There are those who believe that “you are what you eat” and dutifully have five servings of vegetables per day, and there are those who grab a bag of chips and claim that healthy eating doesn’t matter because “it’s all in the genes.”
So who has it right? If you asked a researcher in the budding field of nutrigenomics, which aims to untangle the complex web of interactions between genes and diet, the answer would be, “They both do.”
“We do know that diet does affect our risk of various diseases,” said Professor Ahmed El-Sohemy, a member of U of T’s department of nutritional sciences as well as the Canada Research Chair in Nutrigenomics. But as for the notion of the universal ideal diet, he claims that “what [is ideal] for one person may not be the same for another person.”
Nutrigenomics looks at the genetic basis and physiological effects of differences in the way people process food. Although this may seem straightforward, the mechanisms involved are remarkably intricate.
“If you look at a complex food,” said El-Sohemy, “there are hundreds of chemicals, if not thousands, and each is being metabolized or acted on by many different genes, and each of those genes can exist in various forms.”
This high level of complexity means that potential areas of nutrigenomic research are extremely diverse. El-Sohemy’s own interests, for instance, include gene-based variability in carbohydrate metabolism, genetic determinants of caffeine consumption and withdrawal, and even the genetic basis of preferences in taste. In the field at large, some of the most actively investigated gene-diet interactions are those related to complex chronic diseases such as obesity, heart disease, diabetes, and cancer.
Given the marketability of everything diet-related and the cachet of anything personalized, it should come as no surprise that a few companies-including U.S.-based GeneLink and Vancouver-based One Person Health-already offer gene-based dietary recommendations to consumers.
Typically, this personalized advice relies on the analysis of a handful of genes thought to affect the body’s use of certain nutrients. For example, the B vitamin folate is required by a gene that regulates levels of homocysteine, a proposed risk factor for heart disease. A less active variant of the gene requires more folate to do its job, so individuals who possess that variant could choose to adjust their dietary intake to lower their risk of heart attack or stroke.
However, El-Sohemy warned that since the field is “still in its infancy,” companies providing recommendations could be “delivering that information prematurely when we haven’t quite figured out what is going on.” Many of the health claims made by these companies have not yet been examined by regulatory agencies such as Health Canada or the Food and Drug Administration in the United States.
Still, El-Sohemy believes that nutrigenomics holds great promise and what it is capable of offering will become clearer with time.
“As the science unfolds and we begin to demonstrate more examples of the kinds of differences that we find,” said El-Sohemy, “I think people will begin to see that it could really play an important role in affecting the decisions that they make.”
