Enhanced Sensitivity to the Euphoric Effects of Alcohol in Schizophrenia
ABSTRACT The purpose of this study was to determine whether schizophrenia was associated with alterations in alcohol response that might explain the elevated risk for AUDs in this population. In a randomized, double-blind, placebo-controlled, counter-balanced 3 test day laboratory study, the effects of alcohol were compared in 23 subjects with schizophrenia (without any previous alcohol use disorder (AUD) but with some alcohol exposure) and in 14 healthy subjects matched for age, gender, education, and lifetime exposure to alcohol. Standard alcohol drinks in a scheduled design were administered to produce blood alcohol levels of 0, 0.02-0.04 mg%, or 0.06-0.08 mg%. Schizophrenia symptoms, perceptual alterations, stimulant and depressant subjective effects of alcohol, and 'high' were measured before alcohol administration and at several post-drug time points. Verbal learning and recall, vigilance and distractibility, and motor function were assessed once per test day. Relative to healthy subjects, subjects with schizophrenia reported greater euphoria and stimulatory effects in response to alcohol. Alcohol produced small transient increases in positive psychotic symptoms and perceptual alterations without affecting negative symptoms. Alcohol also impaired several aspects of immediate and delayed recall, and vigilance, and distractibility. Schizophrenia patients showed increased euphoric and stimulatory responses to alcohol. These exaggerated positive responses to alcohol doses may contribute to the increased risk for AUDs associated with schizophrenia. The absence of 'beneficial' effects of alcohol does not support a self-medication hypothesis of alcohol use in schizophrenia.
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ABSTRACT: Background and aimsAlcohol use disorders are common among people with psychosis and are associated with poorer prognoses. In psychosis patients, there are inconsistent findings regarding the link between alcohol disorders and clinical symptomatic outcomes. This study examined the relationships between alcohol consumption and specific clinical outcomes, including affective symptoms, in psychosis.Methods Participants were recruited from secondary care services in the UK. Two hundred and ten participants whose substance use met inclusion for an alcohol disorder were compared with other substance users (n=117) on baseline demographic, clinical, and substance use variables. The alcohol sub-group was assessed at three time points, with repeated measures of psychopathology and alcohol use over a 2 year period. Generalised Estimating Equations (GEE) models were used to examine whether change in alcohol use was associated with change in clinical outcomes. We controlled for a wide range of potential confounds, including other substance use.ResultsA small but specific effect was evident for change in the quantity of alcohol consumed on change in depression (adjusted coefficient for 10 total units over 90 days: 0.0015, p=0.047). Alcohol consumption was not associated with subsequent severity of psychotic symptoms (adjusted coefficient for Positive and Negative Syndrome Scale general for 10 average daily units 0.2492, p=0.420) or severity of anxiety symptoms (adjusted coefficient for 10 average daily units 0.0534, p=0.473).Conclusions For people with psychosis, the most detrimental effect of alcohol consumption appears to be its effect on mood. Some of this effect seems to be reversible, with drinking reduction associated with subsequent mood improvement.Addiction 04/2014; 109(8). DOI:10.1111/add.12599 · 4.60 Impact Factor
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ABSTRACT: Background: Alcohol dependence is one of the leading contributors to the burden of disease in the world. A range of genetic and environmental risk factors has been identified to date, and preclinical and clinical studies including imaging studies have identified neuronal networks involved in the development of alcohol dependence. Methods: We review genetic and environmental risk factors for the development of alcohol addiction as well as structural and neuronal changes, including their transmitter systems, due to regular alcohol intake. Results: Stress as well as family background and, in juveniles, the peer group could be identified as environmental risk factors for alcohol dependence. Heritability is estimated at around 50%, and it seems to be comparable in women and men. There is ongoing research on a broad range of putative endophenotypes such as tolerance of the effects of alcohol intake or personal traits like 'impulsivity'. On the neurobiological level, chronic alcohol intake seems to render mesolimbic circuits hypersensitive to alcohol and alter the motivational reward system including dopaminergic neurotransmission. Conclusion: Environmental and genetic risk factors, and especially their interaction, facilitate the development of alcohol dependence. Ongoing alcohol intake results in profound alterations of neuronal systems crucial for motivation, learning, memory and cognition control. Future studies should further combine the knowledge of neurobiological mechanisms and risk factors to develop new prevention strategies. (C) 2014 S. Karger AG, BaselNeuropsychobiology 01/2014; 70(2):67-76. DOI:10.1159/000364825 · 2.30 Impact Factor