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• Published: 08 November 2021

Acute effects of alcohol on social and personal decision making

• Hanna Karlsson 1   na1 ,
• Emil Persson   ORCID: orcid.org/0000-0003-2994-0541 2   na1 ,
• Irene Perini   ORCID: orcid.org/0000-0002-5972-0913 1 ,
• Adam Yngve   ORCID: orcid.org/0000-0003-1012-7286 1 ,
• Markus Heilig 1   na1 &
• Gustav Tinghög   ORCID: orcid.org/0000-0002-8159-1249 2 , 3   na1  

Neuropsychopharmacology volume  47 ,  pages 824–831 ( 2022 ) Cite this article

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• Human behaviour
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Social drinking is common, but it is unclear how moderate levels of alcohol influence decision making. Most prior studies have focused on adverse long-term effects on cognitive and executive function in people with alcohol use disorders (AUD). Some studies have investigated the acute effects of alcohol on decision making in healthy people, but have predominantly used small samples and focused on a narrow selection of tasks related to personal decision making, e.g., delay or probability discounting. Here, we conducted a large ( n  = 264), preregistered randomized placebo-controlled study (RCT) using a parallel group design, to systematically assess the acute effects of alcohol on measures of decision making in both personal and social domains. We found a robust effect of a 0.6 g/kg dose of alcohol on both moral judgment and altruistic behavior, but no effects on several measures of risk taking or waiting impulsivity. These findings suggest that alcohol at low to moderate doses selectively moderates decision making in the social domain, and promotes utilitarian decisions over those dictated by rule-based ethical principles (deontological). This is consistent with existing theory that emphasizes the dual roles of shortsighted information processing and salient social cues in shaping decisions made under the influence of alcohol. A better understanding of these effects is important to understand altered social functioning during alcohol intoxication.

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Introduction.

There is a lack of systematic research on the effects of moderate alcohol intake on decision making in non-clinical populations. This may be related to the difficulties that go into designing these types of studies, and the fact that prior research has been primarily focused on the adverse consequences of alcohol use disorders (AUD) on physiology and behavior. Numerous studies have investigated impairments in interpersonal behavior and decision-making processes in patients with AUD, but these studies cannot disaggregate the direct effects of alcohol from functional consequences of alcohol-induced organ damage, such as e.g., well documented alcohol-induced regional gray matter loss in AUD [ 1 ].

In healthy volunteers, alcohol intake can influence incentive motivation through activation of canonical dopaminergic brain reward system, but these effects vary by gender and genetics [ 2 , 3 , 4 , 5 ]. Enhanced emotional reactivity and increased positive mood have also been linked to alcohol intake in non-threatening environments [ 6 , 7 ]. It is furthermore widely held that alcohol results in broad and non-selective impairments of cognitive function, but this notion has recently been questioned. A meta-analysis of studies that examined the effects of alcohol on event-related potentials suggests that alcohol intake results in relatively selective impairments of attention, automatic auditory processing, and performance monitoring [ 8 ]. Similarly, alcohol is commonly held to increase impulsivity, but available studies make it difficult to disentangle to what extent impulsivity is a cause vs. a consequence of alcohol use, and also point to the moderating influence of emotional states [ 9 ].

Few studies have examined acute effects of alcohol on motivated behavior and decision making under a level of experimental control that allows causal inferences. For instance, many of the existing studies have used survey data to compare the behavior of people who abuse alcohol to those who do not. Although there are also placebo-controlled laboratory studies, most of these have used small samples and focused on a narrow selection of tasks related to personal decision making, primarily risk taking and impulsivity [ 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 ]. Even for these tasks, there is a lack of converging evidence. Some studies found increased risk taking due to alcohol [ 11 , 13 ], while others found no effect [ 10 , 12 , 14 , 15 , 19 , 20 ]. Similarly, waiting impulsivity has been found to increase [ 19 ] or decrease [ 16 ] following alcohol intake, but the majority of studies have found mixed or no effects [ 10 , 11 , 14 , 15 , 17 ]. Prototypical tasks for altruism and moral judgment have only been included in a minority of studies, with mixed results for both types of tasks [ 19 , 20 , 21 , 22 ]. In addition, some studies have used an observational field paradigm, typically approaching people in a bar with a structured questionnaire [ 22 , 23 , 24 ]. Whereas important insights can be obtained from these observational studies, they cannot provide answers about the causal relationship between alcohol intake and behavior, as they are inherently correlational, and also prone to selection bias.

Here, we therefore investigated how moderate acute alcohol intoxication influences basic social and personal decision making central to a wide variety of everyday behaviors: altruistic behavior and distributional preference, moral judgment, waiting impulsivity, and choice under risk. To this end, we conducted a preregistered (see https://osf.io/sf5em ) randomized placebo-controlled study, using a general task paradigm and a substantially larger sample ( n  = 264) than previous studies. We randomized participants to alcohol (0.6 and 0.51 g/kg for males and females, resp.) or placebo, and assessed moral judgment using standard sacrificial dilemmas (trolley problems) thought to probe the interaction between emotional intuitions and controlled cognitive processes in moral cognition [ 25 , 26 , 27 , 28 ]. Prosocial behavior was assessed using modified versions of the dictator game [ 29 , 30 ]. For risk taking, we used two different tasks, covering both intuitive-cognitive aspects of decision making, via standard prospect theory gambles [ 31 ], and more affect-laden decisions from experience, using the Balloon Analog Risk Task (BART; [ 32 ]). Finally, waiting impulsivity was assessed using a prototypical task that captures participants’ preferences for real monetary rewards delivered at different points in time [ 33 , 34 ]. We assessed both general discounting (over relatively short delays) and temporal inconsistency in discounting, known as present bias, which is a characteristic property of discounting models that feature a sharp rise in the discounting rate for rewards delivered closer to today, such as quasi-hyperbolic discounting [ 34 , 35 ].

Materials and methods

Ethics statement.

The study was approved by the Regional Ethical Review Board of Linköping (ref 2016/496-31) and all participants provided written informed consent.

Open science

The preregistration together with data, analysis codes (main analyses), and experimental materials are available via the project’s OSF repository ( https://osf.io/sf5em ). Individual level data for the main analyses are shown in Supplementary materials Fig. S 1 –S 4 . We preregistered six main questions of interest for this data collection; this paper is focused on the first four of them.

Participants

Healthy volunteers were recruited using advertisements in social media, flyers, and the Online Recruitment System for Economic Experiments ORSEE [ 36 ] at Linköping University, Sweden. Eligible participants were randomized to alcohol ( n  = 128) or placebo ( n  = 136). The groups were similar in terms of baseline characteristics, including age, sex, education, alcohol consumption as measured with AUDIT, and personality traits measured with NEO-FFI (Table  1 ). The distribution of AUDIT scores was also very similar in both groups, and shown in Supplementary Materials (Fig. S 1 ). Our final sample size is smaller than the pre-specified target of n = 300 because we had to stop enrolling participants due to the onset of the COVID-19 pandemic.

Study timeline

The study visit consisted of five phases (Fig.  1B ): screening, questionnaires for baseline assessments, treatment phase (intake of drink), decision-making tasks performed at a computer, and a finishing phase with end of session questionnaires. The study was conducted in a computer lab in sessions of up to 15 participants, who were seated in separate cubicles and did not interact with each other.

A CONSORT diagram of study participant. B study timeline. C time course of BrAC (mean ± SD).

Screening and eligibility

During the screening phase, prospective participants were evaluated for eligibility by a research nurse or a physician. Detailed eligibility criteria are provided in Supplementary Materials. In brief, subjects were excluded if they had any psychiatric disorder, were pregnant, had any previous neurological condition or if they were at risk of alcohol or other substance use disorders except nicotine. Alcohol Use Disorder Identification Test [AUDIT; [ 37 ]] was used to assess the presence of AUD or hazardous drinking. Weight and sex were noted. Breath alcohol concentration (BrAC) baseline was measured using a breathalizer. A total of 316 individuals were evaluated, and 265 were included. Of these, 129 were allocated to placebo and 136 were assigned to alcohol (Fig.  1A ).

Baseline assessments

Baseline personality traits were obtained using the NEO Five Factor Inventory [NEO-FFI; [ 38 ]]. The Symptom checklist-90 [SCL-90; [ 39 ]] was used to measure symptoms of anxiety and depression. The Family Tree Questionnaire [FTQ; [ 40 ]] was used to assess family history of alcohol problems. The Biphasic Alcohol Effect Scale [BAES; [ 41 ]] was used to measure stimulant and sedative effects of alcohol.

Alcohol administration

Participants were informed that they would receive alcohol, corresponding to a BrAC of 0.6‰ or placebo, and were randomized to one of these in a parallel group design (see Fig.  1A ). In the alcohol group, male participants received a 0.6 g/kg dose of alcohol using a 12% solution. The solution was made using 95% ethanol mixed with cranberry juice. To adjust for known differences in body water, women received 85% of the alcohol administered to men. In the placebo group participants received a 1% alcohol solution. In both groups, the drink was divided into three glasses. Participants in both the alcohol and placebo group were required to finish each glass within five minutes. After the last glass, participants had a break for 15 min before proceeding with the decision-making tasks. Breath alcohol concentration (BrAC) was measured at baseline, 25 min later, just before the decision-making tasks and after additional appr. 45 min, as soon as the participant finished the session. The Biphasic Alcohol Effect Scale [BAES; [ 41 ]] was performed every time BrAC was measured and the Drug Effect Questionnaire [DEQ; [ 42 ]] was measured the second and third time BrAC was measured.

Decision-making tasks

For detailed task description and instructions, see Supplementary Materials. In brief, tasks focused on four domains of decision making: waiting impulsivity, choice under risk, moral judgment, and prosocial behavior. Tasks were presented on a computer screen using Qualtrics and Inquisit software. Divider screens prevented participants from seeing each other’s responses. Tasks were presented in a block-randomized order. At the end of the experiment, one decision for each subject was randomly selected and paid out for real (using the cell phone payment system Swish) together with the show-up fee of 150 SEK (appr. $15) that participants received for participating in the study.

Waiting impulsivity

This was assessed using a prototypical task that measures participants’ preferences for rewards delivered at different points in time [ 33 , 34 ]. Participants chose repeatedly between smaller rewards delivered sooner (SS) and larger rewards delivered later (LL). We tested for two distinct types of discounting; a general form of impatience, based on the proportion of smaller-sooner choices each person made in the first block of items ( pr. smaller-sooner ), and a specific form of impatience known as present bias, which is based on the difference (for each participant) between choices made in the first and second blocks of items ( diff. pr. smaller-sooner ). Present bias is a characteristic property of discounting models that feature a sharp rise in the discounting rate for rewards delivered closer to today, such as quasi-hyperbolic discounting [ 34 , 35 ].

Risk taking

One of the tasks to examine risk taking used standard prospect-theory gambles [ 31 ]. We used incentivized binary choices between a lottery and a certain amount of money in three different domains: gain, loss, mixed. We used the proportion of choices where the gamble was our main dependent variable for each domain ( pr. risky choices ). Using this task enabled us to characterize choices after the expected patterns of prospect theory [ 31 ], which emphasizes greater risk aversion for gains than losses and disproportionate weighting of the loss component in mixed prospects.

The second task in this domain was the Balloon Analog Risk Task [BART; [ 32 ]], in which participants were presented with a picture of a balloon and could earn money by pumping up the balloon by clicking a button. Each click earned them 0.1 SEK and caused the balloon to incrementally inflate. If the balloon was overinflated, it exploded, and all money earned for that trial was lost. If instead participants had chosen to cash-out prior to the balloon exploding, the money earned for that trial was added to their sum for this task. Our main dependent variable was the average number of pumps per trial, excluding trials where the balloon exploded ( avg. pumps per balloon ).

Moral judgment

This was assessed using four sacrificial moral dilemmas (trolley problems) that involved a conflict between utilitarian and deontological moral foundations [ 25 , 43 , 44 ]. In each dilemma, participants were faced with the possibility of saving a certain number of people by sacrificing one individual. Killing the single person while saving the others is consistent with utilitarian judgment, while not pulling the switch is consistent with deontological judgment, whereby actively causing harm to another person is morally unacceptable regardless of overall consequences. The main dependent variable for moral judgment was based on participants’ responses to four moral dilemmas (switch, footbridge, fumes, and shark; see Supplementary materials for details), presented in random order, and calculated as the proportion of utilitarian choices made by each participant ( pr. utilitarian choices ).

Prosocial behavior

This was assessed using two different tasks, designed to measure both altruistic behavior and preference for equality versus efficiency in distributions. Both were modified versions of the dictator game [ 29 , 30 ].

In the first task, participants were endowed with 50 SEK (appr. $5) and decided how much of it to keep for themselves and how much to donate to a well-known charity organization (Swedish Heart-Lung Foundation). The main dependent variable was the amount donated ( donation to charity ).

In the second task, subjects chose repeatedly between binary allocations of money (for themselves and another anonymous participant). Each item featured a choice between an equal distribution and an unequal but more efficient distribution, for example 40 SEK (appr. $4) each vs 40 SEK for me and 50 SEK for the other participant. We used the proportion (for each person) of choices where the equal allocation was chosen over the more efficient allocation ( pr. equality ).

Statistical analysis

The main analysis plan was specified before data collection begun, see the preregistration for details. STATISTICA 13.0 (Dell Inc, Tulsa, OK) was used for all analyses. One-way ANOVA, with group (alcohol or placebo) as a between-subject factor, and a pre-set alpha=0.05, were the preregistered main tests. Subject-level data for main tests are provided in Supplementary Materials, Fig. S 1 –S 4 . Secondary analyses (not preregistered) additionally assessed the potential influence of baseline subject characteristics (age, sex, personality measures, and alcohol use as measured by the AUDIT). Covariates were retained in analysis models if they were a significant predictor, or if they reduced the residual variance by more than 10%; otherwise, they were excluded. In additional analyses (also not preregistered) we compared self-reported effects of alcohol (stimulant, sedative, strength of drug effect, desirability) across the two conditions, based on subjects’ responses to the Biphasic Alcohol Effect Scale (BAES) and the Drug Effect Questionnaire (DEQ).

No BrAC alcohol was detected in the placebo group at any timepoint, or in the alcohol group at baseline. In the alcohol group, a BrAC of appr. 0.5‰ was reached by the time behavioral testing started, and remained stable at that level until completion of testing (Fig.  1C ). Using the Biphasic Alcohol Effects Scale [ 41 ], the alcohol group showed the expected stimulant as well as sedative effects of alcohol compared to the placebo group. On the Drug Effects Questionnaire [ 42 ], there was a clear effect of alcohol on the “Feel drug” and “High” items (Fig.  2 ). Neither “Like” nor “Want more” items were affected. The proportion of participants who correctly guessed their allocation was 95.5% in the alcohol group, and 69% in the placebo group. No unexpected adverse events were noted.

A – D Mean responses on the Drug Effect Questionnaire (DEQ) before and after the decision-making tasks. Error bars indicate 95% Confidence Intervals. E , F Mean responses to the Biphasic Alcohol Effects Scale (BAES). Error bars indicate 95% Confidence Intervals. Significant alcohol effects for all items are indicated in the Results section.

Moral judgment in sacrificial dilemmas

Preference for utilitarian responding was increased in the alcohol group (one way ANOVA: F 1, 262  = 5.71, p  = 0.02; Cohen’s d = 0.29; Fig.  3A ). This remained unchanged when controlling for potential confounds. In the final ANCOVA, agreeableness ( p  < 0.01), gender ( p  = 0.06) and hazardous alcohol use, as measured with the AUDIT ([ 37 ]; p  = 0.02) contributed to the model, and all correlated negatively with utilitarian choices. Exploratory analyses indicated that the effect of alcohol on moral judgment was driven by the switch and fumes dilemmas, and to some extent the shark dilemma, while no corresponding effect was seen in the footbridge dilemma.

A Moral judgment. Main panel: overall proportion of utilitarian choices. Inset: proportion of participants in each group who chose the utilitarian option, for the respective scenario. B Donation to charity. Main panel: Total amount of money donated. Inset: distribution of amounts donated to the charity, by group. Ten Swedish kronor (SEK) was approximately equal to one USD at the time of the experiment. Tick marks on the x-axis show the midpoints of equally-sized bins (10 SEK wide), except at the endpoints, where bin size is smaller. Error bars indicate 95% Confidence Intervals. Sample size is n  = 128 for placebo and n  = 136 for alcohol.

Participants in the alcohol group donated more money to a charity ( F 1, 262  = 4.83, p  = 0.03; Cohen’s d = 0.27; Fig.  3B ). This remained unchanged when controlling for potential confound of baseline subject characteristics. In the final model, agreeableness ( p  < 0.01) and hazardous alcohol use as measured with the AUDIT ( p  = 0.02) significantly contributed to the model. Agreeableness was positively correlated with donations and AUDIT was negatively correlated.

Equality/efficiency tradeoffs did not differ between groups (0.27 ± 0.38 vs. 0.27 ± 0.39; F 1, 262  < 0.01, p  = 0.98); thus, participants in both groups were reluctant to pursue equality of resources if redistribution had a cost. This result remained unchanged when controlling for potential confounds. In the final model, age ( p  < 0.01), neuroticism ( p  < 0.01), extraversion ( p  < 0.01), openness ( p  = 0.02), conscientiousness ( p  = 0.01) and gender ( p  < 0.01) significantly contributed to the model. Openness correlated negatively with equality. Female gender, age, neuroticism, extraversion and conscientiousness correlated positively with equality.

Risk taking – prospect theory gambles & BART

Behavior in the prospect gambles was similar in the two groups (Fig.  4 ). There was a tendency for decreased risk taking in the alcohol group for gains (0.59 ± 0.29 vs. 0.65 ± 0.22; F 1, 262  = 3.58, p  = 0.06), but no effect, or trend in the loss (0.49 ± 0.22 vs. 0.45 ± 0.22; F 1, 262  = 1.72, p  = 0.19), or in the mixed domain (0.49 ± 0.21 vs. 0.47 ± 0.22; F 1, 262  = 0.64, p  = 0.42). When all three domains were combined, the alcohol and placebo groups were virtually indistinguishable (0.52 ± 0.18 vs. 0.52 ± 0.15; F 1,262  < 0.01, p  = 0.96; Cohen’s d = −0.01). This remained unchanged when controlling for potential confounds. In the final model, age ( p  < 0.01), extraversion ( p  = 0.01), conscientiousness ( p  = 0.03) and agreeableness ( p  = 0.06) significantly contributed to the model or showed a tendency to do so. Age and extraversion were positively correlated with risk taking, while agreeableness and conscientiousness were negatively correlated with risk taking.

A Mean proportion of trials where individuals chose the gamble over the certain option, separated by domain (gain, loss, mixed). Error bars indicate 95% Confidence Intervals calculated from t tests. B Distribution of the average number of pumps per balloon on the Balloon Analog Risk Task (BART). Sample size is n  = 128 for placebo and n  = 136 for alcohol, except for BART where two individuals in placebo and three in alcohol could not participate in the task due to software issues.

Similarly, there was no difference in risk taking on the Balloon Analog Risk Task (BART) between alcohol and placebo (Fig.  4 ; 43.4 ± 14.1 vs. 43.5 ± 14.2; F 1,257  < 0.01, p  = 0.99; Cohen’s d = −0.002). This remained unchanged when controlling for potential confounds. In the final model, neuroticism ( p  = 0.01) and conscientiousness ( p  = 0.05) were significant covariates. Both were negatively correlated with adjusted average number of pumps.

There was no statistically significant difference between groups for waiting impulsivity (0.24 ± 0.31 vs. 0.29 ± 0.31; F 1,262  = 2.21, p  = 0.14), or present bias (0.0007 ± 0.15 vs. 0.03 ± 0.18; F 1,262  = 2.59, p  = 0.11). Results were similar when all individual decisions were combined (0.24 ± 0.30 vs. 0.28 ± 0.29; F 1,262  = 1.25, p  = 0.26; Cohen’s d = −0.14). Thus, any possible effect of alcohol on waiting impulsivity was small and insignificant, and the bound on the 95% confidence interval in the hypothesized direction, i.e., increased waiting impulsivity following alcohol intake, was close to zero. These results remained unchanged when controlling for potential confounds.

We conducted a large, preregistered RCT to assess acute effects of alcohol on measures of decision making in personal and social domains. A 0.6 g/kg dose of alcohol did not influence personal decisions, but robustly moderated social decision making. In particular, subjects in the alcohol group showed an increased utilitarian preference in sacrificial moral dilemmas, and donated more money to charity in a modified dictator-game task. As an internal validation of these findings, we detected the expected effects of personality traits, independently of the alcohol effects. Although participants’ level of alcohol use, as measured by the AUDIT scale, correlated negatively both with their utilitarian decisions and charitable donations, the effects of alcohol on these outcomes did not interact with the level of alcohol use, and thus did not differ across the spectrum of use included in the study. For personal decision making, we did not find an effect of alcohol at the dose given on any of several risk-taking measures or waiting impulsivity. As an internal validation, we reliably replicated known patterns of results with all our tasks, e.g., increased risk seeking for losses and selective sensitivity to harmful actions across different moral dilemmas. Thus, our null findings are unlikely a result of compromised task calibration or unusual sample composition. Our findings are also unlikely to be explained by effects on elements of decision making that are related to impulse control, since, at the moderate level of alcohol intoxication used, we found no effects in tasks specifically designed to capture this dimension of behavior.

Our results for moral judgment, that subjects became increasingly utilitarian, differ from the few previous studies. Francis and colleagues [ 21 ] recently conducted a placebo-controlled study on moral judgment, using both traditional moral dilemmas and an adapted virtual-reality moral behavior task. They found no effects of alcohol on any of these tasks. In contrast, Duke and Bègue [ 22 ] found that alcohol intake correlated with increased utilitarian responding, but only on the footbridge dilemma and not on the switch dilemma, in a study conducted at two bars in France. However, the results from these two studies should be interpreted with caution, given the small sample sizes and the correlational nature of the data in the latter study. Our findings are contrary to what would be expected based on the widely held dual-process theory of moral cognition [ 25 , 28 ]. According to this theory, the effects of alcohol to increase emotional reactivity and weaken cognitive control should give increased preference for deontological rather than utilitarian actions. In fact, we find the opposite, i.e. increased utilitarian responding due to alcohol. A possible account of this finding is that acute alcohol intoxication primarily affects moral judgment through effects on its cognitive elements, and does so by subtly shifting the balance between perceived costs and benefits in the utilitarian calculation. This is broadly consistent with findings indicating an important role of frontocortical brain areas in social decision making [ 45 ], and a higher sensitivity of these neocortical structures to alcohol effects compared to subcortical brain structures that generate incentive salience and affective signals [ 1 ].

Acute effects of alcohol on altruistic behavior using real monetary rewards have hardly been assessed at all previously. Two previous studies found no effect or a tendency for a negative effect on altruism following alcohol intake [ 19 , 20 ]. In contrast, we found that alcohol made people more altruistic, donating a larger proportion of their money (around ten percentage points more than the placebo group) to charity. This is a modest effect size, but appears to be highly specific, as it was found at a modest dose of alcohol at which there were no discernible effects on impulsivity or risk taking. We had no a priori expectation about the direction of the effect on altruism. In principle, these results can also be rationalized using alcohol myopia theory [ 46 , 47 , 48 ], which emphasizes impaired attention and thus increased reliance on salient stimuli following acute alcohol intoxication. The need of the charity recipients is arguably a salient cue in the task that we used, and it is possible that this is what caused increased donations in the alcohol group.

Previous studies on personal decision making for risk and impulsivity have found mixed results [ 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 49 ], but most studies have been limited by a small sample size. Prior to our study, Bernhardt et al. [ 10 ] was probably the most well-powered study to date ( n  = 54 adolescent males in a within-subject design), and their results are similar to what we found, with no effects on waiting impulsivity or on risk taking in gain, loss, or mixed domains. Taken together, this strongly suggests that alcohol taken at moderated doses by healthy social drinkers has small or no effects on risk taking or waiting impulsivity. For the Balloon Analog Risk Task (BART), we are aware of only one previous study that was adequately powered, Rose et al. [ 50 ] with n  = 142 in a between-subjects design; e.g., all other studies reviewed by Harmon et al. [ 51 ] had <33 subjects per treatment cell. Interestingly, whereas Rose et al. found increased risk taking (more pumps) due to alcohol intake (Cohen’s d = 0.40 at a 0.6 g/kg dose of alcohol), our results clearly favored a no-effects interpretation, with the 95% confidence interval bounded at an effect size or appr. Cohen’s d = 0.25 in either direction. Thus, more studies are needed to determine the acute effects alcohol on the BART. Of note, while the BART is commonly viewed as a generic “risk taking task”, its original evaluation suggested that it may in fact be more related to sensation seeking and impaired behavioral inhibition [ 32 ], i.e. facets of the impulsivity distinct from those involved in trading off the magnitude of gains or losses vs. their probability.

Our study has several strengths as well as limitations. Among the former, it had a large sample size and a preregistered analysis plan. This is important given that prior studies are for the most part small and without transparent control of analytical flexibility. The combination of small sample sizes, high analytical flexibility and publication bias has been a perfect storm for generating irreproducible findings [ 52 , 53 , 54 , 55 ]. However, despite a larger sample than previous studies, we had insufficient power to conduct otherwise relevant subgroup analyses, for example based on gender or quantitative traits, beyond using them as covariates in the analysis. For the same reason, we did not attempt to capture biphasic effects of alcohol. Finally, we were not able to control for expectation effects by adding more conditions, while blinding was not successful. These limitations may affect the generalizability of our findings.

Some features of the study are both strengths and limitations. For instance, we ensured a high degree of experimental control, at the expense of assessing the effects of alcohol in a standardized, sterile laboratory environment. As expected under these conditions, while self-ratings of intoxication (“feeling effect” and “high”) were robustly influenced by alcohol, neither “liking” nor “wanting” ratings were affected. On one hand, this suggests that our findings are unlikely to be primarily driven by expectations, since expectations of alcohol effects are linked to experiencing alcohol in a naturalistic context. At the same time, alcohol effects on decision making under laboratory conditions may differ from those “in the wild”. Similarly, although we make a distinction between personal and social decision making in terms of outcomes, all decisions in our study were taken in private in front of a computer. Thus, future studies could extend our findings by investigating the effects of alcohol on social decisions made in a public setting (e.g., observed by an audience), where social signaling and reputational concerns also come into play.

Designing the experiment, we emphasized task comprehension, and all decisions that involved money were incentivized (participants were paid for one randomly drawn decision at the end). Payments were implemented via a standard cell phone transfer system in order to circumvent concerns about differential transactions costs in the waiting-impulsivity task [ 56 ]. However, as a potential side effect, this made the larger-later option in this task more attractive than we had anticipated, resulting in a more than usual amount of upper censoring (people who chose the larger-later option for all trials) for this task. Our results for waiting impulsivity should be interpreted with this limitation in mind. Similarly, our finding that alcohol did not influence impulsivity, may not generalize to higher doses, or other populations. Also, even at the dose used, effects on impulsivity might be present in people with substance use disorders, externalizing psychopathology, or both.

The pattern of our results suggests that alcohol selectively moderates decision making in the social domain, at least for low-moderate doses of alcohol. This is consistent with existing theory that emphasizes the dual roles of shortsighted information processing and salient social cues in shaping decisions under the influence of alcohol [ 46 ]. Our findings are obtained in social drinkers without any AUD, but have potentially important implications for attempts to understand the emergence of AUD. Most prior alcohol challenge studies have focused exclusively on personal decision making, but changes in social cognition, ultimately resulting in social marginalization and exclusion, are at the core of the addictive process [ 57 , 58 ]. It has recently been shown that communicating deontologically rather than utilitarian-motivated decisions may be more advantageous to signal trustworthiness as group member [ 59 , 60 ]. Impairments in the ability to signal trustworthiness caused by alcohol use could contribute to social marginalization. These alcohol-induced effects on social cognition are likely to interact with pre-existing vulnerabilities to influence social functioning. Our findings highlight the importance of taking the social dimension of decision making into account to better understand the process of developing AUD.

Taking a broader perspective, to policymakers and everyday decision-makers alike, it is useful to know that the influence of alcohol on decision making is sensitive to social cues. Whether alcohol is ultimately good or bad for people’s decisions will likely depend on context. Perhaps surprisingly, from the narrow perspective of our sample and the specific tasks that we used, social outcomes were more advantageous among people who were given alcohol compared to people who were not.

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Acknowledgements

We are grateful to Åsa Axén, Sandra Boda, Sarah Gustavson, Lisbet Severin, Lina Koppel, Theodor Arlestig and David Andersson for assisting with data collection.

This work was supported by the Swedish Research Council (MH: 2013-07434; GT: 2018-01755) and the Swedish Research Council for Health, Working Life and Welfare (EP: 2020-00864). Funders had no role in study design, data collection, analysis, decision to publish, or preparation of the manuscript.

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These authors contributed equally: Hanna Karlsson, Emil Persson, Markus Heilig, Gustav Tinghög.

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Hanna Karlsson, Irene Perini, Adam Yngve & Markus Heilig

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Emil Persson & Gustav Tinghög

The National Center for Priority Setting in Health Care, Department of Medical and Health Sciences, Linköping University, 581 83, Linköping, Sweden

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MH and GT provided funding for the study. HK, EP, IP, MH, and GT designed the study. HK, AY and GT collected the data. HK and EP analyzed the data and drafted the manuscript. All authors revised the manuscript and approved the final manuscript for submission.

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Karlsson, H., Persson, E., Perini, I. et al. Acute effects of alcohol on social and personal decision making. Neuropsychopharmacol. 47 , 824–831 (2022). https://doi.org/10.1038/s41386-021-01218-9

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Health Risks and Benefits of Alcohol Consumption

Alcohol consumption has consequences for the health and well-being of those who drink and, by extension, the lives of those around them. The research reviewed here represents a wide spectrum of approaches to understanding the risks and benefits of alcohol consumption. These research findings can help shape the efforts of communities to reduce the negative consequences of alcohol consumption, assist health practitioners in advising consumers, and help individuals make informed decisions about drinking.

Forty-four percent of the adult U.S. population (age 18 and over) are current drinkers who have consumed at least 12 drinks in the preceding year ( Dawson et al. 1995 ). Although most people who drink do so safely, the minority who consume alcohol heavily produce an impact that ripples outward to encompass their families, friends, and communities. The following statistics give a glimpse of the magnitude of problem drinking:

• Approximately 14 million Americans—7.4 percent of the population—meet the diagnostic criteria for alcohol abuse or alcoholism ( Grant et al. 1994 ).
• More than one-half of American adults have a close family member who has or has had alcoholism ( Dawson and Grant 1998 ).
• Approximately one in four children younger than 18 years old in the United States is exposed to alcohol abuse or alcohol dependence in the family ( Grant 2000 ).

Measuring the Health Risks and Benefits of Alcohol

Over the years, scientists have documented the effects of alcohol on many of the body’s organ systems and its role in the development of a variety of medical problems, including cardiovascular diseases, liver cirrhosis, and fetal abnormalities. Alcohol use and abuse also contribute to injuries, automobile collisions, and violence. Alcohol can markedly affect worker productivity and absenteeism, family interactions, and school performance, and it can kill, directly or indirectly. On the strength of this evidence, the United States and other countries have expended considerable effort throughout this century to develop and refine effective strategies to limit the negative impact of alcohol ( Bruun et al. 1975 ; Edwards et al. 1994 ).

In the past two decades, however, a growing number of epidemiologic studies have documented an association between alcohol consumption and lower risk for coronary heart disease (CHD), the leading cause of death in many developed countries ( Chadwick and Goode 1998 ; Criqui 1996 a , b ; Zakhari 1997 ). Much remains to be learned about this association, the extent to which it is due specifically to alcohol and not to other associated lifestyle factors, and what the biological mechanisms of such an effect might be.

Effects on Physical Health

Cardiovascular diseases account for more deaths among Americans than any other group of diseases. Several large prospective studies have reported a reduced risk of death from CHD across a wide range of alcohol consumption levels. These include studies among men in the United Kingdom ( Doll et al. 1994 ), Germany ( Keil et al. 1997 ), Japan ( Kitamura et al. 1998 ), and more than 85,000 U.S. women enrolled in the Nurses’ Health Study ( Fuchs et al. 1995 ). In research studies, definitions of moderate drinking vary. However, in these studies, most, if not all, of the apparent protective effect against CHD was realized at low to moderate levels of alcohol consumption.

Follow-up of another large U.S. survey, the National Health and Nutrition Examination Survey I ( Rehm et al. 1997 ), found that after an average of nearly 15 years of follow-up, the incidence of CHD in men who drank was lower across all levels of consumption than in nondrinkers. Incidence also was reduced among women, but only in those consuming low to moderate levels of alcohol. In fact, an increased risk was observed in women consuming more than 28 drinks per week.

An association between moderate drinking and lower risk for CHD does not necessarily mean that alcohol itself is the cause of the lower risk. For example, a review of population studies indicates that the higher mortality risk among abstainers may be attributable to socioeconomic and employment status, mental health, overall health, and health habits such as smoking, rather than participants’ nonuse of alcohol ( Fillmore 1998 ).

It is also important to note that the apparent benefits of moderate drinking on CHD mortality are offset at higher drinking levels by increased risk of death from other types of heart disease, cancer, liver cirrhosis, and trauma. The U.S. Department of Agriculture (USDA) and the U.S. Department of Health and Human Services (USDHHS), in the U.S. Dietary Guidelines for Americans, have defined moderate drinking as one drink per day or less for women and two or fewer drinks per day for men ( USDA 1995 ). In addition, the NIAAA further recommends that people aged 65 and older limit their consumption of alcohol to one drink per day.

Cerebrovascular disease, in which arteries in the brain are blocked or narrowed, can lead to a sudden, severe disruption of blood supply to the brain, called a stroke. Ischemic stroke, which is by far the predominant type of stroke, results from a blockage of a blood vessel; hemorrhagic stroke is due to rupture of a blood vessel. Alcohol-related hypertension, or high blood pressure, may increase the risk of both forms of stroke. Yet, in people with normal blood pressure, the risk of ischemic stroke may be decreased due to the apparent ability of alcohol to lessen damage to blood vessels due to lipid deposits and to reduce blood clotting. Alcohol’s anticlotting effects, while perhaps decreasing the risk of ischemic stroke, may increase the risk of hemorrhagic stroke ( Hillbom and Juvela 1996 ). These studies are coming closer to providing a clear picture of the relationship between alcohol and risk of stroke.

The relationship between alcohol consumption and stroke risk has been examined in two recent overviews. In a meta-analysis, researchers compared the relationship between alcohol consumption and the risk of ischemic and hemorrhagic strokes ( English et al. 1995 ). They detected no differences in the risk patterns for the two types of stroke, but found clear evidence that heavy drinking was associated with increased stroke risk, particularly in women.

In contrast, the Cancer Prevention Study II found that, in men, all levels of drinking were associated with a significant decrease in the risk of stroke death, but in women, the decreased risk was significant only among those consuming one drink or less daily ( Thun et al. 1997 ). A recent study reported that among male physicians in the Physicians’ Health Study, those who consumed more than one drink a week had a reduced overall risk of stroke compared with participants who had less than one drink per week ( Berger et al. 1999 ).

Among young people, long-term heavy alcohol consumption has been identified as an important risk factor for stroke ( You et al. 1997 ). Very recent alcohol drinking, particularly drinking to intoxication, has been found to be associated with a significant increase in the risk of ischemic stroke in both men and women aged 16 through 40 years ( Hillbom et al. 1995 ).

The relationship between alcohol consumption and blood pressure is noteworthy because hypertension is a major risk factor for stroke as well as for CHD. A national consensus panel in Canada recently conducted an extensive review of the evidence concerning this relationship ( Campbell et al. 1999 ), concluding that studies have consistently observed an association between heavy alcohol consumption and increased blood pressure in both men and women. However, in many studies comparing lower levels of alcohol use with abstention, findings are mixed. Some studies have found low alcohol consumption to have no effect on blood pressure or to result in a small reduction, while in other studies blood pressure levels increased as alcohol consumption increased.

The possibility that alcohol may protect against CHD has led researchers to hypothesize that alcohol may protect against peripheral vascular disease, a condition in which blood flow to the extremities is impaired due to narrowing of the blood vessels. In a 1985 analysis of data from the Framingham Heart Study, alcohol was not found to have a significant relationship, either harmful or protective, with peripheral vascular disease ( Kannel and McGee 1985 ). However, an important recent study produced different results. In an analysis of the 11-year follow-up data from more than 22,000 men enrolled in the Physicians’ Health Study, researchers found that daily drinkers who consumed seven or more drinks per week had a 26-percent reduction in risk of peripheral vascular disease ( Camargo et al. 1997 ).

Two other studies found inconsistent results with regard to gender. One study of middle-aged and older men and women in Scotland showed that as alcohol consumption increased, the prevalence of peripheral vascular disease declined in men but not in women ( Jepson et al. 1995 ). In contrast, among people with non-insulin-dependent diabetes, alcohol was associated with a lower prevalence of peripheral vascular disease in women but not in men ( Mingardi et al. 1997 ).

There is no question that alcohol abuse contributes significantly to liver-related morbidity (illness) and mortality in the United States. The effects of alcohol on the liver include inflammation (alcoholic hepatitis) and cirrhosis (progressive liver scarring). The risk for liver disease is related to how much a person drinks: the risk is low at low levels of alcohol consumption but increases steeply with higher levels of consumption ( Edwards et al. 1994 ). Gender also may play a role in the development of alcohol-induced liver damage. Some evidence indicates that women are more susceptible than men to the cumulative effects of alcohol on the liver ( Becker et al. 1996 ; Gavaler and Arria 1995 ; Hisatomi et al. 1997 ; Naveau et al. 1997 ).

Definitions Related to Drinking

Studies investigating the health effects of alcohol vary in their definitions of “low,” “moderate,” and “heavy” drinking. According to the Dietary Guidelines for Americans , issued jointly by the U.S. Department of Agriculture (USDA) and the U.S. Department of Health and Human Services (USDHHS), moderate drinking is no more than two standard drinks per day for men and no more than one per day for women ( USDA and USDHHS 1995 ). The National Institute on Alcohol Abuse and Alcoholism further recommends that people aged 65 and older limit their consumption of alcohol to one drink per day. Information on drinking levels as they are defined in the individual studies cited in this issue can be found in the original references.

How Much Is a Drink?

In the United States, a drink is considered to be 0.5 ounces (oz) or 15 grams of alcohol, which is equivalent to 12 oz (355 milliliters [mL]) of beer, 5 oz (148 mL) of wine, or 1.5 oz (44 mL) of 80-proof distilled spirits.

Does Abstaining Increase Risk?

Epidemiologic evidence has shown that people who drink alcohol heavily are at increased risk for a number of health problems. But some studies described in this section suggest that individuals who abstain from using alcohol also may be at greater risk for a variety of conditions or outcomes, particularly coronary heart disease, than persons who consume small to moderate amounts of alcohol.

This type of relationship may be expressed as a J-shaped or U-shaped curve, which means that the risk of a disease outcome from low to moderate drinking is less than the risk for either abstinence or heavier drinking, producing a curve in the shape of the letter J or U (see figure ).

By examining the lifestyle characteristics of people who consume either no alcohol or varying amounts of alcohol, researchers may uncover other factors that might account for different health outcomes. For example, gender, age, education, physical fitness, diet, and social involvement are among the factors that may be taken into account in determining relative risk of disease.

Similarly, people may quit drinking because of health problems, or even if that is not the case, former drinkers may have characteristics that contribute to their higher mortality risk, such as smoking, drug use, and lower socioeconomic status. If former drinkers are included in the abstainers group, they may make alcohol appear to be more beneficial than it is. Therefore the best research studies will distinguish between former drinkers and those who have never used alcohol.

Rates of death from all causes, all cardiovascular diseases, and alcohol-augmented conditions from 1982 to 1991, according to base-line alcohol consumption.

SOURCE: Thun et al. 1997 . Reprinted with permission from New England Journal of Medicine , Vol. 337, pp. 1705–1714, 1997. Copyright 1997, Massachusetts Medical Society. Waltham, MA. All rights reserved.

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Alcohol has been linked to a number of cancers, including cancers of the head and neck (mouth, pharynx, larynx, and esophagus), digestive tract (stomach, colon, and rectum) and breast ( World Cancer Research Fund/American Institute for Cancer Research [WCRF/AICR] 1997 ; Doll et al. 1993 ; International Agency for Research on Cancer [IARC] 1988 ).

Alcohol is clearly established as a cause of cancer of various tissues in the airway and digestive tract, including the mouth, pharynx, larynx, and esophagus ( Doll et al. 1993 ; IARC 1988 ; La Vecchia and Negri 1989 ; Seitz and Pöschl 1997 ; WCRF/AICR 1997 ). An increased risk of gastric or stomach cancer among alcohol drinkers has been identified in several, but not the majority, of case-control or cohort studies. The link between alcohol use and chronic gastritis (stomach inflammation) is clear, although progression from chronic gastritis to neoplasia is less well understood and probably involves other factors in addition to alcohol ( Bode and Bode 1992 , 1997 ).

In addition, a link between alcohol and breast cancer has been suspected for two decades but the nature of this association remains unclear. (For a more detailed discussion of the role of alcohol in breast cancer, see the article in this issue on medical consequences pp 27–31.)

Psychosocial Consequences and Cognitive Effects

Alcohol use plays a role in many social activities, from the “business lunch” and parties to special occasions. The benefits to those who drink during social occasions are greatly influenced by culture, the setting in which drinking occurs, and expectations about alcohol’s effects ( Goldman et al. 1987 ; Heath 1987 ; Leigh 1989 ; Leigh and Stacy 1991 ). Stress reduction, mood elevation, increased sociability, and relaxation are the most commonly reported psychosocial benefits of drinking alcohol ( Baum-Baicker 1985 ; Hauge and Irgens-Jensen 1990 ; Leigh and Stacy 1991 ; Mäkelä and Mustonen 1988 ).

There is extensive evidence indicating that people who suffer psychological distress and rely on alcohol to relieve their stress are more likely to develop alcohol abuse and dependence ( Castaneda and Cushman 1989 ; Kessler et al. 1996 , 1997 ). Because vulnerability to alcohol dependence varies greatly among individuals, it is difficult to assess the risk of dependence in relation to how much a person drinks. Two persons exposed to alcohol in exactly the same way may or may not have the same outcome for many reasons, including genetic differences, personality, behavioral features, and environment.

Most mental disorders occur much more often than expected by chance among people who are abusing alcohol or are alcohol dependent ( Kessler et al. 1996 ). Of these individuals, those who are alcohol dependent are more likely than alcohol abusers to have mental disorders. In fact, alcohol dependence elevates the risk for all types of affective and anxiety disorders ( Kessler et al. 1996 ).

Although the relationship between heavy alcohol consumption and cognitive impairment is well established, the effects of moderate drinking on the ability to perform cognitive tasks, including remembering, reasoning, and thinking, are largely unexplored.

Most studies of the relationship between alcohol consumption and other forms of dementia, notably Alzheimer’s disease ( Tyas 1996 ), have failed to find statistically significant associations. However, several recent studies suggest that moderate alcohol consumption may have a positive effect on cognitive function. In an analysis of baseline data (data collected at the beginning of a study) for persons aged 59 through 71 who were enrolled in the Epidemiology of Vascular Aging Study in France, moderate alcohol consumption was associated with higher cognitive functioning among women but not men after a number of possible confounding variables were controlled for ( Dufouil et al. 1997 ). Another study, which followed 3,777 community residents in France who drank primarily wine, found a markedly reduced risk of the incidence of dementia among moderate drinkers relative to abstainers ( Orgogozo et al. 1997 ).

Effects on Society

Researchers have identified and classified a wide variety of adverse consequences for people who drink and their families, friends, co-workers, and others they encounter ( Edwards et al. 1994 ; Harford et al. 1991 ; Hilton 1991 a , b ). Alcohol-related problems include economic losses resulting from time off work owing to alcohol-related illness and injury, disruption of family and social relationships, emotional problems, impact on perceived health, violence and aggression, and legal problems.

The risk of such consequences for the individual varies widely and depends on the situation. However, researchers have found a general trend toward an increased risk of adverse effects on society as the average alcohol intake among individuals increases ( Mäkelä and Mustonen 1988 ; Mäkelä and Simpura 1985 ).

Alcohol use is associated with increased risk of injury in a wide variety of circumstances, including automobile crashes, falls, and fires ( Cherpitel 1992 ; Freedland et al. 1993 ; Hingson and Howland 1993 ; Hurst et al. 1994 ). Research shows that as people drink increasing quantities of alcohol, their risk of injury increases steadily and the risk begins to rise at relatively low levels of consumption ( Cherpitel et al. 1995 ). An analysis of risk in relation to alcohol use in the hours leading up to an injury has suggested that the amount of alcohol consumed during the 6 hours prior to injury is related directly to the likelihood of injury occurrence ( Vinson et al. 1995 ). The evidence showed a dose-response relationship between intake and injury risk and found no level of drinking to be without risk.

Patterns of alcohol consumption also increase the risk of violence and the likelihood that aggressive behavior will escalate ( Cherpitel 1994 ; Martin 1992 ; Martin and Bachman 1997 ; Norton and Morgan 1989 ; Zhang et al. 1997 ). Alcohol appears to interact with personality characteristics, such as impulsiveness and other factors related to a personal propensity for violence ( Lang 1993 ; Zhang et al. 1997 ). Violence-related trauma also appears to be more closely linked to alcohol dependence symptoms than to other types of alcohol-related injury ( Cherpitel 1997 ).

Patterns of moderate drinking, on the other hand, have been associated with a key health benefit—that is, a lower CHD risk. Research is now in progress to clarify the extent to which alcohol itself, or other factors or surrogates such as lifestyle, diet, exercise, or additives to alcoholic beverages, may be responsible for the lower risk. Broader means of quantifying the relationships between relative risks and specific consumption levels and patterns are needed to describe epidemiologic findings more clearly and simply, and translate them into improved public health strategies.

The Overall Impact

The overall impact of alcohol consumption on mortality can be assessed in two ways ( Rehm and Bondy 1998 ): (1) by conducting meta-analyses using epidemiologic studies that examine all factors contributing to mortality, or (2) by combining risk for various alcohol-caused diseases with a weighted prevalence or incidence of each respective disease.

The meta-analysis approach to assessing overall mortality was used by researchers to examine the results of 16 studies, 10 of which were conducted in the United States ( English et al. 1995 ). In this overview, researchers found the relationship between alcohol intake and mortality for both men and women to be J-shaped curves: the lowest observed risk for overall mortality was associated with an average of 10 grams of alcohol (less than one drink) per day for men and less for women. An average intake of 20 grams (between one and two drinks) per day for women was associated with a significantly increased risk of death compared with abstainers. The risk for women continued to rise with increased consumption and was 50 percent higher among those consuming an average of 40 grams of alcohol (between three and four drinks) per day than among abstainers. Men who averaged 30 grams of alcohol (two drinks) per day had the same mortality as abstainers, whereas a significant increase in mortality was found for those consuming at least 40 grams of alcohol per day.

The proposed J-shaped relationship between alcohol intake and mortality does not apply in all cases, however. For example, because most of the physiologic benefit of moderate drinking is confined to ischemic cardiovascular conditions, such as CHD, in areas of the world where there is little mortality from cardiovascular diseases, alcohol provides little or no reduction in overall mortality. Rather, the relationship between intake and all-cause mortality assumes more of a direct, linear shape ( Murray and Lopez 1996 c ), with increasing consumption associated with higher overall mortality. The same holds true for people under age 45, who have little ischemic cardiovascular mortality ( Andréasson et al. 1988 , 1991; Rehm and Sempos 1995 ).

Quantifying the level of disability and morbidity related to alcohol can be difficult, in large part because few standardized measures exist. One way to quantify the relationship between alcohol and health-related consequences is to use a measure called the disability-adjusted life year (DALY), which may prove useful in summarizing the effects of alcohol on the full spectrum of health outcomes.

In the Global Burden of Disease Study ( Murray and Lopez, 1996 , 1997 b ), the researchers combined years of life lost and years lived with disability into a single indicator, DALY, in which each year lived with a disability was adjusted according to the severity of the disability ( Murray and Lopez 1997 b , c ). The study found tremendous differences in alcohol’s impact on disability across different regions of the world. The most pronounced overall effect was observed in established market economies. The researchers found the smallest effect of alcohol in the Middle Eastern crescent, which is not surprising given the region’s high proportion of abstinent Islamic populations ( Murray and Lopez 1997 a ).

Epidemiologic studies have long provided evidence of the harm alcohol can cause to individual health and to society as a whole. Newer studies have identified an association between low to moderate alcohol consumption and reduced CHD risk and overall mortality. The most significant association with lower CHD risk is largely confined to middle-aged and older individuals in industrialized countries with high rates of cardiovascular diseases. Elucidation of the mechanisms by which alcohol affects CHD risk will clarify the relationship and may enable scientists to develop pharmacologic agents that could mimic or facilitate the positive effect of alcohol on health ( Hennekens 1996 ; UK Inter-Departmental Working Group 1995 ; USDA 1995 ). At this point, research clearly indicates that no pattern of drinking is without risks. However, for individuals who continue to consume alcohol, certain drinking patterns may help reduce these risks considerably.

Among teenagers and young adults in particular, the risks of alcohol use outweigh any benefits that may accrue later in life, since alcohol abuse and dependence and alcohol-related violent behavior and injuries are all too common in young people and are not easily predicted. To determine the likely net outcome of alcohol consumption, the probable risks and benefits for each drinker must be carefully weighed.

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