The Addictive Dimensionality of Obesity

Abstract

Our brains are hardwired to respond and seek immediate rewards. Thus, it is not surprising that many people overeat, which in some can result in obesity, whereas others take drugs, which in some can result in addiction. Though food intake and body weight are under homeostatic regulation, when highly palatable food is available, the ability to resist the urge to eat hinges on self-control. There is no homeostatic regulator to check the intake of drugs (including alcohol); thus, regulation of drug consumption is mostly driven by self-control or unwanted effects (i.e., sedation for alcohol). Disruption in both the neurobiological processes that underlie sensitivity to reward and those that underlie inhibitory control can lead to compulsive food intake in some individuals and compulsive drug intake in others. There is increasing evidence that disruption of energy homeostasis can affect the reward circuitry and that overconsumption of rewarding food can lead to changes in the reward circuitry that result in compulsive food intake akin to the phenotype seen with addiction. Addiction research has produced new evidence that hints at significant commonalities between the neural substrates underlying the disease of addiction and at least some forms of obesity. This recognition has spurred a healthy debate to try and ascertain the extent to which these complex and dimensional disorders overlap and whether or not a deeper understanding of the crosstalk between the homeostatic and reward systems will usher in unique opportunities for prevention and treatment of both obesity and drug addiction.

Individual Differences in Cue-Induced Motivation and Striatal Systems in Rats Susceptible to Diet-Induced Obesity

“…Some have proposed that pre-existing hypoactivity of mesocorticolimbic systems produces 'reward deficiency' that drives over-eating (Johnson and Kenny, 2010;Parylak et al, 2011). By contrast, others propose that opposite hyperreactivity of these systems drives elevated cue-triggered motivation to eat (Davis et al, 2009;Gearhardt et al, 2011;Stice et al, 2012;Volkow et al, 2013a). Both hypotheses recognize that individual differences are important (Berthoud, 2012); indeed differences in sensitivity to leptin, insulin, and post-meal satiety have been associated with susceptibility to diet-induced obesity (Levin et al, 2004;Clegg et al, 2005;Cottone et al, 2007).…”

Consequences of Adolescent Ethanol Consumption on Risk Preference and Orbitofrontal Cortex Encoding of Reward

“…Differential consumption among groups is unfortunately a common byproduct of many alcohol self-administration models, and considering the caloric content of the gelatin mixture, could result in differential effects on reward circuitry. The consumption of high fat or other 'rich' diets can alter reward circuitry (eg, Volkow et al, 2013); however, this requires extended access to these foods (Johnson and Kenny, 2010), resulting in differential weight gain between groups. We did not observe any differences in body weight between groups (during adolescence or in adulthood), which therefore suggests that even the 'high' levels of gelatin consumption by our control animals were not high enough to result in physiological differences between groups.…”

Obesity, Dopamine, and Reward Behaviors

“…While no studies of baseline extracellular DA levels and total DA D2 receptor levels, which would require PET studies of DA D2 receptors before and following DA depletion, have been reported in obese humans, animal studies have shown decreased baseline extracellular DA levels, decreased amphetamine induced DA release, and decreased absolute levels of DA D2 receptor levels in obese animals, particularly in those who compulsively consume food (16)(17)(18). Both Stankowska and other investigators have postulated that extreme obesity may be due to a food addiction and that extremely obese humans may have changes in DA neurotransmission similar to those seen in substance abuse (26,27,50). Studies in human substance abusers have shown both decreased extracellular DA levels, and total DA D2 receptor levels as well as decreased psychostimulant induced DA release and available DA D2 receptor levels (21)(22)(23)(24)(25).…”