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PubMed1977

Assessing the alcoholic's disposition to drink.

Reliable and valid techniques for assessing the alcoholic's disposition to drink would allow researchers to address many issues of clinical significance. This paper reviews some basic issues in behavioral assessment techniques, proposes several criteria for a reasonably general technique for assessing disposition to drink, and presents evidence relevant to the validity of one behavioral measure of disposition to drink. A study is presented which focuses on distinguishing good from poor treatment outcome subjects on the basis of their response patterns for alcohol during a simulated drinking binge. Alcoholic subjects were assigned to one of two treatment outcome groups based on treatment success evaluated at follow-up two months after hospital discharge. An analysis of the alcoholic's response patterns for alcohol during a simulated drinking binge revealed that good outcome subjects showed decreases in disposition to drink as their blood alcohol levels (BAL) rose, while poor outcome subjects showed increases in disposition to drink as their BAL increased. These results indicate that individual differences in behavioral response to alcoholization and withdrawal can index the alcoholic's potential for readdiction and relapse subsequent to hospital treatment and illustrate the role which behavioral assessment techniques can play in developing and refining models of human alcohol abuse.

Adult↗
PubMed1984

Life stressors and problem drinking among older adults.

Research on the prevalence of excessive drinking among persons age 60 and older is reviewed, and the inadequacy of general criteria for operationally defining problem drinking in this population is pointed out. We critically examine the empirical evidence relating life stressors (e.g., death of a spouse) to the onset of problem drinking in older age and, to a lesser extent, to the continuation of drinking problems into the later stages of the life cycle. Potential mediators and moderators of the stress-problem drinking relationship (e.g., personal coping methods and social resources) have generally been ignored in this research. Life stress is probably best viewed as a component of one or more of several combinations of factors that may trigger or perpetuate drinking problems. A comprehensive conceptual framework to guide future research is presented. The use of such a framework should serve to integrate research on problem drinking among older persons with work in the general field of adaptation to life stress.

Aged↗
PubMed1987

Social drinking as a health and psychosocial risk factor. Anstie's limit revisited.

This chapter reviews empirical evidence dealing with the risk of using beverage alcohol in quantities generally considered to be within the range of moderate or social drinking. It begins with a discussion of terms and concepts typically employed to define the limits of moderate and social drinking. The historical debate over moderate drinking is considered next, using Francis Anstie's daily limit of 1.5 oz of absolute ethanol as an example of an influential and enduring approach to this issue. The scientific evidence relevant to the association between moderate drinking and damage is reviewed in sections dealing with the risks of acute ingestion of alcohol and the hazards of chronic drinking. In a final section, a multidimensional model of risk is developed to serve as a basis for early intervention and prevention planning. It is concluded that both social and moderate drinking entail risk of health hazards and psychosocial consequences. These risks are not always a direct function of the amount of ethanol consumed but rather reflect complex interactions among a host of antecedent and mediating variables. When these are taken into account, a better estimate of the relative risk of different consequences of drinking can be made.

Alcohol Drinking↗
PubMed1983

Effects of naloxone and naltrexone on the increased water intake and drinking duration in phenobarbitone-treated rats.

In two experiments, phenobarbitone sodium (30 mg/kg) reliably enhanced water consumption and extended the duration of drinking in 24h water-deprived male rats. The opiate receptor antagonists naloxone (0.1-10 mg/kg) and naltrexone (0.1-10 mg/kg) both decreased water intake and reduced the duration of drinking. When the barbiturate was given in conjunction with either naloxone or naltrexone, phenobarbitone and the opiate antagonist exerted opposite effects on the two measures of drinking. While it was true that both opiate antagonists reduced water intake and drinking duration in barbiturate-treated animals, the barbiturate-induced enhancement of drinking was in no way modified by concurrent opiate antagonist treatment. Hence, the effects of phenobarbitone and of the two opiate antagonists upon the drinking measures appeared to be quite independent. There was no evidence, therefore, that the effects of phenobarbitone upon drinking were related to endogenous opioid mechanisms. The possible contrast between benzodiazepine- and barbiturate-induced hyperdipsia is briefly considered in the light of these results.

Animals↗
PubMed1979

Water intake and time course of drinking after single or repeated chlordiazepoxide injections.

Chlordiazepoxide (5.0, 10.0 or 15.0 mg/kg) was given to rats either acutely or for 9 consecutive days. Its effects were examined in a 15-min drinking test in which latency to drink, volume of water consumption and the time-course of drinking were measured. Chlordiazepoxide (10.0 mg/kg) produced the strongest stimulant effect on drinking and enhanced the frequency of occurrence of drinking both at the beginning and at the end of the test period. Chlordiazepoxide (15.0 mg/kg) delayed the onset of drinking and its peak effect was observed later than for other injection conditions. Single and repeated administration of chlordiazepoxide had the same effects on the measures taken in the test. Initial sedation to the drug treatment and subsequent tolerance to this effect were not, therefore, factors influencing the drug effects observed in this experiment. Possible mechanisms underlying the stimulation of drinking by chlordiazepoxide are considered.

Animals↗
PubMed1979

Relationship of sociodemographic and drinking variables to differentiated subgroups of alcoholics.

The results suggest that the sociodemographic variables of age, living arrangements, number of dependents, the drinking variable, and the client's perception of the type of drinker he is are the most strongly related to the derived typology. The exact relationship of these variables, as well as the variables that were moderately related to the typology, is not apparent. There is a pattern, however, that appears to run through the categories of the classification. The evidence suggests that for alcoholics to be in their prime earning years, living with their spouses, perceiving themselves as alcoholic, possessing marketable skills, and a recent history of abstinence seems to increase the likelihood of psychological need satisfaction. The antithesis--to be alcoholic, less than 30 or older than 50 years old, living by oneself or with parents, perceiving oneself as a social or problem drinker, and possessing a recent history of drinking--seems to decrease the likelihood of psychological need satisfaction. There seems to be a relationship between drinking behavior and psychological need satisfaction. As a group, the members of Clusters Two, Three, and Four are unable to abstain for longer than a week; Clusters Two and Three both possess physiological problems of adjustment. The members of Clusters One and Five tend to be able to abstain for longer periods. Cluster One is devoid of physiological difficulties, whereas Five has borderline problems. The physiological subscale of the Human Service Scale assesses the absence of symptoms associated with poor health (Realges & Butler, 1976). It appears that aberrant drinking does not necessarily result in self-perceived physiological-health complaints. These results are at variance with the belief that ethanol ingestion by an alcoholic and the resulting pathological complications are the predominant difficulties encountered by these persons. Thus it seems to us that a distraught life situation (that is, the lack of social and demographic assets--marriage, education, and so on) contributes to self-perceived severity of psychological need deprivation and not solely aberrant drinking. Therefore, in terms of recovery from alcoholism, these results argue against a unidimensional approach toward the treatment of alcoholism; that is, an approach that focuses solely on the drinking as "the" problem. A more strategic approach would include a thorough medical, psychiatric, psychological, social and vocational evaluation of the alcoholic's life situation, which in turn would permit mobilizing the efforts of a multidisciplinary team whose goal would be to maximize the resources and enhance the life situation of the alcoholic. It is hoped that the results of this study serve to increase our understanding of those factors that influence aberrant drinking.

Adult↗
PubMed1992

Familial transmission of alcohol use: V. Drinking patterns among spouses, Tecumseh, Michigan.

This study examined concordance and discordance of self-reported alcohol consumption in 184 spouse pairs drawn from a representative sample of the Tecumseh, MI community. A significant association (tau B = .57, p less than .001) between self-reported alcohol consumption of husbands and that of wives was observed. Drinking daily and high maximum drinking were also significantly correlated between spouses, as were church attendance, smoking, impulsivity, and sociability. A significant association between the drinking of wives and that of their mothers-in-law was noted. The relationship between husbands' drinking and that of their fathers-in-law was marginally significant. However, three-quarters of daughters of heavy-drinking fathers (21 of 28) married abstemious men (never drank or drank lightly), while only 7% married heavy-drinking husbands. These findings lend support to the idea that a network of familial influences--both primary and secondary assortative mating--contributes to regulating adult drinking behavior.

Adult↗
PubMed1997

Opiate agonists microinjected into the nucleus accumbens enhance sucrose drinking in rats.

Previous studies have indicated that central opioid peptides and opiate receptors play an important role in the modulation of ingestive behaviors. The nucleus accumbens (Acb), a forebrain region involved in reinforcement, contains high levels of opiate receptors. The present investigation was undertaken to determine the relative involvement of opiate receptor subtypes in sucrose drinking. Morphine (0, 0.5, 5 micrograms/0.5 microliter), the mu agonist D-Ala2, NMe-Phe4, Glyo 15-enkephalin (DAMGO; 0, 0.025, 0.25 and 2.5 micrograms/0.5 microliter), the delta agonist D-Pen2,5-enkephalin (DPEN; 0, 0.031, 0.31, 3.1 micrograms/0.5 microliter), and the kappa agonists U50488H (0, 0.0186, 0.186, 1.86 micrograms/0.5 microliter), and dynorphin (0, 0.05, 0.5, 5 micrograms/0.5 microliter) were microinfused into Acb. Intake of 5% sucrose, drinking duration, locomotion, rearing, and grooming were measured in a 30-min session in rats previously adapted to sucrose. After microinjection into Acb, morphine induced a robust increase in both sucrose intake and drinking duration at the low dose. DAMGO enhanced sucrose drinking at lower doses, and suppressed drinking at the highest dose. DPEN also increased sucrose intake in a dose-dependent manner. U50488H and dynorphin had no effect on sucrose drinking. In addition, it was demonstrated that intra-Acb administration of DAMGO specifically enhanced palatable sweet solution drinking, leaving water intake unchanged. Although mu and delta agonists tended to increase spontaneous motor activity, the pattern of effects indicated that increases in ingestion could not be simply attributed to general arousal. These findings demonstrate that both mu and delta receptors within the accumbens may have an important modulatory role in ingestion of palatable substances.

Analgesics, Opioid↗
PubMed2005

Sexual maturation in early adolescence and alcohol drinking and cigarette smoking in late adolescence: a prospective study of 2,129 Norwegian girls and boys.

Early sexual maturation has been associated with higher involvement in risk behaviour during early and mid-adolescence. In a prospective study of 2,129 girls and boys, we investigated whether the timing of sexual maturation was associated with cigarette smoking and alcohol drinking in late adolescence and whether this relation differed between boys and girls. Nine hundred and eighty boys and 1,149 girls, who participated in a cross-sectional study in middle school, were included in a follow-up study in high school 4 years later. Self-rating of pubertal status, as registered at baseline in middle school, was used to indicate the timing of sexual maturation. Age-adjusted odds ratios (ORs) with 95% confidence intervals (CIs), estimated by logistic regression, were used to assess the association between sexual maturation and alcohol drinking and daily smoking at follow-up. We found that girls who had matured early (OR 1.7, CI 1.2-2.4) or late (OR, 1.5, CI, 1.1-2.2) were both more likely to report more advanced drinking in late adolescence than were girls who were on time. Boys who had matured late were less likely (OR 0.5, CI 0.3-0.8) than boys who were on time to engage in advanced drinking. In general, daily smoking was more common among girls than boys, and more common among girls who had matured early (OR 1.5, CI 1.1-2.2) than among girls who were on time. Adjustment for social factors, e.g. parental education and marital status and parental drinking and smoking habits, did not substantially influence these results. We concluded that, for girls, but not for boys, early sexual maturation was associated with more advanced drinking and higher frequency of smoking in late adolescence. In boys, late sexual maturation was associated with reduced risk of advanced drinking.

Adolescent↗
PubMed1994

Heavy drinking and the risk of occupational injury.

This study evaluated the association between the frequency of heavy drinking and the risk of occupational injury, using nationally representative data from the 1988 National Health Interview Survey (NHIS). The sample consisted of 29,192 adults who were employed at some time during the year preceding the NHIS interview. Overall, 7.2% reported an on-the-job injury during the preceding year, but the rates were higher--about 13%--for those employed as skilled or unskilled laborers or who reported engaging in repeated strenuous physical activity at work. Slightly more than one-fourth of the employed adults reported at least one occasion of drinking five or more drinks during the preceding year. After adjusting for the effects of age, gender, education, occupation, and strenuous job activity, the odds of occupational injury increased with frequency of heavy drinking, with odds ratios varying from 1.08 (one occasion of heavy drinking) to 1.74 (daily heavy drinking). Odds ratios were decreased slightly by the inclusion of smoking as a control variable, indicating that some of the excess risk of injury among heavy drinkers may reflect their greater propensity to take health-related risks rather than direct effects of ethanol. The odds ratios also were slightly lower when the analysis was restricted to current drinkers, suggesting that the risk of work injury was increased by light or moderate as well as heavy drinking.

Accidents, Occupational↗
PubMed1975

Analysis of various factors involved in EEG synchronization during milk drinking in the cat.

Electroencephalographic (EEG) and multineuronal activity (MUA) from several brain structures were recorded in 11 adult cats during milk drinking. Milk drinking elicited parietal and hippocampal EEG synchronization and inhibited multiunit discharge in several brain regions. The proportion of EEG synchronization varied considerably between animals, but remained more or less constant for each cat after several testing days. Neither modification of milk concentration nor fasting influenced the proportions of EEG synchronization during milk drinking. Adaptation of the animals to the experimental environment facilitated the appearance of EEG synchronization during milk drinking. Chlorpromazine (3 mg/kg) significantly increased the proportion of EEG synchronization observed during milk drinking. By contrast, displacement of the head, neck or postural body adjustments during milk drinking blocked EEG synchronization. Amphetamine also had a suppressive effect on the EEG parietal and hippocampal synchronic activity observed during milk drinking. Our results suggest that development of parietal EEG synchronization in response to pleasant stimulation is a complex phenomenon requiring a relaxed condition of the animal, including its adaptation to the experimental environment and relative immobility with the concomitant diminution of afferent inflow from some of the muscles involved in locomotion.

Amphetamine↗
PubMed1978

Petide antagonists of the renin-angiotensin system in the characterisation of receptors for angiotensin-induced drinking.

The two naturally occurring analogues of angiotensin II (AII), Asp1-Val5-AII and Asp1-Ile5-AII, were equally effective as intracranial dipsogens in the water-replete rat. Renin, synthetic tetradecapeptide renin substrate (SRS) and angiotensin I (AI) also produced copious drinking when injected into the brain, but the naturally occurring renin substrate of rat caused little drinking and was much less effective than SRS. Prior intracranial injection of pepstatin, a competitive antagonist of the renin-angiotensinogen reaction, reduced drinking in response to renin and SRS but not to AI and AII. Renin-, SRS- and AI-induced drinking were inhibited by the converting enzyme inhibitor SQ 20881 injected through the same intracranial cannula in antagonist to agonist ratio of 1000:1, whereas the AII response was enhanced, although not significantly so, and the carbachol response was unaffected. Finally, position 8 aliphatic substituted analogues of AII were competitive antagonists of AII-induced drinking, and also inhibited drinking induced by renin, SRS and AI injected through the same intracranial cannula, but they did not inhibit carbachol-induced drinking. In conclusion, the angiotensin-sensitive receptor for thirst does not accept SRS or AI. It responds best to AII.

Angiotensin II↗
PubMed1991

Potentiation of angiotensin II-induced drinking by glucocorticoids is a specific glucocorticoid type II receptor (GR)-mediated event.

Earlier studies showed that pretreatment (3 and 6 h) of rats with the glucocorticoid hormone, dexamethasone, potentiated the drinking response to either central or peripheral administration of angiotensin II (AII). In the present study the specificity and mechanisms of this potentiation were examined. Intraperitoneal (i.p.) injection of rats with the pure glucocorticoid agonist, RU 28362 (0.4-1.6 mg/kg; 3-24 h), resulted in a time- and dose-dependent potentiation of the drinking responses to either peripherally (100 micrograms/kg, s.c.) or centrally (10 ng) injected AII, similar to the effects of dexamethasone. Drinking induced by central injection of carbachol (200 ng) was unaltered by pretreatment with RU 28362, suggesting that potentiation by this compound was specific for AII. The potentiation of AII-induced drinking by either dexamethasone or RU 28362 was completely abolished by pretreatment with the glucocorticoid Type II receptor (GR) antagonist, RU 38486 (2 mg/kg, i.p.), but not by the mineralocorticoid Type I receptor (MR) blocker, mespirenone (2 mg/kg, i.p.). Taken together, these results indicate that the glucocorticoid-induced potentiation of AII-induced drinking is mediated via GR. Associated with the fact that glucocorticoids potentiate AII-induced drinking is the observation that these steroids also potentiate AII-induced urine output. This enhancement of urine output may explain in part the potentiation in drinking behavior. Possible mechanisms are discussed.

Androstanols↗
PubMed1981

Suppression of drinking by naloxone in the rat: a further characterization.

The effects of naloxone, an opiate antagonist, were examined on drinking induced by various dipsogenic stimuli. In rats deprived of water for 24 h, naloxone (0.1-10 mg/kg) produced a dose-related suppression of drinking immediately following water presentation but did not alter the latency to begin drinking. Naloxone also produced a dose-related suppression of water consumption induced by isoproterenol and angiotensin II, agents simulating conditions of extracellular dehydration. Naltrexone, a congener of naloxone, was more potent than naloxone in reducing isoproterenol-induced water intake. Schedule-induced polydipsia, which occurs in the absence of body fluid deficits, was not altered by either naloxone or naltrexone at doses attenuating drinking induced by the other methods. These data suggest that the suppressant effects of naloxone on water consumption are not a manifestation of an increased latency to drink or an impairment in the motor components of drinking activity. Furthermore, narcotic antagonists appear to attenuate regulatory, but not adjunctive drinking.

Angiotensin II↗
PubMed1989

Altered spontaneous and osmotically induced drinking for fowls with permanent access to dilute quinine.

Fowls were given a dilute quinine solution as their sole source of fluid, and effects on normal ingestion and on drinking responses to dipsogenic stimuli were examined. Compared to controls with water, daily fluid intakes were depressed by 25% with quinine. There was no significant effect of quinine on food intake, but growth was suppressed slightly. Drinking in response to hypertonic NaCl injections was attenuated with quinine, and whereas an initial peak in water intake was seen directly after hypertonic NaCl injection, this was absent with quinine. Moreover, increases in quinine intake after hypertonic NaCl injections were insufficient to restore normal osmolality. Plasma analyses indicated that birds drinking quinine were permanently dehydrated and, unlike birds with water, they appeared to reduce the hyperosmolality induced by hypertonic NaCl injections in the absence of drinking. In contrast, drinking responses to angiotensin were generally similar with quinine and water, although birds drinking quinine tended to stop sooner with the highest dose of angiotensin. These results support previous suggestions that osmotic thirst is of primary importance in control of normal drinking, but also demonstrate that birds tolerate a degree of dehydration if a suitable fluid source is unavailable.

Angiotensin II↗
PubMed1993

Functional mapping of the rat brain during drinking behavior: a fluorodeoxyglucose study.

Autoradiographic techniques using the radiolabeled glucose analog [14C]2-fluoro-2-deoxy-D-glucose (FDG) were used to map the functional activity in the CNS during drinking behavior. Rats were trained to drink water during a 1-h session each day. Half of the rats were injected with FDG and allowed to drink, while the other half were satiated prior to FDG injection. Uptake of FDG for drinking and control groups of rats was quantified in 60 brain structures from frontal cortex to cervical spinal cord. The largest percent increase in activity (96%) during drinking was in the lateral hypothalamus. Limbic structures with significant metabolic increases included the lateral septum (48%), lateral habenula (44%), and nucleus accumbens (32%). Thalamic nuclei activated included intralaminar (60%), zona incerta (51%), ventroposteromedial (50%), anterior ventral (47%), and dorsal medial (40%). Other structures with increases were the caudal caudate nucleus (53%) and the spinal trigeminal nucleus (45%). The findings were interpreted in light of related metabolic mapping studies of the effects of orofacial stimulation, dehydration, ingestion, arousal, and reward. It was concluded that this FDG study revealed primarily the involvement of structures linked to rewarding and arousal components of motivated drinking behavior, as well as sensorimotor correlates of the orofacial stimulation. The findings provide the first comprehensive functional map of brain systems related to drinking behavior in adult animals.

Animals↗
PubMed1976

Effects of angiotensin on drinking.

A series of four experiments was carried out to assess the effects of angiotensin II on drinking elicited by various types of stimulation. Experimental I examined the effects of the interaction of 2 cc/kg of 5% NaCl plus 0.2 mg/kg angiotensin II on ad lib eating and drinking. Results indicate that NaCl plus angiotensin produced an additive enhancement in water consumption. Experiment 2 was conducted to investigate the effects of 0.2, 0.4, 0.8, 1.2, and 1.6 mg/kg of angiotensin II on drinking and eating in 23 hr water deprived animals. Dose related increases in drinking alone were observed. In Experiment 3 the effects of 0.4, 0.8, 1.2, and 1.6 mg/kg of angiotensin II on schedule dependent lever pressing and schedule induced drinking and licking were determined. Results demonstrate that angiotensin II decreased lever pressing and increased schedule induced water consumption without a concomitant increase in licking. Experimental 4 examined the effects of the same doses of angiotensin II on prandal drinking in food deprived animals. Under these conditions angiotensin II increased water consumption. Results were discussed in terms of the differential effects of angiotensin II on drinking, eating, and schedule dependent lever pressing.

Angiotensin II↗
PubMed1983

Patterns of drinking in the rat following the administration of opiate antagonists.

Durations of drinking were recorded for water-deprived rats as they drank to satiety, following SC injections of naloxone (0.1-10.0 mg/kg), naltrexone (0.1-10.0 mg/kg) or saline vehicle. The results provided evidence for the effects of opiate antagonists on the temporal pattern of drinking exhibited by water-deprived animals. A separate, time-sampling procedure was used to supplement the drinking duration data, and showed that the opiate antagonists may suppress water consumption during a period 2.5-7.5 min after the start of the initial drinking bout. A second experiment confirmed that the pattern of drinking displayed during schedule-induced polydipsia in the rat is resistant to any suppressant effect of a moderate dose of an opiate antagonist. The similarity between opiate receptor blockade and water preloading in their effect on drinking in response to water deprivation, and lack of effect on schedule-induced polydipsia is discussed. Opiate antagonists may affect drinking principally by imposing a thirst satiety signal.

Animals↗