No volume of alcohol is safe and consumption raises dementia risk, researchers warn

Any amount of alcohol consumption raises dementia risk, challenging the previously held beliefs on the benefits of light drinking. 

Heavy drinkers who consumed 40 or more drinks a week displayed a 41% higher risk.

Early cognitive decline might lead to reduced alcohol intake, which could explain the supposed “protective” effects of alcohol seen in earlier research.

Consuming any volume of alcohol raises the risk of dementia, suggests the largest combined observational and genetic study on the subject to date. It warns that light drinking, which researchers previously thought was protective, is unlikely to lower the risk.

Researchers note that a common belief is that there is an “optimal dose” of alcohol for brain health. However, many studies on this subject matter have focused on older people or didn’t differentiate between former and lifelong non-drinkers.

“The pattern of reduced alcohol use before dementia diagnosis observed in our study underscores the complexity of inferring causality from observational data, especially in aging populations,” say the researchers.

“Our findings highlight the importance of considering reverse causation and residual confounding in studies of alcohol and dementia, and they suggest that reducing alcohol consumption may be an important strategy for dementia prevention.”

Diverse cohorts

The researchers studied data from two large biological databases for the entire dose range of alcohol consumption. Their observational analyses looked at 559,559 participants from both groups. Over 90% of participants reported they drank alcohol.

The first cohort was the US Million Veteran Program (MVP), which includes people of European, African, and Latin American ancestry. The second was the UK Biobank (UKB), comprising people of predominantly European ancestry.

The analysis tracked the participants, who were aged 56–72 at baseline, beginning from their recruitment until their first dementia diagnosis, death, or the date of last follow-up (December 2019 for MVP and January 2022 for UKB).

On average, the monitoring period was 4 years for the US cohort, and 12 for the UK cohort.

The study reveals 14,540 of participants developed dementia of any type during the monitoring period, specifically 10,564 in the US group and 3,976 in the UK group. By the end of the study, 48,034 had died — 28,738 in the US group and 19,296 in the UK group.

The observational analyses revealed U-shaped associations between alcohol and dementia risk.

Compared to “light” drinkers (fewer than seven drinks a week), non-drinkers and “heavy” drinkers who consumed 40 or more drinks a week displayed a 41% higher risk, which rose to a 51% higher risk among those who were alcohol-dependent.

Genetic link

The researchers also studied the genetic link between alcohol use and dementia risk, based on Mendelian randomization genetic analysis.

This segment of the study examined multiple large genome-wide association studies of dementia, involving the data of 2.4 million participants in total.

The researchers found that the risk of dementia went up in a linear fashion, the more a person’s genes indicated they were likely to consume alcohol.

For example, a genetic predisposition to having just one to three extra drinks per week was linked to a 15% higher risk of dementia, while a doubled genetic risk for alcohol dependency was associated with a 16% increase in dementia risk.

These findings also challenged the belief that low levels of alcohol might be protective. The study found no evidence of this “U-shaped” curve. Instead, the risk of dementia simply increased with more alcohol.

Three genetic measures related to alcohol use were used as different exposures to study the impact on dementia risk of alcohol quantity, as well as problematic and dependent drinking.

Moreover, participants who went on to develop dementia typically drank less over time in the years preceding their diagnosis. The scientists say this suggests that reverse causation — in which early cognitive decline leads to reduced alcohol consumption — is behind the supposed protective effects of alcohol found in previous observational research.

One important limitation of their findings is that participants of European ancestry demonstrated the strongest statistics because of their numbers in the study, they highlight. Mendelian randomization also relies on assumptions that can’t be verified.

The study is published online in BMJ Evidence Based Medicine.

Industry has responded to the demand for risk-mitigation among drinkers. Quantum BioPharma recently announced clinical findings from a study supporting that its hangover supplement Unbuzzed accelerates alcohol metabolism “dramatically and rapidly.”