Cigarette smoking topography in smokers with schizophrenia and matched non-psychiatric controls

Brown University Center for Alcohol and Addiction Studies, Box G-BH, Providence, RI 02912, USA.
Drug and Alcohol Dependence (Impact Factor: 3.42). 12/2005; 80(2):259-65. DOI: 10.1016/j.drugalcdep.2005.04.002
Source: PubMed


Smoking is highly prevalent among people with schizophrenia, and little is known about factors that affect smoking in these patients. One basic question is whether smoking behavior differs for smokers with schizophrenia compared to equally nicotine-dependent smokers who do not have a major mental illness. In this study, 20 smokers with schizophrenia or schizoaffective disorder (SCZ) and 20 non-psychiatric smokers (CON) underwent smoking topography assessments. The groups were matched on age, gender, daily smoking rate, years of regular smoking and nicotine dependence rating. Results indicate that, compared to the CON participants, the SCZ participants smoked significantly more total puffs (SCZ: 58.5 +/- 48.3; CON: 21.3 +/- 9.4) and puffs per cigarette (SCZ: 12.3 +/- 6.0; CON: 8.9 +/- 2.3) and had shorter inter-puff intervals (SCZ: 21.9 +/- 9.7 s; CON: 42.0 +/- 21.5 s), larger total cigarette puff volumes (SCZ: 583 +/- 169 ml; CON: 429 +/- 159 ml) and higher carbon monoxide boosts (SCZ: 3.8+/-5.4 ppm; CON: 1.0 +/- 2.5 ppm). Test-retest reliabilities were good to excellent for most smoking measures in both groups. These findings suggest that smokers with schizophrenia smoke more intensely than matched non-psychiatric smokers and that their smoking behavior is reliable when assessed under laboratory conditions.

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    • "However, as noted previously, only one study of which we are aware has examined the effects of abstinence on smoking-reinforced responding in a psychiatric sample of smokers and reported that even brief abstinence (5–6 h) increased responding for smoking opportunities in adult smokers with schizophrenia (Tidey et al. 1999). Other studies have compared samples of smokers with and without psychiatric disorders and have generally shown that smokers with psychiatric illness (e.g., depression, schizophrenia) smoked more or valued cigarette smoking more than non-psychiatric controls (MacKillop and Tidey 2011; Spring et al. 2003; Tidey et al. 2005, 2008; Weinberger et al. 2007). "
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    ABSTRACT: RATIONALE: Individuals with attention deficit hyperactivity disorder (ADHD) have a more difficult time quitting smoking compared to their non-ADHD peers. Little is known about the underlying behavioral mechanisms associated with this increased risk. OBJECTIVES: This study aims to assess the effects of 24-h smoking abstinence in adult smokers with and without ADHD on the following outcomes: smoking-reinforced responding, withdrawal, and cognitive function. METHODS: Thirty-three (n = 16 with ADHD, 17 without ADHD) adult smokers (more than or equal to ten cigarettes/day) were enrolled. Each participant completed two experimental sessions: one following smoking as usual and one following biochemically verified 24-h smoking abstinence. Smoking-reinforced responding measured via a progressive ratio task, smoking withdrawal measured via questionnaire, and cognition measured via a continuous performance test (CPT) were assessed at each session. RESULTS: Smoking abstinence robustly increased responding for cigarette puffs in both groups, and ADHD smokers responded more for puffs regardless of condition. Males in both groups worked more for cigarette puffs and made more commission errors on the CPT than females, regardless of condition. Smoking abstinence also increased ratings of withdrawal symptoms in both groups and smokers with ADHD, regardless of condition, reported greater symptoms of arousal, habit withdrawal, and somatic complaints. Across groups, smoking abstinence decreased inhibitory control and increased reaction time variability on the CPT. Abstinence-induced changes in inhibitory control and negative affect significantly predicted smoking-reinforced responding across groups. CONCLUSIONS: Smokers with ADHD reported higher levels of withdrawal symptoms and worked more for cigarette puffs, regardless of condition, which could help explain higher levels of nicotine dependence and poorer cessation outcomes in this population. Abstinence-induced changes in smoking-reinforced responding are associated with changes in inhibitory control and negative affect regardless of ADHD status, a finding that may lead to novel prevention and treatment programs.
    Full-text · Article · Dec 2012 · Psychopharmacology
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    • "One such target is the nicotinic acetylcholine (ACh) system. Schizophrenia patients smoke at a remarkably high rate and volume relative to the general population (Tidey et al., 2005; Dome et al., 2010; Williams et al., 2010). Numerous studies confirm that the primary psychoactive chemical in cigarette smoke, nicotine , improves a wide-range of cognitive functions and enhances emotionality and motivation (Stolerman et al., 2000; Adan et al., 2004; Harris et al., 2004; Newhouse et al., 2004; Levin et al., 2006). "
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    ABSTRACT: Schizophrenia is a neurodevelopmental disorder featuring complex aberrations in the structure, wiring, and chemistry of multiple neuronal systems. The abnormal developmental trajectory of the brain appears to be established during gestation, long before clinical symptoms of the disease appear in early adult life. Many genes are associated with schizophrenia, however, altered expression of no one gene has been shown to be present in a majority of schizophrenia patients. How does altered expression of such a variety of genes lead to the complex set of abnormalities observed in the schizophrenic brain? We hypothesize that the protein products of these genes converge on common neurodevelopmental pathways that affect the development of multiple neural circuits and neurotransmitter systems. One such neurodevelopmental pathway is Integrative Nuclear FGFR1 Signaling (INFS). INFS integrates diverse neurogenic signals that direct the postmitotic development of embryonic stem cells, neural progenitors and immature neurons, by direct gene reprogramming. Additionally, FGFR1 and its partner proteins link multiple upstream pathways in which schizophrenia-linked genes are known to function and interact directly with those genes. A th-fgfr1(tk-) transgenic mouse with impaired FGF receptor signaling establishes a number of important characteristics that mimic human schizophrenia - a neurodevelopmental origin, anatomical abnormalities at birth, a delayed onset of behavioral symptoms, deficits across multiple domains of the disorder and symptom improvement with typical and atypical antipsychotics, 5-HT antagonists, and nicotinic receptor agonists. Our research suggests that altered FGF receptor signaling plays a central role in the developmental abnormalities underlying schizophrenia and that nicotinic agonists are an effective class of compounds for the treatment of schizophrenia.
    Full-text · Article · Dec 2012 · Schizophrenia Research
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    • "Individuals with schizophrenia have a high risk for tobacco dependence. Epidemiological studies estimate that as many as 80% of individuals diagnosed with schizophrenia smoke cigarettes and clinical reports indicate that those with schizophrenia are particularly heavy smokers (Hughes et al, 1986; Glassman, 1993; Olincy et al, 1997; Kalman et al, 2005; Tidey et al, 2005; Williams et al, 2005, 2007; McKee et al, 2009). In support of a self-medication hypothesis, some studies have shown that smoking enhances cognition, improves sensory-gating deficits, and relieves side effects of neuroleptic therapeutics (Leonard et al, 1998, 2007; Sacco et al, 2005; Levin and Rezvani, 2007; D'Souza and Markou, 2011). "
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    ABSTRACT: Individuals diagnosed with schizophrenia have an exceptionally high risk for tobacco dependence. Postmortem studies show that these individuals have significant reductions in α7 nicotinic acetylcholine receptors (nAChRs) in several brain areas. Decreased α7-mediated function might not only be linked to schizophrenia but also to increased tobacco consumption. The purpose of this study was to determine whether pharmacological blockade of α7 nAChRs would increase motivation of rats to intravenously self-administer nicotine (NIC) during a progressive ratio schedule of reinforcement (PR). Before PR, rats received local infusions of 0, 10, or 20 pmol of a selective α7 nAChR antagonist, α-conotoxin ArIB [V11L,V16D] (ArIB) into the nucleus accumbens (NAc) shell or the anterior cingulate cortex, brain areas that contribute to motivation for drug reward. We additionally sought to determine whether local infusion of 0, 10, or 40 nmol of a selective α7 nAChR agonist, PNU 282987, into these brain areas would decrease motivation for NIC use. Infusion of ArIB into the NAc shell and anterior cingulate cortex resulted in a significant increase in active lever pressing, breakpoints, and NIC intake, suggesting that a decrease in α7 nAChR function increases motivation to work for NIC. In contrast, PNU 282987 infusion resulted in reductions in these measures when administered into the NAc shell, but had no effect after administration into the anterior cingulate cortex. These data identify reduction of α7 nAChR function as a potential mechanism for elevated tobacco use in schizophrenia and also identify activation of α7 nAChRs as a potential strategy for tobacco cessation therapy.
    Full-text · Article · Dec 2011 · Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology
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