Physical consequences of schizophrenia and its treatment

Food Intake and Reward Mechanisms in Patients with Schizophrenia: Implications for Metabolic Disturbances and Treatment with Second-Generation Antipsychotic Agents

“…Finally, stress-induced hypercortisolemia contributes to the development of obesity as a result of visceral fat accumulation (Ryan and Thakore, 2002) consequentially to more abundant intra-abdominal adipose tissue's (vs subcutaneous fat mass) concentration of glucocorticoid receptors that activate cortisol-sensitive lipoprotein lipase (Rebuffe-Scrive et al, 1985;Pedersen et al, 1994;FernandezReal et al, 1997), an anabolic enzyme promoting buildup of fat (Bjorntorp, 1996 Figure 3 Schematic overview of the interface between biopsychological factors governing eating behaviors. Appetite, that is, incentive motivational drive to seek and consume food, is derived from interrelated psychobiological factors including food's rewarding properties, individual's homeostatic needs, and cognitive ability to favor alternative (to eating) behaviors (Saper et al, 2002;Hinton et al, 2004;Kelley, 2004b).…”

“…Besides negative psychosocial impacts (distorted selfesteem and societal stigmatization) and medications noncompliance, schizophrenics appear to be particularly susceptible to the detrimental medical sequelae of obesity such as the 'Metabolic Syndrome', which is a cluster of cardiovascular risk factors, including abdominal adiposity, insulin resistance, impaired, glucose tolerance, dyslipidemia, and hypertension (McKee et al, 1986;Mukherjee et al, 1996;Brown et al, 2000;Haupt and Newcomer, 2002;Ryan and Thakore, 2002;Ryan et al, 2003;Holt et al, 2004;Kohen, 2004;Marder et al, 2004;Lieberman et al, 2005).…”

“…Furthermore, stress-related negative affective states drive comfort or palatable food consumption as it can alleviate these states (ie, 'selfmedication') via temporary normalization of reward function (Wang et al, 2001), via inhibition of hypothalamic CRF secretion involved in stress-induced anxiety and depression (Dallman et al, 2003) or via priming effects (Wise, 2004) on the mesocorticolimbic dopaminergic system (Thierry et al, 1976;Imperato et al, 1989). Finally, stress-induced hypercortisolemia contributes to the development of obesity as a result of visceral fat accumulation (Ryan and Thakore, 2002) consequentially to more abundant intra-abdominal adipose tissue's (vs subcutaneous fat mass) concentration of glucocorticoid receptors that activate cortisol-sensitive lipoprotein lipase (Rebuffe-Scrive et al, 1985;Pedersen et al, 1994; FernandezReal et al, 1997), an anabolic enzyme promoting buildup of fat (Bjorntorp, 1996 Figure 3 Schematic overview of the interface between biopsychological factors governing eating behaviors. Appetite, that is, incentive motivational drive to seek and consume food, is derived from interrelated psychobiological factors including food's rewarding properties, individual's homeostatic needs, and cognitive ability to favor alternative (to eating) behaviors (Saper et al, 2002;Hinton et al, 2004;Kelley, 2004b).…”

Abnormal glucose metabolism in patients treated with antipsychotics

“…In addition to diabetes per se, milder glucose dysregulation has been described in numerous patients receiving atypical antipsychotics, such as impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT) assessed during an oral glucose tolerance test (OGTT) [9][10][11]. A higher risk of developing a metabolic syndrome, which includes IFG in its various definitions, has also been stressed in recent studies [12][13][14][15]. Both diabetes and metabolic syndrome may contribute to the higher incidence of cardiovascular disease (CVD) in patients with schizophrenia and schizoaffective disorders.…”

Early treatment-related changes in diabetes and cardiovascular disease risk markers in first episode psychosis subjects

“…Compared to the general population, people with schizophrenia have increased risks of developing cardiovascular disease (CVD) and type 2 diabetes (T2DM) (Brown et al, 2000;Ryan and Thakore, 2002;Susce et al, 2005), and their life expectancy is shorter by 15 years primarily because of coronary heart disease (Hennekens et al, 2005). Two important factors contributing to this increased morbidity and mortality are inherent susceptibility and antipsychotic medication side effects.…”