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Stressful stimuli have been reported to trigger increased smoking. The present experiment involved induction of differing levels of performance anxiety in 10 male smokers. In the high anxiety condition, subjects performed mental arithmetic with competitive pressure; in the low anxiety control condition, no competitive pressure was applied. Both sessions included smoking and sham smoking trials. Scores on the Profile of Mood States showed significantly more anxiety on the day of the high anxiety session than on the day of the low anxiety session, confirming the effectiveness of anxiety-induction procedures. Nicotine intake as inferred from topographical measures was significantly greater under conditions of high anxiety. Greater post-smoking decreases in anxiety in the high-anxiety condition, as compared to the low-anxiety condition and the two sham-smoking conditions, were also observed. Both smoking and anxiety level significantly increased heart rate; lack of statistical interaction suggests additive rather than potentiating effects. Peripheral skin temperature rose in response to mental arithmetic, a trend counteracted by smoking. No significant smoking-related changes in performance were found.

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.

Different ways of modifying the aide-patient relationship to promote improvement in psychiatric patients were investigated. Psychiatric aides were given information about the behavior of assigned patients, cash awards based on the improvement of assigned patients, and different kinds of supervision by the psychology staff; the effects of these variables on a large number of psychiatrically relevant behaviors were measured. Appropriate behavior of patients increased when the aides were given quantitative information about the improvement of assigned patients. Cash awards for aides, which were not contingent on the behavior of patients had little effect, while cash awards contingent on the behavior of assigned patients were associated with more appropriate behavior. Direct supervision of aide-patient interactions was associated with an increase in appropriate behavior, while required consultation for the aides about assigned patients was not. Behavior of patients deteriorated when the program was terminated.

EKG’s of chair-restrained Rhesus monkeys were recorded using 1. implantation of subdermal electrodes, and 2. surface electrodes. Both procedures resulted in reliable registration of EKG’s in experiments involving both Pavlovian and instrumental conditioning and recording. The advantages and disadvantages of the methods are discussed and detailed instructions for implementation are given.

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.

The effects of Pavlovian conditioning on diurnal cardiac rate were studied in four rhesus monkeys. A three-hour conditioning period, consisting of 18 CS-UCS pairings with UCS an aversive tail-shock, produced cardiac-rate elevation which persisted for as long as 12 hours after the session.

Acute administration of mecamylamine, a centrally active nicotinic cholinergic agonist, has been shown to increase amount of smoking as indicated by smoking topography (e.g., puff rate, puff duration), expired carbon monoxide changes, and other inferential measures. In the present study, subjects showed significantly greater increases in plasma nicotine following smoking of two high-nicotine research cigarettes when pretreated with mecamylamine than when pretreated with placebo, even though no significant differences in puff volume or puff number were detected. Interestingly, none of our subjects reported nausea, although some achieved plasma nicotine levels at which nausea would typically be expected. We attribute the observed increases in nicotine intake to compensatory behavior designed to overcome mecamylamine's blocking effects.

The antinociceptive and anxiolytic consequences of smoking a nicotine-containing cigarette or a zero-nicotine cigarette were investigated in minimally deprived habitual smokers, using a within-subject design. Five subjects were studied in each of two experiments. In one, pain was induced using the cold pressor test; in the other, anxiety, using unsolvable anagrams. All subjects exhibited pain- and anxiety-reduction after smoking a nicotine-containing cigarette. The results support the hypothesis that nicotine from smoking can produce psychological changes that are independent of the state of nicotine withdrawal.

This laboratory has previously reported increases in arginine vasopressin, neurophysin I, and beta-endorphin/beta-lipotropin in conjunction with relatively high plasma nicotine levels in subjects not experiencing nausea. The present study further explores the hormonal and neuropeptide responses provoked by nicotine from smoking. Nausea was induced in deprived smokers by having them smoke 2 high-nicotine cigarettes (2.87 mg.) in succession. Subjects who reported nausea showed a less selective release of pituitary hormones than previously observed at sub-nausea: Plasma levels of adrenocorticotropic hormone, arginine vasopressin, beta-endorphin/beta-lipotropin, growth hormone, neurophysin I, and prolactin increased over baseline; no increases were seen in follicle-stimulating hormone, luteinizing hormone, or thyroid-stimulating hormone. Nausea and significantly elevated pituitary hormone release were consistently associated with plasma nicotine levels exceeding 60 ng/ml produced by smoking high-nicotine cigarettes, but did not occur in response to low-nicotine (0.48 mg.) cigarettes (plasma nicotine levels below 10 ng/ml). Because the hormonal profile associated with nicotine-induced nausea resembles that of nausea produced by other manipulations (motion sickness, administration of other drugs), it is likely that the observed hormonal pattern at this level of stimulation is characteristic of nausea and not unique to nicotine.

Recent scientific research challenges a number of traditional assumptions in the treatment of alcoholism. Two major tenets, the disease conception of alcoholism and mandatory abstinence as a goal of treatment are reviewed, and insufficient evidence is found to support a dogmatic position on either.

The relationship among changes in plasma nicotine, ACTH, and cortisol secretion after smoking were investigated. Ten male subjects smoked cigarettes containing 2.87 mg nicotine and 0.48 mg nicotine. No rises in cortisol or ACTH were detected after smoking 0.48 mg nicotine cigarettes. Cortisol rises were significant in 11 of 15 instances after smoking 2.87 mg nicotine cigarettes, but ACTH rose significantly in only 5 of the 11 instances where cortisol increased. Each ACTH rise occurred in a subject who reported nausea and was observed to be pale, sweaty, and tachycardic. Peak plasma nicotine concentrations were not significantly different in sessions when cortisol rose with or without ACTH increases, but cortisol increases were significantly greater in nauseated than in non-nauseated smokers. Our data suggest that smoking-induced nausea stimulates cortisol release by stimulating ACTH secretion and that cortisol secretion in non-nauseated smokers may occur through a non-ACTH mechanism. It is not clear whether nicotine or some other stimulus inherent in smoking is responsible for cortisol secretion without ACTH secretion.

Groups of middle-income outpatient problem drinkiers were randomly assigned to one of two treatments: a multicomponent positive reinforcement procedure emphasizing moderation, or "traditional" denial-confrontation therapy emphasizing abstinence. There were no significant differences between participants assigned to the two procedures with respect to pretreatment characteristics. Participants reduced their alcohol consumption significantly in both treatments. Behavioral participants reduced alcohol consumption significantly during therapy, whereas traditional participants reduced significantly prior to therapy. Significantly more traditional participants dropped out of therapy than did behavioral. The data suggested that the effects of traditional therapy were mixed, helping those participants who were receptive, driving out those who were not; moreover, reduced consumption seemed to be more the result of compliance with initial therapist demands (made during the screening period) than the effect of denial-confrontation in subsequent therapy. Behavioral treatment was more successful in several indicators of outcome; the improvement observed seemed to be attributable to the active therapeutic techniques employed.

Various psychological procedures for treating problem drinking have been proposed over the years (Pomerleau, 1977). Few suggestions have been as controversal as behavioral treatment using controlled drinking — the idea the alcoholics might be able to learn to moderate their drinking as a result of therapy. Interest in controlled drinking was started by reports of “spontaneous” moderation in former alcoholics (Davies, 1962) and has received considerable momentum from the lack of scientific support for the theoretical basis for mandatory abstinence (Lloyd and Salzberg, 1975; Pomerleau, Pertschuk, and Stinnett, 1976). While much careful investigation still needs to be done, initial results on controlled drinking have been promising.

Nausea was induced by having subjects smoke two high nicotine cigarettes in quick succession. Plasma levels of prolactin, adrenocorticotropic hormone, beta-endorphin/beta-lipotropin, growth hormone, arginine vasopressin, and neurophysin I increased without changes in thyroid stimulating hormone, luteinizing hormone, or follicle stimulating hormone. Nausea and pituitary hormone release correlated with high nicotine intake (smoking 2.87 mg nicotine cigarettes) but did not occur during lower nicotine intake (smoking 0.48 mg nicotine cigarettes). Individual differences in nausea and related hormonal responses may provide an objective method for predicting receptivity to smoking.

To assess the psychological effects of smoking cessation, 21 subjects in a smoking treatment program were evaluated at the beginning of therapy and 4 months later. No differences were observed in reported affect, use of mental health facilities, psychotropic medications, or alcohol. A statistically but not clinically significant weight increase was observed. It is concluded that within some contexts smoking cessation need not be as stressful as popularly depicted.

The present study explored neuropeptide responses to nicotine from smoking. Habitual smokers smoked research cigarettes of known strength under controlled laboratory conditions while blood samples were withdrawn unobtrusively for subsequent biochemical analysis. To provide a metric that reflected total nicotine intake and total neurohormonal output, data were integrated over time. Subjects were relatively unresponsive in the low-nicotine (0.48 mg) condition. In the high-nicotine (2.87 mg) condition, there were significant positive correlations between integrated plasma nicotine and plasma arginine vasopressin (r = +0.985), its carrier protein neurophysin I (r = +0.944), and beta-endorphin-beta-lipotropin (r = +0.977), but not adrenocorticotropic hormone. Data from an experiment that used an extraction step to remove beta-lipotropin corroborated the functional relationship between plasma nicotine and beta-endorphin implied by the original findings. Taking into account recent research on the role of neuropeptides in the modulation of affective states and cognitive function as well as of other CNS activity, the present findings were interpreted as strengthening the hypothesis that nicotine-stimulated neuropeptide release provides positive reinforcement for smoking.

Alteration in neuroendocrine activity associated with the regulation of energy metabolism and food intake may play a role in characterizing the alcohol dependent state. Alcoholics, when compared to controls, demonstrated significantly larger and more rapid glucose and insulin responses following the consumption of a placebo beer, which they believed contained alcohol. The existence of significant correlations between peak neuroendocrine responses and desire to drink, anxiety, as well as psychophysiological responses in alcoholics suggests the potential multivariate nature of the biological/behavioral state associated with alcohol dependence.

1. 1. The behaviorally based constructs of DSM-III have differentiated alcohol abuse and dependence, wherein the latter has been characterized by: (1) a history of tolerance and physical dependence; and (2) a history of pathological drinking patterns and/or problems consequent to drinking behavior (APA-DSM III 1980). In contrast, ICD-9 refers to an alcohol dependence syndrome which follows the model proposed by Edwards and Gross in 1976. The WHO memorandum on nomenclature and classification of drug and alcohol related problems has further proposed that alcohol dependence be defined along a continuum of severity, and that dependence be differentiated from severity of alcohol related disabilities (Edwards et al. 1981). In many respects, the alcohol dependence syndrome construct is consistent with Jellinek's disease concept of alcoholism which had its antecedents in medical writings of the late eighteenth and early nineteenth centuries (Lender 1979). 2. 2. Commencing in the early 1960's, many behavioral and social scientists were critical of the disease model of alcoholism. Behavioral researchers found that the drinking behavior of alcoholic subjects could be controlled by its consequences in the laboratory, suggesting that drinking behavior was like any operant. Longitudinal studies of drinking practices suggested that relapse to dependent drinking did not appear to be inevitable. In general, these researchers have utilized behavioral and epidemiological data to prove the null hypothesis: that there was no biological disease behind alcohol addiction. 3. 3. In contrast to the operant studies which served to rebut the disease construct, Ludwig and associates employed a model of Pavlovian conditioning which suggested a relationship between an alcoholic's desire to drink and an increase in autonomie arousal associated with the presence of alcohol (Ludwig et al. 1977). These investigators hypothesized that the arousal represented a subclinical conditioned withdrawal syndrome, and that the elicited psychophysiological responses were opposite from those elicited by actual alcohol consumption. Our group, Kaplan et al. 1983, at the University of Connecticut has confirmed Ludwig's findings regarding the relationship between physiological arousal and craving in the presence of alcoholic beverages (in alcoholic but not control subjects), and has further extended research in this area. The authors have postulated that dependent alcoholics experience a “state change” which may be defined on the basis of subjective and biological responses to alcohol related stimuli and beverage consumption. They have found that there is a significant relationship between severity of alcohol dependence in the last 30 days prior to admission to a treatment program and: (1) increase in skin conductance in response to the presentation of a glass which the subject presumes to contain beer; (2) likelihood of responding to a placebo beverage as though it contained real beer; (3) likelihood of choosing beverage alcohol as a reward for the completion of an operant task. Our colleagues at The University of Connecticut have also demonstrated a relationship between increase in skin conductance and increase in subjective desire to drink in alcoholics but not in control subjects; as well as a relationship between increase in desire to drink and increase in salivation in alcoholic but not control subjects (Pomerleau et al. 1983). 4. 4. In pilot studies designed to further define the biological dimensions associated with craving in the alcoholic, the authors have been examining certain endocrine responses in alcoholic and control subjects as they anticipate beer consumption, and after they consume a placebo beverage which they believe to be real beer. Alcoholics, but not controls, experience a significant decrease in serum testosterone as they hold and smell a glass of beer (Morse et al. 1985). Subsequent administration of placebo beer was followed by a return of testosterone levels to baseline, while alcoholics then demonstrated a sharp elevation in plasma insulin and a moderate increase in plasma glucose during this time period (Dolinsky et al. 1985). Changes in glucagon and Cortisol did not adequately account for the changes observed in insulin and glucose. There was a satistically significant correlation between changes in insulin and changes in craving and anxiety. 5. 5. The authors believe that the use of psychophysiological and biochemical data to assess some of the biological dimensions of craving represents a promising approach to defining the alcohol dependent state. Traditionally, alcohol dependence has been defined clinically, and more recently has been defined in the context of questionnaire data. At this writing there is a need to define biological and behavioral criteria which can be used to quantify alcohol dependence, and to clarify the relationship between the development of alcohol dependence and the various risk factors (including genetic) and consequences which influence its course.

The present study was conducted to examine the effects of acute aerobic exercise on smoking behavior. On alternate days, 10 healthy young smokers were subjected to half an hour of sustained high exercise (about 56% of maximum work capacity) or of low exercise (about 28% of maximum, simulating normal daytime activity). During the high-exercise condition, there were pronounced increases in physiological markers of physical activity such as mean work, heart rate, and lactic acid as well as elevations in circulating hormones (norepinephrine, epinephrine, and immunoreactive beta-endorphin and cortisol) known to be affected by vigorous exercise. Despite a trend toward decreased desire for cigarettes after the high exercise condition, there were no differences in plasma nicotine levels following the smoking of a usual-brand cigarette 35 min later. The sustained effects of the two exercise conditions were also similar: plasma cotinine levels 24 hr later (reflecting nicotine intake over the entire exercise day) revealed no significant differences between hight and low exercise.

Cardiac rates of rhesus monkeys were observed in a variety of different conditioning procedures, each of which involved a visual stimulus (CS) followed by an electric shock (US). With a 30-sec CS, cardiac rate accelerated rapidly after CS onset, reached a maximum in the middle of CS, and decelerated thereafter, with a terminal CS rate often at the level of, or below, pre-CS levels. A similar biphasic cardiac rate response in CS was also observed under subsequent exposure to intermittent pairings of CS and US, avoidance of US, response-produced termination of US, and when CS-US pairings were superimposed upon an avoidance baseline, even when CS duration was varied from 12 to 60 seconds. The unusual regularity of cardiac rate responses in several different procedures may result from one or more of these factors: (a) characteristics of the rhesus monkey, (b) initial exposure to Pavlovian conditioning, or (c) the uniformity of measurement of cardiac rate employed in this study.

The use of three electrodes to produce digitizable EKG’s and to deliver shocks to the tail of the monkey is described. Cardiac signals are taken from a head electrode and a “ground” tail electrode. Shock is administered through a “hot” tail electrode and the “ground” tail electrode.