Nutritional Genomics: Exploring the evidence

By Pantelis Konstantoulakis*PhD and Andreas Zourdos

I have to admit that when I first heard about “nutritional genomics” I was  excited to see what it is all about, that is why I decided to do my own research on this topic.  Genetic tests are held by clinical geneticists and usually will look for rare and incurable diseases. However, some took this idea a bit further.

Is nutritional genomics a science based method?

To explore the relation between genes and diet, we have to understand how the genotype is connected to the phenotype. More than 600 genes, from a total of around 20.000 of the human genome have been correlated with obesity. At this point, it is important to stress that correlation does not imply causation. Some extremely rare mutations of the DNA do indeed lead to increased food intake, and due to this, obesity. Some  well controlled clinical trials that have been published by highly recognised scientific journals and have been criticised but confirmed, have identified the role of three genes. More precisely, the gene of the Melanocortin 4 receptor (MC4r), the  peroxisome proliferator-activated receptor γ (PPARG) and the pro-opiomelanocortin gene(1). In other words, these rare mutations influence our appetite and subsequently they influence calorie consumption, again obesity is a product of overfeeding (2). Nevertheless, no genetic disorder has been confirmed to play a pivotal role on who becomes obese or overweight (3). It is also well recognized by the World Health Organization that obesity is caused by chronic caloric surplus(4). This comes in agreement with fundamental scientific theories , such as the first and second law of thermodynamics.

The genetic disorders related to nutrition are rare or without any scientific significance. A common genetic mutation has to do with folic acid, and who responds well to the supplement form of the vitamin or the chemical form found in nature. It is obvious that this is of little importance and does not determine weight or health.  One common genetic disorder connected with diet is lactose intolerance. Because lactose cannot be digested and absorbed , therefore it cannot cause obesity since it does not affect energy balance. Phenylketonuria is another well known example that can be treated with excluding phenylalanine from the diet.  Again it is becoming obvious that diet-gene interactions are the exception rather than the rule (3,5).

The propaganda of  nutritional genomics also declares that many diseases such as obesity, diabetes, cardiovascular disease and hypertension are due exclusively to nutrition or to isolated nutritional preferences. This is a huge scientific fallacy since it is more than well proven that these diseases depend on the interaction of multiple factors. News flash – but environmental causes and more precisely low socio-economic profile is linked to obesity(3).

This means that people who do not have much to spend will buy and eat the choices that are calorie dense, creating a cheap way to satisfy their appetite, and will get obese due to this , not because there is some diet-gene interaction. Again, the mechanism of storing or losing adipose tissue can be very well understood by the laws of thermodynamics, which are considered fundamental to science , just as the law of gravity. To cut a long story short,  the phenomenon of losing weight is as reproducible as a glass falling on the floor, getting smashed to little pieces. It happens every time. Or maybe those who make a living out of nutritional genomics think that if their clients eat a hyper-caloric diet , they will not gain fat because there is some form of diet-gene interaction.That would be a scientific revelation.

Now, it is really worth to  examine what the other side has to say on the topic:  A Greek study (6) explored the effectiveness of a “nutritional genomics” diet compared to a typical Mediterranean diet and concluded that the “nutritional genomics” group lost  significantly more weight compared to the Mediterranean diet. By carefully reading this study it is striking that it does not take in account energy balance and fails to report the calories of both diets.That is, if there was a difference at this variable then increased weight loss should not be attributed to some hypothetical diet-gene interaction but to the plain obvious, increased negative energy balance. If it was a ceteris paribus comparison – meaning all other variables were equal, then the laws of thermodynamics have failed. Finall, it comes  as a diabolic coincidence that the man in charge of this trial is the distributor of nutrigenomic tests in Greece.

From a psychological aspect, “nutritional genomics” are nothing more than a way to forgive our sins: it is not our fault that we gain fat, some genetic curse is haunting us. In conditions such as obesity, sometimes it is hard for the individual to face reality with honesty and take responsibility. Those on the business of  “nutritional genomics” know that, and that is why the goal post is moved to the genes – by that way lifestyle, personal responsibility and psychological matters are non-significant. Then,  DNA becomes the scapegoat for the guilty past and the Trojan horse for a present time nutritional intervention. In the name of genetics from now on, nutritional advice has a whole new different meaning, since it carries the potential to manipulate one’s genes! How can one not stand in awe? Time now for a reality check:  the evidence for the effectiveness of “nutritional genomics” is non-existent (3,5), just like  the regulation and laws on these matters. It is pretty fair to say that this story is more science fiction than science based. Pompous scientific terminology is not evidence. The truth is that  “nutritional genomics” is the answer to an irrelevant question.

Please check the related article discussion on Colby Vorland's blog here

Bibliography

1. Jackson, JF (1998).Obesity-Leanness included. Online Mendelian Inheritance in Man. www.ncbi.nlm.nih.gov/omim/601665 (accessed July 26 2010).

2. Prentice, AM (2001) Overeating: the health risks. Obesity Research, 9, 234S-238S.

3. Wallace, H. (2006).Your diet tailored to your genes: preventing diseases or misleadingmarketing?GeneWatchUK.www.genewatch.org/uploads/f03c6d66a9b354535738483c1c3d49e4/Nutrigenomics.pdf (accessed July 25 2010).

4. Obesity and Overweight (2010).World Health Οrganization. www.who.int/mediacentre/factsheets/fs311/en/(accessed July25 2010)

5. Sauko, PM et al. (2010). Negotiating the boundary between medicine and consumer culture: Online marketing of nutrigenetic tests. Social Science & Medicine.70(5): 744–753

6. Arkadianos, I. et al. (2007). Improved weight management using genetic information to personalize a calorie controlled diet. Nutrition Journal. 6:29 doi:10.1186/1475-2891-6-29