Lipids, Homocysteine and Vitamin A: Perspectives and new hypotheses from patients with cardiovascular disease

Abstract

Vitamin A is an essential fat-soluble nutrient with important functions in growth, development and the visual process. The major bioactive form of vitamin A, retinoic acid, can stimulate expression of genes involved in the regulation of many important metabolic processes and can influence risk factors of cardiovascular disease (CVD) such as apolipoproteins and the amino acid homocysteine. We investigated whether circulating vitamin A can modify risk of myocardial infarction associated with blood concentrations of apolipoproteins B and A1, and homocysteine in a large cohort consisting of more than 4000 patients with established CVD. In the first two studies, we observed an increased risk of myocardial infarction in patients with higher concentrations of apolipoprotein B and homocysteine ​​and low concentrations of apolipoprotein A1. The risk was highest in patients who also had higher blood concentrations of vitamin A. In the most recent work, we observed that markers of impaired renal function (creatinine), the amino acid cysteine and the inflammatory marker uric acid were positively associated with vitamin A concentrations in the blood. Although vitamin A is a nutrient, there was little evidence indicating that intake of specific food groups or nutrients were associated with vitamin A concentrations in the blood. Taken together, we can conclude that vitamin A can modify the risk of acute myocardial infarction associated with traditional risk factors such as apolipoproteins and homocysteine. In addition, renal function but also amino acids and inflammatory markers are associated with vitamin A concentrations in blood, while diet appears to play a minor role, suggesting that vitamin A concentrations are under homeostatic control. The clinical relevance of the work is unknown, and replication is essential.