A brief summary of the articles appearing in this issue of biological psychiatry.

IN THIS ISSUEVolume 73, Number 9, May 1, 2013A brief summary of the articles appearing in this issue of Biological Psychiatry.
Food Addiction: Theories, Concepts, and Evidence synaptic transmission onto dopamine neurons. Using whole-cell The notion of ‘food addiction’ has been suggested to help patch clamp electrophysiology, they determined that leptin acts explain the global surge in obesity over the last thirty years. Here, presynaptically to depress excitatory synaptic transmission.
Smith and Robbins (pages 804–810) critically investigate this Leptin-induced weakening of synaptic strength onto dopamine proposal using the established theoretical framework of drug cells may underlie its inhibitory effects on appetitive behavior for addiction models, examining the underlying similarities and The gut-derived hormone ghrelin increases food intake by signaling in the brain. Kanoski et al. (pages 915–923) used a rat The concept of food addiction has become a common, but model to examine whether ghrelin signaling in the ventral controversial feature in the scientific literature. Mesolimbic and subregion of the hippocampus, a brain region that controls nigrostriatal dopamine systems are often cited as brain mechan- motivational and memory processes, affects feeding behavior.
isms that contribute to the establishment of food addiction. In this Results show that ghrelin administration increased motivation to review, Salamone and Correa (pages e15–e24) provide a critical seek out food and stimulated food intake, suggesting that this discussion of recent findings and current theoretical views of neuroendocrine system plays a role in the ability of environ- dopaminergic involvement in food motivation and consumption.
mental cues to trigger excessive feeding.
Volkow et al. (pages 811–818) review the growing evidence for the existence of an addictive dimension in obesity and other Food Addiction: Risk Factors and Susceptibility eating disorders that interferes with the body’s homeostatic Stice et al. (pages 869–876) tested whether individual process to regulate satiety and food intake. They also discuss differences in reward-related brain regions predicted onset of how the implementation of a more cross-disciplinary approach in overweight/obesity or substance use among initially healthy- research, one that considers the rewarding components of food, weight and abstinent adolescents. Functional magnetic reso- could improve opportunities to help prevent and treat obesity.
nance imaging (fMRI) results showed that elevated caudate and Common brain mechanisms may mediate the acquisition and putamen reward responding predicted substance use onset, but development of overeating and drug addiction. The drug-reward not overweight/obesity, over 1 year follow-up. These findings paradox stems from findings that show brain stimulation of the suggest that increased reward responsivity increases risk for same region can induce different behavioral effects. In his review, future substance use onset but not unhealthy weight gain.
Wise (pages 819–826) discusses and provides insights into the Sinha and Jastreboff (pages 827–835) review the research drive-reward paradox from the perspective of the dual roles of linking stress to overeating and weight gain. They also present an dopamine – motivation and reinforcement – in both food and integrative heuristic model to describe how high stress alters the biology of stress and appetite/energy regulation, which in turnaffects neural mechanisms contributing to stress- and food cue- induced craving for highly palatable foods and increased over- Newman et al. (pages 843–850) explored whether reward- consumption of such foods, leading to an increased risk of driven feeding can produce drug-like plasticity in the brain and report that repeated, intermittent bouts of palatable feeding inrats produced a hypersensitivity of gamma-aminobutyric acid Food Addiction: Neural Circuits and Correlates of Reward and (GABA) systems in the nucleus accumbens shell, a crucial brain reward site. This neuroplasticity appeared to be related to The patterns of self-control and food consumption observed repeated mu-opioid receptor activation. These results may aid in individuals with eating disorders appear to extend to their understanding of clinically observed links between binge-like abuse of alcohol and drugs, with increased rates of substance eating disorders and substance abuse, which is known to activate abuse in bulimia nervosa and decreased rates in anorexia both opioid and GABA systems in the nucleus accumbens shell.
nervosa. This suggests there may be overlapping neural circuits Tellez et al. (pages 851–859) assessed the extent to which the for foods and substances of abuse. Kaye et al. (pages 836–842) caloric content of fats, independently of oral palatability, pro- review dopamine positron emission tomography and fMRI duces the main behavioral and neurobiological hallmarks of studies, which suggest that similar alterations in brain regions psychostimulant self-administration in mice. Their results support important for reward and inhibition of behaviors may contribute the hypothesis that self-stimulation of the gastrointestinal tract to food over- or under-consumption and substances of abuse in with calorically dense fats generates the expression of addiction- related behavioral and neurochemical markers.
Identifying factors that distinguish groups of obese people Leptin signaling in the ventral tegmental area, a critical site for may help advance prevention and treatment approaches for neuroadaptations to rewarding stimuli, can modulate reward- obesity. Here, Balodis et al. (pages 877–886) used fMRI to study seeking behaviors. Because plasticity of glutamatergic synapses brain correlates of reward processing in obese people with and onto ventral tegmental area neurons can encode predictive without binge eating disorder (BED) and lean controls. Relative to information about reward, Thompson and Borgland (pages the control group, the no-BED obese group demonstrated 860–868) hypothesized that leptin can decrease excitatory increased ventral striatal and ventromedial prefrontal cortex & 2013 Society of Biological Psychiatry activity during reward anticipation. The obese group with BED, measures of adverse consequences and other correlates of the compared to those without BED, showed relatively diminished two disorders were quite similar, suggesting that BED represents striatal activation during reward anticipation, similar to findings a public health problem at least equal to bulimia nervosa.
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 Using a rodent model of voluntary running, Dubreucq et al.
stimuli in obese individuals with moderate binge eating who (pages 895–903) have shown previously that the cannabinoid received placebo or GSK1521498, a mu-opioid receptor antago- type-1 receptor increases wheel running. Using pharmacology nist, for four weeks. Compared with placebo, individuals who and conditional mutagenesis in mice, they now report that this received drug showed a clear reduction in brain responses to permissive control is exerted through cannabinoid type-1 recep- high calorie (compared to low calorie) food images, which was tors located on GABAergic nerve terminals in the ventral associated with reduced motivational responding to such foods.
These results provide further evidence of a link between the Naltrexone for Smoking Cessation-Related Weight Gain opioid system and food-related behavior in binge-eating obese 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 Kessler et al. (pages 904–914) describe results of a large antagonist naltrexone on weight gain through one year of follow epidemiologic study comparing DSM-IV BED to bulimia nervosa up in abstinent smokers. Compared with placebo, weight gain in 14 countries in the World Health Organization World Mental was lower in women, but not men, treated with naltrexone. The Health surveys. Prevalence estimates were found to be consis- results support the first potential pharmacotherapy to reduce tently higher for BED than bulimia nervosa across countries, while womens’ weight gain after smoking cessation.

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