Vitamin D deficiency is a very common problem in the U.S., and especially in an aging population. Older individuals are at greater risk for deficiency because aging lowers the amount of 7-dehydrochlesterol in the skin and thus lowers the ability to produce vitamin D, as well as lower absorption. Most of our vitamin D comes from sun exposure, and only a small amount typically, obtained from food or supplements. Due to our decreasing exposure to sun, with spending so much time indoors, wearing clothing and/or sunscreen, the majority of us just don’t get enough vitamin D anymore, whether we live in Alaska or Arizona.
Vitamin D deficiency is associated with increased parathyroid secretion, increased bone turnover, osteoporosis, and increase risk of hip and other fractures. Lower levels of vitamin D as measured in the blood, is also associated with risks of cancers of the colon, breast and ovary in several observational studies. Vitamin D deficiency has other serious implications and has been associated with multiple sclerosis, type-1 diabetes, Chrohn’s disease , and even increases in the risk of hypertension and cardiovascular disease.
Causes of vitamin D deficiency include hereditary disorders, reduced skin synthesis and absorption of vitamin D, and acquired disorders of vitamin D absorption, metabolism and responsiveness.
We get our vitamin D from exposure to sunlight, from our diet and from supplementation. Vitamin D3 is produced in the skin on exposure to ultraviolet radiation, and vitamin D2 is derived from plants and enters our body only through the diet or supplementation. There are two major supplemental forms of vitamin D; vitamin D2 (ergocalciferol) and vitamin D3 (holecalciferol). Vitamin D2 is manufactured through the ultraviolet irradiation of ergosterol from yeast. Vitamin D3 is made through the ultraviolet irradiation of 7-dehydrocholesterol from lanolin. Vitamin D2 is considered to be vegetarian suitable, and vitamin D3 is animal derived, from the lanolin. Both forms are often added to foods such as milk, orange juices, infant formulas, cheeses and breakfast cereals. Natural food sources of vitamin D3 include salmon, sardines, mackerel, tuna, shiitake mushrooms, egg yolks, cod liver oil and exposure to sunlight. Both vitamin D2 and vitamin D3 are available in over the counter supplements, including low doses, and moderately higher doses, typically not more than 5,000 IU. High and higher doses of vitamin D2 are available by prescription.
The back story on whether or not vitamin D2 and vitamin D3 are equally effective, goes back to studies in the 1930s where they were assumed to be equally effective in humans. Over time, human studies comparing the increase in blood levels of vitamin D with the supplementation of vitamin D2 vs vitamin D3 have been inconsistent in their results and few in number. They have also been wrought with problems in small sample sizes, lack of vitamin D stability of the products used, wide variations in the seasons the blood was drawn (serum levels of vitamin D are naturally higher in the sunnier months), variable intestinal absorption amongst individuals, variable baseline serum levels of vitamin D, previous history of vitamin D supplementation and variations in age (older people have less vitamin D absorption). While it is common thought that vitamin D2 is about a third of the potency of vitamin D3, these variables in the studies, make it extremely difficult to make comparisons and draw accurate conclusions. One small study done in 1998 did demonstrate that vitamin D3 yielded a small increase in serum 25-hydroxyvitamin D over the vitamin D2. A study of 30 men in 2004, between the ages of 20 and 61, demonstrated that the rise in blood levels within the first few days of receiving a single high dose was the same for both forms, indicating equivalent absorption. However, the vitamin D3 treated individuals had a continued rise over two weeks and peaked at 2 weeks, while the vitamin D2 treated men, had a decline to their baseline, by day 14. One might conclude from these two well designed studies, that the rise in serum levels with vitamin D3 might be only a very small amount, as in the first study. Or, rather than give one dose to last 2 or more weeks where there was a greater effect with vitamin D3, as in the second, this same study showed that within the first 3 days of either form, the rise in blood levels, was the same, indicating that a daily dose of either form of vitamin D would be equivalent.
The newest study addressing this question, challenges the long held belief that vitamin D2 is less potent or less effective than vitamin D3 in raising and maintaining blood levels. This was a randomized, placebo-controlled, double-blinded study of healthy individuals ages 18-84 years who received either placebo, 1,000 IU of vitamin D3, 1,000 IU of vitamin D2, or 500 IU of vitamin D2 plus 500 IU of vitamin D3 daily for 11 weeks at the end of the winter. Sixty percent of the study subjects were vitamin D deficient at the start of the study (< 20 ng/ml). This three month study of 68 individuals found that supplementation with both forms produced similar results. Neither 1,000 IU of vitamin D2 or vitamin D3 raised 25-hydroxyvitamin D levels in vitamin D deficient subjects to a level above 30 ng/ml. The authors concluded that vitamin D2 is equally as effective as vitamin D3 in maintaining 25-hydroxyvitamin D status. My main point in this article is not to prove that the vegetarian supplementation of vitamin D2 is as potent as the non-vegetarian supplement vitamin D3, but rather, that we cannot state with reasonable certainty that D3 is a third more potent, as is generally thought. Vegetarians may find some comfort in this article about vitamin D2 and vitamin D3 yielding similar results, at least when taken daily. If not, then the most we could assert, is that we may need a one third higher dose of vitamin D2 to yield the same results. References
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