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Nicotine intake and smoking topography in smokers with bipolar disorder
Author(s) -
Williams Jill M,
Gandhi Kunal K,
Lu ShouEn,
Steinberg Marc L,
Benowitz Neal L
Publication year - 2012
Publication title -
bipolar disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.285
H-Index - 129
eISSN - 1399-5618
pISSN - 1398-5647
DOI - 10.1111/j.1399-5618.2012.01047.x
Subject(s) - topiramate , carbamazepine , nicotine , oxcarbazepine , cotinine , lamotrigine , bipolar disorder , cyp2a6 , medicine , smoking cessation , mood , psychology , metabolite , psychiatry , endocrinology , cytochrome p450 , cyp3a4 , epilepsy , metabolism , pathology
Williams JM, Gandhi KK, Lu S‐E, Steinberg ML, Benowitz NL. Nicotine intake and smoking topography in smokers with bipolar disorder. Bipolar Disord 2012: 14: 618–627. © 2012 The Authors. Journal compilation © 2012 John Wiley & Sons A/S. Objectives: Cigarette smoking behavior in bipolar disorder (BPD), including the effects of mood‐stabilizing medications, has not been well characterized. Methods: We compared serum nicotine, nicotine metabolite levels, and smoking topography in 75 smokers with BPD to 86 control smokers (CON). For some comparisons, an additional control group of 75 smokers with schizophrenia (SCZ) were included. Results: There were no differences between the BPD and CON groups in baseline smoking characteristics or serum nicotine or cotinine levels. Fifty‐one smokers with BPD (68.9%) were taking one of the following mood stabilizers: valproic acid, lamotrigine, carbamazepine, oxcarbazepine, lithium, or topiramate. The 3‐hydroxycotinine‐to‐cotinine ratio, a marker of cytochrome P450 2A6 (CYP2A6) metabolic activity, was significantly higher in BPD versus CON and versus SCZ (0.68 versus 0.49 versus 0.54; p = 0.002). The difference between groups, however, was no longer significant when the analysis was repeated with those taking hepatic enzyme‐inducing drugs (carbamazepine, oxcarbazepine, and topiramate) included as a covariate. The time between puffs, or interpuff interval (IPI), was shorter in BPD versus CON by an average of 3.0 sec (p < 0.05), although this was no longer significant when we removed smokers from the analysis of those taking hepatic enzyme inducers. Conclusions: Smokers with BPD are not different from CON on most measures of nicotine intake and smoking topography. We found an increased rate of nicotine metabolism in smokers taking mood stabilizers that are hepatic enzyme inducers, including carbamazepine, oxcarbazepine, and topiramate. Smokers with rapid nicotine metabolism might be expected to smoke more intensely to compensate for the more rapid disappearance of nicotine from the blood and brain, and may have more difficulty in quitting smoking, although this requires further study.