12.06.21
Vitamin D deficiency may nearly double one’s risk of developing cardiovascular disease (CVD), and also increases the chances of hypertension, a new observational study conducted by researchers at the University of South Australia suggests.
The study, which compared 44,519 CVD cases with 251,269 controls, all sourced from the UK Biobank, was a statistical analysis breaking down CVD risks based on a range of serum vitamin D concentrations.
Globally, CVD is linked to 17.9 million deaths annually, the leading cause of death worldwide. Meanwhile, 55% of UK Biobank participants have low levels of vitamin D (<50 nmol/L) and 13% of these participants have severe deficiency, which is categorized as <25nmol/L.
Low levels of vitamin D are recorded by an estimated 23% of people in Australia, 24% of people in the U.S., and 37% of people in Canada.
Levels of vitamin D, which were measured using 35 confirmed genome-wide significant variants, had a linear correlation with CVD risk in the study population after genetic predictions were made. CVD risk initially decreased steeply with increasing concentrations and appeared to level off around the 50 nmol/L mark, with similar associations seen for systolic and diastolic blood pressure.
It could be inferred from the study that lowest blood concentrations of vitamin D could nearly double the risk of CVD compared to what was seen in the healthy control group. Further, correcting blood concentrations of vitamin D was predicted to result in a 4.4% reduction in CVD incidence.
“Severe deficiency is relatively rare, but in settings where this does occur it is very important to be proactive and avoid negative effects on the heart,” Elina Hyppönen, chief investigator, said. “For example deficiency can be a problem for people living in residential care who may have limited exposure to the sun […] our results are exciting as they suggest that if we can raise levels of vitamin D within norms, we should also affect rates of CVD.
Because of the ethical issues associated with recruiting people with a vitamin D deficiency and leaving them without treatment for long periods, a genetic approach to analyze the data was warranted, Hyppönen said. “It is exactly this type of difficult setting which demonstrates the power of our genetic approach, given we can show how improving concentrations affects the risk in those most in need, without exposing participants to any harm.”
The study, which compared 44,519 CVD cases with 251,269 controls, all sourced from the UK Biobank, was a statistical analysis breaking down CVD risks based on a range of serum vitamin D concentrations.
Globally, CVD is linked to 17.9 million deaths annually, the leading cause of death worldwide. Meanwhile, 55% of UK Biobank participants have low levels of vitamin D (<50 nmol/L) and 13% of these participants have severe deficiency, which is categorized as <25nmol/L.
Low levels of vitamin D are recorded by an estimated 23% of people in Australia, 24% of people in the U.S., and 37% of people in Canada.
Levels of vitamin D, which were measured using 35 confirmed genome-wide significant variants, had a linear correlation with CVD risk in the study population after genetic predictions were made. CVD risk initially decreased steeply with increasing concentrations and appeared to level off around the 50 nmol/L mark, with similar associations seen for systolic and diastolic blood pressure.
It could be inferred from the study that lowest blood concentrations of vitamin D could nearly double the risk of CVD compared to what was seen in the healthy control group. Further, correcting blood concentrations of vitamin D was predicted to result in a 4.4% reduction in CVD incidence.
“Severe deficiency is relatively rare, but in settings where this does occur it is very important to be proactive and avoid negative effects on the heart,” Elina Hyppönen, chief investigator, said. “For example deficiency can be a problem for people living in residential care who may have limited exposure to the sun […] our results are exciting as they suggest that if we can raise levels of vitamin D within norms, we should also affect rates of CVD.
Because of the ethical issues associated with recruiting people with a vitamin D deficiency and leaving them without treatment for long periods, a genetic approach to analyze the data was warranted, Hyppönen said. “It is exactly this type of difficult setting which demonstrates the power of our genetic approach, given we can show how improving concentrations affects the risk in those most in need, without exposing participants to any harm.”
