Effects of a History of Heavy Alcohol Consumption on Alzheimer's Disease

1993 ◽  
Vol 163 (3) ◽  
pp. 358-363 ◽  
Author(s):  
Jules Rosen ◽  
Angela Colantonio ◽  
James T. Becker ◽  
Oscar L. Lopez ◽  
Steven T. Dᴇkosky ◽  
...  

Neuropsychological and psychiatric evaluations were made of 39 subjects with possible Alzheimer's disease and a history of excessive alcohol consumption (AD + ETOH), who had been abstinent or had drunk minimally for at least three months before evaluation, and 225 patients with probable Alzheimer's disease (PAD) of comparable age, years of education, and baseline global impairment. At baseline, there were no significant differences between the groups in terms of age of onset of dementia, neuropsychological test scores, or current behavioural or psychiatric symptoms. One year later, no differences in rates of decline between 20 abstinent AD + ETOH patients and 88 PAD subjects could be shown. Thus, past heavy alcohol consumption does not appear to modify the presentation of dementia of the Alzheimer's type, nor does it modify progression over a one-year interval.

2020 ◽  
Vol 21 (7) ◽  
pp. 2316 ◽  
Author(s):  
Bin Peng ◽  
Qiang Yang ◽  
Rachna B Joshi ◽  
Yuancai Liu ◽  
Mohammed Akbar ◽  
...  

Neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS), increase as the population ages around the world. Environmental factors also play an important role in most cases. Alcohol consumption exists extensively and it acts as one of the environmental factors that promotes these neurodegenerative diseases. The brain is a major target for the actions of alcohol, and heavy alcohol consumption has long been associated with brain damage. Chronic alcohol intake leads to elevated glutamate-induced excitotoxicity, oxidative stress and permanent neuronal damage associated with malnutrition. The relationship and contributing mechanisms of alcohol with these three diseases are different. Epidemiological studies have reported a reduction in the prevalence of Alzheimer’s disease in individuals who drink low amounts of alcohol; low or moderate concentrations of ethanol protect against β-amyloid (Aβ) toxicity in hippocampal neurons; and excessive amounts of ethanol increase accumulation of Aβ and Tau phosphorylation. Alcohol has been suggested to be either protective of, or not associated with, PD. However, experimental animal studies indicate that chronic heavy alcohol consumption may have dopamine neurotoxic effects through the induction of Cytochrome P450 2E1 (CYP2E1) and an increase in the amount of α-Synuclein (αSYN) relevant to PD. The findings on the association between alcohol consumption and ALS are inconsistent; a recent population-based study suggests that alcohol drinking seems to not influence the risk of developing ALS. Additional research is needed to clarify the potential etiological involvement of alcohol intake in causing or resulting in major neurodegenerative diseases, which will eventually lead to potential therapeutics against these alcoholic neurodegenerative diseases.


2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S220-S220
Author(s):  
Sakshi Bhargava ◽  
Nikki Hill ◽  
Jacqueline Mogle ◽  
Tyler R Bell ◽  
Rachel Wion

Abstract Understanding individual factors (e.g., personality) associated with self-reported memory problems is important to refine identification of individuals at a higher risk of developing Alzheimer’s disease (AD). Using multilevel modeling, we examined the association of family history of AD and personality traits with self-reported memory problems in older adults (n = 421; 72.21% White; 62.95% female; Mage = 76.69). Results showed that individuals with a family history of AD reported more frequent memory problems and greater one-year memory decline. Similar findings were reported for individuals with higher extraversion scores. Further, older adults with higher neuroticism scores reported greater one- and ten-year memory decline. Neuroticism was positively related to frequency of memory problems, but only among participants with a family history of AD. Findings suggest that higher neuroticism and lower extraversion may increase older adults’ reports of memory problems. Family history of AD may further exacerbate this tendency.


1991 ◽  
Vol 159 (4) ◽  
pp. 524-530 ◽  
Author(s):  
H. Karlinsky ◽  
E. Madrick ◽  
J. Ridgley ◽  
J. M. Berg ◽  
R. Becker ◽  
...  

A family with a multigenerational history of proven or suspected early-onset Alzheimer's disease (AD) consistent with autosomal-dominant inheritance is described. To date, the pedigree comprises five generations in which there are 13 known affected individuals. The mean age of onset of cognitive deficits in those for whom data are available (n = 11) is 47.6 (s.d. 3.0) years and the mean age of death (n = 10) is 58.8 (s.d. 4.0) years. The variability in the extent and quality of available data illustrates the diagnostic difficulties encountered in ascertaining such an extended pedigree, and the need for caution in interpreting the evidence.


2020 ◽  
Vol 35 (6) ◽  
pp. 800-800
Author(s):  
Alexander C ◽  
Suhr J

Abstract Objective Traumatic brain injury (TBI) is potentially a risk factor for Alzheimer’s disease (AD). This relationship may depend on the severity of TBI as well as other risk factors including APOE. We examined whether TBI status affects age of onset of AD, while improving on prior literature’s methodological issues. Method Data from the National Alzheimer’s Coordinating Centers were used. Inclusion criteria included: normal cognition at baseline; eventual diagnosis of AD; adults aged 50 and older; at least 3 years of follow-up data. Covariates included age at baseline and history of TIA, stroke, or hypertension. The resulting sample (N = 485) was 65.2% female; 89.1% White, 9.1% Black; and 4.5% Hispanic; 8% with TBI; and 42% with APOE4. Average age at baseline was 79.2 (SD = 7.6). ANCOVAs were used to determine whether TBI status (no TBI; TBI with brief LOC; TBI with extended LOC) was associated with earlier age of diagnosis for AD, controlling for age at baseline and health factors. APOE status was added to a second ANCOVA. Results Age at baseline (p < .001), but not health history (p = .777), was related to age of AD diagnosis. TBI status was not associated with age of AD diagnosis (p = .737). When APOE and the interaction between APOE and TBI status were added to the model, neither was significant (p’s = .150, .647). Conclusions When controlling for baseline cognition, age at baseline, and health factors, there was no relationship between TBI status and age of diagnosis of AD. However, use of more stringent inclusion criteria as compared to previous studies may have reduced power significantly.


1999 ◽  
Vol 174 (1) ◽  
pp. 39-44 ◽  
Author(s):  
Tony Hope ◽  
Janet Keene ◽  
Christopher G. Fairburn ◽  
Robin Jacoby ◽  
Rupert McShane

BackgroundAlzheimer's disease and other types of dementia are characterised by numerous psychiatric and behavioural changes. Little is known of their natural history.AimsTo investigate the sequence and pattern of these changes throughout the course of dementia.MethodOne hundred people, initially living at home with carers, entered a prospective, longitudinal study. At four-monthly intervals, behavioural and psychiatric symptoms were assessed using the Present Behavioural Examination and Mini-Mental State Examination. Follow-up continued for up to nine years (mean 3.3 years; s.d. 2.4). Patterns of onset and disappearance of these symptoms, their sequence and association with time of death and cognitive decline were analysed. Autopsy confirmed a diagnosis of pure Alzheimer's disease in 48 subjects. Data for this subgroup are presented.ResultsSome changes tend to occur earlier than others but changes can occur at almost any time in the course of dementia.ConclusionsThe natural history of behaviour changes in Alzheimer's disease shows great individual variation although some changes tend to follow a recognisable sequence.


2017 ◽  
Author(s):  
Shea J. Andrews ◽  
Alison Goate ◽  
Kaarin J. Anstey

AbstractINTRODUCTIONObservational studies have suggested that light-moderate alcohol consumptions decreases the risk of Alzheimer’s disease, but it is unclear if this association is causal.METHODSTwo-sample Mendelian randomization (MR) analysis was used to examine whether alcohol consumption, alcohol dependence or Alcohol Use Disorder Identification Test (AUDIT) scores were causally associated with the risk of Late Onset Alzheimer’s disease (LOAD) or Alzheimer’s disease age of onset survival (AAOS). Additionally, γ-glutamyltransferase levels were included as a positive control.RESULTSThere was no evidence of a causal association between alcohol consumption, alcohol dependence or AUDIT and LOAD. Alcohol consumption was associated with an earlier AAOS and increased γ-glutamyltransferase blood concentrations. Alcohol dependence was associated with a delayed AAOS.DISCUSSIONMR found robust evidence of a causal association between alcohol consumption and an earlier AAOS, but not alcohol intake and LOAD risk. The protective effect of alcohol dependence is potentially due to survivor bias.Research in ContextSystematic ReviewThe authors reviewed the literature using online databases (e.g. PubMed). Previous research links light-moderate alcohol consumption to a decreased risk of Alzheimer’s disease (AD), however, prior studies based on observational study designs may be biased due to unmeasured confounders influencing both alcohol consumption and AD risk.InterpretationWe used a two-sample Mendelian randomization (MR) approach to evaluated the causal relationship between alcohol intake and AD. MR uses genetic variants as proxies for environmental exposures to provide an estimate of the causal association between an intermediate exposure and a disease outcome. MR found evidence of a causal association between alcohol consumption and an earlier AD age of onset, suggesting that light-moderate alcohol consumption does not reduce risk of Alzheimer’s disease.Future DirectionsFuture studies should use alterative study designs and account for additional confounders when evaluating the causal relationship between alcohol consumption and AD.HighlightsWe evaluated causal relationships between alcohol intake and Alzheimer’s diseaseAlcohol consumption is causally associated with an earlier Alzheimer’s age of onsetNo evidence of causal assocations between alcohol intake and Alzheimer’s risk


2020 ◽  
pp. 140349482091180
Author(s):  
Kia K. Egan ◽  
Maja B. Jørgensen ◽  
Anne I. Christensen ◽  
Maja Bramming ◽  
Cathrine J. Lau ◽  
...  

Aims: This study aimed to test the hypothesis that heavy alcohol consumption and problem drinking is associated with a higher risk of becoming unemployed and a lower chance of entering the job market across socioeconomic positions. Methods: A sample of 84,474 men and women aged 18–60 years from the Danish National Health Survey 2010 participated in the study. Information on alcohol consumption and problem drinking was obtained by questionnaire. The primary outcomes were becoming unemployed and entering the job market. The follow-up period was five years. Information on labour market transitions and socioeconomic position (educational level) was obtained through nationwide registers. Multiplicative analyses were performed. Results: Heavy alcohol consumption and problem drinking were associated with a higher risk of unemployment among low-educated (hazard ratio (HR)=1.5; 95% confidence interval (CI) 1.3–1.9) and medium-educated (HR=1.3; 95% CI 1.1–1.5) individuals in comparison to individuals with a similar educational level drinking one to seven drinks per week. Excessive alcohol consumption and problem drinking were associated with a lower chance of entering the job market for individuals with a medium or high level of education: medium-educated individuals drinking >28 drinks per week had a HR of 0.82 (95% CI 0.69–0.98) when compared to medium-educated individuals drinking one to seven drinks per week. The corresponding HR among high-educated individuals was 0.71 (95% CI 0.49–1.0). Conclusions: Heavy alcohol consumption and problem drinking are associated with a higher risk of unemployment in some social strata, whereas excessive alcohol consumption and problem drinking are associated with a lower chance of entering the job market in other social strata.


2021 ◽  
Author(s):  
Grace Marion Power ◽  
Jess Marion Tyrrell ◽  
Apostolos Gkatzionis ◽  
Si Fang ◽  
Jon Heron ◽  
...  

Background: Weight change is a major indicator of adverse health outcomes. This study aims to examine factors contributing to weight change over a one-year interval in midlife. Methods: Observational and one-sample Mendelian randomisation (MR) analyses were conducted to estimate effects on weight change compared to one year previously (mean age: 56.5 years) using data from the UK Biobank study (n=453,169). Risk factors included alcohol consumption, smoking intensity, body mass index (BMI), educational attainment and Alzheimer's disease liability. Results: Observational analyses indicated strong evidence of an association between greater educational attainment and family history of Alzheimer's disease with weight loss. In contrast, smoking intensity and higher BMI were associated with weight gain. MR analyses were consistent with observational estimates for educational attainment and Alzheimer's disease liability on weight loss and provided strong evidence of a genetically predicted effect between higher overall BMI and weight gain. Whilst there was little evidence of a genetically predicted effect between smoking intensity and weight change in those who had ever smoked, when stratified, smoking intensity was associated with weight loss in current smokers and weight gain in previous smokers. There was little evidence of an association between alcohol consumption and weight change in the one-year period. Inverse probability weighting was used to account for non-random selection on smoking and alcohol status and further stratification by smoking status, indicating that our results were largely robust to collider bias. Conclusions: Individuals who have been in education for longer, may have more opportunity to reduce their weight in midlife. The effect of Alzheimer's disease liability on weight loss could be indicative of early signs of dementia. The relationship between smoking intensity and weight change is complex, reinforcing the importance of combining interventions aimed at controlling weight and smoking cessation among cigarette smokers.


2020 ◽  
Author(s):  
William Conlin ◽  
Kenneth J. Sher ◽  
Alvaro Vergés ◽  
Michaela Hoffman ◽  
Douglas Steinley

Objective: Alcohol Use Disorder (AUD) has traditionally been viewed as a chronic, progressive, relapsing disorder (Jellinek, 1960; National Institute on Drug Abuse, 2018). However, little is known about the course of individual AUD criteria. To the extent that individual symptoms represent the focus of some treatments (e.g., withdrawal, craving), understanding the course of specific symptoms, and individual differences in symptom course, can inform treatment efforts and future research directions.Method: The current study examined 34,653 participants form Wave 1 (2001-2002) and Wave 2 (2003-2004) of the National Epidemiological Survey on Alcohol and Related Conditions (NESARC; Grant, Moore, & Kaplan, 2003; Grant, Kaplan, and Stinson, 2005), using logistic regression to analyze the extent to which AUD symptom course is predicted by heavy alcohol consumption, family history of alcoholism, and lifetime diagnosis of Conduct Disorder. Results: The course of all AUD symptoms was significantly influenced by all four external criteria, with the magnitude of the prediction varying across different symptoms and different aspects of course. Conclusion: The strength of the relationship appeared to be related to the theoretical proximity of a given predictor to AUD symptomatology, with heavy drinking being the strongest and family history of AUD being the weakest. The course of all AUD symptoms was strongly associated with the prevalence of the given symptom in the overall sample. Future work should include examining the interchangeability of AUD symptoms and considering heavy alcohol consumption as a criterion for AUD diagnosis.


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