Georgia Lenihan-Geels on eating for our genes

In 2001, the finalisation of the Human Genome Project gave scientists new enthusiasm for genetics and how we could use the knowledge of the human genome sequence in understanding, preventing and curing disease. One particular topic was the exploitation of the genome in relation to diet – was there a way in which dieticians and general practitioners could offer specific dietary advice based on patients’ DNA? The use of such a tool would have a huge, positive impact on health and economy, as the burden of non-communicable diseases (NCDs), namely cancer, metabolic syndrome, cardiovascular and inflammatory disease, are at an all-time high. Complete genetic-based dietary advice is probably a long way off, but as we better understand the complex relationship of diet and genetics we can improve the way this association plays with our health.

Over the past 10-15 years, our genome has emerged as a huge role-player in the development of diet-related disease, which has given birth to the field Nutritional Genomics, a science encompassing two main fields: nutrigenomics and nutrigenetics (Sales et al, 2014). Research has shown how gene activity can be influenced by diet (nutrigenomics), how genetic differences lead to different responses to diets (nutrigenetics), as well as how early-life nutrition (pre and post-natal) can influence health in later life, a phenomenon explained by the ability of certain food compounds to influence the type and number of chemical groups attached to genes. Known as the study of epigenetics, we now understand how these chemical groups form a sort of ‘imprint’ that marks the level of activity of a gene. One of the most famous examples of epigenetic changes came from the Dutch Famine Birth Cohort study, a prospective study on people born during or just after the famine that occurred during the end of World War II. The low-caloric diets of pregnant mothers during this time lead to epigenetic changes of their children’s genes, and as a result these children (now adults) have a higher risk of diabetes and obesity (Heijmans et al, 2008).

Very small differences in our DNA code may predispose us to certain diseases, but only within a certain environment, like in the presence of a particular food component. These small differences, called single nucleotide polymorphisms (SNPs) are just a single base-pair difference in our DNA chain, where one person might have a guanine base instead of an adenine, or a thymine in place of a cytosine. These SNPs explain how one person may benefit more from taking fish oil supplements than someone else, or how the consumption of processed meat may increase the risk of bowel cancer in one person but not in the other. For example, a particular SNP in a gene involved in cholesterol transport in the blood showed an increase in HDL (known as the beneficial cholesterol) when eating a diet high in polyunsaturated fatty acids (Hesketh, 2013). On the other hand, those without the particular SNP showed a decrease in HDL. Higher HDL levels have been associated with a lower risk of cardiovascular events like heart attacks. This is one example of how a SNP, with the interaction of diet, can influence the outcome of disease. Unfortunately, the effects of SNPs are not always so clear.

The relationship between genetics, diet and phenotype (the presence or absence of a risk factor / disease) is hugely complex. Within our 22,000 genes are thousands of SNPs. One SNP may associate with a particular syndrome, for example elevated serum lipid levels, when the person eats sufficient levels of fats. However, the combination of this SNP with another may alter that association. The complexity in these gene-gene and gene-diet interactions makes it difficult to actually pinpoint outcomes and therefore give appropriate dietary advice.

Because there is such variety in response to foods between individuals, the ultimate goal would be nutritional guidelines based on the whole genome of an individual, taking into account all the interactions that occur in response to diet, as well as between genes. In an ideal world, each individual would be able to go to a doctor or even stick a customised chip into a computer to get his or her very own personal dietary advice. We now know that this idea of ‘optimal nutrition’ is a bit far-fetched and not really achievable, due to the multiple interactions and the constant changing variables that contribute.

However, the use of current dietary recommendations is out of date; if a person’s cholesterol levels respond differently to high amounts of polyunsaturated fats, we can easily see how different amounts or types of foods can have completely opposing effects within the bodies of different people. This calls for changes to our guidelines. In fact, there are already online-based companies offering genetic based lifestyle advice if you send in a sample of your DNA (e.g. saliva). For a small price (around USD 100) you can get information about your metabolism, certain food compounds to avoid etc. Unfortunately, the science has not quite reached the level where it can dictate a substantial portion of our dietary recommendations.

Companies like 23andMe recently withdrew their genome-based health advice due to new regulations by the United States Food and Drug Administration, supporting the notion that we are not yet at the point where we can give sufficient dietary advice, at least not at that level. On the other hand, what we do know is relevant and can be used to our advantage. Studies have already unveiled useful associations between SNPs and certain risk factors, which can be used to prevent disease in those at a higher risk. For example, a specific SNP in a gene called TCF7L2 associates with type II diabetes mellitus and more specifically with abnormal blood lipid levels and excess abdominal fat (Phillips, 2013). Those carrying this SNP are predisposed to type II diabetes and can reduce this risk by modulating their diet. Other disease-SNP relationships have been found in obesity, cancer and cardiovascular disease.

The downside of personalised nutrition is the effect it could have on the way we view food and the value of meal times. Preparing and eating a meal is a great way for humans to interact and the social aspects are just as important as the nutritional. Although our modern busy lives generally mean breakfast and lunch are rushed and eaten alone, dinner or weekend meals are usually the time when you get together with your friends or family. If people had to follow strict dietary rules, would these traditions completely deteriorate?

A survey was recently published in which experts in the field of nutrigenomics and nutrigenetics were asked about the expected outcomes for nutrigenomics and personalised nutrition. Only 22% of these experts proposed that nutrigenomics would alter food to a more medicinal view and 25% thought it would place too much responsibility on the individual to follow such strict guidelines for health (Hurlimann et al, 2014). On the other hand, 54% were either unsure or in disagreement that personalised diets would increase the compliance of individuals to their dietary advice. Even if the science behind personalised nutrition is robust, it is just as important to make sure that individuals actually follow their advice.

Between the few surveys conducted amongst several European countries, we can see that consumers show a general willingness for personalised nutrition approaches (de Roos, 2013). However, before we can actually use this tool we need to make sure there is enough consumer support, appropriate scientific evidence as well as privacy protection of individual data. We also need to assess the possible impacts on the social and mental wellbeing of those being treated.


Georgia Lenihan-Geels was born in Wellington, New Zealand and grew up in Vanuatu, Switzerland and China. She has been studying Biomedical Science since 2007 and is currently doing her Masters in Molecular Nutrition at Wageningen University in the Netherlands. Read more by Georgia.