Category Archives: Food & Diet


Dr Neil D Burman MBChB(UCT) 1966, MRCP(UK 1974) Senior  Family General (all-ages) & Internist  practitioner in Claremont Cape Town,  has left Grove Bldg moved his rooms to
 13 Stafford St Harfield  Village, 50m down from Harfield station subway above corner of 1st Ave. .
Consultations  by appointment only 1600-1800, sometimes from 0900 weekdays and public holidays/weekends.   .  Holistic integrative chronic natural medicine practice (HRT, pain relief, infection eg HIV AIDS, TB, /cancer/obesity screening & prevention) .
(No emergencies or surgery- these must go to nearest polyclinic or hospital ER). .

or consultations by Telephone/email  where appropriate.

appts: ph Reception office hrs  021 6717797.   .
doctor personal email  or sms or whatsapp (or as last resort  try ph) 0836299160 all hrs 07.00 – 21.00. .   or    or fax 0865657215
Fellow of  Kronos Longevity Research Foundation Phoenix Arizona.

MEMBER OF  Royal Society SA; Kidney Association;Faculty of Consulting Physicians of South Africa; Kingsbury Hospital Forum;  and Local & International Societies for Study of: ; Menopause and Aging Males, Hypertension, Sexual Health, Vitamin D3-Autoimmune Disease  CGCoimbra network;  SASIM SA Society of Integrative Medicine; LDN Trust; .  Insurance, and Professional Driving Permit Assessments. mornings SASSA Disability Grant med officer Cape Town Clinics.  (formerly practicing/lecturer  in Port Elizabeth;  Hypertension, Renal & Transplant  med   GSH UCT, Leeds Hospital  England: Tygerberg Hospital Univ Stellenbosch; Libertas Hospital G/wood; and Univ W Cape.

Preferred Provider: Discovery Health & FedHealth


update 10 Dec 2016   remember that quotations from experts are in italics:

Note noteworthy timeous new reviews: in the latest 7 dec BMJ   :

    Advice on sugar and starch is urged in type 2 diabetes

advising on low sugar low starch to treat obesity diabetes,

    and  correction The scientific report guiding the US dietary guidelines: is it scientific?

   of the extensive comment on bad new USA guidelines by Nina Teicholtz of 2015 ,

together with reviews of Gary Taubes new book Dec 2016  on The Case against Sugar     ,  being a bigger disaster than even smoking and other drugs..

These help  to  back up Tim  Noakes, Zoe Harcomb, Richard Feinman, Peter Wise  and at least two dozen  other scientific teams around the world, and  Integrative medicine, against the fastfood-pharma – hightech medicine – hospital  industry trying to discredit Banting diet and  needed proven supplements for deficiencies – of natural vits D+C+ iodine +magnes   + multisupps , cannabinoids, fishoil  + BID HRT  (eg melatonin, cholecalciferol, progesterone etc), and other natural supps, and homeopathy,-

so as to keep people profitably sick by the sugary lowfat diet and smoking,  vaccines ,  and patent Big Pharma-raincheck prescription antimicrobials, statins, fosamaxes and ranelates,  antithrombotics, designer hormone substitutes,screening mammo and chemotherapy, bariatrics , nsaids, ACEIs and ARBs,  antidementia, patented antidiabetics, analgesics, opiates,calcium,  aluminium, mercury, and  psycho-pharmaceuticals- none of which address the CAUSES of disease as do coaching on better diet, lifestyle and integrative medicine.  …

      Even more remarkable is the total ignoral of the 25 +  scientific RCTs done and published since 2000 that validate  very low carbs high fat  Banting  (calorie distribution: 8.5% carbs, 62% fat, 30% protein) as much better than the current USA – RSA low fat (54% carbs, 29% fat, 17% protein) generous PUFA and carbs diet. See update review  of the experts below at

       The Universities Stellenbosch+Cape Town 2014 Naude, Volmink  ea critique of Banting   Low carbohydrate versus isoenergetic balanced diets for reducing weight and cardiovascular risk: a systematic review and meta-analysis   notoriously ignored      most of these scientific studies among numerous other errors noted at the time .

            Harcombe and Noakes have now published Mistake or mischief:  The universities of Stellenbosch/Cape Town low-carbohydrate diet review: debunking the Naude, Volmink  ea critique             A major error of the US/UCT analysis was that it missed the point, did not even consider the very low carbs high fat  (+- 8.5% vs 62% fat)  intake of the ketogenic Banting regime.         The  Naude review classified low carbs as diet cals  below 45% carbs, high fat as diet cals above 35% from fat. So they did not analyse at all the  ketogenic +-8% very  low carbs, 60%+ ie very high fat Banting diet.

           The latest is Prof Richard David Feinman’s series of papers from the prestigious SUNY State Univ. NY  . on the benefits of Warburg ketogenic ie low carbs diet for cancer,  never mind obesity  diabetes, and epilepsy ( which goes back to 1931 on Pubmed) , the latest eg Nel ea 2014 Jefferson Med College USA perhaps Autism Spectrum Disorder https ://www.ncbi.nlm.nih.govpubmed/27841033

.       Now Prof Peter Wise emeritus oncologist from ImperiaL College London has thrown a cat among the pigeons,   in his November 2016 BMJ critique of Cancer drugs, survival, and ethics, pointing out how ‘Despite considerable investment and innovation, chemotherapy drugs have had little effect on survival in adults with metastatic cancer’.  A meta-analysis 2004 explored the contribution of cytotoxic chemotherapy to five year survival in 250 000 adults with solid cancers from Australian and US trials.3-important effect was shown on five year survival only in testicular cancer (40%), Hodgkin’s disease (37%), cancer of the cervix (12%), lymphoma (10.5%), and ovarian cancer (8.8%).  In the remaining  patients—including those with the commonest tumours of the lung, prostate, colorectum, and breast—drug therapy increased five year survival by less than 2.5%—an overall survival benefit of  1 to 3  months., as in Europe.  Drug treatment can therefore only partly explain the 20% improvement in five year survival mentioned above. The approval of drugs with such small survival benefits raises ethical questions, including whether recipients are aware of the drugs’ limited benefits, whether the high cost:benefit ratios are justified, and whether trials are providing the right information.      In search of ethics : Many irregularities and competing interests—in pharma, in trials, in government approval, and in the clinical use of cancer drugs—impact ethically on the care and costs of patients with cancer. . Spending a six figure sum to prolong life by a few weeks or months is already unaffordable, and inappropriate for many of the 20% of the (Western) population who will almost inevitably die from solid tumour metastases.    Ethical cancer care demands more prompt and radical treatment of localised and regional disease, together with highly skilled, earlier, supportive care are the important yet underfinanced priorities in cancer control. Finally, aggressively targeting the less than ethical actions of stakeholders in the heavily veiled medical-industrial complex may be the only way forward: current market driven rather than health driven priorities and practices do not benefit cancer patients.

He provoked counterattack from vested interests: Twenty UK medical oncologists retort in BMJ: UK health professionals specialising in the drug treatment of cancer, we think that Wise’s analysis strays into the territory of unbalanced opinion.

    So we come back to addressing the causes of disease for both prevention and treatment, by  integrative ie combining natural  and hightech means.

updated 29 Aug 15    

Six  months later after the first World fat>carbs HFLC groundbreaking congress in Cape Town, Pubmed and Google search show no obvious new information on this life-and-death topic that the February  Cape Town International  Banting Congress   highlighted. .

but the publication of Real Food Revolution II Raising Superheroes now  provides much new evidence and impetus.

While carnivores ( mammals and pterodactyls-birds) from ~300million years ago survived the extinction of the carnivorous  big dinosaurs sixty million years ago, so have current  carnivorous primates- tarsiersand us carnivorous humans nurtured from conception on animal protein and animal fats:

  Top anthropologist    Prof Gail Kennedy (of UCLA and much work at Olduvai Gorge)   in    her classic 2005  Journal of Human Evolution article From the ape’s dilemma to the weanling’s dilemma:  early weaning and its evolutionary context           summed up >2million years of evolution of exclusive human breastmilk ie animal-protein-and-fat>carbs -based  infant feeding:  ” Although humans have a longer period of infant dependency than other hominoids, human infants, in natural fertility  societies, are weaned far earlier than any of the great apes: chimps and orangutans wean, on average, at about 5 and 7.7 years, respectively, while humans wean, on average, at about 2.5 years. Assuming that living great apes demonstrate the  ancestral weaning pattern, modern humans display a derived pattern that requires explanation, particularly since earlier weaning may result in significant hazards for a child. Clearly, if selection had favored the survival of the child, humans  would wean later like other hominoids; selection, then, favored some trait other than the child’s survival. It is argued here  that our unique pattern of prolonged, early brain growth and the neurological basis for human intellectual ability  cannot  be sustained much beyond one year by a human mother’s milk alone, and thus early weaning by one year, when accompanied by   supplementation with more nutritious adult foods, is vital to the ontogeny of our larger brain, despite the associated  dangers.                             Therefore, the child’s intellectual development, rather than its survival, is the primary focus of selection.    Consumption of more nutritious foods derived from animal protein  increased by ca. 2.6M yrs ago when a group of  early hominins displayed two important behavioral shifts relative to ancestral forms: the recognition that a carcass represented a new and valuable food sourced potentially larger than the usual hunted prey;  and the use of stone tools to  improve access to that food source. The shift in the hominin ‘‘prey image’’ to the carcass and the use of tools for butchery  increased the amount of protein and calories available, irrespective of the local landscape. However, this shift brought  hominins into competition with carnivores, increasing mortality among young adults and necessitating a number of   social responses, such as alloparenting. The increased acquisition of meat ca. 2.6 M yrs    ago  had significant effects on the later  course of human evolution and may have initiated the origin of the genus Homo.”

The thesis of Raising Superheroes by Kennedy’s summation of human brain dietary evolution  from babies nurtured on animal meat and fat is supported by serious studies:  a 2010 critique in The Keto Diet for Health;  in the textbook Guts and Brains ,2007   ed paleoarcheologist Wil Roebroeks  at Univ Leiden .; and University Michigan anthropologist John Speth’s Springer Verlag  2010 The Paleoanthropology and Archaeology of Big-Game Hunting – Protein, Fat, or Politics?

Many sensible voices including locally  like Kath Megaw encourage breastfeeding till at least a year in South Africa.   Certainly doesnt say anything different from what sense and the authorities quoted below say-  breast milk and then mushy whole food.
       NICUS the Nutrition Info Centre of University Stellenbosch  recommendations on line for 6-12mo infants certainly advocate  increasing  meats, fish, vegs, fruits & pulses.  But the SA Guidelines on weaning 2012 Introducing solid foods from Stellenbosch University Dietetics says plainly “Complementary food is semi-solid porridges & milk that are given from six to eight months, then vegetables or fruit and then progressing to a mixed diet in mashed form small portions of solid food given until 12 months, when family foods are integrated”. ie NICUS advocates while weaning off breast, get baby (hooked) only on cereals for 2 months. where is the evidence to justify solely cereals as started diet? There is no good science  published to justify this belief, marketeering; and no parallel in the non-primate infant world. .
NICUS say further:   “Both early (< 4 months) and late (> 7 months) introduction of gluten should be avoided. Gluten should be gradually  introduced while the infant is still being breastfed as this may reduce the risk of celiac disease, type 1 diabetes mellitus and wheat allergy.
     “More than 14% of energy from proteins in the eight- to  24-month period may cause an early adiposity rebound  and the development of overweight in young children.  A dietary fat intake of 30-45% of total energy is recommended. The American Heart Association (AHA)  has a limit of 40% fat of total energy with an emphasis on a more liberal intake of unsaturated fat and a focus onensuring adequate intakes of omega-3 fatty acids in infants and children.

In fact scientific evidence has never supported the obsession against eating (animal) saturated fat, triglycerides; nor human need for promoting the plant protein  gluten. As we  were and are taught in basic biology, only water, essential aminoacids- protein, essential fatty acids- fats-  and the trace ~two dozen vitamins and minerals are, as eg  all textbooks say,  essential nutrients required for normal human body function that either cannot be synthesized by the body at all, or cannot be synthesized in amounts adequate for good health (e.g., niacin, choline), and thus must be obtained from a dietary source.[1] .        So its  marketing hype that gluten is any more of an essential macronutrient than sugar, carbohydrates .

Wiki succinctly lists essential ie indispensable macronutrients (like the trace ~two dozen micronutrient vitamins and minerals) as: Essential fatty acids (EFAs) and essential amino acid EAA nutrients
The Wiki entry on gluten has a major paragraph on the common problem of gluten intolerance (especially wheat) , but no claim that it is an essential nutrient- for the simple reason that the gluten-containing cereals eg wheat and related grains, (including barley and rye) are like carbs not essential foodstuffs, and commonly cause distant health problems.

But the  alarming disinformation is  in that  RSA article Introducing solid foods table 1  and the NICUS table Nutrient requirements @ 6 to 12 mo. Their recommended figures are: “total fat RDA 30gm/d ie ~270kcals and protein 13.5gm ie 54kcals  on a total average RDA calorie intake of 710kcals”. That leaves the majority ie the balance of the energy intake- 385kcals  to be made up by carbohydrates  – ie 385/4 = ~ 95gm carbs. That gives their recommended (non-protein) carbs:fat energy ratio as 385:270  ie >1.4– which they imply can come also from plant oils. This RDA contrasts with the long-known (see below) (white and black) mothers’ s breast milk carbs:(animal) fat energy ratio of almost half (of what NICUS recommends 1.4:1):   30:38 kcals/gm ie ratio~0.8.

And even more dangerously, that Univ Stellenbosch  table gives the RDA of vitamin D as 5mg/d ie 40 000iu/d. Neither that gross overdose, nor 5mcg/d = 400iu/d, are near the modern proven necessity of perhaps  1000 iu/d in swaddled urban babies – the vast majority of whom in Africa  are black  and therefore make even less vit D3.

rice milk: as rice / and Noakes’ team says, Rice/ricemilk – like the vast profitable fast food industry in baby purees and formulae-  is ( like the killer Food mega-industry carbs and plantoil-based food pyramid  of the past 40 years of Ancel Keyes ea )  a marketing (Gerber’s)  legend, but not a necessity or good for babies- it lacks fat and protein; and may be contaminated with eg arsenic!

As the Real Food Revolution book  II  Raising Superheroes says, promoting natural real food  is not about banning carbs or promoting high protein intake  – thats impossible and unnecessary on mixed real food- but eating more  fresh unprocessed energy, as mostly animal incl  fish fat more  than natural ie plant carbs, as in breast milk; with rarely  if ever processed foods including synthetic transfats and refined carbs like  sugars, “white” flours and starches,  and the derived alcohols.

17 May 2015    ADAPTING AND ADOPTING BANTING FOR BABIES a la Canadian-WHO recommendations and age-old good practice. canada-guidelines-advise-meat-as-baby-first-food/ Health Canada clarifies stance on meat for babies

Prof Tim Noakes’ team asks for all to sign petitions supporting his argument. We can  doubt he needs it since he knows better than most how strong the evidence is.

When us Seniors’ generation was born around WW2, as in ancient times we were from > 6 months age  gradually weaned off  breast onto and brought up on real fresh food- butter, cream, home-grown veggies, fresh fish and pasture-fed meat /hens (and thus eggs and whole cows’ milk); with a tsp of codliver oil a day as the quintessential brainfood for those of us not brought up on oily ie pelagic  sea fish..

Food was produced  (like us humans) – especially by us mostly  poor – without  antibiotics, GMO,   pesticides; and packaged, dressed  without plastic, let alone massive electromagnetic exposure (microwave, TV, computers, cellphones and then WiFi). Like most on the planet, we had no cars or TV, so we also got plenty of sunshine- vits cholecalciferol D3, and ascorbic acid C (from abundant organic sun-drenched fresh fruit) – and exercise walking/ cycling to transport/ school/ sport or outdoor work as herders, farm/ building  labourers etc if not the minority of us in shops/ factories/ office. Basic education and care – literacy-numeracy and hygiene – was provided mostly by state schools competing widely with mission schools, staffed from dedicated teachers’ /nurses/theological training colleges with intensive community experience; and (if mostly from the bible) literate parents from church/ libraries and radio.

But in our >50 years in medicine, all those aeons-old social foundations have increasingly  been wiped out , especially in  Africa   by the ever-more corrupt advertising (especially on TV) and  Fast Food- GMO- Disease   Industry in partnership with corrupt oligarchy government that closed teachers’ and nurses training colleges; and rural /farm depopulation with mass migration driven by government-led poverty to city ghettoes. .. .

Already by 1970, teaching hospitals- following USA -devised corrupt industry factory-farm-food marketeering  (not science and nutritional evidence-based) – started (by the non-medical Ancel Keys)  nagging us via our medical school cholesterol clinics  to start cutting cholesterol ie meat- dairy- fat  intake in exchange for increasing intake of  factory mass-produced refined and then genetically modified and insecticide-laden carbohydrates (sugar, maize, soya) and  unproven synthetic hydrogenated seed-oils;   and cholesterol-busting drugs like clofibrate, the statins,  and aspartame – none of which were ever scientifically validated, and have been increasingly incriminated like sugar, fructose and  smoking  the past 30 years as major health pollutants. .

The scientific evidence has never the past 50 years shown benefits even matching harms from the profit-driven junk marketing of cholesterol-busting drugs and diets – artificial  low-animal -fat cholesterol high carbs diets , and  synthetic omega6  hydrogenated plant oils like “margarines” and Cremora, and sunflower cooking oils  – for any common disease let alone average lipidemias. But the American public was bludgeoned into obeyance/obeisance and then silence, and have suffered increasing obesity and disease ever since – to the joy of the profiteering Fast Food and Disease Industry and their lobbyists in and outside governments. Now the  SA Dieticians’ Association   attack Noakes       (and thus pre-1960s healthy normal world practice, and still Canadian  guideline)  diet promotion of more animal fat calories than carbs calories for weaning infants;

but the milk comparison the Dieticians quote in their attack- like the figures in the breastmilk Wiki review  –   shows remarkable conformity between UK mothers’ breast milk and eg Bantu mothers (1950)- milk has   about 26% more calories/100gm  from  animal fat ie +- 38cals than from milk carbs +- 30cals, with protein ~1.1g%..   Obviously, LCHF promoters do not preach no-carbs diets since there is no such real food free of carbs.

The message has always been to take more fat calories than carbs calories, especially not refined empty calories like sugar and commercial fructose-laden drinks and GMO maize. Laymen have difficulty grasping that these refined simple  sugars are slow cumulative poisons like longterm smoking, aspartame (Canderel) , oral synthetic sexhormones, fluoride, aluminium, mercury, lead, excess iron, etc. And obviously with poverty  and dependency increasing  in RSA due to almost  worst- in-the -world State schooling  since 1994,  infant mortality  from  joblessness  and thus stress, violence , malnutrition are increasingly rife in the Born-Frees  ie those born in the new South Africa since 1990.

The Diet Association fails to ask simply: where are the references for promoting  protein-and fat-rich food for weanlings?  They are listed abundantly in the social and medical literature of the past century, especially the current literature we seniors in health science practice  have read  weekly the past 50 years from the 1960s;         and conveniently now  analyzed in depth by medical journalist Nina Teicholz and her numerous experts of the past 50 years she interviewed, in chapters 5 and 6 of The Big Fat Surprise 2014 (Scribe Pubs, Australia & UK); 

following in the footsteps of contrarian ie high-carbo-sceptic  investigative nutritionists  like the archetypal insulin-resistant  William Banting 1869 (ironically a distant kinsman of Fred Banting the Nobel-winning discoverer of insulin 50 years later) and his physician Dr William HarveyVilhjalmur Stefansson from 1923;  Arthur Pennington 1949; Robert Atkins since 1963, Gerald Reaven from 1965 (Syndrome X);  WPU Jackson & George Campbell in Cape Town  from 1968,  Denis Burkitt and Tom Cleave in Africa from 1970,  James le Fanu since 1984 (the Rise and Fall of Modern Medicine 2001); Gary Taubes since 2001 (Good Calories Bad Calories 2007); Rooseboom ea 2006 (The Dutch Winter Famine of 1944-45);   and  Sam Feltham  Slimology 2014, the 25 RCTs so far from many universities reported between 2000  and 2014  that Feltham  et al detail eg   ( in his book Slimology) by numerous contrarian  academic clinician experts; all these authorities  show that for health and reversing obesity in adults, the LCHF diet is uniformly more  successful than the HCLF diet.

 By contrast, Zoe Harcombe and colleagues at W Scotland University 2015-in  Evidence from randomised controlled trials did not support the Keys- McGovern USA   introduction of dietary fat guidelines in 1977 and 1983: Harcombe ea’s  systematic review and meta-analysis  have confirmed what we practitioners have read consistently  in the science journals and experienced for the past  50 years, that the USA-led switch from our till post-WW2  healthy natural farmfresh high fat low carbs diet  (to the factory-food low fat low cholesterol high carbs diet with cholesterol-busters) was never based on any good scientific studies, merely on wrong beliefs and profiteering; and has aggravated the obesity-diabetes -cancer pandemic.
BABY DIET EVIDENCE? And similar  Canadian-and WHO paediatrician -led studies reported below  in weanling babies and animals have confirmed that, contrary to the excellent development always seen in nature  in weanlings on the natural highfat>carbs animal protein diet that we seniors were brought up on,  the still-heavily marketed junk food commercial  low-fat low-meat high cereal weanling diets  (which the SADA dieticians insist is best) stunts growth and development and promotes the epidemic childhood obesity and diabetes we are seeing. .

Increasing adverse experience with antibiotics, multiple vaccines, factory foods eg formula milk powders, GMO crops, tap water, doctored dairy milk, aspartame, pesticides like DDT and Roundup glyphosphate, crops grown in heavily polluted but  nutrient-exhausted soil,   and grain/antibiotic/hormone grown foods partly explains why we should avoid as far as possible exposing (future and current) pregnant women and infants to  antibiotics, sugar, concentrated fructose, commercial dairy and processed refined cereal products, and aluminium-mercury-tainted vaccines,  as far as possible.

In conclusion: it is sad  that ADSA  the Association for Dietetics in SA,  attacks evidence-based Banting proponents  personally instead of rebutting in academic scientific robust debate – the scientific media-  the best scientific  references and policies as thoroughly assessed and promoted by real-world experts below.     Clearly, ADSA cannot quote any good science to support its  contrary destructive commerce-based  policy  (of the past ~40 years ) about diet providing the majority of energy as sugars and hydrogenated omega6 – (it and the local medical schools havent done so) instead of low carbs high animal-fat natural food-  so now it hides behind the sub judice rule.



Gwyneth Paltrow 2013 has provoked the wrath of the dietetic establishment by saying that she avoids feeding her children bread, rice and pasta, because she believes that these carbohydrate foods aren’t good for them. Paltrow was writing in her new low-carb, gluten-free cookbook, It’s All Good, which is out in April, and whose recipes are said by her publisher to “form the basis of the diet Gwyneth goes back to when she’s been overindulging, when she needs to rebuild, or lose weight.”     Dieticians who subscribe uncritically to government nutritional guidelines have been wheeled out to testify to how ‘vital’ carbohydrate is in the diet, and warn in the bleakest terms of the dangers of restricting it. “Paltrow is putting her children, aged eight and six, “at risk of nutrient deficiencies”, warns one. Her children “won’t be able to think straight as their brain won’t be functioning”, says another. In the same Daily Mail piece, it is even observed that Paltrow’s children are thin – shock horror! – as if this was automatically cause for concern. So accustomed are we to the sight of overweight children, thin ones are beginning to look unusual …… read on

Dr Sheila Innis’  recent review  Impact of maternal diet on human milk composition and neurological development of infants   Am J Clin Nutr. 2014;99:734S-41S. from Univ British Columbia, Vancouver, Canada concludes unequivocally what vast evidence shows: that animal fat especially Omega3  marine DHA & EPA are crucial for neurodevelopment and all membranes – such natural saturated animal fats make up some 20% of adult brain. Maternal nutrition has little or no effect on many nutrients in human milk; for others, human milk may not be designed as a primary nutritional source for the infant; and for a few, maternal nutrition can lead to substantial variations in human milk quality. Human milk fatty acids are among the nutrients that show extreme sensitivity to maternal nutrition and are implicated in neurological development. Extensive development occurs in the infant brain, with growth from  350 g at birth to 925 g at 1 y, with this growth including extensive dendritic and axonal arborization. Transfer of n-6 (omega-6) and n-3 (omega-3) fatty acids from the maternal diet into human milk occurs with little interconversion of 18:2n-6 to 20:4n-6 or 18:3n-3 to docosahexaenoic acid (DHA) and little evidence of mammary gland regulation to maintain individual fatty acids constant with varying maternal fatty acid nutrition. DHA has gained attention because of its high concentrations and roles in the brain and retina. Studies addressing DHA intakes by lactating women or human milk amounts of DHA at levels above those typical in the United States and Canada on infant outcomes are inconsistent. However, separating effects of the fatty acid supply in gestation or in the weaning diet from effects on neurodevelopment solely due to human milk fatty acids is complex, particularly when neurodevelopment is assessed after the period of exclusive human milk feeding   

    . The   Canada guidelines    The Canadian  statement 2013 reads unequivocally: POSITION STATEMENT Weaning from the breast:    Barbara Grueger; Canadian Paediatric Society , Community Paediatrics Committee  Paed Child Health 2013:  updates the similar previous Canadian Paediatric Society position statement  2004.[3] ”  – “North American parents have traditionally introduced rice cereal as a first food.  There seems to be a movement away from this practice in the general mama community, especially white rice cereal.    Baby-led weaning is a method of  foods introduction wherein the baby is offered whole foods.  The baby has complete control with this method.  For example, you steam a whole artichoke, place it on baby’s tray and allow him to decide what to do with it.    Infant cereal, pureed meats and fish are recommended as first foods by the American Academy of Pediatric AAP, Canadian Paediatric Society (CPS), Dieticians of Canada, Breastfeeding Committee for Canada, Public Health Agency of Canada, and Health Canada. CPS also identifies poultry, cooked egg yolk and well-cooked legumes (beans, lentils, chick peas) to be good sources of iron and suitable for first foods”.) Exclusive breastfeeding provides optimal nutrition for infants until they are six months old. After six months, infants require complementary foods to meet their nutritional needs. This is when weaning begins. Weaning is the gradual process of introducing complementary foods to an infant’s diet while continuing to breastfeed. The timing and process of weaning need to be individualized by mother and child. Weaning might be abrupt or gradual, take weeks or several months, be child-led or mother-led. Physicians need to guide and support mothers through the weaning process. “Breast milk is the optimal source of nutrition in infancy. Breastfeeding protects infants from a wide array of infectious and noninfectious diseases. With few exceptions,[1] healthy term infants require only breast milk (with vitamin D supplementation) [2] to meet all their nutritional requirements until they are about six months old. The Canadian Paediatric Society, Dietitians of Canada, Health Canada and the WHO recommend exclusive breastfeeding for the first six months of life and continued breastfeeding with complementary foods for up to two years and beyond (no upper limit has been defined). Iron from meat has the best bioavailability[4][17] and can be readily absorbed from the gastrointestinal tract. After six months of age, when breastmilk alone cannot provide enough, additional protein sources (such as meat, fish, egg yolk, tofu, lentils and cheese) are needed. Roughage should also be introduced to the diet, although it is not clear when adding fibre becomes necessary. There is no conclusive evidence that delaying the introduction of eggs, fish and nuts (including peanuts) beyond four to six months of age helps to avoid food allergies.[13][18][19] As a greater variety of solids and liquids are introduced to a baby’s diet, weaning will progress. “A review of the literature using MEDLINE (1966 to 2012), the Cochrane database and relevant websites,  WHO, the Canadian Paediatric Society, Health Canada and the American Academy of Pediatrics, concluded:  Given the limited nature of  evidence on weaning, the recommendations in this statement are based largely on expert opinion and consensus.  “Generally, infants were breastfed longer in ancient times[8] than in Western societies today.  Mothers in Zulu societies have traditionally breastfed their infants until 12 to 18 months, at which point a new pregnancy would be anticipated. Ancient Hebrews completed weaning at about three years. Around the world it is not uncommon for children to be completely weaned at two to four years of age.[9] Anthropological studies have described final weaning at the following points: when the infant reaches four times his birth weight; when the infant’s age is six times the length of gestation (ie, 4.5 years); or when the first molar erupts.[9][10] “The early introduction of mixed feedings began in early 19th-century Western society. Prominent contemporary physicians such as American Pediatric Society founders Drs. Luther Emmett Holt and  Job Lewis Smith recommended that weaning begin at around nine to 12 months of age or when the canine teeth appeared. Smith recommended against weaning during the summer months because of the risk of “weanling diarrhea”. As weaning was recommended earlier and earlier, infant mortality increased. Introduction of weaning foods was an important cause of infant mortality in the 19th century. In the early 20th century, mothers were encouraged by the medical community to raise their children scientifically or “by the book”. In the 1920s, the United States government published Infant Care, referred to at the time as the “good book” and read by women from all socioeconomic groups. It recommended cod liver oil, orange juice and artificial feeding.[8] “In 2008, according to the Public Health Agency of Canada, 87% of children were breastfed for some period of time while only 16.4% were exclusively breastfed for six months. Still, this figure represents a steady increase in breastfeeding rates over the previous five years. Breastfeeding duration varies depending on maternal age. Only 11% of infants of mothers aged 25 to 29 years continue to breastfeed exclusively for six months, compared with 20% of infants of mothers 35 years or older.[11] The most common reason mothers give for weaning is a perceived insufficiency in milk supply. Women who breastfeed for longer than three months most often cite return to work as their reason for weaning.[11] Canadian breastfeeding practices may continue to improve because many mothers receiving employment insurance can delay their return to work for 12 months postpartum.         Nutritional and developmental issues :   At around four to six months of age, most infants are developmentally ready to handle puréed foods. They are developing the oral motor coordination necessary to accept different food textures. However, they are at risk for choking on chunky food pieces such as nuts, whole grapes and hot dog wheels that require advanced oral motor coordination not achieved before three years of age. “Sucking and chewing are complex behaviours with reflex and learned components. The learned component is conditioned by oral stimulation. If a stimulus is not applied while neural development is occurring, an infant may become a poor eater. There is a relationship between prolonged sucking without solids and poor eating.[7]     While it is ideal for infants to be exclusively breastfed for six months, it is also true that after a certain age, human milk alone cannot supply all of an infant’s nutritional requirements.[6][13] Individual circumstances may make it appropriate for some infants to start complementary feedings as early as four months of age.[13][14] “Age-appropriate intake of calories and micronutrients is important for growth, motor and mental development.[12][13] Delaying the introduction of nutritional solid foods much beyond six months of age puts an infant at risk for iron deficiency anemia and other micronutrient deficiencies.[15] Picciano et al followed older weaning infants (12 to 18 months of age) by collecting data on dietary intake and growth. Many of the study children were ingesting less than the recommended levels of fat (less than 30% of total calories), iron and zinc. Grains, whole milk, dairy products and meats were identified as important sources of iron, vitamin E and zinc.[16] By four to six months of age, iron stores from birth are diminishing, necessitating the introduction of iron-containing foods at six months of age for all infants.[4] Iron supplementation after the first weeks of life or at four months of age for the exclusively breastfed infant has been recommended by some groups.[14] When there is a delay in introduction of iron fortified foods, oral iron supplementation needs to be considered.[14] The process of weaning  While the best method for transitioning from fully breastfeeding to complete nutritional independence is not known, the process should meet the needs of both baby and mother.[20] Physicians may refer mothers to the La Leche League’s website and the Canadian Paediatric Society’s Caring for Kids website (see Resources for parents, below). Weaning can be either natural (infant-led) or planned (mother-led).   Gradual weaning (infant-led weaning) occurs as the infant begins to accept increasing amounts and types of complementary food while still breastfeeding on demand. With gradual weaning, the complete wean usually occurs between two and four years of age.[8] In Western cultures, there remains a relative intolerance to this type of weaning and many mothers who breastfeed their older baby or child become “closet nursers”. Closet nursing takes place privately, at home. This relative secrecy tends to compound erroneous beliefs about appropriate breastfeeding duration.[7]

2012: .                                 and’give_that_baby_some_meat’_new_canadian_guidelines_advise.html    : Megan Ogilvie Health Reporter,   2012 Forget squash and sweet potatoes; steak is now recommended for baby’s first solid food. In a major departure, new Canadian guidelines say parents should be offering their six-month-old infants meat, fish, poultry or meat alternatives two or three times a day.. these iron-rich foods should be the first that babies consume when being introduced to solids.  The recommendations, part of a joint statement quietly released last week by Health Canada, are sure to give some parents pause.  Previously, it was recommended that babies start out eating infant cereals, followed by fruits and vegetables, as they transition to solid foods.

Healthy Pregnancy, Baby & Child  by Sarah TheHealthyHomeEconomist One of most misguided and damaging pieces of advice coming from the vast majority of pediatricians, dieticians, and other “experts” is to give rice cereal as a baby first food around the age of 4-6 months.  This advice is extremely harmful to the long term health of the child, contributing greatly to the epidemic of fat toddlers and the exploding problem of childhood obesity. Rice cereal is never a healthy baby first food. Not only is it an extremely high glycemic food when eaten alone (spikes the blood sugar) but it also contains ample amounts of double sugar (disaccharide) molecules, which are extremely hard for such an immature digestive system to digest. The small intestine of a baby mostly produces only one carbohydrate enzyme, lactase, for digestion of the lactose in milk. It produces little to no amylase, the enzyme needed for grain digestion until around age one.Now, at least one governmental body is waking up to the harmful notion of cereal grains as the “ideal” baby first food.  Health Canada in collaboration with the Canadian Pediatric Society, Dietitians of Canada and Breastfeeding Committee for Canada has issued new guidelines for transitioning a baby to solid food and two of the first weaning foods recommended.  Meat and eggs! While these guidelines are certain to rile vegetarian and vegan groups, the fact is that meat and eggs are indeed perfect weaning foods for a baby. Not only are these animal foods extremely easy to digest compared with cereal grains, but they also supply iron right at the time when a baby’s iron stores from birth start to run low. The inclusion of meat in these baby first food guidelines is in line with the wisdom of Ancestral Cultures which frequently utilized animal foods for weaning.  A traditional first food in African cultures is actually raw liver which the mother would pre-chew in small amounts and then feed to her child. The guidelines specifically note the role that ancient wisdom played in the decision to no longer recommend cereal grains and instead suggest meat: “While meat and fish are traditional first foods for some Aboriginal groups, the common practice in North America has been to introduce infant cereal, vegetables, and fruit as first complementary foods.” Soft boiled egg yolks are also an ideal choice as a baby first food as they supply ample iron as well as choline and arachidonic acid which are both critical for optimal development of the baby’s brain which grows as its most rapid rate the first year of life. Unfortunately, while the suggestion of meat and eggs is a good one, the joint statement from Health Canada also inexplicably includes tofu and legumes which are both a terrible choice as a baby first food.   The starch in legumes would cause the same digestive problems as rice cereal and the endocrine disrupting isoflavones in tofu would be a disaster for baby’s delicate and developing hormonal system. But, let’s give credit where credit is due.  At least meat and eggs are appropriately included on the baby first food list. Good on you Health Canada! Perhaps your neighbor country to the South will wake up and get a clue about how to properly feed babies based on your lead. I’m not holding my breath.     Sarah, The Healthy Home Economist

Int J Obes (Lond). 2005;29 Suppl 2:S8-13.   How much protein is safe?   Agostoni C1, Riva E. ea University of Milan, Italy    Since breastfeeding and human milk seem to prevent, while high dietary proteins in the first 2 yr of life seem to promote later overweight, questions have been raised on the safe levels of proteins in the early years. How much protein (as a percentage of total calorie intake) is safe    RESULTS:   We should move from the figure of 7-8% in the 4-month exclusively breastfed infants up to the maximum acceptable levels of 14% in 12-24-month-old infants. When protein supply represents less than 6% and energy is limited, fully breastfed infants are likely to enter a status of negative nutrient balance. Over the limit of 14% energy from proteins in the 6-24 months period, some mechanisms may begin to operate, leading young children towards an early adiposity rebound and overweight development, beyond any genetic predisposition. Preliminary data seem to indicate a causal role for whole cow’s milk proteins.    CONCLUSION:    We suggest maintaining breastfeeding as long as possible, and, in case human milk is insufficient, to introduce infant formulas, appropriate for age, up to 18-24 months, in order to keep protein intakes in the safe range of 8-12% within a diet adequate in energy and balanced as far as macronutrients.

Health Canada clarifies stance on meat for babies  By Global News with files from Jennifer Tryon Health   September 25, 2012   Health Canada is clearing the air about what kind of solid foods babies should be introduced to.         The clarification comes after some media outlets reported Tuesday that the agency changed its list of recommended first foods for Canadian babies to include meat and meat alternatives – like eggs, tofu and legumes – to help meet nutritional needs.   For the record, Health Canada has not recently modified these guidelines. Since 2004, the agency has recommended iron-rich foods, such as meat and iron-fortified cereal, as a baby’s first solid foods, because iron is crucial to brain development. Most baby cereals now contain iron. There is no scientific evidence suggesting meat is harder on a baby’s digestive system, but parents are reminded to puree the meat with water or breast milk, so it’s easier for the child to swallow.  Registered dietitian Cora Rosenbloom also tells Global National‘s Jennifer Tryon that there’s no reason to withhold eggs. “There’s really no evidence to say that food allergies are going to be more common if eggs are introduced earlier.”       Link to Health Canada’s current recommendations. Follow Jennifer on Twitter: @JenTryon


update 16 May 2016.   to our health:


  introduction:     Cape Town is the world epicenter of epidemics (of poverty – malnutrition- HIV- HAART- TB –Diabetes, asthma-COPD,  and vitamin D  and iodine deficiency). And we  are seeing neuroarthropathy with a vengeance in our township clinics, where a majority of such diabesity or/and HIV patients  admit if questioned to chronic burning cramping legs  and sore muscles/joints if not also consequent insomnia, falls and leg ulcers.

Poor ill patients  seem to  accept it- neuroarthropathy-  as a way of life since it  usually has no visible signs (for anyone to see) till late– poor circulation, ulcers, falls,  arthritis- , and  malnourished diabesity patients  have bigger worries with uncontrolled diabetes and often uncontrolled hypertension despite even insulin; and the HIV+-Tuberculosis patients  have the multiple toxic burdens of antiretroviral and antituberculous therapy.

Because the burden of these diseases as well as stress from corruption and violence  here  is amongst the highest in a major city in the world, affecting especially the poorest and most illiterate labourers, state clinics rarely have budgets to cover the necessary vitamin and mineral supplements the poor  also need on their poverty fast food diet.

Our patients  accept that in return for life extension by designer antimicrobials and antidiabetic/ antihypertensives, all they will get for pain relief  is the combination of physiotherapy, and  designer synthetic palliative drugs- paracetamol, ibrufen /diclofenac, tramadol, amitryptiline, and if lucky some ung meth sal . These factory-synthesised drugs  give little relief,  and no improvement in prognosis since they do not address the proximate causes of the neuroarthropathy,  associated depression and  work incapacity (and later strokes, arthritis, dementia, ulcers, gangrene, chronic lung/heart/ liver/ kidney/visual disease)- respective causes including stress,  infective, drug-induced, tissue glycogenation, the misguided fast-food high carbohydrate-low fat diet  obesity; and manual labour/multiple trauma  wear and tear, and nutritional deficiency including much-needed marine and saturated fats, vitamins and minerals..

The pioneer  work discussed below in Pakistan(Salahuddin ea, Basit ea), Italy (Cipriani ea) and Brazil (Coimbra ea) in using respectively Vit D3 ~700 000iu loading dose and chronically up to 1000iu /kg/day ie average 70 000iu/day, up to 120000iu per day to reverse deadly acute and chronic disease,  is comparable in its simplicity safety and low cost to :

*Semmelweis’ revolutionary discovery  Vienna in the mid 19thC  of hand disinfection to decimate childbirth sepsis deaths; and

*Pauling’s landmark lifesaving escalation of Vit C dose to a gm  per kg per day for all severe disease; and

*the parallel discovery in UK and USA of the crucial role of not just the RDA preventative microdose but also the pharmacological anti-disease benefits of 10 to 100times bigger doses of all the vitamins B complex 1 to 12.

Cipriani ea 2010 seems to be the first report on Pubmed of deliberate oral dosing with  megadose     600 000iu vit D3 ie 10 000iu/kg, albeit only in health to assess bloodlevel response and safety. Since then, as we previously noted, 2 million unit single overdose in nonagenarians in Netherlands  has been shown to do no harm – ie about 40 000iu/kg. .

And as the Australians and others report below, there is no hint of vigorous vitamin or mineral  supplements being stigmatized as performance enhancing for eg sport –  despite vitamin D3 having the distinction of being truly an anabolic ie performance-enhancing (seco)steroid .

There is no point in giving vitamin D by injection (except in those in ICU on prolonged nil per mouth) since it is so well absorbed provided given with fat eg in fishoil/coconut/DMSO oil. And obviously the higher the dose given, the more important to avoid more than a traditional multisupplement pill a day  with low calcium and vitamin A retinol; combined with a low calcium diet (ie low dairy low peanut) ; and supplementing plenty fresh green produce [providing magnesia a few hundred mgs a day, and vitamin K2 perhaps 35mcg/d].

Dr  Mike Holick Prof of Medicine at Boston University interviewed by Dr Joe Mercola Dec 2015 details  the  rationale underpinning the (eg Coimbra) massive vit D3 dose regime for severe immune disease, “as opposed to  plenty of sensible sun exposure for general good health and lower deathrate from all diseases and infections.                 Most melanoma occurs on the least sunexposed skin, with lower melanoma and all other deaths with high sun exposure. Dark days promote melatonin and thus daytime sleepiness and depression- which bright light in the morning for an hour reverses, and elevates b-endorphan, which has many times the painkilling effect of morphines ie opioids, and antidepressants. Vitamin D deficiency more than doubles the risk of all diseases; even 2000iu vit D3 a day in the 1st yr of life in Finland halved the risk of type 1 diabetes– with loss of protection if vit D dose dropped to 400iu/day. Vitamin D/ sunlight reverse leukemic cells. But maximum sunlight exposure nearer the tropics still only elevates 25OHvit D level to a maximum of about 50ng/ml- whereas increasing evidence proves that it may take more than 10 times that bloodlevel to prevent and treat deadly diseases- depending on your genetic vitamin D receptors.

 Even 1000iu/d vit D with bld level about 30ng/ml halves risk of many cancers, with doubling benefit as 25OHvit D level is doubled serially  eg by 10 000iu/d or 50 000iu/d. The kidneys however limit production of the hypercalcemic 1,25vit D, thus avoiding hypercalcemia provided calcium intake is not supplemented by calcium pills, nuts. vit A  etc. The higher the vit D level above 30ng/ml (up to >? 500ng/ml), the more  of our 2000 enzyme systems are activated  to fight all disease without hypercalcemic risks. Hunter gatherers had levels twice as high as dressed housed people today, around 50ng/ml, with increasing anticancer and antiinfection/antiautoimmune benefit from vit D up to safe levels eg 100ng/ml and higher. .”

At this is multiple sclerosis  March 2016 seems to be the latest from neurologist  Dr Cicero Coimbra  via grassroots health. He stresses that to cure degenerative/ autoimmune disease eg  MS, Parkinson’s, SLE, RA, vitiligo ie to overcome genetic Vit D resistance may require vit  D titration up to 1000iu/kg/d ie up to even 40000iu/d to 200000iu/d,
And 25OHvitD blood level to 1000ng  and even 4000ng / ml for a few years to produce cure, before reducing to maintenance vit D3  eg 100iu/kg/day ie ~ 50000iu/wk.
Hypercalcemia and thus calcinosis  is avoided provided PTH level is maintained in the low normal range, not suppressed. Optimal support includes low calcium and  high water diet and  Vit B2, magnes selenium zinc phosphor  supps.


The spectrum of vitamin D3 adult dose thus extends from the

traditional prevention RDA 10iu/kg/ ie~700iu/d against rickets (infants start with 1000iu/d or 25000iu ie ½ scoop/month of standardized vit D3  100iu/mg powder)

to  vigorous 100iu/kg/day (ie 50 000iu scoop /wk ) for common disease prevention/treatment (toddlers 2000iu/d/ ½ scoop/fortnight));

 to  massive  1000iu/kg/day eg 60 000iu/dy for severe autoimmune/immunodeficiency diseases – with mandatory monitoring of levels of calcium, creatinine, 25OHvitD3 and now PTH levels;

to mega 10 000iu/kg eg 650 000iu as a loading dose for eg TB or meningitis or severe trauma—which dose may maintain  25OHvit D3 blood levels in a “sufficiency” range above ~40ng/ml for a month or two, so obviously requires appropriate maintenance dosing.

Imported vitamin D3 100cwt concentrate powder (100iu/mg) per kg from an importing pharmacist costs about R500/kg ie R0.50/100 000iu- far lower than the cost of the highrisk plant xenocalciferol vitamin D2. Thus to the State (excluding packaging and dispensing cost) , the wholesale cost of vit D3 is about R0.15 per 50 000iu per week for maintenance dose; or for 50 000iu/day R10( US $0.6)/month ie retail abt R60pm ie US$5  for megadose therapy; compared to the quoted retail US$20/month in Brazil. .


PERIPHERAL NEUROPATHY:  Already in 2006 Oh-Park ,Sheehan .ea,  Lancet. Albert Einstein College of Medicine, New York wrote about AIDS-ARV neuropathy Charcot neuroarthropathy in the era of HAART.

Young, Dancho ea Tucson, Arizona, wrote 2012,   ” Charcot arthropathy is a devastating joint condition that affects persons with neuropathy. With HIV/AIDS treatments prolonging the lives of these persons, it is likely that long-term sequelae of the disease will become more evident in the near future. Patients with this disease frequently develop peripheral neuropathy. A high index of suspicion must be raised in any patient with peripheral neuropathy of any cause and a red, hot, swollen, painful foot for Charcot neuroarthropathy to give these patients proper treatment to help prevent the devastating effects of Charcot neuropathy with its potential consequences including foot ulceration and amputation. We know only too well the same applies to diabesity, as it did in the days of heavy smoking.”
In 2013 Zubair ea in India showed that diabetics with foot ulcers had vitamin D levels 1/4 of that of matched diabetics without foot ulcers; and “factors which predict the risk of developing ulcer independent of 25(OH)D status were A1c (>6.9%) [OR 4.3), neuropathy [OR 6.9retinopathy [OR 3.3;  nephropathy [OR 3.1) and smoking [OR 4.5]. It is not clear whether the suppression of delayed wound healing seen during 25(OH)D deficiency is a secondary effect or is a direct action of vitamin D on certain components of the immune system.”  

Tiwari, Singh, Swain  ea at Hindu Universities Uttar Pradesh,India have shown elegantly in                          

    *2012 Tiwari ea   Vascular calcification in diabetic foot and its association with calcium homeostasis.      Vascular calcification (VC), long thought to result from passive degeneration, involves a complex process of biomineralization, frequently observed in diabetes and an indicator of diabetic peripheral vascular disease.. ..In  74 patients with diabetic foot ulcer,   Vascular calcification was present in 42% of patients. Significant difference in vitamin D, HbA1C, and eGFR  levels was observed in VC +ve compared to VC -ve.  Severe vitamin D deficiency was more common in VC +ve (51%) compared to in VC -ve (18%). Sub-group analysis showed that the risk of VC was significantly higher (RR = 2.4, P < 0.05) in patients with vitamin D < 10 ng/ml compared to others. .and        

     * Br J Nutr. 2013. Tiwari  ea  Prevalence and severity of vitamin D deficiency in patients with diabetic foot infection.   In Diabetic Patients with and without  infection (n289), 25(OH)D (nmol/l) was significantly lower (16) v. 20ng/ml  P < 0·001) in cases than in controls. Risk of severe vitamin D deficiency (25(OH)D < 10ng/ml) was significantly higher in cases than in controls (OR 4·0, P < 0·0001). Age, duration of diabetes and HbA1c were significantly higher in cases than in controls and therefore adjusted to nullify the effect of these variables, if any, on study outcome. The study concluded that vitamin D deficiency was more prevalent and severe in patients with diabetic foot infection. ;  and the need for vitamin D supplementation in such patients for a better clinical outcome

*.in  Br J Nutr.. 2014 Tiwari ea  show Vitamin D deficiency is associated with inflammatory cytokine concentrations in patients with diabetic foot infection  . Vitamin D is a potent immunomodulator and  a common deficiency  in different population groups including patients with diabetic foot infection.   in 112 diabetic foot infection cases and 109 diabetic controls , cases had significantly higher concentrations of IL-6 (P≤ 0.001), IL-1β and TNF-α (P≤ 0.006) than controls. Risk of severe vitamin D deficiency (25(OH)D <10ng/ml) was significantly higher in cases than in controls (OR 4·0, P < 0·0001). A significant negative correlation was also observed between 25-hydroxyvitamin D concentration and circulating concentrations of IL-1β (r -0.323; P≤ 0.001) and  IL-6 but not between 25-hydroxyvitamin D and TNF-α and IFN-γ concentrations.


This year  2016     Wukich , Sadoskas  ea. University of Pittsburgh & Georgetown USA  in Diabetes Metab Res Rev.  show that (Charcot) neuroarthropathy (CN) of the ankle and hindfoot  is challenging to treat surgically or nonsurgically. Deformities associated with ankle/hindfoot CN are often multiplanar, resulting in  malalignment; and  shortening of the limb often occurs from collapse of the distal tibia, and ankle, with  significant alterations in the biomechanics of the foot. eg predisposing the patient to lateral foot ulceration. Collapse of the talus, secondary to avascular necrosis or neuropathic fracture, further accentuates these deformities and contributes to a limb-length inequality   CONCLUSION:  Surgical reconstruction of ankle and hindfoot CN is associated with a high rate of infectious and noninfectious complications. Preoperative measures that can improve outcomes include assessment of vascular status, optimization of glycemic control, correction of vitamin D deficiency and cessation of tobacco use. 

Now 2016 Basit A,  Malik RA5 ea in  Universities Karachi Pakistan & Manchester UK ,  show that A single intramuscular dose of 600000IU vitamin D in  143 participants with predominantly type 2 diabetes, aged ~ 52.3years, with high Douleur Neuropathique 4 (DN4) score  by  20weeks gave significant increase in 25(OH)D (from 31.7 to 46.2±10.2ng/mL, p<0.0001) and  significant  reduction (p<0.0001)  in positive symptoms on the DN4 , and total pain score (p<0.0001, The Basit – Malik Pakistan-Manchester paper showing great efficacy of 600 000iu vit D3 load dose in peripheral neuropathy diabetics matches the huge 40% improvement benefit of similar loading and monthly vit D3 dose against severe PTB shown by Salahuddin ea in Pakistan in 2013 that we have previously analyzed in this column

ie  apart from smoking; the very low vitamin D levels common in most but especially ill people  associate   with about 5 fold  risks of uncontrolled diabetes, infections,  retinopathy , progressive leg ulcers, peripheral neuropathy  and arthritis- Charcot arthroneuropathy- -and thus  gangrene and amputation; and vigorous safe (supraphysiological) vit D boost reverses the risks. .


And a reminder that a 2015 study in Cape town from Coussens ea Universities in W Cape and Penn State confirm what we see daily in practice, that vitamin D deficiency is endemic  in our population


while as we have pointed out repeatedly, the State here continues to dispense the inferior vitamin D2 (as the fraudulently labeled “strong calciferol”, not disclosing that it is ergocalciferol  D2) despite this plant xenohormone vit D2 having been rejected by world authorities in favour of the much cheaper and effective  human D3 cholecalciferol.



       And now 2016 Cadegiani , Brasilia, Brazil another  landmark massive-vit D dose report ;  Remission of Severe Myasthenia Gravis After Massive-Dose Vitamin D Treatment.Vitamin D has been shown to be related to autoimmune diseases, such as multiple sclerosis and psoriasis. Correlations have been reported between vitamin D levels and prevalence and severity of other autoimmune disorders, and also between vitamin D therapy and disease improvement and remission. This reports a patient with severe and refractory myasthenia gravis (MG) who followed a massive-dose treatment (80,000 to 120,000 IU/day) promoted by a medical center in Brazil  (Coimbra ea) and she had her first complete remission after this type of treatment  for at least 18 months (ie at least 50 million iu) with increased vitamin D serum levels (400 to 700 ng/mL) and major fall in her AChR antibodies – but acute relapse when vit D was inadvertently stopped and her vit D level halved; with again recovery when megadose vit D was resumed  CONCLUSIONS: This case may reinforce the reported correlation between vitamin D level and disease severity and introduces a possible new use for vitamin D as a potential target for treating autoimmune diseases. We recommend large, double-blind, placebo-controlled, randomized studies using high-dose vitamin D treatment for refractory autoimmune diseases to reliably assess this pharmacotherapy target for these diseases


     The above case concurs with previous reported massive dose daily vitamin D3: Finamor , Coimbra ea , Universities of Brazil  2013 A pilot study assessing the effect of prolonged administration of high daily doses of vitamin D on the clinical course of vitiligo and psoriasis. Autoimmunity has been associated with vitamin D deficiency and resistance, with gene polymorphisms related to vitamin D metabolism frequently described. High doses of vitamin D3 may conceivably compensate for inherited resistance to its biological effects. Nine patients with psoriasis and 16 patients with vitiligo received vitamin D3 35,000 IU once daily for six months ie ~7million iu  in association with a low-calcium diet (avoiding dairy products and calcium-enriched foods like oat, rice or soya “milk”) and hydration (minimum 2.5 L daily).. After treatment 25(OH)D3 levels significantly increased (from ~15 to 106-132ng/mL. PTH and 25(OH)D3 serum concentrations correlated inversely. The PASI score significantly improved in all nine patients with psoriasis. Fourteen of 16 patients with vitiligo had 25-75% repigmentation. Serum urea, creatinine and calcium (total and ionized) did not change and urinary calcium excretion increased within the normal range. High-dose vitamin D3 therapy may be effective and safe for vitiligo and psoriasis patients.



     neurologist Prof Dr Cicero Coimbra from Univ Sao Paulo  presents their results since 2002 in over 4000 pts ( 1000 patients each with multiple sclerosis and Parkinson’s diseases), who have been well controlled without other therapies,  provided the dose is high enough- 10 000iu/d up to about 1000iu/kg/d eg >70 000iu/d for the obese, on a low calcium ie low dairy/peanuts diet, high fluid intake and high exercise, to normalize blood calcium,  and titrate  PTH level to  the low normal range. Dr Cicero Coimbra discusses  high dose vitamin D toxicity: PTH level should not be completely suppressed. In their clinic ( of 7 doctors)  for Autoimmune chronic diseases incl MS, RA, SLE, psoriasis, vitiligo, type 1 diabetes ,  they have treated over 4500 pts on this high quality vit D3 high fluid  low calcium diet  protocol, with only 14 cases of reversible vitamin D toxicosis (hypercalcemia) so far detected ie 0.3%. Babies of mothers thus treated in pregnancy  have high psychomotor development. (Vitamin C supplement should not be concurrently excessive to avoid oxalosis). They define success as being disease-free or non-progressive old fixed disabilities- 95% reach full cure. There vit D3 therapy  costs only ~US $20/mo, to optimize the immune system against both infections and autoimmune disease let alone cancer. Optimal dose of vit D3 replacement becomes at least 10 000iu/day for adults especially with autoimmune diseases  due to common vitamin D resistance. Ideally testing baseline blood and urine at baseline and after a few months on at least 10 000iu/d.



     In Effect of a single oral dose of 600,000 IU of cholecalciferol on serum calciotropic hormones in young subjects with vitamin D deficiency:. 2010. Cipriani ,Minisola ea .University of Rome  Italy tested    48 young subjects with vitamin D deficiency with a single oral dose of 600,000 IU of cholecalciferol. The 25(OH)D level was ~15.8ng/ml at baseline and became ~77ng/ml at 3 d (P < 0.001) and ~62 ng/ml at 30 d (P < 0.001). The trends were maintained in a subgroup followed up to 90 d (P < 0.001). Mean serum Ca and P significantly increased compared to baseline, whereas serum Mg decreased at 3 d. CONCLUSIONS: A single oral dose of 600,000 IU of cholecalciferol rapidly enhances 25(OH)D and reduces PTH in young people with vitamin D deficiency.


       Looking at some new alarmist myth refs about vit D3 overdose :

Moderate  ie physiological increase in just vitamin D levels and intake  (from average diet and sunshine and a traditional supplement) within the average population bloodlevel range understandably has modest  benefit- reversing at least rickets-  in an  indoor living clothed population, even  1st world middleaged:  from Wisconsin Univ, Karen Hansen ea’s recent RCT – JAMA 2015- Treatment of Vitamin D Insufficiency in Postmenopausal Women confirmed this, showing little practical benefit shortterm (ie over 12mo) between placebo, and supplemented vit D3  5600iu/wk and 25000 iu a week, (~3600iu/d);  the highest dose perhaps doubling the baseline 20ng/ml  25OH vit D level. ie into the low “adequate” range average around 40ng/ml.

Be aware again that  the same university’s group published in 2014   An Evaluation of High-Dose Vitamin D 2  for Rheumatoid Arthritis Karen Hansen ea that vit D2 ~100 00iu/month  for a year actually worsens patients and lowers vit D3 levels  , so there is no longer excuse for using vitamin D2 supplement when it blocks D3 receptors and lowers blood vit D3.

The inferiority of vit D2 was confirmed in eg    Clinical Trial of Vitamin D2 vs D3 Supplementation in Critically Ill Pediatric Burn Patients.  Gottschlich, Kagan U Cincinnati Ohio 201550  patients  aged 1 to 18yrs with burns  were enrolled. All participants received multivitamin supplementation ,  plus , 100 IU/kg D2, D3, or placebo daily  RESULTS: There were no significant differences in serum vitamin D levels between groups, but >10% of patients had low 25OHD  at discharge, and %deficiency worsened by the 1-year follow up for the placebo (75%), D2 (56%), and D3 (25%) groups. There were no statistical differences in clinical outcomes between treatment groups, although vitamin D supplementation demonstrated clinically relevant decreases in exogenous insulin requirements, sepsis, and scar formationThe high incidence of low serum 25OHvit D levels 1 year following serious thermal injury indicates prolonged compromise. Continued treatment with vitamin D3 beyond the acute phase postburn is recommended to counteract the trajectory of abnormal serum levels and associated morbidity. 

The perception seems to be that up to 40 000iu vit D3 a day, a bld level below abt 150-350ng/ml  is safe, ie unsafe above that. The evidence for such ceiling ie  higher dose harm in fact is lacking since as we have previously discussed here,  healthy people have taken up to 150 000iu a day for decades without evidence of harm…  provided they took adequate fluids, and did not take supplements of calcium, or also take high  vitamin A which notoriously causes acute hypercalcemic toxicity, or have rising calcium levels . .

But note that vit K2 improves absorption of vit D3 CHOLECALCIFEROL , and vit K2 and magnesia improve benefit of vit D3,while protecting against overdose effects ie calcification, stones  and confusion.  Problem in many  toxicity reports is that they used either vit D2 ergocalcif (WHICH BLOCKS THE NEEDED D3) , or used accidental massive overdose (millions of units vit D ) daily for months- or massive INJECTIONS) or combined vit D WITH CALCIUM REPLACEMENT AND/ OR EXCESSIVE VITAMIN  A  – which combinations are  dangerous;  we need magnesium (not calcium  or high vitamin A supplements).

    Vitamin D3: What’s the Latest? recent 2015 reviews from  Univ California and CommonHealth contrast the Instit Medicine IOM (Big-Pharma-sponsored)  conservative target of  vit D3 800 to max 4000iu/d with much evidence that safe optimal D3 dose may be up to 10 000 to 50 000iu/d, and up to  1 000 000iu as an acute eg antiinfection  loading dose; with risk of toxicity only if blood level exceeds 150-500ng/ml. the evidence-based IOM recommendation of optimal blood level 20-40ng/ml, up to 2000iu a day promoted by conservatives like Prof JoAnn Manson, contrasts with the more proactive view of eg Prof Michael Hollick and the Vitamin D Council promoting double that dose as supplements, safely up to 10 000iu/day.


   SO  I continue to take vit D3 ~70 000iu/wk ie ~10 000iu/d,  with vit K2 supp ~700mcg a wk ie 100mcg/dy and a balanced multisupplement incl. magnesia in addition to a multisupplement A-Z, and fish oil and Lugols iodine 15% 2 drops a day; with if I do get a “flu” attack during bad weather, prompt abolition by a few antibiotic doses of topup Lugols iodine 15% a few tsp (ie ~1000mgs iodine),  and vitamin D3 eg 300 000iu, and vitamin C a few tsp orally and by sniffing. .

The problem with many adverse effect reports of vit D3 overdose eg the Dominican Republic Soladek  2011 report Lowe ea below, and Prof Heaney’s response,  is that they failed to even consider the massive associated  overdose of the far more hypercalcemic vitamin A let alone calcium supp reported by most  patients. It becomes apparent that NO calcium supplement should be encouraged on a prudent diet; but instead supplements of  Vit D3, magnesia, vits K2 and C, CoQ10, and fish oil ; in addition to a balanced (A to Z) RDA-based multisupplement for seniors  like eg Solal’s,  Vital’s Multitime, Centrum etc.. with a low calcium diet if massive dose vitamin D3 is indicated as in autoimmune diseases (Coimbra ea).



the Australian Govt  Supplement Overview   has an intriguing report on vit D in sports, with no hint of vit D supplement being a steroid abuse. .        Vitamin D is classified as a fat soluble vitamin which acts functionally as a steroid hormones. There are 2 different isoforms of Vitamin D: D3 (cholecalciferol) which is the important isomer formed in human   skin and D2 (ergocalciferol) which is the plant-derived ie xeno-equivalent. D2 was the first isoform to be characterised   and was first used in Vitamin D supplements and for food fortification. D3 is now considered preferable. D3 is   biologically inert until converted in the liver to 25(OH)D and to 1,25(OH)D in the kidney.  Vitamin D plays an important role in calcium and phosphorous homeostasis (bone health),but more so in  gene expression and cell growth. The recent recognition of Vitamin D receptors in most body tissues indicates a role for Vitamin D in  many aspects of health and function. Vitamin D is now known to be important for optimal muscle function.

         The principal source of circulating vitamin D comes from exposure to ultraviolet B (UVB) radiation from sunlight.   In 2010, the Institute of Medicine issued new Dietary Reference Intakes for Vitamin D, assuming no sunlight exposure: this included a Recommended Dietary Intake of 600 IU/d and an Upper Level intake of 4000 IU/d  ( BUT no evidence has ever been published to support this ceiling intake.

Whereas Vitamin D deficiency can lead to several health issues including increased risk of bone injuries, chronic musculoskeletal pain and viral respiratory tract infections. There is also emerging evidence that supplementing Vitamin D in athletes with sub-optimal Vitamin D levels may   have beneficial effects on athletic performance in particular strength, power, reaction time and balance.

         There is no universally accepted definition of vitamin D deficiency however, the following definitions based on  serum levels of 25(OH) Vitamin D are often cited:

Vitamin D deficiency: serum levels < 20 ng/ml (50 nmol/L);  Vit D insufficiency: serum levels < 30 ng/ml

Vit  D sufficiency: serum levels > 30 ng/ml    Ideal Vit D range*: 30-50ng/ml 

Toxicity: > 150ng/ml, when combined with raised serum calcium

(*Higher status may be preferred for athletes to allow a greater safety margin and to optimize performance;   some agencies working with elite athletes often set their own thresholds for desired Vitamin D concentrations)

Ie they quote no evidence for the 25OH vit D ceiling of 50ng/ml.


Confirmed in

  Owens DJ1, Close GL ea .  UK Universities  . 2015..A systems-based investigation into vitamin D and skeletal muscle repair, regeneration, and hypertrophy. Skeletal muscle is a direct target for  vitamin D. Observational studies suggest that low 25[OH]D correlates with functional recovery of skeletal muscle following eccentric contractions in humans and crush injury in rats. However, a definitive association is yet to be established. To address this gap in knowledge in relation to damage repair, a randomised, placebo-controlled trial was performed in 20 males with insufficient concentrations of serum 25(OH)D (~18ng/ml). Prior to and following 6 wk of supplemental vitamin D3 (4,000 IU/day) or placebo (50 mg of cellulose), participants performed 20 × 10 damaging eccentric contractions of the knee extensors.  Supplemental vitamin D3 increased serum 25(OH)D and improved recovery of peak torque at 48 h and 7 days postexercise. Together, these preliminary data are the first to characterize a role for vitamin D in human skeletal muscle regeneration and suggest that maintaining serum 25(OH)D may be beneficial for enhancing reparative processes and potentially for facilitating subsequent hypertrophy.


2016 Is there an optimal vitamin D status for immunity in athletes and military personnel?  He CS1, Gleeson M ea .Vitamin D is mainly obtained through sunlight ultraviolet-B (UVB) exposure of the skin, with a small amount typically coming from the diet.It is now clear that vitamin D has important roles beyond its well-known effects on calcium and bone homeostasis. Immune cells express the vitamin D receptor, including antigen presenting cells, T cells and B cells, and these cells are all capable of synthesizing the biologically active vitamin D metabolite, 1, 25 hydroxy vitamin D.There has been growing interest in the benefits of supplementing vitamin D as studies report vitamin D insufficiency (circulating 25(OH)D < 50 nmol/L) in more than half of all athletes and military personnel tested during the winter, when skin sunlight UVB is negligible. The overwhelming evidence supports avoiding vitamin D deficiency (25(OH)D< 30 nmol/L)to maintain immunity and prevent upper respiratory illness (URI) in athletes and military personnel.Recent evidence supports an optimal circulating 25(OH)D of 75 nmol/L to prevent URI and enhance innate immunity and mucosal immunity and bring about anti-inflammatory actions through the induction of regulatory T cells and the inhibition of pro-inflammatory cytokine production. We provide practical recommendations for how vitamin D sufficiency can be achieved in most individuals by safe sunlight exposure in the summer and daily 1, 000 IU vitamin D3 supplementation in the winter.


Sarris J1, Ng CH1. Ea, Universities  of Melbourne, & Deakin, Australia;  &  Harvard Boston; 2016  show in   Adjunctive Nutraceuticals for Depression: A Systematic Review and Meta-Analyses.  Adjunctive  standardized pharmaceutical-grade nutrients, known as nutraceuticals, has the potential to modulate several  neurochemical pathways implicated in depression. A systematic search up to 2015 for clinical trials using adjunctive nutrients for depression    RESULTS: Primarily positive results were found for studies testing S-adenosylmethionine (SAMe), methylfolate, omega-3 (primarily EPA or ethyl-EPA), and vitamin D,.  Mixed results were found for zinc, folic acid, vitamin C, and tryptophan. . No major adverse effects were noted in the studies  adjunctive omega-3 versus placebo revealed a significant and moderate to strong effect in favor of omega-3. CONCLUSIONS: Current evidence supports adjunctive use of SAMe, methylfolate, omega-3, and vitamin D with antidepressants to reduce depressive symptoms.

Raina AH1, Bhat FA1 ea ., India.. 2016 Association of Low Levels of Vitamin D with Chronic Stable Angina: A Prospective Case-Control Study.  Coronary artery disease (CAD) is a major cause of death and disability in developed countries. Chronic stable angina is the initial manifestation of CAD in approximately 50% of the patients. Recent evidence suggests that vitamin D is crucial for cardiovascular health. The prevalence of vitamin D deficiency in our region is 83%. METHODS: a prospective case-control study in  100 cases of chronic stable angina compared controls. Vitamin D deficiency was defined as <20 ng/mL, vitamin D insufficiency as 20-30 ng/mL and normal vitamin D level as 31-150 ng/mL.RESULTS: The prevalence of vitamin D deficiency among cases and controls was 75% and 10%, respectively. 13% had normal vitamin D levels (31-150 ng/mL). None had a toxic level of vitamin D. Among the controls, 10% were vitamin D-deficient, 57% had normal vitamin D levels. The mean vitamin level among cases and controls was 15.53 ng/mL and 40.95 ng/mL, respectively, statistically significant (P ≤ 0.0001). Among the cases, we found that an increasing age was inversely related to vitamin D levels (P = 0.027). Low levels may be an independent, potentially modifiable cardiovascular risk factor.

Jetty , Glueck   Kumar  ea . Jewish Hospital Cincinnati, Ohio, USA  2016  show 12mo Safety of 50,000-100,000 Units of Vitamin D3/Week in Hypercholesterolemic  Vitamin D-Deficient,   Patients with Reversible Statin Intolerance. :   Such Vitamin D3 therapy (was safe and effective when given for 12 months to reverse statin intolerance in patients with vitamin D deficiency. Serum vitamin D rarely exceeded 100 ng/mL, never reached toxic levels, and there were no significant change in serum calcium or eGFR As we explore the healing power of higher doses of vitamin D3 at the Riordan Clinic, we have found it prudent to partner the safety and effectiveness of this dynamic duo. For every 5,000–10,000 units of D3 being recommended and tested for, we are recommending 100 mcg of K2 mk7 to be sure and prevent the inappropriate calcification that higher doses of D3 alone could cause.     is a recent book by Jeff T Bowles .

 Newsletter: Gary Null and vitamin D toxicity    2010 by John Cannell, MD     “Warning: If you intend to take massive doses of vitamin D based on this newsletter, which I highly recommend you do not, read the entire newsletter. In addition, accurate determination of side effects of massive doses of vitamin D was not available in the early 1930s, nor was accurate determination of the true amount in each pill possible.    Is 2,000,000 IU/day of vitamin D toxic?   Ask Gary Null, alternative medicine guru and entrepreneur. He took his own supplement, Ultimate Power Meal, for a month and became extremely ill; one batch of Power Meal apparently contained 1,000 times more vitamin D than it should. That is, it contained 2,000,000 IU of vitamin D3 per serving instead of 2,000 IU per serving. Mr. Null became sicker and sicker as he gulped it down.

After suing his own supplier for permanent physical damage, Mr. Null then reported it took 3 months to get the extra vitamin D out of his system and that he is now alive and well. If Mr. Null took it for the full month that he claims, and if his Power Meal contained 2,000,000 IU per dose, Mr. Null consumed 60,000,000 IU in one month. Could he really be fine now with no lasting injuries?  In an attempt to answer that question, I went back to the 1930s and 40s.  Massive doses in the 1930s  The earliest references I could find to enormous doses of vitamin D were in the 1930s. In 1935, Drs. Dreyer and Reed, of the University of Illinois School of Medicine, published their observations on 700 patients treated with “massive” doses of vitamin D for up to two years.1  ….” read on..

Vitamin D Overdose   Dr. Liji Thomas, MD  2016   vitamin D toxicity can occur from high intakes of supplements containing vitamin D, but not from dietary intake. Prolonged sun exposure also does not result in vitamin D toxicity because the previtamin D3 is degraded as the skin heats up, and also because of the formation of various other non-functional forms of vitamin D from the thermally activated compound.   Long term intakes of vitamin D above the upper limit recommended causes symptoms of toxicity. However, the intakes must be higher than about 40,000 IU/day, or the serum level of 25-hydroxy above 500-600 ng/mL, and the patient is usually also taking excessive amounts of calcium as well.

Dietary Supplement–Induced Vitamin D Intoxication  Klontz KC, Acheson DW.  To the Editor 2004:    Vitamin D intoxication that is associated with the consumption of dietary supplements is reported rarely. In 2004, the Food and Drug Administration (FDA) learned of the following case. A 58-year-old woman with diabetes mellitus and rheumatoid arthritis began taking a dietary supplement called Solutions IE Ageless Formula II on January 12, 2004. Fatigue, constipation, back pain, forgetfulness, nausea, and vomiting soon developed. On March 15, 2004, she was hospitalized because her speech was slurred, and a blood glucose reading taken at home was 30 mg per deciliter. On admission, her serum levels were as follows: calcium, more than 3.75 mmol per liter; 25-hydroxyvitamin D, 460ng/ml (normal range, 9-5);; parathyroid hormone, 12 ng per liter (normal range, 10 to 65); and creatinine, 265 μmol per liter.   The patient was treated with intravenous normal saline, furosemide, and pamidronate. On March 19, 2004, while still hospitalized, she was informed by the product distributor of an error in product formulation such that 188,640 IU of vitamin D3/d  had been added to the daily serving size of six capsules instead of the intended 400 IU. IE SHE HAD TAKEN ~12.2MILLION IU OF VIT D3 IN 2 MONTHS. At discharge on March 24, the patient’s serum levels were as follows: calcium, 2.60 mmol per liter; blood urea nitrogen, 10.0 mmol per liter; and creatinine, 221 μmol per liter. The patient died from a cause unknown to us on January 8, 2005.   Laboratory analysis of the product by the FDA, obtained from one of two lots reportedly overfortified with vitamin D3, revealed 186,906 IU of vitamin D3 in each serving size of six capsules, indicating that the patient had consumed roughly 90 times the recommended safe upper limit of 2000 IU per day. Long-term daily vitamin D consumption of more than 40,000 IU (1000 μg) is needed to cause hypercalcemia in healthy persons.2     In March 2004, the product distributor announced that during the previous month it had received three complaints from customers who had been hospitalized for hypercalcemia and vitamin D toxicity

2011 Vitamin D toxicity due to a commonly available “over the counter” remedy from the Dominican Republic. Lowe H1, Bilezikian JP. ea  Columbia Univ, NY..   Hypercalcemia in ambulatory patients is occasionally caused by vitamin D toxicity. We report nine patients presenting to Columbia University Medical Center with hypercalcemia due to a supplement from the Dominican Republic containing massive amounts of vitamin D. All reported recently taking Soladek readily available in the Dominican Republic and in Upper Manhattan. serum calcium values before the ingestion of Soladek were not elevated  According to the manufacturer’s label, each 5-ml vial of Soladek contains vitamin D3 (600,000 IU), vitamin A (120,000 IU), and vitamin E (5 mg). Laboratory analysis by HPLC revealed that the supplement actually contained vitamin D(3) (864,000 IU) and vitamin A (predominantly retinyl palmitate 123,500 IU) per vial.IE 864000 IU VIT D /day FOR UNKNOWN DURATION. a similar case was reported earlier

Comments by Prof Robert P. Heany    Creighton University, Omaha, Nebraska  on Lowe et al:   Hypercalcemia in vitamin D intoxication JCEM        The report by Lowe et al. on vitamin D intoxication from an OTC supplement (1) is instructive and useful. I comment on the authors’  suggested mechanism of hypercalcemia in such cases. The authors propose that the elevated concentration of serum 25- hydroxy-vitamin D [25(OH)D] is the responsible agent, through loose binding to the vitamin D receptor. While my colleagues and I have shown that 25(OH)D can improve calcium absorption (2), I believe there is a simpler explanation for hypercalcemia in vitamin D intoxication, particularly as the reported values of 25(OH)D were not uniformly high in these nine cases. [In fact the patient with the highest serum calcium had actually the lowest value for 25(OH)D.] Instead, as Vieth suggested several years ago in a paper actually referenced by Lowe et al. (3), elevation of free circulating 1,25(OH)2D (calcitriol) is the most parsimonious explanation. This level is not commonly measured, and was not reported in the cases described by Lowe et al. Vieth has estimated the binding capacity of the D-binding protein (DBP) at approximately 4700 nmol/liter, and it is generally recognized that fewer than 5% of its binding sites are occupied at typical cholecalciferol inputs. However, in the face of huge cholecalciferol doses, as in the nine cases described here, it can easily be calculated that most or all of the binding sites on the DBP would be occupied by cholecalciferol itself as well as by 25(OH)D and 24,25(OH)2D, all of which are bound to the DBP more avidly than is calcitriol. Lowe et al. did not measure serum cholecalciferol, but it is virtually certain that its concentration would have been elevated, if for no other reason than that the capacity of the hepatic 25-hydroxylase is limited, and serum cholecalciferol concentration rises steeply for cholecalciferol inputs in excess of the saturation level of the 25-hydroxylase [which typically occurs at serum cholecalciferol levels of about 10 nmol/L and serum 25(OH)D of about 80 nmol/liter (4)].Even if all of the binding sites of the DBP were not continuously occupied by less polar metabolites, high occupancy would shift the equilibrium between the free and the bound calcitriol, so that free calcitriol concentration would likely have been substantially above normal values continuously. The authors speculate as to the origin of the elevated total calcitriol concentrations, given the down-regulation of the renal 1-á- hydroxylase in such cases. 


     2016.Deficient serum 25-hydroxyvitamin D is associated with an atherogenic lipid profile: The Very Large Database of Lipids (VLDL-3) study. Lupton JR1Michos  ea .  Cross-sectional studies have found an association between deficiencies in serum vitamin D, as measured by 25-hydroxyvitamin D (25[OH]D), and an atherogenic lipid profile. These studies have focused on a limited panel of lipid values including low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG).OBJECTIVE: Our study examines the relationship between serum 25(OH)D and an extended lipid panel (Vertical Auto Profile) while controlling for age, gender, glycemic status, and kidney function.METHODS: We used the Very Large Database of Lipids, which includes US adults clinically referred for analysis of their lipid profile from 2009 to 2011. Our study focused on 20,360 subjects who had data for lipids, 25(OH)D, age, gender, hemoglobin A1c, insulin, creatinine, and blood urea nitrogen. Subjects were split into groups based on serum 25(OH)D: deficient (<20 ng/mL), intermediate (≥20-30 ng/mL), and optimal (≥30 ng/mL). The deficient group was compared to the optimal group using multivariable linear regression.RESULTS: In multivariable-adjusted linear regression, deficient serum 25(OH)D was associated with significantly lower serum HDL-C (-5.1%) and higher total cholesterol (+9.4%), non-HDL-C (+15.4%), directly measured LDL-C (+13.5%), intermediate-density lipoprotein cholesterol (+23.7%), very low-density lipoprotein cholesterol (+19.0%), remnant lipoprotein cholesterol (+18.4%), and TG (+26.4%) when compared with the optimal group.CONCLUSION:  Deficient serum 25(OH)D is associated with significantly lower HDL-C and higher directly measured LDL-C, intermediate-density lipoprotein cholesterol, very low-density lipoproteins cholesterol, remnant lipoprotein cholesterol, and TG


  1. Low-Level VitaminD Is strongly Associated with Atrial Fibrillation in Patients with Chronic Heart Failure.Belen E1, , Cetin M2ea. Atrial fibrillation (AF) freuently accompanies heart failure (HF), and causes exacerbation of symptoms and treatment failure in such patients. Vitamin D was recently suggested to be an important mediator of cardiovascular disease, including HF.OBJECTIVES: The aim of this study was to evaluate the relationship between vitamin D deficiency and AF in patients with chronic HF. METHODS: The study included 180 chronic HF patients that were divided into 2 groups based on having sinus rhythm [AF (-) group] or chronic AF [AF (+) group]. Vitamin D status was assessed via measurement of the serum 25-hydroxyvitamin D (25[OH]D) concentration.RESULTS: Mean age of the patients was 66 ± 8.7 years and 53.9% were male. There weren’t any significant differences in age, gender, body mass index, etiology or chronic HF stage between the 2 groups. The vitamin D level in the AF (+) group was significantly lower than in the AF (-) group (11.05 ng/mL vs. 20 ng/mL, p < 0.001) The left atrium to body surface area ratio (LA/BSA) was significantly higher in the AF (+) group (45.03 mm/m2 vs. 42.05 mm/m2, p < 0.01). Independent predictors (based on multiple regression) of AF were vitamin D level (OR = 0.854, 95% CI: 0.805-0.907, p < 0.001) and LA/BSA ratio (OR = 1.077, 95% CI: 1.003-1.156, p < 0.05). The optimal vitamin D cut-off value for the prediction of AF was 16.50 ng/mL, with a sensitivity of 76.0% and specificity of 65.5% (AUC = 0.75, 95% CI: 0.67-0.82).


Vitam Horm. 2016;100:255-71. doi: 10.1016/bs.vh.2015.10.001. Epub 2015 Nov 30. Molecular Approaches for Optimizing Vitamin D Supplementation.   Carlberg C1.Vitamin D can be synthesized endogenously within UV-B exposed human skin. However, avoidance of sufficient sun exposure via predominant indoor activities, textile coverage, dark skin at higher latitude, and seasonal variations makes the intake of vitamin D fortified food or direct vitamin D supplementation necessary. Vitamin D has via its biologically most active metabolite 1α,25-dihydroxyvitamin D and the transcription factor vitamin D receptor a direct effect on the epigenome and transcriptome of many human tissues and cell types. Different interpretation of results from observational studies with vitamin D led to some dispute in the field on the desired optimal vitamin D level and the recommended daily supplementation. This chapter will provide background on the epigenome- and transcriptome-wide functions of vitamin D and will outline how this insight may be used for determining of the optimal vitamin D status of human individuals. These reflections will lead to the concept of a personal vitamin D index that may be a better guideline for an optimized vitamin D supplementation than population-based recommendations.


  1. Comparative efficacy of vitamin D status in reducing the risk of bladder cancer: A systematic review and network meta-analysis.Zhao, , Huang J3. The optimal concentration of individual vitamin D intake for preventing bladder cancer has not, to our knowledge, been defined. To evaluate the comparative efficacy of different serum 25-hydroxyvitamin D concentrations in preventing bladder cancer, we conducted a systematic search of the literature published up to April 2015.METHODS: We applied a pairwise meta-analysis to estimate direct evidence from intervention-control studies and a network meta-analysis within a Bayesian framework to combine direct and indirect evidence. Moreover, a dose-response curve was utilized to predict the optimal median serum 25-hydroxyvitamin D concentration based on the odds ratio (OR) for each quintile concentration.: Seven studies of a total of 90757 participants, including 2509 bladder cancer patients, were included. Two prospective cohort studies with 57 591 participants and 494 bladder cancer patients, and five case-control studies with 33 166 participants and 2264 bladder cancer patients. From the network meta-analysis, we observed that sufficient serum 25-hydroxyvitamin D concentrations (>75 nmol/L) were superior to all other 25-hydroxyvitamin D concentrations in decreasing the risk of bladder cancer: OR = 0.68 and 95% credible interval (CrI) 0.52 to 0.87 compared with severely deficient concentrations (<25 nmol/L); OR = 0.65 and 95% CrI 0.49 to 0.86 compared with moderately deficient concentrations (25-37.5 nmol/L); OR = 0.61 and 95% CrI 0.47 to 0.80 compared with slightly deficient concentrations (37.5-50 nmol/L); and OR = 0.65 and 95% CrI 0.48 to 0.85 compared with insufficient concentrations (50-75 nmol/L). In addition, we noted a roughly inverse correlation between bladder cancer risk and 25-hydroxyvitamin D concentrations (R(2) = 0.98, P = 0.007).CONCLUSIONS:   Ensuring sufficient serum 25-hydroxyvitamin D concentrations might play an important role in decreasing the risk of bladder cancer. The serum 25-hydroxyvitamin D concentration ≥30ng/ml  was associated with a 60% lower risk of bladder cancer incidence.

the Ides of March 2016:  Where have we been the past 5 years in ignoring the crucial role of K2 supplement  with vit D3? against cancer, fractures, infections, vascular disease and diabetes , 

      like the crucial role of Lugols iodine + selenium, and magnesium (not calcium), coQ10, and animal, marine and coconut ie saturated fat oil- supplement  for all chronic disease prevention?

     Considering that our western processed food staple diet, and the diet of the poor majority everywhere,  is increasingly deficient especially in these nutrients,  with by profit-motivated industrial design  disease-promoting cholesterol-depletion, refined sugars, transfats, antibiotics, hormones,  and noxious at-any-dose elements from fluorine and aluminium upwards.


I see I was  promoting K2 in my emails 4 years ago,  and since 2009, on my Healthspanlife blog  ie in  my lectures  and thus in my healthspanlife blends .

     But  I indeed don’t seem to have published a review of K2 on my blog- till now!
– and there are so many refs out there since the first K2 mention on Pubmed in 1946,
and its first Pubmed  human supplement mention in 2002  Improvement with maternal supplement of vitamin K2  of vitamin K status of breastfeeding infants  (MK40).  Nishiguchi T, Terao T ea.   Semin Thromb Hemost. 2002 : 28533-8.

Unlike the Big Pharma-Disease-Industry- controlled denialists of conservative safe  natural phamacological vitamin therapy  like the   Linus Pauling Institute   and   Wikipedia       ,

the vitamin  K2 Polish scientist Dr Katarzyna Maresz PhD     2015 writes (see abstract below)  Proper Calcium Use: Vitamin K2 as a Promoter of Bone and Cardiovascular Health.  Maresz K1. International Science and Health Foundation Krakow, Poland    Inadequate calcium intake can lead to decreased bone mineral density, thus  increase the risk of bone fractures. Recent scientific evidence, however, suggests that elevated consumption of calcium supplements may raise the risk for heart disease and can be connected with accelerated deposit of calcium in blood-vessel walls and soft tissues. In contrast, vitamin K2 is associated with the inhibition of arterial calcification and arterial stiffening. Dosing of K2 was supported by a population-based study with 16 000 healthy women aged 49 to 70 years drawn from EPIC’s cohort population. After 8 years ,it showed that a high intake of natural vitamin K2 (ie, not synthetic K2, but not of vitamin K1) was associated with protection against cardiovascular events. For every 10 mcg of dietary vitamin K2 consumed (in the forms of menaquinone 7 (MK-7), menaquinone 8 (MK-8), and menaquinone 9 (MK-9), the risk of coronary heart disease was reduced by 9%. … The researchers found that a daily dose of 180 mcg was enough to improve bone mineral density, bone strength, and cardiovascular health. They also showed that achieving a clinically relevant improvement required at least 2 years of supplementation.
      While vit D3  cholecalciferol soltriol  was the multiprevention megavitamin   of the past decade, and CoQ10 the decade before that, catching up with the protean benefits of increasingly diet- deficient vitamins published (350 000 Pubmed citations) the past century, and of vitamin K since 1936, and K2 since 1946,
vit K2 is the most publicized ie advancing megavit of the current decade:
Adequate intake ie ~45 to ~150mcg/d is crucial with magnesium, boron etc to balance vigorous  vit D3 supplement,
for both bone, immune/cancer, and cardiovascular health.
Thus even just ~55mcg/d K2 supplement HALVES the risk of cardiovascular disease – very important in overweight/stressed/ aging people. 

BUT The authorities quoted have assessed safety and optimal longterm effective doses of vitamin K3 and vitamin D3 IN ISOLATION  for major prevention. However, we know that optimal nutrition is balanced nutrition, not one or two nutrient is superdose with an average fastfood mediocre diet. 

This finally convinces me to add vit K2 ~ 35 to 100mcg/day ie 200 to 700mcg/wk  to my own  vit D3 supplements. at a trivial bulk wholesale cost of  ~10mg/d 1% K2 ie ~R0.1/day or R14 – ( US$1)   bag  per 40 weeks of vit D3 @ 50 000iu vit D3 twice a month.

Like  Mercola 2010,             Byron Richards already in 2010 wrote a major review promoting K2 multipurpose:

As a recent BBC review   details,    “Vitamin K1 has a relatively short half-life and is rapidly cleared from the blood  by the liver within eight hours. In comparison vitamin K2 has a longer half-life of up to 72 hours, meaning it remains biologically active in the body for longer.   Vitamin K2 is also absorbed better by the body, and is linked to cardiovascular health. It directs calcium to the bones, and prevents it from being deposited where it shouldn’t be, for example arteries and organs, where it can cause harm.

The Kansas Riordan Clinic  promotes the Superhuman Duo  of D3+K:   they point out that ” Because an accurate LD50 for vit D in humans has never been determined (thank God!) most researchers use the LD50 for dogs as an estimate for humans, using a hypothetical human subject weighing  50kg, 110 pounds: in order to reach the LD50 dose, that subject would need to consume over 3,500 of the 50,000 IU D3 caps in a 24 hour period (146 capsules an hour,  total  175million iu) in order to have a 50% chance of dying. By conscientiously using vitamin K2 in conjunction with D3, this issue of “metastatic calcium” is thoroughly avoided.  Finally, like vitamin D3, strong evidence demonstrates vitamin K’s amazing ability to reduce cancer risk. For example, men taking vitamin K2 mk7 (a naturally occurring long acting form of K2) at 45 mcg a day can statistically reduce their risk of prostate cancer by 60%! That is just one of many cancer risks that are reduced significantly by regular K2 ingestion.      As we explore the healing power of higher doses of vitamin D3 at the Riordan Clinic, we have found it prudent to partner the safety and effectiveness of this dynamic duo. For every 5,000–10,000 units of D3 being recommended and tested for, we are recommending 100 mcg of K2 mk7 to be sure and prevent the inappropriate calcification that higher doses of D3 alone could cause.

            For the safety of vigorous dose of vitamin D3, the masses of D3  evidence we assembled by August 2015   is that 2million units as a single oral dose does no harm to nonagenarians, nor has over 100 000iu a day for 28 years ie over a billion  iu  in middle-aged women.  

 In 2015,    Like *Joe Leech                                          and             *Hogne Vik   ,                                                    *Angela Pifer nutritionist notes the essensiality of balancing vit D3 with K2  “Vitamin D3 should never be taken alone. Always take a combination Vitamin D3/ Vitamin K2 liquid emulsion, at night for best absorption. This is because vitamin D3 improves calcium absorption across the GI tract and vitamin K2 is the cofactor needed to transfer calcium into your bones, and not your arteries.   (Eur J Clin Nutr. 2016 Feb 24. doi: 10.1038/ejcn.2016.3. Steady-state vitamin K2 (menaquinone-7) plasma concentrations after intake of dairy products and soft gel capsules.   KnapenVermeer  ea . Maastricht University, Netherlands.   In a previous human intervention study, we observed an improved vitamin K status after 8 weeks of intake of a yogurt  fortified with vitamin K2 (as menaquinone-7, MK-7) and vitamins C and D3, magnesium and polyunsaturated fatty acids. It was hypothesized that the added nutrients contributed to this improvement. Here we report on a study in which we compared the fasting plasma concentrations of MK-7 from (a) yogurt enriched with MK-7, vitamins D3 and C, magnesium, n-3 poly unsaturated fatty acids (n-3 PUFA) and fish oil (yogurt Kplus), (b) yogurt fortified with MK-7 only (yogurt K) and (c) soft gel capsules containing only MK-7, For 42 days in healthy men and postmenopausal women between 45 and 65 years of age daily consumed either yogurt K, yogurt Kplus or capsules.  RESULTS: The increase in plasma MK-7 with the yogurt Kplus product was more pronounced than the increase in MK-7 with the capsules, reflecting vitamin K status improvement. No significant differences in fasting plasma concentrations of various biomarkers between the yogurts were found.   CONCLUSIONS: Dairy matrix and nutrient composition may affect MK-7 delivery and improvement of vitamin K status. Yogurt fortified with MK-7 is a suitable matrix to improve the nutritional status of the fat-soluble vitamins.)

Some recent of the other 5000 K2 refs on Pubmed, apart from the abundant reviews by Garry Gordon, Joe Mercola, Mike Howard, Jeff Dach, Townsend letter, ea  , are

Integr Med (Encinitas). 2015;14; 34-9.  Proper Calcium Use: Vitamin K2 as a Promoter of Bone and Cardiovascular Health.  Maresz K1. International Science and Health Foundation Krakow, Poland    Inadequate calcium intake can lead to decreased bone mineral density, thus  increase the risk of bone fractures. Supplemental calcium promotes bone mineral density and strength and can prevent osteoporosis. Recent scientific evidence, however, suggests that elevated consumption of calcium supplements may raise the risk for heart disease and can be connected with accelerated deposit of calcium in blood-vessel walls and soft tissues. In contrast, vitamin K2 is associated with the inhibition of arterial calcification and arterial stiffening. An adequate intake of vitamin K2 has been shown to lower the risk of vascular damage because it activates matrix GLA protein (MGP), which inhibits the deposits of calcium on the walls. Vitamin K, particularly as vitamin K2, is nearly nonexistent in junk food, with little being consumed even in a healthy Western diet. Vitamin K deficiency results in inadequate activation of MGP, which greatly impairs the process of calcium removal and increases the risk of calcification of the blood vessels. An increased intake of vitamin K2 could be a means of lowering calcium-associated health risks.    “  Calcium ConcernsIf at least 32 mcg/d of vitamin K2 is present in the diet, then the risks for blood-vessel calcification and heart problems are significantly lowered, the elasticity of the vessel wall is increased. Moreover, the beneficial effects of vitamins D and K on the elastic properties of the vessel wall in postmenopausal women has been seen in clinical trials. If less vitamin K2 is present in the diet, then cardiovascular problems may arise. Dosing of K2 was supported by a population-based study with 16 000 healthy women aged 49 to 70 years drawn from EPIC’s cohort population. After 8 years ,it showed that a high intake of natural vitamin K2 (ie, not synthetic K2, but not of vitamin K1) was associated with protection against cardiovascular events. For every 10 mcg of dietary vitamin K2 consumed (in the forms of menaquinone 7 (MK-7), menaquinone 8 (MK-8), and menaquinone 9 (MK-9), the risk of coronary heart disease was reduced by 9%. A study on 564 postmenopausal women also revealed that intake of vitamin K2 was associated with decreased coronary calcification, whereas intake of vitamin K1 was not.  ”  A recent, double-blind, randomized clinical trial investigated the effects of supplemental MK-7, MenaQ7 (NattoPharma ASA, Hovik, Norway) for a 3-year period in a group of 244 postmenopausal Dutch women. The researchers found that a daily dose of 180 mcg was enough to improve bone mineral density, bone strength, and cardiovascular health. They also showed that achieving a clinically relevant improvement required at least 2 years of supplementation.It showed a significant improvement in cardiovascular health as measured by ultrasound and pulse-wave velocity, which are recognized as standard measurements for cardiovascular health. In that trial, carotid artery distensibility was significantly improved for a 3-year period as compared with that of a placebo group. Also, pulse-wave velocity showed a statistically significantly decrease after 3 years for the vitamin K2 (MK-7) group, but not for the placebo group, demonstrating an increase in the elasticity and reduction in age-related arterial stiffening.” 

*     Nutrients. 2015 Oct ;7;8905-15.  Menaquinone-7 Supplementation to Reduce Vascular Calcification in Patients with Coronary Artery Disease: Rationale and Study Protocol (VitaK-CAC Trial).Vossen, Kroon ea  Coronary artery calcification (CAC) develops early in the pathogenesis of atherosclerosis and is a strong and independent predictor of cardiovascular disease (CVD). Arterial calcification is caused by an imbalance in calcification regulatory mechanisms. An important inhibitor of calcification is vitamin K-dependent matrix Gla protein (MGP). Both preclinical and clinical studies have shown that inhibition of the vitamin K-cycle by vitamin K antagonists (VKA) results in elevated uncarboxylated MGP (ucMGP) and subsequently in extensive arterial calcification. This led us to hypothesize that vitamin K supplementation may slow down the progression of calcification. To test this, we designed the VitaK-CAC trial which analyses effects of menaquinone-7 (MK-7) supplementation on progression of CAC. The trial is a double-blind, randomized, placebo-controlled trial including patients with coronary artery disease (CAD). Patients with a baseline Agatston CAC-score between 50 and 400 will be randomized to an intervention-group (360 microgram MK-7) or a placebo group. Treatment duration will be 24 months.  We hypothesize that treatment with MK-7 will slow down or arrest the progression of CAC and that this trial may lead to a treatment option for vascular calcification and subsequent CVD.
Ugeskr Laeger. 2015 Aug;177:V12140700. Vitamin K2 influences several diseases]. Hey H1, Brasen CL. Lillebælt, Kabbeltoft, In this paper we discuss the evidence of vitamin K2 deficiency which is a factor in several chronic diseases like diabetes, osteoporosis, cancer, inflammatory and cardiovascular diseases. This deficiency is very common in the mentioned diseases although it is rarely treated by clinicians. Randomized clinical trials have shown that patients witr can benefit from vitamin K2 supplement. Further studies are needed to ascertain the effect of vitamin K2 supplement in patients with diabetes and inflammatory bowel diseases.
*           Oman Med J. 2014;29;172-7. Vitamin k dependent proteins and the role of vitamin k2 in the modulation of vascular calcification: a review.  El Asmar, Arbid  ea, American University of Beirut, Lebanon. Vascular calcification, a cause of cardiovascular morbidity and mortality, is an actively regulated process involving vitamin K dependent proteins (VKDPs) among others. Vitamin K is an essential micronutrient, present in plants and animal fermented products that plays an important role as a cofactor for the post-translational γ-carboxylation of glutamic acid residues in a number of proteins. These VKDPs require carboxylation to become biologically active, and they have been identified as having an active role in vascular cell migration, angiogenesis and vascular calcification. calcification.
*             Dermatoendocrinol. 2015 Jan;6e968490. Vitamin K: an old vitamin in a new perspective.   Gröber U, Reichrath J, Holick MF, Kisters Essen, Germany.&  Boston, MA USA. The topic of “Vitamin K” is currently booming on the health products market. Current research increasingly indicates that the antihaemorrhagic vitamin has a considerable benefit in the prevention and treatment of bone and vascular disease. Vitamin K1 (phylloquinone) is more abundant in foods but less bioactive than the vitamin K2 menaquinones (especially MK-7, menaquinone-7). Vitamin K compounds undergo oxidation-reduction cycling within the endoplasmic reticulum membrane, donating electrons to activate specific proteins via enzymatic gamma-carboxylation of glutamate groups before being enzymatically reduced. Along with coagulation factors (II, VII, IX, X, and prothrombin), protein C and protein S, osteocalcin (OC), matrix Gla protein (MGP), periostin, Gas6, and other vitamin K-dependent (VKD) proteins support calcium homeostasis, inhibit vessel wall calcification, support endothelial integrity, facilitate bone mineralization, are involved in tissue renewal and cell growth control, and have numerous other effects.

4 August 2015 VITAMIN D: FOR INDOOR TYPES, HOW MUCH eg 50 000iu/d IS ENOUGH, AND SAFE? & 2million iu loading dose is not toxic for adults. Especially for infants, acute illness- ICU, INFECTIONS:


see previous vit D updates:  at  23 Mar 2015 womens’ day: the crucial role of vitamin D as HRT in reducing all major diseases . Salute Dr Walter Stumpf



PREFACE WARNING: nb black italics are abbreviated quotes; for the link click on blue italics  eg McKenna ea.            NB conclusions depend, are based on, apparently reliable formal  randomized controlled RCTs trials  and team experiences, (but RCTs, metaanalysis, reviews and case reports   are also notoriously  vulnerable to vested interests of authors and sponsors, statistical errors, omission of inconvenient results, even subtle blatant fraud and fabrication;  to small numbers, heuristics and bias   – confusing causality, type 2 statistical errors ie sheer random chance; per  eg per Nobel prizewinner – the American  Daniel Kahneman : Thinking, Fast and Slow: New York 2011; the Briton   Oliver  Gillie 2014; Vit D, Sunlight, mortality, causality  and The Scots   Paradox, the Swiss Paradox;  the Flu, MERS, AIDs-TB-ebola epidemics: Can Sun Exposure, or  Lack of it, Explain Major Paradoxes in Epidemiology;;biography); the Semmelweis Paradox;  the current epidemics in Central and South Africa, Saudi Arabia, South Korea, cities & refugee camp  ghettos, 1918-19 et seq;  the German Gerd Gigenzer

4 August 2015 update: why do new trials/ reviews keep referring to mediocre dose vitamin D3 as high dose?    Karen Hansen’s  Univ Wisconsin  trial compared placebo, with baseline  vit D3  24000iu /month and as high dose 5 fold more ie  124000iu/month- finding no significant benefits. BUT  124000iu/month is still only about 4000iu/day, which on average increases 25OH Vit D3 only by about 40ng/ml. This is hardly high dose when vigorous levels are at least double this ie close to 100ng/ml; and vigorous safe dose long term is around 50 000iu/day ; with up to 150 000iu/day, up to above 250ng/ml blood level,  having been taken for decades, or single dose of 2million units,  without toxicity... Of course safety depends on adequate water, magnesium and vit K2 intake, and not adding  calcium supplements since average city diet is low in magnesium, iodine  and vit K2, not calcium or toxic fluoride or bromine. 

                      2015 Aug 3  JAMA Intern Med. . Treatment of Vitamin D Insufficiency in Postmenopausal Women: A Randomized Clinical Trial. Hansen, Marvdashti ea . Experts debate optimal 25-hydroxyvitamin D (25[OH]D) levels for musculoskeletal health. Objective  randomized, double-blind, placebo-controlled clinical trial was conducted at a single center in Univ Wisconsin   from  2010, completed 2014. A total of 230 postmenopausal women 75 years or younger with baseline 25(OH)D levels of 14 through 27 ng/mL and no osteoporosis were studied.  Interventions: Three arms included daily white and twice monthly yellow placebo (n=76), daily 800 IU vitamin D3 and twice monthly yellow placebo (n=75), and daily white placebo and twice monthly 50,000 IU vitamin D3 (n=79). The high-dose vitamin D regimen achieved and maintained 25(OH)D levels ≥30 ng/mL. Main  Results:  After baseline absorption was controlled for, calcium absorption increased 1% (10 mg/d) in the high-dose arm but decreased 2% in the low-dose arm (P = .005 vs high-dose arm) and 1.3% in the placebo arm (P = .03 vs high-dose arm). We found no between-arm changes in bone mineral density, trabecular bone score, muscle mass, and Timed Up and Go or five sit-to-stand test scores.  High-dose cholecalciferol therapy increased calcium absorption, but the effect was small and did not translate into beneficial effects on bone mineral density, muscle function, muscle mass, or falls. We found no data to support experts’ recommendations to maintain serum 25(OH)D levels of 30 ng/mL or higher in postmenopausal women. Instead, we found that low- and high-dose cholecalciferol were equivalent to placebo in their effects on bone and muscle outcomes in this cohort of postmenopausal women with 25(OH)D levels less than 30 ng/mL.
26 JULY 2015 UPDATE:
1,   Calcium supplements are no longer recommended for adults:  they promote vascular calcification and worse.

J Intern Med. 2015 Jul 14. Calcium supplements: benefits and risks. Reid , Bristow , Bolland .University of Auckland, New Zealand. Calcium is an essential element in the diet, but Calcium Study demonstrates no relationship between dietary calcium intake and rate of bone loss over 5 years in healthy older women with intakes varying from <400 to >1500 mg day. Thus, supplements are not needed within this range of intakes to compensate for a demonstrable dietary deficiency, but might be acting as weak anti-resorptive agents via effects on parathyroid hormone and calcitonin.  As a result, anti-fracture efficacy remains unproven, with no evidence to support hip fracture prevention (other than in a cohort with severe vitamin D deficiency) and total fracture numbers are reduced by 0-10%, depending on which meta-analysis is considered. Five recent large studies have failed to demonstrate fracture prevention in their primary analyses. This must be balanced against an increase in gastrointestinal side effects (including a doubling of hospital admissions for these problems), a 17% increase in renal calculi and a 20-40% increase in risk of myocardial infarction. Each of these adverse events alone neutralizes any possible benefit in fracture prevention. Thus, calcium supplements appear to have a negative risk-benefit effect, and so should not be used routinely in the prevention or treatment of osteoporosis.
        Rather it is vits D3, C,  K2 ;  and magnesia supps that are recommended for multisystem benefits-  magnesia especially for prevention of common renal stones- since the classic paper from Harvard  Am J Clin Nutr. 1967;20:393-9. Effect of daily 200mg MgO   and 10mg vitamin B6   administration to patients with recurring calcium oxalate kidney stones. Gershoff & Prien.
2. for preventing eg calcium stones and mortality etc, vit D3 in high enough dose to switch off hyperparathyroidism. eg Clin Nutr. 2015 Mar 24.    Vitamin D3 supplementation and body composition in persons with obesity and type 2 diabetes in the UAE Sadiya , Abusnana ea The study was executed in 3 phases in two arms vitamin D arm (n = 45) and placebo arm (n = 42); in Phase 1 the vitamin D arm received 6000 IU vitamin D3/day (3 months) followed by Phase 2 with 3000 IU vitamin D3/day. During follow up (phase 3) both the arms were un-blinded and supplemented with 2200 IU vitamin D3/day for another 6 months . On supplementation no significant changes in anthropometric dimensions was observed. S-25(OH) D peaked in phase 1 (77.2 ± 30.1 vs 28.5 ± 9.2, p = 0.003) followed by a decrease in phase 2 (62.3 ± 20.8, p = 0.006) paralleled by a decrease in parathyroid hormone in phase 2 (5.9 ± 2.4 vs 4.5 ± 1.8, p < 0.01) compared to baseline in vitamin D group. Supplementation was safe, improved s- 25 (OH)D also reducing the incidence of eucalcemic parathyroid hormone elevation.
      Crit Care Med. 2015 Jul 16.   A Randomized Study of a Single Dose of Intramuscular Cholecalciferol in Critically Ill Adults.  Nair, Center ea   Univ Sydney & Brisbane, Australia.  LMU, Munich, Germany.    To determine the effect of two doses of intramuscular cholecalciferol on serial serum 25-hydroxy-vitamin-D levels and on pharmacodynamics endpoints.Prospective randomized interventional study.
Fifty critically ill adults with the systemic inflammatory response syndrome.Patients were randomly allocated to receive a single intramuscular dose of either 150,000 IU (0.15 mU) or 300,000 IU (0.3 mU). Secondary hyperparathyroidism was manifested in 28% of patients at baseline. Parathyroid hormone levels decreased over the study period with patients achieving vitamin D sufficiency at day 7 having significantly lower parathyroid hormone levels (p < 0.01).  Although in-hospital mortality rate did not differ between the groups, patients who did not mount a parathyroid hormone response to vitamin D deficiency had a higher mortality (35% vs 12%; p = 0.05). No significant adverse effects were observed.
     3  universal vitamin D3 deficiency:   our local population, as in virtually all populations worldwide who no longer work and live bare in the sun and eat plenty of raw fish(eg unfiltered cod liver) (oil) have average blood 25 OH vit D levels at or below 20ng/ml, whereas it is  incontestable that all diseases decline steadily as this marker vit D3 level is elevated by sunshine to the probable maximum natural achievable level around 40ng/ml- and with vigorous supplements eg 50 000iu/wk  up to around 80ng/ml, but in sickness to around >100ng/ml.
 4.    But the vit D overdose literature shows that while the highest adult vit D3 doses that have been prescribed are about 640 000iu as monthly dose (Salhuddin N ea , Karachi Pakistan 2013- with 40% improvement in TB recovery after only 2 months compared to TB pts given antiTB Rx alone), and 40 000iu/day in South America for months  for serious pemphigus and albinism. The Pakistan Endocrine Society is a pioneer professional group in endorsing vigorous vit D3 dosing.
But the threshold for toxicity- hypervitaminosis D– seems to be above 2million units single dose in nonagenarians (Netherlands 2 pts) or 88 000iu/day longterm (Canada); and blood 25OHvit D above 250 – 500ng/ml. one 70yr old women was reported to present with Hypervit D only after 10 years  taking 100 000ium/d ie over ~300million iu.. Another women was reportedly  unharmed after 5  times that ie @ 150 000iu/day ,  1.5 billion vit D2 iu over 28yrs –Stephenson & Peiris 2009.
small Subcontinent people–  Pakistanis, Indians etc may be more prone to overdose with vit D, often from massive doses given by injection weekly ie no chance of reducing absorption plateauing as oral overdose increases, as normally happens.
VIT D2 VS D3:  note that as one of the most backward Govts in the world, RSA   STATE  authorities- at least in W Cape eg state hospitals and  day hospitals- still distribute and promote vit D2 for osteoporosis, altho these tabs falsely labelled Strong Calciferol are in fact fraudulently labelled,  only their manufacturer website Lennons-Aspen reveals that they are in fact ergocalciferol vit D2, which experts have long condemned as only about 1/4 the strength of vit D3, and which D2 in two studies actually worsens not improves rheumatoid arthritis. This in contrast to the all-disease beneficial  anabolic steroid vit D3 which wholesales in bulk at around R200/kg.a different independent website eg does reveal that Strong calciferol is in fact D2, but not that it is a xenohormone manufactured only by yeasts, not animals; and that it elevates 25OH vit D2– not D3- in our blood, thus blocking both our D3 receptors and formation.   Wiki does detail that it is made only by lichen, mushrooms and alphalpha- but not by any animals.
Already in 2006 Houghton and Veith (Univ Toronto Canada) published The Case Against vitamin D2.. Vitamin D2, or ergocalciferol, should not be regarded as a nutrient suitable for supplementation or fortification… no successful clinical trials to date have shown that vitamin D2 prevents fractures..The poorer stability of and greater impurities in vitamin D2 powders may also lead to a higher risk of toxicity than that associated with the vitamin D3 metabolites. However, it is more likely that the weaker affinity of vitamin D2 metabolites to DBP produces higher and more biologically available proportions of free 25(OH)D2 and 1,25-(OH)2D2 and may thus be responsible for the greater risk of D2 toxicity .  Taken together, the most plausible explanations for the greater bioefficacy of vitamin D3 are conceivably due to the higher affinities of vitamin D3 and its metabolites than vitamin D2 for hepatic 25-hydroxylase, DBP, and VDR and because vitamin D3 is not directly metabolized to 24(OH)D as is vitamin D2.”D2may be safe in mega-overdose, but this  2009 abstract from a Tennessee Veterans’ Admin unit  begs the question of whether the D2 tablets were indeed genuine vitamin D, of any benefit to the patient? who apparently consumed over a billion iu of vit D2 in  half a lifetime – at least 20 times the aggressive dose of 50 000iu/week. :

South Med J. 2009 Jul;102:765-8..  The lack of vitamin D toxicity with megadose of daily ergocalciferol (D2) therapy: a case report and literature review.   Stephenson & Peiris .The maximum daily dose of vitamin D currently recommended is 2000 IU. Ergocalciferol (D2) 50,000 IU orally weekly for 8-12 weeks is often used to treat vitamin D deficient patients (25(OH) vitamin D <20 ng/mL). The lack of vitamin D toxicity after massive doses of ergocalciferol has yet to be reported in the literature. We report a case of a 56-year-old woman who received supratherapeutic doses of ergocalciferol (150,000 IU orally daily) for 28 years without toxicity. We discuss the possible mechanisms which may account for a lack of toxicity despite intake of massive daily doses of ergocalciferol in this patient.
                    1 July 2015 update:  The  2008  report from Kimball & Veith, Toronto concludes:  The lowest observed adverse effect level for vitamin D, said to cause hypercalcaemia in normal adults, is officially 95 mg/day ie 4 000iu/d. But collective  reports  indicate that serum 25(OH)D concentrations need   to exceed 700 nmol/L ie 280 ng/ml chronically   before vitamin D3 toxicity becomes  evident ie from at least ~40 000iu D3 /day or perhaps a million iu monthly. .

update 30 June 2015: The Univ Toronto team  in the previous decade published more evidence of safety and benefit  of vit D3 up to 40 000iu a day 280 000iu/week; but   not 88 000iu/day: the warning is that calcium supplement should be avoided in such high vit D3 dosage. They were not yet advising supplement vit K2 and magnesium.                       Neurology . A phase I/II dose-escalation trial of vitamin D3 and calcium in multiple sclerosis.   Burton JM1, Kimball S, Vieth R   ea  St  Michael’s Hospital, Toronto, Canada.     Low vitamin D status has been associated with multiple sclerosis (MS) prevalence and risk; .  to assess the tolerability of highdose oral vitamin D prospectively, an open-label randomized prospective controlled 52-week trial matched patients with MS to treatment or control groups. Treatment patients received escalating vitamin D doses up to 40,000 IU/day (280 000iu/wk) over 28 weeks to raise serum 25-hydroxyvitamin D [25(OH)D] rapidly and assess tolerability, followed by 10,000 IU/day (12 weeks).. Calcium (1,200 mg/day) was given throughout the trial. Endpoints were mean change in  biochemical measures,  biomarkers, relapse events, and Expanded Disability Status Scale (EDSS) score.    RESULTS:   Forty-nine patients (25 treatment, 24 control) were enrolled [mean age 40.5 years, EDSS 1.34, and 25(OH)D 78 nmol/L]. All calcium-related measures within and between groups were normal. Despite a mean peak 25(OH)D of 413 nmol/L 164ng/ml, no significant adverse events occurred. Although there may have been confounding variables in clinical outcomes, treatment group patients appeared to have fewer relapse events and a persistent reduction in T-cell proliferation compared to controls.   Highdose vitamin D (approximately 10,000 IU/day) in multiple sclerosis is safe, with evidence of immunomodulatory effects.    This trial provides Class II evidence that highdose vitamin D use for 52 weeks in patients with multiple sclerosis does not significantly increase serum calcium levels when compared to patients not on highdose supplementation. The trial, however, lacked statistical precision. , providing only Class level IV evidence for these outcomes.

          Ann Clin Biochem. 2008;.   Self-prescribed highdose vitamin D3: effects on biochemical parameters in two men.     Kimball S1, Vieth R.   , University of Toronto, Toronto, Canada. ..  The lowest observed adverse effect level for vitamin D, said to cause hypercalcaemia in normal adults, is officially 95 microg/day 4000iu/d. Serum 25-hydroxyvitamin D (25[OH]D) concentrations associated with hypervitaminosis D remain undefined. Reported 25(OH)D concentrations resulting from prolonged excessive vitamin D3 intakes have exceeded 700 nmol/L 280ng/ml. We report self-prescribed high dose of vitamin D3 over 5-6 years by two men.               Subject 1 had been taking 100 microg/4000iu day for 3 years followed by 3 years of 200 microg/8000iu/day. Serum 25(OH)D concentrations averaged 130 nmol/L 52ng/ml while taking 100 microg/4000iu day of vitamin D3. While taking 200 microg/8000iu/day of vitamin D3, mean serum 25(OH)D concentrations were 260 nmol/L 102ng/ml with no hypercalcaemia or hypercalcuria over the 6 years of vitamin D3 intake.                                                  Subject 2 was a 39-year-old man diagnosed with multiple sclerosis.  his own dose-escalation schedule  increased from 200ugm 8000iu  to 2200 microg/ 88000iu/day over 4 years. The  evidence of a potential adverse effect was that urinary calcium:creatinine ratios showed an increasing trend, which preceded serum calcium concentrations above the reference range (2.2-2.6 mmol/L). His serum 25(OH)D concentration was 1126 nmol/L 450ng/ml  when total serum calcium reached 2.63 mmol/L. He stopped vitamin D3 supplementation at this point. Two months later, all biochemistry values were within reference ranges; serum 25(OH)D concentrations fell by about one-half, to 656 nmol/L 260ng/ml . These results help to clarify the human response to higher intakes of vitamin D3. Close monitoring of biochemical responses confirmed that an increase in urinary calcium:creatinine ratio precedes hypercalcaemia as serum 25(OH)D concentrations rise.

update 28 June : a landmark trial in Brazil 2 years ago finally shows what a really high dose of Vit D3 – 35000iu/d  can do safely over 6 months, a cumulative safe dose of 6million iu A pilot study assessing the effect of prolonged administration of high daily doses of vitamin D on the clinical course of vitiligo and psoriasis:  Dermatoendocrinol. 2013  Finamor,  Coimbra ea    University São Paulo, Brazil     Autoimmunity has been associated with vitamin D deficiency and resistance, and vitamin D metabolism gene polymorphisms   frequently described. May high dose vitamin D3  compensate for inherited resistance to its biological effects?.  To assess the efficacy and safety of prolonged high-dose vitamin D3 treatment of patients with psoriasis and vitiligo, 25 patients with psoriasis or  vitiligo received vitamin D3 35,000 IU once daily for six months ie >1million iu/mo,  >6 million iu over 6mo  in association with a low-calcium diet (avoiding dairy products and calcium-enriched foods like oat, rice or soya “milk”) and hydration (minimum 2.5 L daily). Psoriasis patients were scored according to “Psoriasis Area and Severity Index” (PASI) . All patients presented low vitamin D status (serum 25(OH)D3 ≤ 30 ng/mL) at baseline. After treatment 25(OH)D3 levels significantly increased (from~16 to ~120ng/mL)  ie increase of +- 100ng/ml by 35000iu dly – a flattened highdose response curve, only 10ng/ml rise per 3500iu/d;    and PTH levels significantly decreased (from ~57 to 27 pg/mL. PTH and 25(OH)D3 serum concentrations correlated inversely. The PASI score significantly improved in all nine patients with psoriasis. 14 of 16 patients with vitiligo had 25–75% repigmentation. Serum urea, creatinine and calcium (total and ionized) did not change and urinary calcium excretion increased within the normal range. High-dose vitamin D3 therapy may be effective and safe for vitiligo and psoriasis patients. WHAT WAS THEIR BMI? my 25OHvit D level runs at ~90ng/ml on ~9000iu vit D3 a day; and my  patient’s level runs at ~150ng/ml on ~15000iu/d… so perhaps the Brazilians with these skin disorders (unlike us) have  resistance genes that block higher levels of 25OHvit D. So without doing costly genotyping, we in practice need to check vit D level response early where very high dose is indicated in severe disease. .

Mediocre chronic dose vit D3 supp  eg 2000iu/d , 25OHvitD well > 30ng/ml-   is not enough– it needs high loading eg >400 000- 600 000iu  for acute illness, and good maintenance dose eg >5o 000- 75 000iu/wk  for blood level >60ng/ml, for chronic prevention, to maintain good vit D level and thus real protection:    BMJ Open Respir Res. 2015 Jun   Association between prehospital vitamin D status and incident acute respiratory failure in critically ill patients:  retrospective cohort study.  Thickett , Christopher ea:      Boston, Massachusetts , USA     Intensive care units of Boston teaching hospitals.  1985 critically ill adults admitted between 1998 and 2011    Exposure of interest was prehospital serum 25(OH)D categorised as ≤10 ng/mL, 11-19.9 ng/mL, 20-29.9 ng/mL and ≥30 ng/mL.  In the cohort, the mean age was 63 years,     25(OH)D was ≤10 ng/mL in 8% of patients, 11-19.9 ng/mL in 24%, 20-29.9 ng/mL in 24% and ≥30 ng/mL in 44% of patients. Eighteen per cent (n=351) were diagnosed with acute respiratory failure.  Prehospital 25(OH)D  30ng/ml  in our critically ill patient cohort.  

Thorax. 2015 Jun 10.Double-blind randomised controlled trial of vitamin D3 suppl for the prevention of acute respiratory infection ARI  in older adults and their carers (ViDiFlu).    Martineau , Griffiths ea.Univ London.  clinical trial of high-dose versus low-dose vitamin D3 supplementation for ARI prevention in residents of sheltered-accommodation housing schemes and their carers in London, UK.    137 individuals were allocated to the active intervention (vitamin D3 2.4 mg = 100 000iu once every 2months +10 μg =400iu daily for residents= 62 000iu/mo; carers 3 mg once every 2 months =60 000iu/mo);  and 103 participants to placebo once every 2 months +vitamin D3 10 μg daily = 12000iu/mo for residents, placebo once every 2 months for carers) for 1 year. RESULTS:Inadequate vitamin D status was common at baseline:  92% of 240  participants had serum 25(OH)D concentration < 30ng/ml. The active intervention did not influence time to first ARI (adjusted HR (aHR) 1.18, 95% CI 0.80 to 1.74, p=0.42). When URI and LRI were analysed separately, allocation to the active intervention was associated with 50% higher  risk of URI (aHR 1.48, 95% CI 1.02 to 2.16, p=0.039) and increased duration of URI symptoms (median 7.0 vs 5.0 days for active vs control, adjusted ratio of geometric means 1.34, 95% CI 1.09 to 1.65, p=0.005), but not with altered risk or duration of LRI.   CONCLUSIONS: Addition of intermittent bolus-dose vitamin D3 supplementation to a daily low-dose regimen to average  ~2000iu/d did not influence risk of ARI in older adults and their carers, but was associated with increased risk and duration of URI  over 400iu dly ie 12000iu spread over the month.

Thorax. 2015 May.   Double-blind randomised placebo-controlled trial of bolus-dose vitamin D3 supplementation in adults with asthma (ViDiAs).  Martineau ,Griffiths ea    London  University UK. Asthma exacerbations are commonly precipitated by viral upper respiratory infections (URIs). Vitamin D insufficiency associates with susceptibility to URI in patients with asthma.  randomised controlled trial of vitamin D3 supplementation for  prevention of asthma exacerbation and URI. 250 adults with asthma in London, UK were allocated to receive six 2-monthly oral doses of 120 000iu 3 mg vitamin D3 (n=125) or placebo (n=125) over 1 year.   206/250 participants (82%) were vitamin D insufficient at baseline. Vitamin D3 did not influence time to first severe exacerbation (adjusted HR 1.02, 95% CI 0.69 to 1.53, p=0.91) or first URI (adjusted HR 0.87, 95% CI 0.64 to 1.16, p=0.34). No clinically important effect of vitamin D3 was seen on any of the secondary outcomes listed above. The influence of vitamin D3 on coprimary outcomes was not modified by baseline vitamin D status or genotype. Bolus-dose vitamin D3 supplementation – 60 000iu/mo = average 2000iu/d – did not influence time to exacerbation or URI in a population of adults with asthma with a high prevalence of baseline vitamin D insufficiency.

update 27 June 2015  another review Safety of vitamin D3 in adults in multiple sclerosis  Kimball ,Vieth ea  2007 University  Toronto, Canada confirms that  up to at least 40 000iu daily for 28 weeks  is safe. Patients’ serum 25(OH)D concentrations reached twice the top of the physiologic range without eliciting hypercalcemia or hypercalciuria. The data provide objective evidence that vitamin D intake beyond the current upper limit is safe by a large margin.

      update  20 June 2015 : the  10th  HIGHDOSE VIT D STUDY  (100 000 to  600 000iu stat, or up to 55 000iu/day):       Quraishi,  Bhan ea 2009 Harvard Univ Boston: Effect of  Highdose VIT D Supplement on Vitamin D Status and Cathelicidin Levels in Sepsis: Crit Care Med. 2015 Jun 17: RCT  to compare changes in vitamin D status and cathelicidin (LL-37) levels in 30  adult ICU patients given  Placebo (n = 10) vs 200,000 IU cholecalciferol (n = 10) vs 400,000 IU cholecalciferol (n = 10), within 24 hours of new-onset severe sepsis or septic shock in a single Boston, MA teaching hospital.  Blood samples  at baseline (day 1) and on days 3, 5, and 7. At baseline, median (interquartile range) plasma 25-OHvitD  was 17 ng/ml,  peaked by day 5 in  intervention groups.  On day 5, median change in biomarkers for placebo, 200,000 IU vit D3 cholecalciferol , and 400,000 IU vit  D3 groups, respectively, were as follows: 1) total 25OHvitD, 3% (-3% to 8%), 49% (30-82%), and 69% (55-106%) (p < 0.001); 2) bioavailable 25OHvitD, 4% (-8% to 7%), 45% (40-70%), and 96% (58-136%) (p < 0.01); and 3) LL-37 : -17% (-9% to -23%), 4% (-10% to 14%), and 30% (23-48%) (p = 0.04). Change in high-sensitivity CRP levels did not differ between groups. A positive correlation was observed between bioavailable 25OHvit D and LL-37 (Spearman ρ = 0.44; p = 0.03) but not for total 25OHvitD and LL-37. CONCLUSIONS:High-dose vitD3 supplement rapidly and safely improves total  and bioavailable 25OHvitD  levels in patients with severe sepsis or septic shock. Changes in bioavailable 25OHvitD are associated with concomitant increases in circulating LL-37 levels.

Clin Nutr. 2015 Apr 14.    Increases in pre-hospitalization serum 25(OH)D concentrations are associated with improved 30-day mortality after hospital admission: A cohort study in Boston, Mass.. Amrein , Christopher ea   in two Boston univ. hospitals .Pre-hospital vitamin D status may be a modifiable risk factor for all-cause mortality among hospitalized patients.  4344 adults hospitalized between 1993 and 2011..  INTERVENTION(S):  None.  The main outcome was 30-day all-cause mortality.  In an adjusted logistic regression model, absolute changes of ≥10 ng/mL in patients with initial 25(OH)D  < 20 ng/mL (n = 1944) decreased the odds of 30-day all-cause mortality by 48% (adjusted OR 0.52, P = 0.026).  A causal relation may not be inferred from this observational study.
      Conversely, another new study this month confirms the hazard of gross overdose of anything:   Kaur, Mithal ea .India Vitamin D toxicity resulting from overzealous correction of vitamin D deficiency  Clin Endocrinol (Oxf). 2015 Jun “Vitamin D toxicity, wrongly  considered rare, can be life-threatening,  with substantial morbidity, if not identified promptly. In 16 patients with vitamin D toxicity seen between January 2011 and January 2013  Clinical manifestations included nausea, vomiting, altered sensorium, constipation, pancreatitis, acute kidney injury and weight loss. Median (range) age was 64.5 (42-86) years. Median  serum 25(OH)D level  371 (175-1161) ng/ml, serum total serum calcium level  13.0 (11.1-15.7) mg/dl . Irrational Overdose of vitamin D caused by prescription of mega doses of vitamin D was the cause of vitamin D toxicity in all cases. Median (range) cumulative vitamin D dose was 3,600,000 (2,220,000-6,360,000)”– but the abstract doesnt mention the timespan . Generally, after loading dose for urgent risk,  maintenance dose  need  not exceed about 80 iu/kg/d eg 7000iu/day ie ~50 000iu/wk or 2500 000 iu/yr, ideally with ideally occasional blood vit D, calcium & creatinine tests. .

           UPDATE FOR KIDS: Pediatr Rheumatol Online J. 2015 May .  Vitamin D-update for the pediatric rheumatologists.    Vojinovic J1, Cimaz R2. University of Nis, Serbia.   ” So in accordance with new vitamin D recommendations, we recommend that a child with rheumatic disease, especially if treated with steroids, needs at least 2-3 time higher doses of vitamin D than the dose recommended for age (approximately 2000 UI/day). Vitamin D supplementation has become an appealing and important adjunct treatment option in PRD

      17 June update : Proc Natl Acad Sci U S A. 2015 Jun 15. pii: 201500909.           High-dose vitamin D3 reduces deficiency caused by low UVB exposure and limits HIV-1 replication in urban Southern Africans.  .Cape Town, South Africa, has a seasonal pattern of UVB radiation and a predominantly dark-skinned urban population who suffer high HIV-1 prevalence. This coexistent environmental and phenotypic scenario puts residents at risk for vitamin D deficiency, which may potentiate HIV-1 disease progression. Coussens ,  Jablonski   ea  from Univ. Cape Town & Stellenbosch conducted a longitudinal study in two  Cape Town ethnically distinct groups of healthy young adults, supplemented with 50 000iu weekly  vitamin D3  for 6 weeks  in winter, to determine whether vitamin D status modifies the response to HIV-1 infection and to identify the major determinants of vitamin D status (UVB exposure, diet, pigmentation, and genetics). Vitamin D deficiency was observed in the majority of subjects in winter and in a proportion of individuals in summer, was highly correlated with UVB exposure, and was associated with greater HIV-1 replication in peripheral blood cells. High-dosage oral vitamin D3 supplementation attenuated HIV-1 replication, increased circulating leukocytes, and reversed winter-associated anemia. Vitamin D3 therefore presents as a low-cost supplementation to improve HIV-associated immunity.
    16 June 2015  REVIEW: ADULTS: WHAT VIT D DOSE IS ENOUGH? Because of our increasingly government-encouraged soporific  TV lifestyle and western processed- food-factory low-fat high-carbs HCLF diet, vitamin D has turned out to be as important as >vitamin C as the seriously deficient primary major nutrients in far higher than scurvy/rickets prevention doses.
Just as we ‘only’ need vitamin C 10mg/d to prevent scurvy, the historical DAILY recommended allowance RDA dose of vitamin D for rickets is ‘only’ ~10mcg 400iu/d.
But current expert opinions advocate  effective multisystem chronic prevention against infections, cancer, neurological, cardiovascular and bone disease in adults  vit C between 1gm  and 30gm/day; and

       vit D between 100mcg 4000iu and 250mcg 10 000iu/d (ie 80-100iu/kg/d); or about 25000 to 70 000iu/week or equivalent spacing;
to a blood 25hydroxyvit D 25OHvitD level of ~60 (40 to 80ng)/ml for global prevention; but around ~100ng/ml depending on severity of illness being targeted.

     DONT REJECT A SUPPLEMENT AS OF NO VALUE JUST BECAUSE IT TESTED INEFFECTIVE  IN  LOW DOSE:   eg Martineau , Griffiths ea.Univ London Thorax. 2015 Jun   Double-blind randomised controlled trial of vitamin D3 supplementation for the prevention of acute respiratory infection in older adults and their carers (ViDiFlu). CONCLUSION: Addition of intermittent bolus-dose vitamin D3 supplementation to a daily low-dose regimen did not influence risk of ARI in older adults and their carers, but was associated with increased risk and duration of URI.   BUT like so many trials,this trial in  240 London Seniors and carers is not about high dose, but mediocre dose, in small numbers: it  confirms that 100 000iu vit D3 every 2 mo ie average ~extra  1666iu/d is no better protection than just 400iu dly ie 12000iu spread over the month.

Since like all steroids the many vitamin Ds are vitamin C-cholesterol-derived oils stored and carried in fat, the fatter the patient the higher the maintenance dose vit D3 (eg 100 iu/kg/d) to maintain a good steady optimal bloodlevel.                                Fortunately, unlike the other essential physiological human anabolic steroids (eg androgens, progesterone and estrogens that are poorly absorbed , and trans-hepatically dangerous if swallowed), vitamin D3 is well absorbed either by mouth, by injection; or transdermally / intranasally; and apparently not degraded to risky byproducts in the liver as are the “sex” steroids. .

And of course for best absorption, fat-soluble essentials like vits A, D, E , K; CoQ10 & alphalipoic acid ALA are best eaten with fat not carbs eg veggies, cereals or on empty.
To minimize risk of stones and vascular calcification from imbalance, it is important to take vit D3 with                                                                                      *liberal water, magnesia and vitamin K2; perhaps                                                 *~30gms fresh marine oil /wk eg a tsp of cod liver oil 3 x a week; and                       * a few tsp/d of virgin coconut oil (and for cooking/frying in);
*at least half of daily non-protein energy as FATS- animal, dairy and avocado &
*while minimizing moderate omega6 as nuts and raw olive/ oil; and avoiding/minimizing diabesogenic insulin-resistance-causing refined carbs, and synthetic junk fats like margarine, and other seed oils- eg sunflower and canola – certainly not for frying.

A new university study from Ireland ( Endocr Connect. 2015 June. McKenna ea) confirms that average vitamin D levels there are still well below sufficiency let alone good levels, although it finds Rising trend in vitamin D status from 1993 to 2013: “The Institute of Medicine 2011 Dietary Report specified higher Vitamin D intakes for all age groups compared to 1997, but also cautioned against spurious claims about epidemic vitamin D deficiency and against advocates of higher intake requirements. 40 years have seen marked improvement in vitamin D status, but we are concerned about hypervitaminosis D. Time series sequence chart demonstrated a steady upward trend with seasonality. The average 25OHD increased by ~50% from ~15ng/ml in 1993 to ~23ng/ml in 2013. CONCLUSIONS: Vitamin D status improved over the past 40 years, but there is a dual problem:                             *groups at-risk of vitamin D deficiency, who need public health preventative measures; and                                                                                                     *random members of the public  taking unnecessarily high vitamin D intakes for unsubstantiated claims. “

       Last year Autier, Mullie ea from Lyon France and Bolland, Reid ea from Auckland NZ published major reviews concluding that “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 “vitamin D supplementation with or without calcium does not reduce skeletal or non-skeletal outcomes in unselected community-dwelling individuals by more than 15%. Future trials with similar designs are unlikely to alter these conclusions
But Gillie from Health Research Forum, London 2014 in Controlled trials of vitamin D, causality and type 2 statistical error  rebuts Autier ea, Bolland ea:    “In Lancet Diabetes Endocrinol, Autier, Mullie ea. (2013) , and Bolland, Reid ea. (2014) , concluded that low levels of vitamin D are not a cause but a consequence of ill health brought about by reduced exposure to the sun, an association known as ‘reverse causality’ Denial of the possible benefits of vitamin D, as suggested by insistent interpretation of studies with reverse causation, may lead to serious harms, some of which are listed.” So Gillie affirms the focus of this June 2015 review on vigorous dose vit D without chronic toxic overdose, that Autier ea and Bolland ea overlook, that their conclusions were based on lowdose vitamin D, not vigorous dose eg loading dose 600 000iu  monthly with or without ~50 000iu weekly that has been increasingly validated.

While  human sex hormones in good youthful balance are all essential physiological anabolic ie growth-promoting steroids, Atif ea at Emory University, Atlanta, 2009  and 2015   showed that in rats, Vitamin D with progesterone P4 supplement affords significantly better brain protection against excitotoxicity in cultured cortical neurons  and in traumatic brain injury in vivo than progesterone or vit D alone. In their 2009 braincell culture experiment, the optimal ratio of the hormones given was Prog:Vit D 1000:1 (Prog 20 umol/L: vitD 20nmol/L); whereas in their 2015 in life study the ratio was 8000:1– the rats were injected intraperitoneally  Prog 16mg/kg and VitD 1ug  one and 6 hours after the brain injury, and at 24 hours after brain injury they were killed and the brain damage compared. The optimal ratio, balance of the two steroid  hormones  for rat brain protection (1000:1 in a bench cellculture  and 8000:1 in an acute living rat model) is noteworthy for human dosing although the absolute doses cannot be extrapolated to living humans.   In humans this review below shows that the optimal acute dosing thus far reported seems to be  about 1000mg progesterone injection ie ~13mg/kg (some disputed trial evidence for protecting human brain injury after 50 years of research), and vit D for acute global protection about  600 000iu = 10 000iu/kg= 250 ug /kg ie P:vitD ratio about 50:1.

But vit D3, & androgens, and progesterone (eg Roeder 1986 & Starkov 1997), are the classic muscle-bone anabolic (ie growth- protein-water-salt-retaining) steroids. So we should always combine them in appropriate dose if needed for men, and even women. Estrogen is essential for reproduction, bone strength and femininity, but is muscle-anabolic only for the female reproductive tract; and for fat and glandular tissue ie breasts: estrogenic  dominance doubles cancer; adiposity;  sarcopenia;  and urinary incontinence ie weakens the pelvic floor; so should never be given unopposed by progesterone/androgen and vigorous vit D3 .

          ACUTE LOADING DOSE OF VIT D?: Like antibiotics, for acute (antimicrobial or ICU metabolic eg vascular, brain, cancer ) disease, adult vitamin D3 LOADING dose 540 000 to 600 000iu monthly – but not much lower loading dosing – has been recommended and proven major benefit, eg

1. New Zealand 2009 Osteoporos Int. ;20:1407-15.. Bacon ea :              High-dose 500 000iu oral vitamin D3 supplementation in the elderly were concerned that: vitamin D doses are frequently inadequate; compliance with daily medication is likely to be suboptimal; large loading doses of vitamin D(3) rapidly and safely normalize 25OHD levels; and monthly dosing is similarly effective only after 3-5 months. With baseline 25OHD > 20ng/ml, vitamin D supplement does not reduce parathyroid hormone PTH levels. This randomized double-blind trial RCT compares “high-dose” vitamin D3 regimens and estimates optimal 25OHD levels, from changes in PTH & procollagen type I propeptide (P1NP) in relation to baseline vit D . Sixtythree elderly participants were randomized to three regimens of vitamin D supplementation: a 500,000-IU loading dose; the loading dose plus 50,000 IU/month; or 50,000 IU/month. the Loading and Loading + Monthly groups showed increases in 25OHD of 23+/- 11ng/ml from baseline to 1 month. Thereafter, levels gradually declined to plateaus of 27 +/- 2 ng/mlL and 36 +/- 2 nmol/l, respectively. In the Monthly group, 25OHD reached a plateau of ~32 +/- 8 ng/dl at 3-5 months. There were no changes in serum calcium concentrations. PTH and P1NP were only suppressed by vitamin D treatment in those with low baseline 25OHD level.. CONCLUSIONS: Large loading doses of vitamin D(3) rapidly and safely normalize 25OHD levels in the frail elderly. Monthly dosing is similarly effective and safe, but takes 3-5 months for plateau 25OHD levels to be reached.

2, Pakistan 2013 Salahuddin N ea:  600 000IU Vitamin D monthly for 2 doses improves clinical recovery from tuberculosis. 259 patients with pulmonary TB were randomized to receive either 600,000 IU of Intramuscular vitamin D3 ie ~20 000iu/day, or placebo for 2 doses. After just 12 weeks, the vitamin D supplemented arm demonstrated significantly greater ~40% improvement: mean weight gain (kg)+3.75, (3.16-4.34) versus+2.61 (95% CI 1.99-3.23) p 0.009 and lesser residual disease by chest radiograph; number of zones involved 1.35 v/s 1.82 p 0.004 (95% CI 0.15, 0.79) and 50% or greater reduction in cavity size 106 (89.8%) v/s 111 (94.8%), p 0.035.

3. Austria 2014  Amrein ea, 540 000iu loading dose in 475 ICU pts significantly reduced morbidity and mortality by 40% in 492 vit D deficient pts,  ie is anabolic ie reverses muscle wasting – sarcopenia. as also found by Aganostis 2015 metanalysis

4. Canada/USA universities 2014 Ekwaru, Holick ea: “in a survey, 17,614 Healthy volunteers reported vitamin D supplement ranging from     0 to    55000iu/day= ~1.65million iu/mo; and had serum 25(OH)D levels ranging from 4 to 160ng/ml. The dose response relationship between vitamin D supplementation and serum 25(OH)D followed an exponential curve. On average, serum 25(OH)D increased by 5ng/ml per 1,000 IU in the supplementation interval of 0 to 1,000 IU /day; and by 92% less eg 0.4ng/ml per 1,000 IU in the supplementation interval of 15,000 to 20,000 IU per day. BMI, relative to absolute body weight, was found to be the better determinant of 25(OH)D. Relative to normal weight subjects, obese and overweight participants had serum 25(OH)D that were on average 8 and 3 ng/ml lower, respectively (P<0.001). We observed no increase in the risk for hypercalcemia with increasing vitamin D supplement.”

5. Pakistan 2015 April 22nd Endocrine Society seminar RCT : Vit D3 up to 600 000iu loading dose : Prof Muhammad Masood, Consultant Endocrinologist of Aga Khan University : “ How Much Vitamin D We Need?” vit D deficiency VDD has resurfaced as significant health problem in recent years. In Pakistan region, VDD is very prevalent despite adequate sunshine throughout the year. A huge number of studies associate Vitamin D deficiency with almost any disease. Recently, concerns about the safe upper level of vitamin D have been raised and a reverse J or U shaped relation has been described with 25-OHD level and mortality. Increasing number of patients are being reported with vitamin D toxicity because of excessive intake of vitamin D resulting from misinterpretation of prescription, manufacturing errors, inappropriate prescription of excessive vitamin D doses for vague musculoskeletal complaints without monitoring 25-OHD concentrations. A study conducted at our center revealed important implications, first a dose of VD3 ranging from 200,000-600,000 IU given orally or IM will correct the deficiency in more than 70% of individual at 2 months. A dose of vitamin D 600,000 IU given IM will correct the deficiency in more than 90% of individuals and maintained levels > 20ng/ml in 84% of individuals at 6 months. Multiple mega doses may pose the risk of toxicity.”
6 Belgium 2014.:Vitamin D status after a 100 000iu highdose cholecalciferol in healthy and burn subjects. Rousseau ea Burns patients are at risk of vitamin D (VDD) deficiency and may benefit from its pleiotropic effects in acute phase. Two groups received an oral dose of 100,000IU VD3 RESULTS:A total of 49 subjects were included: 29 in GHealth and 20 in GBurns. At D0, prevalence of VDD was higher in GB: 25OH-D was 21.5 (10.1-46.3) ng/ml in GH vs 11 (1.8-31.4) ng/ml in GB. DBP and ALB were lower in GB. At D7 In GB, changes in 25OH-D extended from -36.7% to 333.3% with a median increase of 33.1%. This study highlighted the differences in VD status and in response to a high dose VD3 in burn patients when compared to healthy patients. 25OH-D measurement needs cautious interpretation, should not prevent burn patients to receive VD supplements during acute care. Higher doses than general should probably be considered

7 Canada 2015 Jan; up to 300 000iu vit D3 loading: McNally Univ Ontario ea Rapid normalization of vitamin D levels: a meta-analysis.. systematic review of pediatric clinical trials of high-dose vitamin D with 25[OH]D.., selected 88 Uncontrolled and controlled trials reporting 25(OH)D levels after high-dose (≥1000 IU) calciferol. 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 >30ng/dl within 1 month. Nine of 10 studies evaluating loading therapy (>50 000 IU) achieved group 25(OH)D levels >30ng/dlL. Adverse event analysis identified increased hypercalcemia risk with doses >400 000 IU, but no increased hypercalcemia or hypercalciuria with loading doses 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). Loading doses >300 000 IU should be avoided until trials are conducted to better evaluate risk and benefit.
Australia: some Australians are fearful in claimed cautious ignorance: Sanders ea University of Melbourne 2013 ask Is high dose vitamin D harmful? With potential to minimize risk of many chronic diseases, and apparent biochemical safety of ingesting doses of oral vitamin D several-fold higher than current recommended intakes, recent research has focused on supplementing intermittent, high-dose vitamin D. However, two recent randomized controlled trials (RCTs) both using annual high-dose vitamin D reported an increase, rather than a decrease, in the primary outcome of fractures.” So annual megadose doesnt help in prevention?.
but they are planning bold highdose trial:                                                                                    8. BMC Cancer. 2014 Saw ea Melanoma Institute, SydneyAdjuvant therapy with 500,000 IU high dose vitamin D following primary treatment of melanoma; Patients with primary cutaneous melanomas that are ulcerated and >2 mm in thickness, or nodal micrometastases, have few options for adjuvant treatment. Recent studies suggest a role for vitamin D to delay and improve overall prognosis. This pilot placebo-controlled randomised phase II trial will assess feasibility, safety and toxicity of an oral loading dose of Vitamin D (500,000 IU) followed by an oral dose of 50,000 IU of Vitamin D monthly for 2 years in patients treated by wide excision…”

        9 INDIAN PEDIATR 2014 :   300,000 IU or 600,000 IU RCT. Mittal ea Delhi. 76 children (median age 12 mo) with rickets. Oral vitamin D3 as 300,000 IU (Group 1; n=38) or 600,000 IU (Group 2; n=38) in a single day. 25(OH)D levels increased from baseline to 12 weeks after therapy :[Group 1: 7.58 to 16.06 (12.71– 20.29) ng/mL, P<0.001]; Group 2: 6.57 (4.66–9.25) to 17.60 . ie 25(OH)D levels were deficient (

But while all the data above are too heterogenous to do a metaanalysis, we now know as well as the South Africans, Pakistanis, Indians, Americans, Canadians, ANZIOs and Austrians do from this literature analysis and collective experience that a level of 25OHvit D of 20 or 40ng/ml is not adequate protection; conversely a bloodlevel of ~>200ng/ml has to be exceeded long term to incur risk. And a loading adult dose orally in adults of at least 600 000iu vit D3 – more likely >1 million iu- (that’s 6gm of 100cwt vit D concentrate powder, costing perhaps $0.25 in South Africa) taken with fat -may be needed to achieve safe high enough bloodlevel to have acute protective effect- and the vit D bloodlevel will drop below vigorous levels within weeks without maintenance doses, as the Austrian study used after their loading dose 540 000iu..

so even 50 000iu every week – my standard chronic illness adult maintenance dose that I take- is ineffective initially for acute protection in eg TB adults (Daley ea India 2015) or ICU . It seems such adults (pneumonia, TB, acute AIDS, ICU) need ? 600 000iu (or ? a ~ million iu orally) to start, then eg 100 000iu/wk till better, then drop to maintenance. .

Infantile bronchiolitis is a severe and common occurrence and killer under a year of age in South Africa as in the northern hemisphere; especially in tiny premmies; in the majority due to RSV respiratory syncytial virus rather than coronavirus, ‘flu etc; with no conventional therapy except support- leaving the doctor actively doing nothing except comfort, while the nurse nurses…
BUT eight papers since 2011 on Bronchiolitis strongly support vit D: that vitamin D deficiency/ polymorphism plays a major role from pregnancy on:
Three studies from 2011-2014 show that such bronchiolitis infants have low vitamin D or vitamin D polymorphisms that make them vulnerable; Two studies in 2014, from Harvard (Randolph ea ) and Ottawa (McNally ea) Universities in RSV bronchiolitis infants show vit D-binding haplotype, or Vitamin D receptor (VDR) polymorphisms;      And a 2011 study from Belderbos ea Utrech Univ Netherlands 2011 that Cord blood vitamin D deficiency is associated with respiratory syncytial virus bronchiolitis- Neonates born with 25-OHD concentrations <20ng/ml had a sixfold (95% confidence interval: 1.6-24.9; P = .01) increased risk of RSV LRTI in the first year of life compared with those with 25-OHD concentrations ≥ 30ng/dl. These studies thus point to brisk vitamin D supplement as likely major benefit against both RSV and subsequent asthma./COPD.

and Five recent team reviews 2011 to 2014 of RSV bronchiolitis from Italy—Baraldi ea ;   Canada- Poon ea ; Ireland – Clancy ea; and USA: Herzog ea-Cornell Univ NY, and Massachusetts-Maxwell ea – thus encourage the use of vigorous vitamin D and A and omega3 supplements in pregnancy or infancy to prevent  our  high RSA risk of bronchiolitis and future asthma/COPD.  eg
Curr Drug Targets. 2011.Herzog ea Cornell Univ. Immunologic impact of nutrient depletion in chronic obstructive pulmonary disease. Maternal smoking may diminish interferon response secondary to micronutrient deficiency, particularly of Vits A & D, and support persistence of RSV into adult life , Muscle wasting and cachexia systemic features of COPD. Nutritional depletion is related to poor survival and is a rational target for therapeutic intervention also in advanced and critically ill patients. Preliminary studies and suggest that supplementation with omega-3 and Vitamin A, Vitamin D3, and zinc may have beneficial effects in COPD.

now    2015  Salimi ea in Iran show in  Association between vitamin D receptor polymorphisms and haplotypes with pulmonary tuberculosis  in  Biomed Rep.   “The vitamin D receptor (VDR) is an important factor in activating immune response in different infectious diseases. Case control study on 120 PTB patients and 131 healthy controls with  Genetic analysis  by polymerase chain reaction.. The VDR Fok1 Ff genotype was associated with TB and the risk of PTB was two times higher in individuals with the Ff genotype. A higher frequency of f allele was observed in PTB patients and therefore, the f allele may be a risk factor for PTB susceptibility. In addition, haplotype analysis showed that the f-T-B and f-t-b haplotypes (Fok1, Taq1 and Bsm1) may have the potential to increase PTB susceptibility. In conclusion, the Ff genotype and f allele of the VDR Fok1 polymorphism were associated with PTB susceptibility. In addition, the f-T-B and f-t-b haplotypes may be the susceptible haplotypes for PTB.”

     THE RSA HOLOCAUST ESPECIALLY FOR WOMEN AND KIDS:  This new cumulative data above  is crucial given that while men fight ruthlessly for power, sex, money- even wars- the high birthrate in poor malnourished teenage girls in RSA, (especially with prevalent violence, alcohol, smoking and other drug abuses, AIDS and pulmonary and abdominal/ meningeal TB), who are thus ill-equipped both to breastfeed and parent with the myriad burdens of illiteracy and joblessness poverty, single parenting, starvation, male violence, refugee squatter survival, and then having to take ARVs, antiTB drugs or at least INH, cotrimoxazole and frequent other antimicrobials.

It is controversial, but Marks DF1.Br J Health Psychol. 2007 Department of Psychology, City University, UK argues that Literacy not intelligence moderates the relationships between economic development, income inequality and health: ” Kanazawa (2006) presented data allegedly supporting a racist version of evolutionary psychology that claims that the populations of wealthier and more egalitarian societies live longer and stay healthier, not because they are wealthier and more egalitarian, but because they are more intelligent. The objectives of this study are: (i) to determine the relationship between IQ and literacy in Kanazawa’s sample of countries and (ii) to reanalyse Kanazawa’s dataset using measures of literacy in lieu of national IQ test scores. RESULTS:National literacy scores across the countries in the sample are highly skewed. In spite of this, the literacy measures are highly correlated with alleged differences in national IQ (r = .83-.86). The measure of literacy together with economic development (GDPpc) and income inequality (Gini coefficient) control at least 59-64% of the variance in national life expectancy at birth.CONCLUSIONS:There is no scientific justification for believing that alleged intelligence differences play any role in explaining international differences in health status. Measures of alleged national IQ scores are highly confounded with differences in literacy. Literacy is a key factor in the health of any community and policies designed to enhance the literacy of a population are expected to lead to significant improvements in health status.
For these intellectually challenged illiterate women from remote rural villages  – many of whom cannot even write their initials let alone a signature, or understand English or Afrikaans-   anything but their tribal dialect-  pregnancy and AIDS/TB are the only relative escape from starvation and manual ie servile labour- which marginally paid drudgery is disappearing with the government-caused collapsed SA economy, power supply and industry. But the disability grant of ~R1500 ($125pm ie <$1/work hour) ) pm, and child welfare grant of perhaps R300 ($25)pm, is a drop in their ocean of despair. And given the mushrooming STD rates and costs thereof from male recklessness , from worsening corrupt central-government- led illiteracy and effective mass unemployment – state HIV-TB clinics and hospitals seldom have a little B6 or C to give these women, let alone regular supplies of ARVs or essential healing nutritionals eg vits A, Bco, minerals D, iodine, zinc, and biologicals eg  cod liver oil etc.

In the private sector, medical aid schemes also dont pay for supplements, only synthetic designer drugs that ignore underlying causal immunodeficiencies – since Only Disease Pays.
OVERDOSE? Between the two topic headings Hypervitaminosis D and Vitamin D toxicity, there are already 1798 refs on Pubmed alone. Hypervitaminosis D  428 reports on Pubmed since the first, from Harris & Moore, The Nutrition Lab, Cambridge 1929; Hypervitaminosis and vitamin balance: ..        and there are 1436 entries under Vitamin D toxicity since the first Vitamin D Toxicity by Leake 1936 at  UCLA .
ADULTS: But experts and numerous overdose reports ( only a few of which are noted below) reveal the truth,  that at least oral DAILY, well over 50 000iu to 1 MILLION iu/d of vitamin D for months, LONGTERM to up to 100 000IU/D for months to 365 million iu over 10 years has to be taken to cause illness ie symptomatic hypercalcemia .
Conversely, Chakraborty ea at Roy Research Center, Kolkata, India, report (Lab Med. 2015) A nontoxic case of vitamin d toxicity, a woman who developed very high serum Vitamin D levels (746 ng/mL, RI: 20 to 50) as a result of medication error. In spite of such high serum concentrations the patient was without any clinical symptoms and had normal serum calcium. The evidence base regarding the safety profile of Vitamin D supplementation in humans has been build through case reports, not dose titration RCTs to astronomical levels- which would be unethical.

So while routine maintenance dose eg 600 000iu/month, or 4000- to 10 000iu/d, or 100 000iu/wk in adults has never been reported to cause overdose toxicity,
on vigorous chronic vitamin D3 (not calcium or D2) dosing for disease, obviously ideally baseline (or at least after say 2-3 months of trial of conservative vitamin D replacement) calcium, vitamin D and kidney function levels should be measured since very rarely, unexpected silent hypercalcemia may already be present. .
But numerous reports eg from Netherlands 2014 show that a single overdose of even 2million iu vit D (=~100 000iu/d over 30days given the T 1/2 of vit D of 2 wks to 2 months), while kicking the bloodlevel up a few hundred ng/ml, does no harm even in two Dutch nonagenarians.

Relative hypovitaminosis D (bloodlevel below 30ng/ml) is prevalent locally and internationally in an indoor-working sunburn-fearing over-dressed city population not taking supplements more than the usual 400iu vit D in a daily multivite – especially in alcoholics, and the undernourished poor, and those following the government -recommended disease- promoting diabesogenic high- carbs low- fat diet marketed by commercial interests and bad science the past 50 years..

Already in 1999 Vieth at Univ Toronto wrote in Am J Clin Nutr. “Vitamin D supplementation, 25-OH vit D concentrations, and safety. . for adults, the 5-microg (200 IU) vitamin D RDA may prevent osteomalacia in the absence of sunlight, but more is needed to help prevent osteoporosis and secondary hyperparathyroidism, and prevention of some cancers, osteoarthritis progression, multiple sclerosis, and hypertension. Total-body sun exposure easily provides the equivalent of 250 microg (10000 IU) vitamin D/d, suggesting that this is a physiologic limit. The assembled data from many vitamin D supp. studies reveal a curve for vitamin D dose versus serum 25(OH)D response that is surprisingly flat up to 250 mcg (10000 IU) vitamin D/d. To ensure that serum 25(OH)D concentrations exceed 40ng/ml, a total vitamin D supply of >100 microg (4000 IU)/d is required. Except with conditions causing hypersensitivity, there is no evidence of adverse effects with serum 25(OH)D concentrations <55ng/ml, which require a total vitamin D supply of 250 microg (10 000 IU)/d to attain. Published cases of vitamin D toxicity with hypercalcemia, for which the 25(OH)D concentration and vitamin D dose are known, all involve intake of >/= 1000 mcg (40 000 IU)/d. Because vitamin D is potentially toxic, intake of >1000 IU/d has been avoided – even though the weight of evidence shows that the currently accepted, no observed adverse effect limit of 2000 Iu)/d is too low by at least 5-fold ie >10 000iu/d long term.”
O/Dose INFANTS: to avoid vitamin D poisoning and permanent damage to infants, of course dose needs to be scaled down accordingly on the 100iu/kg/d basis; but infants have a much bigger body surface area and thus meds requirement & tolerance. Human breast milk vit D is usually inadequate especially for swaddled darker-skinned babies and mothers; so conventionally at least 1000iu/d supplement vit D is for babies up to 6 months, 2500iu/d above 1year, and 4000iu/d from 9 years; or a pro rata loading dose, is advised eg Canada and USA Heaney ea Conversely, serum 25(OH)D concentration consistently >200 ng/mL is considered to be potentially toxic [5].” Without a fingerprick vit D and calcium assay (lab cost here is ~R300 ie $25), monitoring here is tedious and costly…
ALLERGY TO VITAMIN D3? That vigorous vitamin D3 replacement can improve immunodeficiency and even relieve dermatitis is common cause.
But since Vit D’s discovery in 1914 (USA McCollum and Davis) and soon commercial production and marketing the past 90 years, not a single documented verified ALLERGY case (not overdose) can be found on Pubmed or Google?.Such true allergy cannot be anything but very very rare, since with vit D3, like all other bioidentical human hormones, and vitamins, allergy (unlike overdose) is almost inconceivable- although receptor loss or blockade may create resistance to eg thyroid, testosterone, vit D etc. . Allergy could conceivably occur to some carrier/ additive to the vitamin D3- but not even in the lungs from inhalation of old high-vit D oil droplets in fish factory workers
VitaminDwiki puts it in perspective. Designer ie prescription synthetic meds, and common foods, and tap water, are more likely to cause problem.

None of the 14 refs on Pubmed reports allergy to vitamin D. Google merely notes some anecdotes from users.

The last and urgent word today  -on medical and parental responsibilities- is by Wolfgang Högler ,Birmingham Children’s Hospital, UK ,Clin.Endoc. 2015: Complications of vitamin D deficiency from the foetus to the infant: One cause, one prevention, but who’s responsibility? The supplier of bone Calcium and phosphorus is the hormone calcitriol, which originates from vitamin D, itself made by sunshine in human skin. Requirement for bone minerals is highest during phases of rapid growth, and no one grows faster than the foetus and the infant, making them particularly vulnerable. Deprivation of calcium, whether through low calcium intake or low vitamin D, leads to serious health consequences throughout life, such as hypocalcaemic seizures, dilated cardiomyopathy, skeletal myopathy, congenital and infantile rickets, and osteomalacia.                                                                                                                    These 5 conditions are often summarised as ‘symptomatic vitamin D deficiency’, are fully reversible but also fully preventable. However, the increasing prevalence of rickets and osteomalacia, and the deaths from hypocalcaemic cardiomyopathy, demand action from global health care providers. Clarification of medical and parental responsibilities is a prerequisite to deliver successful prevention programmes.     The foetus and infant have the human right to be protected against harm, and vitamin D supplementation has the same public health priority as vaccinations.

And Dr John Cannell of The Vitamin D Council comments today : Dr. Hogler does not discuss the growing evidence that maternal and infantile vitamin D deficiencies may lead to neurodevelopmental disorders such as autism. I have always thought that the only way obstetricians and pediatricians will prescribe adequate doses of vitamin D is if they are charged for malpractice from failing to identify and treat vitamin D deficiency. If it is established that vitamin D deficiency causes autism, the malpractice attorneys will swarm like sharks to blood. Given increasing evident harms from numerous vaccinations, and often lack of real longterm supporting evidence of good eg the (swine and seasonal) flu and cervix HPV vaccines, we must consider vitamin D supplementation as far more proven benefit and safety than intensive multiple vaccinations.
-And on sepsis and brain salvage:  Dr Cannell promotes   –  vitamin D is a viable treatment for sepsis?, the landmark work of Drs William Grant and Ray Matthews.

The evidence is strong that vigorous natural supplements (vits, minerals, human hormones and some natural biological like marine oil and chondroglucosamine) are priorities especially in both acute emergencies, chronic diseases and prevention, from conception at all ages, over vaccinations and antibiotics and all synthetic designer drugs. .

BMC Cancer. 2014 ;14:780 Adjuvant therapy with high dose vitamin D following primary treatment of melanoma at high risk of recurrence: a placebo controlled randomised phase II trial Saw RP1, Thompson JF. ea Melanoma Institute Australia,North Sydney , Australia. .

  Indian Pediatr. 2014 ;51:265-72. 300,000 IU or 600,000 IU of oral vitamin D3 for treatment of nutritional rickets: a randomized controlled trial. Mittal , Gupta ea University College Medical Sci,, New Delhi.
Calcif Tissue Int. 2013 ;92(2):191-206. Is high dose vitamin D harmful? Sanders KM1, Nicholson GC, Ebeling PR., University of Melbourne

Med J Aust. 2005 Jul 4;183(1):10-2. Annual intramuscular injection of a megadose of cholecalciferol for treatment of vitamin D deficiency: efficacy and safety data. Diamond TH1, Ho KW, Rohl PG, Meerkin M.University of New South Wales, Australia.

Geriatr Orthop Surg Rehabil. 2011 May;2(3):94-9. . Improving mobility and reducing disability in older people through early high-dose vitamin d replacement following hip fracture: a protocol for a randomized controlled trial and economic evaluation. Mak JC1,  Cameron ID ea. , University of Sydney, Australia .Hypovitaminosis D is particularly common among older people with a proximal femoral (hip) fracture and has been linked with poorer lower extremity functioning, falls, and fractures.

     J Nutr. 2014;144:2002-8. Vitamin D deficiency is associated with progression of knee osteoarthritis. Zhang FF1, McAlindon TE EA2.usa uNIVERSITIES

    Lin Chung Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2014 ;28(14):1031-3. [Effect of nasal instillation of vitamin D3 on patient with allergic rhinitis symptoms]. [Article in Chinese] Gong, Jiang Y EA

      Nutrients. 2014 ;6(9):3403-30. doi: 10.3390/nu6093403. Does sufficient evidence exist to support a causal association between vitamin D status and cardiovascular disease risk? An assessment using Hill’s criteria for causality.Weyland PG1, Grant WB2, Howie-Esquivel J3., University of California,
Eur J Clin Nutr. 2014 ;68(5):632-4..Pharmacokinetics of daily versus monthly vitamin D3 supplementation in non-lactating women.Meekins ME1,, Thacher TD2Mayo Clinic, Rochester,& University of Witwatersrand, Johannesburg,
Mol Med. 2009 ;15(9-10):328-36. Vitamin D affords better neuroprotection against excitotoxicity in cultured cortical neurons than progesterone alone. Atif F1, Sayeed I, Ishrat T, Stein Emory University, Atlanta, Georgia, USA
Am J Clin Nutr. 2008 ;87(6):1952-8. Vitamin D intake to attain a desired serum 25-hydroxyvitamin D concentration. Aloia, Yeh ea Winthrop University Hospital, NY.
Am J Clin Nutr. 2008:87(3):688-91.Pharmacokinetics of a single, large dose of cholecalciferol.  Ilahi M1, Armas LA, Heaney Creighton University Omaha, .
Curr Opin Lipidol. 2007 ;18(1):41-6. Vitamin D and vascular calcification.Zittermann Schleithoff Koerfer Ruhr University Bochum, Germany.
J Am Coll Nutr. 2003 Apr;22(2):142-6. Calcium absorption varies within the reference range for serum 25-hydroxyvitamin D. Heaney RP1, Dowell MS, Hale CA, Bendich A.Creighton University, USA.

         Diabetes Care. 2015 May. pii: dc150323. Effect of LOWDOSE Vitamin D Supplementation on Glycemic Control in Patients With Type 2 Diabetes (SUNNY Trial): A Randomized Placebo-Controlled Trial. Krul-Poel YH1, Simsek S7 eu .

          Horm Metab Res. 2015 May 4 Effects of High-Dose Vitamin D Supplementation on Metabolic Status and Pregnancy Outcomes in Pregnant Women at Risk for Pre-Eclampsia. Karamali M1, Asemi Z ea.
J Am Geriatr Soc. 2014 ;62(8):1546-50..Effectiveness and safety of a high-dose weekly vitamin D (20,000 IU) protocol in older adults living in residential care. Feldman F1, Green TJ.ea. Simon Fraser University, Burnaby, BC, Canada.

    Maturitas. 2015 Mar 27. Sarcopenia in post-menopausal women: Is there any role for vitamin D? Anagnostis P1, Goulis DG ea Greek Universities
J Adolesc Health. 2015 Apr 11. Vitamin D =<2000iu/d Fail to Increase 25-Hydroxyvitamin D Levels or to Alter Cardiovascular Risk Factors in Obese Adolescents: A Pilot Study.
Shah S1, Wilson DM2, Bachrach LK2.

     Lancet Infect Dis. 2015 May;15(5):528-34.Adjunctive vitamin D 400 000iu in 6 weeks for treatment of active tuberculosis in India no benefit : a randomised, double-blind, placebo-controlled trial. Daley P1, Vieth R4, , Mathai D ea .
Thorax. 2015 May;70(5):451-7. doi: 10.1136/thoraxjnl-2014-206449. Epub 2015 Feb 27.
PLoS One. 2015 Feb 23;10(2):e0117123. doi: 10.1371/journal.pone.0117123. eCollection 2015. Vitamin D₃ supplementation in Batswana children and adults with HIV: a pilot double blind randomized controlled trial. Steenhoff AP1, Stallings ea .
Eur J Endocrinol. 2015 Mar;172(3):235-41. doi: 10.1530/EJE-14-0870.Vitamin D3 increases in abdominal subcutaneous fat tissue after supplementation with vitamin D3. Didriksen , Jorde R3 ea

44-9987.12279. Epub 2015 Feb 6. Effects of a single, high oral dose of 25-hydroxycholecalciferol on the mineral metabolism markers in hemodialysis patients. Merino , 2, Quereda ea, .
Pediatr Neurol. 2015 ;52:160-4.Vitamin D supplementation in children with epilepsy and intellectual disability. Snoeijen-Schouwenaars , Majoie MH ea .:.
J Acad Nutr Diet. 2015 Feb;115(2):225-30. .Dietary fat increases vitamin D-3 absorption.Dawson-Hughes B, Rasmussen H.
Eur J Clin Nutr. 2015 ;69(2):193-7 The effect of a single, large bolus of vitamin D 250,000 IU in healthy adults over the winter and following year: a randomized, double-blind, placebo-controlled trial.Kearns MD1, Tangpricha V3

Sleep Breath. 2015 May;19(2):579-83. doi: 10.1007/s11325-014-1049-y. Epub 2014 Aug 23. The effect of vitamin D supplements on the severity of restless legs syndrome. Wali S1, Krayem A.

Endocr Pract. 2014 ;20(12):1258-64..The vitamin d dose response in obesity.Dhaliwal R1, Aloia JF1.

BMC Infect Dis. 2013;13:22. Vitamin D accelerates clinical recovery from tuberculosis: Salahuddin N ea.
Curr Drug Targets. 2011;12(4):489-500. Immunologic impact of nutrient depletion in chronic obstructive pulmonary disease. Herzog R1, Cunningham-Rundles , Cornell University, NY.

    Ital J Pediatr. 2014 Oct 24;40:65. Inter-society consensus document on treatment and prevention of bronchiolitis in newborns and infants. Baraldi , Corsello EA -Società Italiana per le Malattie Respiratorie Infantili, Italy.
Pharmacol Ther. 2013;140(2):148-55.Vitamin D deficiency and severe asthma. Poon AH1, Mahboub B, Hamid Q. McGill University,
Clin Exp Allergy. 2014 Feb;44(2):231-7. doi: 10.1111/cea.12247.Vitamin D-binding protein haplotype is associated with hospitalization for RSV bronchiolitis. Randolph, Bont EA Harvard Medical School.
Pediatr Pulmonol. 2014;49(8):790-9. Vitamin D receptor (VDR) polymorphisms and severe RSV bronchiolitis: a systematic review and meta-analysis. McNally1, Little ea. Univ Ottawa, Canada.
Pediatrics. 2011;127):e1513-20. Cord blood vitamin D deficiency is associated with respiratory syncytial virus bronchiolitis. Belderbos, Bont ea, University Utrecht,Ndl.

     J Matern Fetal Neonatal Med. 2013;26;639-46.Vitamin D and neonatal immune function. Clancy ea Ireland
Nutr Rev. 2012;70:548-52. Better newborn vitamin D status lowers RSV-associated bronchiolitis in infants.Maxwell CS1, Carbone ET, Wood RJ. University of Massachusetts, Amherst, USA.
Am J Clin Nutr. 1999 ;69:842-56.Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety. Vieth.   University of Toronto, Canada.

     Clin Endocrinol (Oxf). 2015 Jun . doi: 10.1111/cen.12836. Vitamin D toxicity resulting from overzealous correction of vitamin D deficiency. Kaur, Mithal ea Delhi.

     J Steroid Biochem Mol Biol. 2015 Apr;148:14-8. Iatrogenic vitamin D toxicity in an infant–a case report and review of literature. Ketha, Singh EA

    Einstein (Sao Paulo). 2014;12(2):242-4. Vitamin D intoxication: case report.
[Article in English, Portuguese] Marins TA1, Korkes H1.ea Hospital Israelita Albert Einstein, São Paulo, Brazil.
J Clin Endocrinol Metab. 2011;96(12):3603-8. .Vitamin D intoxication with severe hypercalcemia due to manufacturing and labeling errors of two dietary supplements made in the United States.Araki T1, Holick MF, Newman LG.ea

Ann Pharmacother. 2011 ;45(10):e52. Hypervitaminosis D associated with a vitamin D dispensing error. 4.5million iu over 3 mo. Jacobsen , Schilling ea.

Am J Public Health. 1995 ;85(10):1418-22. Subclinical health effects in a population exposed to excess vitamin D in milk. Scanlon, Falk H.ea
N Engl J Med. 1992 ;326(18):1173-7. Hypervitaminosis D associated with drinking milk. Jacobus CH1, Holick MF, Seely EW.:ea .

Q J Med. 1986 Oct;61(234):911-9. The osteodystrophy of hypervitaminosis D 365million iu over 10 years: a metabolic study. Davies M, Mawer EB, Freemont AJ. A patient received 2.5 mg vitamin D2 ie 100 000iu/d daily for 10 years ie 365 million iu total, presented with increasing skeletal pain and hypercalcaemia. The limbs were painful to touch especially at the insertions of ligaments and tendons, and radiographs showed osteosclerosis with calcification in the periosteum, blood vessels, tendoachilles and plantar fascia. A negative external calcium balance was documented in the presence of enhanced intestinal calcium absorption and an increase in urinary hydroxyproline excretion. Cortisone improved calcium balance and corrected the hypercalcaemia by reducing serum 1,25-dihydroxyvitamin D levels and urinary hydroxyproline excretion.

Nouv Presse Med. 1981;10(36):2965-7.[Vitamin D metabolites in a new case of drug-induced hypercalcemia (author’s transl)]. [ French] Ulmann A, Bourdeau A, Lair M, Bader C. the authors report on a new case of severe hypercalcaemia induced by prolonged oral treatment with high doses of vitamin D2. (6 mg ie 240 000iu/day ie for 9 months ie 23million iu).

     Lancet. 1978 ;2(8090):621-3. The continuing risk of vitamin-D intoxication.
Davies, Adams . Eight cases of vitamin-D poisoning are described.
Arch Intern Med. 1975 Jul;135(7):986-8. Protracted vitamin D intoxication.
Shetty , Hagen ea   A 56-year-old woman underwent subtotal thyroidectomy for Graves disease in 1963. After the operation, hypoparathyroidism developed and therapy was begun with vitamin D2 (ergocalciferol), 100,000 units daily.  Four months later, ie 12 million iu vit D, after hypercalcemia (14 mg/100 ml) had been noted, vitamin D therapy was discontinued

    Dtsch Med Wochenschr. 1975 ;100(9):415-6, 419-23. [Observations in vitamin D and dihydrotachysterol poisoning]. [German] Ziegler R, Delling ea. In three women intoxication with vitamin D or dihydrotachysterol occurred. Two patients died from complications despite successful lowering of the serum calcium, the third died after a pulmonary embolus during hypercalcaemia 5 months after cessation of vitamin D. .

    Br Med J. 1972 ;3(5820):205-7. Vitamin D intoxication treated with porcine calcitonin. Buckle RM, Gamlen TR, Pullen IM.Southampton UK Porcine calcitonin was used to treat three Southampton women in their sixties with hypercalcaemia due to accidental chronic vitamin D intoxication with 30 000 to 500 000iu/d for 4 to 13 weeks (vit D 9 million iu over 4wks; 4.5million iu over 13 week; and 29 million iu over 2 months). Normocalcaemia was achieved in 3 to seven days, with rapid full recovery.


guest opinion by neuro-orthopaedic surgeon and tutor Dr JP Driver-Jowitt FRCS (UK),

Metabolic pathways are the succession of chemical changes which convert one compound into another within the body. There are many: the entire number is probably not known and there are even more subsidiary and partial pathways by which biochemical processes proceed.  The pathways themselves are highly complex and depend upon routing through enzymes, co-enzymes as well accelerating and retarding factors. These routes change with different ingestants and external factors, even unlikely factors such as sunlight, in their complexity as a manufactory.

That these pathways can “learn” to take increased loads and can be trained to be more efficient and act more rapidly can be demonstrated in enhanced metabolism (“adaption”) of drugs and alcohol. Mitochondria engineer these intra-cellular modifications. This “training” might be the basis of athletic fitness (other factors such as muscle hypertrophy and muscle memory training are clearly also involved)

At simplest these pathways allow the assembly of those carbon based substances which form biological structures and allow degradation of material in order to provide energy. Disassembly of “organic” components to be reused in growth, repair, adaptation and excretion of “waste” is further role.

These biochemical pathways can be compared with complex railroad transit systems having junctions, points, lay-bys, regular sites of loading and unloading as well as the ability to regulate the load carried.

Many disease processes can be attributed to aberrations or failures of these metabolic “transport systems”.  Many diseases probably occur as a result of unknown happenings in these biochemical pathways.

Therefore, if one considers nutrition, one must consider these pathways, by which ingestants are disassembled, transported through (usually) the intestinal boundaries.  In themselves, these intestinal transits are highly complex, selective and prone to disease or abnormality.

21st century humans ingest in very different fashions from their evolutionary predecessors.  Ingestants have changed and have become complex by a variety of manufacturing and industrial events.  What then is the likelihood that the biochemical pathways have become altered, “confused” or overloaded beyond design specification?  This would seem not only highly likely but to be accepted and guaranteed.

Therefore, let us look at the common ingestants, the basic feedstock of humans, and the source of their fuel-energy dynamics.  Preeminent is carbohydrate.   For practical purposes all carbohydrate is grown as vegetation.  ( some sugars, exemplified by lactose, have animal origins) So important is food to human behaviour and existence that the wealthiest nations have, as their economic foundation, successful agriculture.

The vegetative production of carbohydrate has been substantially altered over the centuries.  In broad terms, carbohydrate is not palatable and not an attractive ingestant but it has been altered to be more enticing, primarily by increasing the sugar.  The fruit which we eat now has been selectively bred and is considerably sweeter than the fruit provided to primitive man (as a generalisation).  Even substances like corn have been made softer, sweeter and probably fattier by selective breeding.  More recently the changes of selective breeding have been accelerated by genetic engineering, but the perspective must be retained that genetic engineering has had less influence on palatability than selective breeding.  Much of genetic engineering relates to enhanced production efficiency with greater yields and resistance to adverse events such as drought and disease.  Shelf life has been improved and methods of removing contaminants (including contaminating infections and their by-products such as the flavo-proteins) have been forcibly and successfully addressed.

Probably the single most influential change has been the enhanced production of sugars.  Not only has the feedstock been made sweeter but the sugars themselves have been produced in enormous quantities as a stand-alones or additives.

One result  of the “industrialisation” of food is that carbohydrate has been changed from the highly fibrous and cellulose wrapped (and therefore relatively unpalatable). Carbohydrate is now an easily accessed and addictively attractive substance with a long shelf life, made immediately available to millions of households. Because it does not deteriorate (assisted by long-life additives) it can be snacked at will, on impulse, as a consolation or a habit from the readily available stock in most households.

Other attracting and seductive foods have been mixed with carbohydrate to make carbohydrate relatively inexpensive and highly, if not addictively, desirable. Eminent are salt and fat.  Carbohydrate has been introduced into the diet of infants and children in this way and so probably changing their taste and purchase preferences forever.  One has only to look at breakfast cereals where the bulk is cheap carbohydrate but “flavoured” (and for the word flavour think behaviour changing) with the two most powerful enticers, fat and sugar.

Of concern also is the industrial removal of substances from food, such as “de-bittering”. That bitterness, nature’s negative attractant is caused by a variety of substances such as tannins. These would “normally” have the effect of binding molecules and making some foods non-digestible. Removing them will increase absorbable calories, and reduce colon bulk. There is evidence that some of these lost “bitter” components could prevent cancers.

Atheroma demonstrates an analogy with gout. The “pathological substance” of atheroma is cholesterol. This is a normal constituent of the biology of humans. Cholesterol plays a vital part in the structure of the neurological system, and much more. To suggest that cholesterol can be removed from human metabolism (by reducing intake) is ludicrous. What needs to be corrected is the deposition in arterial walls. Now look at gout where the pathological substance is uric acid – a perfectly normal constituent of human metabolism. In humans uric acid is converted, by a metabolic pathway, to urea. Urea is soluble and readily excreted in urine. However if the metabolic pathway is disrupted, uric acid accumulates and disease (gout) results. This metabolic pathway disruption can be caused by genetic factors, overload by ingestion, and other physical factors. Not unlike atheroma.

The physical factor in atheroma is reflected by vascular damage by high pressures of blood, areas of blood turbulence and perhaps loss of blood vessel wall elasticity. Yet another factor might be direct damage to the arterial wall by tiny shards of metal generated in the opening of metal cans. This might explain the high incidence of atheroma in young GIs in Viet Nam: They lived on canned food, probably ingesting these metal shards which might be expected to damage arterial walls, especially in areas of is high turbulence of the blood.

Could excessive food volume alone confuse the metabolic pathways and produce disease? Could mixing different types of food taken at the same meal confuse the metabolic pathways and produce disease?


What about dieting? The analogy with the law of physics, “matter cannot be created or destroyed”, has lead to a dieting illusion. It is often held that losing weight can be worked on the basis “calories in = calories out (by exercise)”. Hence calorie counting. But that can be shown that is invalid as a way of reducing fat. More likely exercise (which undoubtedly can lead to loss of weight, particularly fat loss) changes the metabolic pathways (perhaps from glucose catabolism to fat catabolism), allowing selective burn of fat.



28 January 2014    guest author  orthopaedic surgeon and instructor  Dr Jon Driver-Jowitt FRCS   opined:

This is not scientific precision.  This is not peer reviewed.  This might not resist the rigor of an editor.  These are simply observations intended to spur thought and look laterally.

Much advice about food appropriate for health has been given. Much of that has been based upon (often marginal) statistics. Many are deduced from self-reporting surveys. However the variables are so great that it is impossible to accommodate these into meaningful statistics. A few of these variables include quantum of food, types of mixtures of food, frequency of these foods, plus multiple variables related to micro-nutrients ingested simultaneously, and more.

When in doubt, it has been said, look in the instruction book. The instruction book for  animals (including the human)  exists in the animal. It is the inclination to eat some foods and the abhorrence of others.

Without the instruction book, one has to look at design specifications. Unfortunately the animal-machine-design did not consider the possibility of limitless food, or great food variety, or types of current cultivars. So selection by appetite might be flawed, and one is left guessing (somewhat) about the design specification. That is what is addressed here.

But before that, if one wants to live longer, the method has been (scientifically) available for the better part of a century. Simply, eat less. Eat less than your appetite drive. Eat less than your cohorts.

But let us look at design. Suppose humans were to be designed from scratch, which fuels (i.e. foods) should be selected, bearing in mind the limitations of availability, and knowing that the human is a mobile device with defined functional requirements and a limited life-span? Consider these options, and consider how they fit with current eating patterns:

Fat is probably the most desirable and quintessential food for humans.  It is the supreme appetiser.  It carries essential vitamins. Fat the highest calorific gain of all foodstuffs whilst it has a low energy cost for ingestion and digestion. It is the most cost effective source of energy. Yet fat has powerful negative feedback mechanisms.  Therefore, although fat stimulates appetite it also produces satiation relatively rapidly. Rapid satiation allows food to be spread to the entire pack, in keeping with expectations of le milieu exterior which demands survival of the group, not the greedy individual. However the satiation of fat can be strongly altered by salt.  Therefore, salted fat and perhaps salted protein can become “compulsive” foods, inducing the eater to keep eating until gorged.  So we have yet another factor, the “additions” to food which induce compulsive feeding, prompted by those intent on making money out of food.

Protein is probably neutral tasting without the fat and salt, is not particularly palatable and does not have the “addictive” quality of carbohydrate. But it contains “essential” components which the human cannot manufacture, including amino-acids and vitamin C (curiously a “water-soluble” vitamin). It is also heavily mechanically bound to fat, and often inseparable.

Carbohydrate, on the other hand, was never particularly attractive to early humans.  Yes, I know well enough that some carbohydrates, the sugary carbohydrates, are exceedingly attractive.  But in primitive societies, all carbohydrates were not attractive.  Pure sugar is a relatively new evolution. The current sweet fruits and even potatoes are the product of intentional selective breeding to make those carbohydrates more palatable.

The metabolisms of carbohydrate, the sugars, are again very different from fat, in that the same metabolic pathways are used for both the anabolism and the catabolism of carbohydrate. The control of carbohydrate metabolism lies outside the direct metabolic pathways, relying on end-organ control. These includes insulin receptors.   This is distinct from fat where the anabolic and catabolic pathways are different, and so allowing feed-back to curb appetite and metabolic direction.

Carbohydrate’s prime quality is that it is cheap.  As a consequence commerce has “wrapped” carbohydrate in both fats and sugar in order to make it compulsive eating at a cheap price.  Amongst the most tempting ingestants are those that have both sugar and fat, as in chocolate.

Refined and manufacturer altered carbohydrate once ingested, prompt the desire to keep on eating it. Carbohydrate can have a long shelf life, is easily stored and so lends itself to easy snacking. No surprise that it is perfect to fuel “habituation eating”, and ultimately obesity.

Sugar is impregnated into cake carbohydrate or spread on the top as icing.  Fat is used as a layer to make bland carbohydrates or even carbohydrates and protein more palatable, as in deep fried foods – where salt is added for good measure. Cheap beans are made more palatable for sale by adding the salt and sugar of ketchup.Salt is impregnated into carbohydrate ( chips and French fries).

Water, the foundation nutrient.  Many children are metabolically confused because the water offered to them is laced with calories, primarily sugar and some metabolically noxious colourants. They then lose the distinction between thirst and hunger. When thirsty they might attempt to satisfy themselves  by choOsing “food” rather than fluid (sugar laden drinks, iced cream ). The outcome is hypercaloric habituation.

It therefore might not be what you eat, but which combination one eats, that influences the health or disease of individuals.  There is some evidence that individuals like to eat the same food and will repeat eating that ingestant by choice.

“Humans like variety, humans need variety, and humans need a balanced diet”.  This may not have been the case with evolutionary man and it is certainly not the case with many animals.  Those animals can adapt to a particular foodstuff (obviously one that is available) and then continue eating that foodstuff by choice, even where alternatives become available.

The legend has arisen that individuals need a “mixed and balanced” diet.  As far as I am aware there is no evidence that this mixing needs to occur in the same meal.  True enough, one needs the vitamins and one needs the different proteins, fat and carbohydrate.  But does one need them simultaneously, wrapped around each other and made into tempting compotes?

Editorial comment:  The science concurs:

The evidence  for higher water intake, moderate protein and low sugar/salt no-smoking   intake is self-evident except to sugar, beverage  and cigarette manufacturers, marketeers and addicts.          But the fraudulent promotion of the low saturated fat (ie meat), low-cholesterol , high carbs regime for all remains a big problem.

Dr Ancel Keys  PhD (1904-2004) was a revered polymath  traveler, oceanographer biologist turned physiologist nutritionalist (Biology of Starvation; the K Ration) , who correctly  recognized and  promoted the Mediterranean Diet (>35% fat), and long outlived his critics. But he and his followers  set USA-led  nutrition and health  back 50 years with his  wrongly interpreted Seven Countries study  claiming that atheroma was caused by saturated fat- related hypercholesterolemia, thus   promoting  the Omega6PUFA low cholesterol diet and cholesterol-busting statins- but not explaining the question  of fatal sudden death- coronary thrombosis posed by Sir George Pickering in 1964.

Keys  may  still be laughing  his head off at the  $billions he made  for the  Fast-Food industry & Big Pharma, and the millions  of quality health years he cost gullible Americans and their ilk  with his wrong  high-omega6 diet and thence  the money-spinning statins-for-all poison myth.

After the decades of derision poured  as a result on the ketogenic high-fat-protein  low sugars Atkins diet, the Disease-monger (Food,  Sugar, Disease, Big Pharma)  Industries  will scoff,  as they recently mocked  sports physiologist  Prof Tim Noakes’ conversion to high-fat ketogenic diet for those  with the appropriate physiology, his Real Meal Revolution . .   Some cardiologists and dieticians even attacked him publicly for promoting scientific evidence against the  high-carbs lowfat  diet, including the Womens Health Initiative , not Big Pharma wishful thinking  taught  by the academics  and clinicians  whose livelihoods depend on their promoting Big Pharma and other new-tech products.. 

Read Noakes’ modern  nutrition bible, the American science writer   Gary Taubes’  The Diet Delusion(2009);  and read  the British Dr James le Fanu’s earlier Rise and Fall of Modern Medicine (1999 London pp 323-376),  that dissected Keys’  toxic cholesterol-busting mythology,  including statins  that are now promoted for all seniors.

Its not a question of statin denialism  since such drugs may have an appropriate  place in severe hypercholesterolemia. Over all, the majority of hypercholesterolemic and CVD patients will do better on multisystem-beneficial metformin (antioxidant, antiinfective, antithrombotic, antidiabetic, insulin-sensitizing, appetite-reducing, weighloss-promoting),  titrated to tolerance; with modest other essential multibeneficial  supplements- (water; fish oil, coconut oil,   DMSO, all vitamins especially BCo, C,D and K2;  minerals especially magnesium, zinc, chromium, selenium and iodine; and other aging-and -diet-conditioned deficiencies of eg CoQ10, arginine, alphalipoic acid, carnitine, ribose, carnosine, acetylcystine, garlic, cinnamon, proline  etc.  )  than  a multisystem-toxic statin.

THE SYDNEY HEART DIET STUDY    And now the truth emerges yet again, that debunked Keys’ high Omega6 diet theory: as it did in the original ignored  but landmark  Sydney Heart Diet Study report in an elite 1978 journal (Adv Exp Med Biol.)  aboutLinoleic Acid with Low fat, low cholesterol diet in secondary prevention of coronary heart disease. Woodhill JM, Leelarthaepin B, ea) discrediting  Keys’ (and the USA Govt) postulate.                                                                                                                                The new 35year followup  2013 BMJ multicentre  paper (Ramsden,  Leelarthaepin B ea) from the Universities of Sydney, N Carolina and  Illinois and the  USA NIH :    Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study  reevaluated effectiveness of replacing diet saturated fat (from animal fats, margarine,  shortenings)  with omega 6 linoleic acid Om6LA  (safflower oil/margarine )  for a mean of 39months;  in a  single blind, parallel  randomized controlled trial  in 1966-73  in 458 men 30-59 years, with recent coronary event. Controls received no specific diet instructions. Non- dietary aspects equivalent in both  groups.                                  Results The intervention group (n=221) after only 3.25 years  had 62-70% higher rates of death  and CHD and CVD than controls (n=237; P=0.04-0.05)) (all cause 17.6% v 11.8%),                  Conclusions Advice to substitute PUFA for saturated fats is a key component of worldwide dietary guidelines for CHD risk reduction. However, clinical benefits of the most abundant PUFA Om6LA , have not been established. In this cohort, substituting dietary  LA  in place of saturated fats increased the rates of death from all causes, CHD and CVD. Updated meta-analysis of linoleic acid intervention trials showed no evidence of CVD benefit. These findings (could) have important implications for worldwide dietary advice to substitute Om3LA , or PUFA  in general, for saturated fats.

THE MESA STUDY:  The Sydney Diet Heart Study outcome  has just been confirmed again by the Dec 2013 Harvard USA MESA study (de Olivera, Mozaffarian  ea J Am Heart Assoc.) Circulating and Dietary Omega-3 and Omega6 PUFA  and Incidence of CVD in the Multi-Ethnic Study of Atherosclerosis. in 6 USA centres,  which confirms that  higher intake and levels of fish oil (but not ALA or Om6PUFA) halves CVD: Over 10 years, in a multiethnic cohort of 2837 US adults- mean  age 61.4yrs at outset-  plasma  PUFAs  measured at baseline (2000-2002),  and dietary PUFAs ,  through 2010 during 19 778 person-years of follow-up,  circulating n-3 eicosapentanoic acid EPA and docosahexanoic acid  DHA inversely associated with incident CVD, with extreme-quartile hazard ratios (95% CIs) of 0.49 for EPA  (0.30 to 0.79; Ptrend=0.01) and 0.39 for DHA (0.22 to 0.67; Ptrend<0.001).  No significant associations with CVD were observed for circulating n-3 alpha-linolenic acid ALA or n-6 PUFA (linoleic acid, arachidonic acid). Associations with CVD of self-reported dietary PUFA were consistent with those of the PUFA biomarkers. Both dietary and circulating eicosapentaenoic acid and docosahexaenoic acid, were inversely associated with CVD incidence. These findings suggest that increased consumption of n-3 PUFA from seafood (but not alpha-linolenic acid or n-6 PUFA), may prevent CVD development in a multiethnic population.

But then we senior medics born around WW2  were schooled  in the English /Scottish (not American) medical tradition of Drs Cleave, Burkitt,  Painter & Campbell’s  Saccharine Diseases, refined sugar, boozing,  smoking  and physical indolence-TV sloth as the chief causes of the burgeoning post-WW2 epidemic of obesity, diabetes, vascular disease, cancer and violence. 

Humans rarely  need what Big Pharma, science  invents for megaprofits. We have known for 50 years that  the current pandemic of degenerative and modern infectious diseases  is due to bad diet – fast-food  – and slothful lifestyle,  tampering for megaprofit with food production and the environment, and reversible by correcting these factors with exercise, fresh whole food and organic farming, and avoidance of boozing,  smoking, TV sloth, and continuous wars for profit, especially the Breast-and -Prostate Screening wars for the $billions  to be made from screening aging men and women for early ie silent cancer. 

The Sydney and MESA studies quoted thoroughly debunk  the fast-food high  Om6/carbs  low fat  diet promoted the past 50 years by the Food and Disease Industry, and by  the Peskin-Rowen Om6 PEO  and the statins-for-all hypotheses;  and the nonsensical UK Wald and Law Polypill including high-risk statin-aspirin-betablocker -diuretic-ACEI   for all senior citizens. . Even an advertorial Wikipedia entry promoting  such nonsense has been allowed…

BALANCING INTAKE OF ANIMAL/DAIRY  PROTEIN -SFA WITH MARINE Om3 PUFA, PLANT MCT & Om6, without added refined/concentrated  sugars like fructose and cornstarch:                                                              As Mike Howard the Health Ranger writes this week, healthful pasture-fed butter is back, and margarine debunked even by its manufacturers; and almost half the USA states moving to enforce labeling of GMO foodstuffs so that consumers can choose what they buy. .

and biochemist  GD  Lawrence from Dept  Biochemistry, Long Island University, NY  writes in  May 2013 Adv Nutr.   Dietary fats and health: dietary recommendations in the context of scientific evidence:  Early studies showed that saturated fat SFA  diets with very low levels of PUFAs increase serum cholesterol, whereas other studies showed high serum cholesterol increased the risk of coronary artery disease (CAD). The evidence of dietary SFA  increasing CAD or causing premature death was weak. Over the years, data revealed that dietary SFAs are not associated with CAD and other adverse health effects or at worst are weakly associated in some analyses when other contributing factors may be overlooked. Several recent analyses indicate that SFAs, particularly in dairy products and coconut oil, can improve health. The evidence of ω6 polyunsaturated fatty acids (PUFAs) promoting inflammation and augmenting many diseases continues to grow, whereas ω3 PUFAs seem to counter these adverse effects. The replacement of  SFA in the diet with carbohydrates, especially sugars, has resulted in increased obesity and its associated health complications. Well-established mechanisms have been proposed for the adverse health effects of some alternative or replacement nutrients, such as simple carbohydrates and PUFAs. The focus on dietary manipulation of serum cholesterol may be moot in view of numerous other factors that increase the risk of heart disease. The adverse health effects that have been associated with SFA  in the past are most likely due to factors other than SFAs.  This review calls for a rational reevaluation of existing dietary recommendations that focus on minimizing dietary SFAs,   for which mechanisms for adverse health effects are lacking.

The University Oregon Linus Pauling Micronutrient Centre website on EFAs has not apparently been updated with the latest MESA and Sydney trial reports; but it advocates (from Japan, and American Heart Association recommendations) Om3 fishoil intake of 2-4gm/day and Om6LA perhaps three times that- rather than the Keys-based 20:1 Om6:Om3 low SFA high carbs  balance that has done so much harm in our lifetime. 

BENEFITS OF FISH OIL AND COCONUT  (MCT) OIL:           are  achieved by taking a tsp of clean (eg Baltic) codliver oil or a gm of fish oil concentrate a day; and no Om6LA supplement other than as a salad/pasta dressing; combined with liberal virgin coldpressed coconut oil for massage, cooking, and food dressing, or as a desertspoon+  a day.. 

The Wiki Health entry for coconut oil usefully still notes the historical deliberate- profiteering- fallacious marketing bias against coconut oil- SFA- which has now been again debunked by the Sydney and MESA studies:  Advocacy against coconut and palm oils in the 1970s and 1980s due to their perceived danger as a SFA saturated fat caused companies to substitute trans fats instead of  them.  Many health organizations (still) advise against the consumption of high amounts of coconut oil due to its high levels of SFA, including the USA FDA & ADA, the UK NHS,  the WHO,[3] International College of Nutrition, and American Heart Association,[7]  Coconut oil contains a large proportion of lauric acida SFA that raises blood cholesterol levels by increasing the amount of high-density lipoprotein (HDL) cholesterol and low-density lipoprotein (LDL) cholesterol. Most of the increase is however  HDL cholesterol, hence the ratio of total to HDL cholesterol is decreased.[30] A decreased ratio indicates reduced risk for heart disease.[31] It is also found in significant amounts in laurel oil, palm kernel oil (not to be confused with palm oil), and human and animal breast milk. This may create a more favourable blood cholesterol profile… Because much of the saturated fat of coconut oil is in the form of lauric acid, coconut oil may be a better alternative to partially hydrogenated vegetable oil when solid fats are required.[34] In addition, virgin coconut oil (VCO) is composed mainly of medium-chain triglycerides,[35] which may not carry the same risks as other saturated fats.[34][36

Similarly, the Wiki entry on  Medium-chain triglycerides ie coconut oil-  states its nutritional benefits without any harms: MCTs are  considered good biologically inert source of energy that the humans find reasonably easy to metabolize. MCTs have potentially beneficial attributes in protein metabolism … and..  their tendency to induce ketogenesis Due to their ability to be absorbed rapidly by the body, MCT have use in the treatment of malabsorption ailments. and  neurodegenerative disorders (e.g. Alzheimer’s, Parkinson’s disease)[14] and epilepsy through the use of ketogenic dieting.[15][16] Serum high-density lipoprotein is increasingly elevated as the chain-length of triglyceride decreases.[17]

We should not be relying  on heavily marketed,  factory-processed and poison-laced (margarines, Roundup GMO, exogenous sexhormone -laden meat ) foods, TV-armchair  lifestyle; exploiting and burning fossil fuels; and Big Pharma’s synthetic new designer wannabe drug $$$ rainchecks-  like statins, antidiabetics, antiobesity, antianxiety, antiosteoporosis, antiplatelet, antidepressant, antiinflammatory,  antihypertensive, memory, analgesic  and antibiotic  drugs  for quick fixes, which treat symptoms but not causes, do not reverse the consequences of environmental destruction, bad and deficient diet and unhappy slothful lifestyle.

Dr Driver-Jowitt pragmatically  and succinctly puts healthy diet balance in perspective.