Abstract

The physical manifestation of a trait is a constant interplay between one’s genetic makeup and environmental factors. This notion has been substantiated by nutrigenomic studies demonstrating the benefits of nutritional supplements along the continuum between health and disease.1 More importantly, these studies have revealed the plasticity by which the genetic substrate can interact with various environmental components to either exacerbate or mitigate the manifestation of a disease process in those genetically predisposed. Focusing on cardiovascular disease, a vast literature has demonstrated that this disease process is associated with impaired energy production, increased oxidative stress, and cell calcium overload. To these ends, both clinical and animal studies have demonstrated nutrient deficiencies, integral to these processes, to be associated with cardiovascular disease and that these deficiencies represent independent predictors of increased morbidity and mortality.2,3 One cellular component that has received considerable attention regarding function and nutrient supplementation is the mitochondria. Mitochondria are responsible for cellular bioenergetics via oxidative phosphorylation. However, the perpetual transfer of electrons from one molecule to another within the mitochondria renders this organelle a major site for the genesis of reactive oxygen species (ROS).4 Although the mitochondria have antioxidant defenses,4 the disequilibrium between ROS production and ROS neutralization paves the way for disease manifestation. ROS damage to mitochondrial proteins, lipids, and DNA poses …

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