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.