Alcohol consumption and risk of dementia: 23 year follow-up of Whitehall II cohort study

There is a J-shaped relationship between alcohol use and cognitive impairment and evidence shows that one-quarter of the dementia population have alcohol related problems. It is estimated that alcohol-related dementia (ARD) contributes for about 10% of all cases of dementia, especially early-onset dementia, but is largely overlooked or seen as a comorbid factor. Next, analyses were repeated in the subsample of cohorts that allowed adjustment for all additional demographic and clinical covariates considered (i.e. education, BMI, depression, stroke, diabetes, myocardial infarction, hypertension and high cholesterol). These ‘fully adjusted’ analyses were conducted to determine whether the relationship between dementia and alcohol use was robust to potential confounders. If you stop drinking, it’s possible to at least partially reverse the effects of alcohol-related dementia.

Prevalence of alcohol-related cognitive disorders

This heterogeneity in outcome operationalization may have contributed to the contradictory findings with respect to light to moderate drinking mentioned above. Therefore, there is also a need for the use of standardized objective measures of dementia and cognitive decline, using current consensus criteria. More rigorous studies using newer dementia, genetic, and neuroimaging biomarkers are needed to establish clearer guidelines for frontline clinicians in an era in which dementia prevention is a public and individual health priority. Consumption of large amounts of alcohol is known to have negative effects, but drinking smaller amounts may have a protective effect in adults of all ages. Second, we cannot exclude the potential influences of including former drinkers, who may quit drinking due to underlying diseases and have a high risk of dementia, in the reference group due to data restrictions.

Cross-Sectional Studies

A review of clinical and epidemiological data suggests that criteria and nomenclature of dementia subtypes need improvement. Neuropsychological and biological markers that can differentiate dementia subtypes are in progress but currently limited. Whether alcohol misuse contributes to an added burden on pre-existing Alzheimer’s disease remains an open and ongoing research question, which may be approached in animal models. Indeed, basic science strategies that can control alcohol exposure may help clarify controversies, including whether alcohol in the context of genetically induced Alzheimer’s disease pathology changes the extent, distribution, or signaling pathways of relevant biomarkers. This scoping review was limited by the large amount of heterogeneity in the operationalization of outcomes and the small degree of overlap of underlying studies between reviews (Additional file 1).

Abstaining and increased dementia risk

Supporting information, Tables S3–S8 include detail on the assessment, harmonization and distribution of all demographic and clinical covariates. Given variability across the contributing cohorts in terms of data collected on dementia subtypes, as well as the low population incidence of dementia, the main outcome variable for the current study was all‐cause dementia. Date of death data were also provided for 13 of the 15 cohorts included in this study, allowing the implementation of competing risks models in these datasets (date of death data were not available for the PATH and SPAH cohorts). In recent decades, the estimated global prevalence of dementia has nearly tripled, from 20.2 million in 1990 to 57.4 million in 2019 1.

• The majority of cohorts allowed the separation of current abstainers into former drinkers and life‐time abstainers, allowing the exclusion of former drinkers from the abstainer category.
• This literature review indicates that chronic alcohol misuse accelerates brain aging and contributes to cognitive impairments, including those in the mnemonic domain also affected in Alzheimer’s disease.
• This section collects any data citations, data availability statements, or supplementary materials included in this article.
• The Lancet review by Livingston et al. 1 showed that the risks of heavy drinking and AUDs for dementia have been underestimated.

Recent research indicates drinking any alcohol could increase dementia risk.

Note that alcohol-related dementia is sometimes confused with Wernicke-Korsakoff syndrome. Wernicke-Korkasoff syndrome is caused by a thiamine (Vitamin B1) deficiency, though heavy alcohol use can be an underlying cause of this deficiency. “Alcoholic dementia” is an older term commonly used to describe the medical condition now known as alcohol-related dementia or alcohol-induced major neurocognitive disorder. These terms are used interchangeably and describe a severe form of alcohol-related brain damage (ARBD).

• For the current study, baseline year of data collection for each cohort was the first assessment occasion where both alcohol use and dementia status were assessed, and ranged from 1975 to 2011.
• The present paper is a critical review of research on the effect of alcohol on cognitive function and dementia in the elderly.
• Furthermore, cohort studies in twins may contribute to identifying genetic variations 85.
• Current CDC guidelines of no more than one drink per day for women and two drinks for men are likely to disappoint those who think any drinking is terrible and those who think moderate drinking improves longevity.
• Systematic reviews on the association between alcohol use and brain structures were also included.

This excessive consumption puts a person at risk of various brain diseases, including AD, stroke, and heart disease. Most cases of WKS in developed countries relate to the misuse of alcohol, although WKS syndromes following gastrointestinal disorders and systemic diseases can also contribute. While there is no direct correlation between the prevalence of WE and per capita consumption of alcohol, the introduction of thiamine supplementation programs in some countries, as well as general dietary habits, also influences overall rates 16.

Current drinking and dementia risk

Finally, these socially isolated patients are often hospitalized for another health condition and this presents an ideal opportunity for screening, identification, and intervention. The meta-analysis will be conducted using STATA version 12.0 (STATA Corp, College Station, TX). The study quality will be evaluated with the Newcastle-Ottawa Quality Assessment Scale (NOS).25 The NOS contains 8 items, categorized into 3 dimensions including selection, comparability, and outcome (cohort studies). A star rating system will be used to semi-quantitatively evaluate the quality of the study, which allows a total star of up to 9 and studies with more than 6 stars will be evaluated as high quality. If you’ve been drinking alcohol for a long time, you might experience alcohol withdrawal symptoms, including disorientation, agitation, and mood changes. Ultimately, due to these confounding influences, proving a direct causal link between moderate drinking and health benefits/harms is not possible.

• Analyses first focused on the categorical alcohol use variable and were conducted in the full sample with current abstainers as the reference category.
• A star rating system will be used to semi-quantitatively evaluate the quality of the study, which allows a total star of up to 9 and studies with more than 6 stars will be evaluated as high quality.
• Other contentious issues center around recommendations for red meat, sugary beverages, and environmental sustainability.
• In summary, while a number of studies have reported experimental findings to explain risk reduction through alcohol consumption for vascular dementia, data regarding the impact of alcohol on Alzheimer´s pathophysiology is more contradictory.
• Dementia affects memory, thinking, behavior, and the ability to perform everyday activities 2, and is a leading cause of disability in older individuals 3.
• To increase diagnostic accuracy of WE, refined operational criteria specify a minimum of two symptoms for diagnosis, a guideline recently endorsed by the European Federation of Neurological Societies (EFNS) 18, 19.

Excessive alcohol use may put a person at risk of developing certain health problems relating to the brain. In this context, the subgroup analysis about dementia types can’t be conduct because of the lack of the sample size. In future, we will explore the dose-response relationship between alcohol and dementia in different dementia types, alcohol measurements, and definitions. The 2 researchers will independently screen literatures, conduct data extraction, and quality evaluation. Any disagreement regarding inclusion will be resolved by discussion among all review authors. Researchers will screen titles and abstracts of the studies base on inclusion/exclusion criteria, and select the full text of can alcohol cause dementia potentially relevant studies for further assessment.

None of the cohorts reported participant exclusion criteria on the basis of alcohol use. Individuals were excluded from the current study if they were diagnosed with dementia at baseline, if they were missing baseline dementia status data, if they did not have any follow‐up dementia status assessment or if they were missing baseline alcohol use, age or sex data. For the current study, baseline year of data collection for each cohort was the first assessment occasion where both alcohol use and dementia status were assessed, and ranged from 1975 to 2011. The cohorts had various assessment schedules (two to 19 waves), follow‐up durations (4–40 years) and methods for establishing consensus diagnosis of dementia (Supporting information, Table S1).

Imaging studies of ‘uncomplicated alcoholics’ – individuals with no history of nutritional deficiency, hepatic failure, or other indirect forms of brain injury – confirm structural abnormalities, including changes to the corpus callosum, pons, and cerebellum 12. However, the permanence of such changes, and whether they relate to neurotoxicity in isolation, remains to be established 1. While the evidence base for the alcohol–dementia relationship is large, prior meta‐analyses of published results have several limitations. There is a lack of standardization throughout studies in terms of alcohol categorization, with definitions of ‘light’, ‘moderate’ and ‘heavy’ alcohol use varying widely across studies and impeding cross‐study comparison. The abstaining group is often comprised of both former drinkers and life‐time abstainers, with former drinkers (or ‘sick quitters’) potentially driving the relationship between abstention and poorer health outcomes (i.e. reverse causation) 11. Importantly, studies of the alcohol–dementia relationship are largely based on samples from high‐income countries 9, 10.