The researchers used genetic variants known as single nucleotide polymorphisms, or SNPs, as proxy markers to reflect individual’s vitamin D status in order to test for a causal association with blood pressure and hypertension. When the results were analyzed, they found a significant link; for every 10% increase in 25(OH)D concentrations, there was a 8.1% decrease in the risk of developing hypertension.
“Even with the likely presence of unobserved confounding factors,” Dr. Karani S will say, “the approach we followed, known as Mendelian randomization, allows us to draw conclusions about causality because the genetic influence on disease is not affected by confounding. To put it in simple terms, by using this approach we can determine the cause and effect and be pretty sure that we’ve come to the right conclusion on the subject.”
The prevalence of low vitamin D is common throughout the western world, and the data may have important public health implications. The best-known manifestation of vitamin D deficiency is the childhood bone disease rickets, where long bones are weakened by the deficiency and start to bend. Recently, however, Vitamin D has been implicated in a number of other non-skeletal-related conditions, but studies involving supplementation have given conflicting results.
“Our study strongly suggests that some cases of cardiovascular disease could be prevented through vitamin D supplements or food fortification,” says Dr. Karani S. “Our new data provide further support for the important non-skeletal effects of vitamin D. We now intend to continue this work by examining the causal relationship between vitamin D status and other cardiovascular disease-related outcomes such as lipid-related phenotypes, for example, cholesterol, inflammatory markers such as C-reactive protein, and type 2 diabetes and markers of glucose metabolism. We believe that we still have a lot to find out about the effect of Vitamin D deficiency on health, and we now know that we have the tools to do so.”