Background: The specific pathogenesis of increased vulnerability to cocaine-induced paranoia/psychosis is unknown. Weight loss has been long observed in patients abusing stimulants (including cocaine and the amphetamines). In the current study, we compared Body Mass Index (calculated as weight in kilograms divided by the square of height in meters) in Cocaine-Induced Psychosis cases, referred to as "Cocaine-Induced Psychosis-prone" (n=40) and non-Cocaine-Induced Psychosis cases, referred to as "Cocaine-Induced Psychosis-resistant" (n=29) consecutively admitted to a research substance abuse unit to determine whether Body Mass Index is associated with Cocaine-Induced Psychosis. Height and weight were measured and Body Mass Index calculated by a licensed nutritionist using a standardized protocol. Cocaine-induced psychosis and cocaine use patterns were assessed using the Cocaine Experience Questionnaire.
Results: Body Mass Index in the Cocaine-Induced Psychosis-prone patients was significantly lower than in the Cocaine-Induced Psychosis-resistant patients (i.e., 23.1 kg/m2 +/-2.5 vs. 25.4 kg/m2 +/-3.5 (P=.003), respectively). Percentage of Ideal Body Weight also differed significantly between the two groups.
Conclusions: The data suggest that lower Body Mass Index may be associated with increasing proneness to developing psychotic symptoms in the context of crack cocaine use or that higher Body Mass Index might be associated with some protection against Cocaine-Induced Psychosis in the context of similar use patterns. In the Discussion the authors speculate as to why Cocaine-Induced Psychosis is more commonly observed in the patient population with lower Body Mass Index and lower percentage of Ideal Body Weight. They evoke possible involvement of cocaine's influence on the anorexigenic cytokine Tumor Necrosis Factor, Cocaine-and-Amphetamine-Regulated Transcript, or suppression of the appetite stimulating Neuropeptide Y, or cocaine-induced deficits in nicotinic cholinergic neural-transmission, all of which have not only been linked to weight and appetite, but also to idiopathic psychosis. It could be speculated that one or more of these systems might be differentially affected by cocaine addiction in the psychosis prone Cocaine-Induced Psychosis group vs. the psychosis resistant non-Cocaine-Induced Psychosis group. Further exploration of these possible associations seem warranted. Such findings would have implications for the cocaine model of psychosis proneness and perhaps for the stimulant model of psychoses in general.