Genetic, dietary, and other lifestyle determinants of serum homocysteine levels in young adults in Costa Rica

Abstract

Since 1970, researchers have linked hyperhomocysteinemia to cardiovascular disease (CVD), and hyperhomocysteinemia is now considered a CVD risk factor (1). Low serum concentrations of folate, vitamin B12, vitamin B6, and vitamin B2 have been identified as risk factors for hyperhomocysteinemia (2). Folate is considered the micronutrient with the greatest impact on homocysteine metabolism (2). Several genetic defects in the enzymes participating in the homocysteine metabolic cycle have also been associated with hyperhomocysteinemia (3). Frosst et al. (4) identified a common point mutation (C677T) in the methylenetetrahydrofolate reductase (MTHFR) gene that correlated with reduced MTHFR activity. Homozygotesfor this enzyme variant have significantly elevated total homocysteine (tHcy) levels, suggesting that this mutant gene may be a risk factor for developing hyperhomocysteinemia (3, 4). Moderate hyperhomocysteinemia is equivalent to hypercholesterolemia as a cardiovascular risk factor. Given that, some researchers have pointed to the importance of knowing and reducing the tHcy concentrations in a population in order to lower CVD mortality (5). This is important in Costa Rica, where CVDs constitute the leading cause of death among adults, with a mortality rate of 80.4/10 000 in 2001, and where approximately 2.5% of those deaths occurred among relatively young persons, that is, under 40 years of age (6). Some researchers have studied the traditional CVD risk factors among adults in Costa Rica (7), but there are no data available on the prevalence of hyperhomocysteinemia and its determinants in the country. This is the first study that describes the distribution of tHcy and its determinants among Costa Rican adults.