Personalizing B Vitamin and Omega-3 Fat Recommendations with Genetic Testing
Heart disease is the number one cause of death globally (WHO, July 2013). 7 million people died from heart disease (CHD) in 2011. 450,000 deaths in the US. More than 13 million Americans are affected with coronary heart disease and the direct health care costs exceed $150 billion annually. Doesn’t it make you wonder what to do nutritionally to prevent becoming included in these statistics? Is it more omega-3 fatty acids? Or B vitamins? The answer may lie in genetic screening.
A lack of B vitamins, especially folic acid, vitamin B6 and vitamin B12, contributes to high plasma homocsysteine levels. Elevated homocysteine levels are associated with increased risk of CHD. A proposed mechanism of action is via DNA methylation pathways. Fiorito and colleagues studied the relationship between candidate genes and B vitamin intakes in 206 individuals with previous heart attacks and 206 matched controls identified from the EPIC cohort. They found significantly lower intakes of folic acid, B6, riboflavin and niacin in cases versus controls. They also found several candidate genes with statistically different DNA-methylation patterns which were associated with CHD risk.
In another paper, Verdoia and colleagues assessed homocysteine levels and genetics in 778 patients with heart disease. They found that patients with the C>T polymorphism in the B vitamin enzyme, methylenetetrahydrofolate reductase (MTHFR), had higher homocysteine levels. Previously, Solis and associates found MTHFR polymorphisms affected serum folate and plasma homocysteine concentrations. In other words, nutrient recommendations may need to be personalized based on our genetic makeup.
The cardiovascular health story isn’t restricted to B vitamins. Omega-3 fatty acid intakes are known to be important for heart health. The apolipoprotein E (APOE) gene helps make lipoproteins, primarily very low-density lipoproteins (VLDL), to remove cholesterol to the liver for processing. There are 3 genes: e2, e3, and e4. People with the e4 genotype are at increased risk of atherosclerosis and Alzheimer’s. Chouinard-Watkins and colleagues report that the metabolism of long-chain fatty acids is influenced by genetics. They evaluated the metabolism of a single oral dose (40mg) of isotopically-labeled docosahexaenoic acid (DHA) in 40 volunteers over 28d. Mean plasma labeled DHA levels were 31% lower in people expressing the apoE ε4 allele (E4+) than those without (E4-) genotype.
These 3 new papers highlight potential interactions between nutrition and genes. As genotyping becomes more commonly available, it will be applied by health professionals to personalize national nutrient recommendations to optimize the health of their client.
Fiorito G, Guarrera S, Valle C, Ricceri F, Russo A, Grioni S, Mattiello A, Gaetano C, Rosa F, Modica F, Iacoviello L, Frasca G, Tumino R, Krogh V, Panico S, Vineis P, Sacerdote C, Matullo G. B-vitamins intake, DNA-methylation of One Carbon Metabolism and homocystein pathway genes and myocardial infarction risk: the EPICOR study. 2013 Nutr Metab Cardiovasc doi:10.1016/j.numecd.2013.10.026
Verdoia M, Schaffer A, Cassetti E, Barbieri L, Di Goivine G, Marino P, De Luca G. MTHFR polymorphism and risk of periprocedural myocardial infarction after coronary stenting. 2013 Nutr Metab Cardiovasc doi:10.1016/j.numecd.2013.10.027
Solis C, Veenema K, Ivanov AA, Tran S, Li R, Wang W, Moriarty DJ, Maletz CV, Caudill MA. Folate intake at RDA levels is inadequate for Mexican American men with the methylenetetrahydrofolate reductase 677TT genotype. 2008 J Nutr 138:67
Chouinard-Watkins R, Rioux-Perreault C, Fortier M, Tremblay-Mercier J, Zhang Y, Lawrence P, Vohl MC, Perron P, Lorrain D, Brenna JT, Cunnane SC, Plourde M. Disturbance in uniformly 13C-labelled DHA metabolism in elderly human subjects carrying the apoE ε4 allele. 2013 Br J Nutr 110:1751-1759