Midlife Alcohol Consumption Research Articles

Sustained Hypothetical Interventions on Midlife Alcohol Consumption in Relation to All-Cause and Cancer Mortality: The Australian Longitudinal Study on Women's Health.

No randomized controlled trial has evaluated the effect of long-term alcohol interventions on mortality. Results reported in existing observational studies may be subject to selection bias and time-varying confounding. Using data from the Australian Longitudinal Study on Women's Health 1946-1951 birth cohort, collected regularly from 1996-2016, we estimated all-cause and cancer mortality had women been assigned various alcohol interventions (in categories ranging from 0 to >30 g/day ethanol, or reduced to ≤20 g/day if higher) at baseline, and had they maintained these levels of consumption. The cumulative risks for all-cause and cancer mortality were 5.6% (10,118 women followed for 20 years) and 2.9% (18 years), respectively. For all-cause and cancer mortality, baseline ethanol up to 30 g/day showed lower risk and >30 g/day showed higher risk relative to abstention. Had women sustainedly followed the interventions, a similar relationship was observed for all-cause mortality. However, the negative association observed for intakes ≤30 g/day and positive association for intakes >30 g/day was not evident for cancer mortality. Our findings suggest that all-cause mortality could have been lower than observed if this cohort of women had consumed some alcohol (no more than 30 g/day) rather than no consumption, but cancer mortality might not.

Mid-life alcohol consumption and survival to age 90 in men: The Tromsø Study 1979-1980 with follow-up to 2019.

The Tromsø Study 1979-1980 collected information on alcohol (beer, wine and spirits) consumption frequency and inebriation frequency, and the oldest male participants (aged 50-54 years) were followed for all-cause mortality. This study aimed to identify the impact of habitual alcohol consumption in mid-life on reaching up to 90 years of age. Among the study sample of 778, a total of 120 (15.4%) men reached the age of 90. The most common reported alcohol consumption frequency was 'never or a few times a year', and 18.9% of those in this group reached 90 compared with 11.9% of those who reported a more frequent beer consumption. Fifty per cent survival in these groups was 80.5 and 76.9 years, respectively. The pattern was similar for spirits consumption and for inebriation but not for wine consumption. Number of deaths increased gradually with increasing beer and spirits consumption frequency and with inebriation frequency. We observed no J-shape or pattern that revealed a beneficial influence of light alcohol consumption. Daily smoking, physical inactivity, marital status, blood pressure and total cholesterol reduced the contribution of alcohol consumption to a small degree. This study shows that all beer and spirits consumption frequencies in mid-life affect later life and total lifespan. Refraining from alcohol consumption or drinking only a few times a year increases one's chances of living longer, and the chance of reaching 90 years of age is 1.6-fold higher than in those with more frequent alcohol consumption.

Midlife alcohol consumption and later life cognitive impairment: Light drinking is not protective and APOE genotype does not change this relationship.

IntroductionMuch debate exists about the role of light to moderate alcohol intake and subsequent cognitive function. The apolipoprotein E genotype may modify the relationship.MethodsUsing data from the Honolulu-Asia Aging Study, a longitudinal population-based cohort (n = 2,416), Cox proportional hazards regression analyses were performed to measure midlife alcohol intake (average age = 52 years) and later life cognitive function (average age = 87 years) and to explore the role of apolipoprotein E genotype.ResultsNo protective effect of light drinking (>1 drink/month– 1 drink/day) or moderate drinking (>1–2 drinks/day) was observed in the cohort in adjusted models (HR = 1.013, CI:0.88–1.16; HR = 1.104, CI:0.91–1.34, respectively). Heavy drinking (>2–4 drinks/day) and very heavy drinking (>4 drinks/day) increased the risk for incident moderate cognitive impairment (HR = 1.355, CI:1.09–1.68; HR = 1.462, CI:1.04–2.05, respectively). When examining the relationship by apolipoprotein E ε4 carrier status, a similar dose-response pattern was observed in both groups with higher hazard ratios for those carrying at least one copy of the apolipoprotein E ℇ4 allele. As alcohol level increased, the age at incident moderate cognitive impairment decreased, especially among those with at least one apolipoprotein E ℇ4 allele.DiscussionWe did not observe a significant protective effect for light to moderate drinking in midlife and subsequent cognitive impairment in this cohort. Heavy drinking increased the risk for moderate cognitive impairment and decreased the age at incidence, as did carrying at least one allele of the apolipoprotein E ℇ4 gene.

Methods used in 'ALDH2*2 association with longevity and reduced risk of cognitive decline in Japanese-American men'

ALDH2*2 is a loss of function mutation common in East Asian populations associated with facial flushing on exposure to alcohol and increased risk of certain cancers. Conversely, absence of the ALDH2*2 mutation is associated with increased risk of hypertension and cerebral microbleeds, and two recent studies report a higher frequency of ALDH2*2 alleles in nonagenarians compared to population control samples. We used survival analysis to investigate the association between ALDH2*2 and risk of cognitive impairment and death after controlling for midlife alcohol consumption and other covariates. Participants are 621 Japanese-American men (72 to 92) enrolled in the Honolulu Asia Aging Study (HAAS) and assessed for cognitive impairment for up to 20 years. Impairment was defined as crossing below a threshold score of 74 on the Cognitive Assessment Screening Instrument (CASI). Age at death was determined by Hawaii state death certificate. Ounces of ethyl alcohol consumed per month was assessed by structured interview (number, frequency, and type of beverage) conducted 25 years prior to baseline cognitive assessment. Persons heterozygous for the ALDH2*2 variant have reduced risk of cognitive impairment and reduced risk of death, compared to homozygote non-carriers. Covarying by alcohol exposure had no effect on observed associations. This study replicates previous findings associating ALDH2*2 with longevity, and provides evidence the protective effect extends to cognition. This poster details the statistical analysis carried out to obtain these results.

Association between alcohol consumption in midlife and cognitive function in old age: Findings from the China health and Nutrition Survey

Background and aimsAlcohol consumption has been reported to impair the physical and mental health of the elderly. This study aimed to explore the association between alcohol consumption patterns in midlife and cognition in the elderly among the Chinese population. Methods and resultsStudy subjects were individuals aged ≥45 years in the shared database of the China Health and Nutrition Survey in 1997, who were followed up in 2006. A questionnaire was used to collect information about alcohol consumption (frequency, amount and type). Alcohol consumption (grams/week) was classified into none, light (≤84), light-to-moderate (84.01–168), moderate-to-heavy (168.01–336) and heavy (≥336.01) categories in men, and none, light (<42) and moderate (≥42) categories in women. Cognitive function was measured in 2006 using a subset of items from the modified Telephone Interview for Cognitive Status. The lowest quintile was used as the cut-off point for cognitive impairment. A multivariate logistic regression model was applied. The study involved 1926 participants with a mean age of 56.91 years, and men accounted for 51.66% of the total participants. Drinking behaviours and cognitive scores had significant sexual difference (P < 0.001). Cognitive impairment was identified in 135 men and 237 women. Compared with light drinking, heavy drinking and non-drinking were associated with cognitive impairment in men [adjusted odds ratio (aOR) and 95% CI were 2.19 (1.59–3.00), 1.54 (1.21–1.96), respectively; P < 0.001]. Compared with light drinkers, female non-drinkers and moderate drinkers were associated with cognitive impairment [aOR and 95% CI were 1.54 (1.16–2.03) and 1.75 (1.08–2.85), respectively; P < 0.001]. ConclusionsScientific evidence on the adverse effects of heavy drinking on elderly cognition and the possibly protective effects of light drinking could influence policy decisions on alcohol consumption in China.

Midlife alcohol consumption and longitudinal brain atrophy: the PREVENT-Dementia study

Background and aimsConsensus is lacking on whether light to moderate consumption of alcohol compared to abstinence is neuroprotective. In this study, we investigated the relationship between self-reported alcohol use and brain volume change over 2 years in middle-aged subjects.MethodsA sample of 162 subjects (aged 40–59 at baseline) from the PREVENT-Dementia programme underwent MRI scans on two separate occasions (mean interval 734 days; SD 42 days). We measured longitudinal rates of brain atrophy using the FSL Siena toolbox, and change in hippocampal volume from segmentation in SPM.ResultsControlling for age and sex, there were no significant associations of either total brain, ventricular, or hippocampal volume change with alcohol consumption. Adjusting for lifestyle, demographic and vascular risk factors did not alter this.ConclusionsWe did not find any evidence of influence of alcohol consumption on changes in brain volume over a 2-year period in 40–60-year-olds.

HEAVY ALCOHOL CONSUMPTION IN MIDLIFE IS ASSOCIATED WITH ACCELERATED BRAIN AGING SIX YEARS LATER

Excessive alcohol consumption is associated with cognitive decline, exacerbated brain atrophy, and dementia in older adults, but associations with midlife brain health are less well understood. We hypothesized that heavy drinkers would have older-looking brains in late midlife. We examined alcohol consumption at mean age 56 (range 51-59) in 364 men from the Vietnam Era Twin Study of Aging (VETSA) and their predicted brain age at mean age 62 (range 56-67). We created five midlife alcohol consumption groups based on drinks consumed over the past two weeks: never, former, light (1-14), moderate (15-28), and heavy (>28). Participants underwent structural magnetic resonance imaging at mean age 62. Predicted brain age was measured using the Brain-Age Regression Analysis and Computation Utility software (BARACUS). Models adjusted for age, scanner, race/ethnicity, SES, smoking, health, depressive symptoms, alcohol dependence, general cognitive ability at age 20, and non-independence of twins within pairs. Heavy drinkers had a significantly older predicted than chronological brain age (M= 5.93, SE= 0.88) compared to each of the other four groups (p’s < 0.05). There were no significant differences among the never (M= 2.88, SE= 0.98), former (M= 2.76, SE= 0.74), light (M= 3.00, SE= 0.94), or moderate (M= 5.93, SE= 0.88) consumption groups. Heavy alcohol consumption at age 56 was associated with an approximately 3-year greater predicted brain age difference at age 62. There was no evidence of protective effects of light/moderate drinking over non-drinking. The neurotoxic effects of excessive alcohol may exacerbate brain aging in late midlife.

Light Alcohol Consumption Does Not Protect Cognitive Function: A Longitudinal Prospective Study

Studies show that light to moderate alcohol consumption is related to better health and higher cognitive performance. However, it has been suggested that this association is caused by a systematic bias in the control group as many people abstain from drinking or quit because of health issues. Therefore, the group of non-drinkers is biased towards poor health and may not be suitable as a control group. The present study examined the effect of alcohol on cognitive performance while addressing this bias by excluding the non-drinkers. Thus, instead of comparing different levels of alcohol consumption to a non-drinking control group, a dose-response association was calculated between all levels of alcohol intake and cognitive performance. The study used information from a sample of people in the Swedish Twin Registry, who in their midlife (1967) participated in a survey on alcohol intake and 25 years later participated in a longitudinal study on cognitive aging (N = 486). The cognitive aging study took place on five occasions, at 2-year intervals, and included the Mini Mental State Examination (MMSE), tests of episodic memory, semantic memory and spatial ability. The association between midlife alcohol consumption and later cognitive performance was analyzed using growth curve models, adjusting for background variables. The findings showed that there was a significant negative dose-response association between alcohol intake in midlife and the MMSE, and the tests of episodic memory, such that higher intake in midlife was related to lower performance in old age. The associations between alcohol and semantic memory, and spatial ability respectively, were not significant. In contrast to findings from other studies, which show that low to moderate alcohol intake promotes cognitive function, the current study showed that alcohol intake was related to lower cognitive performance in a dose-response manner, even at low levels. The results from this study indicate that the observed benefits of moderate alcohol intake for cognitive function reported by others might be solely due to comparisons to an inappropriate control group, a group that is biased towards poor health. Hence, it is concluded that light alcohol intake may not protect cognitive function.

Alcohol consumption in midlife and old age and risk of frailty: Alcohol paradox in a 30-year follow-up study.

alcohol consumption has many harmful health effects, but also benefits of moderate consumption on frailty have been reported. We examined this relationship longitudinally from midlife to old age. data of reported alcohol consumption in midlife (year 1974) and in old age (years 2000 and 2003) were available of a socioeconomically homogenous sample of 2360 men (born 1919-34, the Helsinki Businessmen Study). Alcohol consumption was divided into zero (N = 131 at baseline), light (1-98 g/week, N = 920), moderate (99-196, N = 593), and high consumption (>196, n = 716). Incidence of phenotypic frailty and prefrailty was assessed in 2000 and 2003. Alcohol consumption (reference 1-98 g/week, adjusted for age, body mass index and smoking) was related to frailty both longitudinally (from 1974 to 2000, and from 2000 to 2003) and cross-sectionally in 2000 and 2003. during a 30-year follow-up, high consumption clearly decreased whereas lighter consumption remained stable. High consumption in midlife predicted both frailty (odds ratio = 1.61, 95% confidence interval = 1.01-2.56) and prefrailty (1.42; 1.06-1.92) in 2000, association with zero and moderate consumption was insignificant. Cross-sectionally in 2000, both zero (2.08; 1.17-3.68) and high consumption (1.83; 1.07-3.13) were associated with frailty, while in 2003 only zero consumption showed this association (2.47; 1.25-4.88). the relationship between alcohol and frailty is a paradox during the life course. High, not zero, consumption in midlife predicts old age frailty, while zero consumption in old age is associated with frailty, probably reflecting reverse causality.

Adverse Childhood Experiences and Alcohol Consumption in Midlife and Early Old-Age.

To examine the individual and cumulative effects of adverse childhood experiences (ACEs) on alcohol consumption in midlife and early old-age, and the role of ACEs in 10-year drinking trajectories across midlife. Data were from the Whitehall II study, a longitudinal British civil service-based cohort study (N = 7870, 69.5% male). Multinomial logistic regression was used to examine the individual and cumulative effects of ACEs on weekly alcohol consumption. Mixed-effect multilevel modelling was used to explore the relationship between ACEs and change in alcohol consumption longitudinally. Participants who were exposed to parental arguments/fights in childhood were 1.24 (95% CI 1.06, 1.45) times more likely to drink at hazardous levels in midlife (mean age 56 years) after controlling for covariates and other ACEs. For each additional exposure to an ACE, the risk of hazardous drinking versus moderate drinking was increased by 1.12 (95% CI 1.03, 1.21) after adjusting for sex, age, adult socio-economic status, ethnicity and marital status. No associations between ACEs and increased risk of hazardous drinking in early old-age (mean age 66 years) were found. In longitudinal analyses, ACEs did not significantly influence 10-year drinking trajectories across midlife. The effect of exposure to parental arguments on hazardous drinking persists into midlife.

Midlife Alcohol Consumption and the Risk of Stroke in the Atherosclerosis Risk in Communities Study.

Alcohol consumption is common in the United States and may confer beneficial cardiovascular effects at light-to-moderate doses. The alcohol-stroke relationship remains debated. We estimated the relationship between midlife, self-reported alcohol consumption and ischemic stroke and intracerebral hemorrhage (ICH) in a biracial cohort. We examined 12,433 never and current drinkers in the Atherosclerosis Risk in Communities study, aged 45 to 64 years at baseline. Participants self-reported usual drinks per week of beer, wine, and liquor at baseline. We used multivariate Cox proportional hazards regression to assess the association of current alcohol consumption relative to lifetime abstention with incident ischemic stroke and ICH and modification by sex-race group. We modeled alcohol intake with quadratic splines to further assess dose-response relationships. One third of participants self-reported abstention, 39% and 24%, respectively, consumed ≤3 and 4 to 17 drinks/wk, and only 5% reported heavier drinking. There were 773 ischemic strokes and 81 ICH over follow-up (median≈22.6 years). For ischemic stroke, light and moderate alcohol consumption were not associated with incidence (hazard ratios, 0.98; 95% CI, 0.79-1.21; 1.06, 0.84-1.34), whereas heavier drinking was associated with a 31% increased rate relative to abstention (hazard ratios, 1.31; 95% CI, 0.92-1.86). For ICH, moderate-to-heavy (hazard ratios, 1.99; 95% CI, 1.07-3.70), but not light, consumption increased incidence. Self-reported light-to-moderate alcohol consumption at midlife was not associated with reduced stroke risk compared with abstention over 20 years of follow-up in the Atherosclerosis Risk in Communities study. Heavier consumption increased the risk for both outcomes as did moderate intake for ICH.

Midlife Alcohol Consumption and Risk of Dementia Over 43 Years of Follow-Up: A Population-Based Study From the Swedish Twin Registry.

Midlife alcohol consumption (beer, wine, and spirits) was examined in relation to dementia incidence over 43 years. Participants were 12,326 members of the population-based Swedish Twin Registry born during 1907-1925 who responded to items about alcohol consumption in 1967/1970, subsequently classified as nondrinking (0 grams of ethanol per day), light (1-5g/d), moderate (5-12g/d), heavy (12-24g/d), and very heavy (>24g/d) drinking. Dementia was identified from the National Patient and Cause of Death Registries. Cox proportional hazard models adjusted for cluster-correlated data were used in cohort analyses. Conditional logistic regression (dementia-discordant pairs) and mixed effects models (dementia-concordant pairs) were used in twin analyses. Overall, nondrinkers did not differ from light drinkers in dementia risk. Heavy drinking (hazard ratio = 1.10, p = .028) and very heavy drinking (hazard ratio = 1.18, p = .033) were associated with increased dementia risk controlling for sociodemographic, lifestyle, and cardiovascular factors. More alcohol from spirits was related to increased risk of dementia, whereas more alcohol from wine with decreased risk, although the association for wine reversed direction at high amounts. Relative to co-twins drinking light amounts, moderate-to-heavy drinking twins had (a) greater risk of dementia by 57% (p = .006, 300% in monozygotic pairs only) and (b) reduced time to dementia by 4.76 years (p = .019, 4.78 years in monozygotic pairs only). Averaging more than 12 grams of alcohol per day may increase risk of dementia. Alcohol from spirits appears particularly important for the increased dementia risk. Genetic and/or familial factors do not explain these associations. Alcohol use reduction may be a useful population-wide intervention strategy.

Alcohol consumption at midlife and risk of stroke during 43 years of follow-up: cohort and twin analyses.

Although alcohol-stroke association is well known, the age-varying effect of alcohol drinking at midlife on subsequent stroke risk across older adulthood has not been examined. The effect of genetic/early-life factors is also unknown. We used cohort and twin analyses of data with 43 years of follow-up for stroke incidence to help address these gaps. All 11 644 members of the population-based Swedish Twin Registry born 1886 to 1925 with alcohol data aged ≤60 years were included. The interaction of midlife alcohol consumption by age at stroke was evaluated in Cox-regression and analyses of monozygotic twins were used. Covariates were baseline age, sex, cardiovascular diseases, diabetes mellitus, stress reactivity, depression, body mass index, smoking, and exercise. Altogether 29% participants developed stroke. Compared with very-light drinkers (<0.5 drink/d), heavy drinkers (>2 drinks/d) had greater risk of stroke (hazard ratio, 1.34; P=0.02) and the effect for nondrinkers approached significance (hazard ratio, 1.11; P=0.08). Age increased stroke risk for nondrinkers (P=0.012) and decreased it for heavy drinkers (P=0.040). Midlife heavy drinkers were at high risk from baseline until the age of 75 years when hypertension and diabetes mellitus grew to being the more relevant risk factors. In analyses of monozygotic twin-pairs, heavy drinking shortened time to stroke by 5 years (P=0.04). Stroke-risk associated with heavy drinking (>2 drinks/d) in midlife seems to predominate over well-known risk factors, hypertension and diabetes, until the age of ≈75 years and may shorten time to stroke by 5 years above and beyond covariates and genetic/early-life factors. Alcohol consumption should be considered an age-varying risk factor for stroke.

Midlife Alcohol Consumption and the Risk of Stroke in the Atherosclerosis Risk in Communities Study

Midlife Alcohol Consumption and the Risk of Stroke in the Atherosclerosis Risk in Communities Study

Alcohol consumption and cognitive decline in early old age

Objective:To examine the association between alcohol consumption in midlife and subsequent cognitive decline.Methods:Data are from 5,054 men and 2,099 women from the Whitehall II cohort study with a mean age of 56 years (range 44–69 years) at first cognitive assessment. Alcohol consumption was assessed 3 times in the 10 years preceding the first cognitive assessment (1997–1999). Cognitive tests were repeated in 2002–2004 and 2007–2009. The cognitive test battery included 4 tests assessing memory and executive function; a global cognitive score summarized performances across these tests. Linear mixed models were used to assess the association between alcohol consumption and cognitive decline, expressed as z scores (mean = 0, SD = 1).Results:In men, there were no differences in cognitive decline among alcohol abstainers, quitters, and light or moderate alcohol drinkers (<20 g/d). However, alcohol consumption ≥36 g/d was associated with faster decline in all cognitive domains compared with consumption between 0.1 and 19.9 g/d: mean difference (95% confidence interval) in 10-year decline in the global cognitive score = −0.10 (−0.16, −0.04), executive function = −0.06 (−0.12, 0.00), and memory = −0.16 (−0.26, −0.05). In women, compared with those drinking 0.1 to 9.9 g/d of alcohol, 10-year abstainers showed faster decline in the global cognitive score (−0.21 [−0.37, −0.04]) and executive function (−0.17 [−0.32, −0.01]).Conclusions:Excessive alcohol consumption in men (≥36 g/d) was associated with faster cognitive decline compared with light to moderate alcohol consumption.

The Relationship Between Midlife and Late Life Alcohol Consumption, APOE e4 and the Decline in Learning and Memory Among Older Adults

The aim of the study was to determine whether the trajectory of learning and memory is modified according to an interaction between midlife or late life alcohol consumption status and the presence of one or more APOE e4 alleles. This was a secondary analysis of cognitive, genetic and alcohol consumption data collected from members of the Framingham Heart Study Offspring Cohort. Light and moderate alcohol consumption during late life was associated with greater decline in learning and memory among APOE e4 carriers, whereas light and moderate alcohol consumption was associated with an increase in learning and memory among non-APOE e4 carriers. There was not a significant interaction between midlife alcohol consumption status and APOE e4 on the trajectory of learning and memory. Light to moderate alcohol consumption during late life may protect against a decline in learning and memory for non-APOE e4 allele carriers, but not for older adults who carry one or more APOE e4 alleles.

Alcohol consumption in midlife and cognitive performance assessed 13 years later in the SU.VI.MAX 2 cohort.

BackgroundAssociations between alcohol consumption and cognitive function are discordant and data focusing on midlife exposure are scarce.ObjectiveTo estimate the association between midlife alcohol consumption and cognitive performance assessed 13 y later while accounting for comorbidities and diet.Methods3,088 French middle-aged adults included in the SU.VI.MAX (1994) study with available neuropsychological evaluation 13 y later. Data on alcohol consumption were obtained from repeated 24h dietary records collected in 1994–1996. Cognitive performance was assessed in 2007–2009 via a battery of 6 neuropsychological tests. A composite score was built as the mean of the standardized individual test scores (mean = 50, SD = 10). ANCOVA were performed to estimate mean differences in cognitive performance and 95% confidence intervals (CI).ResultsIn women, abstainers displayed lower cognitive scores than did low-to-moderate alcohol drinkers (1 to 2 drinks/day) (mean difference = −1.77; 95% CI: −3.29, −0.25). In men, heavy drinkers (>3 drinks/day) had higher cognitive scores than did low-to-moderate (1 to 3 drinks/day) (mean difference = 1.05; 95% CI: 0.10, 1.99). However, a lower composite cognitive score was detected in male drinkers consuming ≥90 g/d (≈8 drinks/d). A higher proportion of alcohol intake from beer was also associated with lower cognitive scores. These associations remained significant after adjustment for diet, comorbidities and sociodemographic factors.ConclusionIn men, heavy but not extreme drinking was associated with higher global cognitive scores. Given the known harmful effects of alcohol even in low doses regarding risk of cancer, the study does not provide a basis for modifying current public health messages.Trial RegistrationClinicalTrials.gov NCT00272428

Association between alcohol consumption in healthy midlife and telomere length in older men. The Helsinki Businessmen Study

There are scarce data of alcohol consumption and telomere length, an indicator of biological age. In 1974, detailed alcohol consumption was available for a socioeconomically homogenous cohort of middle-aged men (The Helsinki Businessmen Study). Their alcohol use, divided into 5 groups (zero, 1-98, 99-196, 197-490, >490g/week) has been repeatedly assessed until old age. In 2002/2003, leukocyte telomere length (LTL) and the proportion of short telomeres (less than 5 kilobases) were measured in a random subcohort of 499 men (mean age 76years) using the Southern blot. Age-adjusted mean LTL in the 5 midlife alcohol consumption groups were 8.33, 8.24, 8.12, 8.13, and 7.87 kilobases, respectively (P<0.001). The respective proportions (%) for short telomeres were 11.24, 11.52, 11.89, 12.08, and 13.47 (P=0.004). The differences remained after further adjustments (ever smoking, body mass index, cholesterol, perceived fitness) for LTL (P=0.03) and tended to remain for proportion of short telomeres (P=0.07). Neither LTL, nor proportion of short telomeres, were associated with contemporary alcohol consumption groups in old age. Even minor alcohol consumption in midlife was significantly associated with shorter telomere length in old age. The differences represent an up to 10year gap in biological age between zero and highest consumption.

Heavy Episodic Drinking in Early Adulthood and Outcomes in Midlife

This study assessed to what extent drinking patterns of young adults persist into midlife and whether frequent heavy episodic drinking as a young adult is associated with educational attainment, labor market, and health outcomes at midlife. Using the National Longitudinal Survey of Youth 1979, we grouped individuals into three baseline drinking categories using data on the number of occasions they consumed six or more drinks on one occasion from the 1982-1984 surveys. Categories were frequent heavy episodic drinker, occasional heavy episodic drinker, and other drinker/abstainer. We used propensity score matching to compare baseline drinking groups on midlife alcohol consumption, educational attainment, and labor market and health outcomes. Frequent heavy episodic drinkers substantially reduced alcohol consumption between baseline and follow-up 25 years later. However, they were much more likely to abuse alcohol and be alcohol dependent in 1994 and be heavy episodic drinkers at the 25-year follow-up compared with the other drinking groups. After matching, there was little indication that being in a higher consumption baseline alcohol group was adversely associated with years of schooling completed by middle age, the probability of being employed, earnings conditional on being employed in midlife, and health problems in midlife. Results on the probability of surviving to follow-up were mixed. Frequent heavy episodic drinking at ages 17-25 years was associated with higher rates of alcohol dependence and abuse at a 10-year follow-up and alcohol consumption 25 years following baseline but not with other study outcomes at midlife. Lack of differences in outcomes at midlife may be because of decreased heavy episodic drinking among the heaviest baseline drinkers.

Midlife Alcohol Consumption and Later Risk of Cognitive Impairment: A Twin Follow-up Study

In this prospective follow-up study, we monitored the effects of midlife alcohol consumption and drinking patterns on cognitive impairment risks in late life. 1,486 subjects recruited from the Finnish Twin Cohort were included in the analyses. Alcohol consumption data was obtained with structured questionnaires in 1975 and 1981, and subjects were contacted between 1999 and 2007 to conduct a telephone interview evaluating cognitive function. The mean follow-up period was 22.8 years (standard deviation 2.1 years). Both abstainers and heavy drinkers were found to have an increased risk of cognitive impairment in comparison to light drinkers (relative risk ratios 1.44; 95% confidence interval: 1.02-2.10 and 1.94, 1.10-3.44, respectively. Also, binge drinking at least monthly in 1975 and 1981, as well as more than two pass-outs due to excess drinking in 1981 were associated with an increased risk of cognitive impairment (1.98, 1.08-3.64 and 3.85, 1.51-9.83, respectively), even when excluding abstainers and controlling for total alcohol consumption. Subgroup analyses based on apolipoprotein E ε4 status suggest that the increased risk of cognitive impairment associated with being an abstainer is limited to subjects without an ε4 allele. Our results add to the evidence that light to moderate alcohol use is associated with a lower risk of cognitive impairment compared with higher levels of consumption. In addition, binge drinking was found to be an independent risk factor for cognitive impairment.