The large-scale genetic study clarifies the link between high blood pressure (hypertension) and vitamin D deficiency - confirming that low levels of the vitamin can trigger hypertension and an increased risk of cardiovascular disease (CVD).
Led by Dr Vimal Karani from the University College London, UK, the research team noted that while observational studies have already suggested such a link, large-scale genetic study was necessary before any cause and effect could be proven.
“We knew from earlier observational studies that low 25(OH)D concentrations were likely to be associated with increases in blood pressure and hypertension, but correlation is not causality," said Karani.
“Additionally, randomised controlled trials of vitamin D supplementation in humans have produced inconsistent effects on cardiovascular outcomes."
"The whole picture was somewhat confused, and we decided to try to figure it out once and for all."
Presenting their findings at the annual conference of the European Society of Human Genetics (ESHG), Karani and his team added that their new study 'strongly suggests' that some cases of cardiovascular disease "could be prevented through vitamin D supplements or food fortification."
The new data - from the D-CarDia collaboration - involving 35 studies, and information from over 155,000 individuals at numerous centres in Europe and North America.
Karani and his team revealed that the people with high concentrations of 25-hydroxyvitamin D (25(OH)D) had reduced blood pressure and therefore a reduced risk of hypertension.
The research team used genetic variations - known as single nucleotide polymorphisms, or SNPs - as 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 analysed, 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.
Karani explained that even with the 'likely presence' of unobserved confounding factors, the approach the team followed - known as Mendelian randomisation - allowed them 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,” said Karani.
The lead researcher revealed that the team now intend to further their work by examining the causal relationships between vitamin D status and other cardiovascular disease-related outcomes including cholesterol, inflammatory markers like C-reactive protein, 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," said Karani.