Alcohol, Cannabis, Nicotine, and Caffeine Use and Symptom Distress in Schizophrenia

Department of Social Sciences, University of Maryland Eastern Shore, Maryland, United States
Journal of Nervous & Mental Disease (Impact Factor: 1.69). 10/1995; 183(9):559-65. DOI: 10.1097/00005053-199509000-00001
Source: PubMed


The high prevalence of substance use, e.g., alcohol and illegal and nonprescribed drugs, in schizophrenia is widely recognized. One explanation for this high prevalence is that substance use may be a self-initiated method for managing symptoms. To test whether the intake of four substances--alcohol, cannabis, nicotine, and caffeine--would increase with increases in symptom distress, daily self-reports of symptom distress and substance intake over 12 weeks were analyzed with pooled time series analyses. Compliance with neuroleptic medication was added to the analyses to control for any changes in prescribed medication compliance while using nonprescribed drugs or alcohol. Of the four substances studied, only nicotine was significantly related to symptom distress. Higher distress with prodromal symptoms was related to decreases in nicotine use. Analysis of caffeine did not meet the criteria for significance but does provide direction for further research. Higher distress, with neurotic symptoms, was related to increases in caffeine use. Further research is needed to clarify the relationship between nicotine and symptoms.

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    • "Schizophrenia patients who smoke have higher blood levels of cotinine than smokers without psychiatric comorbidity, indicating a higher level of consumption or deeper inhalation [213]. The number of cigarettes consumed daily in this patient group correlates positively with the dose of neuroleptic drugs [104] [154] and also with the occurrence of prodromal symptoms of schizophrenia [48] [116]. People with schizophrenia who had lower functioning were also found to smoke more cigarettes per day [171]. "
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    ABSTRACT: Tobacco dependence is the most common substance use disorder in adults with mental illness. The prevalence rates for tobacco dependence are two to four times higher in these patients than in the general population. Smoking has a strong, negative influence on the life expectancy and quality of life of mental health patients, and remains the leading preventable cause of death in this group. Despite these statistics, in some countries smokers with mental illness are disadvantaged in receiving intervention and support for their tobacco dependence, which is often overlooked or even tolerated. This statement from the European Psychiatric Association (EPA) systematically reviews the current evidence on tobacco dependence and withdrawal in patients with mental illness and their treatment. It provides seven recommendations for the core components of diagnostics and treatment in this patient group. These recommendations concern: (1) the recording process, (2) the timing of the intervention, (3) counselling specificities, (4) proposed treatments, (5) frequency of contact after stopping, (6) follow-up visits and (7) relapse prevention. They aim to help clinicians improve the care, health and well-being of patients suffering from mental illness.
    European Psychiatry 01/2014; 29(2). DOI:10.1016/j.eurpsy.2013.11.002 · 3.44 Impact Factor
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    • "Neurotransmitter pathways in schizophrenia Hamera et al. 1995). a7 subunit mRNA and protein levels are lower in schizophrenic nonsmokers compared to control nonsmokers and are brought to control levels in schizophrenic smokers (Mexal et al. 2010). "
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    ABSTRACT: Schizophrenia alters basic brain processes of perception, emotion, and judgment to cause hallucinations, delusions, thought disorder, and cognitive deficits. Unlike neurodegeneration diseases that have irreversible neuronal degeneration and death, schizophrenia lacks agreeable pathological hallmarks, which makes it one of the least understood psychiatric disorders. With identification of schizophrenia susceptibility genes, recent studies have begun to shed light on underlying pathological mechanisms. Schizophrenia is believed to result from problems during neural development that lead to improper function of synaptic transmission and plasticity, and in agreement, many of the susceptibility genes encode proteins critical for neural development. Some, however, are also expressed at high levels in adult brain. Here, we will review evidence for altered neurotransmission at glutamatergic, GABAergic, dopaminergic, and cholinergic synapses in schizophrenia and discuss roles of susceptibility genes in neural development as well as in synaptic plasticity and how their malfunction may contribute to pathogenic mechanisms of schizophrenia. We propose that mouse models with precise temporal and spatial control of mutation or overexpression would be useful to delineate schizophrenia pathogenic mechanisms.
    Advances in Experimental Medicine and Biology 01/2012; 970:493-516. DOI:10.1007/978-3-7091-0932-8_22 · 1.96 Impact Factor
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    • "Psychotic disorders involve disturbances in the dopamine neurotransmitter systems since drugs that increase dopamine release produce psychotic symptoms when given in large doses, and neuroleptic drugs that reduce psychotic symptoms also reduce dopamine levels [93]. Cannabinoids, such as THC, increase dopamine release [92]. "
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    ABSTRACT: This paper reviews evidence on two hypotheses about the relationship between cannabis use and psychosis. The first hypothesis is that heavy cannabis use may cause a cannabis psychosis-a psychosis that would not occur in the absence of cannabis use, the symptoms of which are preceded by heavy cannabis use and remit after abstinence. The second hypothesis is that cannabis use may precipitate schizophrenia, or exacerbate its symptoms. Evaluation of these hypotheses requires evidence of an association between cannabis use and psychosis, that is unlikely to be due to chance, in which cannabis use precedes psychosis, and in which we can exclude the hypothesis that the relationship is due to other factors, such as other drug use, or a personal vulnerability to psychosis. There is some clinical support for the first hypothesis. If these disorders exist they seem to be rare, because they require very high doses of THC, the prolonged use of highly potent forms of cannabis, or a pre-existing (but as yet unspecified) vulnerability. There is more support for the second hypothesis, in that a large prospective study has shown a linear relationship between the frequency with which cannabis has been used by age 18 and the risks over the subsequent 15 years of a diagnosis of schizophrenia. It is still unclear whether this means that cannabis use precipitates schizophrenia, whether it is a form of self-medication, or whether the association is due to the use of other drugs, such as amphetamines, which heavy cannabis users are more Likely to use. There is stronger evidence that cannabis use can exacerbate the symptoms of schizophrenia. Mental health services should identify patients with schizophrenia who use alcohol, cannabis and other drugs and advise them to abstain or to greatly reduce their drug use.
    Drug and Alcohol Review 01/2009; 17(4). DOI:10.1080/09595239800187271 · 1.55 Impact Factor
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