Effects of single doses of alcohol and caffeine on cigarette smoke puffing behavior

Puffing behavior (number of puffs, puff duration, puff volume, peak pressure, peak flow, peak latency, and puff interval) and pre- to postsmoking delta tidal CO difference were measured in female subjects in order to assess separate and combined effects of ethanol and caffeine. The subjects smoked two cigarettes of their habitual brand in a preliminary familiarizing session and in each of the subsequent four test sessions. The treatments administered after smoking the first cigarette in the test sessions were: alcohol placebo and caffeine placebo; alcohol placebo and caffeine; alcohol and caffeine placebo; alcohol and caffeine. Test-retest reliability across the first cigarette of each session (which was not smoked under the influence of the treatments) was remarkably high for all the puffing parameters. Ethanol in the dose of 0.7 g/kg intensified cigarette smoking of the second cigarette by increasing delta tidal CO, average puff volume, and total puff volume per cigarette, whereas 0.5 g/kg ethanol and 5 mg/kg caffeine given alone or combined with ethanol failed to influence puffing behavior consistently.     

Marihuana attenuates the rise in plasma ethanol levels in human subjects.

This study was conducted to determine if plasma ethanol levels are altered as a result of smoking marihuana. Fifteen healthy adult male volunteers who used ethanol and marihuana on a casual basis participated in this study. Subjects were randomly assigned to one of three groups: placebo, low-dose, or high-dose marihuana. The marihuana dose was held constant and each subject drank three different doses of ethanol on 3 separate days spaced at least 1 week apart. Subjects drank either placebo or ethanol at doses of 0.35 g/kg (7.60 mmol/kg) or 0.70 g/kg (15.19 mmol/kg). Thirty minutes after drinking they smoked either a placebo marihuana cigarette, or one containing either 1.26% or 2.53% delta 9-tetrahydrocannabinol. Plasma ethanol levels rose sharply after the 0.7 g/kg dose and peaked at 50 minutes after drinking began (78.25 +/- 4.95 mg/dl). When subjects smoked the high-dose marihuana cigarettes after the 0.7 g/kg dose of ethanol, peak plasma ethanols levels were only 54.80 +/- 8.32 mg/dl at 105 minutes after drinking began. These alterations in plasma ethanol levels paralleled a reduction in the duration of ethanol- and marihuana-induced subjective effects after high doses of both drugs. These data suggest that marihuana may alter ethanol bioavailability.     

Modeling the effect of alcohol on smoking lapse behavior

Objective

The primary aim of this project was to examine the role of alcohol use in smoking lapse behavior, as alcohol consumption is a known risk factor for poor smoking cessation outcomes.

Materials and methods

We have developed a novel human laboratory model to examine two primary aspects of alcohol-mediated tobacco relapse: (1) Does alcohol facilitate the initiation of the first cigarette? (2) Once the first cigarette is initiated, does alcohol facilitate subsequent smoking? Using a within-subject design, 16 daily smokers who were also heavy social drinkers received a priming drink (0.03 g/dl or taste-masked placebo) and then had the option of initiating a tobacco self-administration session or delaying initiation by 5-min increments for up to 50 min in exchange for monetary reinforcement. Subsequently, the tobacco self-administration session consisted of a 1-h period in which subjects could choose to smoke their preferred brand of cigarettes using a smoking topography system or receive monetary reinforcement for cigarettes not smoked. Alcohol craving, tobacco craving, subjective reactivity to alcohol, and nicotine withdrawal were assessed as secondary outcomes.

Results

Results demonstrated that after consuming the alcohol beverage, subjects were less able to resist the first cigarette and initiated their smoking sessions sooner, and smoked more cigarettes compared to the placebo beverage. These findings have implications for smoking cessation in alcohol drinkers and model development to assess smoking lapse behavior.     

Varenicline,low dose naltrexone,and their combination for heavy-drinking smokers: human laboratory findings

Rationale

Heavy-drinking smokers constitute a sizeable and hard-to-treat subgroup of smokers, for whom tailored smoking cessation therapies are not yet available.

Objectives

The present study used a double-blind, randomized, 2?×?2 medication design, testing varenicline alone (VAR; 1 mg twice daily), low dose naltrexone alone (L-NTX; 25 mg once daily), varenicline plus naltrexone, and placebo for effects on cigarette craving and subjective response to alcohol and cigarettes in a sample (n?=?130) of heavy-drinking daily smokers (≥10 cigarettes/day).

Methods

All participants were tested after a 9-day titration period designed to reach a steady state on the target medication. Testing was completed at 12 h of nicotine abstinence, after consuming a standard dose of alcohol (target breath alcohol concentration?=?0.06 g/dl) and after smoking the first cigarette of the day.

Results

The combination of VAR?+?L-NTX was superior to placebo, and at times superior to monotherapy, in attenuating cigarette craving, cigarette and alcohol “high,” and in reducing ad-lib consumption of both cigarettes and alcohol during the 9-day medication titration period.

Conclusions

These preliminary findings indicate that clinical studies of the combination of VAR?+?L-NTX for heavy drinkers trying to quit smoking are warranted and may ultimately improve clinical care for this sizeable and treatment-resistant subgroup of smokers.     

Alcohol and the reward value of cigarette smoking

People who drink alcohol are more likely to smoke, and experiments have shown that alcohol can increase cigarette smoking. However, it is not clear why alcohol consumption should increase smoking. To address this issue the current experiment looked at the effects of alcohol on a range of behavioural and subjective measures intended to assess the reward value of smoking. These included a preference test carried out after subjects had smoked cigarettes of one colour after consuming alcohol, and cigarettes of another colour after consuming non-alcoholic drinks. In the preference test, subjects were offered the choice of smoking the alcoholic or non-alcoholic drink-paired cigarette. It was hypothesised that if alcohol increased the reward value of smoking, subjects would choose to smoke the alcohol-paired cigarette. Consumption of alcohol increased the length of time people spent smoking, increased the number of puffs taken on each cigarette, and increased the amount of tobacco burnt. There were also strong subjective effects, with subjects looking forward more to smoking after alcohol and reporting greater smoking satisfaction after alcohol. However, subjects did not show a preference for the cigarettes they had smoked after alcohol.     

Smoking Topography in a Nonlaboratory Environment

The relationships between the number of cigarettes smoked/day and the number of puffs/cigarette, puff duration, and total puff time/cigarette were studied. Data were collected on 12 regular smokers for all cigarettes smoked over a 3-day period in a nonlaboratory environment. Between-subject variability was substantial on each of the topographical measures. Neither the number of cigarettes smoked per day nor the classification of Heavy (> 25 cigarettes/day) vs Moderate (< 25 cigarettes/day) smoking levels was related to the intensity with which cigarettes were smoked. Within-subject consistency on the topography measures indicates that smokers may have relatively unique smoking patterns.

Most studies of smoking in the natural environment employ number of cigarettes/day as their estimate of smoke exposure. However, total smoke exposure is determined by an interaction of various topographical features, including frequency (number of cigarettes/day, number of puffs/cigarette), durational (puff duration, interpuff interval, intercigarette interval), and volumetric (puff volume, inhalation volume) components. Employing cigarettes/day to estimate smoke exposure assumes a consistent relationship between cigarettes/day and other topographical features which contribute to total smoke exposure, but it is not clear that such a relationship exists. Laboratory studies of smoking behavior have found that cigarette frequency may vary independently of these other topographic components of smoking, lichtenstein and Antonuccio (1981) examined smoking topography in 24 male smokers while they smoked a cigarette during two 45-minute sessions. They found that cigarette rate was significantly related to intercigarette interval, but not to puff frequency, puff duration, cigarette duration, and amount of tobacco burned.

Results found in laboratory settings, however, have been found not to necessarily generalize to nonlaboratory environments. For example, OssipKlein, Martin, Lomax, Prue, and Davis (1983) examined six subjects smoking adlib in three settings: natural, clinical, and laboratory. They found that cigarette durations were shorter and that subjects took significantly longer and more puffs in a clinical or laboratory setting compared to a naturalistic setting. Thus, examination of the relationship between topographical features in naturalistic smoking would appear to require direct study outside the laboratory.

The present study is to our knowledge the first to examine topographical features of smoking and the relationship between number of cigarettes smoked/ day and other measures of smoking topography while the subject smoked ad-lib in a nonlaboratory environment. This information would potentially be important in examining the extent of individual differences in smoking topography, in assessing the extent to which cigarettes/day is related to other aspects of smoking behavior, and in determining whether categorizing smokers into smoking groups (e.g., moderate and heavy) on the basis of number of cigarettes/day accurately reflects the amount of total smoke exposure/day.     

The influence of nicotine dose and nicotine dose expectancy on the cognitive and subjective effects of cigarette smoking

This study investigated the independent and interactive effects of nicotine dose and nicotine dose expectancy on smoking outcomes using a 2 (given nicotine vs. placebo) × 2 (told nicotine vs. placebo) Balanced Placebo Design (BPD). Smokers (N = 148) completed the Rapid Visual Information Processing Task (RVIP) and measures of smoking urge, mood, and cigarette ratings (e.g., satisfying) after smoking a nicotine or placebo cigarette crossed with instructions that the cigarette contained either nicotine or no nicotine. Nicotine cigarettes (0.6 mg nicotine) produced better sustained attention performance than placebos as indicated by RVIP reaction time, hits, and sensitivity (A'). Nicotine cigarettes also produced better mood and greater rewarding subjective effects of the cigarettes on 11 of 11 dimensions compared to placebos. Nicotine instructions resulted in fewer RVIP false alarms, better mood, and greater rewarding subjective effects of the cigarettes on 9 of 11 dimensions compared to placebo instructions. Nicotine dose by nicotine dose expectancy interactions were also observed for urge and tension-anxiety, such that the dose expectancy manipulation produced differential effects only among those who smoked placebo cigarettes. In contrast a significant interaction for self-reported vigor-activity demonstrated that the dose expectancy manipulation produced effects only among those who smoked nicotine cigarettes. This study provides additional evidence that nicotine improves cognitive performance, and provides initial evidence that denicotinized cigarettes smoked under the guise that they contain nicotine influence cognitive performance, albeit with less robust effects than nicotine. These data may inform the development of expectancy-based interventions for tobacco dependence.     

Potentiation of cigarette craving and satisfaction by two types of meals

This study investigated the effects of consuming different meal types on cigarette craving and satisfaction. Twelve heavy smokers were tested on three evenings. Each day, they smoked three cigarettes and received either a solid meal, an equicaloric liquid meal, or no meal. Subjects smoked the first cigarette one half hour after the experiment began, the second immediately after finishing the meal, and the third 35 min after smoking the second cigarette. Cigarette craving increased most after the solid meal, less so after the liquid meal, and least after no meal. Subjects reported that the cigarette after the solid meal tasted the best, was the most satisfying, enjoyable, and desirable as compared to the cigarette following no meal at all. These results indicate that there is a robust postprandial enhancement of cigarette smoking after a solid meal but less after a liquid meal.     

State-dependent learning effects with a combination of alcohol and nicotine

An experiment was carried out to investigate whether nicotine ingestion (via cigarette smoking) interacted with alcohol (vodka and tonic) in its effect on state-dependent learning (SDL) in humans. On Day 1 of the 2-day experiment 24 subjects were required to learn a simple route map previously found to be SDL sensitive with alcohol. All subjects ingested 0.66 g alcohol/kg body wt. and smoked two medium tar cigarettes (average nicotine content 1.4 mg). Twenty-four hours later, subjects attempted recall under one of the following drug states; (i) alcohol and nicotine (A+N); (ii) alcohol and smoking placebo (A+O); (iii) Nicotine and placebo drink (O+N); and (iv) no drugs (O+O). Highest recall scores were observed in the A+N subjects, with O+N and O+O subjects recalling the least. A+O subjects had intermediate recall performance. Thus the combination did produce a clear SDL effect, with alcohol possibly contributing the major influence.     

Bidis--hand-rolled, Indian cigarettes: effects on physiological, biochemical and subjective measures

Bidis, hand-rolled cigarettes imported from India, have become increasingly popular among US teenagers. These cigarettes are perceived as a safer, more natural alternative to conventional cigarette smoking. The present study was conducted to determine whether the acute effects of bidis and conventional cigarettes are similar. Undergraduate cigarette smokers with a history of bidi smoking were tested in two experimental sessions, using a within-subject design. Subjects smoked both a bidi and a conventional cigarette. Physiological and biochemical measures, subjective evaluations, and smoking behavior characteristics were obtained before, during, and after smoking each experimental cigarette. Although time to smoke and puffs per cigarette were significantly higher after the bidi, physiological and biochemical effects of bidi smoking were similar to those of smoking conventional cigarettes. Bidis were rated less satisfying than the conventional cigarette. However, there were no significant differences between the cigarettes in other subjective measures. Our results do not support the belief that bidis are a safe alternative to conventional cigarettes. Furthermore, bidi smoking, like conventional cigarette smoking, may lead to nicotine dependence.     

Neural Substrates of Alcohol-Induced Smoking Urge in Heavy Drinking Nondaily Smokers

A strong link exists between cigarette smoking and alcohol use, which may be explained by the experimental observation that alcohol ingestion promotes cigarette craving and precipitates smoking. At the neuroanatomic level, it is unclear where and how alcohol exerts these effects, although the process likely involves the ventral striatum given its function in motivational salience and appetitive reinforcement. In a double-blinded, placebo-controlled, crossover study, heavy drinking nondaily social smokers (ie, light smokers or ‘chippers'') were examined using functional magnetic resonance imaging after they ingested an acute dose of alcohol or placebo. We probed reactivity in the ventral striatum and other brain regions during exposure to visual smoking vs nonsmoking control cues. We found that alcohol enhanced self-reported ratings of desire to smoke, and in this context, significantly increased ventral striatum responses to smoking compared with control cues. In exploratory analyses, we observed that alcohol dampened orbitofrontal activity across both cue types, whereas dorsolateral prefrontal and anterior cingulate cortex activation to smoking cues was not affected by alcohol. This study bridges a pharmacological challenge approach to the study of brain reactivity to smoking cues, extends prior cigarette cue imaging studies to nondependent smokers, and elucidates a potential neurobiological mechanism to explain the co-consumption of alcohol and cigarettes in nondependent users.     

Acute doses of d-amphetamine and bupropion increase cigarette smoking

RATIONALE: Bupropion is used clinically as a treatment for smoking cessation, but the processes by which it reduces smoking are poorly understood. Bupropion shares some neurochemical actions and behavioral effects with the psychostimulant amphetamine, and it has been shown that amphetamine increases smoking when administered acutely. The effects of single doses of bupropion on smoking have not been studied but, based on its similarities to amphetamine, we postulated that acute bupropion would also increase smoking. OBJECTIVE: To measure the effects of single doses of amphetamine and bupropion on smoking and craving for cigarettes in smokers. METHODS: Cigarette smokers who were not trying to quit participated in a three-session study in which they received placebo and a single dose of either d-amphetamine sulfate (10 and 20 mg; n=10) or bupropion hydrochloride (150 and 300 mg; n=12) after overnight abstinence. The three outcome measures were: i) subjective and behavioral effects of amphetamine and bupropion after a period of acute abstinence, ii) effects of amphetamine and bupropion on subjective responses to a single, smoked cigarette, and iii) effects of the drugs on number of cigarettes smoked during an ad libitum smoking period. RESULTS: After the acute abstinence and before smoking, both amphetamine and bupropion increased self-reported mood and euphoria, but did not change ratings of craving or withdrawal. After subjects smoked a single smoked cigarette, they reported that bupropion reduced ratings of "buzzed" and "intensity". During the period of ad libitum smoking both amphetamine and bupropion increased the number of cigarettes smoked. CONCLUSION: Acute doses of both bupropion and amphetamine increase smoking in non-treatment-seeking smokers without altering ratings of craving or withdrawal. Bupropion reduced some of the sensory responses to the smoked cigarette. It remains to be determined why bupropion increases smoking when administered acutely under controlled conditions, while it helps to reduce smoking in patients trying to quit.     

Acute effects of low and high dose alcohol on smoking lapse behavior in a laboratory analogue task

Rationale

Smoking lapses (i.e., returns to smoking after quitting) often occur following alcohol consumption with observational data suggesting greater quantities of alcohol lead to greater risk. However, a causal dose-dependent effect of alcohol consumption on smoking lapse behavior has not been established, and the mechanisms that might account for such an effect have not been tested.

Objectives

In a within-subjects design, we examined the effects of low- (0.4 g/kg) and high-dose (0.8 g/kg) alcohol, relative to placebo, on smokers’ ability to resist initiating smoking after acute smoking abstinence.

Methods

Participants were 100 heavy alcohol drinkers, smoking 10–30 cigarettes per day. Across three separate days, participants consumed placebo, low-dose, or high-dose alcohol following 3 h of smoking abstinence and, 35 min later, were offered the opportunity to smoke while resisting smoking was monetarily reinforced proportional to the amount of time delayed.

Results

Consistent with a dose–response effect, participants smoked 3.35 min (95 % confidence intervals (CI) [?7.09, 0.40], p?=?.08) earlier following low-dose alcohol and 6.36 min (95 % CI [?9.99, ?2.73], p?=?.0006) earlier following high-dose alcohol compared to drinking a placebo beverage. Effects of dose on smoking behavior were partially mediated by increases in urge to smoke. There was no evidence that alcohol’s effects on urge to smoke or ability to resist smoking were mediated through its stimulating or sedating effects.

Conclusions

Alcohol can reduce the ability to resist smoking in a dose-dependent fashion, in part, due to its effect on increasing the intensity of smoking urges.     

Alcohol drinking and cigarette smoking: an exploration of the association in middle-aged men and women

The association of alcohol and cigarette consumption was explored among 13,673 black or white persons aged 40-49 years, who received check-ups from mid-1979 to 1985. Alcohol use was strongly associated with number of cigarettes smoked per day, but not with tar-yield, mentholation and presence of filters. Duration of cigarette use, frequency and depth of inhalation, proportion of cigarette smoked and greater time from arising to first cigarette were significantly related to alcohol use in some but not all race-sex groups. Among smokers who consumed alcohol, liquor drinkers smoked the most cigarettes per day and wine drinkers the least. Thus, the association between alcohol drinking and cigarette smoking is strong in middle-aged persons but there are race- and sex-related disparities when specific aspects of smoking behaviour are considered.     

Cigarette smoking by women: interactions with alcohol use

Cigarette smoking increased during alcohol self-administration in comparison to an alcohol-free baseline in 24 women given access to alcohol for 21 days. Heavy smokers (25 or more cigarettes per day) increased smoking significantly during drinking (P<0.05). Analysis of tobacco smoking by level of alcohol consumption showed that both heavy and moderate alcohol users increased smoking significantly during alcohol availability (P<0.05, 0.01). The heavy and moderate smokers smoked significantly more between noon and midnight (P<0.001) than at other times when alcohol was available. The rate of cigarette smoking (defined by inter-cigarette intervals) was faster during alcohol self-administration than during the alcohol-free baseline. Heavy smokers smoked most cigarettes at intervals of 11–20 min during heavy or moderate drinking. During the pre-alcohol baseline, these women smoked most cigarettes at intervals of 21–30 or 31–40 min. Most women (70–74%) also increased tobacco smoking at the premenstruum. Both heavy and occasional smokers increased smoking at the premenstruum significantly more than the moderate smokers (P<0.05). All women reported increased psychological discomfort at the premenstruum on the Premenstrual Assessment Form (PAF) but reports of physical discomfort were more marked in women who smoked less at the premenstruum. These data extend previous findings in men that alcohol consumption is associated with increased cigarette smoking to female social drinkers.     

The effects of cigarette smoking on human sexual potency

Forty-two male cigarette smokers, age 18 to 44, were randomly assigned to high-nicotine, low-nicotine, or control groups in a study relating cigarette smoking to sexual response. Subjects watched erotic film segments while their penile diameters, heart rates, and finger pulse amplitudes were continuously recorded by a polygraph. Subjects in the smoking groups smoked relatively high-nicotine (.9 mg) or very low-nicotine (.002 mg) cigarettes prior to watching the last two films, while control subjects ate candy. Smoking two high-nicotine cigarettes in immediate succession significantly decreased the rate of penile diameter change relative to the other conditions. These effects were not seen after a single cigarette was smoked. High-nicotine cigarettes caused significantly more vasoconstriction and heart rate increase than did low-nicotine cigarettes, which did not differ from control conditions.     

Phenotypic and genetic relationship between BMI and cigarette smoking in a sample of UK adults

In addition to the health hazards posed individually by cigarette smoking and obesity, the combination of these conditions poses a particular impairment to health. Genetic factors have been shown to influence both traits and, to understand the connection between these conditions, we examined both the observed and genetic relationship between adiposity (an electrical impedance measure of body mass index (BMI)) and cigarettes smoked per day (CPD) in a large sample of current, former, and never smokers in the United Kingdom. In former smokers, BMI was positively associated with cigarettes formerly smoked; further, the genetic factors related to a greater number of cigarettes smoked were also responsible for a higher BMI. In current smokers, there was a positive association between BMI and number of cigarettes smoked, though this relationship did not appear to be influenced by similar genetic factors. We found a positive genetic relationship between smoking in current/former smokers and BMI in never smokers (who would be unmarred by the effects of nicotine). In addition to CPD, in current smokers, we looked at two variables, time from waking to first cigarette and difficulty not smoking for a day, that may align better with cigarette and food ‘craving.’ However, these smoking measures provided mixed findings with respect to their relationship with BMI. Overall, the positive relationships between the genetic factors that influence CPD in smokers and the genetic factors that influence BMI in former and never smokers point to common biological influences behind smoking and obesity.     

Peer modeling influences on smoking behavior of heavy and light smokers

Twelve heavy (>20 cigs/day) and twelve light (< cigs/day) male smokers were individually exposed to a high rate smoking confederate model in one session and a low rate smoking confederate model in another session. In both conditions, the model was “warm and friendly” to enhance his effectiveness. Cigarette frequency, inter-cigarette interval, and the various topographical components of smoking (puff frequency, percent tobacco burned, cigarette duration, puff duration, and average inter-puff interval) served as the dependent measures. Subjects smoked more cigarettes and took less time between cigarettes when exposed to a high rate model compared with exposure to a low rate model. Topography measures were not significantly influenced by the modeling conditions. There were no significant differences between heavy and light smokers with respect to any of the dependent measures.     

Assessing individual differences in ethanol preference using a cumulative dosing procedure

Preference for ethanol versus a placebo was assessed in 12 normal volunteers using a cumulative dosing preference test. The test consisted of four sampling sessions followed by three choice sessions. During the sampling sessions subjects received either five cumulating oral doses of ethanol (0.1g/kg per dose) or equal volumes of placebo, at 15-min intervals. Subjective and observer-rated drug effects, psychomotor performance, drug liking ratings, and breath ethanol levels were measured at regular intervals. During choice sessions, subjects first chose which of the two substances (drug or placebo) they wished to take and ingested one unit dose. Then, at 15-min intervals throughout the session, they could ingest up to ten additional unit doses of the same substance (i.e., up to 1.1 g/kg ethanol). On average, the subjects chose the ethanol-containing beverage on 75% of the choice sessions, and they self-administered a mean total dose of 0.8g/kg per session. Subjects varied in the amount of ethanol ingested on choice sessions, and the amount they chose was related to their subjective responses to the drug during sampling. Subjects who chose the most ethanol reported experiencing stimulant-like effects from the ethanol, whereas the subjects who chose ethanol less frequently and ingested lower doses reported primarily sedative-like effects from the drug. The results demonstrate that the cumulative dosing procedure can be used effectively to evaluate drug preferences and dose preferences in normal volunteers.