .    

  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 died. .Is ebola falling there? or are patients simply hiding, dying outside hospitals?

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

25 Nov 2014 the MERS toll mounts in KSA- the past week only 4 new cases but 5 deaths. so this month its 21 cases, 11 deaths.

20 Nov 2014 Now 808 cases ie 18 this month, only 5 the past running week; with 9 deaths this month; so 12 cases under management.

13 November 2014   The rates pick up again- KSA declares 16 cases under treatment, 447cases recovered,  804 cases, 342 deaths; ie this month 15 cases and 5 deaths  .

4 November 2014:  KSA declares 15 Cases Under Treatment, 440 Cases Recovered,  793 Cases,  338 deaths, ie in the past week 13 new (9 Saudis, 4 expats)  and 5 deceased cases of MERS.

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.  Croft  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 KSA 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…....continue..

            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...continue..

​​​​​​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.

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 Salahuddin’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

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 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 ultraOrthodox 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  Tabbouleha “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 .

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23 MARCH 2015: THE CRUCIAL ROLE OF ANABOLIC PROHORMONES – MELATONIN, VITAMIN C AND steroids- PROGESTERONE, SUNSHINE and SOLTRIOL=D3 – AS HRT IN REDUCING ALL MAJOR DISEASE. Salute Dr Walter Stumpf.

 REVERSE THE POST-WW2  GLOBAL SHIFT FROM  HEALTHY ANABOLIC  OUTDOOR (VIT D AND ANDROGEN ie DIET CHOLESTEROL– FAT  DOMINANCE) EXERCISE ABUNDANCE TO THE RECENT LETHAL CARBOHYDRATE-SUGAR- ESTROGENICS- CORTISOL INDOOR TV DOMINANCE AND FAMINE.

update 22 MARCH 2015: VIGOROUS DOSE VITAMIN D UPDATE

NEW STUDIES:

More Canadian and USA studies confirm that vigorous vitamin D  need  applies especially to those living in far northern USA-Canada  and  EurAsia etc;    but also to all of us  globally who spend little time well exposed to the sun- especially the more driven  who both live/work indoors and cover even our limbs and heads outdoors as eg more ‘observant’ adults of many faiths do. As a new Creighton Univ study shows, we are at minimal risk of kidney stones on vigorous supplement vit D3 provided we balance it with enough water and magnesium supplement,

This is why in this age of increasing stress, longevity, epidemics, and pollution of both environment and the food and medicine chains, we have for a couple of years now   been advocating   and taking  vitamin D3  – on a  century of voluminous evidence (62500 papers on Pubmed alone) since 1914  from top nutritional scientists like Drs Jack Drummond, Linus Pauling, Walter Stumpf, Chris Nordin, Chris Gallagher, Rob Heaney, John Cannell, Bill Grant,  Mike Holick, Cedric Garland,  ea  – at least  vit D3  50 000iu a week (~7000iu/d)  ie a million units every 20 weeks;   retail costing  R30 ie R6pm  for us aging frailer types (half that dose ie 50 000iu twice a month @R3/month for the poor/ well or small kids).. at R12/US$, that costs all of $3 to $6 a year.

On about 9000iu vit D3 average supplement/day, my total 25OH vit D bloodlevel runs about 90-100 ng/ml ie 220-250 nmol/l.  so only 400- 1000iu vit D /day will boost the vit D  bloodlevel and benefits little if not  trivially.

But  vigorous D3 dose must be buffered by vit K2  about >100mcg/day , magnesium about 400mg/d, and the usual basket of other ~50 vits, minerals and other natural supplements, to protect us from kidney and arterial calcification etc. We have previously  highlighted trials eg from Pakistan showing that even 600 000iu vit D3 a month ie ~20 000iu/day safely and greatly improves recovery and healing from severe PTB+- AIDS in eg frail Pakistatin patients; whereas overdose of 90year old patients with a  2million iu  vit D3 dose (in Netherlands)  produced no toxicity. Hence we load sick patients with (an antibiotic-like )  200 000 to 400 000iu dose before continuing weekly or fortnightly maintenance- with the sickest fattest getting the highest dose, and infants scaled down accordingly (after a loading dose of eg 25 000iu)   to eg 1000-2000iu/d,  or 50000iu 1/2 scoop ie 25000iu every 2 weeks- the older extrapolation (as for adults)  of ~100iu/kg/day.

For the concerned vegan, vitamin D is vegetarian:  supplement of vit D2 is extracted from yeast or mushrooms;  vit D3 by UV irradiation of cholesterol from lanolin. Like all life, since vitamin D soltriol  is a sun-induced sterol oil product (in this case of cholesterol which in turn is built via  vitamin C ascorbic acid from plant glucose-sugar),   vitamin D does not contain or be made from animal flesh ie animal protein nitrogen  any more than does fish oil.

          Vitamin D may keep low-grade  cancer from becoming aggressive:
http://www.sciencedaily.com/releases/2015/03/150322080155.htm    Taking vitamin D supplements could slow or even reverse the progression of less aggressive, or low-grade, prostate tumors without the need for surgery or radiation, scientists say. Taking vigorous vits C & D does this for all cancers, all disease.

 

               VITAMIN D DEFICIENCY IS ASSOCIATED WITH INSULIN RESISTANCE INDEPENDENT OF INTRACELLULAR CALCIUM, DIETARY CALCIUM AND SERUM LEVELS OF PARATHORMONE, CALCITRIOL AND CALCIUM IN PREMENOPAUSAL WOMEN.   Da Silva Ferreira T,  Sanjuliani AF ea .   Nutr Hosp. 2015 Apr 1;31(n04):1491-1498.

25-Hydroxyvitamin D in the range of 20 to 100 ng/mL doesnt increase  kidney stones.    Am J Public Health. 2014 Sep;104(9):1783-7  Garland, Heaney ea Creighton Univ, USA   Increasing 25-hydroxyvitamin D serum levels can prevent a wide range of diseases. There is a concern about increasing kidney stone risk with vitamin D supplementation. The study included 2012 participants followed prospectively for a median of 19 months. Thirteen individuals self-reported kidney stones during the study period. Multivariate logistic regression was applied to assess the association between vitamin D status and kidney stones.We found no statistically significant association between serum 25-hydroxyvitamin D and kidney stones (P = .42). Body mass index was significantly associated with kidney stone risk (odds ratio = 3.5; 95% confidence interval = 1.1, 11.3).           We concluded that a serum 25-hydroxyvitamin D level of 20 to 100 nanograms per milliliter has no significant association with kidney stone incidence.       

A Statistical Error in the Estimation of the Recommended Dietary Allowance for Vitamin D. Letter to Veugelers, P.J. and Ekwaru, J.P.,           Nutrients. 2015 Mar 10;7(3):1688-90. doi: 10.3390/nu7031688.  Nutrients 2014, 6, 4472-4475; doi:10.3390/nu6104472.   Heaney , Garland ea.    1Creighton University & University of California, San Diego,   GrassrootsHealth, Encinitas, CA .   Recently Veugelers and Ekwaru published data indicating that, in its dietary reference intakes for calcium and vitamin D, the Institute of Medicine (IOM) had made a serious calculation underestimation  [2]. Using the same data set as had the IOM panel, these investigators showed that the Recommended Dietary Allowance (RDA) for vitamin D had been underestimated by an order of magnitude. Veugelers and Ekwaru, using the IOM’s data, calculated an RDA of 8895 IU per day. They noted that there was some uncertainty in that estimate, inasmuch as this value required an extrapolation from the available data, which did not include individuals receiving daily vitamin D inputs above 2400 IU/day.[…].

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4210929/        Nutrients. 2014 Oct; 6(10): 4472–4475.Statistical Error in the Estimation of  Recommended Dietary Allowance for VitaminD     Paul J. Veugelers* and John Paul Ekwaru   University of Alberta, Canada

The Institute of Medicine (IOM) issues dietary recommendations on the request of the U.S. and Canadian governments. One of these recommendations is the Recommended Dietary Allowance (RDA). The RDA is the nutrient intake considered to be sufficient to meet the requirements of 97.5% of healthy individuals [1]. The RDA for vitamin D is 600 IU per day for individuals 1 to 70 years of age and is assumed to achieve serum 25-hydroxyvitamin D (25(OH)D) levels of 50 nmol/L or more in 97.5% of healthy individuals [1]. Serum 25(OH)D is the established proxy for vitamin D status and levels of 50 nmol/L or more have been shown to benefit bone health and to prevent disease and injury [1].

The IOM based their RDA for vitamin D on an aggregation of 10 supplementation studies that were carried out during winter months and at locations with latitudes above the 50th parallel north to minimize the influence of cutaneous vitamin D synthesis [2,3,4,5,6,7,8,9,10,11]. As several of these 10 studies examined more than one supplementation dose, collectively they provided 32 study averages of serum 25(OH)D levels. These are replicated as the green diamonds in Figure 1. The IOM regressed the 32 study averages against vitamin D intake to yield the dose response relationship of vitamin D intake and serum 25(OH)D (green solid line in Figure 1). The IOM further calculated the lower and upper 95% confidence prediction interval based on the 32 study averages and the standard deviation of these 32 study averages (green dashed lines in Figure 1). On the basis of this, the IOM estimated that 600 IU of vitamin D would achieve an average 25(OH)D level of 63 nmol/L and a lower 95% confidence prediction limit (2.5 percentile) of 56 nmol/L. The latter value was rounded downwards to 50 nmol/L to accommodate uncertainty in the estimation [1]. This data point (600 IU vitamin D, 50 nmol/L) is the basis for the current RDA and for the IOM’s conclusion that an intake of 600 IU of vitamin D per day will achieve serum 25(OH)D levels of 50 nmol/L or more in 97.5% of individuals.

The correct interpretation of the lower prediction limit is that 97.5% of study averages are predicted to have values exceeding this limit. This is essentially different from the IOM’s conclusion that 97.5% of individuals will have values exceeding the lower prediction limit. To illustrate the difference between the former and latter interpretation, we estimated how much vitamin D is needed to achieve that 97.5% of individuals achieve serum 25(OH)D values of 50 nmol/L or more. For this purpose we reviewed each of the 10 studies used by the IOM. Eight studies reported both the average and standard deviation [2,5,6,7,8,9,10,11]. These eight studies had examined a total of 23 supplementation doses [2,5,6,7,8,9,10,11]. For each of these 23 study averages we calculated the 2.5th percentile by subtracting 2 standard deviations from the average (depicted by yellow dots in Figure 2). Next, we regressed these 23 values against vitamin D intake to yield the lower prediction limit (red line in Figure 2). This regression line revealed that 600 IU of vitamin D per day achieves that 97.5% of individuals will have serum 25(OH)D values above 26.8 nmol/L rather than above 50 nmol/L which is currently assumed. It also estimated that 8895 IU of vitamin D per day may be needed to accomplish that 97.5% of individuals achieve serum 25(OH)D values of 50 nmol/L or more. As this dose is far beyond the range of studied doses, caution is warranted when interpreting this estimate. Regardless, the very high estimate illustrates that the dose is well in excess of the current RDA of 600 IU per day and the tolerable upper intake of 4000 IU per day [1].

The public health and clinical implications of the miscalculated RDA for vitamin D are serious. With the current recommendation of 600 IU, bone health objectives and disease and injury prevention targets will not be met. This became apparent in two studies conducted in Canada where, because of the Northern latitude, cutaneous vitamin D synthesis is limited and where diets contribute an estimated 232 IU of vitamin D per day [12]. One study estimated that despite Vitamin D supplementation with 400 IU or more (including dietary intake that is a total intake of 632 IU or more) 10% of participants had values of less than 50 nmol/L [13]. The second study reported serum 25(OH)D levels of less than 50 nmol/L for 15% of participants who reported supplementation with vitamin D [14]. If the RDA had been adequate, these percentages should not have exceeded 2.5%. Herewith these studies show that the current public health target is not being met.              We recommend that the RDA for vitamin D be reconsidered to allow for appropriate public health and clinical decision-making.

update 1 March 2015Screening for Vitamin D Deficiency: Is the Goal Disease Prevention or Full Nutrient Repletion? 

                   Since its founding, the  USPSTF has sought to provide a firm evidential base for early detection strategies, evaluating such screening methods as mammography and prostate-specific antigen testing. Although it has also evaluated a few interventions, its predominant focus has been testing for markers that identify persons at risk who are likely to benefit from preventive action. Only recently has the USPSTF ventured into the field—or perhaps the minefield—of nutrition, a territory distant from screening tests and risk assessment, with different and unfamiliar landmarks.

The USPSTF presents its conclusions on testing for vitamin D deficiency (1), reporting that it was unable to find evidence for or against such testing. It noted that one of the likely reasons was the absence of a scientific consensus on both the level of vitamin D status that should be judged “deficient” and what the measurable manifestations of deficiency might be. These are also issues for many other nutrients, such as folate, ascorbate, calcium, and protein. Vitamin D may have seemed to offer a way out of this confusion because serum 25-hydroxyvitamin D [25-(OH)D] concentration is generally recognized as one of the best indices of status for any of a broad array of nutrients. Also, it is now readily measurable and widely utilized.

One of the reasons its promise has not been realized is that most studies of vitamin D efficacy have used a disease-avoidance model, which is the standard approach used by the Institute of Medicine (IOM) for most nutrients (2). Furthermore, disease prevention is the explicit focus of the USPSTF. Nevertheless, the IOM and USPSTF approaches effectively equate health with the absence of disease, an equivalence that nutritionists have long rejected. Instead, nutritionists focus on full nutrient repletion when possible. The inevitable gap between disease prevention and nutrient repletion is still largely unexplored territory. For many nutrients, it can be surprisingly wide, as suggested in this case by studies of the intake required to provide vitamin D in human breast milk in quantities sufficient to meet the needs of infants (3). The IOM’s adult requirement for vitamin D is 600 IU/d (4), which is judged to be sufficient to protect against osteoporotic fracture. In contrast, quantitative and empirical evidence indicates that vitamin D intake from breastfeeding needs to be approximately 6000 IU/d (3, 5). Although high compared with the adult recommendation, such an intake almost exactly reproduces the measured vitamin D status of contemporary Africans leading ancestral lifestyles (6). Such populations provide perhaps our best window on vitamin D levels prevailing during the millennia over which human physiology was adapted to its environment by natural selection.

Whatever the actual requirement or 25-(OH)D cutoff may be, there is another likely reason that the evidence is unclear. The USPSTF drew from systematic reviews and meta-analyses of studies of vitamin D effects, such as the one accompanying the current report (7). In general, the criteria for including studies in such reviews are methodological rather than biological. Of the 6 published biological criteria (8) for including published reports in meta-analyses, the review published in this issue met only 2 (comparable basal status and same chemical form), and several of its component studies met none. Including studies that could never have been informative in the first place (especially when they are large) inevitably biases any review toward the null.

What seems not to have been widely appreciated is that vitamin D exhibits flat response regions at both low and high values of vitamin D status, with a sharp rise in the approximate center of the physiologic range of 25-(OH)D values (8). Studies like the WHI (Women’s Health Initiative), which enrolled women with low vitamin D status values and used a vitamin D dose insufficient to move them into the response range, provide little useful information about vitamin D efficacy. Yet, precisely such studies were included in the review by LeBlanc and colleagues (7). This is not to criticize the WHI, which was designed more than 20 years ago (before vitamin D pharmacology was well-understood), but it is to criticize contemporary reviews and meta-analyses that fail to take advantage of newer information or to use critical biological criteria (8) for selection of studies for analysis of biological effects.

In addition, a disease-avoidance approach becomes problematic for micronutrients in general (and vitamin D in particular) when one understands that micronutrients do not actually cause any of the effects simplistically attributed to them. Although necessary for cell response, such micronutrients by themselves do not initiate or cause the response concerned. For example, vitamin D is a component of the biochemical apparatus that opens the genome to allow access to DNA information needed for a particular cell or tissue response. In terms of cell function, this dependence means that when supplies of the micronutrient are inadequate, cellular response is blunted. This is dysfunction, but not clinically manifest disease. Such dysfunction may indeed lead ultimately to various diseases, but disease prevention remains a dull tool for discerning the defect, and a disease-prevention approach clearly does not measure whether the organism has enough of the nutrient to enable appropriate physiologic responses, such as lactation.

Finally, and aside from the USPSTF’s findings, one must ask whether treating without first testing is sound practice. Certainly, it would be rational to do so if the condition being treated is prevalent and the treatment is safe and inexpensive. That is the case with another micronutrient, iodine, and the iodination of salt. However, the current situation is different because consuming sufficient iodine generally does not require conscious adherence to a particular regimen, whereas taking vitamin D does. Usually, testing improves patient adherence because it provides patient-specific, personally applicable information. General assurances that one probably needs extra vitamin D are not as compelling a motivator as knowing one’s number. Thus, whether the practitioner adheres to the widely divergent guidelines of the IOM (4), the Endocrine Society (9), or the American Geriatrics Society (10), measuring vitamin D status seems to be warranted, not so much to diagnose deficiency but to determine patient status relative to the selected guideline.

update  20 Jan 2015 a new USA study Ng et al. Vitamin D status and survival of metastatic colorectal cancer patients  at the 2015 Gastrointestinal Cancers Symposium found that patients with metastatic colorectal cancer with higher vitamin D levels survived a third longer than those with lower levels – 32.6 months compared to 24.5.

update 12 Jan 2015        As the poet Juvenal (died 130AD) wrote: Mens sana in sano corporis– a healthy mind in a healthy body. Its great how the prime  antistress homeostatic hormones- a pinch of natural  melatonin at night, with ENOUGH  daytime  anabolic soltriol calciferol vitamin D3, restores good sleep, orchestrate homeostasis of all other hormones especially of  the crucial adrenals and gonadals and thus thyroid hormones. ..

Sleep. 2015 Jan 12. Massa ea, Harvard.  Low Vitamin D and Poor Sleep in Older Community – Dwelling Men   :  vitamin D3 is important for sleep duration and quality. 16% of this study population had very low levels of vitamin D (< 20ng/mL 25(OH)D). Lower serum vitamin D levels linked with short (< 5 h) sleep duration,doubled the odds ratio [OR] 2.15 for the highest (≥ 40ng/mL) versus lowest (< 20 ng/mL) quartile of 25(OH)D,; Ptrend = 0.004) and lowering  sleep efficiency. And low vitamin D is a major associate of  major depressionJózefowicz ea Univ Lodz, Poland 2014..

Thanks to global human (mostly male)  greed enslaving the masses the past 7 millennia ie since at least Sumerian times, we have moved rapidly in our lifetime post WW2  from  global homeostatic (food, commodities) plenty to a world of dyshomeostasis- cacostasis stress chaos – in most countries  from Afghanistan to Zimbabwe. Just a few years ago South Africa led Africa in productivity and skills, and still has the biggest reserves of riches- minerals-  in the world; with boundless natural power (sun, sea) and manpower to drive industry and food production. But in  20 years post apartheid, the ruling ANC under Mbeki and the Zumas  has with  selfserving treasonous greed  brought South Africa to its knees with cacostasis, destruction of continuous water, electricity ; school education,  organized and quality  food provision ie agriculture, social security, the post office, the national airline, health services, Home Affairs and pensions). Now there are  rapidly increasing functionally illiterate or  old  16 million on state grants supported by the 6 million capable of meaningfully working and paying taxes if they dont emigrate. And state grants have now been extended to age 23yrs because state school leavers are practically unskilled for  anything but being labourers. .

The national powergrid and oil reserves have been degraded so that total indefinite blackouts are now imminent, never mind weekly “outages” crippling work-  the economy – and destroying appliances. Never mind increasingly pandemic influenza and HIV, antibiotic resistance puts us in the post-antibiotic era in this age of deadly resistant TB and STDs, with  reckless immoral  leaders  like Zuma and Vavi leading the mob in extramarital sex and provoked violence. .

So as never before, everyone from conception to grave needs realistic regular vitamin D3 supplement at about R3 a month to bolster mental and physical health of children, mothers and the working , never mind the ailing aging, to reduce illhealth costs. . Stress- through raised thyroid, sympathetic and cortisol levels and depressed gastrointestinal, cardiovascular, musculoskeletal and immune control, grossly disrupts homeostasis and shifts victims into catabolic estrogen-dominance , insulin resistance mode- which only the hormone supplements  D3 and melatonin, and the essential vitamins and minerals  if not  risk-laden androgenics can try to balance,

George Chrousos ea.  University Athens, Greece since Nat Rev Endocrinol. 2009 and now   Neuroimmunomodulation. 2015 write: Stress – glucocorticoids – and disorders of the stress system- cacostasis vs homeostasis.      All organisms must maintain complex dynamic equilibrium-  homeostasis- which is constantly challenged by internal or external adverse forces – stressors. Stress occurs when homeostasis is threatened or perceived; homeostasis is re-established by various physiological and behavioral adaptive responses. Neuroendocrine hormones have major roles in the regulation of both basal homeostasis and responses to threats, and are involved in the pathogenesis of diseases characterized by cacostasis – dyshomeostasis. The stress response is mediated by the stress system, partly located in the central nervous system and partly in peripheral organs. The central, greatly interconnected effectors of this system include the hypothalamic -pituitary-adrenal (HPA) axis and hormones arginine vasopressin, corticotropin-releasing hormone  and autonomic norepinephrine centers in the brainstem.  Optimal basal activity and responsiveness of the stress system is essential for a sense of well-being, successful performance of tasks, and appropriate social interactions. By contrast, excessive or inadequate basal activity and responsiveness of this system might impair development, growth and body composition, and lead to a host of behavioral and somatic pathological conditions.. Glucocorticoids, the end-products of the HPA axis, play a fundamental role in the maintenance of both resting and stress-related homeostasis and, undoubtedly, influence the physiologic adaptive reaction of the organism against stressors. If the stress response is dysregulated in terms of magnitude and/or duration, homeostasis is turned into cacostasis with adverse effects on many vital physiologic functions, such as growth, development, metabolism, circulation, reproduction, immune response, cognition and behavior. A strong and/or long-lasting stressor may precipitate and/or cause many acute and chronic diseases. Moreover, stressors during pre-natal, post-natal or pubertal life may have a critical impact on our expressed genome.

VITAMIN D ECONOMY & GOAL OF SCREENING: Heaney and Armas, Creighton University  QUANTIFYING THE VITAMIN D ECONOMY: Nutrition Reviews  Dec 2014; and Screening for Vitamin D Deficiency: Is the Goal Disease Prevention or Full Nutrient Repletion? Ann Intern Med. Nov 2014   write:  sunlight and food  contribute only modestly  to the relevant optimal total serum vit D and 25OHvit D levels: unsupplemented individuals who average blood 25OHvit D of 20 ng/mL are receiving about 2,000 IU/day from nonsupplement sources (i.e food and sun) – whites double the amount  compared to dark blacks  from skin. . It has been established for 30 years that in fair-skinned individuals, a single exposure to UV-B at one whole-body minimum erythema dose can produce a rise in serum 25D that is equivalent to an oral dose of D3 in the range of 10,000 to 25,000 IU, ie by as little as 10–15 min of whole-body exposure at mid-day in mid-summer in a pale-skinned individual. Pale-skinned northern Europeans show a rise in serum 25D of 9 ng/mL (23 nmol/L) at the end of 4 weeks of exposure. By contrast, in dark-skinned individuals, the rise was  half  ie 4.5 ng/mL . Meat  eaters exhibit higher human 25D status . Input gaps left after estimating solar inputs (on the order of 1,300–1,600 IU/day, as noted above) could well be filled by hitherto unrecognized food sources. For example, Taylor et al.21 report a combined (D3 plus 25D) content of 112 IU vitamin D equivalents for 200 g of beef tenderloin or  an egg, associated with 2 ng/mL greater level of serum 25D.      The Grassroots Health project collects data on supplement type and has found no difference in the 25D concentration achieved with either 5,000 or 10,000 IU daily doses, irrespective of whether the D3 was delivered via a gel cap in oil or as dry powder in a tablet (unpublished data; S. McDonnell, personal communication). vitamin D could be absorbed from orange juice. On the other hand, fat malabsorption syndromes are known to lead to vitamin D deficiency, and the mechanism is generally considered to be a specific impairment in the absorption of fat-soluble vitamin D. However, poor absorption may reflect not so much mucosal dysfunction, as simple sweeping of any fat-soluble compound out of the gut, dissolved in the unabsorbed fat. Dawson-Hughes et al.,35 using pharmacokinetic methods in individuals with normal absorptive function, reported equal absorbability for D3 under fasting and high-fat meal conditions, with slightly better absorption from a low-fat meal. Mulligan and Licata,36 in an observational study of 17 poor responders to oral D preparations, reported greater absorption from a large meal containing fat than from intake on an empty stomach. However, the limited data, taken as a whole, suggest that the effects of dosage form or vehicle are probably small.

Finally, the issue of D2 versus D3 needs brief mention. Formerly considered controversial, there now seems to be a growing consensus37 that, for equimolar quantities, orally administered D3 raises serum 25D by about twice as much as D2.38–42 This has been shown for bolus doses, short-term continuous administration (12 weeks), and long-term continuous administration (12 months).

Intestinal absorption of D3 is mainly from the jejunum and ileum. Absorbed vitamin D can be found in both the portal venous blood and the lymph that drains the small intestine.  The lymphatic pathway may have particular physiological significance for orally acquired vitamin D, since it avoids a first pass of the absorbed vitamin D through the liver. This suggests that the quantitative relationship between vitamin D and 25D will be the same regardless of whether vitamin D enters from the skin or the gut.

Diffusion from the skin into the blood is slow, with a half-time of about 3 days.7 This half-time means that when regular sun exposure is the principal source of D3, serum D3 concentration will be essentially constant.

it is reasonably certain  that the concentration of vitamin D in fat tissue is substantially higher than the concentration in serum. – a given volume of fat tissue contains approximately 12 times as much vitamin D as the same volume of serum. However, a several-fold gradient is not surprising as D3 solubility in fat is effectively limitless, while DBP capacity, which is large, is finite.

Assuming a diffusional mechanism and a total body fat mass of 35% of body weight,  total body stores in an individual weighing 70 kg would range from 900 to 2,800 µg (37,000 to 113,700 IU). Using the calculations set forth in the prior section and applying them to an individual with a serum 25D level of 20 ng/mL, whose metabolic consumption would be ∼2,000 IU vitamin D/day, the total amount in the reservoir would provide enough of a reserve for 18–57 days at that same rate of utilization. At a serum 25D level of 40 ng/mL, that same reserve would support consumption for only 9–28 days. Neither estimate comes close to compensating for the “vitamin D winter” of most temperate latitudes. The smallness of this reserve explains why even outdoor summer workers who had high daytime skin exposure experienced reductions in 25D averaging approximately 20 ng/mL (50 nmol/L) by late winter. Of note, their 25D values had reached >50 ng/mL (125 nmol/L) by late summer, which is roughly the same as that reported for East Africans living ancestral lifestyles.48 This study indicates both that existing stores at the end of summer were not adequate to maintain the achieved summer level and that the late winter level (∼30 ng/mL) represented a utilization of approximately 3,000 IU/day.

Chemical partition
Extracellular 25(OH)D  The first step in the chemical conversion of D3 is 25-hydroxylation.Bikle et al.51 showed that skin cells contain all the requisite enzymatic apparatus to produce both 25D and 1,25D. However, it is doubtful that under ordinary circumstances, skin is a major source of the extracellular 25D measured in serum (D. Bikle, personal communication). Other sources remain to be identified.

The efficiency with which D3 is converted to 25D varies widely from individual to individual.  Various reasons can be put forth for these inter-individual differences that, though studied in somewhat less detail, have been reported by many investigators. One example is the variable methylation of the CYP2R1 gene and, hence, variable expression of the hepatic 25-hydroxylase.53 While there is currently no final answer, it is clear that differences in intestinal absorption of D3 could not explain the slow rise in participant B, relative to participant A. Moreover, the internal consistency in the shape of the respective curves virtually excludes methodological variability as a cause of the difference.

Extracellular 1,25(OH)2D  The second hydroxylation, which produces extracellular 1,25D, occurs predominantly in the proximal convoluted tubular cells of the kidney. While 25-hydroxylation is not highly regulated, the opposite is true for 1,25D, the synthesis of which is upregulated by parathyroid hormone and low serum inorganic phosphorus concentration and downregulated by fibroblast growth factor-23. Note that 1,25D is a principal regulator of intestinal absorption of calcium; during this process, it acts by upregulating expression of the calcium transport apparatus of the enterocyte. This is an endocrine effect as it is mediated through serum endocrine-like activity and exhibits a typical negative feedback control loop. Under usual conditions, 1,25D is necessary for regulation of calcium absorption. However, it is not the only factor involved in this process. It should also be noted that in the absence of other vitamin D metabolites, 1,25D by itself has been reported not to be sufficient to elevate intestinal calcium absorption.55,56

As would be expected for regulator molecules, the serum half-time of 1,25D is short (hours). Its concentration in serum is a reflection mainly of relative calcium need—being high in individuals on low-calcium diets or in those with calcium malabsorption and low in individuals with high calcium intakes. Also, 1,25D has long been recognized to be calcemic when used therapeutically. The mechanism is generally attributed to intestinal calcium absorption, but this cannot be a satisfactory explanation, as increased metabolic input alone (i.e., without considering output) is rarely sufficient to elevate the serum concentration of any metabolite. Moreover, 1,25D and its analogs do not elevate calcium absorption in patients with end-stage renal disease,57 a condition in which the calcemic effect of 1,25D is often readily apparent. While not adequately explored, there remains another possibility, i.e., an effect of 1,25D on bone-lining cells, where a fall in bone fluid pH to just below 7.0 is enough to solubilize bone mineral sufficiently to elevate serum calcium.58
Physical partition

The distinction between the endocrine and the autocrine pathways is one aspect of the physical partition between extracellular and intracellular processing of the vitamin. The prevailing assumption seems to be that most or all of the D3 entering the body is 25-hydroxylated and that the resulting 25D circulates in the blood, where it serves as the substrate for both renal and extrarenal 1 -α-hydroxylation, with the renal 1,25D product circulating in the blood like 25D and with the extrarenal 1,25D never being expressed in the only accessible body compartment, i.e., the blood.

As Hollis and Wagner59 have pointed out, D3 enters cells more readily than does 25D and, as noted above, there are several enzymes other than the hepatic CYP2R1 that are capable of 25-hydroxylation of D3.49,50 Hence, a physical partition of the vitamin D pathways prior to the 25-hydroxylation step has to be given serious consideration. That this is more than just a theoretical possibility is suggested by the fact, noted earlier, that oral 25D elevates serum 25D to a substantially greater extent than does oral D3.28–30 This was shown first by Barger-Lux et al.28 in a 10-week dosing study involving the two molecules. Figure 9 plots the 25D response to the two agents observed in a group of 54 healthy adults and shows a clear divergence of the dose response curves, with a greater than seven-fold difference in slopes. Cashman et al.,30 using a different design, found an approximate five-fold difference in response after 10 weeks of dosing, and Bischoff-Ferrari et al.,29 an approximate four-fold difference after 17 weeks of dosing.

Figure 9
Change in serum 25D plotted as a function of intake for varying oral doses of 25D and D3. Data from Barger-Lux et al.28
That there should be a greater rise in 25D when oral 25D is the source is, in a sense, trivial, as oral 25D is immediately reflected in the serum, while oral vitamin D must first be 25-hydroxylated, a process that, as described above, is necessarily slower, sometimes substantially so. Only a proper pharmacokinetic study that compares area-under-the-curve values for the two agents can fully quantify this difference. Such a study must either be long enough to allow the 25D plateau to be reached while on continuous dosing of D343 or, if using a bolus dose design, must follow the time course for the two agents for probably 4 months so as to allow full 25-hydroxylation of the administered D3 and full consumption of the administered 25D. No such data are currently available, and this aspect of the physical partition must remain speculative. Nevertheless, the issue is an important one, not just for the therapeutics of 25D but also for a full understanding of the vitamin D economy (see below).

The 25D half-time (as measured by Clements et al.60–62 using tracer-labeled 25D) presents certain puzzling features in its own right. A half-time of, say, 20 days (toward the lower end of the range found by Clements et al.) translates to a daily turnover of about 3.47% of the total mass of extracellular 25D. If the size of daily utilization is known, it is possible to calculate the size of the 25D mass from that fractional utilization rate. If all of the vitamin D input to the body is converted to extracellular 25D, then at a serum 25D concentration of 20 ng/mL (requiring, as shown above, a daily input of ∼50 µg), that 50-µg input is numerically equal to the daily turnover. So, total 25D mass would be 50/0.0347, or close to 1,500 µg. This figure is larger by an order of magnitude than that of the measurable total serum content of 25D, and the discrepancy becomes even larger at higher serum 25D concentrations or longer half-times. This seeming discrepancy has not been noted previously, with one potential reason being the computational difficulty of harmonizing biological units (IU), first with mass concentrations (µg/mL), then with SI units (nmol). However, if a substantial fraction of daily input of D3 is 25-hydroxylated intracellularly, after which it is immediately activated to 1,25D, then only the 25D in the extracellular compartment would be labeled by a tracer-based approach to kinetic analysis, and the calculated daily utilization of the circulating 25D would be lower and the corresponding 25D mass estimate would be closer to what is known from blood and soft tissue content. These calculations provide support for the suggestion of Hollis and Wagner59 that “parent compound D” has more functional significance than has usually been thought.

There is one quantitative aspect of the physical partition, whether occurring prior to or after the 25-hydroxylation step, which seems inescapable. Whether one takes as optimal a serum 25D concentration of 20 ng/mL or 40 ng/mL, the molar equivalent D3 inputs required to sustain either level are far higher than the moles of 1,25D required to support the calcium economy. As noted above, a serum 25D of 40 ng/mL requires approximately 4,000 IU/day, or 100 µg/day, and a serum 25D of 20 ng/mL requires approximately 2,000 IU/day, or 50 µg/day. By contrast, the calcium economy requires between 0.5 µg and 2.0 µg of 1,25D/day. (Higher doses, as noted above, produce hypercalcemia.) It follows that >90% of D3 utilization is occurring along the intracellular/autocrine pathway. If that is not the case, then most of the D3 input to the body is degraded metabolically and not used at all. The latter possibility seems quite improbable, particularly in view of the marginal or subadequate vitamin D status that seems nearly universal. Answering this question of the relative potency of oral D3 and 25D will illuminate the partition of D3 between the extracellular and intracellular pathways and will be an important step in unraveling the puzzle of the physical partition.

One instance in which the pre-25D intracellular pathway is operative is the transfer of vitamin D activity into human breast milk.59,63 25D does not transfer across the secretory mucosa of the mammary gland with sufficient efficiency to produce enough vitamin D activity in milk to nourish the infant, while D3 does. However, for this to occur, D3 must be present in the blood that bathes the mammary secretory apparatus. In earlier work, Hollis et al.63 showed that the concentration of vitamin D in human milk was about 28% of the concentration of D3 in maternal blood. In subsequent work (B. Hollis, personal communication), that figure was shown to be closer to 32%, and a recent study by Oberhelman et al.64 showed a transfer fraction that can be calculated to be about 44%. Based on recommendations of both the American Academy of Pediatrics and the Institute of Medicine for infant intake (400 IU vitamin D/day, which requires a milk concentration of about 520 IU/L, i.e., ∼34 nmol/L), these transfer fractions would require a maternal serum vitamin D concentration of about 30–40 ng/mL (78–120 nmol/L). (The corresponding 25D concentration would be >50 ng/mL [125 nmol/L]; see Figure 8.) Hollis and Wagner59 estimate that the total input of D3 needed to maintain a milk concentration sufficient to meet the infant’s needs for vitamin D was approximately 6,000 IU/day. The equivalence value derived above produces a needed input of approximately 6,000 IU/day, which is essentially identical to the empirical estimate of Hollis and Wagner.
Dosing schedules and serum D3 concentrations

Dosing frequency for oral vitamin D supplementation regimens will affect serum concentration of D3 in predictable and often very striking ways. This fact has been largely overlooked to date, as the serum concentration of D3 has been generally considered to be of no particular interest in its own right. The rationale for infrequent (or bolus) dosing is that it leads to better adherence and that an excess amount ingested today will be stored in fat for use tomorrow. However, this assumption overlooks the effect of infrequent dosing regimens on D3 blood concentrations.

Serum D3 has a half-time variously estimated to be in the range of 0.5–3.5 days, with most investigators favoring a value of about 1.0 days. In contrast, D3 produced in skin moves into the blood with a half-time of about 3 days. This means that when skin synthesis is the principal source of D3, serum D3 concentration will be essentially constant around the clock, as D3 input to the blood from the skin (though produced mainly at mid-day) is effectively constant. With oral ingestion, intestinal absorptive input of D3 occurs mainly during a 4-h period following ingestion. (In one study, a TMAX of as much as 12 h was reported.65 As this is well beyond the usual mouth-to-cecum transit time, the 12-h figure, if confirmed, would suggest appreciable colonic absorption, or small bowel mucosal retention, or a delay pool in the intestinal lymphatics.) In any case, assuming a 1.0-day half-time, serum D3 concentration will inevitably follow a sawtooth pattern, particularly if oral ingestion is the principal input. Figure 10 displays the patterns for purely cutaneous input and for daily, weekly, and biweekly oral administration. With a once-a-week schedule, as is evident from Figure 10, serum D3 concentrations are close to zero for several days each week and below the reference level for most of the interdose interval. Thus, in the practical order, a nursing woman who takes her total weekly dose of vitamin D once each week would produce milk with little or no D content for roughly 4 of the 7 days in each week. This irregular delivery will be even more pronounced with biweekly or less frequent dosing schedules.

Figure 10
Calculated time courses for serum D3 concentration for varying oral dosing intervals. The reference level is the serum concentration for continuous (as contrasted with intermittent) dosing. Each dosing scheme provides the same cumulative intake, according to one of the following regimens: once daily, or 7 times the daily intake once weekly, or 14 times the daily intake once every 2 weeks.
It should be stressed that Figure 10 illustrates the concept and is not a depiction of actually measured serum concentrations of D3. Under input conditions in excess of daily use, unused D3 will accumulate in fat, and its concentration there would be predicted to damp the oscillations of D3 concentration in serum to some extent.

An additional feature of interval dosing is the high D3 concentration peaks achieved in the days following each dose. The impact of such high D3 levels is unclear, although Vieth66 has pointed to the induction of the 24-hydroxylation pathway as a likely consequence, with a corresponding reduction in effective vitamin D activity. Further, as the binding capacity of DBP is approximately 4.7 µmol67 (or ∼78,000 IU/L), with true Stosstherapie, as in several recent studies,68,69 the DBP will be fully saturated by the ingested D3, resulting in displacement of both 1,25D and 25D off DBP and into circulation as free or unbound moieties for several days after dosing (i.e., until fat uptake lowers serum D3 sufficiently). This effect amounts to a transient vitamin D intoxication of uncertain physiological import. Unfortunately, there is essentially no published information about vitamin D concentrations in the immediate post-dosing period following large bolus doses. Whatever else may be said of Stosstherapie, it certainly is not physiological.
Factors influencing serum 25D concentration

Aside from the possible importance of D3 concentration as the substrate for autocrine activity of vitamin D, there is general agreement that serum 25D concentration is currently the principal indicator of vitamin D status.70 This is because extrarenal conversion of 25D to 1,25D operates at concentrations below the kM for the tissue 1 -α-hydroxylases; hence, serum 25D concentration limits the amount of 1,25D a tissue can synthesize when its cells are stimulated to produce a vitamin D-dependent response. While there is no consensus as to the optimal serum 25D concentration, there is also no disagreement about the importance of the substrate, regardless of which concentration may be deemed optimal.

Input of D3, a factor that manifestly affects 25D concentration, has been the subject of much of the previous discussion. Attention is now focused on the effect on serum concentration of 25D produced by variations in body size and in D3 output, i.e., utilization and/or degradation of the 25D in serum.
Obesity

One widely recognized influence on 25D concentration is obesity, with serum 25D being lower in obese individuals. This was originally attributed to a phenomenon termed “sequestration” (implying trapping of vitamin D in adipose tissue of obese individuals).71 However, Drincic et al.72 have shown that simple volumetric dilution is both a more logical explanation and one that fully explains the weight-based difference. Curiously, body mass index works in various regression models almost as well as body weight (and somewhat better in some datasets). This is surprising as body mass index is not a measure of mass but of fatness. The reason is presently unclear, and this observation suggests the possible existence of further mechanisms operating in obese individuals.
Parathyroid hormone-1,25D axis  Clements et al.60–62 showed that 25D half-time in serum ranged from 15 to >35 days, with 25D half-time being inversely related to parathyroid hormone concentration. The parathyroid hormone effect, noted both in patients with hyperparathyroidism and in animals subjected to calcium deprivation, was, in turn, mediated by serum 1,25D concentration. Why 25D utilization (or degradation) should rise in the face of calcium need is physiologically unclear, particularly as renal 1,25D synthesis is not as dependent on 25D concentration as the autocrine functions of vitamin D.

Inflammation.  The other major influence on serum 25D concentration is inflammation. It has been reported that vitamin D status is reduced in the face of systemic inflammatory processes.73–78 For example, Duncan et al.75 reported an inverse correlation of 25D with serum C-reactive protein, with 25D being 40% lower as serum C-reactive protein rose from <5 mg/L to >80 mg/L. Autier et al.,79 in a metaanalysis of the several reports on this relationship, confirmed the existence of the association but attributed the reduced vitamin D status to underlying illness rather than to the inflammation itself. That conclusion may be partly correct, at least for some chronic illnesses, but it cannot apply to the many documented cases in which vitamin D status drops acutely across an inflammatory episode, as with total knee arthroplasty.73,77 In one case study, Henriksen et al.73 reported a 12% drop in 25D by day 2 after total knee arthroplasty and a nearly 80% drop by post-surgery week 8. Reid et al.77 evaluated a series of 33 patients who underwent total knee arthroplasty and reported an approximate 40% drop in total 25D and a 33% drop in calculated free 25D by day 2 after surgery, which was associated with large increases in C-reactive protein.

Decreases in 25D of this magnitude and rapidity cannot be explained by decreased synthesis and must, therefore, reflect increased utilization, degradation, or loss. Depending on which values may be estimated for the total 25D mass (see above), reductions in 25D concentration of the size reported by Reid et al. translate to a loss of several hundred micrograms from the body, which is substantially greater than ordinary daily utilization of vitamin D. While increased utilization cannot be ruled out, it seems unlikely to be the sole explanation. Another possibility, which was suggested by Waldron et al.,76 is the loss of DBP (with its bound ligand) in the urine. In 30 patients undergoing elective orthopedic surgery, the ratio of DBP to creatinine in urine rose 2.5× by the second day post-surgery; this was associated with a >20-fold increase in C-reactive protein. Renal loss could certainly explain much or all of the change in 25D observed in these studies and could be the result of interference with the kidney’s megalin–cubilin system, possibly produced by the anesthesia or inflammatory cytokines associated with the surgery.

Although not directly related to the major focus of this review, the conclusion reached by several of the authors of the studies just reviewed, i.e., that, while inflammation clearly reduced D status, this reduction was without nutritional significance, is in no way supported by data in any of the papers concerned, nor is it consistent with the importance of serum 25D concentration as the principal limiting factor in the autocrine pathway.

METABOLISM AND UTILIZATION   the data assembled here make clear that, even with today’s widespread vitamin D inadequacy, total vitamin D inputs are far higher than previously thought, food sources are greater than previously recognized, and solar input, though theoretically capable of fully meeting any plausible vitamin D requirement, is actually only a minor present-day contributor to total vitamin D input at the population level. That does not mean that the human requirement is more easily met. Rather, it indicates that the requirement is higher than previously recognized, with populations still short of meeting that requirement by the amount needed to move prevailing serum 25D concentrations from current values to putatively healthier levels.

These analyses also make clear that at prevailing inputs (i.e., <4,000 IU/day), D3 is rapidly 25-hydroxylated and little D3 circulates in the blood or is shunted into adipose tissue for storage. Additionally, the recent recognition that oral 25D may raise serum 25D to a significantly greater extent than does oral vitamin D suggests the possibility of a hitherto little recognized or explored intracellular pathway in which the entire metabolic sequence is handled within certain target tissues and is not reflected in blood. A related finding in this respect is the importance of a maternal serum D3 concentration sufficient to support production of human milk capable of meeting infant needs for vitamin D.

Several of these insights have implications for the human requirement. For example, the vitamin D input needed to support an adequate amount of vitamin D in human milk has implications not just for lactation but also for human success as a species under presupplementation conditions. Inadequate vitamin D input in newborns would be expected to lead to skeletal abnormalities (for which the paleo-fossil record provides no evidence), in addition to possible consequences for immune system development.89 A total input of approximately 6,000 IU in modern humans equips them to feed their infants with a nearly full range of the nutrients needed for healthy growth.

CONCLUSION    Precise quantification of vitamin D inputs, transfers, conversions, and compartment sizes are essential for a full understanding of how the human body utilizes this essential micronutrient, why it is important, and what the consequences are of an inadequate vitamin D input.

Since its founding, the U.S. Preventive Services Task Force (USPSTF) has  provided  firm evidential base for early detection strategies, evaluating such screening methods as mammography and prostate-specific antigen testing. Although it has also evaluated a few interventions, its predominant focus has been testing for markers that identify persons at risk who are likely to benefit from preventive action. Only recently has  USPSTF entered  the (mine)field of nutrition, a territory distant from screening tests and risk assessment, with different and unfamiliar landmarks.

The USPSTF now reports it is unable to find evidence for or against vitamin D deficiency testing  (1),  the likely reasons being the absence of a scientific consensus on both the level of vitamin D status that should be judged “deficient” and what the measurable manifestations of deficiency might be. These are also issues for many other nutrients, such as folate, ascorbate, calcium, and protein. Vitamin D may have seemed to offer a way out of this confusion because serum 25-hydroxyvitamin D [25-(OH)D] concentration is generally recognized as one of the best indices of status for any of a broad array of nutrients. Also, it is now readily measurable and widely utilized.                 

One of the reasons its promise has not been realized is that most studies of vitamin D efficacy have used a disease-avoidance model, which is the standard approach used by the Institute of Medicine (IOM) for most nutrients (2). Furthermore, disease prevention is the explicit focus of the USPSTF. Nevertheless, the IOM and USPSTF approaches effectively equate health with the absence of disease, an equivalence that nutritionists have long rejected. Instead, nutritionists focus on full nutrient repletion when possible. The inevitable gap between disease prevention and nutrient repletion is still largely unexplored territory. For many nutrients, it can be surprisingly wide, as suggested in this case by studies of the intake required to provide vitamin D in human breast milk in quantities sufficient to meet the needs of infants (3). The IOM’s adult requirement for vitamin D is 600 IU/d (4), which is judged to be sufficient to protect against osteoporotic fracture. In contrast, quantitative and empirical evidence indicates that vitamin D intake from breastfeeding needs to be approximately 6000 IU/d (3, 5). Although high compared with the adult recommendation, such an intake almost exactly reproduces the measured vitamin D status of contemporary Africans leading ancestral lifestyles (6). Such populations provide perhaps our best window on vitamin D levels prevailing during the millennia over which human physiology was adapted to its environment by natural selection.

Whatever the actual requirement or 25-(OH)D cutoff may be, there is another likely reason that the evidence is unclear. The USPSTF drew from systematic reviews and meta-analyses of studies of vitamin D effects, such as the one accompanying the current report (7). In general, the criteria for including studies in such reviews are methodological rather than biological. Of the 6 published biological criteria (8) for including published reports in meta-analyses, the review published in this issue met only 2 (comparable basal status and same chemical form), and several of its component studies met none. Including studies that could never have been informative in the first place (especially when they are large) inevitably biases any review toward the null.

What seems not to have been widely appreciated is that vitamin D exhibits flat response regions at both low and high values of vitamin D status, with a sharp rise in the approximate center of the physiologic range of 25-(OH)D values (8). Studies like the WHI (Women’s Health Initiative), which enrolled women with low vitamin D status values and used a vitamin D dose insufficient to move them into the response range, provide little useful information about vitamin D efficacy. Yet, precisely such studies were included in the review by LeBlanc and colleagues (7). This is not to criticize the WHI, which was designed more than 20 years ago (before vitamin D pharmacology was well-understood), but it is to criticize contemporary reviews and meta-analyses that fail to take advantage of newer information or to use critical biological criteria (8) for selection of studies for analysis of biological effects.

In addition, a disease-avoidance approach becomes problematic for micronutrients in general (and vitamin D in particular) when one understands that micronutrients do not actually cause any of the effects simplistically attributed to them. Although necessary for cell response, such micronutrients by themselves do not initiate or cause the response concerned. For example, vitamin D is a component of the biochemical apparatus that opens the genome to allow access to DNA information needed for a particular cell or tissue response. In terms of cell function, this dependence means that when supplies of the micronutrient are inadequate, cellular response is blunted. This is dysfunction, but not clinically manifest disease. Such dysfunction may indeed lead ultimately to various diseases, but disease prevention remains a dull tool for discerning the defect, and a disease-prevention approach clearly does not measure whether the organism has enough of the nutrient to enable appropriate physiologic responses, such as lactation.

Finally, and aside from the USPSTF’s findings, one must ask whether treating without first testing is sound practice. Certainly, it would be rational to do so if the condition being treated is prevalent and the treatment is safe and inexpensive. That is the case with another micronutrient, iodine, and the iodination of salt. However, the current situation is different because getting sufficient iodine generally does not require conscious adherence to a particular regimen, whereas taking vitamin D does. Usually, testing improves patient adherence because it provides patient-specific, personally applicable information. General assurances that one probably needs extra vitamin D are not as compelling a motivator as knowing one’s number. Thus, whether the practitioner adheres to the widely divergent guidelines of the IOM (4), the Endocrine Society (9), or the American Geriatrics Society (10), measuring vitamin D status seems to be warranted, not so much to diagnose deficiency but to determine patient status relative to the selected guideline.

THE NEAR-IMPOSSIBILITY  OF OVERDOSING WITH VITAMIN D3 – except  by persistent repeated  injection  A Report  in Feb 2014 from Bansai & Arora ea New Delhi show how  extreme the overdose of vitamin D3 must be to cause hypercalcemic toxicity: an Asian  woman given 6million iu  imi over 10 days  after knee surgery presented 2 months later with 6 wks of persistent vomiting, fatigue, with moderate hypercalcemic renal failure  and 25OHvit D level of 150ng/ml; that normalized in 2 weeks.. So her peak level after the initial 2 weeks on an average ~50 000iu/day may have been around 500-600ng/ml..  Bansai and Arora quote two series from  endemically vit D deficient Kashmir (Pandita ea 2012 in Jammu and 2011  Koul ea Srinagar)   of a total 25 elderly  given chronic overdoses  D3 600 000iu monthly , who were found to have similar moderate hypercalcemia and renal failure with peak 25OHvit D of 100 – 300ng/ml: a mean vit D3 dose of between 20 000iu and >1million iu/day?, mean s. creat 2.5; mean 25OHvitD of 100 – 200ng/ml; mean calcium 13.1mg/dl. 20 000iu a day indefinitely in these frail small elderly averages at least 400iu/kg/day, at least 5 times the chronic recommended dose in the literature the past decades- and to boot, routinely given them with a highdose calcium supplement- when it is rather magnesium that should if any be boosted. .  Koul ea do note that about 100 000iu vit D a day ongoing  is required to cause hypercalcemia, the mean lethal dose being about 8million iu.

By contrast, previous reports below- eg from the Netherlands report of 2million iu single  overdose  in  90 year olds; and planned 600 000iu orally monthly dose in Pakistani men  wasted with TB (Salhuddin ea below)   showed no overdose signs.  So a single loading dose of 1 to 2  million units is unlikely to give overload. By these  precedents (eg 600 000iu p.o monthly- apparently official policy of the Pakistani Endocrine Society) one may  in acute infections  give up to 600 000iu as a loading dose (a million in an obese ill patient) in acute infection situations, then 50 000- 80 000iu weekly depending on weight, to maintain level around 90ng/ml.

Am J Clin Nutr March 2008  Pharmacokinetics of a single, large dose of cholecalciferol 100 000iu  IlahiArmas, and  Heaney   Creighton University Medical Center, Omaha,  Design: followed for 4 mo, 30 subjects were  supplemented with a single oral dose of 100 000 IU cholecalciferol. 10 subjects served as a control group to assess seasonal change of calcidiol.   The subjects were healthy with limited sun exposure (<10 h/wk) and milk consumption (<0.47 L daily);  excluded granulomatous conditions, liver disease, kidney disease, or diabetes or  taking anticonvulsants, barbiturates, or steroids.  Results: Serum calcidiol rose promptly after cholecalciferol dosing from a mean (±SD) baseline of 27.1 ± 7.7 ng/mL to a concentration maximum of 42.0 ± 9.1 ng/mL. Seven percent of the supplemented cohort failed to achieve 32.1 ng/mL at any time point. The highest achieved concentration in any subject was 64.2 ng/mL. The control group had a nonsignificant change from baseline of −0.72 ± 0.80 ng/mL during 4 mo.   Conclusions: Cholecalciferol (100 000 IU) is a safe, effective, and simple way to increase calcidiol concentrations. The dosing interval should be ≤2 mo to ensure continuous serum calcidiol concentrations above baseline.

THE IMPORTANCE OF IMMUNOSYNERGY BETWEEN ADEQUATE ANABOLIC HORMONES- VIT D3, MELATONIN (Berman 1926, Carrillo-Vico 2013), AND PROGESTERONE   in planned and current pregnancy, and aging?  Thangamani, Kim ea Purdue & Indiana Universities in   J Immunol. 2014 Dec 29:  Cutting Edge: Progesterone Directly Upregulates Vitamin D Receptor Gene Expression for Efficient Regulation of T Cells by CalcitriolThe two nuclear hormone receptor ligands progesterone and vit.D play important roles in regulating T cells.., we report that progesterone is a novel inducer of vit.D receptor (VDR) in T cells and makes T cells highly sensitive to calcitriol even when vit. D levels are suboptimal. This novel regulatory pathway allows enhanced induction of regulatory T cells but suppression of Th1 and Th17 cells by the two nuclear hormones. The results have significant ramifications in effective regulation of T cells to prevent adverse immune responses during pregnancy.

A recent review of vitamin D from Mike Holick (Boston Mass.) and a German team  again reminds us of two opposing forces limiting natural sunshine vitamin D supply: on the one hand the skin shuts down active vit D production if the sunlight burns, while on the other, there is simply not enough sunlight  beyond  35degrees latitude from the equator. Thus Germany and Canada-northern USA for example, at >45degrees north,  get far too little sunlight for vit D needs ; eg London is at 51degrees north; Cape Town-Florida-San Diego, Sydney-Buenos Aires, Hawai  and the Med. countries are at the 35degree south latitude. Even this close to the equator, many overdress- especially more observant religious  women-  and thus minimize  benefit from summer sunshine.

J Assist Reprod Genet. 2014 Dec 30.Vitamin D and assisted reproductionvitamin D should be routinely screened and repleted prior to ART? Pacis , Segars ea Dartmouth-Hitchcock Medical CenterLebanon NH  systematic review.  review  current literature regarding the role of vitamin D status & repletion  in pregnancy outcomes in women undergoing assisted reproductive technology (ART).  Thirty-four articles were retrieved, of which eight met inclusion criteria. One study demonstrated a negative relationship between vitamin D status and ART outcomes,  two studies showed no association. The remaining five studies concluded that ART outcomes improved after vitamin D repletion.The majority of reviewed studies reported a decrement in ART outcomes in patients with vitamin D deficiency. Cost-benefit analyses suggested that screening and supplementing vitamin D prior to ART might be cost effective.

25 Dec 2014 ANOTHER AVOIDABLE TRAGIC  TB DEATH:   Dr Nerissa Pather and countless other infectious disease sufferers – health workers and their patients :

 Sunshine Cures:  why did TB  sanatoria work (before there were  antibiotics)? was it indeed the boost of copious sunshine secosteroid antimicrobial soltriol in the skin destroying the M TB porphyrins? or was it belief, then-cleaner  air, high altitude,    rest, care and better nutrition?

Not for nothing was  skin ie CTB  Lupus Vulgaris a relentless scourge  in the clothed  in darker climes and times, except perhaps in ancient sunny Pharanoic medicine, until the Danish Faroe Islander   physician Niels  Finsen-  trying to treat his own Niemann–Pick disease–  used his  invention phototherapy generator on his patients  and found that it magically rolled back skin TB (for which in  1903 he  got the only Nobel prize  apparently ever awarded for dermatology!). This light therapy antimicrobial effect has recently 2005 been attributed by Danish researchers    Møller,  Wulf ea  to the lethal effect of light oxidation on Mycobact  TB porphyrins.    However, this Danish study abstract ignores the antimicrobial benefit of cholecaliferol activated by light on the skin from  the Karolinska Inst in Sweden. A Georgetown Univ paper 2005 details the complexities of   Sunlight, Vitamin D, and the Innate Immune Defenses of the Human Skin , further set out in Optimal Skin Protection with  Vitamin D.    Unfortunately the circle is not yet squared off, there is still no study showing that vitamin D (like bcarotene and likely  melatonin) improves the disease porphyria?

A recent 2009 Mt Sinai NY report of a case of CTB cutaneous TB stresses how rare this skin complication is despite the increasing spread of TB with AIDS- perhaps partly because of the higher prevalence of HIV in poorer peoples in sunnier warmer ie relatively better sunshine-cholecalciferol-endowed climates.

We easily make our optimal vit D3 ~100iu/ kg per day living playing and working outdoors in warm lands. But since we dress more in cooler climates, with aging and dress-conservative cover-up tribal eg Arabic and Hasidic and Mormon customs; and avoid sunburn, and from early middle age lose 3/4 of our skin vitamin D production by 70years, we  aging thus need the bulk of our vit D requirements as supplements ie ~7000iu/day or 50 000iu/week.

A century ago, TB, polio, measles, scarlatina, and syphilis were rampant, and infections rather than wars killed most – ending in the 1919 flu holocaust that devastated the family of Dr Sir  Arthur Conan Doyle (whereas the Flu pandemic took just  one of my   parents’ score of siblings- and polio just left my Mom with a limp..)..

2014  is the centenary  of  recent  recognition of the  cod liver oil  antirickets steroid factor – calciferol/soltriol -briefly misnamed “vitamin”  D – by McCollum, Davis (USA 1913)  and Mellanby(UK); so that in 30 years  by 1945, rickets had been all but abolished in USA. But the recognition of the antirachitic factor was facilitated by discovery in the preceding decade of vitamins A, B and C. The antiscurvy benefit of fresh uncooked coloured crops (and thus their juice)  had indeed been recognized for millennia – eg the Royal  Navy limejuice- , but a specific micronutrient vitamin deficiency  was first only recognized in 1907. Vitamin C ascorbic acid  identification also took another 25years . For 90 years, it has been recognized that a  lightly cooked exclusively fatty meat diet can provide enough vitamin C (let alone all micronutrients)  for  health in eg  atheroma- and scurvy-free Eskimos and anyone who cares to eat thus (Stefansson ) .

Sadly, the lifegiving vitamins have  been diluted,  all but eliminated from retail bottled codliver oil, a ml  of which now generally supplies perhaps only 125iu vit D, and vitamin A 1000iu … So even a tablespoon supplies only about 1200iu vit D.. The Weston Price Foundation discusses  why modern commercial codliver oil is good with its balance of vits A and D– but the vitamin D level is  still  far too low for cooler darker countries.  However we recommend, (apart from far cheaper vit D3 powder 50 000iu/1ml scoop) – a tsp cod liver oil at least 3 times a week because it is the cheapest natural- and with Scandinavian manufacturing controls, safe-  source of vital  EPA+DHA available as well as some vitamins A and E.

As real summer begins here between the southern oceans,  cold winter in the northern hemisphere, we must constantly remind that vitamin D3 cholecalciferol  is NOT an  exogenous vitamin ie a biological  nutrient essential (Funk’s ‘vitamine’, shortened by Jack Drummond  because they are not amines to the more appropriate ‘vitamin’) in the human diet ( like vits A, B, C, E & K) because humans cannot make them. . But since we make  vit D  with light exposure of our skin, since most humans dont get enough sunlight on our skin,  it is certainly  a conditioned essential anabolic steroid, which like other anabolic steroids (the balance especially of androgens) is vital at optimal blood levels through life for optimal health,  healthspan.

Unlike the real vitamins and essential minerals,  Calciferol is (like eg  CoQ10,  alphalipoic acid, nitric oxide, EPA and DHA)   made in limited quantities in humans with adequate organ function and sunshine; but none of them generally in anywhere near optimal quantities for healthspan against all diseases. So given humans’ capacity to live well to a century, we need such supplements from youth to ensure chronic health so as to die of old age in good health. .

How does this relate to the death this month of Dr Nerissa Pather? Multiresistant TB contracted on duty 12 years ago  eventually killed her,    whether or not such  high-risk people are  ever advised to take the best prevention- zinc, selenium, multivites but especially highdose vit C and D3.

D3  bio-insufficiency fragility and  dysimmunity  is further complicated  since to  correct  it requires both plenty of skin sunshine exposure, eaten vitamin C and it’s daughter cholesterol,   and optimal kidney and liver  function. Even then optimal vitamin D3 bloodlevel and effect may be blocked by foolhardy cholesterol blockade eg statins, and  by excess intake and thus bloodlevel of vitamin D2 ergocalciferol – which   authorities eg in South Africa and USA  still negligently promote/ dispense as the dangerously misnamed “strong calciferol”. It is indeed D3 cholecalciferol, not D2   that is the miracle sunshine strong calciferol steroid;  egocalciferol dominance, like insulin and estrogen  dominance,  is  harmful, and can and must  be avoided. .

So it is increasingly apparent that, just as intake/manufacture of  vitamin C the true sunshine vitamin (those colourful veg/ fruit orchards etc) , and  thence cholesterol, should each be at least a few gms a day, the human  (clothed indoor-dwelling) adult synthesis +  intake  of sunshine hormone  vitamin D3 soltriol  should be nearer to 10 000iu ie 250mg/day, or more practically 50 000iu  vit D3 a week  (at a trivial supplement  cost of eg R6/month or $5 a year) for a bigger adult- especially in longer darker winter (starting with perhaps  about 25000iu every fortnight  for babies) .. of course balanced  in most societies with the other supplements especially water, vitamin K2, zinc, selenium iodine  and magnesium (and iron for children and reproductive mothers) .

So, how many more millions must suffer and die from lack of the cheapest, best, safest conditioned essential antimicrobial antioxidant anabolic nutrients available?

An undated (post 2003) Pharmacology Bulletin from Canterbury NZ at least gives conservative  realistic vit D3 advice: a loading dose of D3  500 000iu , then 50 000iu/month. This compares with our routine loading dose of about 200 000 to 400 000iu to start, then 50 000iu every week or two (proportionate to body mass and illness). But Lennons here negligently still continues to  advertise their Strong Calciferol datasheet (updated 2004) as calciferol- last year they in fact confirmed it is D2 ergocalciferol, not cholecalciferol. Only their website http://www.ndrugs.com/?s=lennon-strong%20calciferol confirms that their strong Calciferol is D2;  whereas they also make low strength D3 tabs.

From today’s press “The South African Medical Association (SAMA) extends heartfelt condolences on  the passing of 38yr old Dr Nerissa Pather on  18th December 2014 . Whilst on community service at a  Kwazulu Natal clinic, Dr Pather contracted well-publicised multi-drug resistant spinal TB in 2002 , that rendered her paralyzed and in constant pain. The loss  to a communicable disease acquired in the course of duty is an incalculable tragedy. SAMA reiterates its call to all health departments and facilities to ensure that  basic TB prevention methods are available to all healthcare workers in our facilities. Sadly, this is not the case in many of our hospitals and clinics and continues to place health professionals at enormous risk. The potential consequences of infection and even acquiring drug resistant TB are tragically evident in the death of Dr Pather.  SAMA bows its head to a colleague who has paid the ultimate price in caring for her fellow human beings.”

A current report from Tehran  Calcium and vitamin D plasma concentration and nutritional intake status in patients with chronic spinal cord injury: stresses the  obvious, the  terribly low intake and levels of vitamin D in spinal cord injury patients. Why are we inflicting this further deprivation on the most vulnerable patients?

The tragedy is that with general authoritarian nihilism about universal vitamin supplements- some calling their promotion  quackery- unrecognized  deficiency eg  vit D3, rickets,  and vit C scurvy  are on the increase even in the more affluent eg USA and in sunnier climates- especially with increasing geriatrics and the frail surviving with eg HIV, TB, cancer, chronic bowel disease,   gross overuse of warfarin (vit K deficiency) and  statin (CoQ10 deficiency) etc. .

Vitamin D Deficiency in Critically Ill Patients  is rarely considered or treated .. N Engl J Med 2009 Lee, Eisman & Center   studied vitamin D status in ICU patients  referred to   St. Vincent’s Hospital, Sydney in  2007. Among approximately 1100 ICU patients per year, the mean  25-hydroxyvitamin D in 42 referred patients was ~17ng per milliliter, with a high prevalence of hypovitaminosis D . Moreover, three patients died (from metastatic thymic carcinoma, glioma, and lymphoma), and  had undetectable levels of 25-hydroxyvitamin D.   The current study of  ICU patients reveals high prevalence of hypovitaminosis D that was associated with adverse outcomes, independently of hypocalcemia and hypoalbuminemia. Supplementation with  vitamin D (at a mean dose of 820 IU per day) before admission was not protective.   Vitamin D deficiency is associated with increased mortality.However, vitamin D has pleiotropic effects in immunity, endothelial and mucosal functions, and glucose and calcium metabolism. The association between hypovitaminosis D and common conditions (e.g., the systemic inflammatory response syndrome, septicemia, and cardiac and metabolic dysfunctions) in critically ill patients may be important. Vitamin D–deficient and vitamin D–insufficient states may worsen existing immune and metabolic dysfunctions in critically ill patients, leading to worse outcomes.  A total of 17% of  ICU patients in our study had undetectable levels of vitamin D. hypocalcemia was identified as a reason for referral in only 5% of the patients. These findings highlight the need for consideration of vitamin D status and supplementation in patients in the ICU.

Arch Intern Med. 2008;168:1629-37 25-hydroxyvitamin D levels and risk of mortality in the general population.   Melamed , Astor ea. Albert Einstein College of Medicine, NY tested the association of low 25(OH)D levels with all-cause, cancer, and cardiovascular disease (CVD) mortality in 13 331 nationally representative adults 20 years or older from the NHANES III linked mortality files.  In patients on  dialysis, therapy with  vitamin D agents is associated with reduced mortality. Observational data suggests that low  (25[OH]D) are associated with diabetes mellitus, hypertension, and cancers. However, whether low serum 25(OH)D levels are associated with mortality in the general population is unknown.   Participant vitamin D levels were collected from 1988 through 1994, and individuals were passively followed for mortality through 2000.    RESULTS:  In cross-sectional multivariate analyses, increasing age, female sex, nonwhite race/ethnicity, diabetes, current smoking, and higher body mass index were all independently associated with higher odds of 25(OH)D deficiency (lowest quartile of 25(OH)D level, <17.8 ng/mL , while greater physical activity, vitamin D supplementation, and nonwinter season were inversely associated. During a median 8.7 years of follow-up, there were 1806 deaths, including 777 from CVD. In multivariate models , compared with the highest quartile, being in the lowest quartile (25[OH]D levels <17.8 ng/mL) was associated with a 26% increased rate of all-cause mortality (mortality rate ratio, 1.26; 95% CI, 1.08-1.46) and a population attributable risk of 3.1%.    The lowest quartile of 25(OH)D level (<17.8 ng/mL) is independently associated with all-cause mortality in the general population.

ANABOLIC STEROID SYNERGY?: the steroids cholecalciferol and androgen are both immune and anabolic -switch  protein/muscle/bone promoters, without apparent mutual antagonism or suppression; calciferol also lowers SHBG levels, freeing up more active unbound testosterone ie reducing estrogen dominance.

 Subst Abuse Rehabil. 2014 Dec 10;5:121-7. Effects of different doses of testosterone on gonadotropins, 25-hydroxyvitamin D3, and blood lipids in healthy men. Gårevik, Ekström ea. At the Karolinska Inst Sweden,   Twenty-five healthy male volunteers aged 27-43 years were given 500 mg, 250 mg, and 125 mg of testosterone enanthate as single intramuscular dosesAll doses investigated suppressed the LH and FSH concentrations in serum. LH remained suppressed 6 weeks after the 500 mg dose. These results indicate that testosterone has a more profound endocrine effect on the hypothalamic-pituitary-gonadal axis than was previously thought. There was no alteration in 25-hydroxyvitamin D3 levels after testosterone administration compared to baseline levels. The 250 and 500 mg doses induced decreased concentrations of ApoA1 and HDL, whereas the lowest dose (125 mg) did not have any effect on the lipid profile.

Pediatrics. 2014 Dec . Rapid Normalization of Vitamin D Levels: A Meta-Analysis.  McNally. Menon ea @Univs Ottowa, Thailand & Ireland  systematically reviewed pediatric clinical trials administering high-dose vitamin D to evaluate  (25[OH]D) response and characteristics of  final 25(OH)D levels . Uncontrolled and controlled trials reporting 25(OH)D levels after high-dose (≥1000 IU) ergocalciferol or cholecalciferol were selected. Two of 6 studies that administered daily doses approximating the Institute of Medicine’s Tolerable Upper Intake Level (1000-4000 IU) to vitamin D-deficient populations achieved group 25(OH)D levels >75 nmol/L within 1 month. Nine of 10 studies evaluating loading therapy (>50 000 IU) achieved group 25(OH)D levels >75 nmol/L. In meta-regression, baseline 25(OH)D, regimen type, dose, age, and time factors were associated with final 25(OH)D levels. Adverse event analysis identified increased hypercalcemia risk with doses >400 000 IU, but no increased hypercalcemia or hypercalciuria with loading doses <400 000 IU (or 10 000 IU/kg). Few studies in adolescents evaluated loading dose regimens >300 000 IU.
CONCLUSIONS:   Rapid normalization of vitamin D levels is best achieved by using loading therapy that considers disease status, baseline 25(OH)D, and age (or weight).

Diabetes Res Clin Pract. 2014 Dec A randomised controlled trial of ‘high” dose vitamin D in recent-onset type 2 diabetes .Elkassaby,  Fourlanos ea, Melbourne Australia.  Vitamin D insufficiency is associated with impaired pancreatic beta-cell function. Fifty adults with type 2 diabetes diagnosed less than 12 months, with normal baseline serum 25-OH D (25D), were randomised to 6000IU D (n=26) or placebo (n=24) daily for 6 months. In the D group, median serum 25D (ng/ml) increased from 24 to 60 (3 months). change in FPG (mmol/l) was significantly lower in D (-0.40) compared to placebo (+0.1) (P=0.007), as was the change in PPG in D (-0.30) compared to placebo (+0.8) (P=0.005). Change in HbA1c (%) between D (-0.20) and placebo (-0.10) was not different (P=0.459). At 6 months, changes from baseline in DCP, FPG, PPG and HbA1c were not different between groups.    ie modest Oral D3 supplementation   in type 2 diabetes was associated with transient improvement in glycaemia, but without a measurable change in beta-cell function.  this effect is unlikely to be biologically significant. This modest   dose D3  ie 42000iu/ week to eventual bloodlevel of only 50ng/ml therefore appears to offer little or no therapeutic benefit in type 2 diabetes.   THE DOSE THEY USED IN FACT PRODUCED STEADYSTATE VIT D3 LEVEL HALF THE POSTULATED TARGET LEVEL OF 90-100 ng/ml FOR SERIOUS ILLNESS.

J Asthma. 2014 Nov  Efficacy of high-dose vitamin D in pediatric asthma: a systematic review and meta-analysis.
Pojsupap , McNally ea Univ Ottowa :   studies  suggest a relationship between vitamin D status and asthma-related respiratory outcomes.  benefit of vitamin D supplementation for pulmonary function, symptoms and exacerbations is not well established.   Clinical trials reporting asthma-related respiratory outcomes following vitamin D administration at a dose equal or greater than 500 IU per day were included. Results:  five studies  met study eligibility and assessed final data synthesis. The median trial size was 48 participants (range 17-430) and the average daily dose of cholecalciferol ranged from 500 to 2000 IU/day. Meta-analysis suggested a statistically significant reduction (RR 0.41, CI 0.27-0.63) in asthma exacerbation with vitamin D therapy.

   J Infect Dis. 2013 Feb .  Vitamin D status and incidence of pulmonary tuberculosis, opportunistic infections, and wasting among HIVinfected Tanzanian adults initiating antiretroviral therapySudfeld,  Fawzi ea . Maintaining vitamin D sufficiency may decrease the incidence of pulmonary tuberculosis and other infectious diseases. We present the first prospective study of vitamin D among human immunodeficiency virus (HIV)-infected adults receiving antiretrovirals in sub-Saharan Africa.   Serum 25(OH)level was assessed at antiretroviral therapy (ART) initiation for 1103 HIVinfected adults enrolled in a trial of multivitamins (not including vitamin D) in Tanzania.After multivariate adjustment, vitamin D deficiency (defined as a concentration of <20 ng/mL) had a 3 fold significantly greater association with incident pulmonary tuberculosis, compared with vitamin D sufficiency (HR, 2.89;  [CI], 1.31-7.41; P = .027), but no association was found for vitamin D insufficiency (defined as a concentration of 20-30 ng/mL; P = .687). Deficiency was also significantly associated with incident oral thrush (HR, 1.96; 95% CI, 1.01-3.81; P = .046), wasting (HR, 3.10; 95% CI, 1.33-7.24; P = .009), and >10% weight loss (HR, 2.10; 95% CI, 1.13-3.91; P = .019). Wasting results were robust to exclusion of individuals experiencing pulmonary tuberculosis. Vitamin D status was not associated with incident malaria, pneumonia, or anemia.

update 22 Dec 2014:  as the solstice rolls by,  infections especially viral  flourish north and south,  from flu to gastro , HIV to ebola; HPV  to HZV to childhood exanthems;

so more reason to aim for optimal growth, mental and physical health with the peak anabolic antidepressant energizing anticancer antiinfective steroid –  cholecalciferol D3 – intake and levels.   About 65 000iu a week (with my multivit-multimineral combo)  puts my measured trough 25OHvit D  bloodlevel at 92ng/ml with normal blood calcium. Women can live long  without much androgen apart from frail bones, but not well without vigorous cholecalciferol D3 intake. Humans who live mostly bare  mostly outdoors- us  naked apes-  most of the year closer to the equator  make plenty of D3 from sunshine; but the darker our skins, the sooner vit D production shuts down; so  most of us need vigorous D3 supplement costing perhaps US$6 a year retail. .

update 19 Nov 2014  when this column on vit D started 5 years ago, there were 46000 vit D entries on Pubmed- this has mushroomed 40% to 61000 (compared now to 46000 on vit A; to 53000 on vitamin C; 37000 on vitamin E; 17000 on vit K; and 133000 on all  the 8 B vitamins ); whereas in 2009 there were 272500 entries on all vitamins– now up only 22% to 335 000. ie the papers on the secosteroid  vitamin D have risen at double the rate of the  vitamins.. (D3  C27H44O and D2 C28H44O, vs testosterone C19H28O2).

As the end-of-year solstice approaches, its time to review the crucial role of giving vigorous doses of vitamin D3, whether via   non-burn sunshine, or via the correct lowpressure tanning bed, or directly as vitamin D3  (not vit D2) supplement as appropriate TOGETHER WITH A MULTINUTRIENT PLUS EXTRA MAGNESIUM AND VIT K2. . Ironically, dermatologists would recommend vit D supplement not suntan for what many  consider the wrong reason- that suntanning does more harm than good, which it doesnt. :

at least THIRTEEN   VIT D  studies the past 16 years  SINCE 1998, from ~8 nations-  USA, Canada, Belgium, Spain , Germany, Denmark, UK  &  New Zealand,   – show  POORER   RESULTS  FROM TAKING TOO LITTLE VIT D; OR FROM USING VITAMIN D2 not D3, apparently by suppressing the crucial vit D3 level, and because vit D2 is metabolized faster. :

a new OBSERVATIONAL study in Am J Clin Nutr. Nov 2014  from the Cambridge EPIC-NORFOLK  group by  Kay-Tee Khaw,  Nicholas Wareham ea   Serum 25-hydroxyvitamin D, mortality, and incident cardiovascular disease, respiratory disease, cancers, and fractures: a 13-y prospective population study    examined prospective relation between serum  [25(OH)D] concentrations [which comprised 25(OH)D3 and 25(OH)D2] and subsequent mortality  in 14,641 men and women aged 42–82 y in 1997–2000  in Norfolk, UK followed up to 2012; categorized into 5 groups according to baseline serum concentrations of total vit D from below 30nmol/L to above 90nmol/L..  mean serum total 25(OH)D was 56.6 nmol/L 22ng/ml, which consisted predominantly of 25(OH)D3 (mean: 56.2 nmol/L; 99% of total). The age-, sex-, and month-adjusted HRs  for all-cause mortality (2776 deaths) for men and women by increasing vitamin D category were 1, 0.84 (0.74, 0.94), 0.72 (0.63, 0.81), 0.71 (0.62, 0.82), and 0.66 (0.55, 0.79) (P-trend < 0.0001). When analyzed as a continuous variable and with additional adjustment for body mass index, smoking, social class, education, physical activity, alcohol intake, plasma vitamin C, history of cardiovascular disease, diabetes, or cancer, HRs for a 20-nmol/L increase in 25(OH)D were 0.92 (0.88, 0.96) (P < 0.001) for total mortality, 0.96 (0.93, 0.99) (P = 0.014) (4469 events) for cardiovascular disease, 0.89 (0.85, 0.93) (P < 0.0001) (2132 events) for respiratory disease, 0.89 (0.81, 0.98) (P = 0.012) (563 events) for fractures, and 1.02 (0.99, 1.06) (P = 0.21) (3121 events) for incident total cancers.    Conclusions: Plasma 25(OH)D concentrations predict subsequent lower 13-y total mortality and incident cardiovascular disease, respiratory disease, and fractures but not total incident cancers. For mortality, lowest risks were in subjects with concentrations >90 nmol/L ie 36ng/ml, and there was no evidence of increased mortality at high concentrations, suggesting that a moderate increase in population mean concentrations may have potential health benefit, but <1% of the Norfolk population had concentrations >120 nmol/L 48ng/ml.

Chowdhury , Franco  ea  also University of Cambridge,  UK. BMJ. 2014 Apr .   Vitamin D and risk of cause specific death: systematic review and meta-analysis of observational cohort and randomised intervention studies.    Study specific relative risks from 73 cohort studies (849,412 participants) and 22 randomised controlled trials (vitamin D given alone versus placebo or no treatment; 30,716 participants). In the primary prevention observational studies, comparing bottom versus top thirds of baseline circulating 25-hydroxyvitamin D distribution, pooled relative risks were 1.35 (95% confidence interval 1.13 to 1.61) for death from cardiovascular disease, 1.14 (1.01 to 1.29) for death from cancer, 1.30 (1.07 to 1.59) for non-vascular, non-cancer death, and 1.35 (1.22 to 1.49) for all cause mortality. Subgroup analyses in the observational studies indicated that risk of mortality was significantly higher in studies with lower baseline use of vitamin D supplements. In randomised controlled trials, relative risks for all cause mortality were 0.89 (0.80 to 0.99) for vitamin D3 supplementation and 1.04 (0.97 to 1.11) for vitamin D2 supplementation. The effects observed for vitamin D3 supplementation remained unchanged when grouped by various characteristics. However, for vitamin D2 supplementation, increased risks of mortality were observed in studies with lower intervention doses and shorter average intervention periods.

in a systematic review and meta-analysisTripkovic ,, Lanham-New  ea . Univ Surrey  Am J Clin Nutr. 2012Comparison of vitamin D2 and vitamin D3 supplementation in raising serum 25-hydroxyvitamin D status: In the collective 10 studies, 1016 participants aged 18–97 yrs, men to women  ∼1:3;  vitamin D3 had a significant and positive effect in the raising of serum 25(OH)D concentrations compared with  vitamin D2 (P = 0.001). When the frequency of dosage administration was compared, there was a significant response for vitamin D3 when given as a  BOLUS dose (P = 0.0002) compared with administration of vitamin D2, but the effect was lost with daily supplementation.. The studies were  in the United States, Canada, United Kingdom, Australia, Denmark, and Italy; all studies were single-center studies. Seven studies were conducted in healthy, free-living participants (4, 6, 7, 12, 13, 15, 17);

WE so far FIND AT LEAST 12 RELEVANT COMPARATIVE VIT D3/D2  TRIALS in humans and one in cows:

1.  Karen Hansen ea at Univ Wisconsin 2014  An evaluation of high-dose vitamin D for rheumatoid arthritis   show  that  giving vitamin D2  (not D3)  50 000iu fortnightly for a year is actually adverseIT 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 .

     2. Vitamin D2 supplementation amplifies eccentric exercise-induced muscle damage in  athletes. Nutrients.  Nieman , Luo  EA. A, North Carolina  2013:6:63-75. Six weeks vit D2 (3800 IU/day) increased serum 25(OH)D2 fourfold  and decreased 25(OH)D3   by a fifth  versus placebo (p<0.001, p=0.036, respectively), with no influence on muscle function test scores, AND worsened  muscle damage .

    3. Swanson, Barrett-Connor, ea USA & Belgium May 2014 : In a cohort of older men,   Higher 25(OH)D2 is associated with lower 25(OH)D3 and 1,25(OH)2D3  , suggesting that vitamin D2 may decrease the availability of D3 and may not increase calcitriol.

4.Lehmann,  Dierkes ea  Germany 2013    in the same leading scientific journal  Bioavailability of vitamin D(2) and D(3) in healthy volunteers, a randomized placebo-controlled trial-  giving vit D2 2000iu/day for 8 wks in healthy volunteers actually halves the crucial 25hydroxy vit D3 level;  whereas giving vit D3 2000iu/d  doubles the vit D3 level. Earlier studies have suggested that vitamin D2 is less biologically active  than vit D3.

5. Biancuzzo, Holick ea Boston Mass. 2013 Serum concentrations of 1,25-dihydroxyvitamin D2 and 1,25-dihydroxyvitamin D3 in response to vitamin D2 and vitamin D3 supplementation  in healthy adults 18 to 79 years consuming 1000 IU vitamin D2 or vitamin D3 per day for 11 weeks at end of winter was analyzed.  Of the adults, 82% were vitamin D insufficient (serum 25-hydroxyvitamin D [25(OH)D <30 ng/mL]) at the start of the study. Administration of vitamin D2 and vitamin D3 induced similar increases (from baseline ~20ng/ml 25OH vit D)  in total 25(OH)D as well as in 25-hydroxyvitamin D2 and 25-hydroxyvitamin D3, respectively. Compared with placebo and adjusting for baseline levels, 1000 IU daily of vitamin D2 was associated with a mean increase of 7.4 pg/mL (95% confidence interval, 4.4-10.3) in 1,25(OH)2D2, and  decrease of 9.9 pg/mL (-15.8 to -4.0) in 1,25(OH)2D3. No such differences accompanied administration of 1000 IU daily of vitamin D3.

    6. Leventis P1, Kiely PD. London 2009 in  Scand J Rheumatol. Good Tolerability and biochemical effects of high-dose bolus vitamin D2 and D3 supplementation in patients with vitamin D insufficiency in 69 RHEUMATOLOGY patients with vitamin D insufficiency [25-hydroxyvitamin D (25(OH)D) <40 nmol/L]  50 patients study 1 received 300 000 IU i.m. vitamin D2 (ergocalciferol), 19 patients  in study 2 received 300 000 IU oral vitamin D3 (cholecalciferol) . Bolus i.m. vitamin D2 or oral vitamin D3 was well tolerated.  change from baseline in serum 25(OH)D was significantly greater at 6 and 12 weeks in study 2 (p<0.0001 ). In study 1, a modest increase in mean serum 25(OH)D at 6, 12, and 24 weeks was observed but no patients achieved a serum 25(OH)D concentration > or = 50 nmol/L. PTH remained elevated in 42% of patients with secondary hyperparathyroidism at 12 weeks. In study 2, 100% and 89% of patients had serum 25(OH)D>50 nmol/L at 6 and 12 weeks, respectively. All patients with elevated baseline PTH were fully suppressed at 12 weeks. No hypercalcaemia was observed in either group. The 300 000-IU bolus of vitamin D2 or D3 was practical, well tolerated, and safe. Vitamin D3 had greater potency than equimolar vitamin D2, with a higher, sustained serum 25(OH)D response and efficacious PTH suppression.


    7.  Sempos CT1, Picciano MF ea . USA  J Clin Endocrinol Metab. 2013 Jul;98(7):3001-9..  Is there a reverse J-shaped association between 25-hydroxyvitamin D and all-cause mortality? Results from the U.S. nationally representative NHANES.       A reverse J-shaped association between serum 25-hydroxyvitamin D (25[OH]D) concentration and all-cause mortality was suggested in a 9-year follow-up (1991-2000) analysis of the Third National Health and Nutrition Examination Survey (NHANES III, 1988-1994). We repeated  the analyses with 6 years additional follow-up  in 15 099 participants aged ≥ 20 years with 3784 deaths, to evaluate whether the association persists through 15 years of follow-up. The reverse J-shaped association became stronger with longer follow-up and was not affected by excluding deaths within the first 3 years of follow-up. Similar results were found from both statistical approaches for levels <20 through 119 nmol/L. Adjusted RR (95% confidence interval [CI]) estimates for all levels <60 nmol/L were significantly >1 compared with the reference group. The nadir of risk was 81 nmol/L 32pg/mL (95% CI, 73-90 nmol/L 29-36pg/ml). The association appeared in men, women, adults ages 20 to 64 years, and non-Hispanic whites but was weaker in older adults.  A reverse J-shaped association between serum 25(OH)D and all-cause mortality appears to be real. It is uncertain whether the association is causal.

    8.  Logan  Houghton ea   Br J Nutr. New Zealand 2013;109:1082-8.   Long-term vitamin D3 supplementation is more effective than vitamin D2 in maintaining serum 25-hydroxyvitamin D status over the winter months.  Public health recommendations dont distinguish between vitamin D2 and vitamin D3, yet disagreement exists on whether these two forms should be considered equivalent.  over the winter in healthy adults living in Dunedin, New Zealand (latitude 46°S), Participants aged 18-50 years were randomized   to 1000 IU vitamin D3 (n 32), 1000 IUvitamin D2 (n 31) or placebo (n 32) daily for 25 weeks beginning at the end of summer. After 25 weeks, participants randomised to D2 and placebo had a significant reduction in serum 25(OH)D3 concentrations over the winter months compared with vitamin D3-supplemented participants (both P< 0.001). Supplementation with vitamin D2 increased serum 25(OH)D2 but produced a 9 (95 % CI 1, 17) nmol/l greater decline in the 25(OH)D3 metabolite compared with placebo (P< 0.036). Overall, total serum 25(OH)D concentrations were 21 (95 % CI 14, 30) nmol/l lower in participants receiving vitamin D2 compared with those receiving D3 (P< 0.001), among whom total serum 25(OH)D concentrations remained unchanged. No intervention-related changes in PTH were observed. Daily supplementation of vitamin D3 was more effective than D2;

    9  Seijo M1Oliveri B. ea  Spain  Medicina (B Aires). 2012;72:195-200.  [Is daily supplementation with vitamin D2 equivalent to daily supplementation with vitamin D3 in the elderly?].    equivalence of cholecalciferol (D3) and ergocalciferol (D2) as well as their corresponding doses and administration route remain controversial to date. Twenty-one ambulatory postmenopausal women from Buenos Aires with a mean  age of 77 ± 6.8 years  were randomly assigned to one of the following groups: GD2 (n = 13): 800 IU (drops) and GD3 (n = 8): 800 IU (pills).  Nineteen out of twenty one women showed deficient levels of 25OHD at baseline (< 20 ng/ml): GD2: 14.0 ± 4.8 ng/ml and GD3: 13.2 ± 4.9 ng/ml (NS). Whereas only GD3 exhibited an increase (≈ 25%) at 7 days, both groups showed a significant increase at the end of the study. However, neither attained adequate 25OHD levels (GD2: 17.4 ± 5.5 vs. GD3:22.9 ± 4.6 ng/ml; p < 0.001). Administration of 800 IU of vitamin D3 during 45 days was more effective than D2 in increasing 25OHD, but both failed to achieve adequate levels of 25OHD (= 30 ng/ml). but neither succeeded in achieving adequate levels of 25OHD (= 30 ng/ml).

    10 Holick  Tannenbaum ea usa   J Clin Endocrinol Metab. 2008;93:677-81. Epub 2007 Dec 18.IN LOW DOSE eg 1000iu/d,   Vitamin D2 is as effective as vitamin D3 in maintaining circulating concentrations of 25-hydroxyvitamin A 1000 IU dose of vitamin D2 daily was as effective as 1000 IU vitamin D3 in maintaining serum 25-hydroxyvitamin D levels and did not negatively influence serum 25-hydroxyvitamin D3 levels. Therefore, vitamin D2 is equally as effective as vitamin D3 in maintaining 25-hydroxyvitamin D status.
     11 Armas ,  Heaney ea.Creighton Univ Nebraska.  J Clin Endocrinol Metab. 2004 ;89:5387-91. Vitamin D2 is much less effective than vitamin D3 in humans.Vitamins D(2) and D(3) are generally considered equivalent in humans. Nevertheless, physicians commonly report equivocal responses to seemingly large doses of the only high-dose calciferol (vitamin D(2)) available in the U.S. market. Relative potencies of vitamins D(2) and D(3) were evaluated by administering single doses of 50,000 IU of the respective calciferols to 20 healthy male volunteers, following the  serum vitamin D over 28 d.. The two calciferols produced similar rises in serum concentration, indicating equivalent absorption. Both produced similar initial rises in serum 25OHD over the first 3 d, but 25OHD continued to rise in the D(3)-treated subjects, peaking at 14 d, whereas serum 25OHD fell rapidly in the D(2)-treated subjects and was not different from baseline at 14 d. Area under the curve (AUC) to d 28 was 60 ng.d/ml for vitamin D(2) and 204 for vitamin D(3) (P < 0.002). Calculated AUC(infinity) indicated an even greater differential, with the relative potencies for D(3):D(2) being 9.5:1. Vitamin D(2) potency is less than one third that of vitamin D(3). Physicians resorting to use of vitamin D(2) should beware of its markedly lower potency and shorter duration of action relative to vitamin D(3)

    12 Trang,  Vieth ea  University of Toronto, Am J Clin Nutr. 1998Evidence that vitamin D3 increases serum 25-hydroxyvitamin D more efficiently than does vitamin D2. In all species tested, except humans, biological differences between vitamins D2 and D3 are accepted as fact.  Subjects took 260 nmol (approximately 4000 IU) vitamin D2 (n=17) or vitamin D3 (n=55) daily for 14 d.  With vitamin D3, mean (+/-SD) serum 25(OH)D increased from 41+/-18 nmol/L before to 65+/-17 nmol/L after treatment. With vitamin D2, the 25(OH)D concentration went from 434+/-18 nmol/L before to 57+/-13 nmol/L after. The increase in 25(OH)D with vitamin D3 was 23+/-16 nmol/L, or 1.7 times the increase obtained with vitamin D2 (14+/-11 nmol/L; P=0.03). There was an inverse relation between the increase in 25(OH)D and the initial 25(OH)D concentration.  In the highest tertile [25(OH)D >49 nmol/L] the mean increase in 25(OH)D was 13.3 nmol/L (P < 0.03 for comparison with each lower tertile). Although the 1.7-times greater efficacy for vitamin D3 shown here may seem small, it is more than what others have shown for 25(OH)D increases when comparing 2-fold differences in vitamin D3 dose. The assumption that vitamins D2 and D3 have equal nutritional value is probably wrong and should be reconsidered.

13.  Hymøller L1, Jensen SK.Denmark   J Dairy Sci. 2011;94:3462-6.  Vitamin D₂ impairs utilization of vitamin D₃ in high-yielding dairy cows in a cross-over supplementation regimen.   D(3) given after D(2) is less efficient at increasing the plasma status of 25(OH)D(3) than D(3) given without previous D(2) administration.

A Vitamin D Expert’s Take on the Latest Warning to Stay Out of the Sun to Avoid Skin Cancer

By Dr. Mercola  16/11/2014  The US Surgeon General recently came out with a warning on skin cancer,1 claiming that the sun is dangerous and that you need to stay away out of it.

pioneer Dr. John Cannell, founder of the Vitamin D Council, has dedicated a large part of his professional career to the study of vitamin D and its health benefits, and he has a warning of his own to those who take this narrow-minded advice to heart.

It’s worth noting that the acting Surgeon General, Boris Lushniak, is a dermatologist. And of all the medical specialties out there, dermatologists are clearly the most biased against sun exposure, & as a result, against vitamin D.

This isn’t surprising, since they primarily see the ill effects of sun overexposure. But in taking an overly narrow view, the advice to avoid sun exposure as much as possible can have equally if not greater adverse health effects.                      The Connection Between Sun Exposure and Skin Cancer Unquestionably, UV   radiation can be dangerous; it can increase your risk for certain skin cancers such as squamous cell, basal cell, and melanoma. But there are significant differences even between these cancers, and appropriate sun exposure may actually be more beneficial than detrimental in some cases. Dr. Cannell explains:

“Squamous cell carcinoma is clearly associated with chronic sun exposure. It is more common on the face, the hands, and the scalp.

It is related to radiation burden over your lifetime, and together with basal cell carcinoma, which is sort of intermediate, it accounts for approximately 1,500 deaths a year in the United States…

Basal cell is sort of intermediate. There are studies showing that it is associated with chronic sun exposure, and there are studies showing that it’s not associated with chronic sun exposure.

And then there’s melanoma, which is responsible for almost 9,000 deaths a year and is the deadly skin cancer that is feared. The relationship that melanoma has with the sun is quite complicated.

It is clearly associated with sunburn, especially sunburns when you’re young (that’s incontrovertible) or sunburns in a sun tanning bed.”

However, there are at least two studies showing that melanoma is more common in indoor workers than outdoor workers. And the most likely places for melanoma to appear are actually NOT the face and the hands like squamous cell carcinoma, but rather the lower back and the upper leg—areas that are usually not chronically sun-exposed.

According to Dr. Cannell, there’s a vocal minority in the dermatological community that thinks the emphasis dermatologists have on avoiding sun exposure is wrong, because while sunburn is a risk factor, chronic sun exposure is not.

“A number of studies show that chronic sun exposure is related to melanoma, but they don’t separate out the sunburns, which is very hard to do because you have to do that by memory,” Dr. Cannell says.   Two Decades-Long Study Finds Sun Avoidance Doubles Risk of Death  Dr. Cannell notes a recent study2 done in Sweden, which followed nearly 30,000 middle-aged to older women for up to 20 years. The average follow-up was 15 years.

At the outset, they asked a number of questions about sun exposure, such as: Do you sunbathe? Do you take vacations in sunny areas in the winter? Do you garden with short sleeves and shorts? And, do you use sunbeds?

What they found, and this appears to be the only study of this kind, is that the women who avoided the sun were twice as likely to die over the course of the study. The researchers attributed this finding to a vitamin D mechanism.

What this study actually shows is that chronic sun exposure appears to be associated with less mortality. It’s also the first study to show that women who use tanning beds live longer than those who don’t.

This is in direct conflict to what almost every dermatologist will say, including the Surgeon General. It’s unfortunate, but the danger of almost any specialist is that they don’t take the broader perspective.

What the Surgeon General and almost every other dermatologist fail to take into account is the overall mortality, which is referenced in this recent study.  Risk-Benefit Analysis In addition to this study, dozens of others document the benefits of appropriate sun exposure. This includes a reduced risk of about 16 different cancers of Dr. Garland’s studies suggest this reduction is close to 50 percent.

So many hundreds of thousands of people are put at risk from other cancers as opposed to 10,000 people who are dying from skin cancer caused by sunburn. It’s really a matter of making an educated risk-benefit analysis.

“When you do a risk-benefit analysis and you look at all the data we have, the risk in my opinion appears to be in those who avoid the sun,” Dr. Cannell says.

“Now, if you avoid the sun, your risk for non-melanoma skin cancer goes down. That’s clear. But if you look at studies of either latitude or of 25-hydroxyvitamin D levels in relation to cancer, you find this inverse relationship: the higher the vitamin D level, the lower the internal cancer rate.”

Dr. William Grant of Sunlight, Nutrition, and Health Research Center (SUNARC) estimates that if everyone in the United States had a vitamin D level of 40 nanograms per milliliter (ng/ml), it would save approximately 150,000 lives a year.3

That’s 100 times the rate of squamous cell cancers, which are the only ones that are definitively linked to UV exposure. In Canada alone, it is estimated that 37,000 lives a year are lost due to vitamin D deficiency.4 Also, use of sunscreen has risen in the last 30 years, so if dermatologists were correct, there should be a decrease in stage 1 melanoma. But there’s not. As sunscreen use increased, stage 1 melanoma diagnosis increased…

“It’s thought that by blocking out UVB, patients are able to stay out in the sun longer than they would have otherwise and expose themselves to the more dangerous, or at least potentially dangerous, UVA radiation that’s in the sunshine,” Dr. Cannell says. “What we recommend is what’s called safe, sensible sun exposures. The Australian Cancer Council now recommends the same thing. I think in England there’s now a change in their recommendation from strict sun avoidance to some safe, sensible sun exposure. There are some movements in large organizations to realize that safe, sensible sun exposure is a healthy thing.”            

How Much Sun Exposure Is Sensible?    On its website, Cancer Research UK reports that “by enjoying the sun safely and avoiding sunburn, people can reduce their risk of skin cancer and enjoy the beneficial effects of the sun.” Cancer Research UK’s sun advice is endorsed by the British Association of Dermatologists, Cancer Research UK, Diabetes UK, the Multiple Sclerosis Society, the National Heart Forum, the National Osteoporosis Society, and the Primary Care Dermatology Society. The UK National Health Service5 also recommends sensible, individualized sun exposure to help optimize vitamin D.

It’s important to recognize is how quickly sunlight can make vitamin D in the skin. You don’t need to be outside for hours on end. But you do need more than just a few minutes of sun on your face and arms. According to Dr. Cannell, sunbathing at solar noon in the summer, at most latitudes in the United States you will make between 5,000-10,000 international units (IUs) of vitamin D within 30 minutes.

“You can ask yourself why nature would evolve a mechanism that made so much vitamin D so quickly,” Dr. Cannell says. “When I thought about that question, the only answer I could come up with is nature did it for a good reason. The organism needs vitamin D, so the system in the skin evolved to make it very quickly upon exposure to sunlight.

We recommend full-body sun exposure for up to anywhere from a few minutes to 30 minutes every day. On those days when you cannot get a full-body sun exposure, we recommend a vitamin D supplement or sensible exposure in a low-pressure UVB bed.”

If you’re getting regular sun exposure, I think the need for an oral supplement is really minimal to non-existent. When you swallow a pill, there’s no self-regulating ability. Your body doesn’t have an ability to selectively limit its absorption. But your skin has the ability to control how much vitamin D is being produced based on how much is in your blood.

I personally have not taken oral vitamin D for five years and my level runs from 50-70 g/ml. Lifeguards, roofers, and gardeners who work with their shirt off, all tend to have levels between 40 and 80 ng/ml in the summer. This also brings up an interesting question about the difference between normal and natural. Normal vitamin D levels are an average of what indoor workers have in both winter and summer. Natural are levels of a population with widespread sun exposure. The latter is going to be closer to ideal, or optimal.

vitamin d levels
References for establishment of optimal levelsThere are also other reasons to strive for sun exposure rather than swallowing a pill. As noted by Dr. Cannell, aside from producing vitamin D, sunlight also affects nitric acid levels and endorphins in the skin. Researchers at the University of Wisconsin recently discovered that there may be a system at 311 nanometers that is separate from the vitamin D system (which is at 298 nanometers), and that there may be an entirely new undiscovered biochemical system in the skin that makes yet another substance, besides vitamin D. Time will tell what comes out of that research, but there are indications that sunlight may be responsible for other biological processes that are unrelated to vitamin D production.

Dr. Cannell’s Recommendation on Tanning Beds There are basically two
types of tanning beds:

  1. 1. High-pressure UVA beds. They tan you the quickest because it’s UVA that tans the skin. They contain only a limited UVB spectrum, and will therefore give you color but not much vitamin D
  2. Low-pressure beds, which contain less UVB than sunlight at most latitudes, but still contain a significant amount of UVB. These are the beds Dr. Cannell recommends, provided you’re using a sensible approach that avoids sunburns. It’s important to realize that you can easily get burned after only a couple or a few minutes when using a tanning bed

Another important factor when selecting a tanning bed is the type of ballast it employs, to avoid excessive electromagnetic field (EMF) exposure. Most tanning units use magnetic ballasts to generate light. These magnetic ballasts are well known sources of EMF fields that can contribute to cancer. If you hear a loud buzzing noise while in a tanning bed, it has a magnetic ballast system. I strongly recommend you avoid magnetic ballast beds, and restrict your use of tanning beds to those that use electronic ballasts.

On days you cannot get either regular sun exposure or use of a tanning bed, Dr. Cannell suggests taking 5,000 IUs of vitamin D3. Other vitamin D experts recommend similar amounts. It’s worth noting that, according to the federal government’s Food and Nutrition Board (FNB), the no observed adverse effects level (NOAEL) of vitamin D is 10,000 IUs a day. This means there has never been a replicated reliable study showing that 10,000 units a day is in any way detrimental.

Many individuals who have reported side effects from taking high doses of oral vitamin D have noticed that when they supplemented with magnesium, they were able to tolerate the high oral doses of vitamin D. Dr. Carolyn Dean has written in her book, The Magnesium Miracle, that she has seen this so many times that she doesn’t advise taking more than 2,000 units of vitamin D without magnesium supplementation. Be sure to also have an adequate amount of vitamin K2 along with D to slow the progression of arterial calcification. Remember though that the best form of vitamin D is the one your body produces when it is exposed to sunlight that has sufficient amounts of UVB.

Five Tips to Get an Appropriate, Sensible Amount of Sun  Again, sunshine offers substantial health benefits, including vitamin D production, but you do need to exercise a few simple precautions to protect yourself from overexposure. Virtually all of the harm from sun exposure is related to sunburn. Here are my top five tanning tips:   *  Expose large amounts of your skin (at least 40 percent of your body) to sunlight for short periods daily. Optimizing your vitamin D levels may reduce your risk of as many as 16 different types of cancer, including pancreatic, lung, ovarian, breast, prostate, and skin cancers. If using a sunscreen, give your body a chance to produce vitamin D before you apply it. *When you’ll be in the sun for longer periods, cover up with clothing, a hat, or shade (either natural or shade you create using an umbrella).  *Consider the use of an “internal sunscreen” like astaxanthin to gain additional sun protection. Astaxanthin is a potent antioxidant (and pigment) produced by marine algae in response to their exposure to UV light. Typically, it takes several weeks of daily supplementation to saturate your body’s tissues enough to provide protection. *Consuming a healthy diet full of natural antioxidants is another useful strategy to help avoid sun damage. Fresh, raw, unprocessed vegetables and fruits deliver the nutrients that your body needs to maintain a healthy balance of omega-6 and omega-3 oils in your skin, which is your first line of defense against sunburn. Vegetables also provide your body with an abundance of powerful antioxidants that will help you fight the free radicals caused by sun damage that can lead to burns and cancer.

How Vitamin D Performance Testing Can Help Optimize Your Health  A robust and growing body of research clearly shows that vitamin D is absolutely critical for good health and disease prevention. Vitamin D affects your DNA through vitamin D receptors (VDRs), which bind to specific locations of the human genome. Scientists have identified nearly 3,000 genes that are influenced by vitamin D levels, and vitamin D receptors have been found throughout the human body.

  14  Oct 2014 update:  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 oral overdose of 2,000,000 IU of vitamin D3 in two nonagenarian nursing home patients: a case report.    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. 9 babies between ages of 25 and 105 days were admitted  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 (mean 220: 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.

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 ~63 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. .

29 Sept 2014:       As detailed elsewhere in 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.

 TIME   To SWOP FROM MISNAMED  “STRONG CALCIFEROL” VIT D2 TO THE REAL VIT  D3:     as the winter solstice approaches here, with fierce weather linking to  the expected influenza-like outbreak (while the MERS-CoV outbreak abates with summer in the severely vitamin D deficient Saudi Arabians), a new major study shows the supremacy of vitamin D3 for supplementation, and confirms that vitamin D2 benefit if any  is so mediocre as to be unethical..

Its sad that despite the strong evidence against using vitamin D2 supplement discussed last year,  it seems no one acted on  it despite the confirmatory paper from Bergen of last September.

Thus vit D3 is again confirmed as four times as potent as D2. But crucially, that giving vit D2 may actually SUPPRESS the optimal  serum vit D3  level.

We health professionals with our highly vulnerable populations in South Africa and worldwide   (epidemic/endemic  HIV, TB, cancer, drug addiction, MERS-CoV, asthma, diabetes, cardiovascular,  malnutrition, alcoholism and violence) therefore surely have no choice but to swop promptly from prescribing vit D2 “Strong Calciferol” (a dangerous misnomer) to prescribing vitamin D3 at vigorous dose (with if possible occasional blood level check of 25OHvit D3)- at a trivial imported and distributed cost (100cws)  to South African state clinics  of perhaps<1/4 of the cost of D2 eg  R1 per patient per month for a conservative 100 000iu monthly  (ie  after an appropriate germicidal  loading dose of eg 3000 iu/kg) if not the more realistic dose double that- still at only eg US$0.2 a month.

Health Authorities everywhere have an obligation to enforce the use of vitamin D3 and not vitamin  D2 globally ..

update 3 Sept 2014:  while the MERS outbreak in Arabia may at last be dying down, real highly infections plagues eg ebola malaria cholera typhoid, MRSA,  TB and HIV etc continue rampant, maiming and killing even more than the manmade wars raging on some continents. .

So it is ironic – or typical of the couldnt-care-less greedy politicians and potentates who run the world- that the medical authorities they employ  worldwide apparently continue to ignore the dramatic benefits of at least safe antimicrobial supplements like multivite, zinc, iodine, selenium,   and especially vigorous dose vitamin D3 at negligible cost, and highdose buffered vitamin C to tolerance, and colloidal silver.

Already 35 years ago Italian researchers published on Pubmed that vitamin D3 should be used orally  rather than injected D or as  oral vitamin D2:                   [Behavior of serum vit D in  humans after administration of vitamin D.   Boll Soc Ital Biol Sper. 1979   Coen G, Casciani CU ea.     “evaluated  Serum levels of 25 hydroxy-vit D  following injected and oral vit. D2 and D3 . While no rise in 25OHD3 serum levels was  observed after i. m. administration , a marked rise  was found following the oral administration. However the peak values were largely impredictable.”

We quote above  trials and evidence  that oral vit D2 may be actually harmful, that it is vit D3 in vigorous dose that is needed to at least treble if not quadruple the blood vit D level from the usual deficient levels we find, to between 60 and 100ng/ml during illness.  Unfortunately locally this is not only not grasped, but also the vit D assay kit  being used by  private laboratories measures only total 25OHvit D level, not the needed active 25OH vit D3 level  plus the potentially harmful (vitD receptor-blocking ) 25OHvit D2. This is a crucial omission which has been corrected by eg the Mayo Clini Lab, which routinely reports both D3 and D2 levels.

In the person not on vit D supplements, the mediocre ie insufficient total vit D level may mask that the crucial vit D3 level is actually seriously low- deficient.  In the person on vigorous vit D2 supplement (the spuriously named “strong calciferol” 50 000iu tab no longer prescribed in USA  but commonly in RSA,  that neglects to state it is D2 not D3), the total 25OH vit D assay will be even more misleading if the level  is well up, without the unwary being informed that it is harmful D2 that is elevated, and blocking the needed vit D3 level that the D2 is suppressing.

        15 June  2014 CRUCIAL EFFECTIVE VITAMIN D3 DOSING: A major new  metaanalysis of the benefit of Vitamin D3 and Respiratory Tract Infections RTI in PLOS 2013   at  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 up to 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 asthma”But 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  give a loading dose of about 4000iu/kg, then 10 000 iu/d for an average 70kg adult,  or 50 000iu every 5 days, or more simply 75000iu (about 1.5ml of 100cws vit D3 powder) weekly; or at a stretch, 300000 if not 400 000iu monthly. . As  the common  imported powder concentrate  is 100 000 iu / 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, do not live and work / walk  all day stripped in the sun. The poor malnourished  peasants  live crowded in ghettoes , and  the poorest are generally the darkest 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  $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 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 – is recommended and freely available.

We health professionals with our highly vulnerable populations in South Africa and worldwide   (epidemic/endemic  HIV, TB, cancer, drug addiction, MERS-CoV, asthma, diabetes, cardiovascular,  malnutrition, alcoholism and violence) therefore surely have no choice but to swop promptly from prescribing vit D2 “Strong Calciferol” (a dangerous misnomer) to prescribing vitamin D3 at vigorous dose (with if possible occasional blood level check of 25OHvit D3)- at a trivial imported and distributed cost (100cws)  to South African state clinics  of perhaps<1/4 of the cost of D2 eg  R1 per patient per month for a conservative 100 000iu monthly  (ie  after an appropriate germicidal  loading dose of eg 3000 iu/kg) if not the more realistic dose double that- still at only eg US$0.2 a month.
Health Authorities everywhere have an obligation to enforce the use of vitamin D3 and not vitamin  D2 globally ..

2 February 2014 VITAMIN D 3 DENIALISM:                                                       Dr John Cannell psychiatrist and nutritionalist  of the Vitamin D Council has posted a comprehensive rebuttal of the Autier review’s damnation of vitamin D at http://www.vitamindcouncil.org/blog/a-look-at-the-recent-lancet-review-study/.

Queries  and rebuttals    all over the world are questioning the negative French  (Autier ea)   Vitamin D status and ill health: a systematic review   published last month by the UK Lancet            Low serum concentrations of 25-hydroxyvitamin D (25[OH]D) have been associated with many non-skeletal disorders. However, whether low 25(OH)D is the cause or result of ill health is not known. We did a systematic search of prospective and intervention studies that assessed the effect of 25(OH)D concentrations on non-skeletal health outcomes in individuals aged 18 years or older. We identified 290 prospective cohort studies (279 on disease occurrence or mortality, and 11 on cancer characteristics or survival), and 172 randomised trials of major health outcomes and of physiological parameters related to disease risk or inflammatory status. Investigators of most prospective studies reported moderate to strong inverse associations between 25(OH)D concentrations and cardiovascular diseases, serum lipid concentrations, inflammation, glucose metabolism disorders, weight gain, infectious diseases, multiple sclerosis, mood disorders, declining cognitive function, impaired physical functioning, and all-cause mortality. High 25(OH)D concentrations were not associated with a lower risk of cancer, except colorectal cancer. Results from intervention studies did not show an effect of vitamin D supplementation on disease occurrence, including colorectal cancer. In 34 intervention studies including 2805 individuals with mean 25(OH)D concentration lower than 50 nmol/L at baseline supplementation with 50 μg per day or more did not show better results. Supplementation in elderly people (mainly women) with 20 μg vitamin D per day seemed to slightly reduce all-cause mortality. The discrepancy between observational and intervention studies suggests that low 25(OH)D is a marker of ill health. Inflammatory processes involved in disease occurrence and clinical course would reduce 25(OH)D, which would explain why low vitamin D status is reported in a wide range of disorders. In elderly people, restoration of vitamin D deficits due to ageing and lifestyle changes induced by ill health could explain why low-dose supplementation leads to slight gains in survival.

and the accompanying anonymous Lancet editorialchasing a myth?

Ongoing randomised clinical trials assessing the ability of vitamin D supplementation to reduce the risk of several non-skeletal disorders involve a population larger than that of Cambridge, UK, and will cost millions  of research dollars. VITAL, for example, will enroll 20 000 participants and has US$22 million in funding.  This vast investment of effort by patients, researchers,  and funders is laudable, as it is almost certain that it will be sufficient to answer a question that has long kept the medical community in the dark.
                 Vitamin D first became a medical success story when its importance in bone health and calcium homoeostasis was proven decades ago. Since then, epidemiological  evidence has been accumulating to support a role for vitamin D in the protection of individuals from various   non-skeletal disorders including cancer, cardiovascular diseases, autoimmune and inflammatory diseases, dementia, and diabetes; it might also reduce all- cause mortality. Many of these studies show a strong association between low vitamin D concentrations anddisease. However, the results of myriad recent small randomised controlled trials are almost unanimous in  concluding that vitamin D supplementation provides  protection from few, if any, of these outcomes.
      Vitamin D is a steroid hormone with pleiotropic and tissue-specific effects owing to the wide expression of  the nuclear vitamin D receptor in many different tissues,and the many genes that are targeted by its actions.  In the skeletal system, vitamin D promotes healthy development and remodelling of bone. In other tissues,   vitamin D is postulated to mediate potentially beneficial  effects via a wide variety of mechanisms: some evidence  suggests that it exerts anticancer activity by limiting hyperproliferation of certain cell types, that it promotes metabolic health by regulating lipid metabolism in adipocytes, and that it limits autoimmunity by  suppressing inappropriate immune responses.  In a systematic review in   The  Lancet Diabetes &  Endocrinology editorial , Philippe Autier and colleagues discuss a large number of observational studies suggesting  That high serum concentrations of vitamin D   might be protective.
      For example, those with high vitamin D had decreased risk of cardiovascular events      by up to 58%), diabetes (by up to 38%), colorectal  cancer (by up to 33%), and all-cause mortality (by  up to 29%). However, they also compare these findings with the results of randomised clinical  trials, which reveal a very different picture: no reduction in risk was found, even in trials involving adequate supplementation of participants with lowvitamin D levels at baseline (less than 50 nmol/L). Autier and colleagues also did a new meta-analysis  of 16 trials that assessed the effects of vitamin D supplementation on blood HbA1c, a biomarker mainly   used for monitoring disorders of glucose metabolism.
Although type 2 diabetes is associated with  low vitamin D, the results show that vitamin D supplementation does not reduce HbA1c
. Thus, it looks increasingly likely that low vitamin D is not a cause but  a consequence of ill health.
Despite the growing body of evidence indicating  that vitamin D is unlikely to prevent non-skeletal   disorders, there is strong support for its use from  many prominent members of the research community,  which is fuelled by the relatively low toxicity of vitamin D, the glimmer of positivity from some trials,and the large body of evidence from prospective  observational studies. For those who ‘believe’, the  lack of benefi t found in most trials completed thus  far can be attributed to issues including inadequate  supplementation, testing of a population not  sufficiently vitamin D deficient at baseline, incorrect
formulation, underpowering, or insufficient follow-up.  Vitamin D might not be safe in all settings, however.
Supplementing at high doses could cause harm in  people with already high concentrations of serum  vitamin D, particularly in those with liver, kidney, or  vascular problems. This is a concern, given the large  number of people taking vitamin D supplements (up  to 50% of adults in the USA).
Large clinical trials to assess the effects of vitamin D on non-skeletal health outcomes are  therefore justified. It would be a real boon to patients if the results are positive, but unless effect sizes for clinically important outcomes are large, the results will only confirm the neutral effect reported by most clinical trials thus far. Although this investment might  therefore have little effect on current guidelines, the results will at least allow the research community to  move on.
This French  review of Vitamin D is the sort of tactic regularly concocted by Big Pharma and the Disease Industry for the media,  to discourage patients and doctors  from taking/prescribing  effective doses of supplements (beyond a lowdose  multivite a day), instead force them to take Big Pharma poisons- synthetic new risky designer drugs- like antibiotics, antipain,  anticancer, anticholesterol, antiosteoporosis, antiplatelet,antihypertensive, vaccines, antiflu,  –    to make massive profits for the Disease Industry,  but not address or cure the deficiency causes of disease.     At the behest of Big Pharma like Roche, their lobbyists the FDA, the  European Medicines Authority and the UK NHS are  trying to push through legislation that will make anything but lowdose multisupplements available to the public solely on doctors’ prescription.
Meanwhile, Big Pharma companies are paying fines of over $10 billion  a year for promoting their snakeoil  prescription designer drugs by fraud, when these drugs are allowed to be registered for chronic use after small trials of only 6 to 12 weeks, and the researchers who  publish the trials for megadollar fees are regularly caught out, fired but rarely  jailed.                                                                            ……         The Big Pharma guys simply bill the cost of the fines into their marketing expenses- their bosses, and the politicians they buy off,  are too big to jail… Regulators then allow the drugs to be prescribed for years  until enough patients sicken and die for there to be an uproar and cancellation- as  happened recently with Prot(e)os the synthetic ranelate ‘osteoporosis’  snakeoil;.      Now a top Dutch researcher has been fired for falsifying trials to promote betablockers for hypertension – when these have been discredited as routine therapy  for this purpose  for over a decade.
yet the Regulators led by the FDA – which is massively funded solely  by Big Pharma as their ally- insists that vitamins, minerals and other long-proven natural supplement therapeutics, prime human hormones  like melatonin and physiological human sexhormone creams , have to undergo $multimillion trials before they can be marketed as already  long-evident safe effective therapies.

none of the vit D   trials used the dose of vit D3 now recommended on solid evidence  that we should all take   – 80 (to 100)iu/kg/day or 2400-3000iu/kg/month of vitamin D3- ie about 150 000 – 200 000 iu to start and then per month for average adults –  to maintain healthy 25OH vit D levels around 60-100ng/m (here our bloodlevels are usually between 10 and 20 !  because we take little dairy products, nuts and sunshine- we cover up and live indoors.)  .

Most  of the reported trials used only about 5% of the recommended  vit D  dose ie ~200 to 400iu/day ie 6 iu/kg/day!  this dose does nothing except partly prevent rickets-  in infants!  Pregnant women are still routinely given such weak near-nonsensical doses of vit D.

and as Cannell’s review of the Autier analysis  points out, the vitamin D  trials trials under way – * in USA-Boston VITAL study 20 000pts)   ,           Finland (FIND 18000 pts    and     UK(VIDAL 1600pts ) ,  in some 40 000 subjects, due for publication only  between 2017-2020-  are using only 1600 to  3200iu vit D a day or about 48  000 to 96000iu/month ie perhaps 32iu (25 to 40) /kg/day. So  they are testing still modest doses and blood level targets. .

Read about the fraud of the Disease Industry at https://healthspanlife.wordpress.com/2014/01/20/vitamins-c-d3-avoiding-vitamin-denialism/ – especially about the dodgy ” Strong Calciferol’ tabs (Lennons)- which are not what you expect (vit D3) but vit D2 (the label, and package insert, dont tell you this) . vit  D3 powder is half the price but apparently 4 times as strong as D2.

ideally you should check your 25OH vit D and calcium levels to make sure you are on the right dose- but always taking some magnesia supplement, and at least 2 liter of water/ sodawater/clear fluid a day to avoid dehydration, kidney stones and vascular disease (which  highdose calcium supplement eg 1000mg  & vit D3   400iu/day cause).

8 April 2013  UPDATE: VITAMIN D3 THE AMAZING SUPPLEMENT

It is sad to record that Dr Walter Stumpf died suddenly a few months ago during ongoing correspondence. The world  has lost a teacher  of the century in both biological sciences and the humanities, metaphysics and philosophy,..

This week – as flu mushrooms  in the southern hemisphere autumn- the Canadian Medical Association Journal  April 3-8 features  early-release articles on concerns about the Asian flu viruses and especially the SARS-nCorVirus. Is mass vaccination the answer?  or did this in fact worsen mortality in previous North American  epidemics of eg H1N1?  which brings us back to global protection against infections and all major diseases with lowcost safe VitaminD3 at say 50 000iu(~700iu/kg)/week plus the other all-system protective  supplements – eg multivitamins (especially vit C and K) and minerals especially  magnesium, zinc, idine  and selenium; and during epidemic times, major daily boost in vits D3 and C.

In December 2012 the University of San Diego published a useful researched update on vitamin D3 and breast cancer; pointing out again that while the increase in benefit obviously drops off with increasing dose, safe dose is up to at least 10 000iu a day or 70 000iu a week, to a bloodlevel around 100ng/ml; and toxic dose requires at least 40 000 iu a day chronically (if not 600 000iu/d as other evidence suggests). The projections for breast cancer reduction fit with the same team’s predictions in 2007.

So apart from maintaining good water intake, and avoiding taking ill-advised unbalanced solo calcium supplement, for optimal dosing   in those with cancer or any other high risk, blood levels of both 25hydroxy vit D3,   1,25 calciferol, calcium, phosphate  and creatinine, should be monitored occasionally, to avoid the rare risk of kidney stones and arterial/breast calcinosis.

Remember that magnesia, phosphate and vitamin C  and K2 supplements are amongst the most important of at least 40  to accompany vitamin D3.

Last month three new studies affirmed the importance of vigorous vitamin D3 levels for genetic, heart and all health.

Holick’s group at Boston University   show the profound .Influence of vitamin d status and vitamin d3 supplementation on genome wide expression of white blood cells. No studies have reported on how vitamin D status and vitamin D3 supplementation affects broad gene expression in humans. A randomized, double-blind, single center pilot trial was conducted for comparing vitamin D supplementation with either 400 IUs (n = 3) or 2000 IUs (n = 5) vitamin D3 daily for 2 months on broad gene expression in the white blood cells collected from 8 healthy adults.   in the winter.   CONCLUSION SIGNIFICANCE: Our data suggest that any improvement in vitamin D status will significantly affect expression of genes that have a wide variety of biologic functions of more than 160 pathways linked to cancer, autoimmune disorders and cardiovascular disease with have been associated with vitamin D deficiency. This study reveals for the first time molecular finger prints that help explain the nonskeletal health benefits of vitamin D

Tehran University  http://www.ncbi.nlm.nih.gov/pubmed/23517460  showed clearly that    Vitamin D Supplementation Improve the Severity of Congestive Heart Failure. In  100  heart failure patients with (NYHA) class I ,   Only 6% of the participants had a sufficient serum concentration of 25(OH) D >30 nmol/L. Patients with insufficient or deficient serum levels of 25(OH) D (<30 ng/mL and <20 ng/mL, respectively) received oral vitamin D3 for 4 months. Vitamin D supplement increased mean serum 25(OH) D from 12.6 nmol/L to 54 nmol/L (P<.001). After vitamin D supplement, the serum level of pro-brain natriuretic peptide markedly decreased (P<.001). Cholecalciferol significantly decreased high-sensitivity C-reactive protein level (P<.001). Restoration of serum 25(OH) D level was also associated with substantial improvement in hear tfailure (P<.001) and 6-minute walk distance (P<.001).

 and Robert Heaney’s group at Creighton University   http://www.ncbi.nlm.nih.gov/pubmed/23514768  that .  All-Source Basal Vitamin D Inputs Are Greater Than Previously Thought and Cutaneous Inputs Are Smaller.    

The magnitude of vitamin D inputs in individuals not taking supplements is unknown.. they reanalyzed 3000 subjects’  individual 25(OH)D concentration data from 8 studies involving vitD3  supplement.  The total basal input (food plus solar) was calculated to range from a low of 778 iu/d in patients with end-stage renal disease to a high of 2667 iu/d in healthy Caucasian adults. Consistent with expectations, obese individuals had lower baseline, unsupplemented 25(OH)D concentrations and a smaller response to supplements. Similarly, African Americans had both lower baseline concentrations and lower calculated basal, all-source inputs. Seasonal oscillation in 4 studies ranged from 5.20 to 11.4 nmol/L, reflecting a mean cutaneous synthesis of cholecalciferol ranging from 209 to 651 iu/d at the summer peak. We conclude that: 1) all-source, basal vitamin D inputs are approximately an order of magnitude higher than can be explained by traditional food sources; 2) cutaneous, solar input in these cohorts accounts for only 10-25% of unsupplemented input at the summer peak; and 3) the remainder must come from undocumented food sources, possibly in part as preformed 25(OH).

Update March 2010

August 2009  SUMMARY: Evidence is overwhelming  that the prime sun-induced steroid hormone Vitamin D3 cholecalciferol – soltriol- is  invaluable in  20fold   higher  dose ie   perhaps  5000 to 10 000iu/day rather  than has been preached to date (200- 400iu/d), as part of lifelong  hormone replacement  HRT to prevent all major chronic degenerative diseases in all humans living and working indoors.  Effective dose of vitamin D3 supplement can reduce deathrate and disease by an astonishing 20%- that is indeed a panacea almost as good as other natural micronutrient supplements eg  fish oil, metformin, and appropriate sex hormone replacement SHRT.   It is becoming clear that with rare exceptions everyone- especially those  with serious disease eg cancer, heart, lung, brain, nerve/muscle/bone/joint  or inflammatory bowel diseases or  chronic infections like TB  HIV  influenza  or human papilloma virus –   should take a daily supplement of about 10 000iu (1/4 mg)  vitamin D for as little as ~ R10 US$1  a month ; ideally  under supervision of some  health professional.  All that is required is occasional check of blood chemistry, and good diet and  fluid intake.

And obviously because of vitamin D3’s  benefits in lowering all diseases, when using vigorous dose vitamin D, one must  expect to need to lower  prescription drug treatments for diabetes, hypertension, depression, heart disease, lung disease, arthritis, infections  etc  as these ailments  improve from the vitamin D  replacement over months.

INTRODUCTION:  Battling to help some desperate patients this week – mostly women-  with cancer, vascular, rheumatoid, lupus, diabetic, depressive, osteoporotic  and infective disease- especially now the quadruple perils of infections  influenza; human papilloma virus; AIDS and tuberculosis – let alone nuisances like shingles  candida or  herpes –  prompts a thorough review of the polyfunctional vitamin of this decade- vitamin D3, cholecalciferol, soltriol (Stumpf WE).

This  review is especially appropriate on our Womens’ Day 9 August 2009 for a natural product so important for the health of women , that commemorates the year  1956 when 20 000 women marched in defiance of  male despots’  fascist apartheid pass laws. The ages-old discrimination against women is epitomized by the pragmatic liberal economist Professor Ken Galbraith’s lecture to the Royal Society of Medicine in 1973 on the problem of unequal development and centralization of power in male technostructure – profit maximization.

No-where in business is this better shown than in Big Business creating demand  by saturation marketing,  including the medicalization of health.  This  involves  disease-mongering through creating unnecessary  concerns so as to expand markets among the well  for  patents eg  blanket cholesterol or mammography or colonoscopy  screening,  or remedies   for eg female arousal disorder, anxiety, reactive depression, mild-to-moderate hypercholesterolemia – when very few have been proven to  need or benefit from such labels, procedures and drugs.

VITAMIN D3  SOLTRIOL : INFORMATION EXPLOSION:

The first  of 46200 entries on Medline  on vitamin D is  from Oxford by Heaton 1922 . There are 272 500 entries on vitamins since 1918,  the first specific one by Jack Drummond in 192o, but of course vitamin D was first identified by Mellanby 1919, preceded by vits A, B1 and C between 1909 and 1912. From a recent historical review (table 1) of hormones, vitamin D3  was  perhaps the 7th hormone recognized  after testosterone and  estrogen (China 2600 years ago) ,  thyroid (1891)  epinephrine secretin parathyroid and antidiuretic hormone.

Soltriol is an  exquisite description  for a sun-activated steroid, the  cardinal prohormone vitamin D3  made  from cholesterol via sunlight exposure. Soltriol is not in a 1964 Oxford Dictionary, nor is it’s etymology detectable on Google search; it was indeed invented by  the pioneer polymath neurologist Dr  Walter Stumpf . On Medline search for soltriol, the first result is  Corradino 1973…

It is intriguing to read that Dr Stumpf  graduated in medicine in 1952- and 50 years later  in 2005 he wrote on his website: “From the microautoradiographic target recognition and related actions it follows that vitamin D has healing potential for prevention and treatment of various deficiencies and ailments, including old age: a PANACEA? If there is any compound that deserves being designated a panacea, the multifunctional heliogenic vitamin D appears a suitable candidate.   Philosophical consideration: “Vitamin D”, the term does not reflect its significance. I have used instead SOLTRIOL in several publications as a more appropriate designation. – Is there not a link to Heraclitus emanation of “ ever-living fire ”? The cosmic solar fire (Soltriol) as the sustaining life force, providing wave length energies for Temperature, Visible Light , and Ultraviolet B “. ”  The Main Biological Role of Vitamin D is Seasonal Adjustment of Vital Functions: These include regulation of growth, reproduction, survival stress response; endocrine and exocrine secretion, cell proliferation, cognition and mood; neuro-motor, neuro-endocrine, and neuro-sensory functions, immune response, cardio-vascular and gastro-intestinal functions, regulation of calcium and other mineral levels, cell proliferation and protein synthesis-differentiation.

Considering the decades of vitamin D use for its other benefits, it is ironic that a 1999 University California website on The History of Vitamin D has never been updated to cover more than the anti-rickets protection from vitamin D. But as Prof Stumpf writes to  me today, ultimately it is the sun that is the panacea, transmitting it’s healing powers via the skin-activated messenger hormone vitamin D.

 

It is now almost  a year since this column last reviewed vitamin D3’s benefits against all major diseases   (see table) – during which year  scores of new randomized controlled trials RCTs of vitamin D have appeared- there are now some 1680 RCTs on it since  1965.  Carpenter 1999 reviews Forgotten Mysteries in the History of Vitamin D.

Women have a raw deal:  due to their prime role and innate sense for survival of the species, for nuturing and caring, they live  about 10% longer than their mates, but as a result endure far more illness, as well as assault, disability and murder (mostly  inflicted by the careless male).

PROTEAN STEROIDS, PROTEAN FUNCTIONS: Calcitriol is one of many human steroids that include the sex hormones, aldosterne and digoxin; as well as  nonhuman steroids which also have important medicinal use- like phytosteroids, equine steroids like the equilins eg premarin, and the important ecdysteroids in insects and some plants.   Stumpf has again stressed the wide distribution in humans  of vitamin D receptors VDRs, indicating their importance in protean human functions far beyond calcium regulation.

VITAMIN D AND ALL-CAUSE MORTALITY: it is just a year since Melamed ea from USA showed that  having low vitamin D (as opposed to high level)  increases all-cause mortality by 26%- thus taking submaximum safe dose of vitamin D  can improve chance of survival by about 20%.  This for as little as R10/month – $1-  in South Africa.

In 2000,  the Seven Country Study Group showed that  ” saturated fat,vitamin C and smoking are the major determinants of all-causemortality at the population level” ie the higher the fat and smoking intake and the lower the vitamin C, the higher the deathrate. We now know better-  serious vitamin D deficiency joins the list, which of course includes alcoholism. .

VITAMIN D AND CARDIOVASCULAR DISEASE CVD

Pizzorno 2009 reviews the strong evidence of the importance of balanced vitamins A D and K supplements in reversing the epidemics of both CVD and osteoporosis.

VITAMIN D AND DEPRESSIVE/NEURODEGENERATIVE DISEASE

over 20 articles already this year attest to the importance of vigorous vitamin D levels in reducing these diseases.

VITAMIN D AND AUTOIMMUNE / INFLAMMATORY BOWEL DISEASE AND MUSKULOSKELETAL DISEASE:

The much higher incidence of autoimmune diseases in women – especially SLE systemic lupus erythematosis and RA rheumatoid arthritis-    let alone far higher younger  female  risk for fractures- must have  been obvious for millennia.  So obviously genetic female factors play a major role in these diseases – now surely attributable   largely to  the reproductively necessary absence of the Y chromosome, and thus the 100fold lower testosterone: estradiol T:E2 ratio in women (perhaps 2:1) than in men (in youth, >200:1).. It is common cause that estrogen is immunostimulant whereas testosterone  and progesterone (like vitamin D) are immunomodulating. Hence testosterone and progesterone levels soar during pregnancy to prevent the mother rejecting her foetus. This partly also explains why vigorous vitamin D supplement also greatly improves fertility and pregnancy outcome.

VITAMIN D AND RHEUMATOID ARTHRITIS: many studies  show  the benefits of the prime anabolic steroids- vitamin D and androgen (Devis 1950)  supplements-  in treatment of all inflammatory disease, especially when inflammation itself weakens bone and all other tissues. The latest – last month (Chabchoub 2009)- shows “a possible role for XCI mosaicism in the pathogenesis of RA and thyroid disease  and may in part explain the female preponderance of these diseases”. But the first and only randomized controlled trial of the effect of vitamin D on modifying  RA  appears in  1973 (Brohult)  and the only open  trial (Andjelkovic  1999) in RA  showed that            “alphacalcidiol is a powerful immunomodulatory agent with fairly low hypercalcemic activity”.

VITAMIN D INTOXICATION:  The low toxicity of vitamin D3  is fortunate because while it is ideal to monitor vitamin D levels on effective replacement, the blood test costs about R660- $80- locally;  hence all one needs to do is exclude kidney problems (which may need even higher dose of vitamin D3), and risk of kidney stones- but perhaps checking blood calcium and creatinine  at baseline and occasionally, and ensuring balanced supplement of calcium-magnesium – boron-zinc-manganese-(iron if deficient)  and vitamins B, C, D and K.   Since vitamin D intoxication (toxic rise in blood calcium- hypercalcemia) in some opinions  requires ~>600 000iu/day for months, ths is inconceivable unless one were to swallow say twelve  50 000iu vitamin D every day for months.   So the only recognized form of vitamin D intoxication could be an industrial accident involving mistaken use of vitamin D concentrate in medicine.

HYPERCALCEMIA HIGH BLOOD CALCIUM: medical causes  are rare without gross calcium overdose (milk alkali syndrome) or other specific symptomatic diseases – eg primary hyperparathyroidism, sarcoidosis, tuberculosis, and lymphoma.And fortunately most patients with these diseases and hypercalcemia are far more likely to benefit from therapeutic treatment with vitamin D than worsen on it.

OVERDOSE:      HYPERVITAMINOSIS D: WIKI says   “Vitamin D stored in the human body as calcidiol (25-hydroxy-vitamin D) has a half-life of about 20 to 29 days.[17] Ordinarily, the synthesis of bioactive vitamin D hormone is tightly regulated, and prevalent thinking is that vitamin D toxicity usually occurs only if excessive doses (prescription forms or rodenticide[38] .   Serum levels of calcidiol (25-hydroxy-vitamin D) are typically used to diagnose vitamin D overdose. In healthy individuals, calcidiol levels are normally between 32 to 70 ng/mL (80 to 175 nmol/L), but these levels may be as much as 15-fold greater in cases of vitamin D toxicity. Serum levels of bioactive vitamin D hormone (1,25(OH2)D) are usually normal in cases of vitamin D overdose. Symptoms include Dehydration Vomiting Decreased appetite (anorexia) Irritability Constipation Fatigue.

Overdose of vit D3 has been observed at 1925 µg/d (77,000 IU per day). Acute overdose requires between 600,000 and 1,680,000 IU per day over a period of several days to months, with a safe intake level being 10,000 IU per day.

A 2007 risk assessment suggested that 250 micrograms/day (10,000 IU) in healthy adults should be adopted as the tolerable upper limit.[39] In adults, sustained intake of 100,000 IU can produce toxicity within a few months.[2] For infants (birth to 12 months) the tolerable UL is set at 1000 IU, and 40,000 IU has been shown to produce toxicity within 1 to 4 months.  All known cases of vitamin D toxicity with hypercalcemia have involved intake of or over 40,000 IU)[42].

Although normal food and pill vitamin D concentration levels are far too low to be toxic in adults, people taking multiples of the normal dose of codliver oil may reach toxic levels of vitamin A, not vitamin D, [43] if taken in an attempt to increase the levels of vitamin D. Most officially-recorded historical cases of vitamin D overdose have occurred due to manufacturing and industrial accidents.[42]

Some symptoms of vitamin D toxicity are a result of hypercalcemia caused by increased intestinal calcium absorption. Vitamin D toxicity is known to be a cause of high blood pressure.[45] Gastrointestinal symptoms of vitamin D toxicity can include anorexia, nausea, and vomiting. These symptoms are often followed by polyuria (excessive production of urine), polydipsia (increased thirst), weakness, nervousness, pruritus (itch), and eventually renal failure. Other signals of kidney disease including elevated protein levels in the urine, urinary casts, and a build up of wastes in the blood stream can also develop.[2] In one study, hypercalciuria and bone loss occurred in four patients with documented vitamin D toxicity.[46] Another study showed elevated risk of ischaemic heart disease when 25D was above 89 ng/mL.[47] Vitamin D toxicity is treated by discontinuing vitamin D supplementation, and restricting calcium intake. If the toxicity is severe blood calcium levels can be further reduced with corticosteroids or bisphosphonates. In some cases kidney damage may be irreversible.[2]

Exposure to sunlight for extended periods of time does not normally cause vitamin D toxicity.[42] This is because within about 20 minutes of ultraviolet exposure in light skinned individuals (3–6 times longer for pigmented skin) the concentration of vitamin D precursors produced in the skin reach an equilibrium, and any further vitamin D that is produced is degraded.[48] Maximum endogenous production with full body exposure to sunlight is 250 µg (10,000 IU) per day.[42]”

VITAMIN D AND SEX:

Biologically, the most imperative function for species survival is sex- reproduction.   Vitamin D is clearly a potent  anabolic reproductive steroid like testosterone:   The first paper on this association on Pubmed appears in 1963 from Russia (Gokinaeva).

Stumpf 1989 at Univ N Carolina reported that “vitamin D (soltriol)  regulates and modulates reproductive processes in the female and male, controlling  reproductive processes from onset of puberty to  fertility, pregnancy, lactation, and probably sexual behavior.”

Mirzahossein in 1996 showed that,” given in the critical period of foetal imprinting, vitamin D  may  influence steroid hormone-receptor commanded events for life in a way similar to synthetic steroid hormone analogues”. So as with marine omega3., it is crucial that future parents take enough vitamin D.

Friedrich 2002 showed that  even prostate, colon and   normal cervical tissue and cervical cancer cells have VDRs – vit D receptors- and may be new targets for cancer prevention or cancer treatment.

Kalueff 2005 showed that it influences even neurological receptors eg grooming behaviour in mammals.

And now Blauer 2009 shows that it reduces growth by up to 60% in human uterus muscle and fibroids- leiomyomas.

VITAMIN D AND PAIN: this week Khan ea from Kansas University describe Effect of vitamin D supplement  on  joint pain and fatigue in women starting adjuvant letrozole treatment for breast cancer. But the first Pubmed reference on vitamin D and pain is from von Wendt 1951.  Gerwin 2005 recognized vitamin D deficiency as a cause of fibromyalgia- chronic fatigue syndrome.

and Glueck ea from Cincinnati show that vitamin D supplement for low vitamin D abolishes statin – induced  myalgia.

VITAMIN D AND SLE- SYSTEMIC LUPUS ERYTHEMATOSIS: on medline the first reference to immunosuppression with vitamin D was  by Bourdial  1963 on nasal allergy, and the first  for vitamin D and immunomodulation is by Nagler & Pollack 1986.:

However, the first paper  on the importance of Vitamin D3 deficiency   in  SLE appeared in Germany  1963, but the first paper in English and from an English country  only in 1979 (O’Regan).

The focus throughout has been on the benefit of vitamin D in reversing the hyperimmunity  of SLE, but of course vitamin D is equally important in preventing both the osteoporosis of inflammation, the fracture and wasting risks  of cortisone treatment, and the vascular disease associated with SLE.  In the last year alone there have been 10 such SLE – vitamin D major studies – 7 from the Americas and 3 from Europe.

SLE as well as plain lupus of the skin are  generally regarded as disease that requires protection from the sun.

Now this week Wright 2009 shows that in children,  SLE is  associated with vitamin D deficiency, particularly among those subjects with SLE who are overweight.

VITAMIN D, SUNLIGHT,  SLE AND CANCER:

The first case of SLE associated with cancer ( meningioma and cervix)-  is reported by Williams  1956. The latest – last month- highlights increased risk of  lymphoma, cervix and bronchus cancers.

Search for malignant melanoma MM and SLE finds the first reference in 1963. yet most of the papers are about reactions to interferon therapy, or immune markers- there is one solitary case report (1991 Sulkes, Israel) of a patient with indolent SLE who after 15 years developed and died of rapidly spread of MM. These authors comment on the infrequent association of SLE & solid cancers, the commonest  being uterus and bladder.

So it is exciting that while more sun exposure causes skin cancer and especially cutaneous melanoma  CMM, (Tuohimaa  2007),  sun exposure also improves survival from CMM-  and from a wide range of internal cancers – (especially stomach, colorectal, liver and gallbladder, pancreas, lung, female breast, prostate, bladder and kidney cancers). This favourable effect of more sunshine is obvious when comparing the lower cancer and heart disease deathrates in sunnier southern versus the darker northern countries. Only rare skin diseases eg porphyria cutanea tarda are contraindications to sun exposure of the skin. But at least one study Holme 2008 shows vitamin D deficiency in erythropoetic porphyria.

Professor Halstead 2008 (and many others)  conclude  that the high fructose corn syrup routinely used in fast foods and cooldrinks in first-world manufacturing is rapidly increasing obesity, lipidemia (and metabolic syndrome and cancer);  while folic acid  food fortification is causing low  B12 levels and thus possibly increasing dementia, vascular disease and advanced precancerous colorectal adenomas and breast cancer.   This trend is aggravated by at least  three scientifically unvalidated  obsessions of Regulators and the Medical hierarchy:

1.   low diet cholesterol in those with mild to moderate cholesterolemia;

ii.  low vitamin D –  low intake dairy products and less  sunlight exposure for fear of skin cancer; and

iii. warfarin (which blocks essential vitamin K) to reduce thromboses- whereas it worsens  both fracture risk  and vitamin D and K deficiency, and thus  arterial calcification, cancer and fractures;   all of which are reversed by vigorous vitamin B3-6-9-12 , C, D  & K supplementation.

Protection from both cancers and SLE is probably  associated with higher vitamin D level above ~100nmol/L.  Both lupus and cancers are due to altered immunity.  But SLE is due to increased autoimmunity- hence cancers   are infrequent during active SLE;  whereas cancers are due to reduced immunity – hence are associated with immune suppression, whether by cortisone (including stress) / chemotherapy, or deficiency of vitamin D – dietary and lack of sunshine..

It is now common cause that more  cancers occur with suppressed  blood  cholesterol – whether  the low cholesterol is cause d by or due to the cancer remains to be clarified; and at least one of the major statin cholesterol-lowering trials showed increase in breast cancer cases.

While there is no clear overall  relationship of statins to osteoporosis or cancer,  Kunitomo   1989showed that cholesterol reduces and corticosteroids enhance the toxicity of vitamin D in rats.  Montagnani 1994 showed that pravastain does not  interfere with the circulating levels of the main vitamin D metabolites.

VITAMIN D AND INFECTION:

For an acute infection, Cannell and Hollis 2008    suggest  vitamin D in an antimicrobial  dose of 2000iu/kg eg 120 000 iu a day for 3  days- to produce enough of the naturally occuring antibiotic cathilicidin.  Ginde 2009 show that those with high vitamin D levels have less respiratory infections. This column has previously reviewed the dramatic benefits of vitamin D on infection mortality in AIDs- TB patients.   Obviously one is going to be cautious pushing vitamin D  in a patient with known kidney stones, or hypercalcemia.

VITAMIN D : WHY THE INCREASING DEFICIENCY, NEED FOR SUPPLEMENT ?

Never mind the poor and chronically ill, the aging especially need much more vitamin D, and benefit the most. Even in a sunny fishing nation like Spain, elderly women do not get enough vitamin D from fish or other foods, and most have suboptimal blood levels of it.

Apart from  dietary intolerance and obsession reducing intake of cholesterol and dairy products, the vitamins and minerals in particular have been greatly depleted and imbalanced in commercially produced- and especially genetically-modified  food.   And while increasing longevity,  food scarcity -poverty and   mushrooming prices (cartel pricefixing that is ignored by well-paid politicians and regulators) – are prime causes,  Politicians and Regulators have worsened this by falling decades behind in ignoring the leading 20th pioneer nutritionist/ economists  like the USA’s Professors Linus Pauling the unique double Nobel prizewinner prophet of vitamin C and peace; Ken Galbraith; and  the UK’s  Sir Jack Drummond. The latter two respectively brought the Allies (under FD Rooseveld and WS Churchill)  through  WW2 by putting farming- healthy food production and pricing- as the painfully obvious priority- which selfserving  gluttonous politicians  like Nixon, Bush,  Kissinger, Mugabe and Mbeki, and most others leaders (who support, not just tolerate such despots)  simply ignore since they detest “surplus people”- the honest  poor;  if not also  hardworking farmers.

It is no coincidence that Pauling and Galbraith both graduated from agricultural colleges.  And no coincidence that all three nutritionists were the targets of  politician-business moguls because of the obstacles they posed to the profiteering national economic sabotage that is the lifeblood of ruthless businessmen-capitalists from before Nixon- Connolly- Reagan- Kissinger  and Thatcher, through to the Bushes and Blair and Montsano-GD Searle, Mbeki and Zuma,  and the arms, oil, banking, mining, media,  food, sex, tobacco-alcohol and medical-big pharma industry mafiosi cartel  who make or break  presidents and  governments.

James Ferguson makes a strong case for The Vitamin Murders, that Drummond (and his family) were butchered in  a Vitamin Industry contract  in France as a lesson to do-gooders because his advocacy of the primary role of good natural  nutrition and vitamins  was such an obstacle  to the fast food and synthetic drug industry.    Conspiracy theorists could argue that, like Pauling’s vitamin C, the Drug Industry have through the FDA managed to ensure that only this year is the FDA grudgingly moving to raise the Recommended daily Allowances of vitamin D (and C)  even fractionally above the present rickets- (and scurvy) preventing doses, as opposed  to their   modest 25 to 50fold  fold   higher intakes that have been known already for decades to be both safe and major benefit against all diseases.

John Le Carre’s The Constant Gardner echoes that ongoing conspiracy scenario, the battle between Big Pharma with it’s drug lobbyists (including the USA FDA and the European Union’s European Medicine’s Authority, and leading politicians) to promote their lucrative modern synthetic chronic  drugs (none of which have been shown to reduce all-cause disease and mortality as do natural supplements), versus nutritionists and informed consumers who know that broad natural supplements (vigorous vitamins, minerals and biologicals)  to bolster the failing adulterated food chain are more important and effective  than any patented designer drugs in combating all disease. Unfortunately the necessary advocacy for natural supplements has been muddied by fraudsters  like the Big Pharma- FDA- academia  cartel (who swamp the medical literature with trial and review papers favouring their snake oils), the Rath Foundation, and our local dissidents against reason  like  Mbeki, and Drs Manto Tshabalala-Msimang, Nkosasama Zuma and Olive Shishana.

CONCLUSION: In 2006 Dr Walter Stumpf in THE DOSE MAKES THE MEDICINE wrote:  “in recent years, discussion raged  about the negative effects of   estrogen-replacement therapy and its relationship to cancer.  In numerous articles, the side-effects of estrogen treatment were highlighted in a generalized fashion and, although consideration was given to the duration of treatment, the relationships to dose (let alone type and route of estrogen) were frequently left out. And yet, considerations of dose and time in pharmacology and toxicology are paramount.
Similarly, a
wareness of proper dosage is crucial to the development of future vitamin D therapies. Physiologic dosing of vitamin D does not cause hypercalcemia – hypercalcemia is related  to overdosing ie closer to 100 000iu/day. Considering the many target tissues that are unrelated to systemic calcium regulation, most therapeutic effects of vitamin D occur independently of the high-dose systemic calcium effects. Because of the biased focus on calcium, the many other effects tend to remain unnoticed and hidden.  Future research needs to give more consideration to dose-effect relationships by monitoring target functions independently of systemic calcium regulation.
New therapeutic applications of vitamin D can be established for cardiovascular, neurological, endocrine, immune, gastrointestinal, reproductive and other diseases, including posttraumatic and gerontological deficiencies, in which the polyfunctional effects of  the hormone not only come to bear, but can also be controlled and maximized for optimal health.”

Since the global population shift from rural to   city life and work the past century ie in our lifetispan,  humans have largely gone from being healthy longlived outdoor food-producing  workers living on their own fresh produce including organically grown unadulterated fresh  food and dairy products – or fish- (rich in micronutrients),   to working mostly indoors and consuming largely  micronutrient-depleted  food  as well as multiple noxious deliberate industrial pollutants- from sugar and alcohol  to estrogenics, pesticides, heavy metals, cornsyrup and aspartamate.

Like fish oil is the most important food extract we have (and businessmen are ruthlessly harvesting to extinction), vitamin D3  has become the anti-disease vitamin  of the past decade,  joining vitamins C & B as the  panacea vitamins that can and should be supplemented in far higher dose than anti-vitamin  “Regulators” and professional researchers and associations (with vested interests in protecting  their funder- Big Pharma) approve.

But as the more affluent age and increase in numbers,  the micronutrients that deplete (with longevity, the deteriorating food chain, and unnecessary drugs),- especially  vitamins  K, chondroglucosamine, N-acetyl cysteine, alphalipoic acid, Co-Q10, arginine, carnitine, carnosine,  riboseand the marine  EPA and DHA-   are  fast becoming the “vitamins”  of the next decade.

Tragically, edible marine products especially marine omega3 EPA+DHA are rapidly becoming so scarce that the vast majority of people  can  neither  source nor afford the minimum optimal gram a day, until science breaks through  to synthesize these uniquely beneficial free fatty acids. But at least the supply of minerals, and vitamins including D3, is inexhaustible and therefore freely available at reasonable cost.

ndb

dedicated to Dr Walter Stumpf, whose  >300 papers (~24% on vitamin D) on Medline apparently  span 1963 to 2008- on vitamin D the first  in 1979, the last  30years later appropriately on Vitamin D and the digestive system.  By comparison,  Pubmed lists only 3 papers by Albright,   in 1938-9.