(No emergencies or surgery- these must go to nearest polyclinic or hospital ER). .
or consultations by Telephone/email where appropriate.
update 10 Dec 2016 remember that quotations from experts are in italics:
Note noteworthy timeous new reviews: in the latest 7 dec BMJ :
advising on low sugar low starch to treat obesity diabetes,
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 http://articles.mercola.com/sites/articles/archive/2016/12/11/gary-taubes-the-case-against-sugar.aspx , 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 http://smashthefat.com/science/ 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 https://healthspanlife.wordpress.com/2015/08/29/adopting-low-carbs-high-fat-healthy-diet-for-most/
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. http://www.samj.org.za/index.php/samj/article/view/11605/7753 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 https://feinmantheother.com/ . 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 https://www.ncbi.nlm.nih.gov/pubmed/24675110and 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 http://www.bmj.com/content/355/bmj.i5792, 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: http://www.bmj.com/content/355/bmj.i6487.As 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- tarsiers– and 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 http://www.nhs.uk/conditions/pregnancy-and-baby/pages/solid-foods-weaning.aspx 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. . 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 http://everythingbirthblog.com/2012/01/rice-milk-why-it-says-not-to-give-it-to-children-under-five/ 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 Harvey; Vilhjalmur 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.
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. http://www.ncbi.nlm.nih.gov/pubmed/24500153 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. ” – “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, healthy term infants require only breast milk (with vitamin D supplementation)  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 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. 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 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. 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. “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. “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. 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. 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. 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. Individual circumstances may make it appropriate for some infants to start complementary feedings as early as four months of age. “Age-appropriate intake of calories and micronutrients is important for growth, motor and mental development. 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. 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. 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. 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. When there is a delay in introduction of iron fortified foods, oral iron supplementation needs to be considered. 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. 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. 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.
http://www.thestar.com/news/canada/2012/09/24/hold_the_pablum_’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: email@example.com
HIGH TO MASSIVE DOSE VITAMIN D3 IMPORTANCE – TEN TIMES MORE THAN MAXIMUM SUNLIGHT CAN PROVIDE – IN REVERSING COMMON VIT D DEFICIENCY/RESISTANCE FOUND IN ALL MAJOR DISEASE eg ALL INFECTIONS, INSOMNIA, MULTIPLE SCLEROSIS MS, Myasthenia Gravis, SLE, RA, PARKINSON’S, DEPRESSION, VASCULAR DISEASE, CANCER, VITILLIGO, PSORIASIS, PERIPHERAL NEUROPATHIES, MENTAL ILLNESS.
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 Thisisms.com 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. .
THE NEUROPATHY OF DIABETES, DRUGS/TOXINS, POST-VIRAL,TRAUMA, SPONDYLOSIS, DEMENTIA:
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 6.9; retinopathy [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 600 000 IU vitamin D in 143 participants with predominantly type 2 diabetes, aged ~ 52.3years, with high Douleur Neuropathique 4 (DN4) score by 20 weeks gave significant increase in 25(OH)D (from 31.7 to 46.2±10.2 ng/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 http://www.ncbi.nlm.nih.gov/pubmed/23331510 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: https://www.youtube.com/watch?v=Vxwk-YPrx7o&feature=youtu.be. 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.
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 2015: 50 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 formation. The 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).
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. .http://www.ausport.gov.au/data/assets/pdf_file/0003/594174/CORP_33413_SSF_Vitamin_D_FS.pdf 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 (www.iom.edu/vitamind). 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.
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. http://www.ncbi.nlm.nih.gov/pubmed/27113121 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. http://www.ncbi.nlm.nih.gov/pubmed/27114971 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. : http://www.ncbi.nlm.nih.gov/pubmed/27114973 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
https://riordanclinic.org/2013/10/vitamins-d3-and-k2-the-dynamic-duo/ 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.
Newsletter: Gary Null and vitamin D toxicity 2010 by John Cannell, MD http://www.vitamindcouncil.org/newsletter/newsletter-gary-null-and-vitamin-d-toxicity/ “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..http://www.vitamindcouncil.org/newsletter/newsletter-gary-null-and-vitamin-d-toxicity/ http://www.livescience.com/50765-vitamin-d-supplements-toxicity.html
Vitamin D Overdose Dr. Liji Thomas, MD 2016 http://www.news-medical.net/health/Vitamin-D-Overdose.aspx 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.. http://press.endocrine.org/doi/10.1210/jc.2010-1999?url_ver=Z39.88-2003&rfr_id=ori%3Arid%3Acrossref.org&rfr_dat=cr_pub%3Dpubmed& 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 http://www.thecamreport.com/2009/11/soladek-toxicity-in-a-60-year-old-woman/
Comments by Prof Robert P. Heany Creighton University, Omaha, Nebraska on Lowe et al: Hypercalcemia in vitamin D intoxication JCEM http://press.endocrine.org/e-letters/10.1210/jc.2010-1999 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-Ã¡- 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
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.
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 .
Unlike the Big Pharma-Disease-Industry- controlled denialists of conservative safe natural phamacological vitamin therapy like the Linus Pauling Institute and Wikipedia https://en.wikipedia.org/wiki/Vitamin_K2,
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 http://articles.mercola.com/sites/articles/archive/2010/08/26/this-could-be-even-bigger-than-the-vitamin-d-discovery.aspx, Byron Richards already in 2010 wrote a major review promoting K2 multipurpose: http://www.wellnessresources.com/health/articles/vitamin_k2_bones_cardiovascular_health_blood_sugar_control_cancer_prev/
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. Knapen, Vermeer 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 Concerns: If 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.
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.
SO WHAT FOOD SHOULD WE EAT? READ ON AT https://healthspanlife.wordpress.com/2014/01/29/what-food-should-you-eat/