Vitamin D is not actually a vitamin, but a hormone related to testosterone and oestrogen. Vitamin D is produced naturally in our body by the action of ultra violet light on cholesterol in our skin. Alternatively, we can ingest vitamin D in out diets from a limited number of foods such as fish, fish liver oils and eggs. Once in the blood, the vitamin D is transported on the vitamin D binding protein (DBP) and taken to the liver where it is 25-hydroxylated to form hydroxyvitamin D [25(OH)D]. Plasma levels of 25(OH)D are used to assess the vitamin D status of individuals, and optimal levels are considered to be around 100nmol/L. Plasma 25(OH)D can be further metabolised in the kidney where it is 1α-hydroxylated to form dihydroxyvitamin D [1,25(OH)2D]. This final active form of vitamin D then plays a role in calcium metabolism as well as having important immunomodulatory and cell signalling effects.
Research suggests that the vitamin D status of many individuals is too low and that the recommended intakes should be revised upwards. Because sun exposure is not always possible and most diets contain far too few vitamin D containing foods, supplements should be considered if plasma levels of 25(OH)D are low. However, supplementation is not straightforward, because vitamin D is commercially available in two different forms. Some supplements, including those issued on prescription by the mainstream medical establishment, contain ergocalciferol or vitamin D2. Other supplements contain cholecalciferol or vitamin D3. Both forms are considered equivalent by mainstream health professional, but this viewpoint is based on studies that were conducted during the treatment of children with rickets, over seventy years ago. Research has moved on a great deal since then, and the latest findings suggest that cholecalciferol is the preferred choice for improving plasma levels.
Vitamin D2 was first produced artificially in the 1920’s in a process that was patented by the drug companies. The artificial manufacture of D2 lead to the development of the medicinal preparations called Viosterol. The form available on prescription to this day is the D2 form, and many of the multivitamins on the market also contain the artificial D2 form. The potency of D2 has been questioned by scientist ever since vitamin D2 came to the market all those years ago, but the men in shiny suits continue to sell their patented artificial version in the quest for profit. However, the evidence is now pretty well established that vitamin D3 is a more potent form of the vitamin in humans and the preferred choice for supplements. There are a number of reasons why vitamin D3 is a better choice, but most importantly, it is the form that it produced naturally by the action of ultra violet light.
Vitamin D3 is therefore the natural form of the vitamin found in humans, and evidence suggests the more biologically active of the two. Vitamin D3 is known to have a higher affinity for the vitamin D binding protein, which prevents excessive excretion and maintains higher plasma levels for longer. Because vitamin D2 binds less strongly, it has a shorter circulating half life and is cleared from the blood more quickly. For example, research in the American Journal of Clinical Nutrition in 1998 showed that after supplementation with 4000 IU of vitamin D for 2 weeks, a 70 % greater increase in serum 25(OH)D was seen with vitamin D3 over that of vitamin D2. Vitamin D3 also appears to have a higher affinity for the enzyme vitamin D hydroxylase in the liver. This suggests that vitamin D3 is more likely to be hydroxylated and will more quickly raise plasma levels, when compared to vitamin D2.
In addition, evidence suggests that vitamin D2 and vitamin D3 may possess different metabolic fates which influences their biological activity. For example, as well as 25-hydroxylation, vitamin D can also be 24-hydroxylated in the liver. This hydroxylation reduces the already compromised affinity of vitamin D2 to bind to the vitamin D binding protein. This exacerbates the problem of enhanced clearance of vitamin D2 from the blood compared to vitamin D3. Evidence also suggests that vitamin D2 can be more easily deactivated than vitamin D3. For example, Vitamin D can be hydroxylated to 24,25(OH)2D and then 1,24,25(OH)3D in the kidney. These steps inactivate vitamin D2, but for inactivation of vitamin D3, an additional step may be required. It should not be surprising that vitamin D3 is a more potent form of the vitamin in humans, as vitamin D2 is not a normal part of human biology.
Another potential problem for vitamin D2 is evidence suggesting that in powder form, as found in supplements, it is unstable and degrades rapidly. Analysis of supplements containing vitamin D2 have shown that the actual content of the tablets can be 50% lower than the stated claim on the label. There is also evidence that inert tablet packaging substances may affect the degradation rates of vitamin D2. The inability to acknowledge the poor performance of D2 compared to D3 is highlighted by the refusal of mainstream medicine and the supplement manufacturers to switch to the D3 form of the vitamin. It is already known why the medicine men in shiny suits only sell vitamin D2, and this relates to their shadowy agenda. However, the supplement industry should know better, and they do themselves a disservice by continuing to offer an inferior form of vitamin D. Especially as studies show that vitamin D2 has questionable stability in powder form in supplement.
RdB