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PET probes brain and heart to fathom bulimia, obesity

(PSYCHIATRIC TIMES) - Two studies presented at the Society of Nuclear Medicine meeting in June attempted to explain the mechanisms behind two inversely related disorders: bulimia nervosa and obesity.

Dr. Angela S. Guarda, director of the eating disorders program at Johns Hopkins University, and her radiology colleagues used carbon-11 carfentanil PET to image women with bulimia nervosa before and after a 10-week behavioral treatment program. Compared with healthy controls, women with bulimia have biochemical differences in three areas of the brain associated with addiction and substance abuse.

C-11 carfentanil PET imaging identified reduced micro-opioid receptor binding in the prefrontal cortex and insula of patients who responded positively to a 10-week course of cognitive behavior treatment. The typical pattern of binge eating and purging persisted among patients when micro-opioid receptor binding was reduced in the cingulate cortex.

Patients with relatively high opioid binding in the insula before treatment responded better to behavioral training and counseling than did patients with low binding rates, according to the results of C-11 carfentanil PET. These data could help identify patients who are best suited for specific behavior modification regimens and could provide quantitative measures to guide program design to improve treatment effectiveness.

In another study, researchers from the University of California, Los Angeles found that functional changes in the endothelial lining of the coronary arteries may increase the risk of atherosclerosis and myocardial infarction, especially among people who are obese.

Abnormal endothelium-dependent myocardial blood flow has been shown to independently predict myocardial infarction and other potentially catastrophic cardiac events. In that context, Dr. Thomas H. Schindler, a research associate in molecular and medical pharmacology, and colleagues surmised that dysfunctional endothelium of coronary circulation may be a mechanistic link between cardiovascular events and obesity.

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