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Physical health of patients with schizophrenia
MANAGEMENT ISSUES
Physical health of patients with schizophrenia Jogin H Thakore
General medical comorbidity and schizophrenia The physical health of those with schizophrenia is often poor. Over 50% of those with schizophrenia have a general medical condition. This figure is thought to be an underestimate; it is suggested that the extent and consequences of medical comorbidity in patients with schizophrenia is generally under-recognized. Epidemiological studies have documented higher than expected rates of cardiovascular disease, infectious diseases, type 2 diabetes mellitus, respiratory disease, certain forms of cancer, and a variety of other illnesses in patients with schizophrenia. Though early studies failed to meet methodological standards necessary to provide conclusive evidence, Dixon et al., using rigorous modern criteria, have shown that the prevalence of type 2 diabetes mellitus exceeded those expected in the general population.1 They also showed that the rates of hypertension and heart disease among schizophrenia patients resembled those found in an older cohort in the general population, as measured in the US National Health Interview Survey. In addition to becoming physically sick at younger ages, patients with schizophrenia are rarely treated for their physical illness in the early, less severe phases and appear to present for medical attention only when cardiovascular and pulmonary diseases are severe and potentially life-threatening. This problem is further compounded by reduced detection of comorbid physical illness in schizophrenia by the medical profession despite the fact that medical comorbidity has been linked with more severe psychiatric symptoms. Therefore, it would appear that those with schizophrenia die prematurely and suffer from an excess of cardiovascular illnesses, which they either do not present with or if they do present, tend to go undetected.
Mortality and schizophrenia Nearly two-thirds of those with schizophrenia die of what are euphemistically termed ‘natural causes’ such as cardiovascular disease, diabetes and epilepsy. A number of studies have confirmed the contribution of cardiovascular disease to the increased mortality observed in schizophrenia though these findings are not universally accepted. However, a population-based record linkage study from Western Australia spanning from 1980 to 1998 observed that ischaemic heart disease (IHD) was the major cause of death in the psychiatric patients including schizophrenia.2 Indeed, the rates of death due to IHD remained high in schizophrenia despite a reduction in the general population.
Jogin H Thakore is a Senior Lecturer at the Royal College of Surgeons in Ireland, a lecturer in Psychology at Trinity College, Dublin and a Consultant Psychiatrist at St. Vincent Hospital, Dublin. His research interests include the physical changes in schizophrenia.
PSYCHIATRY 4:11
58
© 2005 The Medicine Publishing Company Ltd
MANAGEMENT ISSUES
Cardiovascular risk factors and schizophrenia
Obesity and schizophrenia
Patients with schizophrenia lead an unhealthy life. For instance, the development of cardiovascular disease is associated with nonmodifiable risk factors (such as age, gender and family history of premature heart disease). Modifiable risk factors include poor diet, physical inactivity, excess alcohol intake, smoking, poverty and various biochemical parameters and physiological events which include obesity, diabetes, insulin resistance, hypertension, platelet abnormalities, dyslipidaemias and hypertriglyceridaemia. Some of these biochemical parameters together form the metabolic syndrome.
There is little doubt that both conventional (older – e.g. haloperidol, zucclopenthixol) and atypical (newer – e.g. olanzapine, risperidone) medications can induce weight gain. However, the potential to do so varies between the different atypical compounds. Large-scale epidemiological studies indicate that there is a clear association between morbid obesity where the body mass index (BMI) is above 40 kg/m2, diabetes and cardiovascular disease. However, the location of the fat is more critical in lesser forms of obesity such as those generally seen in schizophrenia. Significant increases in visceral or intra-abdominal fat (IAF) (Figure 2), termed ‘male obesity’, are linked to the development of dyslipidaemias, atherosclerosis, hypertension and diabetes. Accurate quantification of IAF is possible only at post mortem. However, imaging techniques such as CAT scanning or MRI are suitable alternatives. First-episode, drug-naïve patients with schizophrenia offer a unique opportunity to study the interrelationship between illness and regional fat distribution, without the confounding variable of prior antipsychotic exposure. We have shown, using CT scanning, in two separate studies that such patients have 3–3.4 times as much IAF as matched controls though another study, using MRI, was unable to replicate these findings.5,6 Differences between the three studies may be explained by critical methodological deficits in the paper by Zhang et al. which include a failure to match patients and controls in terms of age, sex, diet, exercise, smoking and alcohol intake and the failure to use radiological determination of the lumbar vertebrae 4/5 junction which is critical if one is using a single CT slice to determine IAF area.6 We have shown that first episode patients with schizophrenia who are psychotropic-naïve have on average normal BMIs, although they have higher levels of visceral fat and are ‘metabolically obese’ as they have high levels of insulin, are insulin resistant, dyslipidaemic and predisposed to type 2 diabetes mellitus. Therefore, the presence of increased visceral obesity would indicate that a critical, potentially pathogenetic component of the metabolic syndrome may be present prior to the development of either diabetes or cardiovascular disease.
Metabolic syndrome and schizophrenia The metabolic syndrome is a cluster of disorders, which include obesity (central – around the abdomen), dyslipidaemias, glucose intolerance, insulin resistance (or hyperinsulinaemia) and hypertension. Its importance lies in the fact that it is highly predictive of type 2 diabetes mellitus and heart disease. Both the World Health Organization and the Third Report of the National Cholesterol Education Program Adult Treatment Panel have provided working criteria for the Metabolic Syndrome in order to improve its detection and thereby rate its prevalence (Figure 1).3,4 The frequency of the metabolic syndrome is 2–4-fold higher in schizophrenia than in an appropriate reference population. Neuroleptics can induce weight gain, with some agents having a greater propensity to do so than others, which may explain why patients with schizophrenia are at a higher risk for developing certain features of the metabolic syndrome.
Diagnostic criteria for the metabolic syndrome WHO criteria 1 or more of the following: • Insulin resistance • Impaired fasting glucose • Impaired glucose tolerance And 2 or more of the following: • WHR > 0.90 (men), 0.85 (women); or BMI ≥ 30kg/m2 • TG ≥ 1.7 mmol/l, or HDL < 0.9 mmol/l (men), 1.0 mmol/l (women) • Blood pressure ≤ 140/90 mm/Hg (or treated hypertension) • Microalbuminuria
A CAT scan showing intra-abdominal fat in an obese patient
National Cholesterol Education Program criteria Any 3 of the following: • Fasting plasma glucose ≥ 6.1 mmol/l • Waist circumference ≥ 102 cm (men), 88cm (women) • TG ≥ 1.7 mmol/l • HDL < 1.0 mmol/l (men), 1.16 mmol/l (women) • BP ≥ 130/85 mm/Hg (or treated hypertension) BMI, body mass index; BP, blood pressure; HDL, high density lipoproteins; TG, triglycerides; WHR, waist-to-hip ratio
White areas are the visceral fat in the abdomen
1
PSYCHIATRY 4:11
2
59
© 2005 The Medicine Publishing Company Ltd
MANAGEMENT ISSUES
buttocks. Screening for diabetes is rather more complicated, in that the gold standard for its diagnosis is the oral glucose tolerance test (OGTT), an impractical procedure for busy clinicians. A fasting or random glucose are alternatives and the latter is preferable, as it requires little effort on behalf of the patient. However, both of these tests are relatively insensitive and the chances of missing genuine abnormalities is large. The glycosylated haemoglobin (HbA1c) is not recommended as a screening test as it lacks sensitivity though is excellent in monitoring glycaemic control following the diagnosis of type 2 diabetes mellitus.
Pre-diabetes, type 2 diabetes mellitus and schizophrenia In support of an independent association between schizophrenia and type 2 diabetes mellitus, we have shown that 15.4% of nonobese, drug-naïve, first-episode patients with schizophrenia have impaired fasting glucose as compared to a well-matched group of normal controls, though this is not a universal finding.7 However, the fact that a family study has indicated that up to 19% of firstdegree relatives of patients with schizophrenia have type 2 diabetes mellitus indicates that this endocrine condition and schizophrenia may have a genetic association, an observation echoed in the following quote by Henry Maudsley (1897); ‘Diabetes is a disease which often shows itself in families in which insanity prevails’. Though the definitions of ‘insanity’ and ‘diabetes’ spoken of by Maudsley would not conform to current diagnostic criteria for either schizophrenia or type 2 diabetes mellitus, the quote is a useful reminder that psychiatric disorders were associated with the occurrence of certain physical conditions prior to the introduction of neuroleptics. Utilizing modern diagnostic criteria, the prevalence of type 2 diabetes mellitus appears to lie between 8.8% and 16.0% (using oral glucose tolerance tests) and 15.8% (using 2 separate samples of fasting plasma glucose).8 A consensus statement by the American Diabetic Association noted an increased prevalence of type 2 diabetes mellitus in schizophrenia, but highlighted the potential role of atypical medication in this association. They acknowledged that much of the evidence has come from case reports, observational epidemiology and crosssectional non-randomized studies.9 A recent study has indicated that the annualized incidence rates of diabetes in schizophrenia is 4.4%, which is much higher than the 6.3 per 1000 observed in the general population.10 Furthermore, the investigators calculated the amount of diabetes caused by various atypical antipsychotics, namely the attributable risk, and found that it was 2.03% for clozapine, 0.80% for quetiapine, 0.63% for olanzapine and 0.05% for risperidone. Even though the annual rates of diabetes were high in schizophrenia, they were not primarily associated with atypical medication. Further studies with greater numbers of subjects with first-episode drug-naïve schizophrenia, high-risk subjects, matched controls and patient controls (type 2 diabetics, lean and obese) need to be conducted in order to elucidate whether the phenotypes are similar between the various groups and to determine if similar plasma biomarkers are also shared.
REFERENCES 1 Dixon L, Postrado L, Delahunty J, Fischer P J, Lehman A. The association of medical comorbidity in schizophrenia with poor physical and mental health. J Nerv Ment Dis 1999; 187: 496–502. 2 Lawrence D M, Holman C D J, Jablensky A V, Hobbs M S T. Death rate from ischaemic heart disease in Western Australian psychiatric patients 1980–1998. Br J Psychiatry 2003; 182: 31–6. 3 Alberti K G, Zimmet P Z. Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: Diagnosis and classification of Diabetes Mellitus, provisional report of a WHO commission. Diabetic Med 1998; 15: 539–53. 4 National Cholesterol Education Program. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III), JAMA 2001; 258: 2486–97. 5 Ryan M C M, Flanagan S, Kinsella U, Keeling F, Thakore J H. Atypical antipsychotics and visceral fat distribution in first episode, drugnaive patients with schizophrenia. Life Sci 2004; 74: 1999–2008. 6 Zhang Z J, Yao Z J, Liu W, Fang Q, Reynolds G P. Effects of antipsychotics on fat deposition and changes in leptin and insulin levels: Magnetic resonance imaging study of previously untreated people with schizophrenia. Br J Psychiatry 2004; 184: 58–62. 7 Ryan M C M, Collins P, Thakore J H. Impaired fasting glucose and elevation of cortisol in drug-naive first-episode schizophrenia. Am J Psychiatry 2003; 160: 284–9. 8 Makherjee S, Decina P, Bocola V, Saraceni F, Scapicchio P L. Diabetes mellitus in schizophrenic patients. Compr Psychiatry 1996; 37: 68–73. 9 American Diabetic Association. Consensus Development Conference on Antipsychotic Drugs and Obesity and Diabetes. Diabetes Care 2004; 27: 596–601. 10 Leslie D L, Rosenheck R A. Incidence of newly diagnosed diabetes attributable to atypical antipsychotic medications. Am J Psychiatry 2004; 161: 1709–11.
Screening Screening for the metabolic syndrome in patients with schizophrenia is a must. All first-episode patients must be screened, as they appear to have higher rates of pre-diabetic states and abdominal obesity than would be expected. Patients already on medication should be offered screening annually and sooner if they become symptomatic. The thorny issue of who should screen is ever present. Ideally, GPs should screen for such metabolic disturbances yet our patients with schizophrenia may be reluctant to attend primary care, which may lead to psychiatrists having to perform such tests. What should one measure? The waist-to-hip ratio is an indirect but reliable indicator of central obesity and all that is required is a simple tape measure. In terms of the ratIo, ‘waist’ is taken as the point midway between the iliac crests and the costal margins, whilst ‘hip’ is considered to be across the most rotund portion across the
PSYCHIATRY 4:11
FURTHER READING Brown S. Excess mortality of schizophrenia. A meta-analysis. Br J Psychiatry 1997; 171: 502–8. Kopelman P G. Obesity as a medical problem. Nature 2000; 404: 635–43. Ryan M C M, Thakore J H. Physical consequences of schizophrenia. Life Sci 2002; 71: 239–57. Thakore J H, Mann J N, Vlahoos J, Martin A, Reznek R. Increased visceral fat distribution in drug-naïve and drug-free patients with schizophrenia. Int J Obes Relat Metab Disord 2002; 26: 137–41.
60
© 2005 The Medicine Publishing Company Ltd
Physical health of patients with schizophrenia Jogin H Thakore
General medical comorbidity and schizophrenia The physical health of those with schizophrenia is often poor. Over 50% of those with schizophrenia have a general medical condition. This figure is thought to be an underestimate; it is suggested that the extent and consequences of medical comorbidity in patients with schizophrenia is generally under-recognized. Epidemiological studies have documented higher than expected rates of cardiovascular disease, infectious diseases, type 2 diabetes mellitus, respiratory disease, certain forms of cancer, and a variety of other illnesses in patients with schizophrenia. Though early studies failed to meet methodological standards necessary to provide conclusive evidence, Dixon et al., using rigorous modern criteria, have shown that the prevalence of type 2 diabetes mellitus exceeded those expected in the general population.1 They also showed that the rates of hypertension and heart disease among schizophrenia patients resembled those found in an older cohort in the general population, as measured in the US National Health Interview Survey. In addition to becoming physically sick at younger ages, patients with schizophrenia are rarely treated for their physical illness in the early, less severe phases and appear to present for medical attention only when cardiovascular and pulmonary diseases are severe and potentially life-threatening. This problem is further compounded by reduced detection of comorbid physical illness in schizophrenia by the medical profession despite the fact that medical comorbidity has been linked with more severe psychiatric symptoms. Therefore, it would appear that those with schizophrenia die prematurely and suffer from an excess of cardiovascular illnesses, which they either do not present with or if they do present, tend to go undetected.
Mortality and schizophrenia Nearly two-thirds of those with schizophrenia die of what are euphemistically termed ‘natural causes’ such as cardiovascular disease, diabetes and epilepsy. A number of studies have confirmed the contribution of cardiovascular disease to the increased mortality observed in schizophrenia though these findings are not universally accepted. However, a population-based record linkage study from Western Australia spanning from 1980 to 1998 observed that ischaemic heart disease (IHD) was the major cause of death in the psychiatric patients including schizophrenia.2 Indeed, the rates of death due to IHD remained high in schizophrenia despite a reduction in the general population.
Jogin H Thakore is a Senior Lecturer at the Royal College of Surgeons in Ireland, a lecturer in Psychology at Trinity College, Dublin and a Consultant Psychiatrist at St. Vincent Hospital, Dublin. His research interests include the physical changes in schizophrenia.
PSYCHIATRY 4:11
58
© 2005 The Medicine Publishing Company Ltd
MANAGEMENT ISSUES
Cardiovascular risk factors and schizophrenia
Obesity and schizophrenia
Patients with schizophrenia lead an unhealthy life. For instance, the development of cardiovascular disease is associated with nonmodifiable risk factors (such as age, gender and family history of premature heart disease). Modifiable risk factors include poor diet, physical inactivity, excess alcohol intake, smoking, poverty and various biochemical parameters and physiological events which include obesity, diabetes, insulin resistance, hypertension, platelet abnormalities, dyslipidaemias and hypertriglyceridaemia. Some of these biochemical parameters together form the metabolic syndrome.
There is little doubt that both conventional (older – e.g. haloperidol, zucclopenthixol) and atypical (newer – e.g. olanzapine, risperidone) medications can induce weight gain. However, the potential to do so varies between the different atypical compounds. Large-scale epidemiological studies indicate that there is a clear association between morbid obesity where the body mass index (BMI) is above 40 kg/m2, diabetes and cardiovascular disease. However, the location of the fat is more critical in lesser forms of obesity such as those generally seen in schizophrenia. Significant increases in visceral or intra-abdominal fat (IAF) (Figure 2), termed ‘male obesity’, are linked to the development of dyslipidaemias, atherosclerosis, hypertension and diabetes. Accurate quantification of IAF is possible only at post mortem. However, imaging techniques such as CAT scanning or MRI are suitable alternatives. First-episode, drug-naïve patients with schizophrenia offer a unique opportunity to study the interrelationship between illness and regional fat distribution, without the confounding variable of prior antipsychotic exposure. We have shown, using CT scanning, in two separate studies that such patients have 3–3.4 times as much IAF as matched controls though another study, using MRI, was unable to replicate these findings.5,6 Differences between the three studies may be explained by critical methodological deficits in the paper by Zhang et al. which include a failure to match patients and controls in terms of age, sex, diet, exercise, smoking and alcohol intake and the failure to use radiological determination of the lumbar vertebrae 4/5 junction which is critical if one is using a single CT slice to determine IAF area.6 We have shown that first episode patients with schizophrenia who are psychotropic-naïve have on average normal BMIs, although they have higher levels of visceral fat and are ‘metabolically obese’ as they have high levels of insulin, are insulin resistant, dyslipidaemic and predisposed to type 2 diabetes mellitus. Therefore, the presence of increased visceral obesity would indicate that a critical, potentially pathogenetic component of the metabolic syndrome may be present prior to the development of either diabetes or cardiovascular disease.
Metabolic syndrome and schizophrenia The metabolic syndrome is a cluster of disorders, which include obesity (central – around the abdomen), dyslipidaemias, glucose intolerance, insulin resistance (or hyperinsulinaemia) and hypertension. Its importance lies in the fact that it is highly predictive of type 2 diabetes mellitus and heart disease. Both the World Health Organization and the Third Report of the National Cholesterol Education Program Adult Treatment Panel have provided working criteria for the Metabolic Syndrome in order to improve its detection and thereby rate its prevalence (Figure 1).3,4 The frequency of the metabolic syndrome is 2–4-fold higher in schizophrenia than in an appropriate reference population. Neuroleptics can induce weight gain, with some agents having a greater propensity to do so than others, which may explain why patients with schizophrenia are at a higher risk for developing certain features of the metabolic syndrome.
Diagnostic criteria for the metabolic syndrome WHO criteria 1 or more of the following: • Insulin resistance • Impaired fasting glucose • Impaired glucose tolerance And 2 or more of the following: • WHR > 0.90 (men), 0.85 (women); or BMI ≥ 30kg/m2 • TG ≥ 1.7 mmol/l, or HDL < 0.9 mmol/l (men), 1.0 mmol/l (women) • Blood pressure ≤ 140/90 mm/Hg (or treated hypertension) • Microalbuminuria
A CAT scan showing intra-abdominal fat in an obese patient
National Cholesterol Education Program criteria Any 3 of the following: • Fasting plasma glucose ≥ 6.1 mmol/l • Waist circumference ≥ 102 cm (men), 88cm (women) • TG ≥ 1.7 mmol/l • HDL < 1.0 mmol/l (men), 1.16 mmol/l (women) • BP ≥ 130/85 mm/Hg (or treated hypertension) BMI, body mass index; BP, blood pressure; HDL, high density lipoproteins; TG, triglycerides; WHR, waist-to-hip ratio
White areas are the visceral fat in the abdomen
1
PSYCHIATRY 4:11
2
59
© 2005 The Medicine Publishing Company Ltd
MANAGEMENT ISSUES
buttocks. Screening for diabetes is rather more complicated, in that the gold standard for its diagnosis is the oral glucose tolerance test (OGTT), an impractical procedure for busy clinicians. A fasting or random glucose are alternatives and the latter is preferable, as it requires little effort on behalf of the patient. However, both of these tests are relatively insensitive and the chances of missing genuine abnormalities is large. The glycosylated haemoglobin (HbA1c) is not recommended as a screening test as it lacks sensitivity though is excellent in monitoring glycaemic control following the diagnosis of type 2 diabetes mellitus.
Pre-diabetes, type 2 diabetes mellitus and schizophrenia In support of an independent association between schizophrenia and type 2 diabetes mellitus, we have shown that 15.4% of nonobese, drug-naïve, first-episode patients with schizophrenia have impaired fasting glucose as compared to a well-matched group of normal controls, though this is not a universal finding.7 However, the fact that a family study has indicated that up to 19% of firstdegree relatives of patients with schizophrenia have type 2 diabetes mellitus indicates that this endocrine condition and schizophrenia may have a genetic association, an observation echoed in the following quote by Henry Maudsley (1897); ‘Diabetes is a disease which often shows itself in families in which insanity prevails’. Though the definitions of ‘insanity’ and ‘diabetes’ spoken of by Maudsley would not conform to current diagnostic criteria for either schizophrenia or type 2 diabetes mellitus, the quote is a useful reminder that psychiatric disorders were associated with the occurrence of certain physical conditions prior to the introduction of neuroleptics. Utilizing modern diagnostic criteria, the prevalence of type 2 diabetes mellitus appears to lie between 8.8% and 16.0% (using oral glucose tolerance tests) and 15.8% (using 2 separate samples of fasting plasma glucose).8 A consensus statement by the American Diabetic Association noted an increased prevalence of type 2 diabetes mellitus in schizophrenia, but highlighted the potential role of atypical medication in this association. They acknowledged that much of the evidence has come from case reports, observational epidemiology and crosssectional non-randomized studies.9 A recent study has indicated that the annualized incidence rates of diabetes in schizophrenia is 4.4%, which is much higher than the 6.3 per 1000 observed in the general population.10 Furthermore, the investigators calculated the amount of diabetes caused by various atypical antipsychotics, namely the attributable risk, and found that it was 2.03% for clozapine, 0.80% for quetiapine, 0.63% for olanzapine and 0.05% for risperidone. Even though the annual rates of diabetes were high in schizophrenia, they were not primarily associated with atypical medication. Further studies with greater numbers of subjects with first-episode drug-naïve schizophrenia, high-risk subjects, matched controls and patient controls (type 2 diabetics, lean and obese) need to be conducted in order to elucidate whether the phenotypes are similar between the various groups and to determine if similar plasma biomarkers are also shared.
REFERENCES 1 Dixon L, Postrado L, Delahunty J, Fischer P J, Lehman A. The association of medical comorbidity in schizophrenia with poor physical and mental health. J Nerv Ment Dis 1999; 187: 496–502. 2 Lawrence D M, Holman C D J, Jablensky A V, Hobbs M S T. Death rate from ischaemic heart disease in Western Australian psychiatric patients 1980–1998. Br J Psychiatry 2003; 182: 31–6. 3 Alberti K G, Zimmet P Z. Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: Diagnosis and classification of Diabetes Mellitus, provisional report of a WHO commission. Diabetic Med 1998; 15: 539–53. 4 National Cholesterol Education Program. Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III), JAMA 2001; 258: 2486–97. 5 Ryan M C M, Flanagan S, Kinsella U, Keeling F, Thakore J H. Atypical antipsychotics and visceral fat distribution in first episode, drugnaive patients with schizophrenia. Life Sci 2004; 74: 1999–2008. 6 Zhang Z J, Yao Z J, Liu W, Fang Q, Reynolds G P. Effects of antipsychotics on fat deposition and changes in leptin and insulin levels: Magnetic resonance imaging study of previously untreated people with schizophrenia. Br J Psychiatry 2004; 184: 58–62. 7 Ryan M C M, Collins P, Thakore J H. Impaired fasting glucose and elevation of cortisol in drug-naive first-episode schizophrenia. Am J Psychiatry 2003; 160: 284–9. 8 Makherjee S, Decina P, Bocola V, Saraceni F, Scapicchio P L. Diabetes mellitus in schizophrenic patients. Compr Psychiatry 1996; 37: 68–73. 9 American Diabetic Association. Consensus Development Conference on Antipsychotic Drugs and Obesity and Diabetes. Diabetes Care 2004; 27: 596–601. 10 Leslie D L, Rosenheck R A. Incidence of newly diagnosed diabetes attributable to atypical antipsychotic medications. Am J Psychiatry 2004; 161: 1709–11.
Screening Screening for the metabolic syndrome in patients with schizophrenia is a must. All first-episode patients must be screened, as they appear to have higher rates of pre-diabetic states and abdominal obesity than would be expected. Patients already on medication should be offered screening annually and sooner if they become symptomatic. The thorny issue of who should screen is ever present. Ideally, GPs should screen for such metabolic disturbances yet our patients with schizophrenia may be reluctant to attend primary care, which may lead to psychiatrists having to perform such tests. What should one measure? The waist-to-hip ratio is an indirect but reliable indicator of central obesity and all that is required is a simple tape measure. In terms of the ratIo, ‘waist’ is taken as the point midway between the iliac crests and the costal margins, whilst ‘hip’ is considered to be across the most rotund portion across the
PSYCHIATRY 4:11
FURTHER READING Brown S. Excess mortality of schizophrenia. A meta-analysis. Br J Psychiatry 1997; 171: 502–8. Kopelman P G. Obesity as a medical problem. Nature 2000; 404: 635–43. Ryan M C M, Thakore J H. Physical consequences of schizophrenia. Life Sci 2002; 71: 239–57. Thakore J H, Mann J N, Vlahoos J, Martin A, Reznek R. Increased visceral fat distribution in drug-naïve and drug-free patients with schizophrenia. Int J Obes Relat Metab Disord 2002; 26: 137–41.
60
© 2005 The Medicine Publishing Company Ltd