The desire for some researchers (Davis et al., 2011) seems to be to make food addiction an instance of a general class of addictions, so that food addiction shares chemical mechanisms with ´conventional addictive drugs´. In this view the task is to uncover the causal path from overeating to changes in brain chemistry or brain physiology that will support an ongoing addiction.
The problem with this strategy is that it presupposes:
a) That conventional drug addiction is in fact supported by changes to the brain that are caused by the addictive drugs themselves.
That this is not the case needs to be argued separately.
b) That we for food addiction can map out a similar causal path
c) That there are no other valid explanations for food addiction
The alternative strategy that we are going to explore is based on the view that food addiction is not primarily supported by changes that are specific to the intake of food - ei. not the effect of changes that can be traced to chemical or physiological effects of the food items ingested.
Instead of assuming that, we are going to have a look at the energy circuits (mainly glucose metabolism) that eating feeds (in the most literal sense) and the consequences that different states of energy supply or depletion has on brain function in general and on self control in particular.
In simple terms the strategy is to explore food addiction for a general mechanism that can be applied in explaining the wider scope of addictions, including those that are now seen as caused by effects of the addictive substance. Instead of treating food addiction as a subspecies of drug addiction we are going to treat drug addiction as a subspecies of resource addiction, or more loosely a kind of food addiction.
Davis, C.ab , Curtis, C.a, Levitan, R.D.b, Carter, J.C.c, Kaplan, A.S.b, Kennedy, J.L (2011) Evidence that 'food addiction' is a valid phenotype of obesity, http://www.ncbi.nlm.nih.gov/pubmed/21907742
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