Recent evidence suggests that the answer is yes. Most people understand that we all have inherent genetic predispositions – some as benign as the shape of our nose and others more dangerous such as the tendency toward certain cancers. However, as research on epigenetics grows, the ability to modulate the expression of certain genes is becoming clearer. Epigenetics is the study of how our genetic expression is affected by factors other than changes in DNA sequence. These factors include our environment, including what we eat, supplements we take, toxins, illnesses, even the amount of sunlight to which we are exposed.
In this study, variations (known by geneticists as polymorphisms) in a specific gene that makes a protein called the zinc transporter 8 (ZNT8), which carries zinc into the hormone insulin, were studied. This protein ZNT8 is responsible for ensuring that pancreatic beta cells (the cells that make insulin which allows us to metabolize blood sugar) have adequate zinc available. If cells in the pancreas do not have enough zinc, they will not function optimally which may ultimately result in higher risk of insulin resistance and the metabolic dysfunction that follows.
When participants with the (CC) genotype ingested more zinc and omega 3 fatty acids, they lowered their risk of metabolic syndrome consequences associated with their genotype. Stated differently, people with this specific genotype (CC) responded well (in terms of improved insulin sensitivity and metabolic health) to higher levels of zinc and omega 3 fatty acids, while other genotypes (CT or TT) did not show a meaningful improvement in metabolism. Since over-supplementation has potentially negative consequences (too much zinc can cause copper deficiency, for example), knowing your genotype may lead to more informed supplementation decisions.
For more details, click here for a link to the abstract entitled Some dietary factors can modulate the effect of the zinc transporters 8 polymorphism on the risk of metabolic syndrome published in the May 2017 issue of Scientific Reports (Abstract 2640). Or read the full paper here. (Full paper 829)
