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A bit of D for CVD

Vitamin D is touted for pretty much every health condition out there. While observational evidence has strongly linked optimal vitamin D levels to cardiovascular disease, the trial evidence has been more mixed. This trial attempts to strengthen that literature base.

Study under review: Vitamin D3 supplementation does not modify cardiovascular risk profile of adults with inadequate vitamin D status


Vitamins are organic compounds (organic chemistry, not organic produce) which are required for an organism to live. They generally serve as cofactors, meaning they help proteins do their job. Vitamins also have the potential to form compounds similar to hormones.

Speaking of hormone-like compounds, previous issues of the ERD go into detail about various aspects of vitamin D research. Vitamin D deficiency is fairly common[1], even in developed countries, and a strong association between serum vitamin D levels and mortality[2] has been repeatably observed[3].

Vitamin D is a fat-soluble vitamin, like vitamins A, E, and K. But unlike these other vitamins, mammals are able to synthesize vitamin D, specifically when exposed to UV-B light (which is shown in Figure 1). UV-B has a wavelength in the 280–315nm range and is produced by the sun, but not by most household lights. This light-induced synthesis has earned vitamin D the moniker “the sunshine vitamin”. While vitamin D is readily stored for rather long periods of time, serum levels of vitamin D can drop considerably during winter time, when UV intensity is low and duration of sunlight is short.

Figure 1: How vitamin D is synthesized using UV light

Vitamin D has several biological functions, including in the innate immune system[4], calcium absorption from the diet, modulating bone calcification[5], adjusting circulating phosphorous levels[6], and working with parathyroid hormone to maintain serum calcium levels. The majority of these functions are mediated by vitamin D binding to the vitamin D receptor (VDR). So, by examining how tissues in the body express this receptor, researchers can begin to determine which tissues vitamin D influences. Within the cardiovascular (CV) system, the endothelial cells (cells within the interior of blood vessels), smooth muscle cells (a type of muscle cell that is found around the blood vessels), and cardiomyocytes (heart muscle) all express VDR.

Thus, it is not surprising that several studies[7] have observed an association between low serum levels[7] of vitamin D and CV events and CV-related mortality[3]. This is likely due to the role that vitamin D plays in preventing vascular calcification[8], reducing blood pressure[9] via the renin-angiotensin-aldosterone system, lowering blood cholesterol levels[10], and reducing excess inflammation[11].

The study under review was designed to allow researchers to better understand the effect of vitamin D supplementation on CV health. Researchers provided individuals with a relatively low dose of vitamin D (20 micrograms (μg) or 800 IU) during the winter months while monitoring a rather comprehensive list of markers of CV health, including blood pressure, heart rate, serum lipids, vascular calcification, and several haematological variables. What separates this study from previous studies is this comprehensive analysis, that the participants were non-obese healthy adults, and a rather low dosage of vitamin D.

Serum vitamin D levels drop during winter months, as UV-B mediated synthesis is reduced. This may be detrimental to health, and several mechanisms (blood pressure, cholesterol, and vascular calcification) have been identified for how vitamin D specifically affects cardiovascular health. The objective of this study was to observe if low-dose vitamin D supplementation during winter months in healthy individuals has an impact on cardiovascular risk markers.

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