The recent announcement from an international team of medical scientists, some based at the PMS in Exeter, of their discovery of a robust statistical association between common genetic variants at a locus of the human genome (in this case called FTO on chromosome 16) with proneness in sample populations to be overweight, attracted widespread comment in the media, much of it heralded by claims for identification of the Fat Gene.
To those of us accustomed to following the media discussion of the periodic announcement of the earmarking of the gene-for-this and the gene-for-that the reception accorded this fat gene seemed predictable.
Views polarised around either the fatalistic “its in your genes so there’s nothing you can do about it”, or around the didactic “self knowledge is the soundest motivation of remedial action and self care”, though not always entirely sensitively.
The Sun (link:http://www.thesun.co.uk/article/0,,2-2007170008,00.html), for instance reflected these poles in encouraging readers to characterise bulkier celebrities either as fat gits (failing to take responsibility) or fat gene (fatalistically genetically determined). Sensibly the scientists interviewed stood back and articulated the third familiar position: the causal projection, which is to say that with knowledge of this genetic association and much more research it may be possible to provide a more extensive understanding of the intrinsic causes of excessive weight gain and to devise novel remedies for its consequences. This causal position is often adopted by scientists to justify why more research (and funding,) is required.
The two positions, the fatalistic and the didactic roughly coincide with arguments about the apportioning of responsibility for the management of obesity and its consequences between public healthcare provision and the individual.
The fat gene has been around now in various forms for a number of years hitting the headlines repeatedly alongside pictures of expanded midriffs, so it is timely to reflect on its progress and the role it plays. Since 1999 various genes and loci have been associated with obesity. The first were genes that were identified as causing fat to be deposited by an identifiable mechanism, according to the function of the genes. These genes were again labelled ‘fat genes’ , but the second group, identified by a correlation between functionally anonymous loci and obese people, were not. The new announcement was based on a study that again correlated having a certain allele oat the FTO locus with being obese, although no mechanism for why that occurs is currently known. The question then is why were these genes labelled fat genes when the previous batch were not? Perhaps it has something to do with the effectiveness with which the new discovery was brought to the attention of the all media and with the competitive need of the media to capture public attention within an easily accessible context for which “fat” served perfectly. Alternatively, the fact that the FTO locus, for entirely unrelated reasons had already been labelled as “fatso” in the genetic databases (possibly because it is a very large gene,) was what did the trick.
Will the discovery of FTO’s correlation with obesity ever lead to any practical applications? Certainly it seems questionable whether a genetic test for this allele would be useful. Around 50% of the population carry the allele, so would a doctor find it a useful way of differentiating obese patients? Even if patients knew they had the gene would it be likely to change their behaviours and lead them to choose healthier lifestyles? The evidence from smoking is bleak: even when smokers develop smoking related illnesses around half still continue to smoke. How useful the discovery of this particular fat gene becomes remains to be seen. In the meantime it seems reasonable to go along with the causal projection and expect to learn more about how our bodies work when overfed.