Comorbidity of metabolic syndrome, diabetes and schizophrenia: theoretical and practical considerations

Abstract

Schizophrenia is a psychiatric disorder characterized by heterogeneous symptoms, affecting 0.8-1% of the population worldwide. It usually begins in early adulthood and demonstrates a chronic course. In recent years research interest has turned to the increased burden of somatic illness in schizophrenia, with special emphasis on metabolic syndrome and diabetes. In this article I review the theoretical and practical aspects of the comorbidity of schizophrenia with metabolic syndrome and diabetes mellitus. Epidemiological studies demonstrate the occurrence of metabolic syndrome between 22% and 66%, while the prevalence of diabetes is at least threefold compared to the non-psychiatric population in all age groups. Etiologically it is not clear to what extent these alterations are caused by direct genetic and biological effects in contrast to environmental factors. Among the latter the role of atypical antipsychotics should be emphasized. Clinical management of prediabetic conditions and diabetes in schizophrenia warrants the close cooperation of professionals working in the areas of psychiatry and diabetology. This cooperation should include close metabolic monitoring, lifestyle and dietary training, moreover careful modification and in some cases switching of antipsychotic medication. Persisting metabolic symptoms or diabetes require treatment with oral antidiabetics, fibrates, and statins.

Metabolic syndrome in psychiatrically hospitalized patients treated with antipsychotics and other psychotropics

“…Metabolic syndrome was identified in 29.5% of hospitalized psychiatric patients with previous antipsychotic treatment versus only 7.20% of those without such treatment, and 23.7% among all subjects (Table ). Such rates accord with other recent reports (ADA et al ., ; Ford et al ., ; Athyros et al ., ; Morrato et al ., ; Aekplakorn et al ., ; Falissard et al ., ; Réthelyi and Sawalhe, ; Fernández‐Bergés et al ., ). Several noteworthy factors were associated with metabolic syndrome: (i) longer treatment‐exposure (adjusted for age); (ii) use of clozapine, olanzapine, quetiapine, or older low‐potency neuroleptics; and (iii) polytherapy with ≥2 antipsychotics or one plus other psychotropic agents (Table ).…”

“…Long‐term antipsychotic treatment is associated with increased central adiposity, type 2 diabetes mellitus, dyslipidemia, and hypertension—a combination of abnormalities often referred to as the metabolic syndrome (Bhuvaneswar et al ., ; De Hert et al ., ; Gothefors et al ., ; Kessing et al ., ; Eapen and John, ). Prevalence of metabolic syndrome in the general population is approximately 23% (22–35%; Athyros et al ., ; Aekplakorn et al ., ; Réthelyi and Sawalhe, ; Fernández‐Bergés et al ., ) compared with approximately 37% (22–66%) in patients treated with antipsychotics (ADA et al ., ; Morrato et al ., ; Falissard et al ., ). Despite recent reporting on obesity and metabolic abnormalities in antipsychotic‐treated psychiatric patients, gaps remain in several relevant details, encouraging this review of a large sample of psychiatrically hospitalized patients.…”

The Wnt Signaling Pathway Effector TCF7L2 Mediates Olanzapine-Induced Weight Gain and Insulin Resistance

“…Schizophrenic patients possess an approximately 20% shortened lifespan compared with the general population. One of the main causes of premature mortality is metabolic syndrome (MetS) ( Hennekens et al, 2005 ; Raedler, 2010 ), which is twice higher in schizophrenia patients, featuring insulin resistance, glucose intolerance, dyslipidemia, hypertension, type 2 diabetes mellitus (T2DM), cardiovascular disease, and obesity ( Rethelyi and Sawalhe, 2011 ). Largely due to MetS ( Ryan et al, 2003 ; Mathieu et al, 2009 ; Rheaume et al, 2009 ), the first-episode, drug-naïve patients present impaired glucose tolerance, insulin resistant, higher levels of plasma glucose ( Ryan et al, 2003 ; Spelman et al, 2007 ), and increased visceral fat distribution ( Thakore et al, 2002 ; Ryan et al, 2004 ).…”