Scientists from France have found that anorexia and the highly addicting club-drug ecstasy activate some of the same brain pathways, a finding that may help explain the addictive nature of anorexia and other eating disorders and lead to new treatments.
In a paper published this week, Dr. Valerie Compan of Centre National de la Recherche Scientifique, Montpellier, and colleagues report that both anorexia and ecstasy reduce the drive to eat by stimulating the same subset of receptors for the neurotransmitter serotonin.
These so-called 5-HT4 receptors are located in a brain structure associated with feelings of reward called the nucleus accumbens.
In mice, Compan and colleagues stimulated these receptors, which are known to play a role in addictive behavior, and found that this led to anorexic-like behavior -- food-fed mice ate less and food-deprived mice showed a reduced drive to eat.
Stimulating these receptors in mice also boosted production of the same enzymes stimulated in response to cocaine and amphetamine use.
Blocking the receptors increased food intake in the animals and mice missing these receptors were less sensitive to the appetite-suppressant effects of ecstasy.
"Our data may converge to open the possibility that anorexia can be a reward-relating problem involving neuronal mechanisms," Compan told Reuters Health.
This research, she added, may have implications for the development of drug treatments for eating disorders. "Our studies over seven years now open the possibility that 5-HT4 receptor could represent an important therapeutic target to treat patients suffering from these disorders," Compan said.
News and recovery-oriented commentary about current controversies, emerging trends and research findings related to drug and alcohol addiction, treatment and recovery.
Friday, October 05, 2007
Anorexia an addiction?
New research provides a peek inside the neurobiology of anorexia:
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1 comment:
Thanks for this. I have often seen addictive type symptoms in eating disorders and this seems to fit my conclusions.
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