Cocaine’s appetite for fat and the consequences on body weight

Abstract

For many individuals in treatment for cocaine dependence, weight gain is a substantial problem during recovery. This weight gain causes significant distress and seems to increase the risk of relapse. The mechanisms underlying cocaine’s effects on weight remain elusive. It is widely assumed that this weight gain reflects a metabolic or behavioural compensatory response to the cessation of cocaine use. Here we challenge this assumption and outline potential mechanisms by which chronic cocaine use produces disturbances in the regulation of fat intake and storage, through its effects on the central and peripheral nervous systems, specifically the sympathetic nervous system. We hypothesize that the cocaine-induced alteration in fat regulation results in cocaine users developing a pronounced appetite for fatty food but keeps their fat mass low. This altered fat appetite subsequently leads to excessive weight gain when individuals enter treatment and stop using cocaine. Our aim is to shed light on the neurobiological mechanisms that may underlie the alterations in eating and fat regulation in cocaine-dependent individuals, to open up potential new avenues to support these individuals in recovery.

• CART
• cocaine
• drug addiction
• eating
• fat
• food
• insulin
• leptin

Acknowledgements

LB is the recipient of a Wellcome Trust Vacation Scholarship and KDE is supported by the Medical Research Council (MRC). The authors thank Hisham Ziauddeen for his comments on the manuscript and the MRC and Wellcome Trust for their joint support of the Behavioural and Clinical Neuroscience Institute, which provided the infrastructure for this work.

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this paper.