Australasian Science Magazine

The long-term impact of what your mother ate and drank, whether she was underweight or overweight and whether she smoked during pregnancy influences your chances of becoming obese, diabetic and even developing certain cancers.

By Helen Truby

Lifestyle factors such as a eating plenty of fruit and vegetables, getting a good night’s sleep and keeping physically active are the best way to help your genes keep you healthy.

The completion of the human genome project heralded an era of possibility that we would be able to predict our risk of developing diseases and design effective preventative initiatives. From a nutritionist’s point of view, direct links between health outcomes and food are tantalising, and beg the question: “Is your health destiny already fixed via our genetic code or can our food and lifestyle choices make a difference?”

Epigenetics, the study of how our genes are expressed when exposed to environmental influences, demonstrates that our journey in utero profoundly influences the risk of developing specific diseases. The long-term impact of what your mother ate and drank, whether she was underweight or overweight and whether she smoked during pregnancy influences your chances of becoming obese, diabetic and even developing certain cancers. Conversely, an optimal maternal nutrition environment, which includes breast-feeding, can bestow a protective effect with the offspring’s genetic expression enabling DNA to repair itself and thus be more resistant to disease.

So, is it worth encouraging healthy eating behaviours and adopting physical activity as part of our usual routine if our genes and intrauterine environment have already programmed us for a lifetime of weight gain?

Evidence that our environment and lifestyle play a crucial role comes from the epidemiology field. The rapid emergence and patterns observed in the global obesity epidemic do not support the concept that it is entirely due to genes – simply because our genetic code cannot alter that rapidly.

But the patterns and prevalence of obesity suggest that what we are eating or doing in our environment interact with our genes, up-regulating ones that encourage us to survive famine by storing body fat. This gene–environment interaction also explains why some people are sensitive to environmental change (such as a high fat diet or lack of physical activity) and easily gain weight while others resist these impacts.

The problem with obesity is that it appears to be both heritable and intractable. We have many proven and effective methods that enable us to lose weight, so weight loss per se is reasonably easy but it is very hard to maintain this lower body weight.

In addition, where we store that fat on our frames is important in predicting the risk of disease. Abdominal visceral fat is not just an innocuous annoyance that stops us from zipping our favourite jeans up, but a metabolically active substance that drives the dysregulation of metabolic processes and hence contributes to obesity-related diseases such as Type 2 diabetes.

Longer-term population studies examining the FTO variant gene, which has been heralded as the “obesity gene”, will help uncover true associations between populations and environmental factors that lead to obesity. In the future it may be possible to determine more specific gene–environment interactions that could lead to tailored obesity prevention advice for specific population groups or individuals. For example, if it was determined that a certain saturated fat in combination with another modifiable behaviour increased the risk of developing Type 2 diabetes, then more specific individualised advice on food choices could be provided to those carrying the FTO allele.

While personalised nutrition could revolutionise how dietary advice is given and alter the way practitioners assess and utilise biochemical and genetic data, nutrigenomics remains a new field with a limited evidence base. A recent international survey of dietitians from the US, UK and Australia demonstrated the current low levels of knowledge and confidence to practice in this new domain. This cohort study also revealed that practitioners were confident in using genetic knowledge that was underpinned with robust evidence, for example in specific monogenic diseases such as cystic fibrosis.

With dietitians understandably waiting until more reliable evidence of benefit is available before adopting personalised nutrition, the market for nutrigenomics has emerged. Direct-to-consumer genetic testing by commercial companies is already available, with companies offering to examine an individual’s genetic profile and providing them with dietary advice based on their test results.

This whole area is fraught with difficulty, not the least because today’s major killers, cardiovascular disease and cancer, have a multifactorial aetiology and genetic variation accounts for only a small proportion of absolute risk. But Pandora’s Box has been opened – it is tantalising to consumers to believe that it’s as simple as their genes being able to predict their health, such as their propensity for obesity.

This is in stark contrast to the message that standard health promotion messages give about reducing risk, but with no absolute guarantee of success. It’s obviously a much easier sell that your genetic code will provide a list of do’s and don’ts to eat and drink and you will stay well.

Can knowing your individual genetic profile help at all? It will be in personalised medicine where genomics will be the most helpful. In the near future it may be able to offer the physician guidance about the effectiveness of particular drugs or the possibility that you might suffer side-effects from the drugs about to be prescribed.

With food and diet, the answers may be harder to find and hidden in the interplay between multiple genes involved and past and present environmental impacts, all combined to make a complex nutritional milieu. It will not be easy to sift through and make sense of it all. Large-scale longitudinal studies are needed to provide the answers we seek via nutritional genomics.

At the moment there is insufficient evidence that obesity can be simply predicted by our genes. We may be more informed by asking our mothers if they can still fit into their jeans. If they can, you are probably on track. If they can’t, then lifestyle advice such as a eating plenty of fruit and vegetables, getting a good night’s sleep and keeping physically active still provides the best way to help your genes to keep you healthy.

Helen Truby is Professor of Nutrition and Dietetics, and Head of Department of Nutrition and Dietetics at Monash University.