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Compared with the general population, it has been shown that patients with schizophrenia have a higher risk of impaired glucose tolerance and diabetes mellitus (DM) (1). A study of 248 patients conducted in Japan reported a type 2 DM prevalence of 8.8%, compared with 5% in a control group matched for age and sex (2). Another study by Mukherjee and others reported an overall prevalence of 15.8% among schizophrenia patients in Italy (3), which is considerably higher than reports from population surveys in Italy. A recent study by Dixon and others, using databases collected by the Schizophrenia Patient Outcomes Research Team (PORT), found that rates of diagnosed diabetes (14.9%) exceeded general population statistics well before the widespread use of the newer antipsychotic drugs (4). Several factors may contribute to schizophrenia patients’ increased susceptibility to developing DM. For example, poor health behaviours are likely to be an important contributing factor. Brown and others evaluated 102 schizophrenia patients living in the community and found that they exercised less, smoked more, and had less healthy diets, compared with normal control subjects (5). Lindenmayer and others proposed an additive risk model to identify risk factors that increase the probability of schizophrenia patients’ developing DM (6). Ethnicity, family history of diabetes, history of glucose dysregulation, and preexisting hypertension were all suggested to increase the risk of type 2 DM. Another putative factor may be psychotropic medications: it has been reported that chlorpromazine and lithium impair glucose tolerance (7). The mechanism of action of these drugs is much debated and includes increased peripheral resistance to insulin, which may be secondary to the weight gain in these patients. However, weight gain is not a prerequisite for the development of hyperglycemia and diabetes (8). The newer atypical drugs may contribute directly to hyperglycemia by inhibiting glucose uptake in different cell types. Recent evidence suggests that the antipsychotics may do so by binding to and blocking the glucose transporter protein (9). This study aimed to establish the prevalence of DM and impaired glucose tolerance in a population of schizophrenia patients and to elucidate some of the factors associated with hyperglycemia. MethodWe surveyed 607 patients; residents of the long-stay wards in Woodbridge Hospital, Singapore. Two psychiatrists independently verified that all the patients fulfilled DSM-IV criteria for schizophrenia. The prevalence of DM (that is, those patients with a chart diagnosis of DM) was found to be 4.9% (n = 30). For this study, we recruited patients who were able to give an informed, written consent and who had no documented chart diagnosis of diabetes, impaired glucose tolerance, significant physical illness, or history of drug or alcohol abuse. We subsequently included 194 patients in the study. None had received any atypical neuroleptics, either in the past or at the time of the study.
We reviewed the case records to obtain information on age, sex, illness-onset age, illness duration, and current medication status. We calculated body mass index (BMI) after using the same scale to record the weight and height of all patients. Patients were given an oral glucose tolerance test after an overnight fast. Fasting blood glucose and insulin levels were determined at the start of the testing period. We used the World Health Organization (WHO) diagnostic classification criterion for the Oral Glucose Tolerance Test (OGTT) to classify DM and impaired glucose tolerance (10). ResultsOf the 194 patients, 155 were men and 39 were women. Their mean (SD) age was 55.5 (8.7) years, with an age range of 33 to 83 years. The mean age at onset of schizophrenia was 22.6 years, and the mean duration of illness was 31.8 years. The overall prevalence of diabetes was 16% (n = 31), and the overall prevalence of impaired glucose tolerance was 30.9% (n = 60). Of the 31 diabetes patients, 22 were men, and 9 were women. There was no significant effect of sex or ethnicity on diabetes (c2 = 1.9, P = 0.17 and c2 = 0, P = 1.0, respectively). Table 1 shows the clinical characteristics of the 194 patients. Patients with DM and impaired glucose tolerance were significantly older than those with a normal glucose profile (P = 0.005, Kruskal–Wallis test). Fasting insulin levels were significantly higher in the patients with DM and in those with impaired glucose tolerance, compared with nondiabetic patients (P < 0.005, Kruskal–Wallis test). However, the 3 groups of patients did not differ significantly in other clinical variables. Overall, 12 patients had a BMI $ 25; that is, 12 patients were overweight according to the WHO recommendations for BMI (11). Analysis of age-specific prevalence revealed that the highest prevalence (50%) occurred in patients belonging to the group aged 50 to 59 years.
DiscussionAccording to the National Health Survey, the DM morbidity rate in the general population of Singapore was 9%, and the rate of impaired glucose tolerance was 15% (12). However, the prevalence rates of DM and impaired glucose tolerance in our study were much higher—16% and 30.9%, respectively. The mean age of patients in our study was 55.5 years; in the comparative population (that is, those aged 50 to 59 years), the prevalence of diabetes was 21.8%. We found age to be associated with diabetes, but we found no association with sex, ethnicity, or daily neuroleptic dosage. Tan and others have reported the increased risk of DM with increased age in the Singapore general population (13). These authors report the highest prevalence of DM to be in Asian Indians, although a significant ethnic difference between Chinese subjects and the other 2 ethnic groups (that is, Malays and Indians) could be demonstrated only in women. Obesity is another well-established risk factor that can lead to insulin insensitivity, glucose intolerance, and subsequently, DM. However, the weight and BMI of patients with disordered glucose homeostasis and of those without did not differ significantly. Almost all the patients had been institutionalized for long periods and within the same environment, and their similar diets and lifestyles could account for this lack of variance in weight and BMI. However, Mukherjee and others, reporting similar findings, suggest that individual biological differences in response to diet, rather than diet per se, may be more critical in determining the risk of DM in these patients (3). Our study highlights a high rate of DM among patients with schizophrenia. This comorbidity is associated with an increased risk of hypertension and coronary heart disease, which in turn may contribute to the higher mortality of patients with schizophrenia. Clinicians should be vigilant for the early symptoms of DM in this population, and regular glucose monitoring should be considered for those who have risk factors for developing DM. References1. Braceland FJ, Meduna LJ, Vaichulis JA. Delayed action of insulin in schizophrenia. Am J Psychiatry 1945;102:108–10. 2. Tabata H, Kikuoka M, Kikuoka H, Bessho H, Hirayama J, Hanabusa T, and others. Characteristics of diabetes mellitus in schizophrenic patients. J Med Assoc Thai 1987;70:90–3. 3. Mukherjee S, Decina P, Bocola V, Saraceni F, Scapicchio PL. Diabetes mellitus in schizophrenic patients. Compr Psychiatry 1996;37:68–73. 4. Dixon L, Weiden P, Delahany J, Goldberg R, Postrado L, Lucksted A, and others. Prevalence and correlates of diabetes in national schizophrenia samples. Schizophr Bull 2000;26:903–12. 5. Brown S, Birtwistle J, Roe L, Thompson C. The unhealthy lifestyle of people with schizophrenia. Psychol Med 1999;29:697–701. 6. Lindenmayer JP, Nathan AM, Smith RC. Hyperglycemia associated with the use of atypical antipsychotics. J Clin Psychiatry 2001;62:30–8. 7. National Diabetes Data Group. Classification and diagnosis of diabetes mellitus and other categories of glucose intolerance. Diabetes 1979;28:1039–57. 8. Henderson DC, Cagliero E, Gray C, Nasrallah RA, Hayden DL, Schoenfeld DA, and others. Clozapine, diabetes mellitus, weight gain and lipid abnormalities: a five-year naturalistic study. Am J Psychiatry 2000;157:975–81. 9. Dwyer DS, Bradley RJ, Kablinger AS, Freeman AM. Glucose metabolism in relation to schizophrenia and antipsychotic drug treatment. Ann Clin Psychiatry 2001;13:103–13. 10. World Health Organization Expert Committee on Diabetes Mellitus. Second report. Geneva: WHO; 1980. Technical Report Series No. 646. 11. World Health Organization: Measuring obesity: classification and description of anthropometric data. Copenhagen: WHO; 1989. 12. National Health Survey Singapore. Singapore: Epidemiology and Disease Control Department, Ministry of Health;1998: p 5–9. 13. Tan CE, Emmanuel SC, Tan BY, Jacob E. Prevalence of diabetes and ethnic differences in cardiovascular risk factors. The 1992 Singapore National Health Survey. Diabetes Care 1999;22:241–7. Author(s)Manuscript received February 2002 and accepted January 2003. 1Research Administrator, Woodbridge Hospital and Institute of Mental Health, Republic of Singapore. 2Consultant Psychiatrist, Woodbridge Hospital and Institute of Mental Health, Republic of Singapore. 3Research Assistant, Woodbridge Hospital and Institute of Mental Health, Republic of Singapore. Address for correspondence: Dr M Subramaniam, Research Unit, Institute of Mental Health and Woodbridge Hospital, 10 Buangkok View, Singapore 539747 e-mail: Mythily_Subramaniam@imh.com.sg
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