Obesity and addiction: neurobiological overlaps

Abstract

Drug addiction and obesity appear to share several properties. Both can be defined as disorders in which the saliency of a specific type of reward (food or drug) becomes exaggerated relative to, and at the expense of others rewards. Both drugs and food have powerful reinforcing effects, which are in part mediated by abrupt dopamine increases in the brain reward centres. The abrupt dopamine increases, in vulnerable individuals, can override the brain's homeostatic control mechanisms. These parallels have generated interest in understanding the shared vulnerabilities between addiction and obesity. Predictably, they also engendered a heated debate. Specifically, brain imaging studies are beginning to uncover common features between these two conditions and delineate some of the overlapping brain circuits whose dysfunctions may underlie the observed deficits. The combined results suggest that both obese and drug-addicted individuals suffer from impairments in dopaminergic pathways that regulate neuronal systems associated not only with reward sensitivity and incentive motivation, but also with conditioning, self-control, stress reactivity and interoceptive awareness. In parallel, studies are also delineating differences between them that centre on the key role that peripheral signals involved with homeostatic control exert on food intake. Here, we focus on the shared neurobiological substrates of obesity and addiction.

Figure 1

Schematic representation of the highly interconnected system that affects the intake of food and drugs. It includes food-responsive peptides and hormones, energy homeostatic structures in the hypothalamus, the core of the dopamine reactive system in the ventral tegmental area and the striatum, and various cortical areas in charge of processing affect, motor and cognitive information. In contrast to drugs whose effects are exerted directly at the level of the brain reward dopamine pathway, food affects first multiple peripheral and central mechanisms that directly and indirectly convey information to the brain’s DA reward pathway. The hypothalamus plays a particularly prominent role in this regard although it is also strongly implicated in drug reward (225).

Figure 2

Obesity and addiction are complex bio-behavioural disorders that exist along various aetiological, pathological and physiological dimensions, all of which are likely to display some similarities as well as differences.

Figure 3

The nested bow tie architectures of complex systems allow for the input of a wide range of elements, be they nutrients (a) or rewarding stimuli (b), and produce a large variety of products/macromolecules (a) or goal-directed behaviours (b) using a relatively few intermediate common currencies. In this case, the common currencies that form the ‘knot’ of the bow tie are the various orexigenic/anorexigenic signals (a) and dopamine (b) (12) (slightly modified with permission from an original presentation by Dr. John Doyle).