Scientists Question Food-Addiction Model for Obesity

A recent opinion piece published in Nature Reviews Neuroscience has questioned efforts to conceptualize obesity and overeating “as a food addiction accompanied by corresponding brain changes,” in the process raising concerns about the rush to adopt this model as a foundation for clinical and policy recommendations. Hisham Ziauddeen, et al., “Obesity and the brain: how convincing is the addiction model?,” Nature Reviews Neuroscience, April 2012.

From the outset, the article distinguishes between two popular views of food addiction, one of which posits that certain foods are addictive and one of which attempts to define food addiction as a “behavioral phenotype” seen in some people with obesity that “resembles drug addiction.” In light of these differing perspectives, the article reviews the “five key pieces of evidence cited in support of addiction model,” that is, (i) “a clinical overlap between obesity (or, more specifically BED [binge-eating disorder]) and drug addiction”; (ii) “evidence of shared vulnerability to both obesity and substance addiction”; (iii) “evidence of tolerance, withdrawal and compulsive food-seeking in animal models of overexposure to high-sugar and/or high-fat diets”; (iv) “evidence of lower levels of striatal dopamine receptors (similar to findings in patients with drug addiction) in obese humans”; and (v) “evidence of altered brain responses to food-related stimuli in obese individuals compared with non-obese controls in functional imaging studies.”

After analyzing the current body of published work, the authors report that,
although animal studies provide the strongest basis for a food-addiction
syndrome, other lines of research are not as conclusive as first suggested
by backers of the food-addiction model. According to the article, not only
have “the vast majority of overweight individuals… not shown a convincing
neurobiological profile that resembles addiction,” but further inconsistencies
in the neuroimaging literature suggest that “the application of a single model
is likely to be more of a hindrance than a help to future research.” Even studies
that limited their data to individuals with obesity caused by binge-eating
disorder (BED) apparently failed to concur that food addiction mimics drug
addiction, yielding evidence described in the article as “weak or inconsistent.”

“[G]iven the absence of good evidence, the ubiquitous influence of the addiction
model of overeating and consequent obesity is remarkable,” observe the
co-authors, who suggest several alternatives for future research that would
better handle the complexity of cognitive responses to food consumption
and possibly involve creating “a more precise neurobehavioral definition
of food addiction” separate from that of drug addiction. As they conclude,
however, “successful development of such a model will demand progression
beyond existing clinical definitions of addiction to ideas that are guided by
the developing neuroscientific literature.”