Weight loss in chronic cocaine users appears to be associated with disturbances in body fat mass, not reduced caloric intake or increased physical activity, researchers have found.
The study challenges the widely held belief that chronic cocaine use suppresses appetite. "The cocaine-dependent men in our study reported increased food intake, specifically in foods that are high in fat and carbohydrates, but there was no concomitant increase in body weight," wrote Dr. Karen Ersche and her colleagues from the University of Cambridge, United Kingdom, in the journal Appetite (2013;71:75-80). [Our findings] "suggest a profound metabolic alteration that needs to be taken into account if we are able to understand the fully deleterious physical consequences of repeated use of this drug."
The cocaine users in the study also had lower levels of the energy-regulating hormone leptin, which ordinarily is equated with weight gain. These findings potentially open a new avenue of therapeutic intervention, since behavior is affected by noradrenergic manipulation of basal metabolism and inhibitory processes. "Such intervention, at a sufficiently early stage, could have the potential to prevent weight gain during recovery, thereby reducing personal suffering and improving compliance during the recovery process," the investigators wrote.
Sixty-five men were recruited from the community, 35 of whom were cocaine dependent, according to DSM-IV-TR criteria, and had been using cocaine either in powdered or freebase forms for an average of 15.3 years since the age of 19.2 years. The mean age of the men was about 36 years in both groups. The other half (n = 30) had no history of cocaine use. Those with a lifetime history of psychotic disorders, neurologic illness or head trauma, metabolic or autoimmune disorders, or HIV infection were excluded.
The investigators decided to focus on men "to avoid confounding factors related to hormone fluctuations that affect appetite and weight in women," Dr. Ersche, also the lead investigator, said in an interview.
All participants were assessed via questionnaire for eating behavior, food and alcohol intake, other substance use, education and verbal intelligence, and impulsivity. Plasma leptin levels were assessed in both groups; X-ray absorptiometry scans were used to determine anthropometric measurements such as fat mass, non-bone lean mass, and bone mineral density. Other measures such as body mass index (BMI), weight, height, waist-hip ratio, and skin-fold thickness also were assessed. The fat mass index (FMI) was derived by dividing the individual’s fat mass, fat free mass, and lean mass by the person’s height squared.
A multivariate analysis for variance was conducted on all findings, and covariates such as tobacco or other substance use also was taken into account.
Dr. Ersche and her associates found no differences between BMI, waist-hip ratio, and skin-fold thickness, although cocaine users had higher rates of fat, carbohydrate, and alcohol consumption, and higher levels of uncontrolled eating (although they were more likely to skip breakfast), while their FMI was significantly less than the nonuser group. Leptin levels were found to correlate significantly in both groups, with BMI and FMI. In the cocaine-user group, leptin levels, but not BMI or FMI, correlated with the duration of cocaine use. Controlling for covariates did not change the results.
The investigators concluded that while current treatment programs promote healthy eating to help recovering cocaine users manage their weight, "We argue that a more nuanced view is needed, one that acknowledges a major disturbance in eating behaviors and metabolism."
This study was funded by a research grant from the Medical Research Council and the Wellcome Trust. Dr. Ersche is supported by the Medical Research Council; neither she nor her colleagues reported any relevant disclosures.