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by Marijana Domazet, Sunday, April 21, 2013 | Categories: Obesity

The causes of obesity can be discussed on many levels, whether it is societal or biological. One neurobiological model that has received significant attention is the so-called food addiction model, which stipulates that the effects of certain foods on the brain are comparable to the effects of drugs. In addition to that, this model argues that there are many similarities between obese individuals’ food behaviours and the way drug-addicted individuals behave. Needless to say, the controversies from these claims have been discussed at length within the research community. The most recent contribution to this debate comes from a review that challenges the usefulness of the food addiction model.

The review, which was published in Obesity Reviews, considered the four key areas of evidence that have been put forth so far. First, they considered the clinical overlaps in addiction behaviour and noted that similarities between the obese and addiction groups were difficult to establish. This is mostly due to the fact that food is an essential part of our survival, and as such is not a habit that can “be kicked” in a similar way to drug addiction. It would be absurd to consider each meal a relapse, as there is no other alternative. Secondly, the authors looked at the genetic vulnerability to both addiction and obesity that family studies had argued exists. In short, the authors argued that there were too many elements of the underlying processes that were dissimilar for it to be consistent. Thirdly, the findings from animal research were reviewed. This is the field that had the strongest evidence for food addiction. Essentially, studies where rats where overfed with high sugar diets or high fat diets pointed to their behaviour rapidly changing to addictive behaviours and overeating. However, the same has not been found in human studies. Lastly, neurobiological research considering how our brains’ reward system reacts to certain foods. These complex findings, which were often obtained using fMRIs, are leaning towards not supporting the food addiction model.

We were not surprised to read about these findings. On the face of it, it is understandable how useful the model would have been clinically if it were found to be valid. However, there are too many disparities that reflect that the model is too limited to explain such a complex phenomenon as obesity. The model, as it is described today, tries too hard to encapsulate several heterogeneous groups into one simplistic, reductionist version of a multi-layered problem. It does not give reasonable weight to the complex and rich interaction between nature and nurture and pathologises obese individuals. Having said this, it still has the potential to be useful for a small sub-group of people if it is defined in depth. However, establishing such a precise model is a long and painstaking process that is not likely to happen within the near future. Until these flaws are addressed, we see little use for comparing obesity to addiction.

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