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• Published: 25 August 2022

Age-related differences in the effect of chronic alcohol on cognition and the brain: a systematic review

• Lauren Kuhns   ORCID: orcid.org/0000-0002-3156-8905 1 , 2 ,
• Emese Kroon   ORCID: orcid.org/0000-0003-1803-9336 1 , 2 ,
• Heidi Lesscher 3 ,
• Gabry Mies 1 &
• Janna Cousijn 1 , 2 , 4  

Translational Psychiatry volume  12 , Article number:  345 ( 2022 ) Cite this article

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Adolescence is an important developmental period associated with increased risk for excessive alcohol use, but also high rates of recovery from alcohol use-related problems, suggesting potential resilience to long-term effects compared to adults. The aim of this systematic review is to evaluate the current evidence for a moderating role of age on the impact of chronic alcohol exposure on the brain and cognition. We searched Medline, PsycInfo, and Cochrane Library databases up to February 3, 2021. All human and animal studies that directly tested whether the relationship between chronic alcohol exposure and neurocognitive outcomes differs between adolescents and adults were included. Study characteristics and results of age-related analyses were extracted into reference tables and results were separately narratively synthesized for each cognitive and brain-related outcome. The evidence strength for age-related differences varies across outcomes. Human evidence is largely missing, but animal research provides limited but consistent evidence of heightened adolescent sensitivity to chronic alcohol’s effects on several outcomes, including conditioned aversion, dopaminergic transmission in reward-related regions, neurodegeneration, and neurogenesis. At the same time, there is limited evidence for adolescent resilience to chronic alcohol-induced impairments in the domain of cognitive flexibility, warranting future studies investigating the potential mechanisms underlying adolescent risk and resilience to the effects of alcohol. The available evidence from mostly animal studies indicates adolescents are both more vulnerable and potentially more resilient to chronic alcohol effects on specific brain and cognitive outcomes. More human research directly comparing adolescents and adults is needed despite the methodological constraints. Parallel translational animal models can aid in the causal interpretation of observed effects. To improve their translational value, future animal studies should aim to use voluntary self-administration paradigms and incorporate individual differences and environmental context to better model human drinking behavior.

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Introduction.

Alcohol use disorder (AUD) is the most prevalent substance use disorder worldwide [ 1 ]. Most AUDs remain untreated [ 2 ] and for those seeking treatment, relapse rates are high [ 3 ]. Adolescence marks a rapid increase in AUD and an earlier onset of AUD is associated with worse long-term outcomes, including greater problem severity and more relapses [ 4 , 5 ]. Loss of control over alcohol use is a core aspect of AUD [ 6 ] and the developmentally normative difficulty to control motivational urges in tempting and arousing situations is thought to put adolescents at risk for developing addictive behaviors [ 7 ]. Moreover, neurotoxic consequences of alcohol use may be more severe for a developing brain [ 8 ]. Paradoxically, adolescence is also a period of remarkable behavioral flexibility and neural plasticity [ 9 , 10 , 11 ], allowing adolescents to adapt their goals and behavior to changing situations [ 12 ] and to recover from brain trauma more easily than adults [ 10 ]. In line with this, the transition from adolescence to adulthood is associated with high rates of AUD recovery without formal intervention [ 13 ]. While the adolescent brain may be a vulnerability for the development of addiction, it may also be more resilient to long-term effects compared to adults. Increased neural plasticity during this period could help protect adolescents from longer-term alcohol use-related cognitive impairments across multiple domains, from learning and memory to decision-making and cognitive flexibility. Therefore, the goal of this systematic review was to examine the evidence of age-related differences in the effect of alcohol on the brain and cognitive outcomes, evaluating evidence from both human and animal studies.

In humans, the salience and reinforcement learning network as well as the central executive network are involved in the development and maintenance of AUD [ 7 , 14 ]. The central executive network encompasses fronto-parietal regions and is the main network involved in cognitive control [ 15 ]. The salience network encompasses fronto-limbic regions crucial for emotion regulation, salience attribution, and integration of affective information into decision-making [ 15 , 16 ], which overlaps with fronto-limbic areas of the reinforcement learning network (Fig. 1 ). Relatively early maturation of salience and reinforcement learning networks compared to the central executive network is believed to put adolescents at heightened risk for escalation of alcohol use compared to adults [ 7 ]. Rodent models are regularly used for AUD research and allow in-depth neurobehavioral analyses of the effects of ethanol exposure during different developmental periods while controlling for experimental conditions such as cumulative ethanol exposure in a way that is not possible using human subjects because exposure is inherently confounded with age. For example, animal models allow for detailed neurobiological investigation of the effects of alcohol exposure in a specific age range on neural activation, protein expression, gene expression, epigenetic changes, and neurotransmission in brain regions that are homologous to those that have been implicated in AUD in humans.

A visual representation of the translational model of the executive control and salience networks in humans and rodents. The executive control and salience are key networks believed to play a part in adolescent vulnerability to alcohol-related problems.

While most of our knowledge on the effects of alcohol on the brain and cognitive outcomes is based on research in adults, several recent reviews have examined the effects of alcohol on the brain and cognition in adolescents and young adults specifically [ 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 ]. Heavy or binge drinking has been associated with reduced gray and white matter. Also, altered task-related brain activity [ 20 ], structural abnormalities [ 25 ], and overlapping behavioral impairment in executive functioning have been identified in adolescent and young adult alcohol users [ 19 ]. While some of the observed neurocognitive differences between drinkers and non-drinkers may be predisposing factors, they may be further exacerbated by heavy and binge drinking [ 21 , 23 ]. Furthermore, reviews of longitudinal studies concluded that adolescent alcohol use is associated with neural and cognitive alterations in a dose-dependent manner [ 17 , 22 ].

Although previous reviews underscore the potential negative consequences of heavy alcohol use on the brain and cognition in adolescence, they do not typically address the question of whether adolescents are differentially vulnerable compared to adults to the effects of alcohol on these outcomes. Explicit comparisons between adolescents and adults are crucial to identify potential risk and resilience factors. In the current review, we aimed to extend previous work by systematically examining this critical question: does the relationship between chronic alcohol use and neurocognitive outcomes differ between adolescents and adults? To address this question, we systematically reviewed human and animal studies that included both age groups and used a factorial design that would allow for the comparison of the effects of chronic alcohol use on cognitive and brain-related outcomes across age groups. We specifically highlight outcomes from voluntary self-administration paradigms when available and discuss the translational quality of the animal evidence base. We conclude with a discussion of prominent knowledge gaps, future research directions, and clinical implications.

Study inclusion criteria and search strategy

We followed the PRISMA guidelines for the current systematic review (The PRIMSA Group, 2009). An initial MedLine, Cochrane Library, and PsycInfo search was conducted during September of 2018 with terms related to alcohol, cognition, adolescence/adulthood, and study type (see Appendix for full search strategy and syntax). Two search updates using the same search strategy were conducted on 31 March 2020 and 3 February 2021. For all searches, the identified citations were split into batches and at least two of the following assessors (GM, LK, JC, or CG) conducted a blinded review to determine whether articles met the inclusion criteria. In the first phase of screening, only titles and abstracts were screened and articles that clearly did not meet the inclusion criteria were excluded. In the second phase, the remaining articles received a full-text review and those that did not meet all inclusion criteria were excluded. The first inclusion criterion that was not adhered to was recorded as the reason for excluding. If there was a discrepancy between authors after initial and full-text screening process, the reviewing authors discussed the article and a consensus was reached.

The inclusion criteria were: (1) Human samples including both adolescents younger than 18 and adults older than 18 and animal samples including adolescent (Post Natal Day (PND) 25–42 for rodents) and adult [ 8 ] animals (greater than PND 65 for rodents); (2) Exploration of alcohol as the independent variable and cognitive, reward-related, or brain outcomes as the dependent variables; (3) Alcohol and cognitive outcomes must meet our operationalization defined below; (4) Study design comparing adults and adolescents on outcome measures; (5) Administering or measuring alcohol use during adolescence or adulthood, not retrospectively (e.g., no age of onset work in humans using retrospective self-reports of alcohol consumption); (6) Primary quantitative data collection (no case studies, or review papers); (7) Solely looking at alcohol-related factors as the independent variables (e.g., cannot explore alcohol-related factors in individuals with psychosis); (8) Written in English; (9) Published in a peer-reviewed journal before February 3, 2021 (see Fig. 2 for a detailed screening process).

The definitions for adolescence are variable, hampering the direct comparison of human and rodent research. In rodents, the end of early-mid adolescence is considered to be approximately PND 42 when rats reach sexual puberty. By contrast, the boundaries for the onset of early adolescence are less clear. Based on the notion that most age-typical physiological changes that are characteristic of adolescence emerge from PND 28 [ 26 ], the conservative boundary for adolescence has been set at PND 28 (e.g., seminal review on adolescence [ 27 ]). The preceding week (PND 21-PND 28) has been described as the juvenile period (e.g., [ 28 , 29 ]) but these same reports consider PND 21-PND 23 as the lower boundary for early adolescence [ 28 , 29 ], further emphasizing that the boundary of PND28 may be too conservative. Indeed, multiple studies (e.g., [ 30 , 31 ]), have chosen to take PND25 as the boundary for early adolescence. Hence, we have decided to also follow this less conservative approach and include all studies where alcohol was administered between PND 25 and PND 42.

The exact boundaries of human adolescence are similarly nebulous. From a neurodevelopmental perspective, adolescence is now often thought of as continuing until approximately age 25 because of the continuing maturation of the brain [ 32 ]. However, the delineation of adolescence and adulthood is also dependent on societal norms, and is commonly defined as the transitional period between puberty and legal adulthood and independence which typically begins around age eighteen. In light of this, we chose a relatively liberal inclusion criteria for the human studies; studies needed to include at least some adolescents below eighteen, the age at which drinking typically begins, as well as ‘adult’ participants over the age of eighteen. We are careful to interpret the results of human studies within the neurodevelopmental framework of adolescence, such that 18–25-year-olds are considered late adolescents to young adults who are still undergoing cognitive and brain maturation.

Notably, we excluded studies that assessed alcohol exposure retrospectively (primarily early onset alcohol studies) because age of onset variables are often inaccurate, with reported age of alcohol onset increasing with both historical age [ 33 ] and current alcohol use patterns [ 34 ]. In addition, we excluded work that has not undergone peer-review to ensure high-quality papers.

In humans, we defined cognition as any construct that typically falls within the umbrella of neuropsychological testing, as well as brain-based studies. We also included more distal constructs of cognition, like craving and impulsivity, because they play a prominent role in addictive behaviors [ 35 , 36 ]. In rodents, we defined cognition as attention, learning, and memory in line with a seminal review paper [ 37 ]. Given the importance of social cognition in patterns of alcohol use particularly in adolescence [ 38 ] and its proposed role in adolescent risk and resilience to addiction [ 39 ], we included social behavior as an outcome. Furthermore, because many rodent studies assessed anxiety-related behaviors and the high degree of comorbidity between anxiety disorders and alcohol addiction [ 40 ], we also included anxiety as a secondary outcome. On the other hand, locomotor activity was excluded as an outcome because even though behavioral sensitization is considered to reflect neurobiological changes that may underlie certain aspects of addictive behavior [ 36 ], the translational relevance for addictive behavior and human addiction in particular remains unclear [ 41 , 42 ]. Across both rodents and humans, general alcohol metabolization and ethanol withdrawal studies were not included except if they included brain-related outcomes. The relevant reported findings (i.e., the results of an analysis of comparing age groups on the effect of alcohol on an included outcome) were extracted by a one reviewer and then confirmed by at least one other reviewer. In addition, the characteristics of the sample, details of alcohol exposure, and study design were extracted by a single reviewer and then confirmed by at least one other reviewer. No automation tools were used for extraction. Within the included studies, peripheral findings that did not relate to cognition were excluded from review and not extracted. The protocol for this systematic review was not registered and no review protocol can be accessed.

Study search

Our searches identified 7229 studies once duplicates were removed. A total of 6791 studies were excluded after initial review of abstracts. Then, 434 studies received a full-text review and 371 were excluded for failing to meet all inclusion criteria. See Fig. 2 for a flow diagram of the full screening process. At the end of the inclusion process, 59 rodent studies and 4 human studies were included. The characteristics and findings of the final studies are detailed in Table 1 (rodents) and Table 2 (humans). Due to the heterogeneity of outcomes, meta-regression was not suitable for synthesizing results. Results are narratively synthesized and grouped based on forced or voluntary ethanol exposure and by outcome within the tables and by outcome only in text. Two authors independently rated the quality of evidence for human studies (Table 2 ) based on criteria used in a similar systematic review [ 43 ]: (1) strong level of causality: longitudinal design comparing adolescent and adults while adjusting for relevant covariates; (2) moderate level of causality: longitudinal design comparing adolescents and adults without adjusting for relevant covariates or cross-sectional designs with matched groups that considered relevant covariates; (3) weak level of causality: cross-sectional design without matched adolescent and adult groups and/or did not adjust for relevant covariates. A methodological quality assessment was not conducted for the animal studies due to a lack of empirically validated risk of bias tools and lack of standardized reporting requirements in the animal literature.

PRIMSA flow diagram detailing the screening process.

Animal studies

Cognitive outcomes, learning and memory.

Human evidence clearly suggests that alcohol is related to learning and memory impairments, both during intoxication [ 44 ] and after sustained heavy use and dependence [ 45 , 46 ]. Paradigms that assess learning and memory provide insight into the negative consequences of alcohol consumption on brain functioning, as well as the processes underlying the development and maintenance of learned addictive behaviors.

Conditioned alcohol aversion or preference: Lower sensitivity to alcohol’s aversive effects (e.g., nausea, drowsiness, motor incoordination) but higher sensitivity to alcohol’s rewarding effects has been hypothesized to underlie the higher levels of alcohol use, especially binge-like behavior, in adolescents compared to adults [ 47 ]. Several conditioning paradigms have been developed to assess the aversive and motivational effects of alcohol exposure.

The conditioned taste aversion (CTA) paradigm is widely used to measure perceived aversiveness of alcohol in animals. Repeated high-dose ethanol injections are paired with a conditioned stimulus (CS, e.g., a saccharin or NaCL solution). The reduction in CS consumption after conditioning is used as an index of alcohol aversion. Two studies examined CTA in mice [ 48 , 49 ] and two in rats [ 50 , 51 ]. Three of the four studies found age-related differences. In all three studies using a standard CTA paradigm, adolescents required a higher ethanol dosage to develop aversion compared to adults [ 48 , 49 , 50 ]. Using a similar second-order conditioning (SOC) paradigm pairing high doses of ethanol (3.0 g/kg) with sucrose (CS), both adolescent and adult rats developed equal aversion to the testing compartment paired with ethanol [ 51 ].

Overall, three studies found support for lower sensitivity to alcohol’s aversive effects in adolescents, whereas one observed no differences. Future research should employ intragastric as opposed intraperitoneal exposure to better mimic human binge-like drinking in order to increase the translational value of the findings.

To measure differences in alcohol’s motivational value, conditioned place preference (CPP) paradigms have been used. This involves repeated pairings of ethanol injections with one compartment and saline injections with another compartment of the testing apparatus. On test days, CPP is assessed by measuring how long the animal stays in the compartment paired with ethanol relative to saline injections. Four studies examined CPP, with two studies observing age-related differences [ 52 , 53 , 54 , 55 ]. In the only mouse study, history of chronic ethanol exposure during adolescence (2.0 g/kg for 15 days) but not adulthood [ 52 ] led to increased CPP after brief abstinence (5 days) before the conditioning procedure (2.0 g/kg, four doses over 8 days). This suggests that early ethanol exposure increases alcohol’s rewarding properties later on. However, two rat studies did not observe either preference or aversion in either age when using lower ethanol doses and a shorter exposure period (0.5 and 1.0 g/kg for 8 days) [ 53 ], nor when using higher doses and intermittent exposure (3.0 g/kg, 2 days on, 2 days off schedule) [ 55 ]. Next to species and exposure-specific factors, environmental factors also play a role [ 54 ], with adolescents raised in environmentally enriched conditions demonstrating CPP (2 g/kg) while adolescents raised in standard conditions did not. In contrast, CPP was insensitive to rearing conditions in adults with both enriched and standard-housed rats showing similar levels of CPP.

Overall, there is inconsistent evidence for age-related differences in the motivational value of ethanol. One study found support for increased sensitivity to the rewarding effects of ethanol in adolescents, whereas one found support for adults being more sensitive and two observed no differences.

Fear conditioning and retention: Pavlovian fear conditioning paradigms are used to investigate associative learning and memory in animals. These paradigms are relevant for addiction because fear and drug-seeking behavior are considered conditioned responses with overlapping neural mechanisms [ 56 ]. Rodents are administered an unconditioned stimulus (US; e.g., foot shock) in the presence of a conditioned stimulus (CS; unique context or cue). Conditioned responses (CR; e.g., freezing behavior) are then measured in the presence of the CS without the US as a measure of fear retention. Contextual fear conditioning is linked to hippocampus and amygdala functioning and discrete cue-based (e.g., tone) fear is linked to amygdala functioning. [ 57 , 58 , 59 ], and fear extinction involves medial PFC functioning [ 60 ]. Five studies investigated fear conditioning, four in rats [ 61 , 62 , 63 , 64 ] and one in mice [ 65 ].

Only one of the four studies observed age-related differences in tone fear conditioning. Bergstrom et al. [ 61 ] found evidence for impaired tone fear conditioning in male and female alcohol-exposed (18d) adolescent compared to adult rats after extended abstinence (30d). However, adolescent rats consumed more ethanol during the one-hour access period than adults, which may explain the observed age differences in fear tone conditioning. Small but significant sex differences in consumption also emerged in the adolescent group, with males showing more persistent impairment across the test sessions compared to females, despite adolescent females consuming more ethanol than males. In contrast, three studies found no evidence of impaired tone fear conditioning in either age group after chronic alcohol exposure (4 g/kg, every other day for 20d) and extended abstinence [ 62 , 63 ] (22d), [ 64 ].

Two of the three studies observed age-related differences in contextual fear conditioning [ 62 , 63 , 64 ]. In two studies with similar exposure paradigms, only adolescents exposed to chronic high dosages of ethanol (4 g/kg) showed disrupted contextual fear conditioning after extended abstinence (22d) [ 62 , 63 ]. Importantly, differences disappeared when the context was also paired with a tone, which is suggestive of a potential disruption in hippocampal-linked contextual fear conditioning specifically [ 64 ]. Furthermore, there may be distinct vulnerability periods during adolescence as contextual fear retention was disrupted after chronic alcohol exposure (4 g/kg, every other day for 20d) during early-mid adolescence but not late adolescence [ 62 ]. In the only study to combine chronic exposure and acute ethanol challenges, contextual conditioning was impaired by the acute challenge (1 g/kg) but there was no effect of pre-exposure history in either age group (4 g/kg, every other day for 20d) [ 63 ].

Only one study examined fear extinction, and found no effect of ethanol exposure (4/kg, every other day for 20d) on extinction after tone conditioning. However, adults had higher levels of contextual fear extinction compared to mid-adolescents while late adolescents performed similar to adults [ 62 ]. Moreover, looking at binge-like exposure in mice (three binges, 3d abstinence), Lacaille et al. [ 65 ] showed comparable impairments in long-term fear memory in adolescents and adults during a passive avoidance task in which one compartment of the testing apparatus was paired with a foot shock once and avoidance of this chamber after a 24 h delay was measured.

In sum, there is limited but fairly consistent evidence for adolescent-specific impairments in hippocampal-linked contextual fear conditioning across two rat studies, while no age differences emerged in context-based fear retention in one study of mice. In contrast, only one of the four studies found evidence of impaired tone fear conditioning in adolescents (that also consumed more alcohol), with most finding no effect of alcohol on tone fear conditioning regardless of age. With only one study examining medial PFC-linked fear extinction, no strong conclusions can be drawn, but initial evidence suggests context-based fear extinction may be diminished in mid-adolescents compared to adults and late adolescents. Research on age-related differences on the effect of alcohol on longer-term fear memory is largely missing.

Spatial learning and memory: The Morris Water Maze (MWM) is commonly used to test spatial learning and memory in rodents. Across trials, time to find the hidden platform in a round swimming pool is used as a measure of spatial learning. Spatial memory can be tested by removing the platform and measuring the time the animal spends in the quadrant where the escape used to be. The sand box maze (SBM) is a similar paradigm in which animals need to locate a buried appetitive reinforcer.

Six rat studies examined spatial learning and memory using these paradigms. Three of the six studies observed age-related differences. Four examined the effects of repeated ethanol challenges 30 minutes prior to MWM training, showing mixed results [ 30 , 66 , 67 , 68 ]. While one found ethanol-induced spatial learning impairments in adolescents only (1.0 and 2.0 g/kg doses) [ 66 ], another found no age-related differences, with both age groups showing impairments after moderate doses (2.5 g/kg) and enhancements in learning after very low doses (0.5 g/kg) [ 67 ]. Sircar and Sircar [ 68 ] also found evidence of ethanol-induced spatial learning and memory impairments in both ages (2.0 g/kg). However, memory impairments recovered after extended abstinence (25d) in adults only. Importantly, MWM findings could be related to thigmotaxis, an anxiety-related tendency to stay close to the walls of the maze. Developmental differences in stress sensitivity may potentially confound ethanol-related age effects in these paradigms. Using the less stress-inducing SBM, adults showed greater impairments in spatial learning compared to adolescents after 1.5 g/kg ethanol doses 30 min prior to training [ 30 ].

Two studies examined the effects of chronic ethanol exposure prior to training with or without acute challenges [ 69 , 70 ]. Matthews et al. [ 70 ] looked at the effect of 20 days binge-like (every other day) pre-exposure and found no effect on spatial learning in either age following an extended abstinence period (i.e., 6–8 weeks). Swartzwelder et al. [ 69 ] examined effects of 5-day ethanol pre-exposure with and without ethanol challenges before MWM training. Ethanol challenges (2.0 g/kg) impaired learning in both age groups regardless of pre-exposure history. Thigmotaxis was also increased in both age groups after acute challenges while pre-exposure increased it in adults only.

In sum, evidence for impaired spatial learning and memory after acute challenges is mixed across six studies. Two studies found support for ethanol having a larger impact in adolescents compared to adults, whereas one study found the opposite and three studies did not observe any differences. Differences in ethanol doses stress responses may partially explain the discrepancies across studies. Importantly, given the sparsity of studies addressing the effects of long-term and voluntary ethanol exposure, no conclusion can be drawn about the impact of age on the relation between chronic alcohol exposure and spatial learning and memory.

Non-spatial learning and memory: Non-spatial learning can also be assessed in the MWM and SBM by marking the target location with a pole and moving it across trials, measuring time and distances traveled to locate the target. By assessing non-spatial learning as well, studies can determine whether learning is more generally impaired by ethanol or whether it is specific to hippocampal-dependent spatial learning processes. A total of six studies assessed facets of non-spatial learning and memory. Two of the six studies observed age-related differences.

In the four studies that examined non-spatial memory using the MWM or SBM in rats, none found an effect of alcohol regardless of dose, duration, or abstinence period in either age group [ 30 , 66 , 67 , 70 ]. Two other studies examined other facets of non-spatial memory in rats [ 65 , 71 ]. Galaj et al. [ 71 ] used an incentive learning paradigm to examine conditioned reward responses and approach behavior towards alcohol after chronic intermittent ethanol (CIE; 4 g/kg; 3d on, 2d off) exposure to mimic binge drinking. To examine reward-related learning and approach behavior, a CS (light) was paired with food pellets and approach behavior to CS only presentation and responses to a lever producing the CS were measured. In both adolescents and adults, the ethanol-exposed rats showed impaired reward-related learning after both short (2d) and extended (21d) abstinence. No effect of alcohol on conditioned approach behavior was observed in either age group during acute (2d) or extended (21d) abstinence. Using a novel object recognition test in mice, Lacaille et al. [ 65 ] assessed non-spatial recognition memory by replacing a familiar object with a novel object in the testing environment. Explorative behavior of the new object was used as an index of recognition. After chronic binge-like exposure (three injections daily at 2 h intervals) and limited abstinence (4d), only adolescents showed reduced object recognition.

Across facets of non-spatial memory, there is little evidence for age-related differences in the effect of chronic alcohol, with four of the six studies finding no age differences. For memory of visually cued target locations in the MWM and SBM paradigms, alcohol does not alter performance in either age. Also, both adolescents and adults appear similarly vulnerable to alcohol-induced impairments in reward-related learning based on the one study. Only in the domain of object memory did any age-related differences emerge, with adolescents and not adults showing reduced novel object recognition after binge-like alcohol exposure in one study. However, more research into object recognition memory and reward-related learning and memory is needed to draw strong conclusions in these domains.

Executive function and higher-order cognition

Executive functions are a domain of cognitive processes underlying higher-order cognitive functions such as goal-directed behavior. Executive functions can include but are not limited to working memory, attentional processes, cognitive flexibility, and impulse control or inhibition [ 72 ]. A core feature of AUD is the transition from goal-directed alcohol use to habitual, uncontrolled alcohol use. Impaired executive functioning, linked to PFC dysfunction [ 73 ], is assumed to be both a risk factor and consequence of chronic alcohol use. A meta-analysis of 62 studies highlighted widespread impairments in executive functioning in individuals with AUD that persisted even after 1-year of abstinence [ 46 ]. Thirteen studies examined facets of executive functioning and higher-order cognition, specifically in the domains of working memory, attentional processes, cognitive flexibility, impulsivity in decision-making, and goal-directed behavior [ 65 , 74 , 75 , 76 , 77 , 78 , 79 , 80 , 81 , 82 , 83 ].

Working memory: Working memory refers to the limited capacity system for temporarily storing and manipulating information, which is necessary for reasoning and decision-making [ 84 ]. In the Radial Arm Maze test (RAM) [ 85 ], some of the equally spaced arms (typically eight) around a circular platform contain a food reward for animals to find. Spatial working memory is measured by recording the number of revisits to previously visited arms (i.e., working memory error) and first entries into unbaited arms (i.e., reference memory). Alternatively, the hippocampus mediated [ 86 ] spontaneous tendency to alternate arms can be used as a measure of spatial working memory. In this case, revisiting an arm in back-to-back trials in close temporal succession is interpreted as a working memory error. Five studies examined the effects of chronic ethanol exposure on spatial working memory [ 65 , 75 , 79 , 80 , 83 ]. One of the five studies observed age-related differences.

Chronic binge-like alcohol exposure had no effects on spontaneous alterations after prolonged abstinence (2d on, 2d off; 3 weeks abstinence) [ 79 , 80 ] in rats or limited abstinence (three injections daily at 2 h intervals; 24 h abstinence) [ 65 ] in mice, nor on RAM performance in rats (2d on, 2d off) [ 75 , 83 ]. However, acute ethanol challenges (1.5 g/kg) after chronic binge-like exposure (2d on, 2d off) resulted in RAM test impairments in both age groups in rats [ 75 , 83 ], with some evidence for increased working memory errors in adolescents [ 83 ].

In sum, there is little evidence for impairments in working memory function in rats after chronic ethanol exposure, with four of the five studies observing no difference between age groups. While acute intoxication impairs working memory function in both ages, there is evidence from only one study that adolescents may make more working memory errors.

Attentional processes: Attentional processing refers to the selection of information that gains access to working memory [ 87 ]. PPI is a pre-attentional cognitive function which provides an index of sensorimotor gating and measures the ability of a lower intensity sensory stimulus to reduce the magnitude of response to a more intense stimulus presented closely afterward. Reduced sensorimotor gating (reduced PPI) can disrupt information processing and thereby impair cognitive function, while enhanced sensorimotor gating (enhanced PPI) may reflect behavioral inflexibility [ 88 ]. For example, lesions in the medial PFC produce both behavioral inflexibility and enhancements in PPI in rats. Two studies assessed attentional processes by measuring prepulse inhibition (PPI) in rats [ 82 , 89 ]. One study observed age-related differences and one did not.

Slawecki and Ehlers [ 82 ] observed age-related differences in sensorimotor gating following ethanol vapor exposure (2w) and brief abstinence (6d), with adolescents showing enhanced PPI at some decibels reflective of behavioral inflexibility, while adults did not exhibit PPI at any of the intensities tested. Slawecki et al. [ 89 ] did not observe any age-related differences in PPI during the acute phase of ethanol withdrawal (7–10 h abstinence) during a period of chronic ethanol exposure (14d).

In sum, there is limited and mixed evidence from two studies of age-related differences in the pre-attentional process of sensorimotor gating. Only one study found support for adolescent sensitivity to ethanol effects.

Cognitive flexibility: Cognitive flexibility refers to the ability to update information based on environmental factors r changing goals in order to adaptively guide decision-making and is linked to the inability to reduce or abstain from drinking [ 90 ]. Three studies examined facets of cognitive and behavioral flexibility [ 79 , 80 , 81 ]. Two of the three studies observed age-related differences.

In two rat studies, cognitive flexibility was assessed using reversal learning paradigms [ 79 , 80 ]. In the reversal learning paradigm, rats were trained on simple (e.g., visual cue) and more complex discriminations (e.g., visual + scent cue) between rewarded and non-rewarded bowls. After learning the discriminants, the rewards were reversed. Ethanol exposure reduced flexibility in both adolescents and adults for simple discriminations in both studies. Age-related differences emerged for the more complex discriminations in one study, with only adults showing reduced flexibility after prolonged abstinence (21d) following binge-like exposure (5 g/kg, 2d on, 2d off) [ 79 ]. In contrast, both age groups showed reduced flexibility for complex discrimination in the other study after prolonged abstinence (21d) despite adolescents consuming more ethanol orally than adults during the 28 week exposure [ 80 ].

In another study, Labots et al. [ 81 ] used a conditioned suppression of alcohol-seeking task after two months of voluntary ethanol consumption (2 months) in rats to examine flexibility around alcohol-seeking behavior. After stratifying the age groups based on levels of ethanol consumption, medium- and high-consuming, adolescents showed higher levels of conditioned suppression compared to similarly drinking adults, indicating greater behavioral flexibility and control over alcohol-seeking in adolescents after chronic voluntary exposure.

Overall, there is limited evidence for adolescent resilience to the effects of chronic alcohol on cognitive flexibility. Two studies found support for adolescent resilience to ethanol’s effect on behavioral flexibility, whereas another study found no differences between adolescents and adults.

Impulsivity: Impulsivity is a multi-faceted behavioral trait that encompasses impaired response inhibition, preference for an immediate reward over a larger but delayed reward, and premature expression of behaviors which may be maladaptive or in conflict with conscious goals. Impulsivity is a risk-factor for the development of addiction and may also be a consequence of sustained substance use [ 35 ]. Pharmacological evidence points towards overlapping neuronal mechanisms in impulsivity and addictive behavior, particularly within the mesolimbic dopamine system [ 91 ]. Two studies examined impulsive decision-making behavior in rats [ 74 , 78 ]. Both studies observed age-related differences.

One study examined impulsive behavior using a delay-discounting task in which choices are made between immediate small rewards and larger delayed rewards [ 78 ]. Regardless of age, chronic intermittent exposure (2d on, 2d off) had no effect on choice behavior in non-intoxicated rats. Following acute challenges, adolescents but not adults demonstrated a reduced preference for the large reward regardless of ethanol exposure history, reflecting a general adolescent-specific heightened impulsivity during intoxication. Another study examined decision-making under risk conditions using an instrumental training and probability-discounting task [ 74 ]. After prolonged abstinence (20d), rats were trained to press two levers for sucrose rewards and were concurrently trained to choose between two levers with different associated probabilities of reward and reward size, creating a choice between a certain, small reward and an uncertain, large reward (i.e., riskier choice). Ethanol consumption was voluntary and while adolescents initially consumed more ethanol than adults at the beginning of the exposure period, the total amount of consumption was similar by the end of the exposure period. Only adolescents showed increased risky and sub-optimal decision-making compared to age-matched controls, while adults performed similarly to controls.

In sum, both studies found support for ethanol having a larger impact on adolescent compared to adults on impulsive behavior.

Goal-directed behavior: Goal-directed behavior refers to when actions are sensitive to both the outcome value (goal) and contingency between the behavior and the outcome [ 92 ]. Two studies used a sign-tracking and omission contingency learning paradigm to examine goal-directed versus habitual behavior [ 76 , 77 ]. One study observed age-related differences and the other did not. Sign tracking refers to tasks where a cue predicts a reward, but no response is needed for the reward to be delivered. Despite this, after repeated pairings of the cue and reward, animals and humans may respond (e.g., via a lever) when the cue is presented anyway, and even when no reward is known to be available. Sign-directed behavior is considered habitual and has been proposed to underlie the lack of control of alcohol use in addiction [ 93 ]. In humans, sign-tracking behavior is difficult to differentiate from goal-directed behavior based on only the observable behavior, i.e., seeing a cue such as a favorite drink or bar and then having a drink [ 94 ]. In the context of alcohol use, reflexively having a drink when seeing an item that is often associated with the rewarding effects of alcohol (e.g., wine glass, bar, smell of alcohol) despite not consciously desiring the alcohol ‘reward’ is an example of how habitual behavior (possibly driven by sign-tracking) can initiate the behavior as opposed to an intentional goal [ 93 ]. Omission contingency refers to a 2nd phase after sign-tracking when the response is punished and the behavior must be inhibited to avoid punishment. After both forced and voluntary ethanol exposure (6w), no alterations to sign-tracking behavior were observed in adolescent and adult rats [ 76 , 77 ]. One study did observe an age-related difference in omission contingency learning, with adolescents performing better than adults after chronic voluntary ethanol exposure [ 77 ]. This preliminarily suggests that adolescents may be more capable of adapting their behavior to avoid punishment compared to adults after chronic use. However, before behavioral testing began, adolescent rats were abstinent for 17 days, while adults were only abstinence for 10 days which may have influenced the results.

In summary, one study found support for adolescents being less sensitive to ethanol effects on goal-directed behavior compared to adults, whereas one study found no effect of ethanol in either age group.

Across the domains of executive function, there is some evidence that adolescents may be more vulnerable to impairments in certain executive and higher-order cognitive functions following chronic alcohol exposure, with increased risky decision-making after prolonged abstinence [ 74 ], impulsivity during intoxication [ 78 ], and reduced working memory function during intoxication after chronic exposure. In contrast, animals exposed to alcohol during adolescence may better retain cognitive flexibility [ 77 , 79 ] and are better able to regain control over alcohol-seeking in adulthood [ 81 ].

Other behavioral outcomes

Anxiety : AUD is highly comorbid with anxiety disorders [ 95 ], especially in adolescence [ 96 ]. While anxiety is not strictly a cognitive outcome, it is related to altered cognitive functioning [ 97 , 98 ]. Many studies assessing the effects of ethanol on the rodent brain and cognition also include anxiety-related measures. Multiple paradigms have been developed to elicit behaviors thought to reflect anxiety in rodents (e.g., rearing, startle, avoidance, etc.). In the open field test (OFT), anxiety is indexed as the tendency to stay close to perimeter walls as animals have a natural aversion to brightly lit open spaces [ 99 ]. In the elevated plus maze paradigm, rodents are placed at the center of an elevated four-arm maze with two open arms two closed arms [ 100 ]. The open arms elicit unconditioned fear of heights/open spaces and the closed arms elicit the proclivity for enclosed, dark spaces. Anxiety is indexed as entries/duration of time in open vs. closed arms, as well as rearing, freezing, or other postural indices of anxiety. In startle paradigms, the startle response is a defensive mechanism reflecting anxiety which follows a sudden, unpredictable stimulus (e.g., tones, light) [ 101 ]. In light-dark box paradigms, anxiety is elicited using a testing apparatus with a light and dark compartment, relying on the conflict between natural aversions to well-lit spaces and the tendency to explore new areas. Percentage of time spent in the light compartment, latency to return to the dark compartment, movement between compartments (transitions), and rearing-behavior are measured as indices of anxiety [ 102 ]. Anxiety can also be assessed using a social interaction test with an unfamiliar partner, with approach and avoidance behaviors measured to index anxiety [ 103 ]. In the novel object test (NOT) [ 104 ], anxiety is elicited by the introduction of a new object in the rodent’s environment. The amount of contacts and time spent in contact with the object is used as an index of anxiety. Similarly, in the marble-burying test (MBT), novel marbles are placed in an environment and the amount of defensive burying of the objects is used as an index of anxiety [ 105 ].

Eleven studies examined anxiety-like behavior in rodents with mixed results across paradigms [ 70 , 78 , 82 , 83 , 89 , 106 , 107 , 108 , 109 , 110 , 111 ]. Overall, five of the eleven studies observed age-related differences.

Two studies used the OFT, finding no effects of voluntary (2w, 4 h/day access) or forced (12/day vapor) ethanol exposure on anxiety-like behavior in adolescents or adult rats during withdrawal (7–9 h) [ 110 ] or after a brief abstinence period (4 days) [ 107 ]. One study used both the MBT and NOT after voluntary ethanol consumption (2 h/d for 2 weeks; no abstinence) and observed higher anxiety in ethanol-exposed adults and reduced anxiety in ethanol-exposed adolescents compared to controls as indexed by marble burying [ 106 ]. However, no age effects were observed in response to a novel object, with reduced interaction with the novel object in both age groups after chronic exposure.

Four studies used the elevated maze paradigm with mixed results. Only one study observed age-related differences in mice after chronic exposure (8–10w vapor) [ 109 ]. Adolescents showed reduced anxiety compared to adults during the acute withdrawal period, but all mice were kept under chronic social isolation and unpredictable stress conditions, which may have affected the results. Two studies in rats found no effect of intermittent (1 g/kg) or binge-like (5 g/kg) exposure in either age group after short (24 h) [ 70 ] or sustained abstinence (20d) [ 83 ]. A third study observed heightened anxiety in both age groups after intermittent exposure (4 g/kg), with anxiety increasing with prolonged abstinence periods (24 h to 12d) [ 108 ].

Three rat studies used a startle paradigm to assess anxiety. Two observed reduced acoustic startle responses after ethanol exposure (12 h/d vapor) in both age groups during acute withdrawal periods (7–10 h) and following more sustained abstinence (6d) [ 82 , 89 ]. In the other study, light-potentiated startle was also reduced in both ages during days 1–10 of withdrawal after binge-like exposure (2d on, 2d off), but age-related differences emerged when the rats were re-exposed via a 4-day binge (1–4/kg). Then, only adults showed higher levels of light-potentiated startle compared to controls [ 78 ], suggesting that ethanol pre-exposure increases anxiety in adults but not adolescents when re-exposed to ethanol after withdrawal.

Two studies used the light-dark box paradigm with mixed results [ 89 , 111 ]. Only adult rats showed increased mild anxiety-like behaviors during early withdrawal (7–10 h) after chronic vapor exposure 12 h/d) [ 89 ]. In contrast, no age-related differences emerged after voluntary ethanol consumption (18 h/d access; 3d/w for 6 weeks), with male mice showing less anxiety-like behavior in both ages [ 111 ]. In contrast, the one study using the social interaction test observed reduced anxiety in adult mice compared to both adolescents and age-matched controls during early withdrawal (4–6 h) after chronic, unpredictable vapor exposure [ 109 ].

In summary, there is inconsistent evidence for age-related differences in the effect of chronic ethanol exposure on anxiety outcomes in rodents. The substantial differences across studies in how anxiety was elicited and measured make it challenging to draw strong conclusions. In the five studies that found age-related differences, adults tend to show higher levels of anxiety, particularly during early withdrawal; however, the opposite was found in the one study examining anxiety in social interactions. Six studies did not observe any age-related differences. Overall, adolescents may be less sensitive to the anxiety-inducing effects of chronic alcohol exposure.

Social behavior: Two studies were identified that examined the effects of chronic ethanol exposure on social behavior in rats [ 112 , 113 ], with both observing age-related differences. After chronic exposure (1 g/kg, 7d), followed by a brief abstinence period (24–48 h), one study found a decrease in social preference in adolescents only [ 112 ], while the other study found no ethanol-related effects on social behavior (2 g/kg, 10d) [ 113 ]. After acute challenges, age and treatment interactions emerged in both studies, but the directions of the results are inconsistent. In the first study, adolescents showed increased social preference, as indexed by the number of cross-overs between compartments toward and away from a peer, across multiple acute doses (0.5–1.0 g/kg) administered immediately before testing, while adults showed no changes in social preference [ 112 ]. In contrast, Morales et al. [ 113 ] found evidence for age-related temporal differences in social activity after acute challenge, with adults showing decreased social impairment five minutes post injection (1 g/kg) and adolescents (1.25 g/kg) after 25 min compared to age-matched controls.

The findings from these two studies paint a complicated and inconsistent picture of the effects of ethanol on social behavior in adults and adolescents warranting further research. One study found support for a larger effect of chronic ethanol on adolescent social behavior compared to adults, while the other did not observe effects of ethanol in either group. One study found support for a larger effect of chronic plus acute ethanol intoxication on social behavior, with the opposite observed in the other.

Brain outcomes

Neurotransmitter systems.

Glutamate is the brain’s main excitatory neurotransmitter and plays a crucial role in synaptic plasticity (i.e., experience-related strengthening or weakening of synaptic connections). Glutamatergic transmission plays an important role in the formation and maintenance of addictive behaviors and the nucleus accumbens (NAc) is considered an important hub in this, receiving glutamatergic input from cortical-limbic areas and dopaminergic input from the midbrain [ 114 ]. Seven studies investigated glutamate functioning in regions of the brain [ 106 , 107 , 108 , 109 , 115 , 116 , 117 , 118 ]. Four of the seven studies observed age-related differences.

Three studies investigated glutamate-related processes in the NAc [ 106 , 107 , 118 ]. Two weeks of voluntary binge drinking (4-h access, no abstinence) did not affect expression of calcium-dependent kinase II alpha (CaMKIIα) and the AMPA receptor GluA1 subunit in the NAc of mice [ 107 ]. In contrast, Lee et al. [ 106 ] showed that voluntary binge drinking (2-h access, no abstinence) increased mGlu1, mGlu5, and GluN2b expression in the shell of the NAc, as well as PKCε and CAMKII in the core of the NAc in adult mice only. In rats, Pascual et al. [ 118 ] showed reduced NR2B phosphorylation in the NAc of adolescents only after two weeks of chronic intermittent ethanol exposure; an effect that also lasted until 24 h after end of exposure. This indicates that adolescents might be less affected by the effects of ethanol on NAc-related glutamatergic neurotransmission than adults. This may in turn mediate decreased withdrawal symptoms and potentially facilitate increased drinking [ 106 ].

Two studies investigated glutamate-related processes in the (basolateral) amygdala [ 107 , 116 ]. In mice, Agoglia et al. [ 107 ] showed decreased CaMKIIα phosphorylation in adolescents, but increased GluA1 expression in adults after two weeks of voluntary binge drinking (4-h access, no abstinence). Also, drug-induced AMPAR activation resulted in increased binge drinking in adolescents but decreased binge drinking in adults, highlighting the potential importance of glutamatergic signaling in age-related differences in alcohol consumption. However, Falco et al. [ 116 ] reported no difference in NR2A mRNA levels in the basolateral amygdala for either age group after 60-day abstinence.

Alcohol’s effects on frontal cortex functioning is thought to be mediated by alterations in NMDA receptor subunit expression [ 119 , 120 ]. Two studies investigated glutamate-related processes in the frontal cortex of rats [ 115 , 118 ]. Pascual et al. [ 118 ] showed reduced NR2B phosphorylation after two weeks of forced intermittent ethanol exposure in adolescents only. Using a 2-week ethanol vapor paradigm, Pian et al. [ 115 ] found different patterns of NMDAR subunit expression. These patterns were highly dependent on abstinence duration (0 h, 24 h, 2w), however, they only statistically compared results within rather than between age groups. Ethanol exposure was associated with decreased NR1 receptor expression in both age groups, but only the adult group showed a decrease in NR2A and NR2B expression. The NR1 and NR2A expression returned to normal during withdrawal, but in adults NR2B expression increased after two weeks of abstinence.

Conrad and Winder [ 109 ] assessed long-term potentiation (LTP) in the bed nucleus stria terminalis (BNST), a major output pathway of the amygdala towards the hypothalamus and thalamus. Voluntary ethanol exposure resulted in blunted LTP responses in the dorsolateral BNST regardless of age. However, all mice were socially isolated during the experiments to induce anxiety, so it is unclear whether the effects were solely due to ethanol exposure.

Two studies looked at glutamate receptor subunit expression in the hippocampus [ 108 , 115 ]. Pian et al. [ 115 ] observed increased expression of NR1, NR2A, and NR2B in adults after 2 weeks of ethanol exposure. In adolescents, a reduction in NR2A expression was observed. After abstinence, adult levels returned to normal, while in adolescents, decreased NR1 and NR2A expression was seen after 24 h but an increased expression of these subunits was seen after 2 weeks of abstinence. These findings support regional specific effects of age group, with potentially increased sensitivity to the impact of alcohol on glutamatergic mediated hippocampal functioning in adolescents. Unlike expected, van Skike et al. [ 108 ] did not find effects of chronic intermittent ethanol exposure or withdrawal on NMDA receptor subunit expression in the hippocampus and cortex as a whole in adolescent and adult rats. The authors speculate that these null results might be associated with the exposure design (limited exposure and route of administration) and lack of withdrawal periods compared to Pian et al. [ 115 ].

In sum, there is limited and inconsistent evidence for age-related differences in glutamate function across seven studies. The direction of the observed age-related differences varies across regions, with evidence of both increased and decreased sensitivity to ethanol effects in adolescents compared to adults in the four studies that observed age-related differences.

GABA is the brain’s main inhibitory neurotransmitter. GABA A receptors are a primary mediator of alcohol’s pharmacological effects [ 121 ]. A total of four studies looked at GABAergic functioning [ 108 , 116 , 122 , 123 ]. Three of the four studies observed age-related differences.

One study investigated GABA-related processes in the (basolateral) amygdala, showing reduced GABA A α1 and GAD67 (enzyme that converts Glutamate to GABA) mRNA expression in adult rats only, 60 days after 18-days ethanol exposure [ 116 ].

Two studies looked at the rat cortex as a whole [ 108 , 122 ]. Van Skike et al. did not find effects of chronic intermittent ethanol exposure on GABA A receptor expression [ 108 ]. Grobin et al. [ 122 ] showed that, while basal GABA A receptor functioning was not affected by 1 month of chronic intermittent ethanol exposure, GABA A receptors were less sensitive to the neurosteroid THDOC in adolescents. This neuromodulatory effect was not found in adults and did not persist after 33 days of abstinence. However, these results indicate that neurosteroids may play an indirect role in age differences in the GABAA receptor’s response to alcohol.

Two studies focused on the rat hippocampus [ 108 , 124 ]. Fleming et al. [ 124 ] found age-specific effects of chronic intermittent ethanol exposure on hippocampal (dentate gyrus) GABA A receptor functioning. Adolescent rats showed decreased tonic inhibitory current amplitudes after ethanol exposure, which was not the case for young adult and adult rats. Also, only the adolescents showed greater sensitivity to (ex vivo) acute ethanol exposure induced enhanced GABAergic tonic currents. The specificity of these effects to adolescent exposure might indicate adolescent vulnerability to ethanol-induced effects on the hippocampus; however, Van Skike et al. [ 108 ] did not find any effects of chronic intermittent ethanol exposure on GABA A receptor expression in the hippocampus.

In sum, given the limited number of studies and lack of replicated effects, no clear conclusions can be drawn about the role of age on the effects of alcohol on GABAergic neurotransmission. Age-specific effects appear to be regionally distinct. The only available study found support for heightened adult sensitivity to ethanol in the amygdala. In contrast, one study found support for greater adolescent sensitivity in the hippocampus and whole cortex, whereas the other found no age-related differences.

The mesocorticolimbic dopamine system, with dopaminergic neurons in the ventral tegmental area (VTA) projecting to the NAc and prefrontal cortex, plays a key role in AUD, particularly through reward and motivational processes [ 14 ]. Only two studies investigated dopaminergic processes, focusing on the frontal cortex, NAc, and broader striatum [ 118 , 125 ]. Both studies observed age-related differences in certain dopamine outcomes.

Carrara-Nascimento et al. [ 125 ] investigated acute effects of ethanol in adolescent and adult mice 5 days after a 15-day treatment with either ethanol or saline. In the PFC, ethanol pretreated adolescents showed reduced dopamine levels (DA) and related metabolites (DOPAC and HVA) in response to an acute ethanol challenge compared to ethanol pretreated adults and adolescent saline controls. In the NAc, there were no differences between pretreated adolescents and adults, but analyses within each age group revealed that ethanol-pretreatment with an acute challenge decreased DOPAC within the adolescent group. Results from the dorsal striatum also showed no differences between adolescents and adults. However, within the adolescent group, ethanol pre-treatment increased DOPAC and, within the adult group, it increased HVA. Pascual et al. [ 118 ] found similar results looking at the expression of DRD1 and DRD2 dopamine receptors after two weeks of chronic intermittent ethanol exposure in rats. In the NAc and dorsal striatum, DRD2 expression was reduced in adolescent compared to adult exposed rats, while both DRD1 and DRD2 expression were reduced in the frontal cortex.

These results suggest reduced alcohol-induced dopamine reactivity in adolescents in the PFC and NAc based on the two available studies, but more studies are warranted for a more detailed understanding of the relationship between age and dopamine receptor expression following chronic ethanol exposure.

Acetylcholine

Acetylcholine is a known neuromodulator of reward and cognition-related processes [ 126 ]. The composition and expression of nicotinic and muscarinic acetylcholine receptors have been implicated in various alcohol use-related behaviors [ 127 , 128 ]. Only one study investigated cholinergic processes and observed age-related differences. Vetreno et al. [ 129 ] showed global reductions in choline acetyltransferase (ChAT; cholinergic cell marker) expression after adolescent onset, but not adult onset of forced intermittent binge-like exposure (20 days – every other day, 25 days abstinence).

Neuromodulatory processes

Neurodegeneration and neurodevelopment.

Chronic alcohol consumption is thought to lead to brain damage by influencing processes involved in neurodegeneration and neurogenesis. The formation of addictive behaviors is paralleled by the formation of new axons and dendrites, strengthening specific neuronal pathways [ 130 ]. While brain morphology is commonly investigated in humans, it is a proxy of the impact of alcohol on the brain and therefore rarely studied in rodents. Five studies investigated facets of neurodegeneration or development in rodents [ 55 , 65 , 131 , 132 , 133 ]. All five studies observed age-related differences.

Huang et al. [ 131 ] showed reduced cerebral cortex mass in adolescent mice, but shortening of the corpus collosum in adults after 45 days of ethanol injections, suggesting some age-specific regional effects. Using an amino cupric silver staining, significant brain damage was revealed for both adolescent and adult rats after 4 days of binge-like ethanol exposure [ 132 ]. However, adolescents showed more damage in the olfactory-frontal cortex, perirhinal cortex, and piriform cortex.

Looking at hippocampal neurogenesis, ethanol exposure has been shown to initially reduce hippocampal neurogenesis in adult rodents, recovering after 1-month abstinence [ 134 ]. Compared to adults, neurogenesis in the dentate gyrus of the hippocampus was found to be reduced in adolescent exposed mice (Bromodeoxyuridine levels) [ 65 ] and rats (doublecortin levels) [ 133 ]. Lacaille et al. [ 65 ] also measured the expression level of genes involved in oxidative mechanisms after binge-like alcohol exposure. In whole brain samples, they found increased expression of genes involved in brain protection (i.e., gpx3, srxn1) in adults, but increased expression of genes involved in cell death (i.e., casp3) combined with decreased expression of genes involved in brain protection (i.e., gpx7, nudt15) in adolescents. Casp3 protein levels were also higher in the whole brain of adolescent exposed mice [ 65 ] and the adolescent dentate gyrus [ 133 ], suggesting more neurodegeneration and less neurogenesis in adolescents versus adults following ethanol consumption.

Cyclin-dependent kinase 5 (CDK5) is involved in axon, dendrite, and synapse formation and regulation. CDK5 is overexpressed in the prefrontal cortex and the NAc following exposure to substances of abuse including alcohol [ 135 ]. Moreover, CDK5 inhibition has been shown to reduce operant self-administration of alcohol in alcohol-dependent rats [ 136 ]. One study reported higher H4 acetylation of the CDK5 promoter in the PFC of adult versus adolescent ethanol-exposed rats during acute withdrawal, however, CDK5 mRNA expression was control-like after 2 weeks of abstinence [ 55 ].

In sum, strong conclusions cannot be drawn due to the limited number of studies and lack of replicated effects. However, preliminary evidence points to adolescent vulnerability to damage in the cortex, reduced neurogenesis, and increased neurodegeneration in the hippocampus and the cortex as a whole based on four of the five studies. In contrast, one study found support for adult vulnerability to ethanol’s effects axon, dendrite, and synapse formation and regulation.

Growth factors

Brain-derived neurotrophic factor (BNDF) and nerve growth factor (NGF) are involved in brain homeostasis and neural recovery [ 137 , 138 ]. While ethanol exposure initially increases BDNF and NGF, chronic ethanol exposure seems to reduce BDNF and NGF levels and can thereby result in long-term brain damage and related cognitive problems [ 139 , 140 ]. Four studies investigated growth factor expression in the frontal cortex [ 54 , 55 , 79 , 80 ] and two studies also investigated the hippocampus [ 79 , 80 ]. All four studies of the frontal cortex observed age-related differences. Neither study of the hippocampus observed age-related differences.

In rats, 30 weeks of chronic ethanol exposure reduced prefrontal mBDNF and β-NGF regardless of age, despite adolescents consuming more ethanol [ 80 ]. Moreover, the reduction of mBDNF was correlated with higher blood alcohol levels and was persistent up to 6–8 weeks abstinence. Interestingly, during acute withdrawal (48 h) adolescents but not adults temporarily showed control-like mBDNF levels. This might indicate an attempt to counteract neurodegeneration as a result of ethanol exposure in adolescents. These results were partially replicated using a shorter intermittent exposure paradigm (13 doses, 2 days on/off) [ 79 ]. While intoxication after chronic ethanol exposure reduced prefrontal BDNF, levels recovered after 3-weeks abstinence regardless of age. However, during acute withdrawal (24 h), BDNF was still reduced in early-adolescent onset rats, increased in adult-onset rats, but control-like in mid-adolescent onset-rats, suggesting slower recovery in younger animals. Looking at BDNF gene regulation, a similar study (8 doses, 2 days on/off) reported higher H3 demethylation but lower H4 acetylation of the BDNF promoter in the PFC of adult versus adolescent ethanol-exposed rats during acute withdrawal [ 55 ]. However, prefrontal BDNF mRNA expression returned to control levels after 2 weeks of abstinence. Interestingly, social housing may be protective, as reduced prefrontal BDNF was no longer observed in alcohol-exposed adolescent mice housed in environmentally enriched relative to standard conditions [ 54 ]. Two studies investigated hippocampal BDNF expression but reported no significant interactions between alcohol exposure and age group [ 79 , 80 ].

In sum, the results of the four available studies suggest lower prefrontal BDNF during chronic alcohol use that recovers after abstinence regardless of age. However, the rate of recovery may be influenced by age with slower recovery in adolescents. In the two available studies, no age-related differences were observed in BDNF expression in the hippocampus.

Transcription factors

The transcription factors cFos and FosB are transiently upregulated in response to substance use, and ΔFosB accumulates after chronic exposure, particularly in striatal and other reward-related areas [ 141 ]. Two studies investigated cFos and FosB [ 55 , 142 ] and one study ΔFosB related processes [ 111 ]. All three studies observed age-related differences.

After chronic ethanol exposure (8 doses, 2 days on/off), adolescent compared to adult rats showed increased prefrontal H3 and H4 acetylation of the cFos promotor region and increased H4 acetylation and H3 dimethylation of FosB promotor regions after acute abstinence [ 55 ]. Moreover, mRNA expression of FosB was elevated in adolescents but not adults after 2-weeks abstinence. The upregulating effects of an acute ethanol challenge on prefrontal cFos appears to reduce after chronic pre-treatment to a larger extent in adolescent than adult exposed mice [ 142 ]. This pattern of results was similar in the NAc, but desensitization to ethanol’s acute effects on cFos in the hippocampus was more pronounced in adults. Faria et al. [ 142 ] also looked at Egr-1 (transcription factor, indirect marker of neuronal activity and involved in neuroplasticity), showing a stronger reduction in Egr-1 expression in the PFC, NAc, and hippocampus of adolescent versus adults after repeated ethanol exposure. Regarding ∆FosB, Wille-Bille et al. [ 111 ] found increased ∆FosB in adolescent compared to adult rats in the prelimbic PFC, dorsomedial striatum, NAc core and shell, central amygdala nucleus capsular, and basolateral amygdala after 3 days per week 18 h ethanol exposure sessions for 6 weeks. In sum, the three available studies provide preliminary evidence for increased adolescent vulnerability to ethanol-induced long-term genetic (mRNA expression) and epigenetic (methylation) changes in mesocorticolimbic areas.

Immune factors

Ethanol is known to trigger immune responses in the brain (e.g., increase production of hemokines and cytokines), causing inflammation and oxidative stress [ 143 , 144 , 145 ]. Three studies examined immune factors [ 146 , 147 , 148 ]. Two of the three studies observed age-related differences.

Microglia remove damaged brain tissue and infectious agents and are key to the brain’s immune defense. Only one study investigated microglia levels [ 146 ]. Although direct comparisons between age groups were missing, both adolescent and adult rats showed less microglia in the hippocampus (CA and DG) and peri-entorhinal cortex, and more dysmorphic microglia in the hippocampus after 2 and 4 days of binge-like ethanol exposure [ 146 ]. Notably, age groups were matched on intoxication scores, with adolescents needing more ethanol to reach the same level of intoxication. An in silico transcriptome analysis of brain samples from mice after 4 days of 4 h/day drinking in the dark, suggest overexpression of neuroimmune pathways related to microglia action (toll-like receptor signaling, MAPK signaling, Jak-STAT signaling, T-cell signaling, and chemokine signaling) in adults that was not observed in adolescents, while adolescents consumed more ethanol [ 147 ]. Similarly, ethanol-exposed adult mice showed higher chemokine expression (CCL2/MCP-1) in the hippocampus, cerebral cortex, and cerebellum and higher cytokine expression (IL-6, but not TNF-α) in the cerebellum, while no chemokine or cytokine changes were observed in ethanol exposed adolescent mice [ 148 ]. Both adolescents and adults showed increased astrocyte levels in the hippocampus (CA1) and the cerebellum after ethanol exposure, but changes in astrocyte morphology were only observed in the adult hippocampus.

In sum, two of the studies found support for increased immune responses after ethanol exposure in adults compared to adolescents, whereas the one other study found no difference between the age groups.

HPA-axis functionality

Chronic stress and HPA-axis functionality have been associated with the maintenance of AUD (e.g., reinstatement drug seeking, withdrawal) [ 149 ]. Two studies investigated corticotropin-release factor (CRF) expression in rats [ 116 , 150 ]. One study observed age-related differences and the other did not.

Falco et al. [ 116 ] found decreased CRF mRNA expression in the adult but not adolescent basolateral amygdala 2 months after 18-day restricted ethanol exposure. In contrast, Slawecki et al. did not find any interaction between age and treatment on CRF levels in the amygdala, as well as the frontal lobe, hippocampus, hypothalamus, and caudate 7 weeks after 10-days of ethanol vapor exposure.

No conclusions can be drawn. One study observed found support for reduced effects of ethanol on HPA-axis functionality compared to adults, whereas the other observed no difference between the age groups. Future studies using different (voluntary) exposure paradigms are needed to further investigate the effects of alcohol on HPA activity in relation to age of alcohol exposure.

Neuropeptides

Neuropeptides are a diverse class of proteins that have a modulatory function in many different processes, including but not limited to neurotransmission, stress, immune responses, homeostasis, and pain [ 151 , 152 , 153 ]. Only one study investigated neuropeptides in rats and observed age-related differences [ 150 ].

Slawecki et al. [ 150 ] specifically investigated neuropeptide-Y, substance-P, and interleukine expression in the frontal lobe, hippocampus, hypothalamus, dorsal striatum, and amygdala 7 weeks after 10-days of ethanol vapor exposure in rats [ 150 ]. Interactions between age and treatment were found for the hippocampus and caudate only. Ethanol-induced reductions in hippocampal neuropeptide-Y and increases in caudate neurokinine were more pronounced in adults compared to adolescents suggesting long-lasting effects of ethanol in adults but not adolescents.

Ethanol metabolism

The first metabolite of ethanol is acetaldehyde, which has been theorized to mediate the effects of ethanol on both brain and behavior [ 154 ]. Only one study investigated ethanol metabolism in the brain and did not observe age-related differences [ 155 ].

Rhoads et al. showed that despite the fact that adolescent rats consumed more alcohol brain catalase levels after 3-weeks of ethanol exposure (no abstinence) did not differ between adolescents and adults [ 155 ]. Although the general role of catalase in ethanol metabolism is small, catalase can oxidize ethanol to acetaldehyde in the brain, affecting elimination of ethanol after consumption [ 156 , 157 ]. These findings may therefore imply that ethanol metabolism may not differ between adolescent and adult animals, which should be studied in a more direct manner.

Full proteome analysis

While the previously described studies focused on specific factors involved in neurotransmission, brain health, and plasticity, proteomics allows for the study of the full proteome in a specific region or tissue type. One study investigated the impact of age on ethanol-induced changes in the hippocampal proteome, observing age-related differences [ 158 ]. In this study, rats intermittently and voluntarily consumed beer for 1 month and the hippocampal proteome was analyzed after 2 weeks of abstinence. The results point to the involvement of many of the factors described above and imply age-specific effects of alcohol. Adult beer exposure increased citrate synthase (part of the citric acid, or Krebs, cycle) and fatty acid binding proteins (involved in membrane transport) compared to controls. Adolescent beer exposure increased cytoskeletal protein T-complex protein 1 subunit epsilon (TCP-1), involved in ATP-dependent protein folding, and reduced expression of a variety of other proteins involved in glycolysis, glutamate expression, aldehyde detoxification, protein degradation, and synaptogenesis, as well as neurotransmitter release. These more extensive changes suggest that the adolescent hippocampus might be more vulnerable to the effects of ethanol exposure, but more studies are needed to clarify and replicate these findings and extend the focus to different brain areas.

Neuronal activity and functioning

Ethanol-induced molecular changes may eventually change neuronal activity. Three studies investigated neuronal activity and functioning [ 89 , 159 , 160 ] using electrophysiological methods. All three studies observed age-related differences.

Galaj et al. [ 159 ] assessed firing patterns and the structure of pyramidal neurons in the L2 and L5 layers of the prelimbic cortex of the rat brain using ex vivo electrophysiological recordings and morphological staining. Following chronic intermittent ethanol exposure and brief abstinence (2 days), adolescents, but not adults, showed reduced amplitudes of spontaneous excitatory post-synaptic currents (sEPSCs) in L5 neurons compared to controls, indicating reductions in intrinsic excitability. In line with this, Dil staining showed increased thin spine ratios in the L5 layer in adolescents only. Age differences were more pronounced after prolonged abstinence (21 days), with adolescents showing reduced amplitude and frequency of sEPSCs in L5 neurons while adult’s L5 neurons showed augmented firing patterns (i.e., amplitude and frequency). Furthermore, adolescent rats showed decreased total spine density and non-thin spines, indicating less excitatory postsynaptic receptors in the L5 layer. In contrast, adults showed increases in spine density and non-thin spines.

Li et al. [ 160 ] examined the functioning of CA1 interneurons, which are important for learning and memory processes [ 161 ], in the rat hippocampus using ex vivo whole-cell recordings. After prolonged abstinence (20 days), voltage-gated A-type potassium channel ( I A ) conductance was measured. Differences emerged between age groups (although no statistical interaction effect was directly assessed): EtOH-exposed adolescents and adults both showed lower I A mean peak amplitude compared to the respective control groups. However, adolescents also showed reduced I A density and increased mean decay time, which decreased in adults. Furthermore, only adolescents showed increased depolarization required for activation compared to controls, which can result in higher interneuron firing rates in the CA1 region that could affect learning processes. Additional research is needed to connect these findings to behavioral measures of learning and memory.

Slawecki et al. [ 89 ] was the only study to use in vivo electroencephalogram (EEG) recordings with rats to examine function in the frontal and parietal cortex at different times during a 14-day vapor exposure period. During acute withdrawal (7–10 h abstinence period), following daily exposure no effects emerged in frontal cortical regions throughout the exposure period. In parietal regions, only adolescents showed increased high frequency (16–32 Hz and 32–50 Hz) power on days 8 and 12 compared to controls. Adolescent hyperexcitability during withdrawal may indicate increased arousal in adolescents compared to adults during withdrawal, but more studies linking brain activity to behavioral indices of withdrawal will allow for clearer interpretations.

Overall, strong conclusions cannot be drawn given the disparate paradigms and outcomes utilized. While adolescents and adults appear to differ in the effect of ethanol on neuronal firing, the meaning of these differences is not clear given the lack of connection between these findings and behavioral outcomes.

Human studies

Four studies examined age-related differences of the effect of alcohol on brain or cognition in humans [ 162 , 163 , 164 , 165 ].

Müller-Oehring et al. [ 162 ] examined the moderating role of age on resting state functional connectivity and synchrony in the default mode, central executive, salience, emotion, and reward networks of the brain in a sample of no/low and heavier drinkers aged 12–21 years old. While the study did not compare discrete groups of adolescents and adults, analyses investigating the interaction between continuous age and alcohol exposure history were conducted which provide insight into the effect of alcohol use on functional brain networks from early adolescence to emerging adulthood. Regardless of age, no differences were observed between matched subgroups of no/low drinkers and moderate/heavy drinkers in the default mode, salience, or reward networks. However, in the central executive network, connectivity between the superior frontal gyrus (SFG) and insula increased with age in the no/low drinkers but not in heavier drinkers. Age-related strengthening of this fronto-limbic connection correlated with better performance on a delay discounting task in boys, suggesting that adolescent alcohol use may interfere with typical development of higher-level cognitive functions. In the emotion network, amygdala-medial parietal functional synchrony was reduced in the heavier drinkers compared to the no/low drinkers and exploratory analyses suggested that weaker amygdala-precuneus/posterior cingulate connectivity related to later stages of pubertal development in the no/low drinking group only. Interestingly, in the default mode (posterior cingulate-right hippocampus/amygdala) and emotional networks (amygdala, cerebellum), connectivity in regions that exhibited age-related desynchronization was negatively correlated with episodic memory performance in the heavy drinkers. These results give preliminary evidence that alcohol might have age-dependent effects on resting state connectivity and synchronization in the central executive, emotion, and default mode networks that could potentially interfere with normative maturation of these networks during adolescence.

Three studies examined age effects in alcohol-related implicit cognitions, specifically attentional bias [ 163 , 165 ], alcohol approach bias [ 165 ], and implicit memory associations and explicit outcome expectancies [ 164 ]. Attentional bias refers to the preferential automatic allocation or maintenance of attention to alcohol-related cues compared to neutral cues which is correlated with alcohol use severity and craving [ 166 ]. McAteer et al. [ 163 ] measured attentional bias with eye tracking during presentation of alcohol and neutral stimuli in heavy and light drinkers in early adolescents (12–13 yrs), late adolescents (16–17 yrs), and young adults (18–21 yrs). Regardless of age, heavy drinkers spent longer fixating on alcohol cues compared to light drinkers. Cousijn et al. [ 165 ] measured attentional bias with an Alcohol Stroop task [ 167 ], comparing the speed of naming the print color of alcohol-related and control words. Consistent with the findings of McAteer et al. [ 163 ], adults and adolescents matched on monthly alcohol consumption showed similar levels of alcohol attentional bias. In the same study, Cousijn et al. [ 165 ] did not find any evidence for an approach bias towards alcohol cues in any age group.

Rooke and Hine [ 164 ] found evidence for age-related differences in implicit and explicit alcohol cognitions and their relationship with binge drinking. Using a teen-parent dyad design, adolescents (13–19 yrs) showed stronger memory associations in an associative phrase completion task and more positive explicit alcohol expectancies than adults. Interestingly, both explicit positive alcohol expectancies and implicit memory associations were a stronger predictor of binge drinking in adolescents compared to adults. It is important to note that adolescents also had higher levels of binge drinking than adults in the study.

Cousijn et al. [ 165 ] also investigated impulsivity, drinking motives, risky decision-making, interference control, and working memory. No age differences emerged in the cognitive functioning measures including risky decision-making (Columbia Card Task – “hot” version), interference control (Classical Stroop Task), or working memory (Self-Ordered Pointing Task). However, adolescents were more impulsive (Barrett Impulsiveness Scale) than adults and reported more enhancement motives. Importantly, impulsivity as well as social, coping, and enhancement motives of alcohol use correlated with alcohol use in both ages. However, age only moderated the relationship between social drinking motives and alcohol use-related problems (as measured by the Alcohol Use Disorder Identification Test), with a stronger positive association in adolescents compared to adults. Importantly, the adolescent group had a different pattern of drinking, with less drinking days per month but more drinks per episode than the adult group.

In summary, human evidence is largely missing, with no studies comparing more severe and dependent levels of alcohol use between adolescents and adults. The preliminary evidence is too weak and heterogeneous to draw conclusions, warranting future studies investigating the impact of age.

The current systematic review assessed the evidence for the moderating role of age in the effects of chronic alcohol use on the brain and cognition. The identified 59 rodent studies (Table 1 ) and 4 human studies (Table 2 ) provide initial evidence for the presence of age-related differences. Rodents exposed to ethanol during adolescence show both increased risk and resilience to the effects of ethanol depending on the outcome parameter. However, due to the high variability in the outcomes studied and the limited number of studies per outcome, conclusions should be considered preliminary. Moreover, brain and behavioral outcomes were mostly studied separately, with studies focusing on either brain or behavioral outcomes. The behavioral consequences of changes in certain brain outcomes still need to be investigated. Table 3 provides a comprehensive overview of the strength of the evidence for age-related differences for all outcomes. Below, we will discuss the most consistent patterns of results, make connections between the behavioral and neurobiological findings when possible, highlight strengths and limitations of the evidence base, and identify the most prominent research gaps.

Patterns of results

Age-related differences in learning and memory-related processes appear to be highly domain specific. There is limited but fairly consistent evidence for adolescent-specific impairments in contextual fear conditioning, which could be related to hippocampal dysfunction. Results for other hippocampus-related memory processes such as spatial memory are mixed and largely based on forced exposure with acute challenge studies rather than voluntary long-term exposure to alcohol. The evidence base is currently insufficient to draw conclusions about the role of age in alcohol’s effects on non-spatial types of learning and memory. Alcohol generally did not impact performance in the non-spatial variants of the MWM and SBM paradigms or in reward-learning, but the results of the limited studies in the object-learning domain highlight potential impairments and the importance of age therein. For example, adolescents but not adults demonstrated impaired object memory in the only study using the novel object recognition task [ 65 ]. Acute challenges after chronic pre-exposure to alcohol also appear to impair performance in the working memory domain, with one study suggesting heightened adolescent sensitivity to working memory impairment [ 83 ]. Thus, although the domain-specific evidence is limited by the relative lack of research, overall patterns suggest that learning and memory functions that are primarily hippocampus-dependent may be differentially affected by adolescent compared to adult alcohol use. Studies focusing on neural hippocampal processes corroborate these findings, reporting more extensive changes in protein expression [ 158 ], less desensitization of cFos upregulation [ 142 ], larger changes in GABAa receptor subunit expression [ 124 ], longer lasting changes in NMDA receptor expression [ 115 ], and larger reductions in neurogenesis [ 65 , 133 ] in the hippocampus of adolescent compared to adult ethanol-exposed rodents. On the other hand, ethanol-induced changes in the hippocampus recovered more quickly in younger animals after abstinence [ 150 ] and adolescent mice showed less signs of ethanol-induced neuroinflammation compared to adults [ 148 ].

Higher rates of adolescent alcohol use, especially binge drinking, may be facilitated by a heightened sensitivity to the rewarding properties of alcohol in combination with a reduced sensitivity to the negative effects of high doses [ 47 ]. In line with this, there is limited but consistent evidence that adolescents show less CTA in response to chronic ethanol and consequently voluntarily consume more ethanol [ 50 ]. Importantly, distinct vulnerability periods within adolescence for altered CTA may exist [ 168 , 169 ], with early adolescents potentially being least sensitive to aversive effects. Future studies using chronic exposure paradigms comparing different stages of adolescence to adults are needed. In contrast to CTA, there is insufficient evidence of age-related differences in the motivational value of alcohol based on CPP paradigms, with only one of five studies reporting stronger CPP in adolescents than adults [ 52 ]. Adolescents may be more sensitive to the effects of environmental factors on the motivational value of alcohol than adults, as adolescents housed in enriched environments acquired CPP while those in standard housing did not, an effect that was not found in adults [ 54 ]. Evidence for environmentally enriched housing being protective against these changes in adolescents provides an important indication that environmental factors matter and are important factors to consider in future research on the motivational value of ethanol on both the behavioral and neural level. Complementary studies on the functioning of brain regions within the mesolimbic dopamine pathway and PFC, which play an important role in motivated behavior, indicate limited but consistent evidence for age-related differences. Adolescents showed less dopamine reactivity in the PFC and NAc compared to adults after chronic ethanol exposure. Furthermore, there is limited but consistent evidence that adolescents are more vulnerable to epigenetic changes in the frontal cortex and reward-related areas after chronic ethanol exposure. For instance, adolescents may be more sensitive to histone acetylation of transcription factors in motivational circuits underlying the rewarding effects of alcohol [ 55 ], which may contribute to addictive behaviors [ 170 , 171 ]. Chronic alcohol use is also associated with lower BDNF levels in the PFC and subsequent increases in alcohol consumption, implicating BDNF as an important regulator of alcohol intake [ 172 ]. While evidence is limited, chronic alcohol use consistently reduced prefrontal BDNF in both age groups. However, the rate of recovery of BDNF levels after abstinence appears to be slower in adolescents.

Regarding executive functioning, there is limited but fairly consistent evidence from animal studies that adolescents are more vulnerable to long-term effects of chronic exposure on decision-making and are more impulsive than adults during acute intoxication and after prolonged abstinence following chronic exposure. Impulsivity is associated with functional alterations of the limbic cortico-striatal systems [ 91 ], with involvement of both the dopaminergic and serotonergic neurotransmitter systems [ 173 ]. While no studies investigating serotonergic activity were identified, the consistent reduction in dopamine reactivity observed in the PFC and NAc in adolescents compared to adults parallel the behavioral findings. There is also limited but fairly consistent evidence that adolescents are more resilient to impairments in cognitive flexibility than adults following chronic exposure to alcohol, and that adolescents may more easily regain control over their alcohol-seeking behavior than adults. These behavioral findings provide preliminary support for the paradox of adolescent risk and resilience in which adolescents are at once more at risk to develop harmful patterns of drinking, but are also more resilient in that they may be more equipped to flexibly change behavior and with time regain control over alcohol consumption. However, studies assessing processes that might be related to brain recovery provide little conclusive evidence for potential underlying mechanisms of these behavioral findings. While adolescents appear more vulnerable to ethanol-induced brain damage [ 131 , 132 ], show reduced neurogenesis [ 65 , 133 ], and show less changes in gene expression associated with brain recovery [ 65 , 133 ], adults show relatively higher immune responses after repeated ethanol exposure [ 147 , 148 ]. The limited evidence for adolescent resilience to alcohol’s effects on cognitive flexibility diverge from the conclusions of recent reviews that focused mostly on adolescent-specific research. Spear et al. [ 18 ] concluded that adolescents are more sensitive to impairments in cognitive flexibility; however, this was based on adolescent-only animal studies. Similarly, the systematic review of Carbia et al. [ 19 ] on the neuropsychological effects of binge drinking in adolescents and young adults also revealed impairments in executive functions, particularly inhibitory control. However, as pointed out by the authors, the lack of consideration of confounding variables (e.g., other drug use, psychiatric comorbidities, etc.) in the individual studies and the lack of prospective longitudinal studies limit our ability to causally interpret these results. This further highlights the difficulty of conducting human studies which elucidate causal associations of the effects of alcohol, and the need for animal research that directly compares adolescents to adults to bolster interpretation of findings from human research.

Only a few studies have investigated age-related differences in cognitive functioning in humans. These studies focused on mostly non-dependent users and studied different outcomes, including cognitive biases and implicit and explicit alcohol-related cognitions. Overall, there was limited but consistent evidence that age does not affect alcohol attentional or approach biases, with heavy drinkers in both age groups allocating more attention to alcohol cues compared to controls [ 163 , 165 ]. In contrast, in line with a recent meta-analysis of the neurocognitive profile of binge-drinkers aged 10–24 [ 23 ], there is limited evidence that age affects alcohol associations. One study found age effects on implicit (memory associations) and explicit (expectancies) cognition in relation to alcohol use. Adolescents showed stronger memory associations and more positive expectancies than adults [ 164 ]. These expectancies were also predictive of higher binge drinking in adolescents but not adults, highlighting the importance of future research into age differences in alcohol-related cognitions and their consequences on alcohol consumption. However, the quality of the evidence was rated as weak based on the methodological design of the included studies.

Regarding anxiety-related outcomes, results are inconsistent across studies and paradigms. When age-differences are observed, adolescents often show reduced anxiety compared to adults during both acute withdrawal and sustained abstinence following chronic ethanol exposure. However, the direction of age-related effects of alcohol may also be anxiety-domain specific. In social settings, adults show reduced anxiety compared to adolescents. Research on the neurocircuitry of anxiety processes implicates the extended amygdala, especially the BNST, in anxiety behaviors with an emphasis on the role of GABAergic projections to the limbic, hindbrain, and cortical structures in rodents [ 174 ]. Despite adolescents showing less non-social anxiety than adults after ethanol exposure, no age-differences were observed for LTP in the BNST [ 109 ]. Also, GABA receptor expression in the hippocampus and whole cortex was not altered by ethanol exposure in either age group [ 108 ]. However, the anxiolytic effects of NMDA antagonists [ 175 ] also highlight the importance of glutamatergic activity in anxiety processes [ 176 ]. In line with behavioral findings, adolescents were less sensitive to changes in glutamate expression: adults showed heightened expression in the NAc, which has been suggested to underlie the higher levels of anxiety observed in adults compared to adolescents [ 106 ]. Importantly, across the various studies, different paradigms were used to assess anxiety, potentially contributing to the inconsistent results. Furthermore, most of the identified studies used a forced ethanol exposure paradigm. As alcohol-induced anxiety is likely also dependent on individual trait anxiety, voluntary consumption studies in high and low trait anxiety animals are important to further our understanding of the interaction between alcohol use and anxiety. Of note, the observed pattern suggestive of reduced anxiety in adolescents compared to adults diverges from conclusions of previous reviews such as Spear et al. [ 18 ] which concluded that adolescents are more likely to show augmented anxiety after alcohol exposure based on animal studies with adolescent animals only. Importantly, anxiety was included as a secondary outcome in this review because of the high comorbidity between anxiety disorders and alcohol addiction, warranting the inclusion of age-related differences in the relation between alcohol and anxiety. However, the search strategy was not specifically tailored to capturing all studies assessing age-related differences in the effect of alcohol on anxiety.

Translational considerations, limitations, and future directions

The reviewed studies revealed a high degree of variability in study designs and outcomes, hindering integration and evaluation of research findings. We were unable to differentiate our conclusions based on drinking patterns (i.e., comparing binge drinking, heavy prolonged use, AUD). The prevalence of binge-drinking in adolescence is very high and is associated with neurocognitive alterations [ 177 ]. Studies investigating the potential differential impact of binge-drinking compared to non-binge-like heavy alcohol use in adolescence and adulthood are critical for understanding the risks of chronic binge-like exposure in adolescence, even if it does not progress to AUD.

It is also important to acknowledge the limitations of the choice of adolescent and adult age ranges in our inclusion criteria. Rodent studies had to include an adolescent group exposed to alcohol between the ages of PND 25–42 and an adult group exposed after age PND 65. Ontogenetic changes may still be occurring between PND 42–55, and this period may more closely correspond to late adolescence and emerging adulthood in humans (e.g., 18–25 years). Studies that compared animals in this post-pubertal but pre-adulthood age range were not reviewed. Studies investigating age-related differences in the effects of ethanol on brain and cognitive outcomes in emerging adulthood are also translationally valuable given the high rates and risky patterns of drinking observed during this developmental period [ 178 ]. Indeed, an important future direction is to examine whether there are distinct vulnerability periods within adolescence itself for the effects of ethanol on brain and cognitive outcomes. Given that emerging adulthood is a period of continued neurocognitive maturation and heightened neural plasticity, studies comparing this age range to older adults (e.g., over 30) are also necessary for a more thorough understanding of periods of risk and resilience to the effects of alcohol.

Furthermore, we did not conduct a risk of bias assessment to examine the methodological quality of the animal studies. The applicability and validity of the risk of bias tools for general animal intervention studies, such as the SYRCLE risk of bias tool [ 179 ], remain in question at the moment. The lack of standardized reporting in the literature for many of the criteria (e.g., process of randomizing animals into intervention groups) would lead to many studies being labeled with an ‘unclear risk of bias’. Furthermore, there is still a lack of empirical evidence regarding the impact of the criteria in these tools on bias [ 179 , 180 ]. This is a significant limitation in evaluating the strength of the evidence for age-related differences based on the animal studies, which highlights the importance of more rigorous reporting standards in animal studies.

Moreover, most work is done in male rodents and is based on forced ethanol exposure regimes. In a recent opinion article, Field and Kersbergen [ 181 ] question the usefulness of these types of animal models to further our understanding of human substance use disorders (SUD). They argue that animal research has failed to deliver effective SUD treatment and that social, cultural, and other environmental factors crucial to human SUD are difficult, if not impossible, to model in animals. While it is clear that more sophisticated multi-symptom models incorporating social factors are needed to further our understanding of SUD and AUD specifically, a translational approach is still crucial in the context of investigating the more fundamental impact of alcohol use on brain and cognition. In humans, comparing the impact of alcohol use on brain and cognition between adolescents and adults is complicated by associations between age and cumulative exposure to alcohol; i.e., the older the individual, the longer and higher the overall exposure to alcohol. Although animal models may be limited in their ability to model every symptom of AUD, they can still provide critical insights into causal mechanisms underlying AUD by allowing direct control over alcohol exposure and in-depth investigation of brain mechanisms.

The intermittent voluntary access protocol resembles the patterns of alcohol use observed in humans, and also result in physiologically relevant levels of alcohol intake [ 182 , 183 , 184 ]. Only a minority of the studies included in this review employed a voluntary access protocol, with one study using beer instead of ethanol in water [ 158 ], which better accounts for the involvement of additional factors (e.g., sugar, taste) in the appeal of human alcohol consumption. Voluntary access protocols can also model behavioral aspects of addictive behavior such as loss of control over substance use and relapse [ 185 , 186 , 187 ], an important area in which little is known about the role of age. Ideally, one would also investigate choices between ethanol and alternative reinforcers, such as food or social interaction, that better mimic human decision-making processes [ 188 ]. However, studies on the effects of ethanol on social behavior are limited and show inconsistent results and studies assessing reward processes often lack a social reward component as an alternative reinforcer.

On a practical level, rodents mature quickly and choice-based exposure paradigms are more complex and time-consuming than most forced exposure paradigms. Consequently, by the time final behavioral measurements are recorded, both the adolescent and adult exposure groups have reached adulthood. To combat this, many of the included studies use forced ethanol exposure, such as ethanol vapor, to quickly expose rodents to very high doses of ethanol. Although the means and degrees of alcohol exposure may not directly translate to human patterns of alcohol use, such studies do allow for the assessment of the impact of high cumulative doses of ethanol within a relatively short period of time which allows for more time in the developmental window to test age-related differences in the outcomes. When considering the translational value of a study, it is therefore important to evaluate studies based on the goal, while not ignoring the practical constraints.

While human research is challenging due to the lack of experimental control and the inherent confounds in observational studies between age and alcohol exposure history, large-scale prospective longitudinal studies offer a gateway towards a better understanding. Comparisons of different trajectories of drinking from adolescence to adulthood (i.e., heavy drinking to light drinking, light drinking to heavy drinking, continuously heavy drinking, and continuously light drinking) could offer insight into the associated effects on cognitive and brain-related outcomes. Of course, different drinking trajectories are likely confounded with potentially relevant covariates which limits causal inference. Direct comparisons of low and heavy adolescent and adult drinkers, supported by a parallel animal model can help to bolster the causality of observed age-related differences in human studies. In addition, changes in legislation around the minimum age for alcohol consumption in some countries provide a unique opportunity to investigate how delaying alcohol use to later in adolescence or even young adulthood impacts cognitive functioning over time. Importantly, future studies investigating the moderating role of age in humans should carefully consider the impact of psychiatric comorbidities. While adolescence into young adulthood is the period in which mental health issues often emerge [ 189 , 190 ], there is some evidence that the prevalence of comorbidities is higher in adults with AUD [ 95 ]. This is an important to control for when considering age-related differences on cognition and the brain given the evidence of altered cognitive functioning in other common mental illnesses [ 191 , 192 ].

Concluding remarks

The aim of this systematic review was to extend our understanding of adolescent risk and resilience to the effects of alcohol on brain and cognitive outcomes compared to adults. In comparison to recent existing reviews on the impact of alcohol on the adolescent brain and cognition [ 17 , 18 , 19 , 22 , 23 ], a strength of the current review is the direct comparison of the effects of chronic alcohol exposure during adolescence versus adulthood. This approach allows us to uncover both similarities and differences in the processes underlying alcohol use and dependence between adolescents and adults. However, due to the large degree of heterogeneity in the studies included in sample, designs, and outcomes, we were unable to perform meta-analytic synthesis techniques.

In conclusion, while the identified studies used varying paradigms and outcomes, key patterns of results emerged indicating a complex role of age, with evidence pointing towards both adolescent vulnerability and resilience. The evidence suggests adolescents may be more vulnerable than adults in domains that may promote heavy and binge drinking, including reduced sensitivity to aversive effects of high alcohol dosages, reduced dopaminergic neurotransmission in the NAc and PFC, greater neurodegeneration and impaired neurogenesis, and other neuromodulatory processes. At the same time, adolescents may be more resilient than adults to alcohol-induced impairments in domains which may promote recovery from heavy drinking, such as cognitive flexibility. However, in most domains, the evidence was too limited or inconsistent to draw clear conclusions. Importantly, human studies directly comparing adolescents and adults are largely missing. Recent reviews of longitudinal human research in adolescents, however, revealed consistent evidence of alterations to gray matter, and to a lesser extent white matter, structure in drinkers [ 17 , 18 ], but also highlight the limited evidence available in the domains of neural and cognitive functioning in humans [ 17 ]. Future results from ongoing large-scale longitudinal neuroimaging studies like the ABCD study [ 193 ] will likely shed valuable light on the impact of alcohol use on the adolescent brain. However, our results also stress the need for direct comparisons with adult populations. Moreover, while the lack of experimental control and methodological constraints limit interpretations and causal attributions in human research, translational work aimed at connecting findings from animal models to humans is necessary to build upon the current knowledge base. Furthermore, the use of voluntary self-administration paradigms and incorporation of individual differences and environmental contexts are important steps forward in improving the validity of animal models of alcohol use and related problems. A more informed understanding of the effects of alcohol on adolescents compared to adults can further prevention efforts and better inform policy efforts aimed at minimizing harm during a crucial period for both social and cognitive development.

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This work was supported by grant 1RO1 DA042490-01A1 awarded to Janna Cousijn and Francesca Filbey from the National Institute on Drug Abuse/National Institutes of Health. The grant supported the salaries of authors Lauren Kuhns, Emese Kroon, and Janna Cousijn. Thank you to Claire Gorey (CG) for running the initial search and aiding in the screening process.

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Kuhns, L., Kroon, E., Lesscher, H. et al. Age-related differences in the effect of chronic alcohol on cognition and the brain: a systematic review. Transl Psychiatry 12 , 345 (2022). https://doi.org/10.1038/s41398-022-02100-y

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Implicit Social Attunement and Alcohol Use: The Effect of Peer Feedback on Willingness to Drink in Social Settings

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• Published: 12 August 2024

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• Emese Kroon   ORCID: orcid.org/0000-0003-1803-9336 1 , 2 ,
• Ran Zhang 2 ,
• Karis Colyer-Patel 2 ,
• Alix Weidema 2 ,
• Doğa Ünsal 2 ,
• Helle Larsen 1 &
• Janna Cousijn 1 , 2  

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Social context plays an important role in alcohol consumption. While most studies focus on explicit social drinking norms, this study aimed to (1) develop an implicit social attunement (ISA) task to experimentally assess how willingness to drink alcohol is affected by social alcohol drinking (SAD), social non-alcohol drinking (SNAD), and social non-drinking (SND) settings and peer feedback on willingness to drink in these settings, and (2) assess how ISA is associated with explicit social attunement, age, alcohol use and related problems. Participants ( N  = 506) aged 16–60 years completed the ISA task and questionnaires assessing alcohol use and alcohol use–related problems, age, and explicit social attunement online. Willingness to drink was highest in the SAD setting (SAD: M ( SD ) = 5.70 (2.68); SNAD: M ( SD ) = 4.03 (2.20); SND: M ( SD ) = 2.02 (1.30)) and—regardless of social setting — lower peer willingness to drink induced higher ISA than higher peer willingness to drink (SAD: t (325) =  − 2.929, p  = .035; SNAD: t (325) =  − 2.888 p  = .036; SND: t (325) =  − 6.764, p  < .001). Higher ISA to higher peer willingness in the SAD ( r  = .15, p  = .001) and SNAD ( r  = .11, p  = .011) settings was associated with higher alcohol use and related problems, while higher ISA to lower peer willingness in the SND setting was associated with lower alcohol use and related problems ( r  =  − .18, p  = .002) and recent alcohol use (standard drinks: r  =  − .14, p  = .011; binge drinking days: r  =  − .16, p  = .005). Explicit social attunement, but not ISA, mediated the association between lower age and higher alcohol use and related problems ( b  =  − .013, p  = .009). Results indicate that peer feedback can be a protective or risk factor for alcohol use, depending on the social setting. Future studies are needed to elucidate differences between implicit and explicit social attunement behaviors in their associations with age and alcohol use and related problems.

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Alcohol use in social settings is very common across age groups (e.g., Mustonen et al., 2014 ) and stronger social motives for use have been associated with higher frequency and quantity of alcohol consumption and alcohol use–related problems (Bresin & Mekawi, 2021 ). Peer drinking is known to be associated with higher alcohol use (Scholte et al., 2008 ), especially during adolescence (Huang et al., 2014 ), potentially due to heightened social reward sensitivity (Beard et al., 2022 ; Foulkes & Blakemore, 2016 ). However, most evidence of peer influence on alcohol use–related behaviors relies on self-report measures of explicit social norms. Hence, we know relatively little of the potential implicit nature of peer influence on alcohol consumption. Furthermore, it is unclear how contextual factors, age, and social attunement—individual tendencies to adapt to and harmonize with one’s social environment—might be associated with peer influence on willingness to drink.

Alcohol use is usually initiated during adolescence and peaks during early adulthood (Johnston et al., 1975 ; Lee et al., 2018 ). Social learning is crucial during this developmental period in which parental influence reduces while peer influence increases (Marshal & Chassin, 2000 ; Sebastian et al., 2008 ). However, peer influence on alcohol use remains prominent in adulthood: Rosenquist et al. ( 2010 ) showed that individuals with a heavy drinking social network are more likely to drink heavily themselves, and that the individuals closest to them have the largest influence on one’s drinking behavior. In line with this, decades of research have shown that both descriptive and injunctive peer norms, especially from proximal peers, are associated with heaviness of alcohol use (e.g., Halim et al., 2012 ; Voogt et al., 2013 ). For example, Leung et al. ( 2014 ) showed that adolescents with heavy drinking peers are more likely to heavily drink themselves due to peer influence and peer group selection. While solitary drinking might pose a higher risk for the development of an alcohol use disorder (AUD; e.g., Creswell, 2021 ; Skrzynski & Creswell, 2020 ), Creswell ( 2021 ) showed that drinking in social settings increases immediate health risks through the consumption of larger amounts of alcohol. For example, a recent ecological momentary assessment study by O’Donnell et al. ( 2019 ) showed that young adults consumed larger amounts of alcohol in social situations where others consumed alcohol. Furthermore, several experimental studies also showed that young adults adapt their drinking behavior to the drinking of other individuals (Larsen et al., 2009 , 2010 , 2012 ) and drink more in group settings (Kuendig & Kuntsche, 2012 ).

Peer influence on drinking can take a variety of forms. Peer pressure in which individuals conform with the group norm to avoid negative consequences is common (e.g., O’Donnell et al., 2019 ), but more positive reinforcement motives, like social attunement, might also play a role (Cousijn et al., 2018 ). Social attunement refers to an individual’s tendencies to adapt to and harmonize with one’s social environment—in the absence of explicit peer pressure—to maximize positive social feedback. Hence, social attunement could play a central role in reducing alcohol use when maturing (Chassin et al., 2004 ; Vergés et al., 2013 ): as reduced reward sensitivity and increased behavioral control only account for part of the reduction in alcohol use when maturing (Heyman, 2009 ), changing group norms and peer influence might be crucial in this process (Dawson et al., 2006 ; Lee et al., 2015 ). Social attunement is a form of social learning that is hypothesized to play an important role in both adolescent risk for excessive use and resilience to persistent heavy use in adulthood (Cousijn et al., 2018 ). While one’s tendency to attune with the social environment might result in excessive use during adolescence when the social value of excessive drinking can be relatively high, this same tendency might result in a reduction of drinking in adulthood by attuning to the new socially devaluated alcohol standards (e.g., due to new responsibilities; Hajema & Knibbe, 1998 ).

Recently, Kroon et al. ( 2022 ) developed a questionnaire to assess explicit self-reported social attunement and assessed the role of social attunement in alcohol use. Results showed that explicit social attunement is associated with alcohol use and related problems, specifically in youngsters (around 16 to 20 years old) with heavy drinking peers. However, it is likely that not all social attunement is explicit: we regularly adjust our behaviors to the social environment without noticing or being able to report on it. Hence, implicit measures of social attunement are crucial to explore the role of social attunement in alcohol use.

As tasks to assess implicit social attunement are currently lacking, we aimed to develop a task to experimentally assess the effects of different social settings (i.e., alcohol drinking, non-alcohol drinking, or no drinking) on willingness to drink, and whether peer feedback—either indicating higher or lower willingness to drink—results in implicit social attunement in the direction of the peers. We expect that implicit social attunement of one’s willingness to drink alcohol is higher in social settings in which other individuals are drinking alcohol, compared to situations with non-alcoholic drinks or no drinks. Furthermore, we expect implicit social attunement to depend on the direction of peer feedback: reducing willingness after lower drinking feedback, increasing willingness after higher drinking feedback, while not changing willingness when peer feedback matches one’s own willingness.

Second, we aimed to evaluate how implicit social attunement, explicit social attunement, and age are associated with alcohol use and whether implicit and/or explicit social attunement might mediate the association between age and alcohol use. Focusing on the task outcomes, we expect higher implicit social attunement when peers have a lower willingness to drink to be associated with lower alcohol use, while we expect higher implicit social attunement when peers have a higher willingness to drink to be associated with higher alcohol use. Also, we expect implicit social attunement to be positively associated with explicit social attunement and expect younger individuals to show higher implicit and explicit social attunement and to report higher alcohol use than their adult counterparts. Furthermore, we expect implicit and explicit social attunement to mediate the association between age and alcohol use.

This study proposes a novel task to measure implicit social attunement complementing the existing measure of explicit social attunement. This will enable us to assess the role of implicit and explicit social processes in alcohol use and how these differ depending on age.

Sample and Procedure

A total of 506 participants aged 16–60 participated in the study, to reach sufficient power for the most complex analyses (i.e., mediation models; Sim et al., 2022 ). The collected data was part of a larger online study including multiple cognitive tasks and questionnaires. Participants were recruited via social media (i.e., WhatsApp, Instagram, Facebook), in-person flyers (Amsterdam and Rotterdam region), and the Erasmus University Rotterdam’s student participant pool. The study advertisement was targeting individuals that use cannabis and/or alcohol, but no inclusion or exclusion criteria aside from age (16–65 years old) and proficiency in English or Dutch applied. Participants were fully informed, had the opportunity to contact the researchers, and signed informed consent before participation. The 1-h online session included two blocks of questionnaires, separated by several experimental tasks, that participants could complete in English or in Dutch depending on their preference. At the end of the study, participants were pointed towards potential ways to seek help for mental health or substance use problems. As compensation, participants could enter a raffle in which one in five participants received a ten-euro gift card. Study protocols were approved by the Ethics Review Committee of Erasmus University Rotterdam (ETH2122-0311) to ensure confidentiality, data protection, and informed consent.

Implicit Social Attunement Task

The Implicit Social Attunement Task (ISAT; inspired by Izuma & Adolphs, 2013 ) was developed to measure implicit social attunement (ISA) to peer feedback in different imagined social situations. In this version, social attunement is operationalized as the extent to which participants adjust their initial willingness to drink in the direction of the peer feedback, controlled for average adjustments made when no feedback is provided.

In the first block, participants were presented with 45 images of social situations (featuring two or more men and/or women) in a fixed order, including 15 images for each of the three social situations: Social Alcoholic Drink (SAD; drinking beer), Social Non-Alcoholic Drink (SNAD; drinking soda), Social Non-Drink (SND; no drinking). Participants were instructed to imagine being in the presented situation and asked to indicate their willingness to drink alcohol in this situation on a scale from 1 to 10 (1 = no willingness, 10 = strong willingness), enabling a large range of responses while using a common grading scale (i.e., Dutch grading system) which has previously been used and validated in similar studies (e.g., Larsen et al., 2022 ). Immediately after their response, they were shown what they were told was the average willingness to drink that their peers (a group of similar age) had indicated for this situation when they completed the task earlier. This “peer feedback” was not real: feedback was semi-randomly generated based on the participants’ response. Peers responded identically to the participants in 2 trials (fixed trials identical for all participants). In the other 43 trials, the chance of receiving “higher” willingness feedback (peer rated higher than participant) or “lower” willingness feedback (peer rated lower than participant) was 50%. In all trials with non-identical feedback, there was a 70% chance that the difference between participants’ and peer response was large (2 to 3 points) and a 30% chance that the difference was small (1 point). After the first block, a working memory task was performed, creating an 11-min delay. In the second block, all pictures were shown again in the same order and participants were asked to rate their willingness to drink in these situations again, without seeing peer feedback.

Questionnaires

Participants completed single-item questions assessing age (in years), gender (male/female/other), nationality (Dutch/Non-Dutch), highest completed education (recoded to four categories based on the Dutch high school (different levels preparing for different higher education levels), and higher education system: (1) less than high school, (2) (pre-) vocational/(pre-) college, (3) (pre-) university, (4) other, age of onset of alcohol use (in years), self-reported (estimated) number of days of binge drinking (> 4 drinks on a single occasion; Courtney & Polich, 2009 ) during the last year, and self-reported (estimated) lifetime drug use (excluding alcohol, cigarettes, and cannabis). The Alcohol Use Disorder Identification Test (AUDIT; Hildebrand & Noteborn, 2015 : α  = 0.92, Saunders et al., 1993 ) was used to assess alcohol use (AUDIT-C: items 1–3) and related problems (AUDIT-P: items 4–10), with full AUDIT (items 1–10) scores over 7 reflecting problematic alcohol use. Furthermore, participants completed a timeline follow-back (TLFB; Robinson et al., 2014 ) calendar assessing last 14-day use of alcohol (number of standard drinks, number of drinking days, number of binge drinking days), cigarettes (number of cigarettes), and cannabis (grams) to assess recent use. The social attunement questionnaire (SAQ; Kroon et al., 2022 : α  = 0.75) was used to assess explicit social attunement. General mental health was assessed using the DSM-5 Cross Cutting Symptoms scale (American Psychiatric Association, 2013 ; Doss & Lowmaster, 2022 : α  = 0.96) and general executive functioning was assessed using a short 6-item self-report questionnaire for online assessment (Buchanan et al., 2010 : α  = 0.79).

Data Analysis

First, to assess the effects of social setting and feedback type on willingness to drink and to evaluate the psychometric properties of the novel ISAT task, internal consistency of the three social conditions was assessed (Cronbach’s alpha) and a repeated measures ANOVA was conducted to compare willingness to drink in block 1 across the three social conditions (SAD, SNAD, SND). Sample t -tests were used to assess the presence of a change in willingness to drink (different from 0) in different social situations (SAD, SNAD, SND) for different feedback types (high, low, same).

Second, to assess the role of feedback type and social setting in implicit social attunement (ISA), ISA scores—controlling for change on same feedback trials—were calculated per participant to quantify individual implicit social attunement when provided with higher willingness to drink feedback (ISA +  = difference score on positive trials − difference scores on same trials) and when provided with lower willingness to drink feedback (ISA −  =  − 1*difference score on negative trials − difference score on same trials). Separate scores were calculated for all social settings (SAD, SNAD, and SND). Repeated measures ANOVAs were conducted to assess the effects of social setting (SAD, SNAD, SND), feedback type (+ , −), and their interaction on ISA.

Third, to assess how ISA scores were associated with explicit social attunement, age, and alcohol use, Spearman’s correlations between ISA + and ISA − scores per social setting, SAQ scores, age, and measures of alcohol use (AUDIT and TLFB outcomes) were calculated. Then, exploratory mediation analyses were conducted to assess whether SAQ and/or ISA scores mediated the association between age and alcohol use measures. Analyses were conducted using the most recent versions of R (version 4.2.2 in RStudio version 2022.12.0) and JASP (version 0.16.4).

Sample Characteristics

The majority of the participants were non-Dutch (66.60%), highly educated (94.47% completed (pre-)university education), and identified as female (60.08%), with an average age of 29.90 ( SD  = 11.85) years old (Table  1 ). Most participants reported lifetime alcohol use (93.87%), on average reporting low-risk alcohol consumption in the last year (AUDIT < 8) (Saunders et al., 1993 ) and drinking about 1 in 3 days during the last 2 weeks (Table  1 ).

Willingness and Change in Willingness to Drink

Social setting (SAD: α  = 0.98, SNAD: α  = 0.97, SND: α  = 0.92) did significantly affect willingness to drink in block 1 ( F (1.42, 802.84) = 989.69, p  < 0.001, η general 2  = 0.33; Fig.  1 A). Holm’s corrected post hoc comparisons showed that there were significant differences in willingness to drink between all conditions (all p  < 0.001), with willingness to drink being highest in the SAD setting and lowest in the SND setting (SAD: M ( SD ) = 5.70 (2.68); SNAD: M ( SD ) = 4.03 (2.20); SND: M ( SD ) = 2.02 (1.30); Table S1 ). Willingness to drink changed in the direction of the peer feedback (all p ’s > 0.001, see Fig.  1 B and Table S1 ), while no change in willingness was observed when presented with peer feedback indicating identical willingness to drink (lowest p  = 0.143).

Willingness to drink per social setting ( A ) and changes in willingness to drink per social setting and feedback type ( B ). SAD, social alcohol drink; SNAD, social non-alcohol drink; SND, social non-drink; high: peer feedback indicating higher willingness to drink, low: peer feedback indicating lower willingness to drink, same: peer feedback identical to own willingness to drink. Error bars represent mean and SE

Implicit Social Attunement: The Effect of Social Setting and Feedback Type

Results showed a significant interaction between feedback type and social setting in their effect on ISA ( F (1.75, 568.53) = 6.846, p  = 0.002, η general 2  = 0.003; Greenhouse–Geisser correction applied) (Fig.  2 ). Holm’ corrected post hoc comparisons showed that there were no differences between social settings in ISA + scores (lowest p  = 0.780) or ISA − scores (lowest p  = 0.302; Table S2 ). Within social setting, feedback type did have an effect: ISA − scores were higher than ISA + scores in the SAD ( t (325) =  − 2.929, p  = 0.035, d  = 0.325), SNAD ( t (325) =  − 2.888, p  = 0.036, d  = 0.320), and SND ( t (325) =  − 6.764, p  < 0.001, d  = 0.750) condition. There were differences between the ISA + and ISA − scores across all social settings, except for the comparisons between the SAD and SNAD conditions (SAD ISA + vs. SNAD ISA − : t (325) =  − 2.449 p  = 0.116, d  = 0.272; SNAD ISA + vs. SAD ISA − : t (325) =  − 1.940, p  = 0.316, d  = 0.215).

The effects of social setting and feedback type on implicit social attunement (ISA). SAD, social alcohol drink; SNAD, social non-alcohol drink; SND, social non-drink; + : peer feedback indicating higher willingness to drink, -: peer feedback indicating lower willingness to drink. ISA + and ISA − scores are corrected for change on same feedback trials. Error bars represent mean and SE

Implicit Social Attunement: Associations with Explicit Social Attunement, Age, and Alcohol Use

Full AUDIT scores were positively correlated with ISA + in SAD ( r  = 0.15, p  = 0.001) and SNAD ( r  = 0.11, p  = 0.011) trials, but not SND trials ( p  = 0.83; Fig.  3 ; full overview in Table S3 ). However, TLFB scores were only positively correlated with ISA + in SAD trials (Standard drinks r  = 0.11, p  = 0.015; Drinking days r  = 0.11, p  = 0.013). Full AUDIT scores were negatively correlated with ISA − in SND trials only (full AUDIT: r  =  − 0.18, p  = 0.002). TLFB scores were negatively correlated with ISA − in the SND trials (Standard drinks: TLFB: r  =  − 0.14, p  = 0.011, Binge days: r  =  − 0.16, p  = 0.005) and SNAD trials (Binge days: r  =  − 0.094, p  = 0.049). There was a strong positive correlation between all TLFB outcomes and full AUDIT scores (Standard drinks: r  = 0.66, p  < 0.001; Drinking days: r  = 0.53, p  < 0.001; Binge days: r  = 0.61, p  < 0.001). Full AUDIT scores ( r  =  − 0.18, p  < 0.001) and binge days ( r  =  − 0.17, p  < 0.001) correlated negatively with age, while there was a positive correlation between age and drinking days ( r  = 0.12, p  = 0.007). SAQ scores were positively correlated with full AUDIT scores ( r  = 0.14, p  = 0.001), but not with any TLFB outcome. SAQ scores were positively correlated with ISA + SND trials ( r  = 0.18, p  = 0.008), but not SNAD ( p  = 0.866) or SAD ( p  = 0.314) trials. SAQ scores were not associated with ISA − in any condition (lowest p  = 0.174). Furthermore, SAQ scores were negatively associated with age ( r  =  − 0.17, p  < 0.001).

Correlations between implicit social attunement, explicit social attunement, age, and alcohol use. Positive correlations highlighted in purple and negative correlations highlighted in red, with darker colors presenting stronger correlations. SAD, social alcohol drink; SNAD, social non-alcohol drink; SND, social non-drink; ISA + , implicit social attunement to peer feedback indicating higher willingness to drink, controlled for same feedback trials responses; ISA − , implicit social attunement to peer feedback indicating lower willingness to drink, controlled for same feedback trials responses; AUDIT, alcohol use disorder identification test; TLFB, timeline follow-back. SAQ, social attunement questionnaire scores of explicit social attunement. Significance levels: * p  < .05, ** p  < .01, *** p  < .001

The Mediating Role of Implicit and Explicit Social Attunement

Whereas none of the ISA scores mediated the association between age and full AUDIT scores (Table S4 ) or age and any of the TLFB scores (Table S5 – S7 ), SAQ scores did mediate the association between age and full AUDIT scores ( b  =  − 0.013, SE  = 0.005, 95% CI  = [− 0.023, − 0.005], p  = 0.009; Fig.  4 ), but not the association between age and TLFB scores (Table S5 – S7 ). Younger individuals showed higher explicit social attunement, which was related to higher full AUDIT scores. Sensitivity analyses showed that this effect was driven by individuals scoring above the full AUDIT cut-off for heavy use (AUDIT > 7; Table S8 ) and separate analyses of the alcohol use (AUDIT-C; items 1–3) and alcohol use–related problems (AUDIT-P; items 4–10) items of the AUDIT confirmed that the effects were guided by the alcohol use related problem items (Table S9 ).

Mediation results: SAQ mediates the association between age and AUDIT scores. *** p  < .001, ** p  < .01

Using the newly developed implicit social attunement task, we assessed the effects of social settings on willingness to drink and whether peer feedback would induce implicit social attunement towards peers. Willingness to drink was highest in social settings where alcohol was being consumed, indicating that perceived norms in social settings affect willingness to drink. Furthermore, task manipulations were effective: individuals adapted their willingness to drink in the direction of the peer feedback provided. Implicit social attunement did not differ between social settings, but social attunement was larger when peers indicated lower willingness to drink compared to higher willingness to drink. However, higher implicit social attunement to peers indicating higher willingness to drink in social drinking settings was associated with higher alcohol use and related problems. Furthermore, while implicit social attunement did not mediate the association between age and alcohol use measures, explicit social attunement did: younger individuals that reported higher explicit social attunement scored higher on alcohol use and related problems.

The implicit social attunement task showed excellent internal consistency (Tavakol & Dennick, 2011 ) in all social settings and willingness to drink changed in the direction of the peer feedback. As expected, willingness to drink was higher in the SAD condition than in the SNAD and SAD conditions, while willingness to drink was also higher in the SNAD than the SAD condition. This could indicate that seeing others drink increases willingness to drink regardless of the type of drink but that the effect is larger when the norm of drinking alcohol is present. This is in line with previous research showing that injunctive and descriptive peer norms (e.g., Halim et al., 2012 ; Voogt et al., 2013 ) and imitation of peer behavior (Larsen et al., 2009 , 2010 , 2012 ) affect people’s drinking behavior. Using this task, we were also able to distinguish the effects of different social settings within the same task. Interestingly, results indicate that people show lower willingness to drink when no alcohol is being consumed, indicating that peer influence and descriptive norms might also be important in reducing alcohol consumption.

Regardless of social setting, individuals did attune their willingness to drink in the direction of the peers. This effect is larger when provided with peer feedback indicating lower willingness to drink, also highlighting the potential importance of peer influence in cutting down alcohol use. This is in line with earlier research by Stevens-Watkins and Rostosky ( 2010 ) highlighting the potential protective factors of lower perceived peer substance use during adolescence on (binge) drinking in later years. Research should be extended, varying the group that provides feedback, to assess whether effects are similar when feedback is provided by proximal peers—usually expected to have greater influence (e.g., Salvy et al., 2014 ; Voogt et al., 2013 )—parents, or health care professionals to assess generalizability and potential prevention effects. Unlike expected, social setting did not affect social attunement. We expected that the presented social setting would affect the perceived drinking norms, resulting in larger attunement when feedback indicating higher willingness to drink is provided in the SAD setting and when feedback indicating lower willingness to drink is provided in the SNAD and SND settings (Halim et al., 2012 ; Voogt et al., 2013 ). These results could be associated with the fact that the norm setting was implicit rather than often studied explicitly reported injunctive and descriptive norms (e.g., Voogt et al., 2013 ) and did not include a real-life drinking situation in which imitation might play a larger role (e.g., Larsen et al., 2012 ). However, these results also highlight the potential irrelevance of social setting in implicit peer influence and/or large individual differences in the relevance of social setting. It could well be that the behavior of peers and the social norm set by this behavior is more important than the specific social setting when it comes to alcohol use, but future studies should replicate these findings to confirm potential utility in intervention settings.

Correlational analyses showed that only in non-alcohol settings (SNAD and SND), implicit social attunement to lower peer willingness to drink was associated to less alcohol use and related problems. This may mean that those with less implicit social attunement in response to peers indicating lower willingness to drink in non-alcohol settings tend to drink more and experience more alcohol use–related problems. In contrast, only in the settings in which drinks were present (SAD and SNAD), implicit social attunement to higher peer willingness to drink was associated with more alcohol use and related problems. This indicates that those that attune less to peers with higher willingness to drink in drink settings consume less and experience less alcohol use–related problems. Although speculative, these results indicate that individuals who reduce their willingness to drink in social settings where peers are not drinking may be more resilient and less likely to develop alcohol-related problems. Conversely, those who increase their willingness to drink in social drinking settings where peers are willing to drink could be at higher risk. These results are in line with recent research showing that those with a higher resistance to peer influence show smaller associations between perceived peer drinking and own alcohol use (DiGuiseppi et al., 2018 ). Interestingly, this study did not find similar associations with actual peer drinking, indicating a need for assessing ecological validity of our task and how results relate to real-life drinking behavior. For example, studies should include measures of perceived peer drinking and actual peer drinking within the individuals’ proximal peer group to assess whether social attunement is involved in the association between real-life peer drinking experiences and real-life drinking behavior (Kroon et al., 2022 ).

Regarding the role of age, we found implicit social attunement in SNAD settings to be higher in younger individuals, indicating that in potentially ambiguous situations (no alcohol drinks, but people are having a drink) younger adults might have a higher tendency to attune to peer feedback regardless of the direction of this feedback (i.e., the drinking norm set). Furthermore, younger adults reported fewer drinking days, but more binge drinking and more alcohol use–related problems, as well as higher explicit social attunement. Explicit social attunement was specifically associated with higher alcohol use and related problems (AUDIT scores) rather than metrics of heaviness of alcohol use only (TLFB outcomes). Explicit social attunement was only associated with implicit social attunement to peer feedback indicative of higher willingness to drink in the SND settings and observed correlation was small ( r  = 0.12), indicating that implicit and explicit social attunement are likely different social processes. In line with these differences, explicit social attunement—but none of the implicit social attunement measures—mediated the association between age and alcohol use and related problems (AUDIT scores). These effects were guided by those with AUDIT scores above the cut-off for problematic alcohol use (AUDIT > 7). Also, in line with the lack of effects found for any of the TLFB outcomes, the effect was guided by higher scores on the AUDIT items indicating problematic use (AUDIT-P; items 4–10) rather than the items indicating heaviness of use (AUDIT-C; items 1–3). Alternatively, the mediating role of explicit, but not implicit social attunement, in the relation between age and problematic alcohol use may in part be explained by social conformity behavior, which is likely to be more closely related to the explicit than implicit outcomes. It is recommended that future studies include more measures to allow differentiation between explicit social attunement and conformity. Although the mediation analyses should be considered exploratory, the results indicate that the association between age and alcohol use and related problems might be partially guided by increased explicit social attunement in younger individuals. Longitudinal studies—assessing the change of these associations during the transition from adolescence to adulthood and beyond—are crucial to confirm these associations.

The new implicit social attunement task showed a couple of clear strengths. The task induced implicit social attunement in the direction of the peer feedback. Furthermore, the use of fictional peers of a similar age prevented potential selection effects. Mundt et al. ( 2012 ) showed that individuals are known to select peers that they relate to in terms of behavior and interests, potentially resulting in peer feedback biased towards one’s own behavior/opinion within those peer groups. To experimentally assess the complexity of peer influence more generally, the stimuli can also easily be adapted to include other drugs (e.g., cannabis) or other social behaviors to assess willingness to participate in those behaviors based on implicit norms presented across conditions (e.g., adding different social settings and/or type of drink, food, or behavior) and whether this willingness changes depending on the provided feedback (e.g., same, higher, or lower).

However, some limitations must be noted. This study is fully cross-sectional and longitudinal studies are needed to confirm the temporal precedence of the observed associations. Furthermore, the fictional nature of the peers and the relative emotional distance to this peer group affects ecological validity. Future research could gather information on one’s social network, providing personal peer group feedback, and consider the drinking norms in one’s social circle in the analysis. Also, due to the response-dependent probabilistic feedback, individuals reporting very low or very high willingness across trials received limited feedback in one of the directions. While general implicit social attunement (regardless of feedback direction) can always be assessed, separating positive and negative influence might not always be an option. Furthermore, results showed remarkable inconsistencies between alcohol use and related problems—as assessed with the AUDIT—and self-reported recent alcohol use—as assess with the TLFB. While it could well be that the effects found are indeed primarily associated with alcohol use–related problems rather than heaviness of recent use, the TLFB results could also be affected by the relatively low variance in the past 2-week drinking with most participants reporting drinking less than 30 drinks, and by age differences in binge drinking. Exploratory assessments revealed that binge drinking was negatively associated with age ( r  =  − 0.113, p  = 0.014) and while regular binge drinking has been associated with higher AUDIT scores it might result in underestimation of use on the TLFB (Collins et al., 2008 ). Also, while the inclusion of participants from a broad age range is a clear strength of this study, we did not manage to recruit an equal number of participants across ages, resulting in an overrepresentation of participants under forty. Replication including a larger number of older adults is warranted. Moreover, research including heavier alcohol users is needed to assess the generalizability to hazardous users as most AUDIT scores were below the at-risk cut-off (Saunders et al., 1993 ) and last 2-week alcohol use indicated less than daily use (Table  1 ). Furthermore, studies are needed to assess associations between implicit social attunement and other types of social learning to evaluate divergent validity of the task.

This study shows the potential of using the implicit social attunement task in unravelling the complex effects of social settings and peer feedback on alcohol consumption across age ranges. Results indicated that peer influence might act as protective or risk factor for alcohol use depending on the social setting and highlights the potential differences between implicit and explicit social attunement behaviors in their associations with age and alcohol use and related problems.

Data Accessibility

The data that support the findings of this study are available from the corresponding author upon reasonable request.

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This research was supported by the ERC-ST grant 947761 awarded to Janna Cousijn.

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Alcohol drinking among college students: college responsibility for personal troubles

• Vincent Lorant 1 ,
• Pablo Nicaise 1 ,
• Victoria Eugenia Soto 1 , 2 &
• William d’Hoore 1  

BMC Public Health volume  13 , Article number:  615 ( 2013 ) Cite this article

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One young adult in two has entered university education in Western countries. Many of these young students will be exposed, during this transitional period, to substantial changes in living arrangements, socialisation groups, and social activities. This kind of transition is often associated with risky behaviour such as excessive alcohol consumption. So far, however, there is little evidence about the social determinants of alcohol consumption among college students. We set out to explore how college environmental factors shape college students' drinking behaviour.

In May 2010 a web questionnaire was sent to all bachelor and master students registered with an important Belgian university; 7,015 students participated (participation = 39%). The survey looked at drinking behaviour, social involvement, college environmental factors, drinking norms, and positive drinking consequences.

On average each student had 1.7 drinks a day and 2.8 episodes of abusive drinking a month. We found that the more a student was exposed to college environmental factors, the greater the risk of heavy, frequent, and abusive drinking. Alcohol consumption increased for students living on campus, living in a dormitory with a higher number of room-mates, and having been in the University for a long spell. Most such environmental factors were explained by social involvement, such as participation to the student folklore, pre-partying, and normative expectations.

Conclusions

Educational and college authorities need to acknowledge universities’ responsibility in relation to their students’ drinking behaviour and to commit themselves to support an environment of responsible drinking.

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In 2007 one young adult in two has entered university education in Western countries and this proportion is likely to increase in the future [ 1 ]. Many of these young students will be exposed to substantial changes in living arrangements and social activities. This kind of transition is often associated with an increase in heavy and risky alcohol use [ 2 ].

Indeed, it is reckoned that college students are particularly exposed to alcohol during their college years. An international study of alcohol consumption among students found wide geographical variation in the prevalence of risky drinking behaviour, with more than 40% of students aged 17-30 having drunk heavily in the U.S.A. and in several European countries [ 3 ]. Risky drinking has also been found to be a common practice [ 4 ].

Risky alcohol consumption among young people is becoming a key public health priority because of its important health and educational consequences. Among those aged 15-29, alcohol accounts for more than 10% of the overall burden of disease and injury [ 5 ]. In addition to morbidity and mortality, alcohol has a significant important effect on student academic performance and on antisocial behaviour [ 6 , 7 ]. The case for alcohol could be weakened if adolescent drinking patterns became more mature in adulthood. However, a review of cohort studies shows that higher consumption in late adolescence continues into adulthood [ 8 ].

Risky alcohol consumption has first been approached from an individual perspective, with a strong emphasis on individual risk factors, such as gender, age, and psychological factors, and on drinking motives [ 3 , 9 , 10 ]. Adolescents often report drinking for motives such as social enhancement, enjoyment, image enhancement, or coping motives; thus, they may drink because of positive consequences that outweigh, at least in the short term, negative consequences [ 11 – 13 ].

International comparison, however, shows there is wide cross-country variation in the prevalence of risky drinking among college students [ 3 ]. Within the U.S.A., there is compelling evidence that college drinking varies dramatically between colleges [ 14 ]. This indicates that alcohol use may be sensitive to contextual factors. Alcohol use among college students occurs in specific social environments characterised by independent living, reduced parental control, increased social homogeneity, wide availability of alcohol-related social activities such as pre-partying [ 15 ] and student folklore (traditional, extra-curricular, and generally recreational activities managed by student organisations) [ 16 ]. The transition to the college environment brings about changes in adolescents’ adjustment to their social environment, which in turns influence alcohol use [ 2 ]. We thus need to better understand upstream factors that shape drinking at college. With some exceptions [ 10 ], there has, however, been little research into the college-related environmental risk factors affecting drinking by college students in Europe. Moreover, research needs to better understand the contribution of the college and university context to alcohol-drinking behaviour. The European university system and legal provisions related to alcohol consumption differ considerably from those in North America. Thus, research of the kind suggested might indicate opportunities for community health preventive interventions.

The study analyses alcohol consumption among college students from a community health perspective. We aim to understand how the college-related environment shapes students’ drinking behaviour. In particular, we assess the role of living arrangements, college social activities, and social norms in drinking patterns. We explore two questions: (1) does the college-related environment influence alcohol use? (2) How do social and normative factors contribute to these college influences on alcohol use?

Design and participants

This study is part of an important multi-method investigation into alcohol drinking among college students. It was carried out in a Belgian university with two main campuses, one in Louvain-La-Neuve, a town of 20,000 inhabitants, half of whom are students living in dormitories. The other campus, mainly devoted to health sciences, is located in Brussels, 30 km away from the main campus.

A web survey was carried out in May 2010. An e-mail invitation was sent to all bachelor and master students registered with the university (n = 18,137), with a link to a web-survey questionnaire. No financial or material incentive was provided. The students could request a copy of the final report, and 62% of the respondents made such request. The form included 31 questions related to socio-demographics, living arrangements, study programmes, involvement in student activities, alcohol use, injunctive and descriptive norms, and positive and negative consequences of alcohol use. On average, filling in the questionnaire took 12 minutes and very few break-offs were recorded. The study was approved for ethical issues by the Social and Student Affairs review board of the university on the 26 th March 2010.

After up to two reminders, 7,015 students (39%) participated, a rate well above the average web survey participation rate [ 17 ]. Compared with a face-to-face survey, our participation rate may look low. But for a web survey it is a very satisfactory result, as it corresponds to the median web-survey participation [ 18 ]. In addition, there is no evidence that online surveys with lower response rates produce biased estimates in higher education evaluation or surveys [ 19 ] or in surveys in general [ 20 , 21 ]. However, to assess the risk of bias we compared the distribution of our sample with the distribution of the population. Analysis of non-participants suggests that women were a bit more likely to participate (OR = 1.10) than men; no differences of participation regarding age or year of study were noted. There is thus little evidence of an important bias linked to factors associated with alcohol consumption.

Alcohol consumption measures came from the Eurostat European Health Interview Survey schedule and from the European School Survey Project on Alcohol and Other Drugs (ESPAD) questionnaire [ 22 ]. We modelled the weekly average number of drinks in the last year, the monthly frequency of drinking, and the monthly frequency of abusive drinking (more than 6 drinks on one occasion [ 23 ]). A drink was defined as a glass of any alcoholic beverage (beer, wine, spirits, other), assuming that a standardised glass of beer, wine, or spirit contains a similar quantity of alcohol (from 10 to 13 g).

College environmental factors included curricular and extra-curricular features. The former consisted of the number of years the student had been studying and the study programme (a student class within a curriculum). The study programme factor was expected to capture the peer effect linked to the culture of alcohol consumption specific to faculties. The extra-curricular features were: living arrangements (living in a dormitory or with parents), living on the campus (yes or no), and the number of room-mates (0 for staying with parents).

Social involvement was measured by involvement in traditional student folklore, pre-partying, and being a student representative. Student folklore shares some similar features with the sororities and fraternities in the U.S.A. It has long played a traditional role in European university social life: traditional students’ organisations contribute to welcoming freshmen and to rites of passage; they organise parties and other recreational activities that may or may not involve drinking. Some student associations also manage student accommodation and sit on consultative bodies related to student social affairs. Involvement in this kind of traditional student folklore was measured by a score ranging from a low of 0 to a high of 3 according to rites of passage or positions of responsibility in student folklore. One point was given for each of the following: participation in hazing activities at the beginning of the academic year, after which one is labelled “baptisé”; participation in another traditional activity that upgrades the student’s prestige and allows him/her to wear a ritual cap called a “calotte”; and participation in the folklore organisation. The score was categorised in three groups (0 = none, 1 = medium, 2-3 = high). Finally, the university provides students with many curricular or extra-curricular social organisations. We asked the students whether they were members of any organisation of that kind.

Pre-partying was defined as the consumption of alcohol with friends while preparing to go out for the night. Pre-partying helps to improve sociability and conviviality, easing the discomfort associated with meeting new people at a party [ 15 , 24 – 26 ]. Students were requested to report their pre-partying frequency per month.

The normative factors included descriptive and injunctive norms. Alcohol injunctive norms were covered by a four-item questionnaire measuring approval by friends of four kinds of drinking behaviour: drinking every weekend, daily, after driving, and enough to be drunk [ 27 ]. Each item had a score ranging from 0 (strong disapproval) to 4 (strong approval). The overall sum of the four items ranged between 0 and 16 and measures “permissiveness”. Descriptive norms measure the perceived drinking behaviour of referent others and were assessed by the Drinking Norm Rating Forms, which ask the student to estimate the average daily number of drinks individuals of three different reference groups consume (students in general, same-sex students, and friends) [ 27 ]. According to social comparison theory proximal comparisons are more relevant than distal comparisons, so we expected that friends’ average consumption would have a greater influence than typical same-sex student consumption [ 28 ].

In order to also include experiential reporting, students’ positive drinking consequences were registered via the Positive Drinking Consequences Questionnaire, a 14-item scale [ 29 ]. This scale measures actual and past perceived positive consequences of alcohol use and differs from expectations. The scale mainly records consequences of drinking in terms of improved social interaction (11 items out of 14) such as social enhancement and stress reduction. This seemed relevant for young people in transition to adulthood and experiencing a dramatic change in their living conditions. We counted the number of times students reported a positive consequence of drinking over the last year.

Data analysis

The analysis was in two stages, according to our two research questions. First, we investigated the role of socio-demographics and college environmental factors. Second, we added to the analysis social-involvement, normative, and experiential factors that might contribute to the influence of college environmental factors. However, cross-sectional analysis of drinking behaviour is vulnerable to selection bias: unobserved heterogeneity across individuals may explain why some vulnerable individuals self-select into an at-risk college environment, as predicted by the theory of increased heterogeneity [ 2 ]. We assessed this kind of bias by sensitivity analysis: we checked the robustness of the models by including age at first drink, a factor strongly linked to poor executive function and an individual risk factor for subsequent drinking and drug abuse [ 30 ]. Because number of drinks and frequency of abusive drinking are not normally distributed and because of over-dispersion (a minority may never drink), we used a negative binomial mixed regression model. All models included a random component capturing the intra-study programme correlation. Statistical procedures were carried with SAS 9.2.

On average, students were aged 21.5 (std = 3.3), and mainly female (Table  1 ). Women were slightly younger compared with men (21.4 vs 21.8, F = 21.5, p < 0.01) but there was no significant association between gender and study year ( χ 2 =1.18, p  = 0.28). On average students have been attending the University for about 2.8 years (std = 1.7) and were pursuing bachelor degrees. A majority of students were staying on the campus (66.9%) and in a dormitory (64%), with an average of 4.4 room-mates (std = 4.2). A minority of the students (12.3%) was highly involved in traditional student folklore with a score of 2 to 3. Most students pre-party (67%), with an average of 2.3 pre-parties per month (std = 3.3).

There were some socio-demographic differences between our sample and the population. Compared with the overall University population, our sample had a higher frequency of females (sample: 57.3%; population: 54.6%), was younger (21.5 y vs 21.9 y), and had a higher proportion of undergraduates (62% vs 59%). Overall, these differences were small and do not indicate a systematic tendency towards more or less frequent drinking: women generally drink less than men and undergraduates generally drink more than postgraduates.

On average, students had their first drink at the age of 15.7 (std = 1.8), while only a small percentage had never drink alcohol (6%). In Belgium, the legal drinking age is 16. On average, a student drank seven times a month (std = 6.6), had 1.7 drinks a day (std = 21), and 2.8 episodes of abusive drinking per month (std = 4.4). Over the last year, the students acknowledged on average 5 positive consequences (std = 3.1). The three most frequent consequences were to “approach a person that I probably wouldn’t have spoken to otherwise” (68%), to “find it easy to engage in a conversation in a situation in which I would usually have stayed quiet” (65%), and to feel “like I had enough energy to stay out all night partying or dancing” (64%).

College students overestimated what a typical student drinks; this overestimation decreased for closer-reference students: 4.2 (std = 4.7) daily drinks for students in general, 3.9 (std = 4.9) for same-sex students, 3.5 (std = 4.4) for friends (to be compared with a self-declared 1.7). College students overestimated their friends’ drinking by 2 drinks a day.

Overall socio-demographic variables played a more important role for abusive drinking and number of drinks than for the frequency of drinking (Table  2 , Model 1). Men drank more, more frequently, and drank abusively more often than women. But the gender difference was somewhat lower for frequency of drinking (OR = 1.58) and higher for abusive drinking (OR = 2.29). Older students were less likely to drink and, in particular, less likely to engage in abusive drinking. For each additional year of age, the frequency of abusive drinking decreased by 9% and the frequency of drinking decreased by 2%.

Higher exposure to college environmental factors meant, in most cases, more frequent, and more abusive drinking (Table  2 , Model 1). These risk factors were, in general, more important for excessive drinking than for frequency of drinking. For each additional year spent at the university, drinking became more frequent and the frequency of abusive drinking increased (OR = 1.11). Compared with not living on the campus, living on the campus meant more frequent and more abusive drinking behaviour (OR = 1.56). The greater the number of room-mates, the higher the risk of frequent and abusive drinking behaviour. Each additional room-mate increased the frequency of abusive drinking by 6%. There was one exception to these college environmental factors: staying in a dormitory was associated with less frequent drinking behaviour. This could be due to the collinearity with living on the campus and the number of room-mates: as 93% of those living in dorms were on the campus, it was difficult to disentangle the campus effect from the dormitory effect. We checked this issue in two ways. First, we ran Model 1 for the number of drinks per day, by excluding the “living on the campus” variable. We found that, indeed, living in a dormitory was associated with an increased number of drinks compared with living with parents (OR =1.12 95% CI: 1.06-1.18). Second, we compared the two campuses, the one in Louvain-la-Neuve, which is mainly a student town and is known to expose students to numerous drinking opportunities, with the one in Brussels, which has a much more mixed population, controlling for all other variables of Model 1. We found that the Brussels campus had a lower risk (OR = 0.68, 95% CI: 0.60-0.76) compared with the Louvain-La-Neuve campus, suggesting that living on the campus is a more potent predictor of frequent abusive drinking than living in a dormitory.

There was a small intra-class correlation linked to the study programme and this was more important for abusive drinking (0.23) than for frequency of drinking (0.03), suggesting a slight programme effect on abusive drinking but not on drinking frequency. We found the Faculty of Engineering and the Faculty of Social Sciences to have a higher number of drinks per day (Engineering mean = 2.2, p  < 0.001; Social Sciences Mean = 2.1, p  < 0.001), with a lower number in the faculties of medicine (1.21, p < 0.001) and psychology (mean = 1.17 NS).

Model 2 adds social-involvement, normative, and experiential factors (Table  2 ). The more a student was involved in traditional student folklore, the more frequent his or her drinking behaviour, even at the intermediate level of involvement. This was particularly obvious for abusive drinking (OR = 2.11), with a somewhat lower risk for drinking frequency (OR = 1.46). More frequent pre-partying was associated with increased drinking: one additional monthly occasion of pre-partying increased abusive drinking by 8%. However, not all university involvement increased drinking frequency. Being elected as a student representative was associated with a lower risk of drinking, particularly of abusive drinking (OR = 0.84).

Drinking was more frequent as the number of positive consequences increased and as drinking norms became more favourable to drinking. The more a student thought his friends were drinking, the more and the more frequently he drank (OR = 1.02). Likewise, the more a student thought his friends were permissive regarding drinking, the higher the risk of all drinking behaviour, particularly for drinking frequency (OR = 1.08). Drinking frequency or quantity increased by at least 10% for each additional positive consequence a college student experienced.

In most cases, controlling for social engagement, normative, and experiential factors led to a reduction in the risk associated with the college environment. The effect of the number of years attending the University on abusive drinking decreased from OR = 1.11 to OR = 1.05, while the effect of the number of room-mates decreased from 1.06 to 1.02. The effect of living arrangements became insignificant or very small.

The model’s robustness was checked by including age at first drink, a factor likely to capture individual vulnerability. In most cases, the ORs were only slightly affected: the effect of time attending the university on abusive drinking decreased from 1.11 (Model 1, without controlling for age at first drink) to 1.109 (Model 1, with control for age at first drink); the effect of living on the campus on abusive drinking frequency decreased from 1.56 to 1.52; the effect of traditional student folklore from 2.11 to 2.09. Pre-partying frequency was not affected by this kind of sensitivity analysis.

Main findings

This study confirmed that excessive alcohol consumption is common among college students, with an average of 3 episodes of abusive drinking per month. Greater exposure to college environmental factors, such as living on the campus, a longer spell at university meant more frequent drinking. These community risk factors were more pronounced for excessive drinking patterns than for the quantity or frequency of drinking. Time had a double and mixed effect: older students drink less and less excessively than younger students; however, the longer the period a student has spent in the university, the higher his/her risk of drinking. These effects of college environmental factors were partly explained by social-involvement, experiential, and normative expectations: college students drank for the positive consequences, because they over-estimate the drinking of their friends, or because of other normative expectations.

Consistency with previous studies

The role of living arrangements has been shown in previous American [ 31 ], European [ 10 , 32 ], and cross-comparative [ 3 , 33 ] studies in which living with parents, not living on the campus, and not living in fraternity and sorority houses protected against heavy or abusive drinking. We found that living on the campus was a more potent predictor of frequent abusive drinking than living in a dormitory (both in model 1 and model 2). On the surface, this might seem to contradict a previous European review [ 10 ]. However, this is in part because of the strong association between living on the campus and living in a dormitory. This is also consistent with the Harvard School of Public Health college alcohol study which found that living off-campus was a stronger and more significant factor than staying in a dormitory [ 31 ]. The finding that the dormitory became non-significant in model 2 suggests that social-involvement, experiential, and normative expectations contribute to explain college environmental factors of drinking behaviours.

Yet, our study shows that the college environment influences drinking behaviour in a much more complex way that involves not only where students live but also the kind of living arrangements, participation in traditional student folklore, the duration of college training, and the type of faculty in which the student is studying. In particular, living in a dormitory with a high number of room-mates and being highly involved in traditional student folklore also play a role in the frequency of abusive drinking. There is thus not one college environmental risk factor but several that relate to different aspects of student life. This may explain why living away from home had a slightly greater effect on heavy drinking in the American (OR = 1.72) or in the international comparison study (OR = 1.61) than in ours (OR = 1.57). The role of dormitory size needs, in particular, to be emphasized and could be explained by innovation diffusion. As adolescent social network studies have shown, teenagers who have a denser social network are more likely to drink than those with less dense social networks [ 34 ]. The finding on that pre-partying contribution to the relationship between college environmental factors and frequency of abusive drinking supports this hypothesis. As in previous studies [ 15 ], pre-partying was revealed to be a common practice contributing to both drinking behaviour and the influence of community factors on drinking behaviour. College students pre-party to ease the discomfort or awkwardness associated with meeting new people. As hypothesized in a qualitative study, the pre-party is a base to build on when you get to a party, a way to bond with friends, and a social lubricant at a later event to help “hook up” with a partner [ 26 ].

Our study shows that abusive drinking increased with the period attending the college, whereas it decreased with age. These two opposite effects were of similar magnitude: this may explain why previous studies have found no clear relationship between age and drinking behaviour [ 10 ]: it all depends on the time spent in the university. Few studies have controlled for the time spent in college, so that the protective maturing effect of age was confounded by the risk attached to the time spent attending college. One important prospective American study found, moreover, that heavy drinking decreased with age [ 35 ], while there is wide evidence of an association between late adolescent drinking behaviour and subsequent drinking into adulthood [ 8 ]. Why did older students drink less while, at the same time, more years at the University were associated with more drinking? Firstly, the correlation between age in years and number of years attending the university was not very high (correlation coefficient = 0.33), suggesting that not all students follow the same trajectory. Some start a postgraduate programme later in life, while working part-time. These “older” students generally spend a shorter period at university (2-3 years) and, possibly, have less time for student activities involving alcohol. Secondly, age and time at the University capture different risks linked to drinking alcohol: age may also capture a cohort effect and, in particular, changes in drinking habits: older students may not only adapt their consumption but may also have started drinking later than the younger age group. This is supported by our data, as we found a small but significant positive correlation between age and age at first drink (correlation = 0.22, p <0.001), although, with our cross-sectional design, these correlations must be approached with caution. A third possible explication is that a significant proportion of students had studied outside the University for their first undergraduate degree and where thus not exposed to the campus for as long as those who followed both under- and postgraduate programmes on the same campus. Our study suggests that the maturing effect on heavy drinking is modest and depends on the time spent attending the University, leaving one particular group of college students at risk: those starting university at a younger age and studying there for longer periods. But these results should be approached with caution. Truncation may affect our results, as younger students who failed to graduate because of heavy alcohol consumption are less likely to be observed at a later stage; this makes the comparison between younger and older students problematic: the latter are observed if they haven’t dropped out of the University.

We found that students overestimate other students’ average number of daily drinks. To compare our results with previous studies of self-other comparison in drinking, we computed the Z Fisher transformation correlation between self-reported daily number of drinks and friends’ numbers of drinks. Our Z Fisher correlation was 0.36 ( p  < 0.001), which compares quite well a Z fisher value of 0.29 from a previous meta-analytic integration of 23 studies [ 29 ]. The college social environment increases drinking through a combination of social activities and normative and motivational expectations. It puts students at risk of frequent and abusive drinking because students expect positive social consequences, because of social activities such as pre-parties, and because of injunctive and descriptive drinking norms. The role of such social and normative influences, evidenced in previous studies [ 36 , 37 ], may result from two different and complementary processes: social learning, in which drinking behaviour is acquired through social interaction, and social control, which emphasizes the role of social expectations such as norms and peer pressure [ 38 ]. We found that college students overestimate other students’ alcohol consumption and this overestimation decreases with social distance: drinking behaviour was more related to the quantities drunk by friends than to the quantities drunk by students overall. Finally, pre-partying and participation in traditional student folklore, both of which provide strong opportunities for social learning, emerged as strong predictors of drinking behaviour. All this suggests that social learning is a key factor that contributes to the effect of the college social environment on drinking behaviour, as found elsewhere [ 39 ].

Limitations

Our cross-sectional study is vulnerable to reversed causality, so the results need to be interpreted with caution. It could be that involvement in student life and drinking behaviour are confounded by unobserved vulnerability. Extraverted individuals are sensitive to positive social rewards and, thus, more likely to engage in socially-motivated drinking, so the relationship between traditional student folklore and drinking behaviour may be biased upwards. Moreover, the dose-response relationship with involvement in traditional student folklore or with the number of room-mates may downplay this risk of confounding without totally removing it. To assess the risk of confounding we replicated the analysis controlling for the age at which the student reported that he or she started drinking, a factor known to predict a heavy alcohol consumption trajectory [ 40 ]. Our results suggest that this kind of self-selection risk may slightly affect our conclusions.

The second limitation has to do with the setting, which unlike other campuses in Belgium or abroad, is much less socially mixed, giving the college environmental factors more clout while mitigating other social control effects. Our results, nevertheless, are in line with a cross-comparative study such as the College Alcohol study in the U.S.A. [ 23 ] or the European Amsterdam-Antwerp comparison, which showed living arrangements to be a strong predictor of problematic alcohol use [ 33 ]. Finally, it could be that our setting provides a pessimistic picture of community factors and is, in that sense, a good model for reflecting on the community risk factors linked to college drinking behaviour.

Conclusion: relevance for community health promotion

It is foreseen that in the future most young adults will attend university where, our study shows, they will be exposed to frequent and intensive drinking behaviour. That experience will have subsequent and important consequences lasting into adulthood [ 8 ]. Colleges need thus to acknowledge their role in this issue and to commit themselves to lower exposure to excessive alcohol consumption. In particular, they need to combine multi-level strategies: individual, group, and organization-level, from a community health promotion perspective. One danger would be a top-down approach of undertaking community actions in ways that do not consider the realities of student life. A first step would be to involve members of the community in identifying realistic objectives, e.g. limiting excessive consumption, and defining targets, e.g. male students involved in traditional and folklore activities in which hazardous alcohol intake peaks. A second step would be to define interventions, e.g. social-norm interventions that could correct gross miss-perceptions and effectively reduce alcohol consumption [ 41 – 43 ]. Third and fourth steps would be to evaluate what has been implemented, to provide feedback in order to improve and extend interventions, which requires sustained funding, and to analyse gaps between national policies and what is locally feasible. More community-based research is needed to face the problem of hazardous alcohol use, which is persistent and pervasive.

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Acknowledgments

This research was supported by the Université catholique de Louvain, in particular the Vice-Rector for Student and Social Affairs.

The research was also carried out with the help of students in the Faculty of Public Health: Anémone Bruneau, Alessandra Ausloos, Anne-Sophie Dehanne, Céline Denis, François Leruth, and Sandrine Race.

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Vincent Lorant, Pablo Nicaise, Victoria Eugenia Soto & William d’Hoore

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VL conceived the study, carried out the survey, performed the data analysis, and drafted the manuscript. PN participated in the design of the study, carried out the survey, contributed to analysis and helped draft the manuscript. VES contributed to analysis and helped draft the manuscript. WD contributed to analysis and helped draft the manuscript. All authors read and approved the final manuscript.

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Lorant, V., Nicaise, P., Soto, V.E. et al. Alcohol drinking among college students: college responsibility for personal troubles. BMC Public Health 13 , 615 (2013). https://doi.org/10.1186/1471-2458-13-615

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eTable 1. Health Deficits of the Frailty Index in the UK Biobank Cohort

eTable 2. Association of Wine Preference and Drinking During Meals With Mortality in Older Drinkers From the UK Biobank Cohort

eTable 3. Association of Average Alcohol Intake Status With Mortality in Older Drinkers From the UK Biobank Cohort, Excluding Participants With Prevalent Cancer at Baseline for Cancer Mortality, or Those With Prevalent CVD at Baseline for CVD Mortality

eTable 4. Association of Wine Preference or Drinking During Meals With Mortality in Older Drinkers From the UK Biobank Cohort, Excluding Participants With Prevalent Cancer at Baseline for Cancer Mortality, or Those With Prevalent CVD at Baseline for CVD Mortality

eTable 5. Association of Wine Preference and Drinking During Meals With Mortality in Older Drinkers From the UK Biobank Cohort, Excluding Participants With Prevalent Cancer at Baseline for Cancer Mortality, or Those With Prevalent CVD at Baseline for CVD Mortality

eTable 6. Association of Average Alcohol Intake Status With Mortality in Older Drinkers From the UK Biobank Cohort, by Drinking Patterns, Excluding Participants With Prevalent Cancer at Baseline for Cancer Mortality, or Those With Prevalent CVD at Baseline for CVD Mortality

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Ortolá R , Sotos-Prieto M , García-Esquinas E , Galán I , Rodríguez-Artalejo F. Alcohol Consumption Patterns and Mortality Among Older Adults With Health-Related or Socioeconomic Risk Factors. JAMA Netw Open. 2024;7(8):e2424495. doi:10.1001/jamanetworkopen.2024.24495

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Alcohol Consumption Patterns and Mortality Among Older Adults With Health-Related or Socioeconomic Risk Factors

• 1 Department of Preventive Medicine and Public Health, Universidad Autónoma de Madrid, Madrid, Spain
• 2 Center for Biomedical Research in Epidemiology and Public Health, Madrid, Spain
• 3 Department of Environmental Health and Nutrition, Harvard T.H. Chan School of Public Health. Boston, Massachusetts
• 4 Madrid Institute for Advanced Studies Food Institute, Campus of International Excellence Universidad Autónoma de Madrid + Spanish National Research Council, Madrid, Spain
• 5 Department of Chronic Diseases, National Center for Epidemiology, Carlos III Health Institute, Madrid, Spain

Question   Do health-related or socioeconomic risk factors modify the associations of alcohol consumption patterns with mortality among older drinkers?

Findings   This cohort study in 135 103 older drinkers found that even low-risk drinking was associated with higher mortality among older adults with health-related or socioeconomic risk factors. Wine preference and drinking only with meals were associated with attenuating the excess mortality associated with alcohol consumption.

Meaning   This cohort study identified inequalities in the detrimental health outcomes associated with alcohol that should be addressed to reduce the high disease burden of alcohol use.

Importance   Alcohol consumption is a leading cause of morbidity and mortality that may be more important in older adults with socioeconomic or health-related risk factors.

Objective   To examine the association of alcohol consumption patterns with 12-year mortality and its modification by health-related or socioeconomic risk factors.

Design, Setting, and Participants   This prospective cohort study used data from the UK Biobank, a population-based cohort. Participants were current drinkers aged 60 years or older. Data were analyzed from September 2023 to May 2024.

Exposure   According to their mean alcohol intake in grams per day, participants’ drinking patterns were classified as occasional: ≤2.86 g/d), low risk (men: >2.86-20.00 g/d; women: >2.86-10.00 g/d), moderate risk (men: >20.00-40.00 g/d; women: >10.00-20.00 g/d) and high risk (men: >40.00 g/d; women: >20.00 g/d).

Main Outcomes and Measures   Health-related risk factors were assessed with the frailty index, and socioeconomic risk factors were assessed with the Townsend deprivation index. All-cause and cause-specific mortality were obtained from death certificates held by the national registries. Analyses excluded deaths in the first 2 years of follow-up and adjusted for potential confounders, including drinking patterns and preferences.

Results   A total of 135 103 participants (median [IQR] age, 64.0 [62.0-67.0] years; 67 693 [50.1%] women) were included. In the total analytical sample, compared with occasional drinking, high-risk drinking was associated with higher all-cause (hazard ratio [HR], 1.33; 95% CI, 1.24-1.42), cancer (HR, 1.39; 95% CI, 1.26-1.53), and cardiovascular (HR, 1.21; 95% CI, 1.04-1.41) mortality; moderate-risk drinking was associated with higher all-cause (HR, 1.10; 95% CI, 1.03-1.18) and cancer (HR, 1.15; 95% CI, 1.05-1.27) mortality, and low-risk drinking was associated with higher cancer mortality (HR, 1.11; 95% CI, 1.01-1.22). While no associations were found for low- or moderate-risk drinking patterns vs occasional drinking among individuals without socioeconomic or health-related risk factors, low-risk drinking was associated with higher cancer mortality (HR, 1.15; 95% CI, 1.01-1.30) and moderate-risk drinking with higher all-cause (HR, 1.10; 95% CI, 1.01-1.19) and cancer (HR, 1.19; 95% CI, 1.05-1.35) mortality among those with health-related risk factors; low-risk and moderate-risk drinking patterns were associated with higher mortality from all causes (low risk: HR, 1.14; 95% CI, 1.01-1.28; moderate risk: HR, 1.17; 95% CI, 1.03-1.32) and cancer (low risk: HR, 1.25; 95% CI, 1.04-1.50; moderate risk: HR, 1.36; 95% CI, 1.13-1.63) among those with socioeconomic risk factors. Wine preference (>80% of alcohol from wine) and drinking with meals showed small protective associations with mortality, especially from cancer, but only in drinkers with socioeconomic or health-related risk factors and was associated with attenuating the excess mortality associated with high-, moderate- and even low-risk drinking.

Conclusions and Relevance   In this cohort study of older drinkers from the UK, even low-risk drinking was associated with higher mortality among older adults with health-related or socioeconomic risk factors. The attenuation of mortality observed for wine preference and drinking only during meals requires further investigation, as it may mostly reflect the effect of healthier lifestyles, slower alcohol absorption, or nonalcoholic components of beverages.

Alcohol consumption is a leading cause of morbidity and mortality, accounting for approximately 5.1% of the global burden of disease and 5.3% of all deaths and being responsible for significant social and economic losses, thus representing a major public health problem. 1 Additionally, the assumed benefits of drinking low amounts of alcohol, especially on cardiovascular disease (CVD) mortality, 2 - 4 are being questioned due to selection biases, reverse causation, and residual confounding, 5 supporting health messaging that the safest level of drinking is no drinking at all or less is better. 6 , 7 Selection biases are often overlooked, but they can lead to a systematic underestimation of alcohol-related burden. That is the case of the abstainer bias, whereby the apparently lower mortality of light drinkers compared with abstainers could be explained by the higher death risk of the abstainers because they include former drinkers who quit alcohol due to poor health, as well as lifetime abstainers, 5 who often have worse lifestyle and health characteristics than regular drinkers. 8 Also, the healthy drinker/survivor bias, caused by overrepresentation of healthier drinkers who have survived the deleterious effects of alcohol, can distort comparisons, especially in older age. 5 In addition, drinking habits may influence the association between the amount of alcohol consumed and health. In this context, wine preference has been associated with lower risk of death, 9 CVD morbimortality, 10 and diabetes, 11 attributing the beneficial associations of wine to its high content in polyphenols. 12 Furthermore, drinking with meals has been associated with lower risk of all-cause, non-CVD, and cancer deaths 13 and frailty, 14 so this might be a safer option for alcohol drinkers along with moderate consumption. 15

The health impact of alcohol consumption may be greater in individuals with socioeconomic or health-related risk factors. On one hand, older adults with health-related risk factors are more susceptible to the harmful outcomes associated with alcohol due to their greater morbidity, higher use of alcohol-interacting drugs, and reduced tolerance. 16 , 17 However, some studies have observed benefits of alcohol on unhealthy aging or frailty, especially of light alcohol intake 18 , 19 and of a Mediterranean alcohol drinking pattern, defined as moderate alcohol consumption, preferably wine and accompanying meals, 14 , 20 suggesting that the protective associations of these potentially beneficial drinking patterns might be greater in individuals with ill health, although they might be due to the aforementioned methodological issues. 5 Therefore, it would be of interest to examine whether health-related risk factors modify the associations between alcohol consumption patterns and mortality.

On the other hand, there is evidence that socioeconomically disadvantaged populations have higher rates of alcohol-related harms for equivalent and even lower amounts of alcohol, probably due to the coexistence of other health challenges, including less healthy lifestyles, and lower social support or access to health care. 21 , 22 Also, the potentially beneficial associations of wine preference and drinking during meals might be more important in individuals with socioeconomic risk factors. However, to our knowledge, no previous research has examined whether socioeconomic status modifies the associations between these potentially beneficial drinking patterns and health.

Therefore, the aim of our study is to examine the associations of several potentially beneficial alcohol consumption patterns, that is, consumption of low amounts of alcohol, wine preference, and drinking only during meals, with all-cause, cancer, and CVD mortality in older adults and their modification by health-related or socioeconomic risk factors, while addressing the main methodological issues deemed to bias such associations. Thus, we restrict analyses to current drinkers and use occasional drinkers instead of abstainers as the reference group to prevent selection biases, exclude deaths in the first 2 years of follow-up to reduce reverse causation, and adjust analyses for many sociodemographic, lifestyle, and clinical variables to palliate residual confounding. We also restrict analyses to older adults because most deaths occur in this population group, which also has a high prevalence of health-related risk factors and because the protective associations of alcohol consumption have been specifically observed in older adults, 6 which is consistent with our aim to study potentially beneficial drinking patterns.

This cohort study was approved by the North West Multi-Centre Research Ethics Committee, and all participants provided written informed consent before enrollment. This study is reported following the Strengthening the Reporting of Observational Studies in Epidemiology ( STROBE ) reporting guideline.

We used data from the UK Biobank cohort, a multicenter, prospective, population-based study with more than 500 000 participants aged 40 to 69 years identified from National Health Service primary care registers and enrolled at 22 assessment sites across England, Scotland, and Wales between 2006 and 2010. At the baseline assessment visit, they completed a computer-assisted interview and a touch-screen questionnaire on sociodemographic, lifestyle, and clinical characteristics, provided biological samples, and underwent physical and medical examinations. They were followed-up for mortality through linkage to national death registries. Additional information on the UK Biobank study has been reported elsewhere. 23 , 24

At the baseline assessment visit, study participants were asked about the frequency and mean amount of the main types of alcoholic beverages that they consumed, and alcohol content was estimated by multiplying the volume ingested (in milliliters) by the volume percentage of alcohol (4.5% for beer and cider, 11.5% for white and sparkling wine, 13% for red wine, 20% for fortified wine, and 40% for spirits) and by the specific gravity of ethanol (0.789 g/mL). According to their mean alcohol intake, drinking patterns were classified into occasional (≤2.86 g/d), low risk (men: >2.86-20.00 g/d; women: >2.86-10.00 g/d), moderate risk (men: >20.00-40.00 g/d; women: >10-20.00 g/d), and high risk (men: >40.00 g/d; women: >20.00 g/d), a categorization based on the recommendations from health authorities that we have used in previous studies. 25 - 27 When more than 80% of alcohol came from a certain type of beverage, drinkers were classified as with preference for wine, with preference for other drinks, or with no preference. 27 Participants were also classified as drinkers only during meals and as drinkers either only outside of meals or at any time. Finally, participants were classified as drinkers with no wine preference nor drinking only during meals, drinkers with wine preference or drinking only during meals, and drinkers with wine preference and drinking only during meals.

Health-related risk was assessed at baseline using the frailty index (FI) developed specifically for the UK Biobank 28 based on the procedure used by Rockwood et al. 29 A total of 49 health deficits were considered, most dichotomously (1 point if present and 0 points otherwise), and a few according to severity (0 points for no deficit, 0.25-0.75 points for mild to moderate deficits, and 1 point for severe deficit). The FI score was calculated as the total sum of points assigned to each health deficit divided by the number of deficits considered and ranged from 0.00 to 0.57. The complete list of health deficits and associated scores can be found in eTable 1 in Supplement 1 . Participants were considered to have health-related risk factors if they were prefrail or frail (FI > 0.12). 28

Socioeconomic risk was assessed at baseline using the Townsend deprivation index (TDI), 30 which measures the level of an area’s socioeconomic deprivation. TDI ranges from −6.26 to 10.16, with higher score indicating greater deprivation. Participants were considered to have socioeconomic risk factors if they lived in more deprived areas (TDI > 0) and not if they lived in more affluent areas (TDI ≤ 0).

Information on mortality was obtained from death certificates held by the National Health Service (NHS) Information Centre (NHS England) up to September 30, 2021, for participants in England and Wales, and by the NHS Central Register Scotland (National Records of Scotland) up to October 31, 2021, for participants in Scotland. 31 , 32 Length of follow-up was estimated as the time from the baseline assessment visit to the date of death or administrative censoring, whichever came first. Cause-specific mortality was ascertained with the International Statistical Classification of Diseases and Related Health Problems, Tenth Revision ( ICD-10 ) classification 33 : codes C00 to C97 as primary cause of death for cancer and codes I00 to I99 for CVD.

We also used baseline information on sociodemographic, lifestyle, and clinical characteristics, including sex, age, self-reported race and ethnicity, education (college or university degree; A levels, AS levels, or equivalent; O levels, General Certificate of Secondary Education, or equivalent; Certificate of Secondary Education or equivalent; National Vocational Qualification, Higher National Diploma, Higher National Certificate, or equivalent; other professional qualifications; and no qualifications), tobacco smoking (never, former, or current), leisure-time physical activity (metabolic equivalents of task-hours per week), time spent watching television (hours per day), and prevalent morbidities (diabetes, CVD, and cancer) that could have a potential effect on the amount of alcohol consumed. In the UK Biobank, race and ethnicity are classified as Asian (Indian, Pakistani, Bangladeshi, any other Asian background), Black (Caribbean, African, any other Black background), Chinese, multiple (White and Black Caribbean, White and Black African, White and Asian, any other mixed background), White (British, Irish, any other White background), and other (any group not specified, eg, Arab).

From 217 462 participants aged at least 60 years in the UK Biobank cohort, we excluded 36 284 with incomplete information on alcohol consumption, 10 456 never drinkers, 8295 former drinkers, and 20 167 known binge drinkers (those who consumed ≥6 units of alcohol in 1 session) to avoid classifying binge drinkers with low mean alcohol intake as low-risk drinkers. We additionally excluded 1140 participants who died in the first 2 years of follow-up and 6017 participants with missing information on the FI (194 participants), the TDI (116 participants), and potential confounders (5707 participants). Thus, the analytical sample included 135 103 individuals.

The associations of alcohol consumption patterns (mean alcohol intake status, wine preference, and drinking during meals) at baseline with all-cause and cause-specific mortality were summarized with hazard ratios (HRs) and their 95% CIs obtained from Cox regression; the models included interactions between alcohol consumption patterns and health-related or socioeconomic risk factors and adjusted for baseline sociodemographic (sex, age, race and ethnicity, education, and TDI [except when stratifying by socioeconomic risk factors]), lifestyle (tobacco smoking, leisure-time physical activity, and time spent watching television), and clinical characteristics (diabetes, CVD, cancer, and FI score [except when stratifying by health-related risk factors]) of study participants. Analyses of alcohol intake were further adjusted for wine preference and drinking during meals, whereas analyses of wine preference and drinking during meals were further adjusted for mean alcohol intake and the other drinking pattern.

To characterize whether wine preference and drinking during meals modified the association of mean alcohol intake with mortality, we tested interaction terms defined as the product of the categories of mean alcohol intake by 3 categories of drinking patterns (no wine preference nor drinking only during meals, wine preference or drinking only during meals, and wine preference and drinking only during meals).

Additionally, we assessed whether sociodemographic and lifestyle variables modified the study associations by testing interaction terms defined as the product of alcohol consumption patterns by categories of such variables (except mean alcohol intake status by sex, as sex was included in the definition of alcohol intake status). Since no interactions were found, the results are presented for the total sample. Finally, we performed additional sensitivity analyses excluding participants with prevalent cancer at baseline for cancer mortality or those with prevalent CVD at baseline for CVD mortality.

Statistical significance was set at 2-sided P  < .05. Analyses were performed with Stata software version 17 (StataCorp). Data were analyzed from September 2023 to May 2024.

A total of 135 103 participants (median [IQR] age, 64.0 [62.0-67.0] years; 67 693 [50.1%] women) were included. Occasional drinkers less often identified as White; were more frequently residents in England, women, and never smokers; were less physically active; had a lower educational level, a lower prevalence of CVD; and had a higher prevalence of diabetes, cancer, and health-related risk factors. Having socioeconomic risk factors was less frequent in low- and moderate-risk drinkers ( Table 1 ).

Over a median (range) follow-up of 12.4 (2.0 to 14.8) years, 15 833 deaths were recorded, including 7871 cancer deaths and 3215 CVD deaths. Compared with occasional drinking, low-risk drinking was associated with higher cancer mortality (HR, 1.11; 95% CI, 1.01-1.22); moderate-risk drinking was associated with higher all-cause (HR, 1.10; 95% CI, 1.03-1.18) and cancer (HR, 1.15; 95% CI, 1.05-1.27) mortality; and high-risk drinking was associated with higher all-cause (HR, 1.33; 95% CI, 1.24-1.42), cancer (HR, 1.39; 95% CI, 1.26-1.53), and CVD (HR, 1.21; 95% CI, 1.04-1.41) mortality ( Table 2 ). Hazards were greater in individuals with health-related or socioeconomic risk factors vs those without across categories of alcohol intake. Interestingly, while no associations with mortality were found in participants without health-related or socioeconomic risk factors among low- or moderate-risk drinkers, low-risk drinkers with health-related risk factors had higher cancer mortality (HR, 1.15; 95% CI, 1.01-1.30) and moderate-risk drinkers with health-related risk factors had higher all-cause (HR, 1.10; 95% CI, 1.01-1.19) and cancer (HR, 1.19; 95% CI, 1.05-1.35) mortality ( Table 2 ). Likewise, both low-risk and moderate-risk drinkers with socioeconomic risk factors showed higher mortality from all causes (low risk: HR, 1.14; 1.01-1.28; moderate risk: 1.17; 95% CI, 1.03-1.32) and cancer (low-risk: HR, 1.25; 95% CI, 1.04-1.50; moderate risk: HR, 1.36; 95% CI, 1.13-1.63) ( Table 2 ).

Wine preference and drinking only during meals were associated with lower all-cause mortality only in participants with health-related risk factors (wine preference: HR, 0.92; 95% CI, 0.87-0.97; drinking only during meals: HR, 0.93; 95% CI, 0.89-0.97), as well as in participants with socioeconomic risk factors (wine preference: HR, 0.84; 95% CI, 0.78-0.90; drinking only during meals: HR, 0.83; 95% CI, 0.78-0.89) ( Table 3 ). Drinking only during meals was also associated with lower cancer mortality in participants with health-related risk factors (HR, 0.92; 95% CI, 0.86-0.99) or socioeconomic risk factors (HR, 0.85; 95% CI, 0.78-0.94) ( Table 3 ). Furthermore, in individuals with socioeconomic risk factors, wine preference was associated with lower cancer mortality (HR, 0.89; 95% CI, 0.80-0.99) and drinking only during meals with lower CVD mortality (HR, 0.86; 95% CI, 0.75-1.00) ( Table 3 ). Adhering to both drinking patterns was associated with lower all-cause, cancer, and CVD mortality in drinkers with health-related or socioeconomic risk factors, and to a lesser extent, with lower all-cause death in drinkers without health-related risk factors (eTable 2 in Supplement 1 ). Importantly, wine preference and drinking during meals modified the association of mean alcohol intake with mortality: the excess risk of all-cause, cancer, and CVD death for high-risk drinkers, of all-cause and cancer death for moderate-risk drinkers, and of cancer death for low-risk drinkers vs occasional drinkers was attenuated and even lost among individuals with these drinking patterns ( Table 4 ). Analyses excluding participants with prevalent cancer at baseline for cancer mortality, or those with prevalent CVD at baseline for CVD mortality showed consistent results (eTables 3-6 in Supplement 1 ).

This cohort study in older alcohol drinkers from the UK found that compared with occasional drinkers, low-risk drinkers had higher cancer mortality, moderate-risk drinkers had higher all-cause and cancer mortality, and high-risk drinkers had higher all-cause, cancer, and CVD mortality. The excess mortality associated with alcohol consumption was higher in individuals with health-related and socioeconomic risk factors, among whom even low-risk drinkers had higher mortality, especially from cancer. Wine preference and drinking only with meals showed small protective associations with mortality, especially from cancer, among drinkers with health-related and socioeconomic risk factors, and these 2 drinking patterns attenuated the excess mortality associated with high-, moderate-, and even low-risk drinking.

In line with recent research on the associations between alcohol use and health, 6 , 34 , 35 our results corroborate the detrimental outcomes associated with heavy drinking in older adults. However, we also found higher risk for all-cause and cancer deaths in moderate-risk drinkers, unlike most previous research, which has reported protective associations of low to moderate alcohol consumption, mainly for all-cause 2 - 4 , 36 and CVD 3 , 36 , 37 mortality, ischemic heart disease, 3 , 6 , 34 and diabetes, 6 or null associations with all-cause mortality, 38 CVD, 39 and unhealthy aging. 20 This discrepancy may be due to the implementation of an important methodological improvement in our analyses, that is, using occasional drinkers as the reference group instead of lifetime abstainers, to prevent selection bias caused by misclassification of former drinkers as abstainers, and to palliate residual confounding because they are more like light drinkers than are never drinkers. 40 , 41 In fact, another analysis of the UK Biobank cohort that also avoided selection biases found an increased CVD risk in the general population for drinking up to 14 units per week. 42

To our knowledge, there are no studies examining the potential modification of health-related risk factors on the association between alcohol use and health. The stronger associations between mean alcohol intake and mortality observed in older adults with health-related risk factors make sense, since they have more morbid conditions potentially aggravated by alcohol and greater use of alcohol-interacting medications than their counterparts without health-related risk factors. 16 , 17 The fact that even low-risk drinkers with these risk factors had higher risk of cancer death is an important finding, which is consistent with the reported increased risk of several types of cancer and cancer mortality even with very low amounts of alcohol. 6 , 36 , 37 , 43

Our results also suggest that socioeconomic status acts as a modifier of the association between the amount of alcohol consumed and mortality, as mortality hazard was much greater in individuals with socioeconomic risk factors than in individuals without, in line with previous research. 21 , 22 , 44 , 45 We even found a detrimental association of low amounts of alcohol with all-cause and cancer mortality in this group, unlike the MORGAM study by DiCasetnuovo et al 44 reporting a lower mortality associated with consuming no more than 10 g/d of alcohol, which was clearer in individuals with higher vs lower education. 44 These discrepant results could again be explained by the different reference groups used: occasional drinkers in our study and never drinkers in the MORGAM study. Importantly, although older adults with socioeconomic risk factors have a higher risk of ill health and death, probably due to the coexistence of other health challenges, especially poorer lifestyles, 21 , 22 the observed associations in our study were independent of lifestyles, suggesting that other factors should account for them.

Regarding the potentially beneficial drinking patterns, that is, wine preference and drinking during meals, the literature is inconsistent. A 2018 pool of studies 34 reported a nondifferential association of specific types of alcoholic drinks with all-cause mortality and several CVD outcomes, whereas other studies have found protective health associations for wine but not other beverages. 15 , 46 Drinking with meals has also shown protective associations with several health outcomes. 15 In our analysis, these drinking patterns modified the association between alcohol intake and death risk. On one hand, the protective association for mortality of these patterns was only observed in individuals with socioeconomic or health-related risk factors, independently of the amount of alcohol consumed. On the other hand, the detrimental association of alcohol intake was more evident in individuals without these patterns. These findings suggest that the less detrimental associations of alcohol intake from wine or during meals are not due to alcohol itself, but to other factors, including nonalcoholic components of wine, such as antioxidants, slower absorption of alcohol ingested with meals and its consequent reduced alcoholaemia, as well as spacing drinks when drinking only with meals, or more moderate attitudes in individuals who choose to adhere to these drinking patterns.

Our study has several strengths, such as the large sample size, the long follow-up, and the methodological improvements implemented to prevent selection biases and reduce reverse causation. However, it also has some limitations. First, alcohol intake was self-reported, and therefore prone to some degree of misclassification. Also, alcohol intake was measured only at baseline and not at multiple time points over the life span, not allowing us to take into account changes in alcohol intake before the baseline assessment or to redistribute former drinkers among categories of current drinkers to reduce selection bias; this may have led to an underestimation of the true effects of alcohol consumption. 5 Second, as in any observational study, we cannot entirely rule out residual confounding, despite adjusting for many potential confounders. And third, this study was conducted in older adults in the UK with a high proportion of White participants, so our results may not be generalizable to other racial ethnic groups or populations with different lifestyles, drinking patterns, or socioeconomic development.

This cohort study among older drinkers from the UK did not find evidence of a beneficial association between low-risk alcohol consumption and mortality; however, we observed a detrimental association of even low-risk drinking in individuals with socioeconomic or health-related risk factors, especially for cancer deaths. The attenuation of the excess mortality associated with alcohol among individuals who preferred to drink wine or drink only during meals requires further investigation to elucidate the factors that may explain it. Finally, these results have important public health implications because they identify inequalities in the detrimental health outcomes associated with alcohol that should be addressed to reduce the high burden of disease of alcohol use.

Accepted for Publication: May 30, 2024.

Published: August 12, 2024. doi:10.1001/jamanetworkopen.2024.24495

Open Access: This is an open access article distributed under the terms of the CC-BY License . © 2024 Ortolá R et al. JAMA Network Open .

Corresponding Author: Rosario Ortolá, MD, PhD, Department of Preventive Medicine and Public Health, School of Medicine, Universidad Autónoma de Madrid, Calle del Arzobispo Morcillo 4, 28029 Madrid, Spain ( [email protected] ).

Author Contributions: Dr Ortolá had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Concept and design: Ortolá.

Acquisition, analysis, or interpretation of data: All authors.

Drafting of the manuscript: Ortolá.

Critical review of the manuscript for important intellectual content: Sotos-Prieto, García-Esquinas, Galán, Rodríguez-Artalejo.

Statistical analysis: Ortolá.

Obtained funding: Sotos-Prieto, Rodríguez-Artalejo.

Administrative, technical, or material support: Rodríguez-Artalejo.

Supervision: García-Esquinas, Galán.

Conflict of Interest Disclosures: None reported.

Funding/Support: This work was supported by the Plan Nacional sobre Drogas, Ministry of Health of Spain (grant No. 2020/17), Instituto de Salud Carlos III, State Secretary of R+D+I and Fondo Europeo de Desarrollo Regional/Fondo Social Europeo (Fondo de Investigación en Salud grants No. 19/319, 20/896, and 22/1111), Agencia Estatal de Investigación (grant No. CNS2022-135623), Carlos III Health Institute and the European Union “NextGenerationEU (grant No. PMP21/00093), and the Fundación Francisco Soria Melguizo (Papel de la Disfunción Mitocondrial en la Relación Entre Multimorbilidad Crónica y Deterioro Funcional en Ancianos project grant). Mercedes Sotos-Prieto holds a Ramón y Cajal contract (contract No. RYC-2018-025069-I) from the Ministry of Science, Innovation and Universities.

Role of the Funder/Sponsor: The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.

Data Sharing Statement: See Supplement 2 .

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• Alcohol Taking by the Teenagers
• Alcohol, Tobacco, and Illegal Drugs: Use Consequences
• Alcohol Use Disorder: Case Conceptualization
• Tobacco and Alcohol Should Not Be Allowed to Be Advertised
• Addiction in “Dragged High on Alcohol” Documentary The “Dragged High on Alcohol” documentary is about an alcohol addict Ryan, and the film crew follows him and his family, showing how Ryan experiences his addiction.
• Whip Whitaker’s Alcoholic Addiction and Its Influence on His Life In this case study, the author dwells on the alcoholic addiction of Whip Whitaker, a fictional character, alongside the impact of this addiction on his way of doing things.
• Social Problems Related to Alcohol and Drugs The present paper will explain the content of three articles relating to the issue of Alcohol and drug use while also providing a personal reflection on the readings.
• Canadians’ Reaction to Alcohol as a Newly-Invented Illicit Drug The possible reaction of Canadians to alcohol, if it was a newly-invented illicit drug, will differ depending on their personal characteristics and external circumstances.
• Alcohol Difference in the United States and Europe The types of alcohol and the patterns of its consumption vary across the countries. The attitude towards depends on the socio-political and the economic situation.
• Alcohol and Wellness: How Alcohol Affects Human Wellness Wellness refers to deliberate actions to live healthy life by eating recommended foods and drinks respectively. This essay describes how alcohol affects human wellness.
• History of Alcohol in Europe Europe and the United States recorded diverse historical developments regarding the distribution, quality, and consumption of alcohol.
• Qualitative Research of Alcoholism in the U.S. According to the Centers for Disease Control and Prevention, 11% of alcohol consumed in the USA is drunk by adolescents, and 90% of it is consumed in the form of binge drinking.
• Effects of Alcohol on Pregnant Women This paper is set out to shed light on the effects of alcohol on expectant women since they are the ones who are at great risk compared to their male counterparts.
• The Influence of Drugs and Alcohol on Date Rape While drugs can affect mental health and make the victim forget everything, the perpetrators indulge in alcohol abuse to escape the blame and deny non-consensual sex.
• 12-Step Mutual Support Groups and Alcoholics Anonymous 12-Step mutual support groups are an effective treatment method for alcohol dependence that should only be used as a secondary or adjunctive treatment.
• Personal Relationship With Alcohol Abuse Given that alcohol abuse affects myriad families, ruining people’s health and harming social life, it is still a sensitive and critical issue to consider.
• Fair Trade: Japan – Taxes on Alcoholic Beverages The WTO indicted Japan for what it described as a violation of the internal taxation and regulations as stipulated in the General Agreement on Tariff and Trade 1994.
• Alcohol Drinking and Ethical Decision-Making People should be prepared to make sacrifices and account for their actions if they expect good results since all good things cost heavily.
• The Alcohol Consumption Rate in Cambridgeshire Cambridgeshire is among the counties in the UK with the highest rates of alcohol consumption. This prevalence is caused by its culture and lack of effective social support.
• Arguments of “No Alcohol Safe To Drink…” by Ives The main idea of “No Alcohol Safe to Drink, Global Study Confirms” by Ives is that there can not be a healthy glass of wine and a moderate level of alcohol consumption.
• Causes and Consequences of Alcohol and Drug Addiction Drug addiction is a psychological and physical disorder that affects the brain of an individual. It is caused by dependence on drugs, alcohol, and specific behaviors.
• Alcohol Oxidation to Aldehydes and Ketones Alcohol oxidation is vital during the synthesis of organic compounds, only bleach can directly oxidize some alcohols to carboxylic acids, ketones, or aldehydes.
• Alcohol Addiction in a 59-Year-Old Man: Case Study The case study concerns Juan, a 59-year-old commercial pilot who has come to visit a clinician at the urging of his son.
• Reflection Paper on Alcoholics Anonymous Alcoholics Anonymous is a self-help group that assists alcohol addicts to break from the drinking habits and stay sober. This paper is a reflection of one of such meetings.
• Drugs and Alcohol Influence on Drivers Excessive amounts of alcohol and drugs deprive the driver of conscious control over the vehicle, leading to catastrophic consequences.
• Alcohol and Drug Abuse in the Workplace Alcohol and drug abuse is one of the major causes of accidents in the workplace. Random alcohol and drug tests would discourage employees of organization from abusing alcohol or drugs.
• Comparing a Behavioral and Chemical Addiction on the Example of Alcohol and Pornography This research examines two alcoholic treatments therapies of both inpatient and out patient addicts with an intention to assess the abuse consequences and monitor their effectiveness.
• The Problem of Teenage Alcoholism The problem of drinking alcohol among teens is an epidemic towards which they spend nearly 5.5 billion dollars a year.
• Alcohol Consumption and Sale Laws in the US Alcohol consumption and sale in the United States are regulated by several laws, each of which may vary depending on the state.
• Tone and Voice in Paisley’s “Alcohol” and Lockward’s “My Husband Discovers Poetry” In the poem, “My Husband Discovers Poetry,” and the song “Alcohol,” there are numerous poetic stylistic devices that are used.
• Alcohol Marketing Failures and Successes On the surface, alcohol might seem to be the easiest product to market since its audience develops an acquired taste, and customers’ purchasing ability is restricted mostly by age.
• Understanding and Preventing Prenatal Alcohol Exposure Learn about the detrimental effects of prenatal alcohol exposure on fetal development and discover effective interventions to prevent PAE and support affected.
• Treatment of Alcohol Dependency Through Cognitive Behavioral Therapy (CBT) Alcohol dependence results from a misconception that drinking alcohol can help to fulfill some needs in the victim’s life be it social, emotional or psychological needs.
• Discussion: Alcohol in Pregnancy It is significant to emphasize that the safe level of alcohol that a woman can drink during pregnancy has not been confirmed.
• Alcohol Use Disorder in a 39-Year-Old Male Patient The most highly suspected diagnosis for Mr. X is alcohol use disorder. The patient has a disrupted mood, cognitive concerns, and physical issues.
• Alcoholism Issue: The Minimum Drinking Age The paper states that alcoholism is a highly responsible step, often more important for life and health than enlisting in the army or getting married.
• Substance-Related Disorders: Opiates and Alcohol The patient was admitted for detoxification from opiates and alcohol. She has a long history of illicit drug use. The patient’s mood suggests she may be depressed.
• How Alcohol Affects Nursing Babies?
• Alcohol Death and Its Effect on Family Life
• How Alcohol Depresses the Central Nervous System
• Alcohol Treatments and Rehabilitation Programs
• How Drinking Alcohol Affects the Brain
• Factors Affect University Students Alcohol Consumption
• How Does Alcohol Affect Our Society and Our Health?
• Alcohol Problems Among Young People in Britain
• Alcohol Around Kids From Childhood
• Alcohol Dependency Among Native Americans
• Alcohol and Its Effects on the Brain
• Alcohol-Related Car Accidents Examples
• Long-Term Effects and Societal Impacts of Alcohol Consumption
• Alcohol Consumption and Metabolic Syndrome
• Alcohol and Its Effects on the Body
• Alcohol Consumption During the European Union
• Australia and Alcohol Prohibition
• Alcohol and the Causes of Student Binge Drinking
• How Alcohol May Affect Human Behaviour
• Drug and Alcohol Use by Student-Athletes
• Alcohol Consumption Crisis and How to Combat It Earl Rochester suggests a national system of licensing to combat the public health crisis of alcohol consumption.
• Alcohol Consumption During the COVID-19 Pandemic The paper raises the topic of increasing adherence to alcoholic beverages. An increasing number of people acquired this bad habit during the lockdown.
• Opinion on Alcohol Consumption The destructiveness of alcohol has been proven by multiple studies. The effect this substance has on people is immense, and sometimes the outcomes are fatal.
• Alcohol and the Negative Consequences of Consumption It is no secret that alcoholism is a problem in society. Some individuals are used to drinking alcoholic beverages for short-term stress reduction and well-being improvement.
• Drug Abuse and Alcohol-Related Crimes in Adolescents The current paper focuses on the topic of drug abuse and alcohol-related crimes among teenagers, showing that substances remain the most notable factor in juvenile crime.
• Overconsumption of Alcohol by a Customer The paper discusses who should be held accountable for the accidents resulting from overconsumption of alcohol by a customer served at a club, bar, or restaurant.
• Fetal Alcohol Spectrum Disorders and Alcohol Consumption The paper states that fetal alcohol spectrum disorders have severe implications for the well-being and health of individuals in all stages of their lives.
• Effects of Parent-Based Teaching of Alcohol Use The approach significantly impacts the struggle to prevent alcohol abuse but requires being informed on the appropriate mechanisms to employ.
• Alcohol in the Drugs and Behavior Context It is no secret that alcohol and human health are incompatible things. The most significant influence of alcohol falls on the cerebral cortex.
• Alcohol and Drug Foundation’s Public Relations The campaign conducted by Alcohol and Drug Foundation is a vivid example of how the theories and practices of PR can help alter people’s behavior.
• Drugs and Behavior: History of Alcohol in America The ordinary colonial American drank roughly twice as much alcohol in 1770 as it does today—about three and a half gallons annually.
• ”US Wooed Alcohol Industry…” Rabin’s Article The article discusses the issue of conducting scientific research aimed at justifying moderate drinking and its benefits for health.
• Alcohol: The Legal Drinking Age There is no significant harm in making the legal drinking age 18. The punishment that those under 21 individuals face when caught taking alcohol affects their daily lives.
• Socialization and Causes of Alcohol Consumption The process of socialization is indispensable for integrating into society, realizing and understanding self-identity, and finding one’s place in modernity.
• Alcoholism: Medical & Philosophical Dimensions The news article considered in the paper is devoted to the changes on the way to which modern medicine is ethical in its aspirations.
• Parental Alcohol Abuse as a Family Issue Parental alcohol abuse is a serious problem in the community that impacts not only one individual but spreads to different social units.
• Alcohol Use Amongst Hispanic College Apprentices The results showed that less assimilated Hispanic percent of boys in the buffer zone could be at greater risk of alcohol addiction than Hispanic masculine apprentices.
• Fetal Alcohol Spectrum Disorder and Care Planning Tyler has had Fetal Alcohol Spectrum Disorder since he was born while his mum was an alcoholic addict while pregnant.
• Statistical Study of Alcoholism Among Students This research paper investigates the relationship between workday alcohol consumption and several characteristics of students’ social, economic, and academic status.
• Alcohol Addiction and Its Effects on the Body and Specific Organs The more an individual use alcohol to cope with pain and adversity, the more the body adapts to it and becomes dependent on its effects.
• Teen Alcohol Consumption Reduction Plan in Long Island Alcohol consumption in adolescence is associated with a high risk of developing suicidal tendencies, unwanted pregnancy, and drug use.
• The Alcoholics Anonymous Group Meeting Open and closed psychological support groups have at all times been an essential mechanism of maintaining a mentally healthy society.
• The 12-Step Alcoholics Anonymous Meeting’s Purpose and Stories Meetings consist of the opportunity to be heard without condemnation, and to learn from the experience of people who abstain from drinking alcohol for a while.
• COVID-19 Epidemic and Alcohol and Drug Addiction The sudden life changes during the COVID-19 epidemic make it difficult for people who suffer from alcohol and drug dependence to fight their addictions.
• Adolescent Addiction and Behavioral-Based Alcoholism Addiction to substances can be difficult to comprehend because, despite the progressively unfavorable consequences, addicted people take drugs and alcohol obsessively.
• Pandemic’s Impact on Mental Health & Substance and Alcohol Abuse While substance use disorder can impose mental health challenges on those who consume drugs, COVID-19 affects the psychology of all humankind.
• Planned Change Process in Alcohol Addiction A social worker at a high school in a midwestern state should work with four teenagers who were suspended for two weeks for drinking alcoholic beverages at school.
• Alcohol Abuse and Self-Management Program The main self-management program for a high school student with alcohol addiction is to set long-term and intermediate goals, and the development of a reward system.
• Meaning of Alcoholics Anonymous The paper discusses Alcoholics Anonymous. It can be referred to as a fellowship of individuals who have decided to solve their drinking problem.
• Impaired Control, Impulsivity, and Alcohol Self-Administration Impaired control is a significant factor in the association between impulsiveness and alcohol consumption in both non-dependent and dependent drinkers.
• Alcohol Abuse: Causes and Solutions Alcohol abuse remains one of the key healthcare concerns around the globe, not least because addicts do not purely injure their own health.
• Alcoholic Yeast Fermentation and Optimal Conditions This laboratory report examines the dependence of bioethanol production on temperature, pH, stirring, and gas composition.
• Health Professionals’ Perceptions of Fetal Alcohol Spectrum Disorder Infants with fetal alcohol spectrum disorder (FASD) symptoms tend to have psychological or physiological deviations.
• Responsibility and Brand Advertising in the Alcoholic Beverage Market The article indicates that the brand advertisements highlight alcohol consumption as socially acceptable, while media advocacy campaigns focus on the role of manufacturers.
• National Association for Alcoholism and Drug Abuse Counselors This paper will consider the fourth principle of the organization’s ethical code, which reads: “Working in a culturally diverse world.”
• Evaluation Using GAS: Alcohol Withdrawal Syndrome Quitting alcoholism is not easy, but it can happen with a well-designed strategy and commitment from both the patient and the interventionist.
• Interaction of the Pharmaceuticals with Alcohol Intake It is important to establish the key value of healthy living based on the interaction with the pharmaceuticals and alcohol intake to avoid developing a dependency on the elements
• The Negative Effects of Drinking Alcohol While Pregnant The paper outlines the domains of child development and the negative effects of alcohol on the fetus, discusses the physical and mental impact of fetal alcohol on an individual.
• Alcoholics Anonymous Organization’s Role and Functions Alcoholics Anonymous unites millions of people. These individuals are alcohol addicts, and they cannot remove this substance from their lives.
• Drug and Alcohol Addiction Treatment Program Successful addiction treatment is comprised of three aspects, constructing the addiction treatment: body, mind, and soul.
• Alcohol Consumption and the Effects
• Drinking Motives and Alcohol Consumption
• How Does Alcohol Consumption Affect Social Attention
• Drug and Alcohol Use Among Adolescents
• Drinking Culture and Alcohol Consumption
• Alcohol Dependency and Its Effects on the Community
• Alcohol Advertisements and College Student Binge Drinking
• Alcohol and Native American Experience
• Alcohol Consumption and Maturity
• College Students and Alcohol Abuse
• Alcohol and the Central Nervous System
• How Alcohol Abuse Affects Aging People
• Alcohol Availability and Violence
• Alcohol Beverage Advertising Should Be Restricted
• How Alcohol Abuse Has Become Part of the Culture in Many Societies
• How Alcohol Causes Mental and Moral Changes
• Alcohol Consumption and Risky Sexual Behaviors
• Alcohol and the Destruction of Families
• Drugs and Alcohol Mask the Pain
• Alcohol Consumption During Pregnancy and Low Birth Weight
• Alcohol Use Disorder and Borderline Personality Disorder: The Case Study Thomas demonstrates at least four symptoms of alcohol use disorder and probably has borderline personality disorder, which prevents him from building long-term relationships.
• Reflections on Alcoholic Anonymous Meeting Alcoholics Anonymous is a nonprofessional and apolitical community that gathers members having problems with alcohol consumption worldwide and supplies them with mutual aid.
• Education Level and HIV Transmission Among Alcoholics in California This research highlights the objective elements and statistical information regarding the relationship between education level and HIV transmission among alcoholics in California.
• Alcohol and Other Drug Use Among the Aboriginal and Torres Islander People The paper evaluates the patterns of alcohol and other drug usage among the Aboriginal and Torres Strait Islanders, and drug-related harms.
• The Effect of Prohibition Alcohol and Drug Use Although Prohibition reduced consumption in the initial period, it does not imply that it realized success; neither did it make the community better.
• Researching of Pregnancy and Alcohol Abuse In order to address the issue of alcohol abuse during pregnancy, the interprofessional team should consider the current trends and recommendations on maternal alcohol consumption
• Alcohol Dependence as a Physical Dependence The paper aims at displaying an aspect of physical alcohol dependence, where alcohol dependence is shown in hardship-related issues in life.
• Substance and Alcohol Misuse among Adolescents Substance and alcohol misuse among adolescents is a considerable bother for the US healthcare system since adolescence is commonly known as a time for experimentation.
• Yeast Alcohol Dehydrogenase Structure Yeast alcohol dehydrogenase refers to a group of enzymes that are found in yeast and have a widespread application in the beer and wine industry where they facilitate the process of fermentation.
• Substance Abuse: Alcohol and Drugs in the Movie “Ray” The movie “Ray” by Taylor Hackford. In “Ray,” the issue of substance abuse helps understand the problems that a person faces when dealing with addiction.
• Alcoholism in Older Adults in America Based on the social, economic, and health problems of alcoholism, it is pertinent to adopt effective ways of minimizing its incidence in society.
• The American Alcohol Problem Studies have shown that, alcohol abuse leads to health complications whereby; the abusers develop digestive, psychological, mental and physical problems.
• Alcohol Addiction: Assessing and Diagnosing the Client This paper considers the case of a 38-year-old welder, who has an alcohol addiction problem: the problem is assessed, diagnosed, and ways in which he can be helped are identified.
• Interpersonal Psychotherapy and Alcohol Addiction Interpersonal psychotherapy (IPT) is a highly adaptable approach to treating an array of disorders, and it has been used to address the needs of various patient groups.
• The Problem of Alcohol Addiction in Russia Russia now acknowledges alcohol addiction as a problem. The health impact of alcohol in Russia is most notable in its contribution to mortality through cardiovascular diseases.
• Impact of Alcohol Abuse on Breast Cancer Risk in Women This paper will examine the effects of alcohol abuse on the development of breast cancer in women to uncover its devastating consequences.
• Defining The Harm of Alcoholism Disease The paper aims to provide a report on the disease of alcoholism based on Čuček Trifkovič’s paper, followed by a comparison with three other studies.
• Alcohol Consumption: Negative Impacts This essay cross-examines the outcomes of alcohol consumption. The paper achieves its objective through carrying out research with specific methodology.
• Alcohol Abuse as It Pertains to High Risk Families The main objections of the promotion and prevention program are to ensure reduced substance abuse among young people to protect their health.
• Alcohol and Its Effects on Domestic Violence Alcohol was invented as a beverage drink just like the others, such as soda and juice. Of late, alcohol has been abused because people are consuming it excessively.
• Biopsychologic Model of Alcohol Consumption This work is devoted to alcohol dependence: the possible causes of occurrence, health risks, as well as the most effective methods of treatment are considered.
• Fetal Alcohol Spectrum Disorders Fetal alcohol spectrum disorders (FASDs) are the spectrum of conditions caused by parental alcohol use during pregnancy that affects the world population’s health
• The Effects of Alcohol on Human Body and Mental State “Drinking: A Love Story” is the story about the relationship between a human and alcohol, the transformation of a person as an addict, and their way to sobriety.
• Dealing With Alcohol Abuse in Adolescents This research evaluates how the public can be incorporated in developing effective interventions aimed at dealing with alcohol abuse and binge drinking among youth.
• Alcohol Dependence in Modern Women Alcohol dependence has become a serious problem in modern women. It is explained by changing social roles, numerous responsibilities, and dissatisfaction with life.
• Exposure to Low Levels of Alcohol During Pregnancy There are no solid reasons for the mother to drink alcohol during pregnancy, and, as the safe dose is hard to establish.
• Fetal Alcohol Syndrome (FAS) Among Pregnant Women Fetal Alcohol Syndrome is a severe disease that has dangerous affects on the fetus and on a born child. The abnormal features of this syndrome accompany a man throughout the life span.
• Paternal Exposure: Alcohol and Offspring Development The experiments related to the influence of fathers’ alcoholism on the development of their children allowed to conclude on the presence of several developmental disorders.
• Developments in Global Tobacco and Alcohol Policy WHO reports that about 8 million people die from smoking every year. Tobacco is a major cause of the emergence and development of multiple complications such as cancer, heart disease.
• Alcohol Negative Effects on Vital Parts of Human Body The paper discusses alcohol abuse. Although alcohol seems harmless to many people, it has a significant negative effect on various vital parts of the human body.
• The Fetal Alcohol Syndrome (FAS) Fetal Alcohol Syndrome (FAS) is a severe disease that has dangerous affects on the fetus and on a born child.
• Hispanic Community: Alcohol & Substance Abuse Among the Female Gender Population This study will focus on alcohol and substance abuse among the female gender population proportion (12-20 years and 25-45 years) in the Hispanic community in California.
• Overcoming Chronic Alcoholism by Patients This work describes the problem of alcoholism, its stages and main symptoms, problems of diagnosis, psychological and physical treatment.
• Article Critique about Alcohol & Society The research efforts of recent years aimed to shed light on the interconnection between alcohol outcomes and socioeconomic factors.
• Alcohol and Depression Article by Churchill and Farrell The selected article for this discussion is “Alcohol and Depression: Evidence From the 2014 Health Survey for England” by Sefa Awaworyi Churchill and Lisa Farrell.
• Drug and Alcohol Abuse in Organizations The purpose of this paper is to analyze the impact of drugs and alcohol on the behavior of the employees and the relationships between business owners and their subordinates.
• Problem Drinking Treatments: A Comparison of Alcoholics Anonymous and Moderation Management This paper will contrast and compare Alcoholics Anonymous (AA) and Moderation Management (MM) and the programs that they offer.
• Support Services and the Case Review: Drug and Alcohol Addiction The article presents a plan to help a 39-year-old patient living in Palm Beach treat his alcohol and drug addiction.
• College Experience and Alcohol Consumption Alcohol use is related to a high number of health problems in the United States. Current statistics show that more than 80% of college students drank on one or more occasions.
• The Money Factor in Drug and Alcohol Treatment A vast number of individuals fail to take up drug treatment because they are unable to raise the money that is required to enroll in such a program.
• Banning Alcohol From Mainstream Consumption
• Alcohol-Related Crimes, How Do We Tackle It
• Alcohol Disadvantages Examples
• Alcohol Use for Disease Control and Prevention
• Alcohol and Its Effects on Social Behavior
• Alcohol Benefits and Demerits
• Alcohol Consumption Among First Time Mothers
• Illegal Alcohol Sale and Consumption
• Alcohol and Its Effect on Society
• Alcohol: The World’s Favorite Drug
• Alcohol Abuse Among College Students at University of South Carolina
• How Alcohol Affects the Brain’s Size
• Alcohol Treatment Save Your Life
• Alcohol and Its Effects on Psychological and Physical Levels
• How Alcohol Affects the Internal Organs
• Alcohol Consumption and the Risk of Dementia
• Alcohol and Its Physiological Effects
• Alcohol and Teenagers Alcoholic Beverage
• Why Should Not Reduce Alcohol Not A Concern For Authorities?
• Alcohol Consumption Among College Students
• Formation of the Alcoholics Anonymous Association Alcoholics Anonymous is an association of different people recuperating from alcoholism who come together to contribute their experiences about alcoholism and its effects.
• Global Trends Affecting a Local Drug and Alcohol Rehab Centers Drug abuse is one of the greatest problems affecting the world today. Rehabilitation centers have been the best institutions in transforming the lives of drug addicts.
• Alcoholism: Causes, Symptoms and Negative Effects Alcohol abuse and alcoholism are associated with a broad range of medical, psychiatric, social, legal, occupational, economic, and family problems.
• Alcoholic Parents’ Effect on Adult Children While effects of being raised by alcoholics in adult children may vary, fear of failure, desire to control, and developing compulsive behaviors are prevalent characteristics.
• Alcohol Abuse Among Students: Reforming College Drinking A large number of works are devoted to the problem of alcohol abuse among students. One of them is Drinking in College: Rethinking a Social Problem by George Dowdall.
• Alcohol Addiction and Its Adverse Effects on the Victim and Family Alcoholism is known to have numerous adverse effects. Alcoholics have wives, husbands, children and other close relatives who are mindful of their welfare.
• Personal Issues: Marriage, Obesity, and Alcohol Abuse The actions of every person have a particular impact on society and its development, and this impact is sometimes underestimated.
• Anti-Drugs, Alcohol and Tobacco Education Programs Many teachers understand that drugs and alcohol use among students is the major reason why many students do not accomplish their educational goals.
• Human Brain. Alcohol Effects on Frontal Lobe Impairment In this paper, various ways of influence of alcohol abuse on frontal lobe impairments are considered with special emphasis on direct frontal lobe impairments.
• Alcoholism and Its Effects: Beyond the Influence In the book “Beyond the Influence”, Ketcham et al. present their proof that the disease of alcoholism is a physiological disease rather than a psychological disorder.
• Alcoholics’ Rights for Organ Transplantation This essay seeks to answer the question as to whether it makes medical and ethical sense to accept organ transplantation within a family.
• Alcohol Cessation in Pregnancy The problem of alcohol use during pregnancy attracts the attention of different researchers. The paper offers evidence-based concepts for promoting alcohol cessation.
• Applied Ethics: Moral Standards of Alcoholic Parents The work aims to discuss the topic of ethics, the moral values which people are supposed to follow, considering the case of Mary, whose parents are alcoholics.
• The Café Bar’s Employee Relations: Illegal Substance and Alcohol Use The Café Bar is committed to offering and preserving a secure and prolific work atmosphere, liberated from the unfavorable consequences of drugs and alcohol.
• Alcohol Addiction Group Manual The present manual offers key information about the formation of a psychotherapeutic group that is focused on addressing the problem of alcohol addiction.
• The Importance of Religion in Understanding the History of Alcohol Although it emerged in specific ancient civilizations, the alcoholic drink gained a unique religious significance from the Ancient Period to the Middle Ages.
• Genetic Predisposition to Alcohol Dependence and Alcohol-Related Diseases The subject of genetics in alcohol dependence deserves additional research in order to provide accurate results.
• Temperament of Children in Alcoholic Families There are many factors that destabilize family relationships, and one of the most devastating problems is the alcohol addiction of one or both parents.
• Alcohol and Its Major Behavioral Effects Alcohol is most widely known for its effects on behavior, for which reason it is currently used as a legal recreational drug.
• Alcohol Abuse: the Economist Approach To an economist, the problem of alcohol abuse is viewed as an externality in both consumption and production. The value to consumers is greater than the value to society.
• Personality Versus Alcohol This dissertation examines the influences of alcohol on personality through a multidimensional study of numerous studies and experiments performed by scientists around the world.
• Alcohol Abuse’ Treatment Among the Elderly This research focuses on finding the best treatment for the problem of alcohol abuse among the elderly as it may pose serious health problems.
• Drug and Alcohol Abuse Treatment Effectiveness The production and consumption of drugs is a core challenge in the modern world. It is the reason why there is an increased need for treatment of people affected by drug addiction.
• The Treatment of Alcohol Abuse among the Elderly Alcohol abuse among the elderly is an issue that has raised concern among medical practitioners and society in general.
• Alcohol Advertisement and Its Impact on Consumption There is a need for restrictions in alcohol advertisements so that the vulnerable youth can be salvaged from underage drinking that risk interfering with their health and career life.
• “Adolescent Alcoholism and Drug Addiction” by Choate The article “Adolescent alcoholism and drug addiction: The experience of parents” revolves around the issue of drug addiction among teenagers and its effects on their families.
• Alcohol Consumption in Children and Public Health Alcohol has long been a big concern for public health, especially its use by children. It negatively influences many aspects of life: health, education, and social relationships.
• Twelve-Step Programs: Alcoholics Anonymous This paper provides an overview of the most effective Twelve-Step Programs in the USA and a more detailed description of an Alcoholics Anonymous meeting.
• Teratogenic Effects of Alcohol and Smoking The teratogen is an umbrella term for substances that can have adverse effects on an embryo. In the situation, a girl continues drinking alcohol and smoking cigarettes despite being pregnant.
• Alcohol Intervention in the Primary Care Setting The paper will discuss and analyze scholarly research on the topic of alcohol intervention to analyze patient outcomes in the primary care setting.
• Miami-Dade Community Needs: Alcohol and Drug Addiction Miami-Dade is one of the counties in the state of Florida. The health needs of the people living in this county are supported using different initiatives and programs.
• Alcohol Culture World History Alcohol consumption is a rather widespread phenomenon, as the culture of liquor drinking exists in nearly every state of the world.
• Problem of the Alcohol Addiction in Modern Families The increasing cases of alcoholism, also known as addiction, have led to a rising concern and a research on its challenges and remedies.
• Manitoba Mothers and Fetal Alcohol Spectrum Disorders Singal et al. focuse on a rather important problem of maternal alcohol consumption during pregnancy resulted in fetal alcohol spectrum disorder in children.
• The Price Role in Alcohol and Cigarettes Consumption This essay is a presentation concerning the facts about price elasticity of demand and the key issues that relate to it. It determine, whether binge drinking is common among college students.
• The Power of Alcohol: Human Inability to Control Demands Alcohol is one of the most dangerous drinks which are available for people. Alcohol has a variety of face, and people cannot even guess how they can be dependent on alcohol.
• Sociology: “Alcoholics Anonymous” by Bill Wilson The book “Alcoholics Anonymous” gives a detailed analysis of the health challenges and decisions made by Bill Wilson. The narrator struggled with alcoholism for many years.
• Substance Abusers Alcoholics – Psychology Alcoholics suffer from a distinct physical yearning to take alcohol past their capability to manage it, irrespective of every law of common sense.
• Sociology: Prevention of Alcohol and Drug Problem Drug prevention program is the process that devotes its efforts towards limiting the use of psychoactive substances and the development of associated problems.
• Fetal Alcohol Syndrome The research study conducted by Mcgee indicated that the tendency towards being passive was more pronounced in children with Fetal Alcohol Syndrome than their peers.
• Alcohol Misuse in Teenagers: New Means to Address the Issue Despite the efforts of healthcare specialists, over the past few years, the rates of alcohol consumption in youth have grown impressively.
• Which Drug Is More Effective in the Treatment of Alcohol Withdrawal?
• How Alcohol Affects the Human Body?
• How Does Alcohol Makes You Drunk?
• Should Alcohol and Tobacco Advertisement Be Banned?
• Should the Alcohol Drinking Age Be Decreased?
• Should the Government Attempt to Reduce Current Levels of Alcohol Consumption?
• What Are the Positive and Negative Effects of Alcohol?
• What Effect Does Alcohol Have on a Person’s Health and Life Expectancy?
• Why Shouldn’t Teenagers Drink Alcohol?
• How Does Alcohol Affect the Brain?
• How Does Drugs and Alcohol Affect Teenage Brain Development?
• Why Alcohol Should Not Be Legal?
• How Much Alcohol Is Ok per Day?
• What Happens When You Drink Alcohol Every Day?
• What Is the Healthiest Alcohol?
• What Alcohol Is Considered Heavy Drinking?
• How Long Does Alcohol Stay In Your System?
• What Are the Benefits of Drinking Alcohol?
• What Is the Least Harmful Alcohol to Drink?
• Which Alcohol Is Lowest in Sugar?
• Which Alcohol Is Healthier: Vodka or Whiskey?
• How Much Alcohol Do Alcoholics Drink?
• Does Alcohol Change Your Body Shape?
• Does Alcohol Raise Blood Pressure?
• Does Alcohol Help You Sleep?
• What Are the Steps in Alcohol Production?
• How Is Alcohol Made Industrially?
• Which Material Is Used for Production of Alcohol?
• How Alcohol Is Produced by Fermentation?
• Which Enzymes Are Necessary for Alcohol Production?

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StudyCorgi. (2021, September 9). 257 Alcohol Essay Topics & Research Titles for Students. https://studycorgi.com/ideas/alcohol-essay-topics/

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StudyCorgi . "257 Alcohol Essay Topics & Research Titles for Students." September 9, 2021. https://studycorgi.com/ideas/alcohol-essay-topics/.

StudyCorgi . 2021. "257 Alcohol Essay Topics & Research Titles for Students." September 9, 2021. https://studycorgi.com/ideas/alcohol-essay-topics/.

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This essay topic collection was updated on June 20, 2024 .

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Health Risks and Benefits of Alcohol Consumption

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

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

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

Measuring the Health Risks and Benefits of Alcohol

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

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

Effects on Physical Health

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

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

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

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

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

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

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

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

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

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

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

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

Definitions Related to Drinking

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

How Much Is a Drink?

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

Does Abstaining Increase Risk?

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

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

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

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

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

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

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

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

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

Psychosocial Consequences and Cognitive Effects

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

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

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

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

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

Effects on Society

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

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

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

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

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

The Overall Impact

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

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

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

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

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

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

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

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Massive biomolecular shifts occur in our 40s and 60s, Stanford Medicine researchers find

Time marches on predictably, but biological aging is anything but constant, according to a new Stanford Medicine study.

August 14, 2024 - By Rachel Tompa

We undergo two periods of rapid change, averaging around age 44 and age 60, according to a Stanford Medicine study. Ratana21 /Shutterstock.com

If it’s ever felt like everything in your body is breaking down at once, that might not be your imagination. A new Stanford Medicine study shows that many of our molecules and microorganisms dramatically rise or fall in number during our 40s and 60s.

Researchers assessed many thousands of different molecules in people from age 25 to 75, as well as their microbiomes — the bacteria, viruses and fungi that live inside us and on our skin — and found that the abundance of most molecules and microbes do not shift in a gradual, chronological fashion. Rather, we undergo two periods of rapid change during our life span, averaging around age 44 and age 60. A paper describing these findings was published in the journal Nature Aging Aug. 14.

“We’re not just changing gradually over time; there are some really dramatic changes,” said Michael Snyder , PhD, professor of genetics and the study’s senior author. “It turns out the mid-40s is a time of dramatic change, as is the early 60s. And that’s true no matter what class of molecules you look at.”

Xiaotao Shen, PhD, a former Stanford Medicine postdoctoral scholar, was the first author of the study. Shen is now an assistant professor at Nanyang Technological University Singapore.

These big changes likely impact our health — the number of molecules related to cardiovascular disease showed significant changes at both time points, and those related to immune function changed in people in their early 60s.

Abrupt changes in number

Snyder, the Stanford W. Ascherman, MD, FACS Professor in Genetics, and his colleagues were inspired to look at the rate of molecular and microbial shifts by the observation that the risk of developing many age-linked diseases does not rise incrementally along with years. For example, risks for Alzheimer’s disease and cardiovascular disease rise sharply in older age, compared with a gradual increase in risk for those under 60.

The researchers used data from 108 people they’ve been following to better understand the biology of aging. Past insights from this same group of study volunteers include the discovery of four distinct “ ageotypes ,” showing that people’s kidneys, livers, metabolism and immune system age at different rates in different people.

Michael Snyder

The new study analyzed participants who donated blood and other biological samples every few months over the span of several years; the scientists tracked many different kinds of molecules in these samples, including RNA, proteins and metabolites, as well as shifts in the participants’ microbiomes. The researchers tracked age-related changes in more than 135,000 different molecules and microbes, for a total of nearly 250 billion distinct data points.

They found that thousands of molecules and microbes undergo shifts in their abundance, either increasing or decreasing — around 81% of all the molecules they studied showed non-linear fluctuations in number, meaning that they changed more at certain ages than other times. When they looked for clusters of molecules with the largest changes in amount, they found these transformations occurred the most in two time periods: when people were in their mid-40s, and when they were in their early 60s.

Although much research has focused on how different molecules increase or decrease as we age and how biological age may differ from chronological age, very few have looked at the rate of biological aging. That so many dramatic changes happen in the early 60s is perhaps not surprising, Snyder said, as many age-related disease risks and other age-related phenomena are known to increase at that point in life.

The large cluster of changes in the mid-40s was somewhat surprising to the scientists. At first, they assumed that menopause or perimenopause was driving large changes in the women in their study, skewing the whole group. But when they broke out the study group by sex, they found the shift was happening in men in their mid-40s, too.

“This suggests that while menopause or perimenopause may contribute to the changes observed in women in their mid-40s, there are likely other, more significant factors influencing these changes in both men and women. Identifying and studying these factors should be a priority for future research,” Shen said.

Changes may influence health and disease risk

In people in their 40s, significant changes were seen in the number of molecules related to alcohol, caffeine and lipid metabolism; cardiovascular disease; and skin and muscle. In those in their 60s, changes were related to carbohydrate and caffeine metabolism, immune regulation, kidney function, cardiovascular disease, and skin and muscle.

It’s possible some of these changes could be tied to lifestyle or behavioral factors that cluster at these age groups, rather than being driven by biological factors, Snyder said. For example, dysfunction in alcohol metabolism could result from an uptick in alcohol consumption in people’s mid-40s, often a stressful period of life.

The team plans to explore the drivers of these clusters of change. But whatever their causes, the existence of these clusters points to the need for people to pay attention to their health, especially in their 40s and 60s, the researchers said. That could look like increasing exercise to protect your heart and maintain muscle mass at both ages or decreasing alcohol consumption in your 40s as your ability to metabolize alcohol slows.

“I’m a big believer that we should try to adjust our lifestyles while we’re still healthy,” Snyder said.

The study was funded by the National Institutes of Health (grants U54DK102556, R01 DK110186-03, R01HG008164, NIH S10OD020141, UL1 TR001085 and P30DK116074) and the Stanford Data Science Initiative.

• Rachel Tompa Rachel Tompa is a freelance science writer.

About Stanford Medicine

Stanford Medicine is an integrated academic health system comprising the Stanford School of Medicine and adult and pediatric health care delivery systems. Together, they harness the full potential of biomedicine through collaborative research, education and clinical care for patients. For more information, please visit med.stanford.edu .

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Older Adults Do Not Benefit From Moderate Drinking, Large Study Finds

Virtually any amount increased the risk for cancer, and there were no heart benefits, the researchers reported.

By Roni Caryn Rabin

Even light drinking was associated with an increase in cancer deaths among older adults in Britain, researchers reported on Monday in a large study. But the risk was accentuated primarily in those who had existing health problems or who lived in low-income areas.

The study, which tracked 135,103 adults aged 60 and older for 12 years, also punctures the long-held belief that light or moderate alcohol consumption is good for the heart.

The researchers found no reduction in heart disease deaths among light or moderate drinkers, regardless of this health or socioeconomic status, when compared with occasional drinkers.

The study defined light drinking as a mean alcohol intake of up to 20 grams a day for men and up to 10 grams daily for women. (In the United States, a standard drink is 14 grams of alcohol .)

“We did not find evidence of a beneficial association between low drinking and mortality,” said Dr. Rosario Ortolá, an assistant professor of preventive medicine and public health at Universidad Autónoma de Madrid and the lead author of the paper, which was published in JAMA Network Open.

On the other hand, she added, alcohol probably raises the risk of cancer “from the first drop.”

The findings add to a mounting body of evidence that is shifting the paradigm in alcohol research. Scientists are turning to new methodologies to analyze the risks and benefits of alcohol consumption in an attempt to correct what some believe were serious flaws in earlier research, which appeared to show that there were benefits to drinking.

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