Elsevier

Biological Psychiatry

Volume 73, Issue 9, 1 May 2013, Pages 836-842
Biological Psychiatry

Review
Does a Shared Neurobiology for Foods and Drugs of Abuse Contribute to Extremes of Food Ingestion in Anorexia and Bulimia Nervosa?

https://doi.org/10.1016/j.biopsych.2013.01.002Get rights and content

Is starvation in anorexia nervosa (AN) or overeating in bulimia nervosa (BN) a form of addiction? Alternatively, why are individuals with BN more vulnerable and individuals with AN protected from substance abuse? Such questions have been generated by recent studies suggesting that there are overlapping neural circuits for foods and drugs of abuse. To determine whether a shared neurobiology contributes to eating disorders and substance abuse, this review focused on imaging studies that investigated response to tastes of food and tasks designed to characterize reward and behavioral inhibition in AN and BN. BN and those with substance abuse disorders may share dopamine D2 receptor–related vulnerabilities, and opposite findings may contribute to “protection” from substance abuse in AN. Moreover, imaging studies provide insights into executive corticostriatal processes related to extraordinary inhibition and self-control in AN and diminished inhibitory self-control in BN that may influence the rewarding aspect of palatable foods and likely other consummatory behaviors. AN and BN tend to have premorbid traits, such as perfectionism and anxiety that make them vulnerable to using extremes of food ingestion, which serve to reduce negative mood states. Dysregulation within and/or between limbic and executive corticostriatal circuits contributes to such symptoms. Limited data support the hypothesis that reward and inhibitory processes may contribute to symptoms in eating disorders and addictive disorders, but little is known about the molecular biology of such mechanisms in terms of shared or independent processes.

Section snippets

Relationship of ED Traits to Substance Use

This issue explores the relationship between food and addiction and overlapping neural circuits of reward and self-control. AN and BN show patterns of extremes of self-control and food consumption that appear to extend to their use of alcohol and illicit drugs. That is, meta-analyses 32, 33 show increased rates of drug and alcohol abuse in BN and decreased rates in AN. Because of space limitations, this review focuses on two areas of research in ED. First, we discuss dopamine (DA) positron

Difficulties Untangling Cause from Consequence in EDs

Studies of EDs must consider the impact of malnutrition on brain function. For example, malnutrition in AN (3) is associated with changes in brain structure (e.g., reduction in gray matter, greater cerebrospinal fluid [CSF] volume, altered white matter integrity) and profound metabolic, electrolyte, and endocrine disturbances. Furthermore, studies in animals suggest that diet and weight can influence DA metabolism 35, 36 One method of avoiding the confounding effects of abnormal nutritional

DA Function in AN and BN

Several lines of evidence suggest that individuals with ED have altered striatal DA function. PET studies with the radioligand [11C]raclopride find that REC AN patients have increased binding of DA D2/D3 receptors at baseline in the anterior ventral striatum (AVS) relative to control subjects 25, 37. Because PET measures of [11C]raclopride binding are sensitive to endogenous DA concentrations (38), this difference could be due to either a reduction in the intrasynaptic DA concentration or an

Higher-order Neural Processes Modulating Reward, Emotionality, and Inhibition

Data support the hypothesis (3) that AN and BN individuals have an imbalance within and/or between ventral limbic and dorsal cognitive circuits. Specifically, a ventral limbic neural circuit, which includes the amygdala, anterior insula (AI), AVS, ventral regions of the anterior cingulate cortex (ACC), and the orbitofrontal cortex (OFC), is involved in identifying rewarding and emotionally significant stimuli and for generating affective responses to these stimuli 61, 62. A dorsal executive

Reward and Interoceptive Function in Regard to Tasting Food in AN and BN

fMRI studies of appetitive behaviors in ED have used designs that either administer a taste of some food or present images of food. This review focuses on studies of taste because much is known about how tastes of food activate reward and interoceptive circuitry in healthy subjects 34, 65. In brief, the AI is the primary gustatory taste cortex and thus responds to tastes of food (3). The AI, as well as the ACC and OFC, code the sensory-hedonic response to taste and innervate a broad region of

Reward and Inhibition Studies

A recent series of fMRI studies based on reward and inhibition tasks has explored the response of ventral and dorsal corticostriatal systems in AN and BN compared with control subjects to better understand the modulation of reward, emotionality, and behavioral inhibition. Using a monetary choice task to investigate response to positive and negative feedback, REC AN (82) and REC BN (83) subjects had a similar abnormal AVS response in that they failed to differentiate wins and losses compared

Summary

It remains conjectural whether years of pathological eating is the sole cause of aberrant neurobiology in AN. Whereas most people find starvation to be unpleasant and recidivism after dieting is high, AN individuals find that food is anxiety provoking and starvation comforting. If AN were merely a consequence of an out-of-control diet, the rate of AN in this society would probably be much higher. Alternatively, underlying traits may be contributory. For example, many of the characteristic

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