alcohol abuse research paper

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• Published: 13 November 2019

Evidence-based models of care for the treatment of alcohol use disorder in primary health care settings: protocol for systematic review

• Susan A. Rombouts 1 ,
• James Conigrave 2 ,
• Eva Louie 1 ,
• Paul Haber 1 , 3 &
• Kirsten C. Morley   ORCID: orcid.org/0000-0002-0868-9928 1  

Systematic Reviews volume  8 , Article number:  275 ( 2019 ) Cite this article

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Alcohol use disorder (AUD) is highly prevalent and accounts globally for 1.6% of disability-adjusted life years (DALYs) among females and 6.0% of DALYs among males. Effective treatments for AUDs are available but are not commonly practiced in primary health care. Furthermore, referral to specialized care is often not successful and patients that do seek treatment are likely to have developed more severe dependence. A more cost-efficient health care model is to treat less severe AUD in a primary care setting before the onset of greater dependence severity. Few models of care for the management of AUD in primary health care have been developed and with limited implementation. This proposed systematic review will synthesize and evaluate differential models of care for the management of AUD in primary health care settings.

We will conduct a systematic review to synthesize studies that evaluate the effectiveness of models of care in the treatment of AUD in primary health care. A comprehensive search approach will be conducted using the following databases; MEDLINE (1946 to present), PsycINFO (1806 to present), Cochrane Database of Systematic Reviews, Cochrane Central Register of Controlled Trials (CENTRAL) (1991 to present), and Embase (1947 to present).

Reference searches of relevant reviews and articles will be conducted. Similarly, a gray literature search will be done with the help of Google and the gray matter tool which is a checklist of health-related sites organized by topic. Two researchers will independently review all titles and abstracts followed by full-text review for inclusion. The planned method of extracting data from articles and the critical appraisal will also be done in duplicate. For the critical appraisal, the Cochrane risk of bias tool 2.0 will be used.

This systematic review and meta-analysis aims to guide improvement of design and implementation of evidence-based models of care for the treatment of alcohol use disorder in primary health care settings. The evidence will define which models are most promising and will guide further research.

Protocol registration number

PROSPERO CRD42019120293.

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It is well recognized that alcohol use disorders (AUD) have a damaging impact on the health of the population. According to the World Health Organization (WHO), 5.3% of all global deaths were attributable to alcohol consumption in 2016 [ 1 ]. The 2016 Global Burden of Disease Study reported that alcohol use led to 1.6% (95% uncertainty interval [UI] 1.4–2.0) of total DALYs globally among females and 6.0% (5.4–6.7) among males, resulting in alcohol use being the seventh leading risk factor for both premature death and disability-adjusted life years (DALYs) [ 2 ]. Among people aged 15–49 years, alcohol use was the leading risk factor for mortality and disability with 8.9% (95% UI 7.8–9.9) of all attributable DALYs for men and 2.3% (2.0–2.6) for women [ 2 ]. AUD has been linked to many physical and mental health complications, such as coronary heart disease, liver cirrhosis, a variety of cancers, depression, anxiety, and dementia [ 2 , 3 ]. Despite the high morbidity and mortality rate associated with hazardous alcohol use, the global prevalence of alcohol use disorders among persons aged above 15 years in 2016 was stated to be 5.1% (2.5% considered as harmful use and 2.6% as severe AUD), with the highest prevalence in the European and American region (8.8% and 8.2%, respectively) [ 1 ].

Effective and safe treatment for AUD is available through psychosocial and/or pharmacological interventions yet is not often received and is not commonly practiced in primary health care. While a recent European study reported 8.7% prevalence of alcohol dependence in primary health care populations [ 4 ], the vast majority of patients do not receive the professional treatment needed, with only 1 in 5 patients with alcohol dependence receiving any formal treatment [ 4 ]. In Australia, it is estimated that only 3% of individuals with AUD receive approved pharmacotherapy for the disorder [ 5 , 6 ]. Recognition of AUD in general practice uncommonly leads to treatment before severe medical and social disintegration [ 7 ]. Referral to specialized care is often not successful, and those patients that do seek treatment are likely to have more severe dependence with higher levels of alcohol use and concurrent mental and physical comorbidity [ 4 ].

Identifying and treating early stage AUDs in primary care settings can prevent condition worsening. This may reduce the need for more complex and more expensive specialized care. The high prevalence of AUD in primary health care and the chronic relapsing character of AUD make primary care a suitable and important location for implementing evidence-based interventions. Successful implementation of treatment models requires overcoming multiple barriers. Qualitative studies have identified several of those barriers such as limited time, limited organizational capacity, fear of losing patients, and physicians feeling incompetent in treating AUD [ 8 , 9 , 10 ]. Additionally, a recent systematic review revealed that diagnostic sensitivity of primary care physicians in the identification of AUD was 41.7% and that only in 27.3% alcohol problems were recorded correctly in primary care records [ 11 ].

Several models for primary care have been created to increase identification and treatment of patients with AUD. Of those, the model, screening, brief interventions, and referral to specialized treatment for people with severe AUD (SBIRT [ 12 ]) is most well-known. Multiple systematic reviews exist, confirming its effectiveness [ 13 , 14 , 15 ], although implementation in primary care has been inadequate. Moreover, most studies have looked primarily at SBIRT for the treatment of less severe AUD [ 16 ]. In the treatment of severe AUD, efficacy of SBIRT is limited [ 16 ]. Additionally, many patient referred to specialized care often do not attend as they encounter numerous difficulties in health care systems including stigmatization, costs, lack of information about existing treatments, and lack of non-abstinence-treatment goals [ 7 ]. An effective model of care for improved management of AUD that can be efficiently implemented in primary care settings is required.

Review objective

This proposed systematic review will synthesize and evaluate differential models of care for the management of AUD in primary health care settings. We aim to evaluate the effectiveness of the models of care in increasing engagement and reducing alcohol consumption.

By providing this overview, we aim to guide improvement of design and implementation of evidence-based models of care for the treatment of alcohol use disorder in primary health care settings.

The systematic review is registered in PROSPERO international prospective register of systematic reviews (CRD42019120293) and the current protocol has been written according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Protocols (PRISMA-P) recommended for systematic reviews [ 17 ]. A PRISMA-P checklist is included as Additional file  1 .

Eligibility criteria

Criteria for considering studies for this review are classified by the following:

Study design

Both individualized and cluster randomized trials will be included. Masking of patients and/or physicians is not an inclusion criterion as it is often hard to accomplish in these types of studies.

Patients in primary health care who are identified (using screening tools or by primary health care physician) as suffering from AUD (from mild to severe) or hazardous alcohol drinking habits (e.g., comorbidity, concurrent medication use). Eligible patients need to have had formal assessment of AUD with diagnostic tools such as Diagnostic and Statistical Manual of Mental Disorders (DSM-IV/V) or the International Statistical Classification of Diseases and Related Health Problems (ICD-10) and/or formal assessment of hazardous alcohol use assessed by the Comorbidity Alcohol Risk Evaluation Tool (CARET) or the Alcohol Use Disorders Identification test (AUDIT) and/or alcohol use exceeding guideline recommendations to reduce health risks (e.g., US dietary guideline (2015–2020) specifies excessive drinking for women as ≥ 4 standard drinks (SD) on any day and/or ≥ 8 SD per week and for men ≥ 5 SD on any day and/or ≥ 15 SD per week).

Studies evaluating models of care for additional diseases (e.g., other dependencies/mental health) other than AUD are included when they have conducted data analysis on the alcohol use disorder patient data separately or when 80% or more of the included patients have AUD.

Intervention

The intervention should consist of a model of care; therefore, it should include multiple components and cover different stages of the care pathway (e.g., identification of patients, training of staff, modifying access to resources, and treatment). An example is the Chronic Care Model (CCM) which is a primary health care model designed for chronic (relapsing) conditions and involves six elements: linkage to community resources, redesign of health care organization, self-management support, delivery system redesign (e.g., use of non-physician personnel), decision support, and the use of clinical information systems [ 18 , 19 ].

As numerous articles have already assessed the treatment model SBIRT, this model of care will be excluded from our review unless the particular model adds a specific new aspect. Also, the article has to assess the effectiveness of the model rather than assessing the effectiveness of the particular treatment used. Because identification of patients is vital to including them in the trial, a care model that only evaluates either patient identification or treatment without including both will be excluded from this review.

Model effectiveness may be in comparison with the usual care or a different treatment model.

Included studies need to include at least one of the following outcome measures: alcohol consumption, treatment engagement, uptake of pharmacological agents, and/or quality of life.

Solely quantitative research will be included in this systematic review (e.g., randomized controlled trials (RCTs) and cluster RCTs). We will only include peer-reviewed articles.

Restrictions (language/time period)

Studies published in English after 1 January 1998 will be included in this systematic review.

Studies have to be conducted in primary health care settings as such treatment facilities need to be physically in or attached to the primary care clinic. Examples are co-located clinics, veteran health primary care clinic, hospital-based primary care clinic, and community primary health clinics. Specialized primary health care clinics such as human immunodeficiency virus (HIV) clinics are excluded from this systematic review. All studies were included, irrespective of country of origin.

Search strategy and information sources

A comprehensive search will be conducted. The following databases will be consulted: MEDLINE (1946 to present), PsycINFO (1806 to present), Cochrane Database of Systematic Reviews, Cochrane Central Register of Controlled Trials (CENTRAL) (1991 to present), and Embase (1947 to present). Initially, the search terms will be kept broad including alcohol use disorder (+synonyms), primary health care, and treatment to minimize the risk of missing any potentially relevant articles. Depending on the number of references attained by this preliminary search, we will add search terms referring to models such as models of care, integrated models, and stepped-care models, to limit the number of articles. Additionally, we will conduct reference searches of relevant reviews and articles. Similarly, a gray literature search will be done with the help of Google and the Gray Matters tool which is a checklist of health-related sites organized by topic. The tool is produced by the Canadian Agency for Drugs and Technologies in Health (CADTH) [ 20 ].

See Additional file  2 for a draft of our search strategy in MEDLINE.

Data collection

The selection of relevant articles is based on several consecutive steps. All references will be managed using EndNote (EndNote version X9 Clarivate Analytics). Initially, duplicates will be removed from the database after which all the titles will be screened with the purpose of discarding clearly irrelevant articles. The remaining records will be included in an abstract and full-text screen. All steps will be done independently by two researchers. Disagreement will lead to consultation of a third researcher.

Data extraction and synthesis

Two researchers will extract data from included records. At the conclusion of data extraction, these two researchers will meet with the lead author to resolve any discrepancies.

In order to follow a structured approach, an extraction form will be used. Key elements of the extraction form are information about design of the study (randomized, blinded, control), type of participants (alcohol use, screening tool used, socio-economic status, severity of alcohol use, age, sex, number of participants), study setting (primary health care setting, VA centers, co-located), type of intervention/model of care (separate elements of the models), type of health care worker (primary, secondary (co-located)), duration of follow-up, outcome measures used in the study, and funding sources. We do not anticipate having sufficient studies for a meta-analysis. As such, we plan to perform a narrative synthesis. We will synthesize the findings from the included articles by cohort characteristics, differential aspects of the intervention, controls, and type of outcome measures.

Sensitivity analyses will be conducted when issues suitable for sensitivity analysis are identified during the review process (e.g., major differences in quality of the included articles).

Potential meta-analysis

In the event that sufficient numbers of effect sizes can be extracted, a meta-analytic synthesis will be performed. We will extract effect sizes from each study accordingly. Two effect sizes will be extracted (and transformed where appropriate). Categorical outcomes will be given in log odds ratios and continuous measures will be converted into standardized mean differences. Variation in effect sizes attributable to real differences (heterogeneity) will be estimated using the inconsistency index ( I 2 ) [ 21 , 22 ]. We anticipate high degrees of variation among effect sizes, as a result moderation and subgroup-analyses will be employed as appropriate. In particular, moderation analysis will focus on the degree of heterogeneity attributable to differences in cohort population (pre-intervention drinking severity, age, etc.), type of model/intervention, and study quality. We anticipate that each model of care will require a sub-group analysis, in which case a separate meta-analysis will be performed for each type of model. Small study effect will be assessed with funnel plots and Egger’s symmetry tests [ 23 ]. When we cannot obtain enough effect sizes for synthesis or when the included studies are too diverse, we will aim to illustrate patterns in the data by graphical display (e.g., bubble plot) [ 24 ].

Critical appraisal of studies

All studies will be critically assessed by two researchers independently using the Revised Cochrane risk-of-bias tool (RoB 2) [ 25 ]. This tool facilitates systematic assessment of the quality of the article per outcome according to the five domains: bias due to (1) the randomization process, (2) deviations from intended interventions, (3) missing outcome data, (4) measurement of the outcome, and (5) selection of the reported results. An additional domain 1b must be used when assessing the randomization process for cluster-randomized studies.

Meta-biases such as outcome reporting bias will be evaluated by determining whether the protocol was published before recruitment of patients. Additionally, trial registries will be checked to determine whether the reported outcome measures and statistical methods are similar to the ones described in the registry. The gray literature search will be of assistance when checking for publication bias; however, completely eliminating the presence of publication bias is impossible.

Similar to article selection, any disagreement between the researchers will lead to discussion and consultation of a third researcher. The strength of the evidence will be graded according to the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach [ 26 ].

The primary outcome measure of this proposed systematic review is the consumption of alcohol at follow-up. Consumption of alcohol is often quantified in drinking quantity (e.g., number of drinks per week), drinking frequency (e.g., percentage of days abstinent), binge frequency (e.g., number of heavy drinking days), and drinking intensity (e.g., number of drinks per drinking day). Additionally, outcomes such as percentage/proportion included patients that are abstinent or considered heavy/risky drinkers at follow-up. We aim to report all these outcomes. The consumption of alcohol is often self-reported by patients. When studies report outcomes at multiple time points, we will consider the longest follow-up of individual studies as a primary outcome measure.

Depending on the included studies, we will also consider secondary outcome measures such as treatment engagement (e.g., number of visits or pharmacotherapy uptake), economic outcome measures, health care utilization, quality of life assessment (physical/mental), alcohol-related problems/harm, and mental health score for depression or anxiety.

This proposed systematic review will synthesize and evaluate differential models of care for the management of AUD in primary health care settings.

Given the complexities of researching models of care in primary care and the paucity of a focus on AUD treatment, there are likely to be only a few studies that sufficiently address the research question. Therefore, we will do a preliminary search without the search terms for model of care. Additionally, the search for online non-academic studies presents a challenge. However, the Gray Matters tool will be of guidance and will limit the possibility of missing useful studies. Further, due to diversity of treatment models, outcome measures, and limitations in research design, it is possible that a meta-analysis for comparative effectiveness may not be appropriate. Moreover, in the absence of large, cluster randomized controlled trials, it will be difficult to distinguish between the effectiveness of the treatment given and that of the model of care and/or implementation procedure. Nonetheless, we will synthesize the literature and provide a critical evaluation of the quality of the evidence.

This review will assist the design and implementation of models of care for the management of AUD in primary care settings. This review will thus improve the management of AUD in primary health care and potentially increase the uptake of evidence-based interventions for AUD.

Availability of data and materials

Not applicable.

Abbreviations

Alcohol use disorder

Alcohol Use Disorders Identification test

Canadian Agency for Drugs and Technologies in Health

The Comorbidity Alcohol Risk Evaluation

Cochrane Central Register of Controlled Trials

Diagnostic and Statistical Manual of Mental Disorders

Human immunodeficiency virus

10 - International Statistical Classification of Diseases and Related Health Problems

Preferred Reporting Items for Systematic Reviews and Meta-Analyses Protocols

Screening, brief intervention, referral to specialized treatment

Standard drinks

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Discipline of Addiction Medicine, Central Clinical School, Faculty of Medicine and Health, University of Sydney, Sydney, NSW, Australia

Susan A. Rombouts, Eva Louie, Paul Haber & Kirsten C. Morley

NHMRC Centre of Research Excellence in Indigenous Health and Alcohol, Central Clinical School, Faculty of Medicine and Health, University of Sydney, Sydney, NSW, Australia

James Conigrave

Drug Health Services, Royal Prince Alfred Hospital, Camperdown, NSW, Australia

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Contributions

KM and PH conceived the presented idea of a systematic review and meta-analysis and helped with the scope of the literature. KM is the senior researcher providing overall guidance and the guarantor of this review. SR developed the background, search strategy, and data extraction form. SR and EL will both be working on the data extraction and risk of bias assessment. SR and JC will conduct the data analysis and synthesize the results. All authors read and approved the final manuscript.

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Correspondence to Kirsten C. Morley .

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Supplementary information

Additional file 1..

PRISMA-P 2015 Checklist.

Additional file 2.

Draft search strategy MEDLINE. Search strategy.

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Rombouts, S.A., Conigrave, J., Louie, E. et al. Evidence-based models of care for the treatment of alcohol use disorder in primary health care settings: protocol for systematic review. Syst Rev 8 , 275 (2019). https://doi.org/10.1186/s13643-019-1157-7

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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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Center for Social and Affective Neuroscience, Department of Biomedical and Clinical Sciences, Linköping University, 581 83, Linköping, Sweden

Hanna Karlsson, Irene Perini, Adam Yngve & Markus Heilig

Department of Management and Engineering, Division of Economics, Linköping University, 581 83, Linköping, Sweden

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

Gustav Tinghög

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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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Article Contents

Introduction, the heritage of the 19th century — a concept of addiction, temperance and degeneration, trying to eradicate alcoholism — different approaches, after prohibition — the creation of a modern disease concept, one or many types of alcoholism — genetic findings and potential subtypes, the core of alcohol dependence — tolerance and withdrawal or sensitization and reward craving, the disease concept revisited, new treatment options and future directions.

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ONE HUNDRED YEARS OF ALCOHOLISM: THE TWENTIETH CENTURY

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Karl Mann, Derik Hermann, Andreas Heinz, ONE HUNDRED YEARS OF ALCOHOLISM: THE TWENTIETH CENTURY, Alcohol and Alcoholism , Volume 35, Issue 1, January 2000, Pages 10–15, https://doi.org/10.1093/alcalc/35.1.10

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The past 100 years witnessed the formation of a disease concept of alcoholism and a rapid increase in the knowledge of its aetiopathology and treatment options. In the first half of the century, public sanctions aimed at the abolition of alcoholism. In the United States, alcohol prohibition was revoked in the economic turmoil of the Great Depression. In Germany, proposed medical procedures to reduce the fertility of alcoholics had catastrophic consequences during the fascist dictatorship. A revived focus on alcoholics as patients with a right to medical treatment came out of self-organized groups, such as Alcoholics Anonymous. The current disease concept includes the psychosocial and neurobiological foundations and consequences of alcoholism. Neurobiological research points to the dispositional factor of monoaminergic dysfunction and indicates that neuroadaptation and sensitization may play a role in the maintenance of addictive behaviour. New treatment options include pharmacological approaches and indicate that behaviour and motivational therapy and the attendance of patient groups may equally reduce the relapse risk. The task of the future will be to apply scientific discoveries in the best interest of the patients and to support their efforts to be respected like subjects suffering from other diseases.

Alcoholism research and treatment underwent significant changes in the 20th century. Within the last 100 years, a disease concept was formed, which is now widely accepted, the psychosocial and neurobiological consequences of alcoholism have been characterized and treatment programmes have been established and continuously refined. First attempts were made to formulate models of the disposition and development of alcohol dependence that integrate both neurobiological and psychosocial findings. In this essay, we will highlight some of the cornerstones of our present understanding of alcoholism and reflect on some of the organizations and research traditions whose activities were crucial in the development of current concepts. Given the scope of the subject, this review will be both incomplete and subjective, and we will be unable to mention many subjects and institutions whose contributions to current alcoholism concepts were as important and fundamental as the ones we are able to discuss.

An uncontrollable, overwhelming and irresistible desire to consume alcohol was described by Benjamin Rush in 1784, and delirium tremens was independently described by both Pearson and Sutton in 1813 ( Kielhorn, 1988 ). Alcohol craving and withdrawal symptoms were integral parts of the concept of addiction and of the destructive effects of alcohol consumption promoted by the temperance movement in the 19th century ( Levine, 1984 ). In several European countries and in the United States, temperance movements were stimulated by the excessive consumption of liquor and other highly distilled alcoholic beverages, which was uninhibited by cultural traditions and appeared especially problematic among poor working class families during industrialization ( Levine, 1984 ; Henkel, 1998 ). There was, however, a fundamental difference to current concepts of alcoholism: the temperance movement suggested that anyone who consumed excessive amounts of alcohol would suffer from alcohol-related problems and did not suggest that alcoholism could affect certain specifically vulnerable individuals primarily ( Levine, 1984 ; Heather, 1992 ).

A focus on the individual was promoted by degenerationism, the theory that biological factors, toxic environmental influences or moral vices may trigger a cascade of social, moral and medical problems, which increase in each generation and will finally lead to the extinction of that family ( Bynum, 1984 ). The theory of degeneration was based on the pre-Darwinian concept that acquired character traits were passed on to the offspring and assumed that an array of different symptoms and diseases, such as impulsivity, alcoholism, strokes, dementia, microcephaly and epilepsy, were all expressions of one underlying pathology — degeneration ( Hermle, 1986 ).

Degenerationism thus offered a medical explanation for the social problems which were so visible at the end of the 19th century, and excessive alcohol consumption played a crucial role in the concept, as it was seen as a vice which also affects the next generation. In the early 20th century, the degeneration theory suffered from an increasing knowledge about modes of transmission of heritable traits, which pointed to the separate inheritance of different mental and physical diseases, and distinguished between heritable traits and toxic effects on the germ plasm or embryo, thus fundamentally questioning the postulate of the inheritance of acquired traits ( Hermle, 1986 ). However, degenerationism substantially contributed to the concerns about the specific alcohol-related problems of certain individuals.

In the first 30 years of the 20th century, degenerationism and the successors of the temperance movement sparked widespread political activities in the field of alcohol addiction. In the United States, the Anti-Saloon League followed the approach of the temperance movement and focused on the general problems of alcohol consumption. It succeeded in the implementation of alcohol prohibition, which was legally enforced from 1919 to 1933. Prohibition was initially successful in reducing alcohol intake; however, illegal alcohol consumption slowly increased in the late 1920s ( Tyrrell, 1997 ). Prohibition was finally abolished not so much because it failed to abolish alcohol intake, but because of shifting priorities in the Great Depression, when it was argued that liquor production would create jobs and that alcohol taxes might help to reduce income taxes ( Levine, 1984 ).

In Germany, the focus on the individual and their heritable vulnerability to alcohol addiction was imbued with alarmist concerns about the proliferation of the mentally ill, which was supposed to threaten the survival of the nation or ‘race.' Consequently, compulsory sterilization of ‘severe alcoholics' was already advocated by some medical doctors before it was legalized during the Nazi dictatorship. The number of alcohol-dependent patients murdered during the Nazi regime is unknown ( Henkel, 1998 ).

It was in the wake of the failure of prohibition that the current concept of alcoholism was formed, and the worldwide shock about the cruelty and inhumanity of Nazi politics may have promoted the modern disease concept with its focus on individual therapy and its emphasis that alcohol addiction is a disease just like any other physical or mental malady ( Levine, 1984 ; Henkel, 1998 ). A decisive point was the foundation of Alcoholics Anonymous (AA) in the late 1930s. Similar to previous temperance movements, Alcoholics Anonymous displayed a sympathetic and supporting attitude towards the addicted person, but unlike previous groups, AA was only for alcoholics and was not concerned with the general level of alcohol consumption in the population. In fact, the view that all it would take to create an alcohol addict would be his excessive alcohol consumption was no longer persuasive after the end of prohibition ( Levine, 1984 ). Likewise, the existence of alcohol tolerance and withdrawal was widely neglected in the 1930s and early 1940s, although delirium tremens due to alcohol withdrawal had clearly been described by Hare 1910 in the British Journal of Inebriety ( Edwards, 1990 ). Jellinek (1942) and the Yale Summer School on Alcohol Studies agreed with AA that alcoholism would be a disease with a progressive character and not a moral failing. The 1954 report of the World Health Organization (WHO) reflected this new focus on the individual and stated that ‘the personal make-up is the determining factor, but the pharmacological action (of alcohol) plays a significant role’ ( Edwards, 1990 ). However, it was not until the mid-1950s that convulsions and delirium tremens regained public attention as symptoms of alcohol withdrawal, largely due to the detailed reports of Victor and Adams (1953) and Isbell et al . (1955). In 1955, the WHO acknowledged that ‘very serious withdrawal symptoms’, such as convulsions or delirium, may follow the discontinuation of a prolonged period of very heavy alcohol intake ( Edwards, 1990 ). In his famous book on the disease concept of alcoholism, Jellinek (1960) referred repeatedly to the WHO reports and placed the adaptation of cell metabolism, tolerance and the withdrawal symptoms at the heart of his alcoholism concept, because they would ‘bring about ‘craving’ and a loss of control or inability to abstain.’; In his review of the perception of alcohol withdrawal symptoms in the scientific literature, Edwards (1990) noted that Jellinek's new focus on withdrawal symptoms was ‘in very sharp contrast to the earlier stance of the Yale school.’ It is possible that it was easier to rediscover the physical complications of alcohol withdrawal, because the new disease concept allowed attribution of these complications to an individual disposition rather than to some general effect that prolonged alcohol intake would have on every consumer.

In Germany, the modern disease concept of alcoholism was promoted by Feuerlein (1967, 1996) and others who emphasized that alcohol-dependent patients should have the same entitlement to medical treatment as other patients. It was not until 1968 that a German federal court formally confirmed full insurance coverage of alcoholism-related medical treatment costs, although alcoholism had already been considered a disease since 1915 ( Jellinek, 1960 ).

While it had long been observed that the familial risk for alcoholism is increased, it was only because of twin and adoption studies that a genetic contribution to alcoholism was confirmed ( Kaji, 1960 ; Cadoret and Gath, 1978 ). The observation that family members who share half of their genes are not more likely to develop alcoholism compared with family members who share only a quarter of their genes was incompatible with the simple genetic mechanism of inheritance ( Bleuler, 1955 ; Schuckit et al ., 1972 ).

Based on adoption studies, Cloninger et al . (1981) suggested the existence of two types of alcoholism, a mostly environmentally triggered, late-onset type 1 and a male-limited type 2 with a high genetic loading, legal problems and moderate alcohol consumption. The attempt to distinguish between two subtypes of alcoholism stimulated considerable research efforts. Many authors, however, questioned the dichotomy and argued that once patients suffering from comorbid antisocial personality disorder were excluded, the distinction between type 1 and type 2 alcoholics no longer offered clinical subtypes with distinct severity ( Irwin et al ., 1990 ). Instead, subgrouping was suggested to be based on age of onset, the presence of childhood risk factors such as hyperactivity, and severity of alcoholism ( Schuckit et al ., 1995 ; Johnson et al ., 1996 ). Alcoholism types may thus vary on a continuum of severity, rather than represent distinctly different disease entities ( Bucholz et al ., 1996 ). The genetic disposition to alcoholism may manifest in such unsuspicious forms as a low level of response to alcohol intake in subjects not yet accustomed to chronic alcohol intoxication ( Schuckit and Smith, 1996 ). A low level of alcohol response has recently been associated with an increased availability of raphe serotonin transporters and a low central serotonin turnover rate ( Heinz et al ., 1998 ; Schuckit et al ., 1999 ). A low serotonin turnover rate is a potential marker of early-onset alcoholism ( Fils-Aime et al ., 1996 ) and may be caused or aggravated by early social stress experiences ( Higley et al ., 1996 a , b ). These findings may help to link the clinical disposition to alcoholism with the growing literature on neurobiological alterations that precede and follow the manifestation of alcohol dependence.

The last three decades of the twentieth century witnessed a rapidly increasing knowledge of the neurobiological correlates of alcohol dependence. Edwards focused on the development of alcohol tolerance and the manifestation of withdrawal when chronic alcohol intake is terminated ( Edwards et al ., 1977 ). His groundbreaking work was used by the WHO in the International Classification of Diseases (ICD-9) and operationalized in the Diagnostic and Statistical Manual of Mental Disorders (DSM-III-R) as criteria of dependence ( Jurd, 1992 ).

Neurobiological research pointed to alcohol-induced stimulation of inhibitory GABAergic, and the inhibition of excitatory glutamatergic, neurotransmission ( Koob, 1992 ; Tsai et al ., 1995 ). To ensure homeostatic regulation, GABA A receptors may be down-regulated and, indeed, brain imaging studies observed reduced cortical GABA A receptors among alcoholics ( Abi-Dargham et al ., 1998 ). When the sedative effects of alcohol are suddenly withdrawn during early abstinence, reduced GABAergic inhibition and increased glutamatergic excitatory neurotransmission may manifest as anxiety, seizures and autonomic dysregulation ( Tsai et al ., 1995 ). Alcohol consumption may then be reinstated to reduce withdrawal, thus acting as a negative reinforcer ( Edwards, 1990 ). Associative learning may transform neutral emotional or environmental stimuli into alcohol-associated cues that induce a conditioned compensatory response to alcohol, ‘conditioned withdrawal’, and craving ( Ludwig et al ., 1974 ; McCusker and Brown, 1990 ). Acamprosate, a drug used to reduce craving in abstinent alcoholics, blocks glutamatergic N -methyl-d-aspartate receptors and may exert its therapeutic effects by decreasing conditioned withdrawal ( Verheul et al ., 1999 ).

However, cue-induced craving is only moderately associated with the severity of physical reactions such as changes in heart rate and skin conductance to cue presentation ( Niaura et al ., 1988 ). A secondary, potentially independent pathway has been suggested that may induce alcohol craving due to the mood-enhancing, positive-reinforcing effects of alcohol consumption ( Wise, 1988 ; Koob and Le Moal, 1997 ). This pathway seems to involve the so-called dopaminergic reward system and its opioidergic stimulation via μ-opiate receptors ( Spanagel et al ., 1992 ; Di Chiara, 1995 ). The role of the dopaminergic system may lie in the direction of attention towards reward-indicating stimuli, rather than in the induction of euphoria or positive mood states ( Schultz et al ., 1995 ; Berridge and Robinson, 1998), which are associated with alcohol consumption and may be mediated by opioidergic neurotransmission ( Volpicelli et al ., 1995 ). Stimulus-dependent dopamine release may be specifically vulnerable to sensitization, thus mediating a stronger behavioural response upon re-exposure to the drug-associated cue ( Robinson and Berridge, 1993 ). These observations may have important implications for our understanding of the ‘addiction memory’ and for therapeutic strategies: systematic cue exposure and response prevention might help to extinguish conditioned craving, although therapeutic study results so far are ambiguous ( O'Brien et al ., 1998 ), and naltrexone medication may prevent cue-induced reinstatement of alcohol craving (Katner, 1999).

The focus on cue-induced craving and the underlying learning mechanisms ( Glautier et al ., 1994 ; Carter and Tiffany, 1999 ) has revived the discussion on whether the disease concept of alcoholism should be replaced by a social learning perspective ( Heather, 1992 ). What was not being denied are the organic consequences of chronic alcohol intake, such as brain atrophy ( Mann et al ., 1995 ) or neuroadaptive processes such as a reduction of central dopamine D2 receptors ( Volkow et al ., 1996 ). Rather, it is argued that cigarette smoking similarly causes physical dependence or neuroadaptation without therefore being considered a disease. The disease concept may label patients and promote apathy associated with the ‘sick role’ ( Heather, 1992 ).

A response to these concerns rests on several arguments. Firstly, it is argued that the sick role per se does not stigmatize patients and that the stigma associated with specific diseases such as ‘consumption’ never promoted similar attempts to deny its disease status, and instead promoted relabelling as tuberculosis ( Keller, 1976 ). Secondly, it is argued that a state may be called a disease even in the absence of abnormalities of anatomic structure. A case in point may be essential hypertension, which is commonly understood as a disease, although the aetiology and pathogenesis are currently unknown. Keller (1976) suggested calling alcoholism a disease, because its behavioural manifestations represent a disablement. This argument resembles the concept of a mental disorder given by the American Psychiatric Association (1987), which argued that a mental disorder is characterized by present distress, disability, or a significantly increased risk of suffering death, pain, disability, or an important loss of freedom. Culver and Gert (1982) added that the state must exist ‘in the absence of a distinct (external) sustaining cause’, so that distress due to political oppression may be distinguished from a mental malady. Applying this definition to cigarette smoking indicates that smoking should be considered a mental disorder, as it is associated with the increased risk of suffering death, and it would thus be considered a malady or disease by Culver and Gert (1982). This brings up the question of whether fast driving then must be called a disease, as it increases the risk of dying in a traffic accident. It could be answered that the association between fast driving and traffic accidents is rather low and that the habit of driving fast might be terminated without experiencing the distress associated with drug withdrawal symptoms.

As aloof as these discussions sometimes appear, they have important implications for the treatment of alcoholism. In 1956, a Board of the American Medical Association (AMA) passed a resolution that urged hospitals to admit patients with alcoholism equally with patients treated for other diseases. This act is usually seen as the moment when alcoholism was formally recognized as a disease in the United States; however, alcoholism was already listed as a disease in 1933 in the Standard Classified Nomenclature of Diseases, which was approved by the AMA and the American Psychiatric Association ( Keller, 1976 ). Yet the 1956 resolution highlights the important legal issues that are associated with the disease status of alcoholism, not least being the question of whether treatment costs should be covered by health insurances ( Jurd, 1992 ). Research in the field of costs and benefits of alcoholism therapy supported the demand to treat alcoholism within the medical system ( Holder, 1998 ).

The last decade of the 20th century witnessed substantial progress in treatment options and strategies. Of special importance is the general practitioner, who sees the vast majority of patients with alcohol problems, while fewer than 10% actually enter specialized treatment programmes ( Wienberg, 1992 ). Brief interventions in primary health care institutions are very often effective in reducing alcohol consumption ( Bien et al ., 1993 ). For those patients who need more extensive treatment, primary health care services have a gatekeeper function. Motivational enhancement in primary health care ( Miller and Rollnick, 1991 ) can effectively increase the participation in treatment programmes and was associated with reduced subsequent relapse rates ( Bien et al ., 1993 ). Specialized treatment programmes were evaluated in project MATCH. Project MATCH examined three treatment options, cognitive behaviour therapy, twelve-step facilitation according to the AA programme and motivational enhancement therapy, and found them similarly effective ( Project Match Research Group, 1998 ). As disappointing as this result may be for the discovery of prospective indicators of treatment response, it shows that the major treatment options available to alcoholics worldwide work successfully and that the eclectic combination of behaviour therapy and the attendance of self-help groups may indeed combine two powerful treatment strategies. With naltrexone and acamprosate, two pharmaceuticals are available that successfully reduce the relapse risk during early abstinence ( O'Malley et al ., 1996 ; Sass et al ., 1996 ). However, even with an accompanying medical treatment, most alcoholics relapse. The goal of the future will therefore be to describe subgroups of patients that may respond positively to specific medications. As acamprosate and naltrexone affect different neurotransmitter systems, neurobiological screening of alcoholics may help to discover predictors of treatment response. Preliminary results indicate that sleep disorders, EEG activity and delayed recovery of dopamine receptor sensitivity during early abstinence are associated with the relapse risk and may help to identify patients who require specific treatment strategies ( Bauer, 1994 ; Heinz et al ., 1996 ; Brower et al ., 1998 ; Winterer et al ., 1998 ).

Basic research has profoundly helped to understand alcohol effects at the level of signal transduction. We now know that drugs affect neurotransmitter release, receptor sensitivity, post-synaptic second-messenger mechanisms and, perhaps most importantly, gene expression ( Koob, 1992 ; Nestler, 1994 ). These observations indicate that human fate is not passively determined by the genetic constitution, but rather that biological and ultimately environmental stimuli regulate gene expression. Increasing knowledge of the molecular mechanisms of dependence may enable us to target these pathological conditions more specifically than we are able today.

Finally, the history of the last 100 years warns us that ‘ethics are not an option,’ as Edwards stated in a 1999 conference at the Central Institute of Mental Health, Mannheim. That alcoholism had been considered a disease in Germany since 1915 ( Jellinek, 1960 ) did not prevent the dehumanizing treatment of patients with alcohol dependence during the Nazi era. It is an integral part of the professional mission to assist patients in their effort to be treated equally inside and outside of medical therapy. Our increasing knowledge about the disposition towards alcohol dependence and a high relapse risk can help to identify patients with demands for special therapeutic efforts, it should never be used to stigmatize these subjects. To monitor the consequences of our research is part of the professional duty.

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Adolescence and Alcohol: a review of the literature

Affiliation.

• 1 Department of Child- and Adolescent Psychiatry, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. [email protected]
• PMID: 23839238
• DOI: 10.1007/s40211-013-0066-6

Up to two thirds of adolescents consume alcohol and about a quarter engage in abusive behavior at some point. Many users begin alcohol use at young ages, and binge drinking is a dominant pattern for a proportion of youth. Because neurogenesis is inhibited by ethanol, consequences of adolescent alcohol abuse include changes in brain development and impairment of neurocognitive performance. A variety of mental and psychosocial problems are also often witnessed in alcohol abusing youth. Apart from the influence exerted by genetic and psychosocial factors, the chance of developing problematic alcohol consumption is increased by consumption in a binge drinking manner and by first contact with alcohol at a young age. Discrimination of alcohol consumption within the frames of normal adolescent behavior from problematic use is still a challenging issue. Different prevention programs provide treatment either directly to the adolescent, in the context of the school, or within the frame of the adolescent's family. Although some of these efforts have been shown to be effective in reducing alcohol misuse in youth, hardly any intervention reveals satisfactory outcomes in a long-term prospect. Successful prevention strategies would need to comprise treatment of current neuropsychological impairment as well as of comorbid mental health problems and concurrent other substance misuse.

Publication types

• Alcohol Drinking / adverse effects
• Alcohol Drinking / epidemiology*
• Alcohol Drinking / prevention & control
• Alcohol Drinking / psychology
• Alcohol-Induced Disorders, Nervous System / epidemiology
• Alcohol-Induced Disorders, Nervous System / prevention & control
• Alcohol-Induced Disorders, Nervous System / psychology
• Alcoholism / epidemiology*
• Alcoholism / prevention & control
• Alcoholism / psychology
• Binge Drinking / epidemiology*
• Binge Drinking / prevention & control
• Binge Drinking / psychology
• Cross-Sectional Studies
• Follow-Up Studies
• Outcome and Process Assessment, Health Care
• Prospective Studies
• Risk Factors
• Temperance / psychology
• Temperance / statistics & numerical data

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Alcohol is dangerous. so is ‘alcoholic.’.

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Researcher explains the human toll of language that makes addiction feel worse 

When Mass General transplant hepatologist Wei Zhang says he wants his colleagues to think before they speak, he has the tragedy of a recent patient in mind.

Admitted to intensive care for advanced alcohol-associated liver disease, the 36-year-old woman hid the truth when asked about her drinking. “She was like, ‘No, I quit over a year ago, I didn’t drink at all,’” said Zhang, also director of the hospital’s Alcohol-Associated Liver Disease Clinic. “But we have tools that can detect the use of alcohol in the past three, four weeks.”

The patient, who had been traumatized by years of physical abuse, was denied a liver transplant, in part because she withheld information about her alcohol use. Her death days later was “a consequence of stigma,” Zhang said. Patients too often “feel they’re being judged and may fear that their condition is seen as a result of personal failing rather than a medical issue that needs treatment.” 

Amid increases in high-risk drinking and alcohol-associated liver disease across the country , he hopes  that new research can help complete the years-long work of erasing that stigma, saving lives in the process. 

For decades, medical terminology has labeled liver disease and other alcohol-related conditions as “alcoholic”: alcoholic liver disease, alcoholic hepatitis, alcoholic cirrhosis, alcoholic pancreatitis. Meanwhile, clinicians and administrators have described patients as addicts and alcoholics. 

More recently, specialists and advocates have sought with some success to revise how we talk about substance use and those struggling to overcome it, not just to reduce stigma but also to combat bias among medical professionals. According to the  National Institute on Alcohol Abuse and Alcoholism , the term “alcohol use disorder” is now preferable to “alcohol abuse,” “alcohol dependence,” and “alcoholism.”

“Emphasizing non-stigmatizing language is crucial not only for fostering honesty but also for supporting the overall treatment process and patient outcomes,” Zhang said. 

The new study is a step toward that goal. Inspired by his patients, Zhang set out to observe whether the terminology used by institutions that treat alcohol-associated liver disease reflects or rejects stigma. He and his team reviewed messages on more than 100 accredited liver transplant center websites, along with language used by addiction psychiatry sites. They found that almost nine of 10 transplant center websites use stigmatizing language such as “alcoholic.” Less than half of addiction psychiatry websites do the same.

“The gap between professional society recommendations and actual practice is concerning, since patients frequently use these online resources for information which can significantly influence their behavior and perceptions about alcohol-associated liver disease,” Zhang said.

Zhang’s anti-stigma efforts are grounded in strong evidence, according to Harvard Medical School psychiatrist  John F. Kelly , who published “Does It Matter How We Refer to Individuals with Substance-Related Conditions?” in 2009.

“Emphasizing non-stigmatizing language is crucial not only for fostering honesty but also for supporting the overall treatment process and patient outcomes.”

“Drug use disorder and alcohol use disorder are among the most stigmatized conditions universally across different societies because people feel that it’s self-induced — that people are to blame because they put it in their body,” said Kelly, also the founder of Mass General’s  Recovery Research Institute . “Just because they made that decision initially, doesn’t mean they plan on becoming addicted.”

In the 2009 study, Kelly and his colleagues described patients to more than 600 clinicians, alternating between “substance abuser” and “having a substance use disorder.” Those in the latter category were viewed more sympathetically and as more worthy of treatment. 

“I was quite surprised just how susceptible they were,” Kelly said. “These were passionate, dedicated clinicians. They were still susceptible to the negative punitive bias.”

They still are today, Zhang’s findings suggest. 

“We are very good at seeing patients with liver disease but if we add this behavioral mental disorder, it is somewhat out of our scope,” he said. “I think education could at least have them be more familiar with this topic and be willing to at least listen to the adoption and use of non-stigmatizing language.” 

“I think education could at least have them be more familiar with this topic and be willing to at least listen to the adoption and use of non-stigmatizing language.”

Building on the new study, Zhang has recommended to healthcare institutions and professional societies that they implement website feedback mechanisms and carry out regular content audits to guard against potentially harmful language. 

“The steps we are recommending should not only help to align clinical practice with sound language guidelines, but also foster a more empathetic and supportive healthcare environment for patients,” he said. 

Zhang also said healthcare institutions should look to leverage technology to support adoption of appropriate standards.

His team is collaborating with Mass General’s Research Patient Data Registry to obtain de-identified patient records, which they plan to review for instances of stigmatizing language. He hopes the process will help researchers quantify the prevalence of such language in clinical notes and identify patterns that can inform interventions. The team will also analyze the association of stigmatizing language with patient outcomes.  

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More From Forbes

The dramatically rising toll of alcohol abuse.

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The toll of alcohol abuse is rising dramatically.

In the United States, the leading preventable cause of death is tobacco and second is poor diet and physical inactivity. Care to guess what comes in third? You can’t be faulted if you guessed opioids such as illicit fentanyl, given all the media attention it gets. But no, it’s something much more accessible, advertised directly to the consumer and having a negative impact across all socioeconomic groups: Alcohol, and specifically the problem of alcohol abuse which is dramatically worsening recently.

From 1999 to 2017, the number of alcohol-related deaths in the U.S. doubled, to more than 70,000 a year. These numbers got much worse at the height of the Covid-19 pandemic. According to the National Institute on Alcohol Abuse and Alcoholism, alcohol-related deaths soared , reaching 178,000 in 2020 and 2021. Comprehensive federal datasets have yet to be released for 2022 and 2023.

In a study published in 2020 in the Journal of the American Medical Association, researchers showed that significant increases in mortality started emerging in the mid 2010s across all racial and ethnic groups. But the steepest rate of acceleration of alcohol-induced deaths occurred among younger, white individuals, especially women. Authors noted that the large increases among younger age groups presaged “substantial future increases in alcohol-related disease.” In light of more recent figures which suggest an intensifying problem, it appears that the researchers’ warning provided more than four years ago was prescient.

What could be compounding the problem of youth drinking are the ways in which advertisers depict alcohol consumption. They emphasize its social acceptability—even its supposed link to social success—and this especially applies when commercials direct their messages at a comparatively young demographic.

The data demonstrate that the marketing works. Researchers publishing in the Journal of Public Health Research found a strong association between the youth-appeal of marketing content of televised alcohol advertisements and the brand-specific consumption of both underage youth and adults.

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Critics of certain commercials that are aimed at a younger demographic, like a beer ad which aired in 2019 promoting “Coors Light. The Official Beer of Saturday Morning,” suggest the companies that sponsor the advertising are going too far.

The negative health effects of alcohol are usually because of excessive drinking over long periods of time. Here, the leading causes of alcohol-attributable deaths are liver and cardiovascular diseases, seven types of cancer—including liver, throat, mouth, esophagus and stomach—as well as alcohol use disorder. NIAAA defines the latter as a “medical condition characterized by an impaired ability to stop or control alcohol use despite adverse social, occupational, or health consequences.” This can encompass alcohol abuse, dependence, addiction and the colloquial term, alcoholism.

But consuming a large amount of alcohol in a short period of time can also be deadly, as it may lead to alcohol poisoning or other dangers like motor vehicle accidents. The Centers for Disease Control and Prevention estimates that 17% of U.S. adults binge drink. Moreover, in 2021 alcohol-impaired driving fatalities accounted for 13,384 (roughly a third) of all motor vehicular deaths. And 40% of violent crimes such as assault, homicide and domestic abuse, were committed by people who had high blood alcohol content at the time of their arrest.

The rise in alcohol abuse certainly isn’t limited to the U.S. In the United Kingdom, for instance, The Guardian reported last month that heavier drinking during the Covid-19 pandemic led to 2,500 more deaths from alcohol in 2022 than in 2019, a 33% jump.

While alcohol can be a toxic, carcinogenic drug, it’s also enjoyed by many people in moderation and often as an accompaniment—a lubricant of sorts—in a variety of social settings. Research psychologists have found that drinking moderate amounts of alcohol in a group setting “boosts people’s emotions and enhances social bonding.”

In addition, there may be physical gains associated with consumption of small amounts of alcohol. The Harvard T.H. Chan School of Public Health and others, like WebMD, still tout certain cardiovascular health benefits related to moderate intake of alcohol.

Nevertheless, other health entities, such as the Mayo Clinic, appear to be taking a different stance lately. The hospital group now says that “drinking alcohol in any amount carries a health risk,” though it qualifies the statement by suggesting that “while the risk is low for moderate intake, the risk increases as the amount you drink goes up.”

And a STAT News article published this month indicates that “alcohol isn’t healthy after all.” The publication asks whether the new dietary guidelines, set by the U.S. Departments of Agriculture and Health and Human Services and scheduled to be released in 2025, will be shaped more by health or (alcohol) industry interests? It’s suggested that changes in guidance are likely if the experts who draft the recommendations take into account the evidence of alcohol-related harms, including “heightened risks of certain cancers, chronic diseases, and injuries.”

While prevention is important, treatment is equally vital. Research published by The Lancet shows that early, preventive strategies in primary care can be effective, and a variety of interventions are available to treat alcohol dependence.

However, access to quality care for alcohol misuse and alcohol-associated diseases is often lacking. Additionally, there may be a stigma attached to seeking help for something as socially acceptable and easily accessible as alcohol.

Public health specialists have therefore asserted that it’s time for a national dialogue about substance misuse of all drugs, legal and illegal, and that this discussion should include alcohol. In this context, experts suggest that efforts need to be centered around research on alcoholism, addiction and abuse, as well as ways to improve access to therapy for alcohol use disorders, possible curbs on advertising and targeted awareness and education campaigns.

However, alcohol abuse and misuse is not (yet) considered a public health emergency. Without declaring it as such, sufficient funding for a concerted nationwide policy is not forthcoming, which means the federal government hasn’t prioritized an alcohol policy in the same way it has done for illicit drugs, or prescription opioids for that matter. Perhaps the latest alarming figures on the rising toll of alcohol abuse will help trigger more urgency.

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