University Of Michigan Health SystemWe had mentioned in our previous article as to how low Vitamin D could result in heart diseases. Now, pertaining to the above topic, a new study claims that patients suffering from high blood pressure who have a gene variant that apparently impacts an enzyme important to standard vitamin D activation, are said to have double the chances to suffer from congestive heart failure as opposed to those without the variant.

This study is claimed to be the first indication of a genetic link between vitamin D action and heart disease.

“This study revealed that a critical enzyme absolutely required for production of the vitamin D hormone has a genetic variant associated with the development of congestive heart failure. If subsequent studies confirm this finding and demonstrate a mechanism, this means that in the future, we may be able to screen earlier for those most vulnerable and slow the progress of the disease,” commented, Robert U. Simpson, professor of pharmacology at the University of Michigan Medical School and one of the authors of the study.

Around 617 participants were included in the study. The genetic profiles of those subjects were examined by study co-authors Russel A. Wilke of the Medical College of Wisconsin and Catherine A. McCarthy of the Marshfield Clinic Research Foundation in Marshfield, Wis. They were analyzed in Marshfield Clinic Personalized Medicine Project, a big DNA biobank.

The scientists apparently searched for variants in around 5 applicant genes selected for their functions in vitamin D control and hypertension. It was seen that around one-third of the participants suffered from both hypertension and congestive heart failure, one-third apparently had hypertension alone and one-third were supposedly healthy controls.

The outcomes illustrated that a variant in the CYP27B1 gene was apparently linked to congestive heart failure in patients suffering from hypertension. It is by now identified that mutations that inactivate this gene could decrease the necessary switch of vitamin D into an active hormone.

Simpson remarked, “This initial study needs to be confirmed with a larger study that would permit analysis of the full cardiovascular profile of the population possessing the gene variant.”

The authors mention that upcoming study could be required to incorporate people of more varied origins as compared to this study’s population which mostly consisted of individuals from European ancestry.

The study was published in the journal Pharmacogenomics.