Depending on their genes, people with cardiovascular disease could significantly lower their blood pressure and, in turn, their risk of heart disease and stroke by increasing their intake of vitamin B2, suggests a study from Northern Ireland.
To investigate the effect of vitamin B2 (riboflavin) on blood pressure for patients with cardiovascular disease who have a certain gene variation (polymorphism), 83 participants with one of three different genotypes received riboflavin (1.6 mg/day for 16 weeks) or placebo in a randomized controlled trial (1). The patients had already participated in an intervention study with riboflavin in 2004 (2). Like in 2004, the current follow-up study showed that patients with a specific variation in the gene encoding, the methylenetetrahydrofolate reductase (MTHFR), had higher systolic blood pressure, with a non-significant trend noted for higher diastolic blood pressure. Despite an increase in the number of antihypertensive medications prescribed since the initial study, elevated blood pressure remained unchanged for these patients at the time of follow-up. The recent study results showed that only riboflavin supplementation produced significant decreases of 9.2 mm Hg in systolic and of 6.0 mm Hg in diastolic blood pressure in these patients.
The researchers concluded that optimizing riboflavin status may offer a low-cost strategy for managing elevated blood pressure among this genetically at-risk group. These findings, if confirmed in the general population, could have important implications for the prevention of hypertension.
Research into the genetic basis of hypertension has enabled a more detailed understanding of the biological processes underlying blood pressure control. One genetic variant under recent investigation is the 677C/T polymorphism in the gene encoding the folate -metabolizing enzyme MTHFR. This polymorphism previously received much attention as the main genetic determinant of increased homocysteine concentrations, but it has also been associated with elevated blood pressure (3, 4) and an increased risk of stroke (5). People with this polymorphism, which has a reported frequency of 10% worldwide, ranging from 4% to 18% in the United States (6), produce an MTHFR enzyme with decreased activity. Riboflavin is required as a cofactor for MTHFR and the decreased enzyme activity results from the loss of its riboflavin cofactor. However, supplementation with riboflavin appears to increase the enzyme variant activity potentially lowering disease risk (7).