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A brief summary of the articles appearing in this issue of Biological Psychiatry.

        Food Addiction: Theories, Concepts, and Evidence

        The notion of ‘food addiction’ has been suggested to help explain the global surge in obesity over the last thirty years. Here, Smith and Robbins (pages 804–810) critically investigate this proposal using the established theoretical framework of drug addiction models, examining the underlying similarities and differences in the brains and behaviors of obese and substance-dependent individuals.
        The concept of food addiction has become a common, but controversial feature in the scientific literature. Mesolimbic and nigrostriatal dopamine systems are often cited as brain mechanisms that contribute to the establishment of food addiction. In this review, Salamone and Correa (pages e15–e24) provide a critical discussion of recent findings and current theoretical views of dopaminergic involvement in food motivation and consumption.
        Volkow et al. (pages 811–818) review the growing evidence for the existence of an addictive dimension in obesity and other eating disorders that interferes with the body’s homeostatic process to regulate satiety and food intake. They also discuss how the implementation of a more cross-disciplinary approach in research, one that considers the rewarding components of food, could improve opportunities to help prevent and treat obesity.
        Common brain mechanisms may mediate the acquisition and development of overeating and drug addiction. The drug-reward paradox stems from findings that show brain stimulation of the same region can induce different behavioral effects. In his review, Wise (pages 819–826) discusses and provides insights into the drive-reward paradox from the perspective of the dual roles of dopamine – motivation and reinforcement – in both food and drug seeking.

        Food Addiction: Neural Adaptations

        Newman et al. (pages 843–850) explored whether reward-driven feeding can produce drug-like plasticity in the brain and report that repeated, intermittent bouts of palatable feeding in rats produced a hypersensitivity of gamma-aminobutyric acid (GABA) systems in the nucleus accumbens shell, a crucial brain reward site. This neuroplasticity appeared to be related to repeated mu-opioid receptor activation. These results may aid understanding of clinically observed links between binge-like eating disorders and substance abuse, which is known to activate both opioid and GABA systems in the nucleus accumbens shell.
        Tellez et al. (pages 851–859) assessed the extent to which the caloric content of fats, independently of oral palatability, produces the main behavioral and neurobiological hallmarks of psychostimulant self-administration in mice. Their results support the hypothesis that self-stimulation of the gastrointestinal tract with calorically dense fats generates the expression of addiction-related behavioral and neurochemical markers.
        Leptin signaling in the ventral tegmental area, a critical site for neuroadaptations to rewarding stimuli, can modulate reward-seeking behaviors. Because plasticity of glutamatergic synapses onto ventral tegmental area neurons can encode predictive information about reward, Thompson and Borgland (pages 860–868) hypothesized that leptin can decrease excitatory synaptic transmission onto dopamine neurons. Using whole-cell patch clamp electrophysiology, they determined that leptin acts presynaptically to depress excitatory synaptic transmission. Leptin-induced weakening of synaptic strength onto dopamine cells may underlie its inhibitory effects on appetitive behavior for rewarding stimuli.
        The gut-derived hormone ghrelin increases food intake by signaling in the brain. Kanoski et al. (pages 915–923) used a rat model to examine whether ghrelin signaling in the ventral subregion of the hippocampus, a brain region that controls motivational and memory processes, affects feeding behavior. Results show that ghrelin administration increased motivation to seek out food and stimulated food intake, suggesting that this neuroendocrine system plays a role in the ability of environmental cues to trigger excessive feeding.

        Food Addiction: Risk Factors and Susceptibility

        Stice et al. (pages 869–876) tested whether individual differences in reward-related brain regions predicted onset of overweight/obesity or substance use among initially healthy-weight and abstinent adolescents. Functional magnetic resonance imaging (fMRI) results showed that elevated caudate and putamen reward responding predicted substance use onset, but not overweight/obesity, over 1 year follow-up. These findings suggest that increased reward responsivity increases risk for future substance use onset but not unhealthy weight gain.
        Sinha and Jastreboff (pages 827–835) review the research linking stress to overeating and weight gain. They also present an integrative heuristic model to describe how high stress alters the biology of stress and appetite/energy regulation, which in turn affects neural mechanisms contributing to stress- and food cue-induced craving for highly palatable foods and increased over-consumption of such foods, leading to an increased risk of weight gain and obesity.

        Food Addiction: Neural Circuits and Correlates of Reward and Motivation

        The patterns of self-control and food consumption observed in individuals with eating disorders appear to extend to their abuse of alcohol and drugs, with increased rates of substance abuse in bulimia nervosa and decreased rates in anorexia nervosa. This suggests there may be overlapping neural circuits for foods and substances of abuse. Kaye et al. (pages 836–842) review dopamine positron emission tomography and fMRI studies, which suggest that similar alterations in brain regions important for reward and inhibition of behaviors may contribute to food over- or under-consumption and substances of abuse in individuals with eating disorders.
        Identifying factors that distinguish groups of obese people may help advance prevention and treatment approaches for obesity. Here, Balodis et al. (pages 877–886) used fMRI to study brain correlates of reward processing in obese people with and without binge eating disorder (BED) and lean controls. Relative to the control group, the no-BED obese group demonstrated increased ventral striatal and ventromedial prefrontal cortex activity during reward anticipation. The obese group with BED, compared to those without BED, showed relatively diminished striatal activation during reward anticipation, similar to findings in alcohol dependence and pathological gambling.
        Cambridge et al. (pages 887–894) used fMRI to explore drug-related changes in motivation and pleasure associated with food stimuli in obese individuals with moderate binge eating who received placebo or GSK1521498, a mu-opioid receptor antagonist, for four weeks. Compared with placebo, individuals who received drug showed a clear reduction in brain responses to high calorie (compared to low calorie) food images, which was associated with reduced motivational responding to such foods. These results provide further evidence of a link between the opioid system and food-related behavior in binge-eating obese individuals.

        Prevalence of Binge Eating Disorder

        Kessler et al. (pages 904–914) describe results of a large epidemiologic study comparing DSM-IV BED to bulimia nervosa in 14 countries in the World Health Organization World Mental Health surveys. Prevalence estimates were found to be consistently higher for BED than bulimia nervosa across countries, while measures of adverse consequences and other correlates of the two disorders were quite similar, suggesting that BED represents a public health problem at least equal to bulimia nervosa.

        Neurobiology of Physical Exercise

        Using a rodent model of voluntary running, Dubreucq et al. (pages 895–903) have shown previously that the cannabinoid type-1 receptor increases wheel running. Using pharmacology and conditional mutagenesis in mice, they now report that this permissive control is exerted through cannabinoid type-1 receptors located on GABAergic nerve terminals in the ventral tegmental area.

        Naltrexone for Smoking Cessation-Related Weight Gain

        Weight gain is a common adverse effect of quitting smoking and the endogenous opioid system may play a significant role. King et al. (pages 924–930) examined the opioid receptor antagonist naltrexone on weight gain through one year of follow up in abstinent smokers. Compared with placebo, weight gain was lower in women, but not men, treated with naltrexone. The results support the first potential pharmacotherapy to reduce womens’ weight gain after smoking cessation.