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.

Conflict of interest statement

The authors report no biomedical financial interests or potential conflicts of interest.

Published by Elsevier Inc.

Figures

Figure 1

In striking contrast to drugs whose actions are triggered by their direct pharmacologic effects in the brain reward dopamine pathway (ventral tegmental area [VTA], nucleus accumbens, and ventral pallidum), the regulation of eating behaviors and hence the responses to food are modulated by multiple peripheral and central mechanisms that directly or indirectly convey into the brain’s reward pathways, including those involved with pleasure, aversion, habituation, and cognitive control [Diagram of the organization of striatocortical connectivity loops reprinted with permission from Haber et al. (112), copyright 2000 Society for Neuroscience]. PYY, peptide YY; s. intestines, small intestines; SN, substantia nigra.

Figure 2

Schematic representation of bowtie architectures in the brain as exemplified by the (A) energy homeostatic (metabolic) and (B) dopamine reactive (reward) systems. The human brain, like most complex biological systems, is characterized by the layered architectures of interactive networks [reprinted with permission from (111), copyright 2004 Elsevier]. These systems display an evolutionarily optimized organization, whereby a narrowing funnel of many potential inputs converges onto a relatively small number of processes before fanning out again into a great diversity of outputs. (C) The homeostatic and reward bowties are good examples of nested layered architectures [reprinted with permission from (111), copyright 2004 Elsevier], since the dopamine bowtie can be viewed as an integral part of the broader energetic network that includes hypothalamic (HYP) signaling and peripheral hormones. NAc, nucleus accumbens; PFC, prefrontal cortex; SN, substantia nigra; VTA, ventral tegmental area (modified with permission from an unpublished presentation, courtesy of Dr. John Doyle, Ph.D.).