Alcohol consumption, dementia and truth ?.
It is good to read a research article on “Alcohol consumption and risk of dementia: 23 year follow-up of Whitehall II cohort study” by Séverine Sabia et al .
This cohort study is similar to an earlier study by Topiwala A et al . Both the research studies [1-2] were epidemiological observational Whitehall II cohort studies. Archana Singh-Manoux & Mika Kivimäki were the common coinvestigators and activily participated in both the studies & CAGE questionnaire was used for alcohol dependence and for follow up [1-2].
The main objective of both the Whitehall II cohort studies was to study the association between alcohol consumption and dementia, but the results of both the cohort studies were dissimilar.
Séverine Sabia and colleagues reported that abstinence from alcohol in midlife, decrease in consumption, and long term abstinence were associated with a higher risk of dementia of 45%, 50% and 67% respectively; also long term consumption of alcohol more than14 units/week was associated with an increased risk of dementia in late life.The risk of dementia was more in patients with chronic diseases & cardiometabolic diseases .
Anya Topiwala and colleagues reported that compared with abstinence, moderate alcohol consumption was associated with cognitive decline, hippocampal atrophy and no protective effect was observed for small amounts of alcohol .
The Whitehall II study is an ongoing ambidirectional cohort study (both retrospective & prospective), hence the epidemiological cohort study by Séverine Sabia et al , is not purely prospective in nature.
Studies revealed that lower risk of dementia was associated with moderate alcohol consumption, and the association was J-shaped or U-shaped [3-4]. Epidemiological studies report better health in moderate alcohol use compared with abstinence .
Baseline characteristics of the patients, confounding variables and biases, in both the Whitehall II Cohort studies had a significant role in variations of research-outcomes & controversial results [1-2].
Harm can result from weekly alcohol consumption as low as 14-21 units. Information was missing about Drinking patterns, whether alcohol consumption was uniformly spread over 7 days or concentrated (heavier drinking), also internal validity was the limitation, hence strength of evidence is weak [1-2].
Tolerance, and physical & psychological dependence occur early with alcohol consumption and a cause of increase rate of drinking. Chronic alcohol consumption affect vital organs and causes tissue damage that result from direct effects of alcohol as well as due to accumulation of acetaldehyde and by oxidative stress. Chronic alcohol consumptionleads leads to mitochondrial damage, cytokine induced injury, growth factor dysregulation and it result in neurotoxicity, wernick-korsakoff and Korsakoff’s psychosis .
Social impact and public message: The main concern is advertisement of results of research studies by media that give wrong message to public, that drink more and prevent dementia , and good for alcohol industry .
2.Topiwala A, Allan CL, Valkanova V, et al. Moderate alcohol consumption as risk factor for adverse brain outcomes and cognitive decline: longitudinal cohort study. BMJ2017;357:j2353. doi:10.1136/bmj.j2353
3. Anstey KJ, Mack HA, Cherbuin N. Alcohol consumption as a risk factor for dementia and cognitive decline: meta-analysis of prospective studies. Am J Geriatr Psychiatry2009;17:542-55. doi:10.1097/JGP.0b013e3181a2fd07
4.Xu W, Wang H, Wan Y, et al. Alcohol consumption and dementia risk: a dose-response meta-analysis of prospective studies. Eur J Epidemiol2017;32:31-42. doi:10.1007/s10654-017-0225-3
5 - Killian W “Alcohol consumption and brain health”. BMJ 2017;357:j2645
6. Caan W. Exogenous drugs and brain damage. In: (Bonner A, Waterhouse J, Ed.s) “Addictive behaviour: molecules to mankind.” London: Macmillan, 1996, 56-68.
Competing interests: No competing interests