Food affects people differently. We all know people who can eat whatever they want, who do not work out, and yet they don’t gain a pound. Similarly, what is good for one person’s diet is not necessarily good for another. Some of these differences in our relationship with food depend on the genetics. DNA influence our eating habits, and nutrients — or the lack of them — affect how DNA is interpreted inside the cell.
The understanding of the food-DNA interplay is the major aim of nutrigenetics, with the ultimate goal to provide a personalized diet based on the genetic makeup. In order to achieve this, nutrigenetics identifies differences in our DNA that are linked to the way we absorb, metabolize and store nutrients. While in some cases it is possible to recognize a single DNA region or even a specific nucleotide (the building blocks of DNA – a difference in one of them is called single nucleotide polymorphism or SNP) responsible for a specific trait, in most of the cases more variables are involved, making it difficult to get a clear prediction.
The easiest case is when variations (SNPs) in one DNA region lead to one intolerance. For example, the digestion of lactose is dependent on the level of a specific enzyme, the lactase. In most mammals, the amount of lactase generally declines in adulthood, but some individuals have a variation in a region of the MCM6 gene that enables high levels of lactase during their entire life. This “acquired tolerance” became frequent in most of the countries, but the variations found in one place are rare in others. For example, the variations found in Europe differ from those in the populations of sub-Saharan Africans. Other well-established variations on a specific gene dictate precise outcomes, such as an increased need for folic acid and vitamins B6 and B12, the intolerance to fructose or a higher sensitivity to alcohol.
However, in other cases, it is the interplay of several DNA regions that determines how we approach and react to a specific nutrient. For example, the cravings for coffee are dictated by two DNA regions (near the CYP1A1 and AHR genes). However, if an amount of caffeine is harmful or not depends on the ability to metabolize it, which is dictated by a single gene (CYP1A2). The same amount of caffeine has a more stimulating effect on slow metabolizers and they might be more likely to suffer from a heart attack due to high (very high!) caffeine intakes. As a consequence, only slow metabolizers that crave caffeine should limit their coffee intake.
A precise advice is not always easy and often we can merely identify a genetic predisposition that can be enhanced or prevented by lifestyle and other factors (i.e. epigenome, microbiome, etc). A well-studied example is a susceptibility to obesity: variations in genes controlling appetite, eating behavior, metabolism (mainly of fats), response to training and weight loss… all together they mediate our weight management and predisposition to obesity. More and more genes are taking part on this complex puzzle and research starts to grasp their interplay that leads to the predisposition.
A host of discoveries in nutrigenetics are around the corner and effective and precise diets based on our DNA are not far away. In the meantime, let’s not forget what we know about lifestyle: a balanced diet and an adequate amount of physical activity have never been proven harmful.