Dr. Arash Hossein-Nezhad, currently a scholar at Boston University has teamed up with senior author Professor Michael Holick to write a spectacular in depth review about vitamin D for the highly respected journal, Mayo Clinic Proceedings.
The publication covers so many things we currently know about vitamin D, it makes a compelling case for a spectacular role of vitamin D in human health. Here were some highlights and questions answered:
Can vitamin D be washed off the skin?
I have speculated on this before, raising the question that maybe vitamin D can be washed off. The authors say, no it can’t.
Approximately 65% of the vitamin D precursor, 7-dehydro-cholesterol, is found in the epidermis. More than 95% of the pre-vitamin D3 that is produced is in the living cells of the epidermis (underneath the hard cornified outer layer) and thus cannot be removed from the skin by washing.
This explains a forgotten 1937 paper (Helmer AC, Jensen CH: Vitamin D precursors removed from the skin by washing. Studies Inst Divi Thomae 1937, 1:207-216.) in which the authors proved that irradiated surface skin oils (sebum) of young men cured rickets in animals and that vitamin D containing sebum was removed by washing. It is probably the 5% of vitamin D made on the surface of the skin that is removed by washing.
Is there a difference between vitamin D derived from sun exposure and from food/supplements?
Ingested vitamin D appears to differ from sun-derived vitamin D only in the fact that ingested vitamin D is first transported away from the gut by chylomicrons before it binds to D binding protein in the lymphatic system.
Otherwise, vitamin D3 is vitamin D3, no matter if it’s coming from your skin or oral intake.
How does vitamin D work during pregnancy?
25(OH)D is transferred across the placenta; fetal cord blood concentration of 25(OH)D is correlated with the mother’s 25(OH)D concentration. However, the active metabolite 1,25(OH)2D does not readily cross the placenta, despite the mother having up to a fourfold increase in her serum 1,25(OH)2D levels.
The fetal kidneys and the placenta provide the fetal circulation with 1,25(OH)2D. This apparently occurs early in gestation, meaning the fetus can activate its own vitamin D.
Epidemiologic evidence has suggested a link between fetal life events and susceptibility to disease in later adult life. This paradigm, referred to as fetal programming, may have a profound effect on public health strategies for the prevention of many illnesses in later life. This may mean that if you were vitamin D deficient as a fetus, taking vitamin in later adult life may not fully protect you from these illnesses.
Can vitamin D help with autoimmune diseases?
Epidemiologic, genetic, and basic science studies indicate a potential role of vitamin D in the pathogenesis of certain systemic and organ specific autoimmune diseases, such as type 1 diabetes mellitus, multiple sclerosis (MS), rheumatoid arthritis (RA), and Crohn’s disease.
Vitamin D suppresses autoimmune disease pathology by regulating the differentiation and activity of CD4+ T cells, resulting in a more balanced TH1/TH2 response that favors less development of self-reactive T cells and less autoimmunity, by increasing the number of T-regulatory cells. This gives hope to the idea that adequate, perhaps pharmacological, doses of vitamin D may have a treatment effect in ongoing inflammatory autoimmune disorders.
The authors point out that treatment of active RA with a high-dose vitamin D3 analogue resulted in improvement of symptoms of RA in 89% of patients, with 45% of patients entertaining a complete remission.
Whether supplemental vitamin D3 can effectively treat active MS is still a matter of debate. In a trial in active MS using escalating doses up to 40,000 IU/d of vitamin D3 for 28 weeks followed by 10,000 IU/d for 12 weeks, there were no significant adverse events, and there seemed to be significantly less progression of disability in the treatment group.
Do genetics influence vitamin D levels?
The genetic contributions to circulating 25(OH)D represent a complex trait for which family studies have estimated heritability ranging from 43% to 80%.
On rare occasions, some patients who deny taking a vitamin D supplement have unexplained high normal 25(OH)D levels in the range of 40 to 80 ng/mL. It is believed that this is due to a genetic mutation of enzyme that breaks down 25(OH)D.
What effect can sun exposure have on mortality?
The authors point out that it was estimated that if all the people in the United States were to double their sun exposure, the net result could be up to 400,000 reduced deaths compared with only 11,000 increased deaths from melanoma and other skin cancer.
Board member Dr Bill Grant calculated that in a span of 24 years (1970-1994), 566,400 Americans died of cancer because of inadequate exposure to solar UV-B radiation.
The paper is free to read in its entirety, and I recommend doing so.