Alcohol Consumption Is No Protection From MS: UK Study

The risk of developing multiple sclerosis (MS) doesn’t seem to be influenced by consuming alcohol, according to a large-scale analysis in the U.K.

After adjusting for known MS risk factors, including smoking, childhood obesity, socioeconomic status, or genetics, the findings remained the same.

The analysis was published in Nature Scientific Reports in the study, “No evidence for an association between alcohol consumption and Multiple Sclerosis risk: a UK Biobank study.”

While MS’s exact causes are unknown, research has found many risk factors that may contribute to developing it, including genetics and demographic characteristics, as well as environmental influences, such as smoking, childhood obesity, and Epstein-Barr virus infection.

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Some studies of Swedish and Danish populations suggest alcohol consumption is linked to lower MS risk, while others have failed to support this connection.

To investigate this relationship in the U.K., researchers examined data from 409,228 people, ages 40–69, enrolled in the U.K. Biobank (UKB) between 2006 and 2010. Among them, 2,100 (0.51%) had received an MS diagnosis; their median age at recruitment was 56 and most (72.3%) were women. Controls had a similar age at recruitment, but had a more even distribution of men and women.

“The prevalence of MS in UKB is slightly higher than contemporary estimates for the prevalence of MS in the UK in this age category,” the researchers noted.

Participants were asked to report alcohol consumption at the time of enrollment in the Biobank, focusing on their average estimated intake for the previous year. Overall, 80 MS patients (3.8%) and 12,781 controls (3.1%) reported no alcohol consumption in the previous year.

After adjusting for age and sex, abstaining from alcohol was not associated with MS status, meaning there was “no evidence for an association between alcohol consumption and MS risk,” the team concluded.

Researchers also explored the relationship between alcohol consumption and known MS risk factors that may have influenced these results, including body weight, cigarette smoking, and socioeconomic deprivation, a measure that incorporates employment status, car or home ownership, and household overcrowding.

While never-drinkers tended to have higher deprivation scores, there was no association with childhood body size at the age of 10, a proxy for childhood obesity shown to correlate with MS risk, the researchers noted. Also, never-drinkers were more likely to be never-smokers. After adjusting for these factors, there was still no significant correlation between never-drinking and MS risk.

As expected, about twice as many MS patients carried the gene for HLA-DRB1*15:01 (49.7% vs. 26.8%), a major risk factor for MS. In this dataset, this genetic risk factor was associated with a 2.7 times greater likelihood of developing MS, after adjustments. There was no association between alcohol consumption and HLA-DRB1*15:01 carriers after adjusting for other risk factors, however.

Final statistical calculations confirmed the study was sufficiently powered, with the number of participants involved to demonstrate a protective effect of alcohol on MS risk similar to previous studies.

“The inconsistent association seen between studies may reflect limited statistical power to detect a weak effect, differences in population characteristics, or the lack of a true causal association,” the researchers wrote. “Further research in population-based studies and more diverse cohorts is required to clarify whether such a relationship is causal or has arisen due to bias.”