Vitamin D nutrition does not cause peripheral artery disease.

Peripheral Artery Disease To the Editor: We wish to point out to readers who look casually through the Brief Review by Norman and Powell1 or who have access only to its abstract that the review is not relevant to vitamin D in the context of nutrition. Furthermore, the authors failed to present evidence that suggests that vitamin D may have cardiovascular benefits. The major difficulty with the Brief Review is that it fails to distinguish between what is physiological nutrition in humans, versus the administration to rats of pharmacological amounts of vitamin D, its derived hormone, calcitriol, or analogs. The vitamin D–nicotine (VDN) model of arteriosclerosis has been used for many years2 in rats using a huge bolus dose of vitamin D (40 000 IU/rat) along with nicotine. Per kg body weight, the vitamin D dose in animal models exceeds by 200-fold what humans can derive through sun exposure (250 to 625 micrograms/d, or 10 000 to 25 000 IU/d). The term “vitamin D” should not have been used in such a generic sense. For example, take the sentence, “In postmenopausal women, vitamin D supplementation (two micrograms per day) increased CD3 and CD8 subsets of lymphocytes.”1 Despite appearances, this does not refer to either the nutrient vitamin D or to nutritional supplementation. Instead, the two micrograms relates to double the physiological replacement dose of one of the most potent hormones in our bodies, calcitriol. Those who read the sentence without checking directly the article cited3 are left the false impression that vitamin D supplementation is risky; if 2 g affects lymphocytes, then so should the 10 g in a multivitamin. In the abstract and in the text they write “Vitamin D is likely to have a role in the paradoxical association between arterial calcification and osteoporosis.”1 However, Norman and Powell fail to mention that there is no effect of vitamin D consumption on circulating levels of the calcitriol that they propose as the agent affecting arteries.4,5 Under the heading of “Vitamin D and Animal Models,” Norman and Powell stated that “Chronic less toxic treatment also results in metastatic calcification and deteriorating renal function. In general, vitamin D results in arterial wall calcification and a variety of other ‘arteriosclerotic’ changes.”1 However, to support this statement they cite drug company–funded research that involved molecular analogs of the vitamin D hormone given at pharmacological doses.6 None of this is pertinent to vitamin D in the context of human nutrition. In the section headed “Epidemiological Studies of Vitamin D and Arterial Disease”, the authors report some of the literature on vitamin D and cardiac disease, but they have omitted articles which provide evidence of an inverse association between serum 25hydroxyvitamin D and myocardial infarction.7,8 They have made no mention of the reported inverse association between vitamin D status and cardiac function.9 There is also a growing literature of an inverse association between vitamin D status and diabetes,10,11 which is a major risk factor for cardiovascular disease. We regret writing such a critical letter, but we do not regard the recently published Brief Report as a balanced summary of the research on vitamin D and cardiovascular disease. To complicate the issue, the Brief Review is ambiguous about whether the “vitamin D” being discussed relates to nutrition, endocrinology, or pharmacology.12