Vitamin D: Answers

There is no such thing as Vitamin D deficiency and no evidence that low levels are the cause of disease. Many inflammatory conditions lead to disruption of Vitamin D production and hence are the cause of low levels rather than the result of them.

Taking supplements can therefore only do harm.

Inflammation and vitamin D: the infection connection – Meg Mangin , Rebecca Sinha, Kelly Fincher.

This paper presents many studies whose findings are contrary to popular belief. The authors claim that they can find no evidence anywhere of insufficient D levels being the direct cause of any disease and that the ‘optimum levels’ set by health authorities have no basis in scientific fact.

Healthy people can have ‘low’ Vitamin D status as well as sick individuals and sometimes disease is associated with high levels. In other cases, disease is associated with high levels of one form of D and low levels of another at the same time.

The results suggest that the problems are arising not from an absolute deficit but rather from a mismanagement of existing resources which is in turn caused by an existing condition or deficit of some other essential nutrient.

Outcomes related to autoimmune disorders, cancer, cardiovascular disease and hypertension, diabetes and metabolic syndrome, falls and physical performance, immune functioning, infections, neuropsychological functioning, and preeclampsia could not be linked reliably with calcium or vitamin D intake and were often conflicting.’’ -Ross et al.

Vitamin D3 is produced by the action of sunlight on cholesterol in the skin.
Dark and light skinned people produce different amounts of D3 in their skin but this was found to be related to differing amounts of cholesterol and not skin pigmentation. – Bogh et al.

  • Racial pigmentation protects against UV but does not prevent the generation of normal levels of active Vitamin D. – Matsuoka et al.
  • People with dark skin also compensate for low 25(OH)D by rapidly converting it to the active 1,25(OH)2D metabolite, thus allowing them to maintain adequate vitamin D status. – Matsuoka
  • Skin pigmentation does not appear to negatively affect vitamin D status – Kelsey
  • Ten to 15 min of sunlight or daylight exposure to a small area of skin (e.g., the forearm or face, etc.) twice a week, without sunscreen, supplies all the vitamin D necessary for health.
  • In dense metropolitan areas tall buildings provide shade but shade gives up to 50 % of UV rays. (Global solar UV index)
  • Indoor workers receive 10–20 % of outdoor workers’ yearly UV exposure and for many, this may be adequate, especially if sunlight exposure is higher when
    they are not working
  • Because over 90 % of UV rays may penetrate clouds Environmental factors are rarely an impediment to photosynthesis of adequate vitamin D.

As the skin ages, there is a decline in the cutaneous levels of 7-dehydrocholesterol, resulting in a marked reduction of the skin’s capacity to produce vitamin D. This can result in a fourfold reduction in vitamin D3 production in a 70-year-old compared to a 20-year-old, but healthy levels are maintained despite this. – MacLaughlin , Holick.

Population levels of Vitamin D seem to correlate with latitude, giving the impression that differences are in fact caused by the difference in light levels. However, this seemingly obvious inference, like almost everything else with Vitamin D, appears to be an illusion, with adaptive skin types being the main determinant of Vitamin D production.

‘‘It may no longer be correct to assume that vitamin D levels in populations follow latitude gradients’’. Kimlin et al.

‘‘Geophysical surveys have shown that UV-B penetration over 24 h, during the summer months at Canadian north latitudes when there are many hours of sunlight, equals or exceeds UV-B penetration at the equator.’’ – Lubin

So storage D is built up over spring, summer and autumn to be stored in the liver and body fat for use over winter. – Ross. Remember that what is usually measured are blood levels which fluctuate with the seasons and are not necessarily an indicator of liver storage.

A study published in The Lancet found little evidence supporting the use of D3 supplements to improve bone density (Reid) and another found instead that increased bone turnover and decreased bone density was associated with high levels of 1,25(OH)2D. – Brot et al.

Adequate vitamin D is essential to prevent rickets, but so is adequate calcium intake; if either calcium or vitamin D is deficient then bone health suffers.

  • Studies find that rickets occurs in sunny countries due to poor calcium intake and is cured with increased consumption
  • Problems with rickets in Inuit children are likewise caused by calcium deficiency.
  • High levels of 1,25(OH)2D stimulate bone osteoclasts, leading to osteoporosis, dental fractures and calcium deposition into soft tissue. – Ishizuka et al.
  • A combination of high 1,25(OH)2D and low 25(OH)D is associated with the
    poorest bone health. – Vanderschueren et al.

Low levels are a result of illness – not the cause.
Decreases in vitamin D levels are a marker of deteriorating health. Ageing and inflammatory processes involved in disease occurrence and clinical course reduce vitamin D concentrations, which would explain why vitamin D deficiency is reported in a wide range of disorders.

Decreases in vitamin D levels are a marker of deteriorating health. Ageing and inflammatory processes involved in disease occurrence and clinical course reduce vitamin D concentrations, which would explain why vitamin D deficiency is reported in a wide range of disorders.

“We postulate that inflammation is the common factor between most non-skeletal health disorders and low 25(OH)D concentrations. Inflammatory processes involved in disease occurrence and clinical course would reduce 25(OH)D, which would explain why low vitamin D status is reported in a wide range of disorders.

“However, increases in 25(OH)D have no effect on inflammatory processes or on disorders at the origin of these processes.

Vitamin D: chasing a myth? Vitamin D status and ill health: a systematic review.
Autier P, Boniol M, Pizot C, Mullie P. Lancet Diabetes Endocrinol. 2013

The magnesium (Mg) connection
As the diagram below shows, the Vitamin D system forms a complex production system with one form of D being converted into another for either storage or usage and where magnesium is involved at every stage of the process. It follows that if magnesium is either itself deficient or badly managed, then quite likely something will go wrong with the vitamin D levels.

In this event, the levels of D are not caused by a lack of supply but rather a dis-regulation of what is already available.

It is claimed that 60% of westerners are deficient in Magnesium and a similar proportion having low levels of Vitamin D. It therefore seems reasonable to ask if the levels of the vitamin are in fact caused by the mineral deficiency.

Supplementation. It appears then that levels of vitamin D are maintained in the body by a complex management system and are result of a multitude of factors.
It seems highly unlikely then that a severe regulatory dysfunction could be cured simply by pumping in more of just one of the substances involved.

“Despite the recent increase in vitamin D supplementation, chronic diseases have increased and are expected to continue increasing. Consequently, more vitamin D experts are beginning to reconsider vitamin D supplementation among the general
population” – Tseng,

Given the variation between populations and the possibility that certain individuals are having trouble regulating the D they already have, recommending higher vitamin D intake to large populations now seems irresponsible to the point of recklessness.

Because adverse effects of vitamin D supplementation may take decades to
be realized, clinicians (mindful of the medical ethics precept ‘First, do no harm’) should err on the side of caution; follow the IOM guideline and wait for the results of long term vitamin D studies.
” – Mangin et al.


Researchers have once more become over-excited by lots of correlation and failed to pay attention to the requirements of causation; they have again confused cause and effect.

  • It is unlikely that anyone is deficient in Vitamin D
  • There is no evidence of a population succumbing to disease for lack of it
  • Measured levels do not and can not characterise the system as a whole
  • Inflammation is the cause of low levels of D not the result
  • Magnesium deficiency is likely to be a causal factor in inflammation
  • We need remarkably little sunlight to get by
  • Supplementation could prove dangerous for a few unlucky individuals
  • There is no scientific basis for the current recommended levels


Inflammation and vitamin D: the infection connection – Meg Mangin, Rebecca Sinha, Kelly Fincher.

Vitamin D production after UVB exposure depends on baseline vitamin D and total cholesterol but not on skin pigmentation – Bogh MK, Schmedes AV, Philipsen PA, Theiden E, Wulf HC.

Racial pigmentation and the cutaneous synthesis of vitamin D. – Matsuoka LY, Worstman J, Haddad JG, Kolm P, Hollis BW.

Global surface ultraviolet radiation climatology from TOMS and ERBE data. – Lubin D, Jensen EH, Gies HP. J Geo Res. 1998;103(D20):26061–91.

Global Solar UV Index: A Practical Guide. Geneva, Switzerland: World Health Organization; 2002. ISBN 9241590076.

Effects of vitamin D supplements on bone mineral density: a systematic review and meta-analysis. – Reid IR, Bolland MJ, Grey A.
Lancet. 2013;383:146–55.

Vitamin D antagonist, TEI-9647, inhibits osteoclast formation induced by 1alpha,25- dihydroxyvitamin D3 from pagetic bone marrow cells. – Ishizuka S, Kurihara N, Miura D, et al. J Steroid Biochem Mol Biol. 2004;89–90(1–5):331–4.

.Dietary reference intakes for calcium and vitamin D. – Ross AC, Taylor CL, Yaktine AL, Del Valle HB. Washington: National Academy of Sciences; 2010. 0-309-16394-3

Skin Pigmentation does not affect vitamin D status in community-dwelling Mexican–American women – Villa M, Kelsey J, Chen J, Marcus R. . J Bone Miner Res. 1994;9(Suppl 1):S418.

Aging decreases the capacity of human skin to produce vitamin D3 – MacLaughlin J, Holick MF. . J Clin Invest. 1985;76(4): 1536–8.

Relationships between bone mineral density, serum vitamin D
metabolites and calcium:phosphorus intake in healthy perimenopausal women.
– Brot C, Jørgensen N, Madsen OR, Jensen LB, Sørensen OH.
J Intern Med. 1999;245(5):509–16.

Active vitamin D (1,25-dihydroxyvitamin D) and bone health in middle-aged and
elderly men: the European Male Aging Study (EMAS)
– Vanderschueren D, Pye SR, O’Neill TW, et al. . J Clin Endocrinol Metab. 2013;98(3):995–1005.

Vitamin D deficiency among northern Native Peoples: a real or apparent
– Peter Frost

Tseng L. Controversies in vitamin D supplementation. eScholarship. 2003.

Vitamin D: chasing a myth? Vitamin D status and ill health: a systematic review.
Autier P, Boniol M, Pizot C, Mullie P. Lancet Diabetes Endocrinol. 2013