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Abstract Antipsychotic drug-induced sexual dysfunction is an important and problematic side effect. We have investigated the effect of chronic antipsychotic treatment on sexual behaviour, sex hormones and genital organ size [...]

Abstract The mechanisms underlying weight gain resulting from antipsychotic drugs are not fully understood, although antagonism of the 5-H[T.sub.2C] receptor is likely to contribute. Animal studies indicate that the drugs [...]

Abstract Many atypical antipsychotic drugs, such as clozapine, can induce significant weight gain which can have serious implications for drug compliance and morbidity. Food intake and weight gain are regulated [...]

Abstract The use of antipsychotic drugs is known to be associated with a number of adverse metabolic side effects, including diabetes mellitus. These side effects could be, at least in [...]

Dopamine in the pathophysiology and treatment of schizophrenia--new findings By Shitij Kapur, Yves Lecrubier, Martin Dunitz, October 2003, 259pp, ISBN 1841843040. Price 32.95 £ The dopamine hypothesis of schizophrenia refuses [...]

Methamphetamine (METH) is an addictive psychostimulant drug commonly leading to schizophrenia-like psychotic symptoms. Disturbances in glutamatergic neurotransmission have been proposed as neurobiological mechanisms and the α-amino-3 hydroxy-5 methyl-4 isoxazole propionic acid (AMPA) glutamate receptor has been implicated in these processes. Moreover, genetic variants in GRIAs, genes encoding AMPA receptor subunits, have been observed in association with both drug dependence and psychosis. We hypothesized that variation of GRIA genes may be associated with METH dependence and METH-induced psychosis. Genotyping of GRIA1 rs1428920, GRIA2 rs3813296, GRIA3 rs3761554, rs502434 and rs989638 was performed in 102 male Thai controls and 100 METH-dependent subjects (53 with METH-dependent psychosis). We observed no evidence of association with METH dependence and METH-dependent psychosis in the GRIA1 and GRIA2 polymorphisms, nor with single polymorphisms rs3761554 and rs989638 in GRIA3. An association of GRIA3 rs502434 was identified with both METH dependence and METH-dependent psychosis, although this did not withstand correction for multiple testing. Combining the analysis of this site with the previously-demonstrated association with BDNF rs6265 resulted in a highly significant effect. These preliminary findings indicate that genetic variability in GRIA3 may interact with a functional BDNF polymorphism to provide a strong risk factor for the development of METH dependence in the Thai population. [ABSTRACT FROM AUTHOR]

There are two issues at the forefront of both clinical concern and research approaches in the treatment of schizophrenia. One reflects a major inadequacy of antipsychotic drugs, namely their lack [...]

Excess deaths from cardiovascular disease are a major contributor to the significant reduction in life expectancy experienced by people with schizophrenia. Important risk factors in this are smoking, alcohol misuse, excessive weight gain and diabetes. Weight gain also reinforces service users' negative views of themselves and is a factor in poor adherence with treatment. Monitoring of relevant physical health risk factors is frequently inadequate, as is provision of interventions to modify these. These guidelines review issues surrounding monitoring of physical health risk factors and make recommendations about an appropriate approach. Overweight and obesity, partly driven by antipsychotic drug treatment, are important factors contributing to the development of diabetes and cardiovascular disease in people with schizophrenia. There have been clinical trials of many interventions for people experiencing weight gain when taking antipsychotic medications but there is a lack of clear consensus regarding which may be appropriate in usual clinical practice. These guidelines review these trials and make recommendations regarding appropriate interventions. Interventions for smoking and alcohol misuse are reviewed, but more briefly as these are similar to those recommended for the general population. The management of impaired fasting glycaemia and impaired glucose tolerance ('pre-diabetes'), diabetes and other cardiovascular risks, such as dyslipidaemia, are also reviewed with respect to other currently available guidelines.These guidelines were compiled following a consensus meeting of experts involved in various aspects of these problems. They reviewed key areas of evidence and their clinical implications. Wider issues relating to primary care/secondary care interfaces are discussed but cannot be resolved within guidelines such as these. [ABSTRACT FROM AUTHOR]

Variation in genes implicated in serotonin neurotransmission may interact with environmental factors to influence antidepressant response. We aimed to determine how a range of polymorphisms in serotonergic genes determine this response to treatment and how they interact with childhood trauma and recent life stress in a Chinese sample. In total, 14 single nucleotide polymorphisms (SNPs) in coding regions of 10 serotonergic genes (HTR1A, HTR1B, HTR1D, HTR2A, HTR3A, HTR3C, HTR3D, HTR3E, HTR5A and TPH2) were genotyped in 308 Chinese Han patients with major depressive disorder. Response to 6 weeks’ antidepressant treatment was determined by change in the 17-item Hamilton Depression Rating Scale (HDRS-17) score, and previous stressful events were evaluated by the Life Events Scale (LES) and Childhood Trauma Questionnaire-Short Form (CTQ-SF). Two 5-HT1B receptor SNPs (rs6296 and rs6298) and one tryptophan hydroxylase2 (rs7305115) SNP were significantly associated with antidepressant response in this Chinese sample, as was a haplotype in TPH2 (rs7305115 and rs4290270). A gene–gene interaction on antidepressant response was found between SNPs in HTR1B, HTR3A and HTR5A in female subjects. The HTR1B SNPs demonstrated interaction with recent stress, while that for TPH2 interacted with childhood trauma to influence antidepressant response. [ABSTRACT FROM PUBLISHER]

Antipsychotic drug-induced sexual dysfunction is an important and problematic side effect. We have investigated the effect of chronic antipsychotic treatment on sexual behaviour, sex hormones and genital organ size in the male rat. The following sexual functions were significantly impaired in both risperidone (2 mg/kg) and haloperidol (2 mg/kg) groups at 3 weeks: Libido (assessed in mounting frequency and intromission), sexual arousability/motivation (in terms of latencies for mounting and intromission) and orgasm (in terms of latency for ejaculation). At 6 weeks, haloperidol also suppressed the 'hit ratio' (intromissions/mounts) as well as the above-mentioned parameters indicating erectile dysfunction. Risperidone had no significant effect on sexual function at 6 weeks. Compared with the control group, haloperidol and risperidone decreased the serum level of testosterone after 6 weeks but not after 3 weeks. The two drugs did not influence the serum level of leutenizing hormone (LH). At 3 weeks, the epididymis was significantly decreased below controls in both risperidone and haloperidol groups. At 6 weeks, the epididymis, seminar vesicle and prostate weights were significantly reduced in the haloperidol group, but not in the risperidone group. The serum concentration of testosterone significantly correlated with sex organ weight, but not with sexual behaviours. These results suggest that sexual function, testosterone revels and genital tissue size in male rats were affected to different degrees by risperidone and haloperidol. These findings contribute to our understanding of antispsychotic drug-induced male sexual dysfunction. [ABSTRACT FROM AUTHOR]