”Battling against one’s biology”: Inherited behavioural susceptibility to obesity
By Susanne F Meisel, on 30 March 2012
As mentioned in one of our previous blog posts, talking about genes in the context of obesity is often not well received. Those discounting their role in the development of obesity often argue that, because genes have not substantially changed over the past 200 000 years, whereas obesity levels have only been soaring over the past 20 odd years (where it became possible to mass-produce cheap, tasty food in combination with a decreased need for physical activity), obesity must be due to changes in the environment, and not genetics.
However, using this argument against the heritability of obesity is somewhat flawed, because it ignores that a condition can be dormant over a period of time until the right circumstances bring it to life. The gardeners among you will know that many plants will adjust their growth according to their surroundings – a plant in a small pot will remain small, whereas a larger pot will allow it to grow. This, however, does not mean that the plant loses its ability to grow larger in a smaller pot; it merely remains small because its surroundings restrict its growth. Similarly, genes predisposing to obesity may be present in an environment where little food is available, but without the right ‘medium’ (i.e. food), this is of little consequence. In the current environment, however, where eating opportunities are plentiful, obesity genes can express their full force.
If obesity was resulting purely from environmental change, all individuals exposed to this change would become overweight. Yet, this is not the case. In fact, the proportion of lean people has not substantially changed, but large people are becoming even larger. This suggests that people respond to the food environment differently. However, undoubtedly, to gain more weight than is healthy, food must not only be available in sufficient quantities, but one must ingest more of it than necessary. Therefore, researchers started to look at differences in eating behaviours, such as how much we are drawn to food and how quickly we feel full, to see what is going on.
Twins can help to untangle the influence of genes and environment on obesity, because identical twins are 100% genetically identical, whereas non-identical twins only share approximately half of their genes (like normal siblings); both, however, grow up in a very similar environment. This means that researchers can compare identical twins’ resemblance for weight with that of non-identical twins; if genetically identical twins are more similar in a trait than non-identical twins, it is evidence for genes being responsible for the trait.
Using twins, researchers from our department wanted to see whether genes that influence weight also influence appetite. If the same genes that influence weight also influence appetite, it suggests that genes influence weight through their effects on appetite – i.e. individuals who inherit more avid appetites might be more susceptible to overeating in the modern food environment, and consequently more likely to gain excessive weight. They looked at this in infants, because infants are exclusively milk-fed, which ruled out that other factors such as preference for certain foods would influence the results. The researchers used questionnaires to ask parents about how fast their twins fed, how easily they got full and how big their appetite was, and related the answers to the babies’ weight. Because they used a sample of identical and non-identical twins the researchers were able to explore the extent to which appetite is heritable, and the extent to which appetite and weight are caused by the same genes.
They found that identical twins were not only very similar in weight, but shared many more similarities in appetite than non-identical twins, suggesting a strong genetic basis to both appetite and weight. In addition, the results showed that a substantial proportion of the genes that are responsible for weight are also responsible for appetite, in line with the idea that genes influence weight through appetite. These findings lend evidence to the idea that some of us are more likely to overeat in the current environment because of a larger appetite, which is ultimately driven by genes.
These discoveries will hopefully contribute to reducing the stigma that surrounds unhealthy weight gain; because it clearly shows that those struggling with weight are in a sense ‘battling against their biology’. This of course, does not mean that there is nothing that can be done about it; however, acknowledging these differences as real and designing strategies to ‘outsmart’ one’s genes is crucial if the battle is to be fought successfully.
Article reference: http://www.ajcn.org/content/95/3/633.long