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The aim of this study is to advance our understanding of how nicotine dependence level, defined by the Fagerström Test of Nicotine Dependence (FTND), relates to nicotine withdrawal features. We classified nicotine dependence in two categories, 1) low dependence (LD; FTND

Background Initial trials of web-based smoking-cessation programs have generally been promising. The active components of these programs, however, are not well understood. This study aimed to (1) identify active psychosocial and communication components of a web-based smoking-cessation intervention and (2) examine the impact of increasing the tailoring depth on smoking cessation. Design Randomized fractional factorial design. Setting Two HMOs: Group Health in Washington State and Henry Ford Health System in Michigan. Participants 1866 smokers. Intervention A web-based smoking-cessation program plus nicotine patch. Five components of the intervention were randomized using a fractional factorial design: high- versus low-depth tailored success story, outcome expectation, and efficacy expectation messages; high- versus low-personalized source; and multiple versus single exposure to the intervention components. Measurements Primary outcome was 7 day point-prevalence abstinence at the 6-month follow-up. Findings Abstinence was most influenced by high-depth tailored success stories and a high-personalized message source. The cumulative assignment of the three tailoring depth factors also resulted in increasing the rates of 6-month cessation, demonstrating an effect of tailoring depth. Conclusions The study identified relevant components of smoking-cessation interventions that should be generalizable to other cessation interventions. The study also demonstrated the importance of higher-depth tailoring in smoking-cessation programs. Finally, the use of a novel fractional factorial design allowed efficient examination of the study aims. The rapidly changing interfaces, software, and capabilities of eHealth are likely to require such dynamic experimental approaches to intervention discovery.

Test strips impregnated with phenylthiocarbamide (PTC) have been used to identify genetic differences based on whether a bitter taste is perceived. To determine whether smokers who perceive PTC as bitter tasting ("tasters") would differ from those who describe it as tasteless ("non-tasters") on smoking-related variables, we studied 464 current smokers (70% female, 79% White; mean age 30.5+/-9 years) recruited to participate in laboratory experiments and clinical trials. Of these, 217 (47%) reported the PTC strips as tasteless and 154 (33%) as tasting bitter. The remaining 93 (20%) described the taste as salty, sweet, or other and were excluded from further analyses. Comparing tasters with non-tasters, we found significant differences in mean (S.D.) total years smoked (14.5 [9.2] for non-tasters, vs. 12.6 [8.4] for tasters, p.05), Fagerstrom Tolerance Questionnaire scores (6.4 [2.1] vs. 5.8 [2.1], p.01), and scores on the Positive Reinforcement scale of the Michigan-Nicotine Reinforcement Questionnaire (8.1 [2.9] vs. 6.8 [3.1], p.05). Results suggest that among smokers, ability to taste PTC may confer some protection from development of nicotine dependence and positive reinforcement from smoking.

To investigate the accuracy of offspring assessments of parental smoking status, we studied 116 parents and 151 adult children (276 parent-child dyads) who provided data on both their own and their parents' smoking status. All currently smoking and all ex-smoking parents were correctly classified as ever-smokers by their offspring (n = 79 and 100, respectively). Of the 97 offspring who reported on never-smoking parents, 88 correctly classified their parents as never-smokers. Thus, sensitivity for detecting ever-smoking in parents was 100%, and specificity, 91%. Because all incorrect classifications involved never-smoking parents, further analyses focused on this group. Too few parents were misclassified to permit testing of parental characteristics. Offspring who misclassified their parents were significantly older than those who did not; neither sex nor smoking status of the offspring was associated with the increased likelihood of misclassification. No significant differences were discovered for dyadic factors (concordance/discordance for sex; parent-offspring age difference). Overall, these results support the utility of proxy reports of parental smoking phenotype by adult informants when self-report is unavailable.

Initial sensitivity to the pharmacological effects of a drug may affect patterns of future use and dependence for a wide variety of drugs. Retrospective reports of sensations experienced upon early experimentation, however, may be limited by recall bias based on time elapsed and subsequent experiences. To validate reports of early experiences with nicotine, we studied 34 smokers who had contributed retrospective data on early experiences with smoking. Half had reported experiencing a buzz from smoking their first cigarette (the "yes" group), the other half had not (the "no" group). To simulate initial sensitivity to nicotine, we asked participants to remain abstinent from smoking for 5 days to allow for the dissipation of tolerance. They then participated in a laboratory session in which they were reexposed to nicotine in an unfamiliar form (nicotine nasal spray) and asked to indicate pleasurable responses by depressing a foot pedal if and when they experienced a "pleasurable buzz." Smokers in the "yes" group were marginally more likely to be male. The two groups did not differ significantly on age or race. The "yes" group smoked significantly more cigarettes/day than the "no" group. When the two groups were compared for response to nasal spray following 5 days' abstinence, smokers in the "yes" group were marginally more likely to have signaled experiencing at least one pleasurable buzz and rated "pleasurable sensation from spray" on a 100-mm visual analogue scale administered 10 min after nicotine dosing significantly higher than were those in the "no" group. To the extent that several days' abstinence can serve as a model for initial sensitivity to nicotine, our findings validate retrospective reports of pleasurable sensations upon early smoking experimentation.

The U.S. Centers for Disease Control defines a never-smoker as someone who has smoked < 100 cigarettes per lifetime. In an attempt to explore differences among nonsmokers and to validate this cutpoint, we surveyed 69 nonsmokers who had smoked between 1 and 200 cigarettes in their lifetime on their experiences during the time they smoked. Of the 7 who classified themselves as ex-smokers, 2 met DSM-IV criteria for nicotine dependence, compared with none who classified themselves as never-smokers. No respondents provided data permitting the computation of a Fagerstrom Test for Nicotine Dependence (FTND) score. Withdrawal effects were minimal, but craving, tolerance, and subjective effects showed a pattern of significant differences that were most prominent between those who smoked only 1 cigarette and those who smoked at least a pack. Our data indicate a graded effect but also suggest that 19 cigarettes per lifetime is a more conservative cutpoint than 99 for defining the never-smoker phenotype. Further investigation of the smoking trajectory and characteristics associated with development of signs of dependence in never- vs. ever-smokers may help refine this cutpoint and shed light on what protects some people who experiment with smoking from becoming chronic users.

Cigarette smokers are known to be overrepresented among adults with Attention Deficit Hyperactivity Disorder (ADHD). To date, however, no attempt has been made to determine the extent to which a lifetime diagnosis of ADHD may be associated with smoking even in the absence of current symptomatology. We hypothesized that nicotine dependence and abstinence effects-especially effects relevant to ADHD symptomatology-would be more pronounced in adult ADHD smokers in comparison with those who reported childhood ADHD symptoms only. Results indicated that, in contrast to controls without ADHD symptomatology, both adult and childhood ADHD groups were significantly more likely to experience a number of nicotine withdrawal symptoms, including irritability and difficulty concentrating; in no instance did the ADHD groups differ from one another in this regard. Thus, studying people with childhood symptoms of ADHD, even in the absence of an adult diagnosis, may shed light on the known association between smoking and ADHD.

To investigate attitudes about weight as they interact with smoking in African American women, we analyzed data from two independent samples of white and African American women smokers--one assembled via a national random-digit-dialing survey, the other consisting of candidates for enrollment in local studies. Findings for the two samples were remarkably consistent. African American women were significantly heavier and significantly more likely to have a self-reported BMI > or = 27. Although the preferred weight for African American women was significantly higher than for white women, the percentage by which they exceeded their preferred body weight did not differ significantly between groups, and the difference between actual and preferred weights was actually greater for African American women. African American women were more likely to be satisfied with their body shape and were significantly less likely to exercise to control weight. They did not differ significantly on binge-eating or dieting. African American women were more likely than white women to be unwilling to gain any weight upon quitting smoking but did not differ significantly on any other smoking-related weight concerns. Our results suggest that weight concerns, though differently conceptualized, may motivate African American women as powerfully as white women. They strongly suggest that race differences need to be considered in designing optimal smoking cessation interventions for weight-concerned women smokers. To accomplish this goal, efforts to identify a vocabulary for the expression of weight concerns in African American women will be needed, as will attention to ways to avoid exacerbating obesity and to encourage exercise.

Although considerable progress has been made towards understanding the role of menstrual cycle phase in smoking, little is known about the possible effects of menstrual phase upon nicotine intake, withdrawal symptomatology, and craving in women with psychiatric cofactors. Fourteen women with and without a history of Major Depressive Disorder (MDD) were studied during five biologically-confirmed phases over the course of one menstrual cycle: smoking logs, salivary cotinine, and ratings of craving and withdrawal were collected daily. During a second cycle, subjects remained abstinent for 3 consecutive days during the postmenses and premenstrual phases. Although a significant omnibus F-test emerged for cigarettes per day across phases during ad libitum smoking, only trends were observed post hoc and supported midcycle rather than premenstrual elevations. There were no significant phase differences for cotinine. Withdrawal symptomatology was markedly elevated during smoking abstinence and in women with a history of depression. but showed no evidence of phase effects. Thus, the hypothesis that depressed individuals would be differentially affected by phase and abstinence was not strongly supported by our results, though overall elevations emphasize the need for special attention to withdrawal severity in this population. Craving was significantly elevated during smoking abstinence and was significantly higher during postmenses, consistent with the midcycle elevation in smoking rate, but showed no group differences. Our findings overall lend little support for the need to control for menstrual phase under conditions of ad libitum smoking. The strong association of self-reported menstrually related dysphoria during abstinence with both craving and withdrawal symptoms, however, is consistent with an exacerbation of smoking abstinence effects in women with severe menstrual symptomatology.

Although most studies of weight gain following smoking cessation assess long-term change, weight gain during the critical period immediately following cessation may be more salient to the smoker for whom fear of weight gain constitutes a serious barrier to cessation. The current study examined weight change in 20 highly dependent women smokers provided with monetary incentives to abstain for 1 week, along with concomitant changes in cotinine. Abstaining smokers (n = 7) gained 3.1 pounds, compared with 0.3 pounds in women who continued to smoke (n = 13). Across all subjects, change was significantly negatively correlated with final plasma cotinine concentration and marginally negatively correlated with percent cotinine reduction. Weight gain in women abstainers in the luteal phase of the menstrual cycle exceeded that in women abstainers in the follicular phase; a significant interaction such that continuing smokers showed no phase-related differences in weight suggests that the effect was not an artifact of perimenstrual increases in eating or fluid retention. Although long-term weight gain has been shown to be positively associated with success in quitting, little is known about the effects of short-term weight gain. Since many weight-concerned individuals either do not attempt to quit or terminate their quit attempts very early, it may be that if weight gain can be postponed beyond the first few fragile days of cessation, women with strong weight concerns may actually be good candidates for success.

The possible impact of menstrual phase upon reactivity to nicotine was investigated in 12 healthy women smokers. Controlled doses of nicotine were administered via an intranasal aerosol delivery device to overnight-deprived women smokers in four hormonally verified menstrual phases. Physiological, biochemical, and subjective measures were collected. Cycle-related symptomatology differed significantly across phase, with lowest values during the mid-follicular phase. No significant differences were found for baseline variables, including withdrawal measures. Nicotine increment was stable across phase, confirming reliability of the dosing method. No significant menstrual phase differences were found for physiological, subjective, or biochemical responses to nicotine. Pending investigations conducted over longer intervals, in a wider variety of subjects, findings suggest that for this type of study, complex strategies to control for menstrual-cycle phase effects may be unnecessary.

Hypothesizing the existence of a subgroup of female smokers for whom nicotine masks, and abstinence unmasks, a tendency toward hyperphagia and perhaps even subthreshold disordered eating, we compared female “weight-control smokers” (WC; n = 46) and “non-weight-control smokers” (NWC; n = 52) on smoking- and eating-related variables. We also examined the relationship between weight-control smoking and withdrawal symptomatology during 48hours of nicotine abstinence (n = 23). Although WC were not more depressed, anxious, or nicotine-dependent than NWC, they were significantly more likely to report weight gain and increased hunger during abstinence; they also scored higher on Cognitive Restraint and Disinhibition (Three-Factor Eating Questionnaire). The expected correlation of cotinine with weight emerged for NWC but not for WC. Weight-control smoking correlated with increased eating during abstinence. Our findings suggest that WC use dietary restraint as well as smoking to manage weight, and that abstinence may precipitate episodes of disinhibited or binge eating. If WC overinclude women vulnerable to excess or unpredictable eating and consequently to substantial weight gain that can be managed by nicotine, highly focused’treatment strategies may be helpful. The peculiar and fascinating combination of pharmacological and sociocultural factors involved in weight-control smoking has generated considerable research over the past few years. Despite these efforts, however, attempts to determine the net impact of weight-control smoking on treatment efficacy, both in terms of attracting such smokers to treatment and achieving sustained abstinence, have produced a somewhat confusing picture. In the current climate of interest in treatment matching, a question no less appropriate than that of whether weightcontrol smoking is likely to deter cessation efforts or promote relapse is that of whether treatment success rates for people motivated to smoke by nicotine’s anorectic properties can be improved upon; an answer to that question will

Nicotine intake, menstrual and smoking withdrawal symptomatology, and baseline cortisol and MHPG were assessed in nine women smokers under conditions of ad lib smoking and overnight abstinence in three menstrual phases (early follicular, mid-to-late follicular, and late luteal). A trend towards higher nicotine intake (p < 0.10) was observed in the mid-to-late follicular phase. Although menstrual symptomatology was not significantly elevated during the smoking abstinence condition overall, abstinence appeared to prevent the normal reduction in symptomatology during the mid-to-late follicular phase that occurred under conditions of ad lib smoking. Menstrual and withdrawal symptoms were highly correlated, and both were most pronounced during the late luteal/abstinence condition. The smoking-specific item "craving" reflected this pattern, though in attenuated form, suggesting that the observed exacerbation of withdrawal symptomatology was not simply due to generalized dysphoria, as queried in both instruments. MHPG was significantly elevated in the late luteal phase, whereas cortisol was significantly higher during ad lib smoking than during abstinence and tended to be highest in the mid-to-late follicular phase. Further investigation will be needed to determine the functional significance of these findings for understanding and treating smoking in women.

The effects of nicotine, like those of other drugs with potential for abuse and dependence, are centrally mediated. The impact of nicotine on the central nervous system is neuroregulatory in nature, affecting biochemical and physiological functions in a manner that reinforces drug-taking behavior. Dose-dependent neurotransmitter and neuroendocrine effects occur as plasma nicotine levels rise when a cigarette is smoked. Circulating levels of norepinephrine and epinephrine increase, and the bioavailability of dopamine is altered as well. Among the neuroendocrine effects are release of arginine vasopressin, beta-endorphin, adrenocorticotropic hormone, and cortisol. Notably, several of these neurochemicals are psychoactive and/or known to modulate behavior. Thus, affective states or cognitive demands may be favorably modified (at least temporarily) by nicotine intake. When nicotine is inhaled, the neuroregulatory effects just described are immediately available and the reinforcing effects of the drug are maximized. On the other hand, nicotine gum and most other nicotine replacement vehicles in current use have a slower onset of action, resulting in less reinforcement value. Recent data suggest that smoking cessation rates may be optimized by tailoring the dose of nicotine replacement (for example, 2 or 5 mg of nicotine gum) to the individual degree of nicotine dependence. In view of the dynamic interactions between the neuroregulatory effects of nicotine and a host of environmental conditions, nicotine replacement therapy is best carried out in combination with behavior modification techniques.

The Tridimensional Personality Questionnaire (TPQ) was developed by Cloninger (1986) to measure heritable variation in three patterns of response to environmental stimuli: novelty seeking, harm avoidance, and reward dependence. Cloninger (1987) used the TPQ to identify two types of alcoholism: Type 1 (low novelty seeking, high harm avoidance and reward dependence; both male and female) and Type 2 (high novelty seeking, low harm avoidance and reward dependence; predominantly male). To determine whether characteristic patterns exist in smokers, we administered the TPQ to 119 female and 121 male smokers, along with the Fagerstrom Tolerance Questionnaire (FTQ, a measure of nicotine dependence), the Russell Motives for Smoking Questionnaire (RMSQ), and the Spielberger State-Trait Anxiety Inventory (STAI/trait). Compared with a normative sample, our sample exhibited elevated scores on the Novelty-Seeking scale; female smokers were somewhat overrepresented in the highest quartile of the Harm-Avoidance scale; both genders tended to be clustered in the lower quartiles of the Sentimentality-Attachment-Dependence subscale of the Reward-Dependence scale and in the highest quartile of the Persistence subscale. Female smokers showed a significant positive association between Harm Avoidance and FTQ scores, and Harm Avoidance was positively correlated with several RMSQ factors (including Additive smoking) in both genders. These findings suggest that the likelihood of becoming a smoker may be a function of novelty seeking and reward dependence, whereas degree of dependence or addiction once the habit is entrained may be linked to harm avoidance. Our observations establish the potential utility of the TPQ as a tool for examining environmental and heritable variation in smoking behavior and may contribute to improved strategies for prevention and treatment of smoking.

Smokers' ability to regulate nicotine intake by varying topographical parameters such as depth of inhalation and number of puffs makes it difficult to administer standardized doses of nicotine as delivered from smoking. A number of studies have claimed to control these parameters without confirming the effectiveness of such procedures by measures of plasma nicotine. The purpose of the present study was to determine whether specifying onset and duration of each puff would result in accurate dosing. Plasma nicotine boosts for five “paced puffers” were compared across two sessions and with similar data for five “free smokers.” Neither between-subject consistency nor within-subject reproducibility was improved by this paced puffing procedure, despite apparent topographical control.

Nicotine dependence implies a pattern of heavy smoking which is resistant to change, as well as nicotine tolerance, withdrawal, and regulation. The present study attempted to develop a coherent model of cigarette smoking by examining responses on several different measures of nicotine dependence. Twenty-seven habitual smokers filled out questionnaires before and after smoking research cigarettes differing in nicotine content in the laboratory. Plasma cotinine was used to estimate nicotine intake from usual brand cigarettes outside the laboratory. Subjects in the high cotinine quartile (heavy smokers) were found to be consistently more nicotine-dependent than subjects in the low cotinine quartile (light smokers). Taking all subjects into account, the six measures of nicotine dependence which exhibited significant correlations with plasma cotinine accounted for about half of the cotinine variance in a multivariate, linear-regression model. Multivariate approaches provide additional tools for assessing biobehavioral mechanisms in substance abuse and may lead to the development of more-comprehensive and sufficient explanations of smoking than are currently available.

The impact of nicotine on the central nervous system is, in an important sense, neuroregulatory, with cascading effects on physiological and biochemical function as well as on behavioral activity. Accordingly, the neurotransmitter and neuroendocrine effects of nicotine constitute a critical part of its biological action, which includes reinforcing as well as pathophysiological consequences. This review focuses on nicotine's effects on cholinergic and non-cholinergic nicotine receptors and on the responses of catecholamines, monoamines, hypophyseal hormones, and cortisol. The contribution of critical variables, such as timing and duration of neuroregulator release and the patterns that make up the total response, is still largely unknown, particularly with regard to the effects of environmental context, history of nicotine use, and mode of administration. The evidence suggests that by altering the bioavailability of the above-listed neuroregulators, nicotine serves as a pharmacological "coping response", providing immediate though temporary improvement in affect or performance in response to environmental demands. Much of what is known to date is based on studies involving the administration of agonists and antagonists under different environmental conditions. Newer technological approaches such as autoradiography and positron emission tomography show potential for determining the neuroregulatory patterns involved and specifying nicotine's locus of action relevant to its behavioral and physiological effects.

Seven subjects with a diagnosis of anorexia nervosa were treated with behavioral contracts in a hospital setting. Behavioral contracts were initiated at different points during hospitalization for each of the subjects. Treatment was defined as 13 days on a behavioral contract. Outcome was evaluated using the Rn statistic for this multiple-baseline approach. The behavioral intervention was found to have a significant effect on weight gain. Improvements made with treatment tended to be maintained in follow-up. A multiple-baseline approach using the Rn statistic permitted a controlled study using a small sample without a control group. This research methodology may be applicable to a wide variety of clinical areas.

In an attempt to determine predictors of success in a multicomponent behavioral treatment program for smoking, data generated from a pre-treatment history questionnaire and treatment records for 100 participants were analyzed by computer. Participants who abstained after eight weeks of treatment were those who had smoked at lower rates and for shorter periods of time, who were less overweight, and who were more compliant with treatment instructions (keeping daily records). In a separate analysis of recidivism, participants who were less likely to have relapsed by the one-year follow-up were those who, prior to treatment, had reported smoking a greater proportion of cigarettes in non-dysphoric (positive or neutral affect) states. The variables which predicted outcome were independent from those which predicted recidivism and vice versa. The research suggests that treatment effectiveness might be enhanced by providing components which take into account individual subject characteristics.

This paper examines findings on the neuroregulatory effects of nicotine in an effort to formulate a unified hypothesis that can explain the remarkable persistence of smoking behavior. Because nicotine alters the bioavailability of several behaviorally active neuroregulators, including acetylcholine, norepinephrine, dopamine, beta-endorphin, and vasopressin, we propose that nicotine is “used” by smokers to produce temporary improvements in performance or affect. Under this formulation, a potentially large number of exteroceptive and interoceptive cues unrelated to the nicotine-dependence cycle may serve as discriminative stimuli for smoking, over and above smoking to terminate or avoid withdrawal. The rapid action of nicotine, and its diverse neuroregulatory effects, render it particularly effective as a “coping response” to the demands of daily living. Of special interest in this regard is a biphasic pattern of arousal/alertness during smoking followed by calming/tension-reduction after smoking, which may result from cholinergic/catecholaminergic activation followed by cholinergic blockade or betaendorphin release. Apparently smokers can adjust nicotine intake to enhance these effects selectively, which may add considerably to the appeal of smoking.

There has been a notable lack of dialogue between neuroscientists, who use nicotine in their work as they would any other pharmacological tool, and public policy and health researchers, who view nicotine dependence with increasing dismay and see the continued use of tobacco products as a modern day scourge. This special journal issue attempts to foster communication among nicotine researchers working along the continuum from basic to applied science. An additional objective is to convey a sense for the special problems and opportunities in the study of nicotine and tobacco use that may be of general interest to those concerned with substance abuse. The articles that follow explore two themes, (1) nicotine as a tool to probe neural activity, and (2) tobacco use as a health hazard and societal problem, by examining nicotine from pharmacochemical, biobehavioral, and econo-social perspectives. The rationale for the integration is that there may be benefits from viewing nicotine in a context broader than those dictated by custom and technological specialization.

The present study is an attempt to identify responses to alcohol-related stimuli which might differentiate alcoholics from non-alcoholics. The assumption was that alcoholics would be more reactive to alcohol cues because of prior conditioning history with respect to alcohol and drinking. Eight alcoholics in treatment were compared with ten non-alcoholic controls and two recovering alcoholics, using swallowing and salivation as the principal dependent measures. (The concordance of swallowing and salivation was validated using dental rolls with an independent group of ten alcoholics.) Five-minute "sniff-trials" were provided in which subjects smelled either cedar chips or their favorite alcoholic beverage, in a labelled container. Swallowing (salivation) and craving (desire to drink alcohol) were significantly elevated in alcohol-sniffing trials for alcoholics in treatment compared with non-alcoholics; cardiac rate and galvanic skin response duration were also elevated in alcoholics in treatment, though not significantly. Recovering alcoholics resembled alcoholics in treatment more closely than they resembled non-alcoholics. The data were examined in the context of conditioned withdrawal resembled non-alcoholics. The data were examined in the context of conditioned withdrawal and homeostatic protective mechanisms. Implications for the stimulus control analysis of drinking were discussed.

Smoking is the most important preventable risk factor for coronary heart disease. Reactivity to psychological stressors is also believed to be cardiopathologic. More recently, evidence has been accumulating that these putative risk factors in combination may be particularly harmful, both because smoking increases in stressful situations and because the cardiovascular effects of smoking combined with those of psychological stress may be greater than those of either alone. This paper reviews the literature on the cardiovascular effects of smoking and psychological stress in the light of epidemiological data and discusses mechanisms by which they may contribute to coronary heart disease.

Recent work on underlying mechanisms in substance abuse is reviewed using cigarette smoking as the focus. Smoking was chosen as an example because current technology makes possible laboratory research on underlying mechanisms without compromising relevance. A stimulus control model of smoking examining the contribution of environmental events is presented; the model is plausible but largely untested. A physiological control model of smoking examining the contribution of internal biochemical events is described; inconsistencies in research findings are discussed. For both models, implications for basic research and/or for treatment research are considered. A key premise is that research on underlying mechanisms may lead to rational therapies—treatments which are more effective than those currently available.

The antinociceptive effects of two different modes of nicotine administration were investigated using a within-subject design. Ten minimally-deprived, habitual smokers and fifteen ex-smokers were studied in separate experiments. Nicotine was delivered in research cigarettes and tobacco snuff. Pain was induced using the cold pressor test. Subjects in both experiments exhibited pain reduction after nicotine administration without changes in nicotine withdrawal. The results suggest that nicotine can produce physiological and psychological changes that are relevant to the reinforcement of smoking but are independent of the state of nicotine withdrawal.

The Fagerstrom Tolerance Questionnaire (TQ) is widely used in both clinical and research settings as a measure of physiological dependence on nicotine. In the light of claims that the efficacy of nicotine gum is related to degree of dependence and that outcomes can be improved by tailoring gum strength to degree of dependence, the availability of a simple, noninvasive test of dependence assumes additional importance. Recently, a number of articles have expressed reservations about various aspects of the TQ: 1) Several TQ items suffer from flaws or ambiguities that undermine their usefulness, and 2) the TQ may not measure what it purports to measure. The present paper reviews these issues, assembles data and observations that bear on the problems, and makes suggestions that may help in refining the TQ or producing a better instrument.

Recent analysis has shown the relevance of social and learning variables in the etiology and maintenance of psychotic behavior. While the token economy represents an improvement over traditional psychiatric treatment, it has been associated primarily with chronic, regressed psychiatric patients. The present paper describes a token economy designed for refractory psychiatric patients whose difficulties have resulted in repeated hospitalization and which has as its primary goal the modification of the behaviors which originally led to commitment. Patients are organized in hierarchies and pairs to promote mutual responsibility, to maintain orderly behavior, and to guarantee that assigned work is done. The psychiatric aide is freed from many of his custodial duties and his work schedule modified to allow him to participate in more therapeutic activities; in particular, aides accept responsibility for working with individual patients and receive cash incentives based on the improvement of assigned patients.