Alcohol use and dementia: a systematic scoping review

Rehm, Jürgen; Hasan, Omer Syed Muhammad; Black, Sandra E.; Shield, Kevin D.; Schwarzinger, Michaël

doi:10.1186/s13195-018-0453-0

Cited by 287 publications

(252 citation statements)

References 77 publications

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“…Recent research has helped elucidate the dose-response relationship between alcohol consumption and some of these outcomes showing that, rather than having protective effect, light to moderate alcohol intake is associated with an increased risk of stroke, other cardiovascular disease subtypes (excluding myocardial infarction), and all-cause mortality [1,2]. Comparable studies examining the doseresponse relationship between alcohol consumption and long-term cognitive outcomes are lacking [5,6].…”

Section: Introductionmentioning

confidence: 99%

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Long-term effects of alcohol consumption on cognitive function: a systematic review and dose-response analysis of evidence published between 2007 and 2018

et al. 2020

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Background: Understanding the long-term health effects of low to moderate alcohol consumption is important for establishing thresholds for minimising the lifetime risk of harm. Recent research has elucidated the dose-response relationship between alcohol and cardiovascular outcomes, showing an increased risk of harm at levels of intake previously thought to be protective. The primary objective of this review was to examine (1) whether there is a dose-response relationship between levels of alcohol consumption and long-term cognitive effects, and (2) what the effects are of different levels of consumption. Methods: The review was conducted according to a pre-specified protocol. Eligible studies were those published 2007 onwards that compared cognitive function among people with different levels of alcohol consumption (measured ≥ 6 months prior to first follow-up of cognition). Major cognitive impairment was excluded. Searches were limited to MEDLINE, Embase and PsycINFO (January 2007 to April 2018). Screening, data extraction, and risk of bias assessment (ROBINS-I) were piloted by three authors, then completed by a single author and checked by a second. Analyses were undertaken to identify and characterise dose-response relationships between levels of alcohol consumption and cognition. Certainty of evidence was assessed using GRADE. Results: We included 27 cohort studies (from 4786 citations). Eighteen studies examined the effects of alcohol consumption at different levels (risk of bias 16 serious, 2 critical). Ten studies provided data for dose-response analysis. The pooled dose-response relationship showed a maximum standardised mean difference (SMD) indicating slightly better cognition among women with moderate alcohol consumption compared to current non-drinkers (SMD 0.18, 95%CI 0.02 to 0.34, at 14.4 grams/day; 5 studies, very low certainty evidence), and a trivial difference for men (SMD 0.05, 95% CI 0.00 to 0.10, at 19.4 grams/day; 6 studies, very low certainty evidence). Conclusions: Major limitations in the design and reporting of included studies made it impossible to discern if the effects of 'lower' levels of alcohol intake are due to bias. Further review of the evidence is unlikely to resolve this issue without meta-analysis of individual patient data from cohort studies that address biases in the selection of participants and classification of alcohol consumption.

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Section: Introductionmentioning

confidence: 99%

“…Rehm and colleagues recently reported an overview of twenty systematic reviews (published 2000-March 2018) that had examined the relationship between alcohol use and dementia or cognitive impairment [6]. Only one of the twenty reviews reported a dose-response analysis.…”

Section: Introductionmentioning

confidence: 99%

Long-term effects of alcohol consumption on cognitive function: a systematic review and dose-response analysis of evidence published between 2007 and 2018

et al. 2020

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“…Studies suggest a U-shaped relationship between regular alcohol consumption and cognitive function: frequent heavy consumption decreases cognitive performance, whereas regular light and moderate consumption may have a protective impact (Gutwinski et al, 2018). Chronic heavy alcohol consumption can cause thiamine (vitamin B1) deficiency and lead to Korsakoff 's syndrome, characterised by symptoms including confabulation, disorientation, severe memory loss and amnesia (Arts et al, 2017;Rehm et al, 2019;Wiegmann et al, 2020).…”

Section: Lifestylementioning

confidence: 99%

Role of nurses in addressing modifiable risk factors for early Alzheimer's disease and mild cognitive impairment

Hope

2020

Br J Nurs

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A multidisciplinary advisory group of health professionals involved in dementia care assessed the current evidence base regarding modifiable risk factors (MRFs) for early Alzheimer's disease and mild cognitive impairment. Based on evidence from the published literature and clinical experience, MRFs in four areas were identified where there is evidence to support interventions that may help delay cognitive decline or reduce the risk of developing Alzheimer's disease: medical (eg cardiovascular risk factors), psychosocial (eg depression, anxiety, social isolation), lifestyle (eg lack of physical activity, smoking) and nutrition (eg poor diet, lack of micronutrients). Practical guidance on how health professionals, but in particular nurses, may actively seek to address these MRFs in clinical practice was also developed. Nurses are at the forefront of patient care and, as such, are ideally placed to offer advice to patients that may proactively help mitigate the risks of cognitive decline and the development of Alzheimer's disease.

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“…Similarly, so-called "blackout" episodes, commonly associated with drinking large amounts of alcohol over short periods of time (Goodwin, Crane & Guze, 1969;White, 2003), are clearly largely defined by and associated with AA (White, 2003;Nelson et al, 2004;Perry et al, 2006), appearing to involve both the frontal lobe and hippocampal regions (White, 2003;Oscar-Berman et al, 2004;Alderazi & Brett, 2007;Vetreno, Hall & Savage, 2011;Wetherill, Schnyer & Fromme, 2012;Hermens & Lagopoulos, 2018). In particular, chronic alcoholism appears to act synergistically with the normal ageing process to exacerbate the memory and other cognitive deficits commonly resulting from the latter (Pfefferbaum et al, 1992;Kim et al, 2012;Sabia et al, 2014;Guggenmos et al, 2017;Rehm et al, 2019).…”

Section: Basal Forebrain Damage In Ad and Arbdmentioning

confidence: 99%

A lipid-leakage model for Alzheimer’s Disease

Rudge

2019

Preprint

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This paper describes a potential new explanation for Alzheimer’s disease (AD), referred to here as the lipid-leakage model. It proposes that AD is caused by the influx of lipids following the breakdown of the blood brain barrier (BBB). The model argues that a principle role of the BBB is to protect the brain from external lipid access. When the BBB is damaged, it allows a mass influx of (mainly albumin-bound) free fatty acids (FFAs) and lipid-rich lipoproteins to the brain, which in turn causes neurodegeneration, amyloidosis, tau tangles and other AD characteristics. The model also argues that, whilst β-amyloid causes neurodegeneration, as is widely argued, its principal role in the disease lies in damaging the BBB. It is the external lipids, entering as a consequence, that are the primary drivers of neurodegeneration in AD., especially FFAs, which induce oxidative stress, stimulate microglia-driven neuroinflammation, and inhibit neurogenesis. Simultaneously, the larger, more lipid-laden lipoproteins, characteristic of the external plasma but not the CNS, cause endosomal-lysosomal abnormalities, amyloidosis and the formation of tau tangles, all characteristic of AD. In most cases (certainly in late-onset, noninherited forms of the disease) amyloidosis and tau tangle formation are consequences of this external lipid invasion, and in many ways more symptomatic of the disease than causative. In support of this, it is argued that the pattern of damage caused by the influx of FFAs into the brain is likely to resemble the neurodegeneration seen in alcohol-related brain damage (ARBD), a disease that shows many similarities to AD, including the areas of the brain it affects. The fact that neurodegeneration is far more pronounced in AD than in ARBD most likely results from the greater heterogeneity of the lipid assault in AD compared with ethanol alone. The lipid-leakage model, described here, arguably provides the first cohesive, multi-factorial explanation of AD that best accounts for all currently known major risk factors, and credibly explains all AD-associated pathologies, including those, such as endosomal-lysosomal dysfunction and excessive lipid droplet formation, that have been too readily overlooked by other accounts of this disease.

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Alcohol use and dementia: a systematic scoping review

Cited by 287 publications

References 77 publications

Long-term effects of alcohol consumption on cognitive function: a systematic review and dose-response analysis of evidence published between 2007 and 2018

Long-term effects of alcohol consumption on cognitive function: a systematic review and dose-response analysis of evidence published between 2007 and 2018

Role of nurses in addressing modifiable risk factors for early Alzheimer's disease and mild cognitive impairment

A lipid-leakage model for Alzheimer’s Disease

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