The Internet has recently brought forth some news about research on  so-called "obesity genes".

Obesity is an increasing problem (no pun intended, of course).  Why it occurs and how it might be mitigated are hot topics in medical science.  One such area of research concerns the genetic contribution to obesity.  Is there an obesity gene or genes and, if so, what might be done about it?

In fact, a number of genes have been found that play some role in obesity.  A new study published in the British Medical Journal challenges the view that these genes actually hinder weight loss, though. 

The study compared people with an FTO gene variant that is found in people who are, on average, 0.89 kg heavier than otherwise similar people.  Contrary to expectations, people with the "heavier" FTO allele responded just as well to weight loss treatments as the other group.

This finding suggests that having the guilty allele does not doom the bearer to a certain Body Mass Index.

Another study challenges the so-called "thrifty gene" hypothesis.  On this theory, people evolved genes that helped them store up fat in good times as insurance against lean ones.  In the modern world where fat, sugar, and salt are ubiquitous in our foods, these genes inevitably make people overweight against a famine that never comes.

Researchers examined 9 of the 115 genes associated with obesity because those 9 have been under "positive selection", that is,  alleles that have become more prevalent among humans because they improve fitness.  They found that only 4 of those alleles seem to favor obesity while 5 seem to favor leanness.

This finding suggests that evolution has not simply promoted genes that make people fat. 

Beside their potential medical implications, both results tend to temper a tendency toward genetic essentialism, the tendency to assume a simple mapping of traits to genes.  One frequent manifestation of genetic essentialism comes in the form of expressions like "The X gene" or "The gene for X", where X may be something like obesity, criminality, autism, etc.

The idea that genes (and, thus, people) can be well understood in this way is well entrenched but is simplistic.  Anna Buchanan explains the difficulty:

"This becomes all the more important when it is considered that most elements in the genome, and in particular most protein-coding regions (‘genes’ in the usual sense of the word), have many different uses even within the same species — even within the same organ or system at any given time and/or during its development. So is a gene expressed in teeth, limbs, and gut a gene ‘for’ teeth? And if the homologous gene in flies — that ‘tooth gene’ — is expressed in (say) limbs and brains in vertebrates, is it now a limb gene? a brain gene?"

The problem is confusing when it comes to genes "for" teeth and limbs.  It becomes arguably worse when applied to matters like obesity, criminality, etc., that have a significant environmental component.  Saying that someone has a gene "for" X makes that trait seem both fixed and ineluctable. 

As the research noted above suggests, the truth is more complicated.

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