Beer and Liquor May Have Positive Effects on Parkinson’s Disease

Beer and liquor may have opposite associations with Parkinson’s disease (PD): moderate beer drinking might lower the risk, whereas consuming liquor might raise it. A new large, prospective, cohort study supports “very preliminary evidence that beer drinking is related to a lower Parkinson’s risk,” Honglei Chen, MD, PhD, head of the Aging and Neuroepidemiology Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina concluded.

“Further, our study suggests that high liquor consumption may be related to a higher risk of Parkinson’s disease.”The study findings were presented here at the American Neurological Association annual meeting. These results also highlight the importance of examining the effects of different types of alcohol when evaluating the health consequences of alcoholic drinks, he added.

NIH-AARP Study Cohort

“Both smoking and coffee drinking have been consistently linked to a lower risk of Parkinson’s,” Dr. Chen told Medscape Medical News.

Because alcohol drinking is common among adults and can have significant behavioural and health consequences, “it’s important to understand the potential relationship of alcohol drinking with Parkinson’s disease,” he added.

It has been hypothesized that alcohol drinking is also related to a lower PD risk, Dr. Chen noted, but epidemiological data on alcohol and PD have been “inconsistent,” and few studies have looked at individual types of alcohol in relation to PD risk.

Dr. Chen’s team analyzed data on 1113 individuals with PD and 305,785 individuals without PD who were enrolled in the National Institutes of Health–American Association of Retired Persons Diet and Health Study. Types of alcohol consumed (beer, wine, and liquor or mixed drinks) were assessed at baseline from 1995 to 1996, and any cases of PD diagnosed between 2000 and 2006 were established by self-report.

After controlling for potential confounders and other types of alcohol consumption, beer drinkers had a lower adjusted odds ratio of PD than nondrinkers.

Table 1. Risk for PD By Beer Intake

Number of Drinks Per DayOdds Ratio 95%Confidence Interval
<1 per day0.790.68 – 0.92
1 – 1.99 per day0.730.50-1.70
 ≥2 per day 0.86 0.60-1.21

For liquor consumption, there was a monotonic increase in PD risk.

Table 2. Risk for PD By Liquor Intake

Number of Drinks Per Day Odds Ratio 95% Confidence Interval
<1 per day 1.06 0.91 – 1.23
1 – 1.99 per day 1.22 0.94 – 1.58
≥2 per day 1.35 1.02 – 1.80

Results for wine consumption were less clear, although a lower PD risk was also observed when comparing drinkers of 1 to 2 drinks daily with nondrinkers.

Table 3. Risk for PD By Wine Intake

Number of Drinks Per Day Odds Ratio 95% Confidence Interval
<1 per day 1.07 0.92 – 1.25
1 – 1.99 per day 0.74 0.53 – 1.02
≥2 per day 1.31 0.89 – 1.94

The biological mechanisms that might link alcohol consumption and PD are not clear, the authors note, but the differential associations with individual types of alcohol suggest the effect is independent of the ethanol in these beverages.

They speculate that the effect relates to urate: Beer contains higher purine levels than wine or liquor, and may work synergistically with ethanol to increase plasma urate, which may decrease Parkinson’s risk. “These findings and potential underlying mechanisms warrant further investigations,” the authors conclude.

A “Welcome Addition”

“This study is a welcome addition to the few longitudinal investigations on lifestyle and risk of [PD],” Alberto Ascherio, MD, DrPH, professor of epidemiology and nutrition, Harvard School of Public Health, Boston, Massachusetts, told Medscape Medical News.

Dr. Ascherio, who was not involved in the study, said its strength is the large sample size, and the main weakness is that consumption of alcoholic beverages was assessed only at 1 point in time, and therefore the study provides only an approximate determination of long-term consumption.

“The results should be interpreted in the context of previous investigations, which had a smaller sample size, but more detailed information on ethanol consumption over time,” Dr. Ascherio added.

He cautioned that the increase in risk with liquor consumption “has not been observed in previous studies,” and should thus be interpreted “cautiously.”

The overall evidence, Dr. Ascherio commented, “is consistent with the conclusion that the urate elevating effect of ethanol probably mediates an inverse association between ethanol consumption and Parkinson’s risk.”

The study was supported by the Intramural Research Program of the National Institute of Environmental Health Sciences and the National Cancer Institute. The authors and Dr. Ascherio have disclosed no relevant financial relationships.

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Hellen Mwithiga

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