Neural substrates of alcohol-induced smoking urge in heavy drinking nondaily smokers.
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SUBMITTER: King A
PROVIDER: S-EPMC2868310 | biostudies-other | 2010 Feb
REPOSITORIES: biostudies-other
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Project description:RationaleEmerging evidence suggests that the ?4?2 form of the nicotinic acetylcholine receptor (nAChR) modulates the rewarding effects of alcohol. The nAChR ?4?2 subunit partial agonist varenicline (Chantix™), which is approved by the Food and Drug Administration for smoking cessation, also decreases ethanol consumption in rodents (Steensland et al., Proc Natl Acad Sci U S A 104:12518-12523, 2007) and in human laboratory and open-label studies (Fucito et al., Psychopharmacology (Berl) 215:655-663, 2011; McKee et al., Biol Psychiatry 66:185-190 2009).ObjectivesWe present a randomized, double-blind, 16-week study in heavy-drinking smokers (n?=?64 randomized to treatment) who were seeking treatment for their smoking. The study was designed to determine the effects of varenicline on alcohol craving and consumption. Outcome measures included number of alcoholic drinks per week, cigarettes per week, amount of alcohol craving per week, cumulative cigarettes and alcoholic drinks consumed during the treatment period, number of abstinent days, and weekly percentage of positive ethyl glucuronide and cotinine screens.ResultsVarenicline significantly decreases alcohol consumption (? (2)?=?35.32, p?<?0.0001) in smokers. Although varenicline has previously been associated with suicidality and depression, side effects were low in this study and declined over time in the varenicline treatment group.ConclusionsVarenicline can produce a sustained decrease in alcohol consumption in individuals who also smoke. Further studies are warranted to assess varenicline efficacy in treatment-seeking alcohol abusers who do not smoke and to ascertain the relationship between varenicline effects on smoking and drinking.
| S-EPMC3438402 | biostudies-literature
Project description:BackgroundThere is a strong bidirectional relationship between the use of alcohol and cigarettes which results in various challenges for treating those who co-use both substances. While varenicline and naltrexone each have FDA-approval for nicotine and alcohol use disorder, respectively, there is evidence that their clinical benefit may extend across the two disorders. Critically, the effect of combined varenicline and naltrexone on neural reactivity to alcohol cues among heavy drinking smokers has not yet been studied. Probing the effect of the combination therapy on alcohol cue-reactivity may give insight to the mechanisms underlying its efficacy.MethodsForty-seven heavy drinking smokers enrolled in two medication studies were randomized to receive varenicline alone (n = 11), varenicline plus naltrexone (n = 11), or placebo (n = 25). Participants completed an fMRI alcohol cue-reactivity task and rated their in-scanner alcohol craving. Whole-brain analyses examined the effect of medication on alcohol cue-elicited neural response.ResultsVarenicline plus naltrexone attenuated alcohol cue-elicited activation in mesolimbic regions relative to varenicline alone and to placebo (Z > 2.3, p < 0.05). The combination varenicline and naltrexone group also endorsed lower in-scanner alcohol craving relative to varenicline alone group (p = 0.04).ConclusionsThese findings provide evidence for the benefit of combined therapy of varenicline and naltrexone over varenicline alone for the attenuation of alcohol cue-elicited neural activation. This study provides a preliminary proof-of-mechanism for this combination pharmacotherapy and suggests that naltrexone may be driving the reductions in cue-elicited alcohol craving in the brain. Further clinical studies using the combined therapy to treat heavy drinking smokers are warranted.
| S-EPMC9059649 | biostudies-literature
Project description:According to evidence from developed countries, age at first alcohol use has been identified as a determinant of heavy episodic drinking (HED). This study aimed to investigate the association between age at first alcohol use and HED using data from the Smoking and Drinking Behavior Survey 2017, a Thai nationally representative survey. Binary logistic regression was used to examine the association. This study used data from 23,073 current drinkers in the survey. The survey participants were chosen to represent the Thai population aged 15 years and older. The prevalence of HED and frequent HED among Thai drinkers was 18.6% and 10.1%, respectively. Age at first drinking <20 years was associated with higher odds of HED (adjusted OR, 1.43; 95% CI, 1.26-1.62) and frequent HED (adjusted OR, 1.31; 95% CI, 1.12-1.53) relative to age at first drinking ≥25 years. Regular drinking, drinking at home, and exposure to alcohol advertising increased the odds of HED. Drinking at home was associated with frequent HED. There was a significant interaction between the effect of age at first alcohol use and sex on HED and frequent HED with a stronger effect of age at first alcohol use observed in females. This study provides evidence from a developing country that early onset of alcohol use is associated with HED. Effective measures such as tax and pricing policy should be enforced to delay the onset of drinking.
| S-EPMC8575245 | biostudies-literature
Project description:IntroductionDespite the strong relationship between smoking and health-related consequences, very few smokers quit. Heavy drinking is a significant risk factor for health consequences, and is implicated in persistent smoking and less success at quitting smoking. Self-efficacy (SE) to abstain from smoking is an important determinant of smoking outcomes and may link alcohol use to poor quit rates. Even though research has demonstrated a strong association between drinking and smoking, and the multiplicative effect of these substances on cancer-related, heavy-drinking smokers has been largely ignored in the literature. Further, research has not taken advantage of innovative methods, such as ecological momentary assessment, to capture the impact of daily factors on smoking cessation outcomes in this particular group. The proposed study identifies daily changing factors that impede or promote SE and future smoking cessation efforts in risky-drinking smokers.Methods and analysisThis is an observational study of 84 regular smokers (≥10 cigarettes per day) who drink at risky levels, report a desire to quit in the next 6 months, and show no evidence of psychiatric disturbance, severe history of alcohol withdrawal or drug dependence (excluding nicotine and caffeine). Participants report on their smoking, alcohol consumption and SE related to smoking twice a day for 28 days using interactive voice response (IVR) surveys. Multilevel regression and path models will examine within-person daily associations among drinking, smoking and SE, and how these variables predict the likelihood of future smoking behaviour at 1 and 6 months follow-up.Ethics and disseminationThis protocol was approved by an accredited Institutional Review Board. The findings will help us understand the factors that promote or impede smoking cessation among a high-risk group of smokers (heavy-drinking smokers) and will be disseminated through peer-reviewed journal articles and presentations at national conferences.
| S-EPMC4289730 | biostudies-literature
Project description:Post hoc analyses of 2 randomized controlled trials suggest naltrexone may reduce alcohol use and improve smoking cessation outcomes among heavy drinkers receiving smoking cessation treatment. However, no studies have been conducted specifically to examine naltrexone for this purpose or to test whether naltrexone has benefit when added to smoking cessation counseling that explicitly addresses heavy drinking.We recruited heavy-drinking smokers from the community and randomized them to receive 10 weeks of either (i) 50 mg naltrexone (n = 75) or (ii) placebo (n = 75) daily. Participants received 6 weeks of transdermal nicotine patch and 6 sessions of counseling that addressed both heavy drinking and smoking. Participants were followed for 26 weeks after their target quit smoking date.Across medication conditions, there were substantial reductions at follow-up in percent heavy drinking days (primary outcome) and average drinks per week (secondary outcome). However, participants receiving naltrexone did not differ significantly from those receiving placebo on percent heavy drinking days (effect size d = -0.04, 95% CI [-0.30, 0.22], p = 0.76) or average drinks per week (d = -0.09, 95% CI [-0.35, 0.18], p = 0.54) during follow-up. Naltrexone compared to placebo was not associated with a significant increase in smoking abstinence rates during follow-up, odds ratio = 0.93, 95% CI [0.46, 1.86], p = 0.83. The effect of naltrexone on these outcomes was not significantly moderated by current alcohol dependence or gender.Results indicate that heavy-drinking smokers, including those with current alcohol dependence, can make substantial reductions in drinking in the context of smoking cessation treatment. However, this study provided no evidence that naltrexone is efficacious for enhancing reductions in drinking or improving smoking cessation in this population. Limitations of this study included lower-than-desired sample size and modest adherence to study medication.
| S-EPMC5485847 | biostudies-literature
Project description:IntroductionPrevious studies have highlighted a strong bidirectional relationship between cigarette and alcohol consumption. To advance our understanding of this relationship the present study uses a behavioral economic approach in a community sample (N = 383) of nontreatment seeking heavy drinking smokers.Aims and methodsThe aims were to examine same-substance and cross-substance relationships between alcohol and cigarette use, and latent factors of demand. A community sample of nontreatment seeking heavy drinking smokers completed an in-person assessment battery including measures of alcohol and tobacco use as well as the Cigarette Purchase Task and the Alcohol Purchase Task. Latent factors of demand were derived from these hypothetical purchase tasks.ResultsResults revealed a positive correlation between paired alcohol and cigarette demand indices (eg, correlation between alcohol intensity and cigarette intensity) (rs = 0.18-0.46, p ≤ .003). Over and above alcohol factors, cigarette use variables (eg, Fagerström Test for Nicotine Dependence and cigarettes per smoking day) significantly predicted an additional 4.5% (p < .01) of the variance in Persistence values but not Amplitude values for alcohol. Over and above cigarette factors, alcohol use variables predicted cigarette Persistence values (ΔR2 = .013, p = .05), however, did not predict Amplitude values.ConclusionsThese results advance our understanding of the overlap between cigarette and alcohol by demonstrating that involvement with one substance was associated with demand for the other substance. This asymmetric profile-from smoking to alcohol demand, but not vice versa-suggests that it is not simply tapping into a generally higher reward sensitivity and warrants further investigation.ImplicationsTo our knowledge, no study to date has examined alcohol and cigarette demand, via hypothetical purchase tasks, in a clinical sample of heavy drinking smokers. This study demonstrates that behavioral economic indices may be sensitive to cross-substance relationships and specifically that such relationships are asymmetrically stronger for smoking variables affecting alcohol demand, not the other way around.
| S-EPMC7976931 | biostudies-literature
Project description:BackgroundMost physiological studies interested in alcohol-dependence examined ethanol as a pharmacological agent rather than a nutrient. We conducted two studies, which assessed the metabolic and endocrine factors involved in the regulation of alcohol and nutrient intake in alcohol-dependent (AD) subjects. We also examined the potential role of a disruption in energy balance in alcohol-dependence.Methods and resultsIn Study-1, quantitative dietetic interviews of eating and drinking habits were conducted with 97 AD subjects. The population was split around a median alcohol intake value of 12.5 kcal/kg/day. The results showed that the "low alcohol" drinking AD subjects had high Body Mass Index (BMI) and Fat Mass (FM) and alcohol intake was compensated for by a decrease in non-alcoholic intakes. "High alcohol" drinking AD subjects, on the other hand, had low BMI and FM and the total caloric intakes were largely above norms. In Study-2, 24 AD inpatients were submitted to dietetic interviews, calorimetry and blood samplings for the measurement of biomarkers of the regulation of metabolism and satiety, on day 2, 5 and 16 of abstinence. These patients were compared with 20 controls matched for age and gender. We observed in AD patients an increase in cortisol, leptin and PYY plasma levels and a decrease in ghrelin, which might explain the observed decrease in non-alcoholic intakes. However, alcoholic and non-alcoholic intakes correlated positively with basal metabolism and negatively with leptin and leptin/BMI.ConclusionFor individuals consuming below 12.5 kcal/kg/day of alcohol, alcohol intake is compensated for by a decrease in non-alcoholic nutrient intakes, probably due to changes in metabolic and satiety factors. For individuals consuming above 12.5 kcal/kg/day of alcohol, alcohol accelerates metabolism and decreases fat mass and leptin levels, and the total caloric intake largely exceeds norms. A dual model for regulation of energy intake in AD subjects is proposed.
| S-EPMC3392266 | biostudies-literature
Project description:Smoking is partly attributed to alterations of reward processing. However, findings on the neurobiological mechanisms that underlie smoking-related and smoking-unrelated reward processing in smokers have been inconsistent. Neuroimaging experiments that used functional magnetic resonance imaging (fMRI) and reported brain responses to smoking-related cues and nonsmoking reward-related cues in smokers and healthy controls as coordinates in a standard anatomic reference space were identified by searching the PubMed, Embase, and Web of Science databases up to December 2018. Three meta-analyses were performed using random-effect nonparametric statistics with Seed-based d Mapping software, with brain activity contrast from individual studies as the input. The striatum showed higher activation in response to smoking-related cues compared with neutral cues in 816 smokers from 28 studies and lower activation in response to nonsmoking reward-related cues in 275 smokers compared with 271 healthy control individuals from 13 studies. The relative reactivity of the putamen to smoking-related cues increased in 108 smokers compared with 107 healthy controls from seven studies. Meta-regression showed that smokers with a greater severity of nicotine dependence exhibited less engagement of the striatum in response to both smoking-related cues and nonsmoking reward-related cues. The present results reveal the disruption of reward system function in smokers and provide new insights into diverging theories of addiction. With the escalation of nicotine dependence, nicotine appears to exert dynamic effects on reward processing, based on incentive sensitization theory and reward deficiency syndrome theory.
| S-EPMC7078287 | biostudies-literature
Project description:BackgroundThis study aims to determine the relationship between expression levels of ALDH2 and SOD2 genes and clinical parameters such as alcohol drinking, tobacco smoking, primary site of HNSCC, and human papilloma virus (HPV) state.MethodsGene expression data were obtained from gene expression omnibus (GEO accession number: GSE65858). Clinical data (N = 270) including survival result, gender, age, TNM stage, primary site of HNSCC, HPV status, alcohol drinking, and tobacco smoking habit were analyzed according to gene expression pattern.ResultsALDH2 gene was expressed in low levels in patients with heavy alcohol consumption. It was expressed in high (p = 0.01) levels in patients with no or light alcohol consumption. ALDH2 gene was also expressed in low levels in patients with oral cavity cancers or hypopharynx cancers. However, ALDH2 gene was expressed in high (p = 0.03) levels in patients with oropharyngeal cancers or laryngeal cancers. HPV-positive patients were found to have high (p = 0.02) expression levels of ALDH2. SOD2 gene was expressed in high (p = 0.005) levels in patients who had greater mean pack-year of tobacco smoking. Based on log rank test, the group of patients with high expression of ALDH2 showed better (p = 0.002) clinical results than those with low expression of ALDH2. Difference of survival results between ALDH2 high-expressed group and ALDH2 low-expressed group was validated in another cohort (GSE39368, N = 138).ConclusionsHeavy alcohol drinking downregulates ALDH2 gene expression level. Heavy smoking up-regulates SOD2 gene expression level in patients with head and neck squamous cell carcinoma. The group of patients with low expression levels of ALDH2 showed significantly poorer survival results compared to those with high expression levels of ALDH2.
| S-EPMC6389042 | biostudies-literature
Project description:Ibudilast, a neuroimmune modulator which selectively inhibits phosphodiesterases (PDE)-3, -4, -10, and -11, and macrophage migration inhibitory factor (MIF), shows promise as a novel pharmacotherapy for alcohol use disorder (AUD). However, the mechanisms of action underlying ibudilast's effects on the human brain remain largely unknown. Thus, the current study examined the efficacy of ibudilast to improve negative mood, reduce heavy drinking, and attenuate neural reward signals in individuals with AUD. Fifty-two nontreatment-seeking individuals with AUD were randomized to receive ibudilast (n = 24) or placebo (n = 28). Participants completed a 2-week daily diary study during which they filled out daily reports of their past day drinking, mood, and craving. Participants completed an functional magnetic resonance imaging (fMRI) alcohol cue-reactivity paradigm half-way through the study. Ibudilast did not have a significant effect on negative mood (β = -0.34, p = 0.62). However, ibudilast, relative to placebo, reduced the odds of heavy drinking across time by 45% (OR = 0.55, (95% CI: 0.30, 0.98)). Ibudilast also attenuated alcohol cue-elicited activation in the ventral striatum (VS) compared to placebo (F(1,44) = 7.36, p = 0.01). Alcohol cue-elicited activation in the VS predicted subsequent drinking in the ibudilast group (F(1,44) = 6.39, p = 0.02), such that individuals who had attenuated ventral striatal activation and took ibudilast had the fewest number of drinks per drinking day in the week following the scan. These findings extend preclinical and human laboratory studies of the utility of ibudilast to treat AUD and suggest a biobehavioral mechanism through which ibudilast acts, namely, by reducing the rewarding response to alcohol cues in the brain leading to a reduction in heavy drinking.
| S-EPMC8197758 | biostudies-literature