This discussion has been about which substances in foods may or may not be dangerously attractive. Now, it is about which qualities in humans can, or might, increase their susceptibility to obesity caused by addictive-like eating behavior. What makes a “prone subject?” We have frequently quoted the 2014 paper by authors from Germany, The Netherlands, Spain, the United Kingdom, and Sweden, which said,
We perceive the necessity, and at the same time the difficulty, to clearly separate known causes of overeating, which without knowledge of the underlying process (e.g. leptin deficiency, hypothalamic tumor) could be labeled as an addictive behavior.
So there is the whole question of the physical characteristics present in the individual, that either potentially or demonstrably exert influence on eating patterns. Dr. Pretlow recently wrote,
In a lecture on addiction by a professor at Columbia, he stated that tolerance develops to the addictive substance (pleasure high). But what causes the addiction is development of hypersensitivity to the cues, i.e. cravings and the drug pushers and paraphernalia. Hypersensitivity to and seeking tempting foods similarly develops, which are likewise needed to trigger the displacement mechanism to get rid of excess brain energy.
How genes complicate matters
The obesity gene was eagerly sought for a while, but of course nothing can be simple. It turned out to be one of those multifactorial cases. The same internationally-authored paper mentioned above, “‘Eating addiction’, rather than ‘food addiction’, better captures addictive-like eating behavior,” said,
Given the increasing number of gene variants known to contribute to the variance in body mass index in the general population, it will be of interest to genotype normal weight and obese subjects with and without “eating addiction…”
In light of the polygenic basis of BMI variance in the general population, we need studies to address if addictive overeating (and obesity) can occur independently of a genetic predisposition to an elevated body weight.
In other words, maybe people who self-identify or qualify as food addicts under various criteria would not be in the same condition if only their genetic inheritance had been different.
We perceive the need to disentangle the mechanisms underlying an “eating addiction” with and without obesity. The differentiation of subjects who overeat due to increased hunger and/or a reduced satiety from those with an “eating addiction” appears difficult…
So, there can be several kinds of people: addicted but not obese; addicted and obese; obese but not addicted; neither obese and nor addicted. This is a lot to think about.
[R]esearch is required to uncover biological, physiological, and psychological differences. Obviously, twin and family studies are required to assess heritability of “eating addiction” (or different subgroups of “eating addiction”)…
As progress is made in uncovering alleles predisposing to diverse substance use disorders or addictive disorders, the overlap with “eating addiction” can be assessed.
Your responses and feedback are welcome!
Source: “’Eating addiction’, rather than ‘food addiction’, better captures addictive-like eating behavior,” ScienceDirect.com, November 2014
Image by Rutger Tuller/CC BY 2.0
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