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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 BMIor = 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.

Smoking is becoming increasingly concentrated in people with co-factors such as depression, attention deficit-hyperactivity disorder, anxiety disorders, and bulimia/bingeing. These behavioral or cognitive patterns may be adaptive or neutral in the conditions under which we evolved but maladaptive in environments requiring alertness for extended periods, where a fully mobilized fight-or-flight response is inappropriate, and where food availability makes lack of an "appestat" a liability. Such conditions are amenable to management by nicotine because of its ability to produce small but reliable adjustments in relevant cognitive and behavioral functions. Moreover, symptomatology may be unmasked or exacerbated by nicotine abstinence, persisting beyond the usual time-course for nicotine withdrawal, which may explain the particular attraction of smoking and the difficulty these individuals experience in quitting without necessarily requiring that they be more nicotine-dependent. The implications are: (1) a better understanding of the evolutionary psychobiology of smoking may promote development of tailored interventions for smokers with co-factors; (2) nicotine may have therapeutic applications for non-smokers with co-factors; (3) because smoking has a fairly high heritability index, and because of evidence of assortative mating, special prevention efforts targeting children of smokers with co-factors, as well as early identification of the co-factor itself, may be needed.

Because initial reinforcement consequences set the stage for subsequent nicotine use, elucidation of the contribution of environmental and inherited factors is crucial to an understanding of nicotine dependence as well as of individual differences in susceptibility to cigarette smoking. A review of some recent animal research and laboratory studies of smokers and never-smokers suggests that vulnerability to nicotine dependence is related to high initial sensitivity to nicotine and that the development of acute pharmacodynamic tolerance in these individuals--particularly to effects of nicotine that are toxic or aversive--may be an adaptation for protecting homeostasis.

Numerous observers have reported that smokers smoke more under stressful conditions. The most frequent explanation is that nicotine reduces anxiety, an intervening variable identified as a negative reinforcer for smoking behaviour. The conditions under which anxiety reduction occurs in response to smoking, however, have not been well defined, nor are underlying mechanisms well understood. There are several possible explanations, including Schachter's theory based on stress-induced changes in urinary pH and the hypothesis of endogenous opioid involvement. The work of Collins and his associates in animals has shown that genetic variations in corticosteroid responsiveness to nicotine are associated with differences in sensitivity to nicotine. Research in our laboratory has extended to humans Collins' findings that sensitivity to nicotine is inversely related to corticosteroid activity. We also found that the combination of a psychological stressor and smoking produced additive effects on cortisol release in humans. These findings suggest a novel way of explaining the interaction between smoking and stress, in that increased nicotine intake in the context of stress may in part reflect behavioural compensation for diminished sensitivity to nicotine when corticosteroid activity is enhanced by the stressor.

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.

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.

The Fagerström 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.