Advances in mapping the human genome have fostered understanding of our genomic blueprint and its influence on molecular processes, health and disease. This has extended to investigations of nutritional genomics.
Proponents hope nutritional genomics will lead to greater understanding of how specific food components influence metabolic pathways and long-term disease-risk, enabling individual tailoring of dietary advice and preventive medicine.
This field consists of two primary areas of investigation:
Nutrigenomics is concerned with how food and nutritional components influence gene expression and gene regulation, and their resulting impact on metabolism. It aims to identify individual nutritional needs.
Nutrigenetics, conversely, investigates individual genetic differences in how people respond to dietary intake, and why people have different reactions to the same nutrient.
Ultimately the aim is to achieve better health outcomes by understanding links between genes and diet. According to Ruth Debusk, “The future of dietetics is unquestionable intertwined with nutritional genomics.”
It cannot be disputed that poor diet plays a pivotal role in modern chronic lifestyle diseases like cancer, diabetes, obesity, heart disease, neurological and inflammatory disorders.
But why do some people gain weight more easily, or develop heart disease when others with similar diets don’t? Nutritional genomics hopes to answer these questions so that therapeutic intervention and nutrition guidelines can be individually tailored.
For instance, the APOE gene has a variant that is associated with high LDL cholesterol – so people with this genetic variant may be more vulnerable to the adverse effects of a high fat diet.
Another genotype has been associated with higher concentrations of the “good” HDL cholesterol, but only if saturated fat from animals is less than 30% of energy intake. People with these genes might benefit from a diet higher in vegetable fat.
Other research found that caffeinated coffee increased the risk of heart attacks in people carrying a particular gene that slows caffeine metabolism, while having no effect on those lucky fast coffee metabolisers.
Inflammation is a common feature underlying chronic diseases. Some individuals may produce more inflammatory markers than others, so anti-inflammatory nutrients like omega-3 or turmeric could reduce their susceptibility.
People also have different nutrition requirements, and these vary at different life stages. A vitamin deficiency could be caused by inadequate intake, or because of a genetic variation that impacts its metabolism. These people may need higher amounts of that nutrient, and that could be further impacted by aging.
Although nutritional genomics is generating much excitement and challenging the “one size fits all” approach to nutrition throughout the lifespan, there is much yet to understand.
Unlike single-gene diseases, diet-gene interactions likely involve multiple genes that have multiple interactions with multiple environmental factors – of which bioactive dietary nutrients are not the only contributors.
For instance, several genes are involved in lipid transport alone – just one factor that can influence heart disease risk – including lipid transport proteins, their receptors and lipid-processing enzymes.
New research on the 100 trillion microbes that live in our gut has added further complexity to the broader picture of genetics and human health. And metabolomics seeks to pinpoint metabolites at each step of metabolic pathways that might also help to fine tune dietary advice.
Finally, the unhealthy diets and sedentary behaviours that dominate modern lifestyles will not be solved by nutritional genomics. They bring epigenetics into the bigger picture – the impact that diet and environment has on our genes.