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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence exists to implicate the monoamine histamine in the control of arousal and cognitive functions. Antagonists of H(3) receptors are postsynaptic and presynaptic modulators of neural transmission in a variety of neuronal circuits relevant to cognition. Accumulating neuroanatomical, neurochemical, pharmacological, and behavioral data support the idea that H(3) receptor antagonists may function to improve cognitive performances in disease states (e.g., Alzheimer's disease and mild cognitive impairment states). Thus, H(3) receptor antagonists have been shown to increase performance in attention and memory tests in nonhuman experiments and prevent the degradation in performances produced by scopolamine, MK-801, or age. In contrast, agonists of the H(3) receptor generally produce cognitive impairing effects in animal models. The role of H(3) receptors in these behavioral effects is substantiated by data indicating a central origin for their effects, the selectivity of some of the H(3) receptor antagonists studied, and the pharmacological modification of effects of H(3) receptor antagonists by selective H(3) receptor agonists. Data and issues that challenge the potential role for H(3) receptor antagonists in cognitive processes are also critically reviewed. H(3) receptor antagonists may also have therapeutic value in the management of obesity, pain, sleep disorders, schizophrenia, and attention deficit hyperactivity disorder.
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PMID:Selective histamine H3 receptor antagonists for treatment of cognitive deficiencies and other disorders of the central nervous system. 1525 Dec 26

BACKGROUND: Metabolic syndrome, a constellation of truncal obesity, dyslipidemia, disturbed insulin and glucose metabolism, and hypertension, is associated with the development of diabetes mellitus and coronary heart disease. However, the prevalence of metabolic syndrome in Hispanic patients with schizophrenia and whether they differ from comparable non-Hispanic patients is uncertain. METHOD: This cross-sectional study, conducted from January 2002 to May 2002, included 48 patients with schizophrenia who were recruited from an outpatient psychiatric clinic. Metabolic syndrome was defined using the criteria of the Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. RESULTS: The prevalence of metabolic syndrome was 63% in all patients with schizophrenia. The metabolic syndrome was present in 41% of non-Hispanic patients and in 74% of Hispanic patients with schizophrenia. Metabolic syndrome was present in 70% of Cuban Americans and 88% of other Hispanic subgroups with schizophrenia. Metabolic syndrome was associated with waist circumference (p <.05) and high-density lipoprotein cholesterol (p <.05) in logistic regression analysis. CONCLUSIONS: These data suggest that schizophrenic patients have a 3-fold greater risk to develop metabolic syndrome than the general population. Hispanic schizophrenic patients have a significantly greater prevalence of metabolic syndrome than non-Hispanic schizophrenic patients (p <.05). An increased waist circumference is the strongest clinical correlate with metabolic syndrome in schizophrenic patients.
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PMID:Prevalence of Metabolic Syndrome in Hispanic and Non-Hispanic Patients With Schizophrenia. 1525

Recently there has been increased concern over the side effects of the atypical antipsychotic drugs, including diabetes, hyperlipidemia and obesity. The relationship between diabetes and antipsychotic drugs requires a careful analysis. Patients with schizophrenia are known to suffer from diabetes more often than the general population. In addition, a number of case reports indicate that the conventional antipsychotic as well as atypical antipsychotic drugs produce diabetes. Clozapine and olanzapine, in particular, have been implicated producing diabetes as well as diabetic ketoacidosis. Epidemiological surveys have supplemented the case reports, finding increased incidence of diabetes in patients treated with atypical antipsychotic agents, but these surveys have not yielded consistent results regarding the differential effects of the various atypical antipsychotic drugs. The mechanism by which antipsychotic agents produce diabetes is not elucidated. Weight gain and consequent alteration in triglycerides and cholesterol have been known to occur frequently with olanzapine and clozapine. The ensuing metabolic syndrome itself may cause insulin resistance and diabetes. In the absence of definitive scientific data on the differential effects of antipsychotic drugs in inducing diabetes, clinical prudence and careful monitoring of all patients on atypical antipsychotic drugs is necessary. Aripiprazole and ziprasidone have not been shown to increase weight or produce diabetes, but more information on the diabetogenic effects of ziprasidone and aripiprazole is needed. In order to assess the differential effects of atypical antipsychotic drugs in producing diabetes and the mechanisms by which they produce this reaction, further research is necessary.
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PMID:Side effects of atypical antipsychotic drugs. 1528 97

This investigation estimates and compares, for the first time, the distribution of body mass index (BMI: kg/m(2)) and the prevalence of obesity among Chinese outpatients with schizophrenia treated with antipsychotics. The BMI of 201 outpatients with schizophrenia-spectrum disorders was studied via a cross-sectional naturalistic study. This investigation also compared the BMI of the subjects with a Taiwanese reference population. This investigation found no significant difference in the prevalence of obesity between male and female subjects. The prevalence of obesity among male and female patients in this investigation was, respectively, 2.74- and 2.51-fold greater than the Taiwanese reference population, and the prevalence of severe obesity among male and female patients was 4.66- and 3.53-fold greater than that in the Taiwanese reference population, respectively. The rate of severe obesity was especially high in patients treated with olanzapine. Atypical antipsychotics other than olanzapine did not seem to be more closely associated with obesity or severe obesity compared to typical antipsychotics.
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PMID:Obesity in schizophrenic outpatients receiving antipsychotics in Taiwan. 1529 54

This is a review of the evidence for a link between exposure to second-generation antipsychotic agents and the development of type 2 diabetes mellitus. Most of this evidence comes from case series and retrospective pharmacoepidemiological studies. Exposure to second-generation antipsychotic agents increases the risk for diabetes mellitus compared to no exposure to antipsychotic drugs. The risk with second-generation antipsychotic agents compared to exposure to first-generation antipsychotics is smaller and not consistent. The differential risk among the second-generation antipsychotic agents has not yet been adequately established. Other risk factors for diabetes mellitus, such as advancing age, non-White ethnicity, family history, obesity, lack of physical activity and the diagnosis of schizophrenia, probably contribute more to the risk than exposure to any single antipsychotic drug. Clinicians are urged to manage risk by regularly monitoring all patients receiving second-generation antipsychotic agents for the emergence of diabetes mellitus.
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PMID:The increase in risk of diabetes mellitus from exposure to second-generation antipsychotic agents. 1531 99

There is compelling evidence that patients with schizophrenia are prone to gain weight. In addition, atypical antipsychotic (AAP) drugs also induce weight gain. All antipsychotic drugs produce weight gain but the potential varies. Many studies overwhelmingly confirm that AAP drugs produce substantially more weight gain in comparison to conventional antipsychotic drugs. Clozapine and olanzapine have the most weight inducing potential. Even ziprasidone, which is considered to be weight neutral, and aripiprazole a dopamine modulator produce weight gain in some. The pathophysiology of weight gain is complicated. Many neurohormones, neuropeptides, gut hormones, as well as adipose tissue and hair root derived hormones interact with environmental factors to produce weight gain. Management of weight gain is a difficult problem. Basic to treatment is an understanding of the etiology. Drug induced obesity provides a unique opportunity to psychiatrists to understand this clinically important problem. In the absence of this knowledge, prevention is the best hope. Education, diet control and simple behavioral measures may prevent excessive weight gain. In those with weight gain, treatment can be attempted with pharmacotherapy with careful monitoring of the side effects.
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PMID:Atypical antipsychotic induced weight gain: pathophysiology and management. 1532 1

Atypical antipsychotics are a major advance in the management of schizophrenia. The reevaluation of widely held risk/benefit assessments of the various atypical antipsychotics provides an opportunity to improve treatment patterns. The best available clinical trial evidence indicates that efficacy among the atypical antipsychotics (at equivalent doses) is very similar, but safety and tolerability profiles differ significantly. Atypical antipsychotics differ markedly in their potential to cause metabolic disturbances, including obesity, diabetes, dyslipidemia, and the metabolic syndrome; clozapine and olanzapine carry the greatest risks, atypical antipsychotics like risperidone and quetiapine have lower risks, and newer agents like ziprasidone and aripiprazole are associated with minimal metabolic risks. Results from the Atypical Antipsychotic Therapy and Metabolic Issues (AtAMI) survey define important opportunities for improving medical and psychiatric outcomes during atypical antipsychotic therapy. (See accompanying article by Newcomer et al) Additional educational and research efforts are required to increase understanding of common conditions such as the metabolic syndrome, increase awareness of uncommon but serious events like diabetic ketoacidosis, and pancreatitis, and identify appropriate strategies for monitoring the risks/benefits of atypical antipsychotic therapy. As clinicians refine practice patterns regarding the atypical antipsychotics, they may require additional knowledge and resources to fully incorporate risk/benefit considerations and optimize long-term psychiatric and medical outcomes.
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PMID:Atypical antipsychotics and metabolic dysregulation: evaluating the risk/benefit equation and improving the standard of care. 1535 15

BACKGROUND: Since the introduction of the first atypical antipsychotics in the early 1990s, this class of medication has been increasingly relied upon for the treatment of a variety of patients with psychotic and mood disorders.DATA SOURCES: The following retrospective review was derived from the MEDLINE database using the search terms metabolic syndrome, insulin resistance, obesity, diabetes, severe mental illness, schizophrenia, bipolar disorder, mood disorders, depression, unipolar depression, and prevalence from 1966 to the present. LITERATURE SYNTHESIS: Coincident with the growing usage of these agents, there have been a growing number of literature reports of changes in metabolic homeostasis among patients taking these medications. These changes have led to interest in evaluating whether there is a relationship among these mental illnesses, their psychiatric treatments, and certain physical comorbidities known collectively as the metabolic syndrome. This article reviews the existing literature around the metabolic syndrome in patients with severe mental illnesses. CONCLUSION: Patients with severe mental illnesses, particularly schizophrenia and chronic mood disorders, demonstrate a higher prevalence of metabolic syndrome or its components compared with the general population. Based upon this increased risk in these patients, baseline and periodic medical evaluations should become a standard component in ongoing clinical assessment.
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PMID:The Metabolic Syndrome in Patients With Severe Mental Illnesses. 1536 18

During the last years, a contribution of antipsychotic drugs in the increase of diabetes prevalence in schizophrenic population has been repetitively suggested. The debate focused mainly on the second-generation antipsychotics. The analysis of the scientific literature indicates however that this discussion is not recent and an increase of diabetes prevalence in schizophrenic populations was already described before the introduction of neuroleptics. Then, after the introduction of the first neuroleptics in the 1950s, an increase of diabetes prevalence was reported among treated patients and the same alarms occurred in the 1990s after the introduction of second-generation antipsychotics. These treatments were related to an increase of glucose tolerance impairment, type II diabetes and diabetic acidoketosis. Recent epidemiological studies have confirmed the increase prevalence of diabetes in schizophrenic patients, particularly in schizophrenic patients before any antipsychotic treatment. Among the suggested mechanisms, there are sedentary life (due to hospitalisation and sedative effects of neuroleptics), food imbalance, shared genetic factors for diabetes and schizophrenia. Moreover, the frequency of the metabolic syndrome is increased in schizophrenic populations. This syndrome associates blood glucose increase, lipid metabolism disorders and android obesity. This could explain--via an increase of the cortisol production--the increase of mortality due to cardiovascular diseases observed in schizoprhenic patients. Thus, it seems well established that schizophrenia is associated with an increased risk for diabetes. It is however more difficult to evaluate the role of antipsychotic treatment as a causative factor of diabetes. Indeed, there are many published case reports or diabetes or diabetic acidoketosis after an antipsychotic treatment, but the level of evidence in controlled trials is low. Many studies were performed on large databases, but were retrospective and subjected to many flaws: concomitant diseases not taken into account, diabetes status evaluated by drug consumption, unknown diabetes status before antipsychotic treatment, etc. In the few prospective studies performed, no significant differences between the atypical versus typical antipsychotics were evidenced for new cases of diabetes. Moreover, in general population, the glucose tolerance impairment is underdiagnosed and it is estimated that people with a glucose tolerance impairment have a 5-10% annual risk of type II diabetes. Thus, this concern has to be replaced among the world epidemic increase of diabetes and in a population of patients whose the disease itself and life style are risk factors for diabetes. Some studies have explored the pathophysiological mechanisms that could support a diabetogenic effect of antipsychotics. Although it does not seem to be a direct effect of antipsychotics on insulin secretion by pancreatic cells, body weight increase has been evidence for both typical and atypical antipsychotics. However, it remains unclear whether this weight increase is responsible for a visceral adiposity, which is a risk factor better fitted to the cardiovascular mortality tha the body weight itself. Other hypotheses involving an effect on the leptin, which regulates the appetite, have been proposed. In waiting of new prospective controlled studies, and without denying the impact of antipsychotics on the glucose and lipid metabolisms (on the weight increase, for example), it should be recognized that the benefit/risk ratio remains largely in favour of the treatment, particularly for the atypical antipsychotics, more effective and better tolerated at the neurological level than the conventional antipsychotics. One of the benefits of the mainly articles in professional media about this concern is to draw attention on the metabolism disorders in schizophrenic patients, which are important risk factor of their frequent cardiovascular surmortality whatever the causes. Consequently, it is advised to monitor glucose and lipid metabolisms of schizophrenic patients before and during their treatment (body weight, fast blood glucose, blood cholesterol and triglycerides). In conclusion, schizophrenic patients are a population with an increased metabolic risk, which is a cause of their increased mortality. Although these data are known since a long time ago, this population does not benefit from the same metabolic follow-up than the non-schizophrenic population. The debate on the possible relationship between diabetes and antipsychotics should be also taken as a helpful recall of the necessity to follow simple rules of prevention and monitoring in this at-risk population. This should make it possible to preserve the benefit of the antipsychotics, the contribution of which in the treatment of schizophrenia is not any more to demonstrate.
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PMID:[Schizophrenia, diabetes mellitus and antipsychotics]. 1553 14

Weight loss outcome for 49 obese patients after 6 months treatment in a behavior modification program was related to Rorschach personality characteristics according to the Comprehensive System (Exner, 2003), also including the Rorschach Oral Dependency Scale (Bornstein, 1996; Masling & Rabie, 1967). Less weight loss was predicted by signs of perceptual and cognitive distortions indicated by the Schizophrenia Index. More weight loss was predicted by Food Contents, suggesting a food preoccupation and possibly a benign dependency orientation. Patients with a focus on food and dependent needs could benefit above all from the treatment program implying learning how to handle food and eating in a supportive setting, as evidenced by more weight loss. Distortions in perception and cognition could constitute more profound difficulties in weight reduction important to recognize in obesity treatment.
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PMID:Rorschach personality predictors of weight loss with behavior modification in obesity treatment. 1554 66


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