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Home > > Science Meeting Summaries & Special Reports > The Science of Addiction: Translating New Insights Into Better Psychiatric Practice > Insights on Obesity and Drug Addiction From Brain Imaging


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SYMPOSIUM

INSIGHTS ON OBESITY AND DRUG ADDICTION FROM BRAIN IMAGING

Co-Chairs:

Nora D. Volkow, M.D.
Director
National Institute on Drug Abuse

Joseph Frascella, Ph.D.
National Institute on Drug Abuse

Overview

Drug addiction and obesity represent major health problems in the United States. Despite a number of different etiologies (e.g., social, environmental, psychological, biological, and behavioral) for both drug addiction and obesity, each can often be characterized as a complex biobehavioral disorder resulting from a loss of control with compulsive or excessive behaviors. Both eating and drug abuse directly involve brain reward pathways; both obesity and drug addiction are chronic, relapsing disorders that represent unique treatment challenges. This symposium explores the commonalities (and differences) between drug addiction and obesity through shared neurobiological processes and brain systems, particularly drawing on insights gained from human brain imaging studies.

Modulators of Orbitofrontal Activation in Response to Food Stimuli
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Modulators of Orbitofrontal Activation in Response to Food Stimuli
Deborah Yurgelum-Todd, Ph.D.

It has been hypothesized that addictive drugs activate the same brain reward mechanisms involved in the control of normal appetitive behavior. The orbitofrontal cortex consistently emerges as a critical convergence zone for the stream of afferent sensory information related to rewarding stimuli, particularly for primary reinforcers such as food. Functional magnetic resonance imaging (fMRI) techniques provide a method for characterizing orbitofrontal response. To clarify the neurobiological mechanisms by which body weight, mood, and age may influence appetitive response, we presented healthy, normal-weight adolescent and adult females with color photographs of foods differing in fat-content/calorie-density (e.g., high-reward or low-reward) while they underwent blood oxygen level dependent (BOLD) functional magnetic resonance imaging (fMRI).

Body mass was observed to be negatively correlated with activity of the orbitofrontal cortex when adult females viewed images of highly rewarding food, suggesting a relationship between weight status and rewarding effects of the food images. In addition, activation of the orbitofrontal cortex was shown to be significantly related to mood ratings. Positive affect was associated with decreased medial orbitofrontal activity during the viewing of high-fat food, whereas negative affect was associated with increased activation of this region during the viewing of high-reward, high-calorie food. These associations suggest that mood may play an important role in moderating the approach to foods that differ in reward salience. In a complementary study, a significant positive correlation was observed between age and activation of the orbitofrontal cortex in adolescent females viewing high-calorie images. Taken together these results indicate that mood state, body mass, and development of the brain circuitry may moderate the reinforcing capacity of rewarding stimuli. These findings have important implications for clarifying models underlying reward response and for the development of more effective therapies of eating disorders and drug addiction.

Hunger as an Addiction
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Hunger as an Addiction
Alain Dagher, M.D.

Drug addiction is an interesting model to try to understand cognitive control. The addict, attempting to abstain from drugs, is under the influence of two contradictory phenomena: a compulsion to use the drug, and a desire to quit. These two thought processes are likely mediated by different, but interacting, brain regions, all of which are innervated by dopamine. It is also instructive to view obesity from the standpoint of addiction neuroscience. There are obvious parallels between attempting to lose weight and abstaining from a drug.

Drugs of abuse are thought to target the same neural systems as natural rewards. The most likely candidate brain region is the mesolimbic and mesostriatal dopamine system. In animals, dopamine is released in the striatum in response to food, sexual mates, and to almost all drugs of abuse. Different theories propose that dopamine acts by mediating the hedonic impact of a reinforcing stimulus, promoting associative learning about the stimulus, or by serving as an incentive to the consumption of the stimulus. Moreover, it has been suggested that the magnitude of the dopamine response to drugs and stressors may be a marker of vulnerability to addiction.

The research described here uses two techniques: functional MRI to measure neural activity during craving induced by drug or food cues, and positron emission tomography to measure dopamine release in human volunteers using [11C] raclopride, a D2 receptor ligand. We have used these techniques to study the brain response to abused drugs (e.g., alcohol, amphetamine, and nicotine) and natural rewards such as food and money.

We review some of the factors that favor the expression of abstinence or relapse in addicts, and the similarities and differences between drugs of abuse and natural rewards such as food.

Neuroimaging Studies of Obesity and Drug Addiction
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Neuroimaging Studies of Obesity and Drug Addiction
Gene-Jack Wang, M.D.

The cerebral mechanisms underlying the behaviors that result in pathological overeating and obesity are poorly understood. The regulation of food intake is a complex balance between excitatory and inhibitory processes. Excitatory processes arise from the body’s needs for nutrients and calories. Studies using positron emission tomography (PET) implicate the involvement of brain dopamine (DA) in non-hedonic motivational properties of food intake in humans. We also found reductions of striatal DA D2 receptors in pathologically-obese subjects, which were similar to those in drug-addicted subjects. We postulated that decreased levels of DA receptors predisposed subjects to search for reinforcers—in the case of drug-addicted subjects, for the drug, and in the case of the obese subjects, for food—as a means to temporarily compensate for a decreased sensitivity of DA-regulated reward circuit. The inhibitory processes arise from satiety signals (e.g., electrical and chemical) after food consumption. We used PET to measure the brain metabolic responses in obese subjects who had an implantable gastric stimulator, which induces stomach expansion via electrical stimulation of the vagus nerve in order to identify the brain circuits responsible for its effects in decreasing food intake. These findings corroborated the role of the vagus nerve in regulating hippocampal activity as well as the importance of the hippocampus in modulating eating behaviors linked to emotional eating and lack of control. The brain regions (orbitofrontal cortex, hippocampus, cerebellum, and striatum) activated by gastric stimulation overlap with those reported during craving responses in addicted subjects, supporting the commonalities in the neurocircuitry that underlie compulsive food intake and compulsive drug intake.


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