In his recent editorial Dr Thakore (Reference Thakore2005) rightly highlights the importance of the association of the metabolic syndrome and one of its consequences, type 2 diabetes, with schizophrenia. Despite acknowledging that antipsychotic drugs can induce substantial weight gain, he avoids ascribing the metabolic disturbances in schizophrenia to drug-induced obesity. His suggestion that untreated schizophrenia is itself associated with metabolic disturbance is based on a study of 19 people who had substantially greater deposits of intra-abdominal fat than a control group (Reference Ryan, Flanagan and KinsellaRyan et al, 2004). This contrasts with other studies showing that 40 antipsychotic-naïve patients with schizophrenia had no elevation in intra-abdominal fat compared with controls (Reference Zhang, Yao and LiuZhang et al, 2004) and that 50 did not differ from a control group in terms of body mass index, fasting plasma glucose or insulin (Reference Arranz, Rosel and RamirezArranz et al, 2004). In attempting to explain discrepancies in terms of methodological differences, Dr Thakore is wrong to state that the control group of Zhang et al consisted of ‘elderly men’; controls were well matched for age and gender with the patient group.
These larger studies also show that antipsychotic drug treatment is associated with increased intra-abdominal fat (Reference Zhang, Yao and LiuZhang et al, 2004) and insulin resistance (Reference Arranz, Rosel and RamirezArranz et al, 2004), despite negative findings from Ryan et al (Reference Ryan, Flanagan and Kinsella2004). The risk of diabetes in schizophrenia is higher in patients receiving olanzapine rather than conventional antipsychotics (Reference Koro, Fedder and L'ItalienKoro et al, 2002); olanzapine is particularly liable to induce weight gain. These and other studies indicate that antipsychotic drug treatment can result in metabolic morbidity. It would thus be misleading, if not dangerous, to imply that obesity resulting from treatment with some antipsychotic drugs is not associated with the development of the metabolic syndrome and type 2 diabetes.
Dr Thakore listed criteria for the metabolic syndrome; these have now been superseded by a more clinically accessible and less stringent definition. The core criterion is central (abdominal) obesity, defined by waist circumference, plus two of four risk factors from elevated triglycerides, reduced high-density lipoprotein cholesterol, raised blood pressure and raised fasting plasma glucose (International Diabetes Federation, 2005).
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