Alcohol use and dementia: a systematic scoping review PMC

link between alcoholism and dementia

Alzheimer’s is caused by specific brain changes called amyloid plaques and neurofibrillary tangles. This makes it harder to develop accurate tests for FTD compared to Alzheimer’s, where recent advancements have greatly improved diagnosis. Two specific types, frontal lobe dementia and alcohol-induced dementia, share some similarities but have distinct characteristics.

  • Understanding the differences is crucial, as it can significantly impact accurate diagnosis and appropriate care.
  • Furthermore, heavy alcohol use may also have a direct role in AD’s pathophysiology by enhancing tau accumulation, delaying its clearance and thereby increasing cell death 40.
  • Subsidiary analyses examining potential bias due to differential misclassification of dementia suggested our main findings on the association of alcohol consumption with dementia to be robust (appendix table S7).
  • Amyloid proteins can clump together in the brain to form plaques, which researchers believe could lead to issues with brain function.

Data Availability Statement

link between alcoholism and dementia

Neuroimaging revealed cerebral atrophy and chronic small vessel ischemic disease. Current drinkers can happily continue with the knowledge that light to moderate drinking has been shown to have mental benefits. Researchers also found that drinking wine had more mental benefits than consuming other types of alcohol. Some point to the anti-inflammatory features of alcohol while others suggest that these positive effects are actually due to the social interactions which occur while the alcohol is being consumed. Progression of cognitive decline with increasing standard drinks of hard liquor, beer and wine. Baseline characteristics of those who were included in the study and those who were excluded due to missing data were compared using t tests for continuous variables and Chi-Square Tests for categorical variables.

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link between alcoholism and dementia

Subsidiary analyses examining potential bias due to differential misclassification of dementia suggested our main findings on the association of alcohol consumption with dementia to be robust (appendix table S7). To tackle some of these limitations, we used repeat data spanning nearly three decades to investigate the association between alcohol consumption and risk of dementia, assessed through linkage to electronic health records for all participants irrespective of their continued participation in follow-up. We examined associations of dementia with alcohol consumption in midlife, alcohol dependence, hospital admission for alcohol related disease, and trajectories of alcohol consumption over 17 years. In addition, we examined whether cardiometabolic disease modifies the association between alcohol consumption and dementia. Table 1 presents details regarding the literature searches conducted in preparation for this review. Similarly, whereas the terms “Alzheimer’s” and “alcoholism” yielded 318 results, “Alzheimer’s” and “alcohol use disorder (AUD)” returned only 40 citations.

  • Some of the genetic markers used for alcohol consumption are problematic as their associations with average volume of drinking and with heavy drinking occasions in overall light drinkers point in opposite directions (80; see also the discussion following 84).
  • These studies don’t separate out the lifetime non-drinkers from those who have quit drinking.
  • The link is strongest with vascular dementia, which is a form of cognitive decline that causes “changes to memory, thinking, and behavior resulting from conditions that affect the blood vessels in the brain,” according to the National Institute on Aging (NIA).
  • Alcoholic dementia encompasses several different alcohol-induced neurological conditions that can affect thinking skills.
  • If you’re buying a bottle or can, it’s helpful to check the ABV content on the label.
  • Accordingly, epidemiological studies have reported a reduction in the prevalence of AD in individuals ingesting low amounts of alcohol, while a moderate consumption of ethanol may protect against Aβ.

Can taking semaglutide drugs Ozempic reduce my risk of Alzheimer’s?

  • Gathering collateral information has shown to be of equivalent legitimacy to self-reporting 24 and therefore may be subject to the same risks of under reporting.
  • Dementia is a clinical syndrome characterized by a progressive deterioration in cognitive ability and the capacity for independent living and functioning 1.
  • The Predictors Study inclusion criteria, exclusion criteria and evaluation procedures are described elsewhere 18, 19.
  • But your care team can prescribe medications to help with withdrawal symptoms.
  • Given the lack of high-quality research on alcohol, AD, and cognitive functioning/impairment, future randomized prevention and secondary prevention trials with alcohol interventions are needed.

Research suggests it’s possible to experience partial recovery of your brain’s white matter, which is accompanied by an improvement in cognitive and motor abilities. Coping with alcoholic dementia can be difficult for a person who is experiencing it, as well as for their loved ones. You don’t have to go through this alone—seeking help from healthcare providers, as well as support groups, can help you as you learn how to manage your alcohol use and how to cope with the effects of alcoholic dementia. Drinking alcohol in moderation has not been considered a cause of health problems or dementia. However, recent studies suggest that even moderate alcohol use can increase the likelihood of dementia.

Moderate drinking and AD

  • (Ivanhoe Newswire) – Dementia, a term encompassing a decline in cognitive function, is a complex and often misunderstood condition.
  • Never or former smokers were more likely to age in a healthy way compared with current smokers (OR 1.72, 95% CI 1.20 to 2.47, I2 87.20%, six studies); however, when we adjusted for publication bias this finding was no longer significant (OR 1.20, 95% CI 0.83 to 1.73, nine studies).
  • Additional adjustment for occupational type or smoking did not change the results either (data not shown).
  • 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.
  • Additionally, we will conduct subgroup analyses to explore the dose-response relationship between alcohol and dementia in different sexes and study types.

Read our tips for supporting a person with ARBD (alcohol-related dementia and Wernicke-Korsakoff’s). A person may consider joining support groups or attending counseling or therapy if alcohol use is impairing their quality of life in the short and long term. A person should consult a doctor if they are experiencing any of these symptoms to receive a prompt diagnosis. According to the Dietary Guidelines for Americans 2020–2025, drinking in moderation consists of no more than one or two drinks daily for females and males, respectively. A standard drink contains 14 grams, or 0.6 ounces (oz), of pure alcohol in the United States. This article will use the terms “male,” “female,” or both to refer to sex assigned at birth.

link between alcoholism and dementia

In addition to a physical examination and medical history, your healthcare provider may order diagnostic testing to help reach specific causes for dementia symptoms. Sometimes, physical changes such as movement disorders or coordination problems can help differentiate types of dementia. A diagnosis of dementia requires a comprehensive physical and psychological evaluation.

Gathering collateral information has shown to be of equivalent legitimacy to self-reporting 24 and therefore may be subject to the same risks of under reporting. However, considering the patients’ memories are intrinsically compromised by the disease process, there may be no simple way to examine alcohol use in a longitudinal study of AD patients that is more valid. Another problem is that we measured alcohol use only in the first six months from entry and therefore did not take into account intrapersonal variation in alcohol use during the follow-up period or earlier in life. Although we controlled for multiple confounding factors, we could not completely rule out the possibility of residual confounding factors such as nutritional factors and exercise. Unfortunately, we do not have dietary or exercise information in this study population so we cannot adjust for these factors. We also did not inquire into the pattern of use, including binge drinking, which is an independent risk factor of AD 5.

Neuropathology and Neuro-Imaging Studies

link between alcoholism and dementia

A sensor-transducer–effector model was proposed as the mechanism for this, which involves N-methyl-D-aspartate (NMDA) receptors as the sensor, multiple protein kinase Cs and focal adhesion kinases as the transducer and heat shock proteins 70 and 27 as the effector 27, 30, 31. We hypothesize that the pathophysiology of AD impairs the upregulation of prosurvival and anti-inflammatory mechanisms, seen by Collins et al. 27, such that moderate alcohol use does not hinder the disease process enough to lead to a significant slower cognitive decline. The hazard ratio for abstinence compared to consumption of 1–14 drinks per week for developing any kind of dementia was 1.47, after adjusting for confounders (extensive assessment of sociodemographic data and cardiovascular health data). Diagnosis was made through linkage with mental health services data set, mortality register and national hospital episode statistics.

In addition, included studies were can alcohol cause dementia restricted to systematic reviews that assessed the relationship between alcohol use and cognitive health, dementia, AD, vascular and other dementias, brain function, or memory. Systematic reviews on the association between alcohol use and brain structures were also included. Studies were included if they were published in 2000 or later in order to include only reviews which were undertaken using methodological standards similar to those used today; however, this does not mean that the original studies underlying these reviews were restricted to 2000 or later (for example, 20) (Additional file 1). From our meta-analysis, we concluded that compared with never drinkers reasonable alcohol consumption is beneficial to healthy ageing; pooled OR for drinkers 1.28 (95% CI 1.08 to 1.52), light drinkers 1.12 (95% CI 1.03 to 1.22), moderate drinkers 1.35 (95% CI 0.93 to 1.97) and high drinkers 1.25 (95% CI 1.09 to 1.44). Nevertheless, associations are marginally statistically significant, while for the moderate category the pooled effect estimate is non-significant, so extra caution is needed before making a final conclusion.