Alcohol consumption and smoking status: the role of smoking cessation

Romberger, Debra J.; Grant, Kathleen M.

doi:10.1016/j.biopha.2003.12.002

Cited by 141 publications

(99 citation statements)

References 79 publications

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“…The prevalence of chronic cigarette smoking among individuals afflicted with alcohol use disorders (i.e., alcohol abuse or dependence) is approximately 50−80% (Durazzo et al, in press;Hurt et al, 1994;Pomerleau et al, 1997;Romberger and Grant, 2004). In 1-weekabstinent, treatment-seeking alcoholics, we observed that chronic cigarette smokers exhibited smaller regional gray matter volumes relative to non-smokers, and alcoholics had smaller regional gray matter volumes compared to light drinking controls, irrespective of smoking status (Gazdzinski et al, 2005).…”

Section: Introductionmentioning

confidence: 51%

Non-treatment-seeking heavy drinkers: Effects of chronic cigarette smoking on brain structure

Durazzo

Cardenas

Studholme

et al. 2007

Drug and Alcohol Dependence

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We previously reported [Cardenas, V.A., Studholme, C., Meyerhoff, D.J., Song, E., Weiner, M.W., 2005. Chronic active heavy drinking and family history of problem drinking modulate regional brain tissue volumes. Psychiatry Res. 138, 115−130] that non-treatment-seeking, active heavy drinkers (HD) demonstrated smaller regional neocortical gray matter volumes compared to light drinking controls; however, the potential effects of chronic cigarette smoking on regional brain volumes were not addressed. The goal of this retrospective analysis was to determine if chronic smoking affected brain structure in the non-treatment-seeking heavy drinking sample from our earlier report (i.e., Cardenas et al., 2005). Regional volumetric comparisons were made among age-matched smoking HD (n = 17), non-smoking HD (n = 16), and non-smoking light drinkers (nsLD; n = 20) from our original sample. Quantitative volumetric measures of neocortical gray matter (GM), white matter (WM), subcortical structures, and cerebral spinal fluid (CSF) were derived from high-resolution magnetic resonance imaging. Smoking HD demonstrated smaller volumes than nsLD in the frontal, parietal, temporal GM, and for total neocortical GM. Smoking HD also demonstrated smaller temporal and total GM volumes than non-smoking HD. Non-smoking HD and nsLD did not differ significantly on GM volumes. Further, the three groups did not differ on lobar WM, subcortical structures or regional CSF volumes. These retrospective analyses indicate neocortical GM volume reductions in non-treatment-seeking smoking HD, but not in non-smoking HD, which are consistent with our studies in recently detoxified treatment-seeking alcohol-dependent samples.

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Section: Introductionmentioning

confidence: 51%

Non-treatment-seeking heavy drinkers: Effects of chronic cigarette smoking on brain structure

Durazzo

Cardenas

Studholme

et al. 2007

Drug and Alcohol Dependence

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“…Finally, a fourth factor likely contributing to ALD, which has not yet received due attention, is tobacco smoke exposure. Epidemiological data show that nearly 80% of heavy drinkers with ALD also smoke tobacco [7,8,9,10]. Our interest in analyzing the contributions of tobacco smoke and related toxins to ALD stems from earlier studies showing that limited lowlevel exposures to nitrosamines such as streptozotocin and N-nitrosodiethylamine cause steatohepatitis with hepatic insulin resistance, oxidative and ER stress, and lipid dyshomeostasis [11,12], similar to the effects of alcohol [13,14].…”

Section: Introductionmentioning

confidence: 99%

Differential Lipid Profiles in Experimental Steatohepatitis: Role for Imaging Mass Spectrometry as a Diagnostic Aid

Yalçın¹,

Nunez²,

Cornett³

2015

J Drug Alcohol Res

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Background. Ethanol, tobacco-specific nitrosamine ketone (NNK), and ethanol+NNK exposures cause steatohepatitis, suggesting that smoking can be a cofactor in alcoholic liver disease. Study design. We used MALDI-TOF imaging mass spectrometry (IMS) to characterize hepatic lipid profiles in steatohepatitis caused by ethanol, NNK, and ethanol+NNK. Results. Ethanol, NNK, and ethanol+NNK increased levels and altered the profiles of hepatic phospholipids. Ethanol caused striking accumulations of m/z 932.7 phosphatidylinositol (PI). NNK increased hepatic levels of PIs with m/z's of 934.8, 960.8, and 962.7. Relative abundance of PIs with m/z's of 857.9 or 883.7 increased progressively from control to NNK, then ethanol, and finally ethanol+NNK, indicating differential and additive effects of these exposures. In contrast, no differences occurred with respect to phosphatidylethanolamine (m/z 766.9), phosphatidylserine (m/z 810.9) or PIs with m/z of 960.8 or 962.7. Principal component analysis generated distinct exposure-related hepatic lipid profiles. Conclusion. MALDI-IMS could serve as a complementary diagnostic aid for differentiating underlying causes of steatohepatitis.

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“…Chronic cigarette smoking is a common comorbid condition in alcohol dependence (Romberger and Grant, 2004;Hurt et al, 1994;Pomerleau et al, 1997), illicit substance abuse, schizophrenia-spectrum and mood disorders (Patkar et al, 2006;Dani and Harris, 2005;Esterberg and Compton, 2005;Fergusson et al, 2003). While nicotine may acutely facilitate learning and memory (Levin and Simon, 1998;Newhouse et al, 2004;Sacco et al, 2004), a growing body of evidence suggests chronic cigarette smoking in non-alcoholic individuals adversely affects multiple domains of neurocognition (e.g., Deary et al, 2003;Razani et al, 2004), including learning and memory (Heffernan et al, 2005;Hill et al, 2003;Richards et al, 2003;Schinka et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Chronic cigarette smoking modulates injury and short-term recovery of the medial temporal lobe in alcoholics

Gaździński

Durazzo

Yeh

et al. 2008

Psychiatry Research: Neuroimaging

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Memory function is largely mediated by medial temporal lobe (MTL), and its compromise has been observed in alcohol dependence and chronic cigarette smoking. The effects of heavy alcohol consumption and chronic smoking on hippocampal volumes and MTL metabolites and their recovery during abstinence from alcohol have not been assessed. Male alcoholics in treatment (ALC) [13 smokers (sALC) and 11 non-smokers (nsALC)] underwent quantitative magnetic resonance imaging and short-echo proton magnetic resonance spectroscopic imaging at one week and one month of sobriety. Outcome measures were compared to 14 age-matched, non-smoking light-drinkers and were related to visuospatial learning and memory. Over one month of abstinence, N-acetylaspartate, a neuronal marker, and membrane-associated choline-containing metabolites normalized in the MTL of nsALC, but remained low in the MTL of sALC. Metabolite concentration changes in both groups were associated with improvements in visuospatial memory. Hippocampal volumes increased in both groups during abstinence, but increasing volumes correlated with visuospatial memory improvements only in nsALC. In summary, chronic cigarette smoking in alcohol-dependent men appears to have adverse effects on MTL metabolite recovery during short-term sobriety. These data may also have implications for other conditions with established MTL involvement and significant smoking co-morbidity, such as schizophrenia-spectrum and mood disorders.

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Alcohol consumption and smoking status: the role of smoking cessation

Cited by 141 publications

References 79 publications

Non-treatment-seeking heavy drinkers: Effects of chronic cigarette smoking on brain structure

Non-treatment-seeking heavy drinkers: Effects of chronic cigarette smoking on brain structure

Differential Lipid Profiles in Experimental Steatohepatitis: Role for Imaging Mass Spectrometry as a Diagnostic Aid

Chronic cigarette smoking modulates injury and short-term recovery of the medial temporal lobe in alcoholics

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