Schizophrenia, smoking and IQ Flashcards
Smoking and mental illness- self medication?
Leon and Diaz (2005) conducted a meta-analysis of studies comparing smoking in psychiatrically healthy adults vs people with mental illness. Forty-two studies across 20 nations consistently demonstrated an association between schizophrenia and current smoking. This showed that patients are up to five times more likely to smoke and schizophrenic patients are particularly likely to smoke (70 - 88%) compared to patients with other forms of mental disorder (c. 50%) and the general population (c. 25%), they smoke more heavily, extract more nicotine from each cigarette and are less likely to succeed in attempts to quit. This suggests that those with SZ also have risk factors for smoking nicotine.
Why are sz patients more likely to smoke cigarettes
Andrews et al
- Nicotine has stimulant properties which are associated with arousing and alerting effects. Research has shown that smokers report smoking in part to enhance their alertness/cognitive function, and there is evidence that they do perform faster/more efficiently immediately after smoking than when acutely abstinent.
- Andrews et al gave participants the N back task, in which the person maintains a number of steps behind in their head. Participants were given a nicotine nasal spray, gum patch etc. and performance improved significantly from ingestion of the nicotine. Therefore, it is theorised that part of what maintains nicotine addiction is the improved cognitive functioning.
- However, this may reflect their dependence rather than a ‘normal’ benefit of smoking as there is very little evidence that non-smokers show performance improvements when given nicotine via routes such as patch or gum (Kassel, 1997).
Why are sz patients more likely to smoke cigarettes
• Fioravanti et al 2005
• Fioravanti et al 2005 This review identified 1275 studies examining cognitive deficits in people with schizophrenia, published between 1990 and 2003. Data from 113 studies (4365 patients and 3429 controls) were combined in a meta-analysis carried out on the five cognitive domains of IQ, memory, language, executive function, and attention.
Why are sz patients more likely to smoke cigarettes
Kumari and Postma (2005)
• With respect to schizophrenia, nicotine has been reported to reduce impairments in visuospatial working memory (e.g. Sacco et al, 2005), ‘sensory gating’ and smooth pursuit eye movements (Kumari and Postma, 2005) and inhibitory control of anti-saccadic eye movements (Larrison-Faucher et al, 2004).
- With respect to schizophrenia, nicotine has been reported to reduce impairments in visuospatial working memory (e.g. Sacco et al, 2005), ‘sensory gating’ and smooth pursuit eye movements (Kumari and Postma, 2005) and inhibitory control of anti-saccadic eye movements (Larrison-Faucher et al, 2004).
- Kumari and Postma (2005) conclude from a review that these deficits may underlie some Sz symptoms such as hallucinations, delusions, social withdrawal and passivity, and that nicotine may therefore be used to self-medicate:It has been suggested that smoking in schizophrenia may be a form of self-medication in an attempt to treat an underlying biological pathology. Smoking normalizes auditory evoked potential and eye tracking deficits in schizophrenia, as well as improving cognitive function. Nicotine acts through a family of nicotinic receptors with either high or low affinity for nicotine. The loci for several of these receptors have been genetically linked to both smoking and to schizophrenia. Smoking changes gene expression for more than 200 genes in human hippocampus, and differentially normalizes aberrant gene expression in schizophrenia. The α7* nicotinic receptor, linked to schizophrenia and smoking, has been implicated in sensory processing deficits and is important for cognition and protection from neurotoxicity. Nicotine, however, has multiple health risks and desensitizes the receptor. A Phase I trial of DMXB-A, an α7* agonist, shows improvement in both P50 gating and in cognition, suggesting that further development of nicotinic cholinergic drugs is a promising direction in schizophrenia research.
- Nicotine “might help to activate psychomotor processes, such as active coping, improved attention and environmental engagement and emotional responding, that commonly are absent in schizophrenic patients with prominent negative symptoms”. Some of these kinds of improvements are addressed in recent therapies for schizophrenia called cognitive remediation with the idea of training individuals with these disorders in terms of their cognitive skills, evidence has suggested that these kinds of therapies are reasonably affective.
Smoking and mental illness- self medication?
The interaction of schizophrenia and nicotine various dependant on the medication.
George et al, 1985
• The interaction of schizophrenia and nicotine various dependant on the medication. Typical antipsychotics such as haloperidol block DA receptors and when the doses increase, patients electively increase the amount of nicotine they consume (Dawe et al, 1995). Atypical antipsychotics such as clozapine or risperidone do not block DA transmission to the same extent and patients smoke less heavily (e.g. George et al, 1985). Therefore there appears to be a relationship with the side effects/ nature of the antipsychotics used. Nicotine may address some of the aversive side effects that antipsychotic medication have.
Smoking and mental illness- self medication?
Gurpegui et al (2007)
• Gurpegui et al (2007) asked 173 Szs and 100 non- psychiatric smokers about benefits of smoking. Schizophrenics consistently reported more so than the controls to greater levels of calmness, cheerfulness, alertness, concentration and agility. Sociability differed only slightly. Probability of reported calming/ cheerfulness effects related to patients’ levels of depression and anxiety.
In conclusion,
In conclusion, when considering the co-morbidity across conditions, it’s possible that people develop an substance use disorder from self-medication of another condition. This could be self-medication of the symptoms of the disorder or to counteract/medicate the effects of the prescribed medication for the original disorder. There is a possibility that substance use disorders change the brain in important ways that put people at risk for other disorders. Chronic substance use might impair aspects of prefrontal cortex functioning or it may make a person more liable to experience stress and negative emotion and less able to deal with stressful events which may trigger feelings of depression. It may be that a illicit substance use disorder that causes social problems (e.g. law, familial breakdown) could trigger the risk of another disorder (e.g. depression). Therefore, the causal direction may be the other way. Psychosocial problems could be a shared vulnerability issue, in that both disorders are affected by this issue. Factors that contribute to any shared vulnerability and this could be intrapersonal risk factors (genes, personality, brain function, etc) and social/situational risk factors (e.g. family problems, stressors). There is a systematic relationship between the interpersonal factors and the situations that people find themselves in e.g. having a highly impulsive personality may put a person into certain environments that increase risks in other ways. Importantly, all of the issues discussed can be related in many different ways and are probably not a set of single simple relationships.
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Meier, Caspi, Moffit et al, (2012) Persistent cannabis users show neuropsychological decline from childhood to midlife:
Meier, Caspi, Moffit et al, (2012) Persistent cannabis users show neuropsychological decline from childhood to midlife:
Recent reports show that fewer adolescents believe that regular cannabis use is harmful to health. Concomitantly, adolescents are initiating cannabis use at younger ages, and more adolescents are using cannabis on a daily basis. The purpose of the present study was to test the association between persistent cannabis use and neuropsychological decline and determine whether decline is concentrated among adolescent-onset cannabis users. Participants were members of the Dunedin Study, a prospective study of a birth cohort of 1,037 individuals followed from birth (1972/1973) to age 38 y. Cannabis use was ascertained in interviews at ages 18, 21, 26, 32, and 38 y. Neuropsychological testing was conducted at age 13 y, before initiation of cannabis use, and again at age 38 y, after a pattern of persistent cannabis use had developed. Persistent cannabis use was associated with neuropsychological decline broadly across domains of functioning, even after control- ling for years of education. Informants also reported noticing more cognitive problems for persistent cannabis users. Impairment was concentrated among adolescent-onset cannabis users, with more persistent use associated with greater decline. Further, cessation of cannabis use did not fully restore neuropsychological function- ing among adolescent-onset cannabis users. Findings are sugges- tive of a neurotoxic effect of cannabis on the adolescent brain and highlight the importance of prevention and policy efforts targeting adolescents.
