Review of Evidence on Alcohol and Health (2025)
Chapter: 7 Neurocognition
7
Neurocognition
Analyses of whether moderate alcohol consumption is positively or negatively associated with cognitive abilities or development of dementia was guided by a 75-year history of rigorous peer-reviewed studies on the effects of alcohol use (Adams and Victor; 1989; Oscar-Berman et al., 2014; Parsons and Nixon, 1993; Sullivan et al., 2023). The mainstay of this work has focused on alcohol dependence, which is now called alcohol use disorder (AUD). Mild, moderate, severe, or profound impairments associated with AUD are detectable with objective quantitative testing conducted after the acutely consumed alcohol has been fully metabolized and is no longer active in the system. Acute alcohol consumption commonly impairs motor control, resulting in postural instability, slurred speech, and eye-to-hand discoordination affecting activities such as driving; memory consolidation for events experienced during intoxication; emotional lability evidenced as unprovoked crying or physical aggression; and poor judgment, for example, deciding to drive while intoxicated. Areas of impairment that persist after acute intoxication and accompanying chronic AUD include specific component processes of memory, such as verbal and spatial working memory, and select cognitive functions, such as problem solving, decision making, and spatial construction.
Myriad demographic, environmental, family history, and genetic factors can influence the course of AUD. For example, high risk for the development of AUD is associated with early initiation of drinking during young adolescence, family history of AUD, poor inhibitory control, binge drinking, history of blackouts, and access to alcoholic beverages. Whether AUD initiated at any age accelerates age-related health declines remains an open question.
Relative to AUD, far less research has been devoted to objective studies of moderate drinking, which is often defined by exclusion from AUD criteria. The few studies of moderate drinking, sometimes referred to as social drinking, that have used objective neuropsychological tests, report performance advantages in some areas, including executive functioning (Hogenkamp et al., 2014), episodic memory (Downer et al., 2015), and working memory (Boissoneault et al., 2016). Along with the apparently positive effects of moderate drinking are cautions, including lifestyle factors that can co-occur with alcohol consumption that are either positive, such as healthful nutrition, regular exercise, and good sleep habits, or negative, such as smoking or interference with medication functions. Other positive lifestyle factors potentially intersect with moderate drinking, such as presenting opportunities for socialization and family interaction.
In addition to studies focused on the cognitive and motor effects of drinking within the limits of low risk, moderate drinkers are characteristically the no-to-low drinking control groups for AUD study groups (Nixon and Lewis, 2019). It must be emphasized that none of these observations, even when an adequate comparison group is examined or with longitudinal assessment, can provide conclusions about causality. Lack of cognitive decline, cognitive improvement, or absence of development of dementia observed in low to moderate drinkers does not mean that these desirable outcomes occurred because of drinking.
Simply focusing on one to a dozen variables as potential moderators of cognitive decline, impairment, or dementia may be inadequate to determine with confidence a direct correlation between current drinking amount by category and cognitive outcome. This includes a consideration of genetic influences that in themselves affect the risk for developing dementia-related disorders. Comorbidities are also common concomitants of drinking. For example, some people may use alcohol to self-medicate against certain psychiatric symptoms, notably depression, anxiety, obsessive-compulsiveness, traumatic stress, learned helplessness, and more. Other comorbidities include infections, such as HIV or hepatitis C, nonalcohol illicit drug use, and misuse of tobacco and cannabis, which is legal in many U.S. states. Aging, sex, race and ethnicity, and socioeconomic status are also leading factors that have been shown to influence cognitive status (Delker et al., 2016; Sullivan et al., 2023).
CHOICE OF OUTCOMES
Outcomes selected for the consideration of alcohol and neurocognitive relations were limited by data available in peer-reviewed publications and the committee’s inclusion and exclusion criteria. In addition, results were restricted to moderate alcohol consumption with reference group outcomes in people who reported never or occasional alcohol consumption. Studies
were excluded if the no-alcohol consumption comparison group included former heavy drinkers; an exception was made when the analyses were stratified such that low-to-light consumption could be directly compared with moderate consumption.
Outcomes were of two types: dementia (total dementia and Alzheimer’s disease) and cognitive decline. Dementia and Alzheimer’s disease were assessed separately because dementia is an umbrella diagnosis that may include Alzheimer’s disease. All considered studies were based on objective, longitudinal measurements that could yield decline, which is necessary evidence for determining dementia generically or categorized as Alzheimer’s disease based on diagnosis by experts, such as clinical neurologists or other clinician diagnosticians using Diagnostic and Statistical Manual of Mental Disorders (DSM)-IV or DSM-5 criteria or International Classification of Diseases (ICD)-9 or -10 criteria for dementia. Determination of dementia could be made from medical charts, nursing home records, or death certificates with the assumption or notation that experienced clinicians made the diagnosis; studies that did not use these criteria were excluded from the analysis.
Cognitive decline was determined with quantitative measures of episodic memory, cognitive screening, or phonemic or semantic word fluency and did not consider dementia as an outcome in longitudinal study. At least two cognitive assessments needed to be made at times separated by several years so a change in cognitive performance could be captured. Too few studies of cognitive decline were available to conduct meta-analyses; rather, findings are based on systematic review with consideration of study quality.
None of the available studies provided adequate evidence to determine causation between drinking and dementia or cognitive outcome. Studies could potentially support conclusions of faster or slower decline associated with moderate alcohol consumption relative to a matched nondrinking group, but absence of association would not necessarily indicate harm or protection from cognitive decline related to moderate alcohol consumption.
BIOLOGICAL PLAUSIBILITY
High alcohol consumption has multiple consequences that may promote or accelerate age-related neurocognitive decline or dementia. A leading speculation is that these disorders feature a chronic inflammatory state that promotes the formation of the amyloid plaques and neurofibrillary tangles associated with neurodegeneration and dementia (Kinney et al., 2018; Sudduth et al., 2013). This inflammation is driven, in part, by the persistent activation of brain microglia that continuously release cytokines that act in a feed-forward loop to further drive inflammation (Pascoal et al., 2021). Alcohol’s proinflammatory properties would preclude the resolution of those signals and further promote this cascade (Wang et al.,
2010). High alcohol intakes also disrupt the blood–brain barrier integrity to enhance neuronal damage (Vore and Deak, 2022) and elevate circulating cholesterol to increase cerebrovascular damage (De Oliveira et al., 2000). Finally, excessive alcohol use combined with inadequate nutrition can culminate in the severe cognitive impairment marking the neurodegenerative disorder Wernicke–Korsakoff syndrome, which is caused by depletion of the essential vitamin thiamine (vitamin B1) (Adams and Victor, 1989). Alcohol-related seizures and withdrawal symptoms can also result in cognitive decline, which may not be fully reversible especially following repeated heavy drinking episodes interspersed with alcohol abstinence.
With advancing age, metabolism of alcohol slows with declining activity of acetaldehyde dehydrogenase, extending the time that this toxic form of alcohol lingers in the older person’s system. Further, with normal aging, blood flow declines (Brodkey and Dugdale, 2022; Mouches et al., 2022) and bodily water distribution lessens (Lu et al., 2023), each contributing to increasing the concentration of consumed alcohol. These factors may heighten risks of moderate drinking in older age not necessarily associated with younger age. Further compounding these concerns are certain drugs, which may be prescribed with higher prevalence in older people. The effects of moderate drinking in older (i.e., 55 years and older) men and women are newly emerging and indicate negative, synergistic effects on cognitive and psychomotor skills relevant to reaction time, working memory, and driving safety (Lewis et al., 2019).
Conversely, moderate alcohol consumption has been posited to reduce the risk for cognitive disorders. At lower levels of consumption, its milder proinflammatory properties might stimulate microglia and enhance their clearance of amyloid and neurofibrillary depositions (Doens and Fernandez, 2014), in a mechanism called hormesis (Calabrese and Baldwin, 2001). Its cardiovascular effects with respect to elevated high density lipoprotein may help to limit cerebrovascular damage (De Oliveira et al., 2000). Moderate consumption levels have been also associated with reduced risk for type 2 diabetes, hyperlipidemia, and obesity, all of which are independent risk factors for cognitive decline and dementia (Neto et al., 2023; Willette et al., 2015). However, associations of moderate drinking with the Mediterranean diet are confounded by the influences of its higher-quality diet, which itself reduces risk factors for cognitive decline and dementia (Charbit et al., 2024). Similarly, the higher socioeconomic status associated with moderate drinking is also associated with a higher-quality diet, access to health care, and higher education; the latter is associated with a greater cognitive reserve that serves as a protective buffer against cognitive decline (Cheng, 2016). Finally, congeners present in some alcohol-containing beverages, most notably phytochemicals such as quercetin and resveratrol, may have antioxidant properties to attenuate neuronal damage (Grabska-Kobylecka et al., 2023). Whether the content in those beverages is sufficient to achieve biological relevance remains in question.
PRIOR DGA RECOMMENDATIONS
2010
The 2010 Dietary Guidelines for Americans (DGA) Subcommittee on Alcohol investigated the question, “What is the relationship between alcohol intake and cognitive decline with age?” This included a systematic review with narrative synthesis of eight publications dating from 1995 to June 2009, seven primary research studies, plus a meta-analysis of 23 studies; 29 additional publications were excluded. Both heavy/binge drinking, and moderate alcohol consumption were evaluated, and the subcommittee defined moderate alcohol consumption using the same definition used in the current analysis. Their evidence summary concluded that “individuals who consume alcohol moderately have a slower cognitive decline with age,” as compared with nonconsumers of alcohol, with a grade of study quality of moderate.
In the meta-analysis that was discussed (Peters et al., 2008), moderate alcohol intake was associated with lower risk for dementia (RR = 0.63, 95%CI [0.53, 0.75]) and Alzheimer’s disease (RR = 0.57, 95%CI [0.44, 0.74]) relative to current nonconsumers but was not significantly associated with risk for vascular dementia (RR = 0.82, 95%CI [0.50, 1.35]) or the risk for cognitive decline (RR = 0.89, 95%CI [0.67, 1.17]). The outcomes of studies discussed in the review were inconsistent. For example, some studies reported a negative association between low-to-moderate intake of wine and lower risk of developing dementia but a positive association between low-to-moderate intake of beer and higher risk of developing dementia. The different outcomes for wine and beer raise the possibility that the association was not with alcohol per se, but with congeners in the alcohol beverage or with lifestyle behaviors that are associated with moderate alcoholic beverage consumption. Additional studies found no associations at low-to-moderate intakes. A significant limitation of most studies from this time period is that the nondrinkers reference group often comprised both never-consumers and former alcohol consumers, and the latter group can introduce substantial bias, as decisions to avoid alcohol consumption may reflect compromised health status.
The 2010 DGAC also investigated the question, “What is the relationship between heavy alcohol intake or binge drinking and cognitive decline with age?” This analysis also included an assessment of moderate alcohol consumption. The analysis concluded that “evidence suggests that heavy or binge drinking is detrimental to age-related cognitive decline,” with a grade of study quality as limited. With respect to low-to-moderate alcohol consumption, studies in the accompanying systematic review with narrative synthesis found greater, lower, or no associations with cognitive decline. Nonconsumers were again the reference group, and the limitations
discussed above were also relevant for these analyses. Another limitation emphasized in the meta-analysis was the heterogeneity within and across studies that contributes to inconsistency of outcomes.
2015
The 2015 DGAC report did not specifically address a potential relationship between neurocognitive decline and alcohol. It notes that a healthier dietary pattern that is associated with reduced risk for neurocognitive disorders, such as a Mediterranean diet, may also be moderate in alcohol; however, this postulated association was not systematically evaluated.
2020
The 2020 DGAC report contains a chapter focused on alcoholic beverages and health. However, this chapter did not consider questions regarding potential associations between alcohol and neurocognitive health and disease. The 2020 report also examined the relationship between dietary patterns and neurocognitive health. Whereas alcohol was not a specific focus of that systematic analysis, it noted the dietary patterns associated with better neurocognitive health did not consistently include alcoholic beverages, and the protective association was not reduced when alcoholic beverages, notably red wine, were included. Conversely, the protective association of those diets was still present when alcohol consumption was excluded from the analysis.
METHODOLOGICAL CONSIDERATIONS
To understand moderate alcohol consumption and neurocognitive health, the committee sought to define alcohol consumption variables as antecedent or associative factors as they influence or correlate with positive or negative cognitive health outcomes. Given the vast number of potential and known moderating factors influencing alcohol and neurocognitive relations, it was practical to reduce the moderators considered, define alcohol consumption parameters, define how cognitive health is measured, narrow the age range considered, and limit reports to those based on longitudinal assessment.
Despite their power, even longitudinal studies of adults (i.e., people ages 21 years and older) have limitations in that they seldom have prospective assessment initiated before the onset of heavy drinking. Further, they are limited in their usefulness without contemporaneously assessed low-to-no drinking control participants to establish normal cognitive trajectories of change with aging against which trajectories of drinkers at identified levels can be compared.
SYSTEMATIC REVIEW
Approach
An evidence scan was completed to describe the extent of the published literature, searching for prior systematic reviews and primary research studies published between 2010 and 2024, and following the last assessment of this topic in the 2010–2015 DGA. Of the 19,997 peer-reviewed papers that were published between 2010 and 2024 and were identified using the search terms noted in Appendix I, 364 articles were reviewed, and 24 articles met the eligibility criteria and were included in the review (Figure 7-1). Of these 24, all were primary research studies; 23 were prospective cohorts, and one was a retrospective cohort (see Appendix I). As defined by the ROBINS-E1 tool, one study had low risk of bias, 16 had some concerns, and seven were at high risk of bias (Table 7-1).
Review criteria strictly applied moderate alcohol consumption as defined as ≤1 drink/day for women and ≤2 drinks/day for men, wherein one drink was equivalent to 14 grams of alcohol. The alcohol intakes for studies outside the United States were harmonized to the U.S. DGA criteria and expressed as 14 grams/day (AND, 2024; Appendix I). Most studies adjusted for confounding variables, including age, smoking, diet, physical activity, or comorbidities. The certainty of the evidence of the studies included in the systematic reviews for dementia and Alzheimer’s disease (AD) are summarized in Table 7-2.
Results
Dementia
Eight studies were reviewed as part of this systematic review and narrative review of dementia. Six cohort studies examined the associations between moderate alcohol consumption and dementia risk, stratified by lower or higher intakes of moderate alcohol consumption (Handing et al., 2015; Jeon et al., 2023; Koch et al., 2019; Langballe et al., 2015; Sabia et al., 2018; Shimizu et al., 2023). Four of these studies found that intakes at the higher range of moderate alcohol consumption had greater risk for developing dementia. Handling et al. (2015) found that men consuming 0.7–2.1 drinks/day had a hazard ratio (HR) of 1.09 (p = 0.01) for developing dementia compared with those consuming >0–0.7 drinks/day. Jeon et al. (2023) evaluated changes in alcohol consumption patterns among adults aged 40 years and older and found that individuals who increased their alcohol
___________________
1 Risk Of Bias In Non-randomized Studies - of Exposures.
NOTES: The diagram shows the number of primary articles identified from the primary article and systematic review searches and each step of screening. The literature dates include articles with the publications between 2010 and 2024. n = number; NLM = National Library of Medicine; PRISMA = Preferred Reporting Items for Systematic Reviews and Meta-Analyses.
SOURCE: Annex I-3 in Appendix I, Academy of Nutrition and Dietetics, 2024.
consumption to moderate drinking (15–29 grams/day or 1.07–2.07 U.S. drinks/day) compared with those who sustained mild drinking (<15 grams/day or <1.07 U.S. drinks/day) exhibited greater risk of all-cause dementia: HR = 1.09, 95%CI [1.03, 1.15] (Table 7-3). The results endured after stratifying by age, sex, and smoking status. Langballe et al. (2015) evaluated the association between alcohol consumption patterns and risk of dementia in Norwegian adults. Results indicated that individuals who consumed alcohol frequently (≥5 times in last 2 weeks) had higher dementia risk than
| Study | Bias Domains assessed as “some concerns” or “high” | Overall Risk of Bias |
|---|---|---|
| Cheng et al., 2023 | Confounding, missing data, outcome measurement | High |
| Garduno et al., 2023 | Confounding | Some concerns |
| Han et al., 2021; Han et al., 2022 | Confounding, exposure measurement, missing data | High |
| Handling et al., 2015 | Confounding, exposure measurement, missing data | High |
| Horvat et al., 2015 | Confounding, missing data, outcome measurement | Some concerns |
| Jeon et al., 2023 | Confounding | Some concerns |
| Kawakami et al., 2023 | Confounding, exposure measurement | Some concerns |
| Koch et al., 2019 | Confounding, exposure measurement, selection of participants | Some concerns |
| Langbelle et al., 2015 | Confounding, outcome measurement | Some concerns |
| Larsson and Wolk, 2018 | Exposure measurement | Some concerns |
| Lee et al., 2022 | Confounding, exposure measurement, missing data, outcome measurement, selection of reported results | Some concerns |
| Love et al., 2020 | Missing data, outcome measurement, selection of reported results | High |
| Nooyens et al., 2014 | Selection of participants, missing data, outcome measurement | High |
| Sabia et al., 2014 | Confounding | Some concerns |
| Sabia et al., 2018 | All domains low risk of bias | Low |
| Salvador et al., 2022 | Confounding, exposure measurement | Some concerns |
| Schaefer et al., 2022 | Confounding, exposure measurement, missing data | Some concerns |
| Shimizu et al., 2023 | Confounding | Some concerns |
| Tian et al., 2022 | Confounding, exposure measurement, missing data | Some concerns |
| Tian et al., 2023 | Confounding | Some concerns |
| Vasiliadis et al., 2019 | Confounding, exposure measurement | Some concerns |
| Zhang et al., 2020 | Confounding, exposure measurement, selection of participants, missing data, outcome measurement | Some concerns |
| Zhou et al., 2014 | Confounding, exposure measurement, selection of participants | High |
NOTE: Overall risk of bias is based on seven domains: (1) confounding; (2) measurement of the exposure; (3) selection of participants into the study (or into the analysis); (4) post-exposure interventions; (5) missing data; (6) measurement of the outcome; and (7) selection of the reported results.
SOURCE: Adapted from Annex I-6 in Appendix I, Academy of Nutrition and Dietetics, 2024.
| Certainty Assessment | ||||||
|---|---|---|---|---|---|---|
| Participants (Studies) Follow-up | Risk of Bias | Inconsistency | Indirectness | Imprecision | Publication Bias | Overall Certainty of Evidence |
| Dementia Moderate Alcohol Consumption vs. Never Consuming Alcohol—not reported | ||||||
| NR | NR | NR | NR | NR | NR | NR |
| Dementia Above Moderate Alcohol Consumption vs. Never Consuming Alcohol | ||||||
| 6,798 (1 nonrandomized study)e | seriousa | not serious | not serious | very seriousc | none | veryd low |
| Dementia Consuming Higher vs. Lower Amounts of Moderate Alcohol Consumption | ||||||
| 9,122 (2 nonrandomized studies)f | seriousa | not serious | not serious | seriousc | none | low |
| Dementia Consuming Alcohol Above Moderate vs. Lower Amounts of Moderate Alcohol Consumption | ||||||
| 6,742 (2 nonrandomized studies)g | seriousa | seriousb | not serious | seriousc | none | veryd low |
| Alzheimer’s Disease Moderate Alcohol Consumption vs. Never Consuming | ||||||
| 193,068 (2 nonrandomized studies)h | seriousa | not serious | not serious | seriousc | none | low |
| Alzheimer’s Disease Above Moderate Alcohol Consumption vs. Never Consuming | ||||||
| 146,288 (2 nonrandomized studies)h | seriousa | not serious | not serious | seriousc | none | low |
| Alzheimer’s Disease Among Alcohol Consumers | ||||||
| 291,200 (2 nonrandomized studies)h | seriousa | seriousd | not serious | seriouse | none | veryd low |
NOTE: NR = not reported.
a Some concerns/high risk of bias in most included studies.
b High heterogeneity in results between studies.
c Wide confidence interval include potential benefits and harms.
d The committee used the phrase “insufficient evidence” to reflect a lower level of certainty of the evidence, as indicated by the assignment of “very low” in the commissioned systematic reviews by the Academy of Nutrition and Dietetics.
f Handing et al., 2015; Koch et al., 2019.
g Koch et al., 2019; Shimizu et al., 2023.
h Larsson and Wolk, 2018; Tian et al., 2023.
SOURCE: Adapted from Table I-2 in Appendix I, Academy of Nutrition and Dietetics, 2024.
| Study and Drinking Frequency Category | Events/Total Sample | Reported Data HR (95% CI) |
|---|---|---|
| Jeon et al., 2023 | ||
| Stopped drinking | 6,153/25,3643 | 1.27 [1.23, 1.32] |
| Sustained mild drinking (<15 g/d) | 6,690/625,723 | 1.00 [reference] |
| Increased to moderate drinking (15.0–29.9 g/d) | 1,471/130,116 | 1.09 [1.03, 1.15] |
| Increased to heavy (≥30 g/d) | 767/39,096 | 1.37 [1.27, 1.47] |
| Koch et al., 2019 | ||
| <1 drink/week | 36/274 | 1.00 [reference] |
| 1–6 drinks/week, 1 drink/d | 24/215 | 0.93 [0.55, 1.57] |
| 1–6 drinks/week, ≥2 drinks/d | 14/85 | 1.54 [0.82, 2.90] |
| 7 drinks/week, 1 drink/d | 23/240 | 0.69 [0.40, 1.19] |
| 7 drinks/week, ≥2 drinks/d | 28/255 | 1.03 [0.61, 1.71] |
| Langballe et al., 2015 | ||
| Occasional (drinking 0× in last 2 weeks, no abstainers) | 529/18,900 | 1.12 [0.95, 1.32] |
| Drinking 1–4× in last 2 weeks | 242/11,182 | 1.00 [reference] |
| Drinking ≥5× in last 2 weeks | 69/2,400 | 1.40 [1.07, 1.84] |
| Sabia et al., 2018 | ||
| Long-term abstinence | 74/837 | 1.67 [1.26, 2.23] |
| Decreased consumption | 36/500 | 1.50 [1.04, 2.16] |
| Increased consumption | 28/1,004 | 0.85 [0.57, 1.26] |
| Long-term consumption 1–14 units/week | 207/5,304 | 1.00 [reference] |
| Long-term consumption >14 units/week | 51/1,282 | 1.36 [0.99, 1.88] |
| Shimizu et al., 2023 | ||
| Long-term abstinence | 2,319/18,102 | 1.61 [1.28, 20.3] |
| Regular drinking over time, <75 g/week | 77/1,381 | 1.00 [reference] |
| Regular drinking over time, 75–150 g/week | 150/1,973 | 1.34 [1.02, 1.77] |
| Regular drinking over time, 150–300 g/week | 314/3,782 | 1.37 [1.06, 1.76] |
| Regular drinking over time, 300–450 g/week | 227/2,938 | 1.41 [1.08, 1.84] |
| Regular drinking over time, ≥450 g/week | 174/2,142 | 1.96 [1.49, 2.59] |
| Study and Drinking Frequency Category | Events/Total Sample | Reported Data HR (95% CI) |
|---|---|---|
| Zhou et al., 2014 | ||
| Occasional drinking | 91/765 | NR |
| Monthly drinking | 51/491 | NR |
| Weekly drinking | 41/402 | NR |
| Daily drinking | 174/1,301 | NR |
NOTES: CI = confidence interval; d = day; g = grams; HR = hazard ratio; NR = not reported.
SOURCE: Table I-4 in Appendix I, American Academy of Nutrition and Dietetics, 2024.
the reference group, which comprised participants who reported drinking alcohol 1–4 times in the last 2 weeks (HR = 1.4, 95%CI [1.07, 1.84]) even after adjusting for age, sex, education, obesity, smoking, and symptoms of depression.
Shimizu et al. (2023) examined alcohol consumption patterns among Japanese adults aged 54–84 years old and found a linear association of weekly regular alcohol consumption with risk for developing dementia. Specifically, regular weekly alcohol consumption of >75–150 grams (5.3–10.7 U.S. drinks/week; (HR = 1.34, 95%CI [1.02, 1.77]) and 150–200 grams (10.7–14.3 U.S. drinks/week; (HR = 1.37, 95%CI [1.06, 1.76]), 300–450 grams (14.3–32.1 U.S. drinks/week; (HR = 1.41, 95%CI [1.08, 1.84]), and ≥450 grams (>32.1 U.S. drinks/week; (HR = 1.96, 95%CI [1.49, 2.59]) were all associated with higher risk for incidence of dementia compared with the reference group who regularly consumed <75 grams alcohol/week (<5.3 U.S. drinks/week). Because their consumption levels were not determined on a per day basis, it is uncertain how these intakes correspond to the DGA recommendations.
By contrast, Sabia et al. (2018) examined alcohol consumption changes from midlife (mean 44.8 years of age) to early old age (mean 61.2 years of age) and its association with dementia risk and found that individuals who maintained long-term abstinence (HR = 1.67, 95%CI [1.26, 2.23]) or decreased their alcohol consumption (HR = 1.50, 95%CI [1.04, 2.16]) had a higher risk of dementia compared to individuals who maintained long-term moderate consumption of 1–14 units/week (0.08–1.14 U.S. drinks/day). The reasons for decreasing alcohol consumption were not provided and could be related to issues related to health or activities of daily living.
Koch et al. (2019) observed a nonsignificant nonlinear relationship (quadratic trend p = 0.07) between greater alcohol consumption and higher dementia risk in people who consumed alcohol. Among those without mild cognitive impairment at baseline, the lowest risk was associated with 1.4 U.S. drinks/day.
Zhao et al. (2023) used sensitivity analysis to compare moderate alcohol consumption of 0.09–1.7 U.S. drinks/day to low alcohol consumption <0.09 U.S. drinks/day and found a greater risk of dementia in the moderate drinking group (HR = 1.10, 95%CI [1.02, 1.18]).
Finally, Kawakami et al. (2023) followed people (age 40 to 70 years for 8 years) who never consumed alcohol (reference) and those who drank moderately. Compared with never drinkers, people who drank at moderate levels (1.0–21.2 grams/day, >0–1.5 U.S. drinks/day) had a lower risk of expressing dementia (HR = 0.69, 95%CI [0.49, 0.98]). Given the consumption ranges for the total group of men and women, it is unclear whether the women’s consumption was moderate (Table 7-4).
Finding 7-1: Four eligible studies with data from 2010 to 2024 reported that the risk of developing dementia was higher among those consuming higher amounts of moderate alcohol than lower amounts of
| Category | N Studies | RR (95% CI) | I2 (%) |
|---|---|---|---|
| Main Analysisa | |||
| Moderate Alcohol Consumptionb | 2 | 0.98 [0.92, 1.04] | 0 |
| Above Moderate Alcohol Consumption | 2 | 1.18 [0.83, 1.69] | 53.4 |
| Sensitivity Analyses with Different Alcohol Intake Categoriesa | |||
| Five Categories (U.S. drinks/day) | |||
| <0.09 | – | 0 | 0 |
| 0.09–1.7 (0.1–1.7 vs. <0.8 U.S. drinks/day) | 3 | 1.10 [1.02, 1.18]c | 0.01 |
| 1.7–3.1 (1.5–3.1 vs. <0.8 U.S. drinks/day) | 1 | 1.01 [0.85, 1.20] | N/A |
| 3.2–4.6 (3.1–4.6 vs. <0.77 U.S. drinks/day) | 1 | 1.13 [0.95, 1.35] | N/A |
| >4.6 (≥4.6 vs. 0.8 U.S. drinks/day) | 1 | 1.34 [1.12, 1.60] | N/A |
| 1 U.S. Drink/Day (Males and Females) | |||
| ≤1 drink/day (0.14–1.0 vs. <0.1) | 2 | 0.98 [0.92, 1.04] | 0 |
| >1 drink/day (>1.14 vs. <1.14) | 4 | 1.18 [1.05, 1.34] | 20.2 |
NOTES: A dash indicates that there were no studies available for this comparison. Results in bold are statistically significant (p < 0.05). CI = confidence interval; I2 = heterogeneity; N = number; N/A = not available; RR = relative risk.
a Meta-analyses of drinking categories were conducted using separate meta-analyses to avoid over-counting participants in comparison groups.
b Moderate alcohol consumption levels are ≤1 drink/day for women and ≤2 drinks/day for men. 1 U.S. drink = 14 grams of alcohol.
c Results in bold are statistically significant (p < 0.05).
SOURCE: Adapted from Table I-3 in Appendix I, Academy of Nutrition and Dietetics, 2024.
moderate alcohol. One study reported that, when compared with long-term moderate consumers, long-term abstinence or decreasing consumption from midlife to older age was associated with higher risk of dementia. Two studies reported that moderate drinkers had a lower risk of developing dementia than never drinkers, and one study found no association between moderate consumption levels of alcohol and the development of dementia.
Conclusion 7-1: The committee concludes there was insufficient evidence about the association between the risk of dementia for those with no alcohol consumption compared to those with moderate alcohol consumption or for those who consume higher versus lower amounts of moderate alcohol.
Alzheimer’s Disease
Three cohort studies reported on associations between moderate alcohol consumption versus never drinking and the development of Alzheimer’s disease (AD) (Koch et al., 2019; Larsson and Wolk, 2018; Tian et al., 2023) (Table 7-5). Tian et al. (2023) reviewed death certificates that indicated AD as a contributing cause of death but did not find a significantly greater risk of AD in moderate drinkers than nondrinkers even after stratifying by sex, age, or smoking. One exception was for white women (0.4 to ≤1.0 U.S. drink/day) whose risk of developing AD was lower in moderate drinkers than in nondrinkers (HR = 0.77, 95%CI [0.64, 0.93]). In contrast to the Tian study, Larsson and Wolk (2018) failed to find significant associations between risk for AD and moderate alcohol consumption. Forest plots (Figure 7-2) indicated high heterogeneity in the two studies and the absence of robust risk ratios linking AD with moderate drinking. Koch et al. (2019) assessed cognitive status and risk for AD in older adults using the Alzheimer’s Disease Assessment Scale (ADAS). This study found no difference in risk of AD in people who consumed 1–6 drinks/week and no more than 1.0 U.S. drinks/day (HR = 0.95, 95%CI [0.57, 1.58]) or 7 drinks/week at no more than 1.0 U.S. drinks/day (HR = 0.93, 95%CI [0.58, 1.51]), as compared with those consuming <1 drink/week (reference group). However, these confidence intervals are quite wide.
Three additional cohort studies examined the association of alcohol consumption stratified as higher or lower level of moderate alcohol consumption and the risk of developing AD (Jeon et al., 2023, Langballe et al., 2015; Zhou et al., 2014) (Table 7-6). Jeon et al. (2023) evaluated changes in alcohol consumption patterns among adults aged 40 years and older residing in Korea. Results indicated that individuals who increased their alcohol consumption to moderate drinking (15–29 grams/day or
NOTES: CI = confidence interval; REML = restricted maximum likelihood; RR = relative risk.
SOURCE: Figure I-4 in Appendix I, American Academy of Nutrition and Dietetics, 2024.
1.07–2.07 U.S. drinks/day; (HR = 1.10, 95%CI [1.03, 1.18]) or heavy drinking (≥30 grams/day or 2.14 U.S. drinks/day; (HR = 1.37, 95%CI [1.25, 1.49]) compared to those who sustained mild drinking (<15 grams/day or <1.07 U.S. drinks/day; reference) over time exhibited higher risk of AD (Table 7-5). Stratified analysis by age, sex, and smoking status were consistent with the above findings.
Langballe et al. (2015) evaluated the association between alcohol consumption patterns and risk of dementia in Norwegian adults enrolled in the HUNT1 cohort. In contrast to individuals who refrained from drinking or drank rarely and did not have a significant AD risk, individuals who consumed alcohol frequently (≥5 times in last 2 weeks) had a significant AD risk (HR = 1.47, 95%CI [1.00, 2.16]) even after adjusting for age, sex, education, obesity, smoking, and symptoms of depression.
Zhou et al. (2014) evaluated the association of alcohol consumption of 0.09–1.7 U.S. drinks/day to never consuming alcohol and risk of AD in China. Men who consumed alcohol daily had a higher risk of developing AD (HR = 2.25, 95%CI [1.43, 3.97]) than those who drank weekly
| Category | N Studies | RR (95% CI) | I2 (%) |
|---|---|---|---|
| Main Analysisa | |||
| Moderate Alcohol Consumptionb | 2 | 0.94 [0.86, 1.03] | 0 |
| Above Moderate Alcohol Consumption | 2 | 0.77 [0.56, 1.07] | 45.5 |
| Subgroup Analysesa | |||
| Moderate Alcohol Consumption | |||
| Males | 2 | 0.97 [0.82, 1.15] | 0 |
| Females | 2 | 0.88 [0.70, 1.11] | 63.2 |
| Above Moderate Alcohol Consumption | |||
| Males | 2 | 0.82 [0.45, 1.49] | 69.7 |
| Females | 2 | 0.68 [0.47, 0.97]c | 0 |
| Moderate Alcohol Consumption | |||
| <60 years | 1 | 0.87 [0.39, 1.94] | N/A |
| ≥60 years | 2 | 0.92 [0.80, 1.07] | 54.7 |
| Above Moderate Alcohol Consumption | |||
| <60 years | 1 | 0.14 [0.02, 1.01] | N/A |
| ≥60 years | 2 | 0.83 [0.59, 1.17] | 48.4 |
| Sensitivity Analyses with Different Alcohol Consumption Categoriesa | |||
| Five Categories (U.S. drinks/day) | |||
| <0.09 | 2 | 0.89 [0.66, 1.20] | 90.3 |
| 0.09–1.7 | 2 | 0.93 [0.80, 1.00] | 0 |
| 1.7–3.1 | 1 | 0.94 [0.74, 1.19] | N/A |
| 3.2–4.6 | – | – | – |
| >4.6 | – | – | – |
| 1 U.S. Drink/Day (Males and Females) | |||
| ≤1 drink/day | 2 | 0.97 [0.89, 1.06] | 0 |
| >1 drink/day | 2 | 1.23 [0.84, 1.80] | 82.5 |
NOTES: A dash indicates that there were no studies available for this comparison. Results in bold are statistically significant (p < 0.05). CI = confidence interval; I2 = heterogeneity; N = number; N/A = not available; RR = relative risk.
a Meta-analyses of drinking categories were conducted using separate meta-analyses to avoid over-counting participants in comparison groups.
b Moderate alcohol levels are ≤1 drink/day for women and ≤2 drinks/day for men. 1 U.S. drink = 14 grams of alcohol.
c Results in bold are statistically significant (p < 0.05).
SOURCE: Adapted from Table I-5 in Appendix I, Academy of Nutrition and Dietetics, 2024.
(HR = 1.31, 95%CI [0.69, 1.43]), monthly (HR = 1.03, 95%CI [0.83, 1.35]), or occasionally (Table 7-6). However, it is uncertain how these drinking patterns relate to the DGA because consumption per drinking occasion was not presented.
Finding 7-2: On the basis of six eligible studies with data from 2010 to 2024, the committee found the risk of AD or dementia among those who consumed higher amounts of moderate alcohol versus lower amounts was inconsistent.
| Study and Drinking Frequency Category | Events/Total Sample | Reported Data HR (95% CI) |
|---|---|---|
| Jeon et al., 2023 | ||
| Stopped drinking | NR | 1.26 [1.20, 1.31] |
| Sustained mild drinking (<15 g/d) | NR | 1.00 [reference] |
| Increased to moderate drinking (15–29.9 g/d) | NR | 1.1 [1.03, 1.18] |
| Increased to heavy (≥30 g/d) | NR | 1.37 [1.25, 1.49] |
| Koch et al., 2019 | ||
| <1 drink/week | 38/NR | 1.00 [reference] |
| 1–6 drinks/week, 1 drink/day | 26/NR | 0.95 [0.57, 1.58] |
| 1–6 drinks/week, ≥2 drinks/day | 12/NR | 1.04 [0.53, 2.02] |
| 7 drinks/week, 1 drink/day | 33/NR | 0.93 [0.58, 1.51] |
| 7 drinks/week, ≥2 drinks/day | 29/NR | 1.02 [0.62, 1.69] |
| Langballe et al., 2015 | ||
| Occasional (drinking 0× in last 2 weeks, | NR | 1.2 [0.96, 1.51] |
| no abstainers) | ||
| Drinking 1–4× in last 2 weeks | NR | 1.00 [reference] |
| Drinking ≥5× in last 2 weeks | NR | 1.47 [1.00, 2.16] |
| Zhou et al., 2014 (all men) | ||
| Occasional drinking | 38/765 | 1.00 [reference] |
| Monthly drinking | 25/491 | 1.03 [0.83, 1.35] |
| Weekly drinking | 18/402 | 1.31 [0.69, 1.43] |
| Daily drinking | 91/1,301 | 2.25 [1.43, 3.97] |
NOTES: CI = confidence interval; d = day; g = grams; HR = hazard ratio; NR = not reported.
SOURCE: Adapted from Table I-6 in Appendix I, American Academy of Nutrition and Dietetics, 2024.
Conclusion 7-2: The committee concludes there was insufficient evidence regarding the association between amounts of moderate alcohol consumption and the risk of developing Alzheimer’s disease.
Cognitive Decline
Heterogeneity among comparison groups and lack of reported data necessary for pooled analysis precluded conducting meta-analysis for this systematic review of the outcomes on immediate and delayed word recall, verbal frequency, Mini-Mental State Examination (MMSE), or other tests of general cognitive ability. Consequently, the results are reported in tables with a narrative synthesis. Quality of studies are presented in figures, tables, and text. Many were listed as having risk of bias and low certainty of evidence (Table 7-7, Table 7-8, and Table 7-9). Unless noted, the 95% CIs for the HRs or relative risk ratios were wide and crossed below and above 1.0.
Two cohort studies (Sabia et al., 2014 and Tian et al., 2022) reported on immediate recall of words. Neither study found robust performance differences between individuals who regularly consumed alcohol within or just above moderate alcohol consumption and those who were never or occasional drinkers (Table 7-6). Sabia et al. (2014) and Horvat et al. (2015) tested differences between people who drank moderately and those who drank infrequently and at lower levels (Table 7-7). Here, the CIs were too wide to draw conclusions about group differences in recall by drinking levels. The Horvat et al. (2015) study also examined frequency of drinking moderately and found that women, but not men, who drank 1–3 times/month showed improved immediate word recall not exhibited by women who drank less than once per month (HR = 0.08, 95%CI [0.03, 0.12]).
Of the two cohort studies reporting on delayed word recall, Love et al. (2020) found no significant differences in performance between people who drank and those who did not, whereas Tian et al. (2022) found that people who drank moderately had lower scores than those who did not drink (β = −0.04, 95%CI [−0.08, −0.01]). These studies had risk of bias, not having stratified for age, smoking, or race/ethnicity. Separate analysis by sex at birth in Horvat et al. (2015) failed to reveal associations between alcohol consumption levels and delayed word recall. Lack of association was also apparent in comparisons between low and moderate drinkers.
Combining immediate and delayed recall performance did not strengthen potential relations between memory scores and drinking levels in the studies by Cheng et al. (2023) and Garduno et al. (2023). By contrast, Zhang et al. (2020) found that people drinking moderately (<1.14 drinks/day women and <2.14 drinks/day men) achieved lower recall scores than their nondrinking counterparts (OR = 0.74, 95%CI [0.69, 0.80]).
TABLE 7-7 GRADE Evidence Profile Describing Relationship Between Amount of Alcohol Intake and Memory
| Certainty Assessment | ||||||
|---|---|---|---|---|---|---|
| Participants (Studies) | Risk of Bias | Inconsistency | Indirectness | Imprecision | Publication Bias | Overall Certainty of Evidence |
| Immediate Word Recall (Alcohol Consumers vs. Never Consumers) | ||||||
| 21,980 (2 studies)f | seriousa | seriousb | not serious | seriousc | none | verye low |
| Immediate Word Recall (Among Alcohol Consumers) | ||||||
| 16,774 (2 studies)g | seriousa | seriousb | not serious | seriousc | none | verye low |
| Delayed Word Recall (Alcohol Consumers vs. Never Consumers) | ||||||
| 7,917 (2 studies)h | very seriousd | seriousb | not serious | seriousc | none | verye low |
| Delayed Word Recall (Among Alcohol Consumers) | ||||||
| 6,608 (1 study)i | seriousa | not serious | not serious | seriousb | none | low |
| Combined Immediate and Delayed Word Recall (Alcohol Consumers vs. Never Consumers) | ||||||
| 24,275 (3 studies)j | very seriousd | not serious | not serious | seriousb | none | verye low |
| Combined Immediate and Delayed Word Recall (Among Alcohol Consumers) | ||||||
| 165,919 (2 studies)k | very seriousa | not serious | not serious | serious | none | low |
a Some concerns.
b Inconsistent results between studies.
c Lack of pooled results.
d High risk of bias.
e The committee used the phrase “insufficient evidence” to reflect a lower level of certainty of the evidence, as indicated by the assignment of “very low” in the commissioned systematic reviews by Academy of Nutrition and Dietetics.
f Sabia et al., 2014; Tian et al., 2022.
g Horvat et al., 2015; Sabia et al., 2014.
h Love et al., 2020; Tian et al., 2022.
j Cheng et al., 2023; Garduno et al., 2023; Zhang et al., 2020.
k Garduno et al., 2023; Nooyens et al., 2014.
SOURCE: Adapted from Table I-13 in Appendix I, Academy of Nutrition and Dietetics, 2024.
| Certainty Assessment | ||||||
|---|---|---|---|---|---|---|
| Participants (Studies) | Risk of Bias | Inconsistency | Indirectness | Imprecision | Publication Bias | Overall Certainty of Evidence |
| Verbal Fluency (Alcohol Consumers vs. Never Consumers) | ||||||
| 17,059 (3 studies)e | very seriousa | seriousb | not serious | seriousc | none | veryd low |
| Verbal Fluency (Among Alcohol Consumers) | ||||||
| 16,774 (3 studies)f | seriousa | seriousb | not serious | seriousc | none | veryd low |
a Some concerns for risk of bias.
b Inconsistency in results.
c Lack of pooled results.
d The committee used the phrase “insufficient evidence” to reflect a lower level of certainty of the evidence, as indicated by the assignment of “very low” in the commissioned systematic reviews by Academy of Nutrition and Dietetics.
e Cheng et al., 2023; Garduno et al., 2023; Han and Jia, 2021.
f Garduno et al., 2023; Han and Jia, 2021, 2022.
SOURCE: Adapted from Table I-16 in Appendix I, Academy of Nutrition and Dietetics, 2024.
| Certainty Assessment | ||||||
|---|---|---|---|---|---|---|
| Participants (Studies) | Risk of Bias | Inconsistency | Indirectness | Imprecision | Publication Bias | Overall Certainty of Evidence |
| Verbal Fluency (Alcohol Consumers vs. Never Consumers) | ||||||
| 5,367 (3 studies)f | very seriousa | not serious | not serious | seriousb | none | verye low |
| Verbal Fluency (Among Alcohol Consumers) | ||||||
| 4,102 (3 studies)g | seriousc | seriousd | not serious | seriousb | none | low |
a High risk of bias.
b Lack of pooled results.
c Some concerns.
d Inconsistency in results.
e The committee used the phrase “insufficient evidence” to reflect a lower level of certainty of the evidence, as indicated by the assignment of “very low” in the commissioned systematic reviews by Academy of Nutrition and Dietetics.
f Han and Jia, 2022; Lee et al., 2023; Salvador et al., 2022.
g Garduno et al., 2023; Han and Jia, 2021, 2022.
SOURCE: Adapted from Table I-19 in Appendix I, Academy of Nutrition and Dietetics, 2024.
Additional domains of cognitive decline beyond recall were also available to assess the association with moderate alcohol consumption. Absence of alcohol level and word fluency testing was not forthcoming in the four alcohol group comparisons (Garduno et al., 2023; Horvat et al., 2015; Love et al., 2020; Salvador et al., 2022). Three studies (Koch et al., 2019; Salvador et al., 2022; Vasiliadis et al., 2019) reported on the MMSE. None found significant associations between moderate alcohol consumption and MMSE performance.
Systematic review provided no consistent association between moderate drinking and cognitive decline in scores on episodic immediate or delayed memory tests, a test of general cognitive functioning (i.e., MMSE), or word fluency tests. With few exceptions, the findings held whether moderate drinkers were compared with no or occasional drinkers or with regular low drinkers. In general, the effect sizes were small, the confidence intervals were wide, and the quality of evidence was low.
Finding 7-3: On the basis of nine eligible studies with data from 2010 to 2024, there was insufficient evidence to support an association between moderate versus never drinking or occasional drinking and the risk of cognitive decline. There were concerns with the studies related to differences in measurement instruments, differences in comparator groups, and imprecise results.
Conclusion 7-3: The committee determined that there was insufficient evidence to draw an association between moderate alcohol consumption versus never or occasional consumption and the risk of cognitive decline.
Summary of Evidence Relative to Past DGA Guidance
Based on the results of the de novo systematic review using data from 2010 to 2024, the committee concludes there is insufficient evidence to evaluate the association of moderate alcohol consumption compared to never consuming alcohol for the outcomes of dementia, AD, and cognitive decline. Thus, there are no findings to compare with the 2010 DGAC report, which was the only past report to directly consider the association of moderate alcohol consumption and neurocognition.
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