Critique #295 – Association between alcohol consumption and mortality in Parkinson’s disease

Authors

Park Y.H., Kim Y.W., Kang D.R., Yoon S.Y.

Citation

J Neural Transm. 2025; July 7; https://doi.org/10.1007/s00702-025-02976-2. Online ahead of print.

Author’s Abstract

Background Previous studies on the association between alcohol consumption and risk of Parkinson’s disease (PD) have produced controversial results. However, the relationship between alcohol consumption and mortality in PD has scarcely been investigated.

Methods Among the nationwide population data from Korea National Health Insurance Service, newly diagnosed PD (ICD-10 code: G20 and a rare intractable disease registration code: V124), between 2009 and 2017, were selected. Alcohol consumption habit was obtained from a self-reported questionnaire on the National Health Screening Program. 32,419 individuals with PD were followed up longitudinally until December 31, 2017, and all-cause mortality was evaluated.

Results During the follow-up period (mean 4.37 ± 2.67 years), 9,049 deaths occurred. When non-drinkers are used as a reference group, there were significant associations between alcohol consumption and all-cause mortality in mild (hazard ratio [HR] 0.78, 95% confidence interval [CI] 0.71–0.84) and moderate drinkers (HR 0.69, 95% CI 0.58–0.82), but not in heavy drinkers (HR 0.84, 95% CI 0.69–1.02). In the sensitivity analysis using never drinkers as the reference group, the results also showed an overall 20% reduced mortality risk among drinkers with PD. Regarding changes in alcohol consumption behavior before and after diagnosis, the mortality rate was higher in former drinkers (HR 1.20, 95% CI 1.02–1.41) and lower in constant drinkers (HR 0.74, 95% CI 0.65–0.83) than in never drinkers.

Conclusion Alcohol consumption appears to be associated with reduced all-cause mortality in PD, suggesting potential neuroprotective effects on disease progression. Although drinking does not appear to be detrimental to all-cause mortality in individuals with PD, alcohol consumption in PD requires attention considering individual motor and non-motor symptoms. Future studies in other ethnic groups are warranted to validate the association between alcohol consumption and disease progression, including mortality, in PD.

Forum Summary

Parkinson’s disease (PD) is a brain disorder that affects movement and mental health. This disease is the second most common neurodegenerative condition after Alzheimer’s disease, and its incidence is expected to rise. Previous studies have identified associations between lifestyle factors and the risk of PD.

This study by Park et al. (2025) is particularly interesting because it does not focus on the association between alcohol consumption and the incidence of PD, but instead on the relationship between alcohol consumption and mortality in PD patients based on a nationwide prospective study in Korea. Although a large number of PD patients were included, alcohol consumption was generally low, and many patients were non-drinkers with imbalances in baseline variables. The associations were evaluated using the non-drinking control group as a whole, as well as using never-drinkers and former drinkers as separate controls. Survival analysis indicated that former drinkers had worse survival rates than never drinkers. In turn, never drinkers had poorer survival than continuous drinkers. While a clear J-shaped relationship was observed between moderate alcohol consumption and mortality in PD patients, comparing these results with those of non-PD patients would have strengthened the findings. Additional limitations include the assessment of alcohol consumption, PD diagnosis, lack of mechanistic insights, and the generalisability of the results to other populations. Nonetheless, this original study offers intriguing hypothesis-generating insights into the association between alcohol consumption and overall mortality in PD patients.

Forum Comments

Background

Parkinson’s disease (PD) is a brain disorder that affects movement and mental health. Common symptoms include tremors, painful muscle contractions, difficulty speaking, as well as cognitive impairment and mental health issues. PD tends to worsen over time, and there is no cure, but treatments and medication can help manage symptoms. This disease usually affects older people, although younger individuals can also be affected. Men are more commonly affected than women. (Pringsheim et al., 2014).

This disease is the second most common neurodegenerative condition after Alzheimer’s disease and its incidence is expected to rise; the global number of PD cases is projected to reach 25.2 million by 2050, indicating a worldwide increase in prevalence with notable differences depending on location, age, sex and socioeconomic status. (Su et al., 2025).

The cause of PD remains unknown, although it is recognised that both genetic and environmental factors contribute. Approximately 15-30% of cases are thought to be due to genetic factors, with the remaining cases likely influenced by a combination of genetic and environmental factors. While most people with PD do not have a family history of the condition, genetic mutations can be important in some families.

Previous studies have identified associations between lifestyle factors and the risk of PD. Physical activity, smoking, coffee, and tea consumption seem to decrease the risk of PD, while dairy consumption and aspirin appear to increase the risk of PD (Tumas et al., 2025).

An association between alcohol consumption and PD risk has also been observed in case-control and cohort studies, associating moderate alcohol consumption with a weak reduction in risk (Palacios et al, 2013), but no effect in women. In fact, a relatively recent systematic review and dose-response meta-analysis of alcohol consumption indicates that drinking alcohol is associated with a lower risk of PD, with a non-linear and nearly U-shaped relationship. There are, however, variations depending on the type of beverage consumed (Shao et al. 2021).

This study by Park et al. (2025) is particularly interesting because it does not focus on the association between alcohol consumption and the incidence of PD, but instead on the relationship between alcohol consumption and mortality in PD patients. For that purpose, Park et al. (2025) conducted a prospective study based on the National Health Insurance Service database of Korea, which contains the medical records of the majority of the Korean population.

Critique

A large number of PD patients (32,419) were included in the study, with a relatively short mean follow-up of approximately 4.4 years and a notable mortality rate of about 28%. PD patients who drank alcohol differed from non-drinkers; drinkers were more likely to be younger and male. While the mortality rate for female PD patients was lower than for males, at 23% versus 33%, respectively, more male PD patients drank alcohol than females, at 26% compared to 8%. The non-drinkers, accounting for over 80% of this population and mainly consisting of women (around 60%), were more likely to have co-morbidities and lead less healthy lifestyles.

Hazard ratios (HR) were calculated based on unadjusted and various adjusted models, showing that the risk of all-cause mortality was lower in mild, moderate, and heavy drinkers, with HRs of 0.72, 0.57, and 0.76 in the unadjusted model, respectively. Similar HRs were obtained in the two additional models. The heavy drinking group did not reach significance in their third model, which adjusted for numerous factors, including various other lifestyle factors. This indicates that, overall, a 20-30% reduction in mortality is observed in mild and moderate drinking PD patients, suggesting a potential neuroprotective effect on disease progression, as concluded by the authors. However, this effect is mainly due to observations in men, as there were few drinking women in the study population.

An important point in this paper is the subdivision made within the non-drinking group. The authors not only analysed the results using the non-drinking group as a whole but also distinguished between never-drinkers and former drinkers. Both survival probability curves and sensitivity analyses were conducted using these different non-drinking groups. Survival analysis showed that former drinkers had poorer survival than never drinkers. In turn, never drinkers had poorer survival than constant drinkers. Sensitivity analysis revealed that HRs were very similar for all-cause mortality in PD patients, whether using the non-drinkers as a whole or using the never drinkers as a reference group. These analyses suggest that former drinkers fare worse in terms of their health, but including these former drinkers in the non-drinking control group does not significantly alter the associations.

The authors state that this association suggests a potential neuroprotective effect on disease progression. While alcohol use disorder has been associated with an increased risk of neurodegenerative diseases like PD (Kamal et a. 2020), various factors have been reported to influence the neuroprotective and neurodegenerative properties of alcohol, including the types of beverages consumed (beer vs. wine vs. liquor). Alcoholic beverages with lower concentrations of ethanol, such as beer, when consumed in low or moderate amounts, are associated with a reduced risk of developing PD (Liu et al. 2013, Zhang et al. 2014).

Interestingly, self-reported alcohol consumption exceeding 56 g per week was associated with higher iron levels in the basal ganglia, which in turn was associated with poorer cognitive function; the basal ganglia is a group of brain regions involved in motor control, procedural learning, eye movements, and cognition. Iron accumulation may be a mechanism underlying alcohol-related cognitive decline, such as in PD (Topiwala et al. 2022). Compounds such as purine, niacin, folic acid, and other phenolic compounds in beer are thought to mediate the neuroprotective effects of alcohol (Sanchez-Muniz et al. 2019). Red wine, known to contain high levels of antioxidants, when consumed at low or moderate levels, may reduce microglial activation, the expression of pro-inflammatory cytokines, and inflammatory mediators, as shown in a rat model (McCarter et al. 2017). Alternatively, low amounts of alcohol consumption may promote the clearance of neurological disease-associated entangled proteins (Cheng et al. 2019) and other waste products from the brain, as occurs during sleep (Smyth et al. 2025). Such waste clearance is mediated by the brain’s system, known as the glymphatic system (Hablitz & Nedergaard, 2021). There is some neuroimaging evidence of glymphatic system dysfunction in patients with PD (Si et al., 2022).

Specific Comments from Forum Members

Forum member Romano considers that “the study by Park et al. (2025) employs a prospective national cohort design, with a large sample size and significant population coverage, which constitute some of its main strengths. These features allow for reliable longitudinal follow-up and provide sufficient statistical power to evaluate the relationship between alcohol consumption and mortality in patients with Parkinson’s disease. The study provides evidence specific to the Korean population, with high internal validity and local relevance; however, its generalizability to other populations is limited. This is important for interpreting the findings and for planning future multicentre or international research. Moreover, the authors applied extensive multivariable adjustments, including age, sex, comorbidities, smoking status, physical activity, and clinical parameters, as well as sensitivity analyses distinguishing former drinkers from never-drinkers, reflecting careful consideration of potential internal biases.

However, the robustness of the study is limited by several methodological issues. Alcohol consumption was measured via self-report at a single time point, without differentiation by type of beverage, consumption patterns, or subsequent changes, introducing a ‘misclassification risk.’ Including former drinkers in the reference group also introduces the well-known ‘sick-quitter’ bias, which may create a false impression of a protective effect in moderate drinkers. Additional limitations pertain to the statistical analysis, such as the absence of proportionality tests in the Cox models and the lack of dose–response evaluation, as well as residual confounding from unmeasured variables, including functional severity or interactions with antiparkinsonian medications. The outcome, defined as all-cause mortality, also does not allow the identification of disease-specific mechanisms. For these reasons, the study’s internal validity is moderate, and the findings do not support reliable causal inferences.

From a statistical standpoint, the study has notable limitations affecting the strength of its conclusions. Exposure classification through self-report, inclusion of former drinkers in the reference group, measurement of alcohol intake after diagnosis, and significant imbalance in baseline variables create clear risks of misclassification bias, residual confounding, and ‘sick-quitter’ bias. Furthermore, the lack of modelling exposure as a time-dependent variable, the absence of proportional hazard checks, and the omission of competing risk considerations reduce the validity of the analysis.

Although adjusted models indicate an association between light/moderate alcohol consumption and lower mortality, the observed pattern is more consistent with statistical artefacts and epidemiological biases than with a true protective effect of alcohol in PD. Establishing causal inference would require additional analyses, such as marginal structural models, splines, multiple imputation, competing risk analyses, and formal control of unmeasured confounding.

The study examines ‘alcohol consumption’ as a global variable without distinguishing between fermented beverages (wine, beer) and distilled spirits (whisky, soju, vodka, etc.). This omission is relevant because fermented beverages often contain polyphenols, antioxidants, and bioactive compounds (e.g., resveratrol in wine), which have been studied for potential neuroprotective effects. In contrast, distilled spirits typically lack these compounds, with risk attributable almost exclusively to ethanol. Failure to differentiate introduces exposure misclassification, diluting potential differences in clinical impact by beverage type and complicating interpretation of whether the observed association is attributable to ethanol itself or accompanying compounds.

Additionally, the study defines alcohol doses as 8 g. The relationship between a single drink and its alcohol content is crucial for evaluating moderate consumption. A standard serving of wine, beer, or spirits typically contains 10–14 g of alcohol, meaning these beverages may exceed the 8-gram threshold considered moderate.

Patients with PD often receive complex pharmacological regimens, including levodopa, dopaminergic agonists, MAO-B inhibitors, COMT inhibitors, and amantadine. Alcohol consumption may produce pharmacodynamic and pharmacokinetic interactions, such as increased somnolence, confusion, or dizziness, raising fall risk, as well as gastrointestinal effects that may alter levodopa absorption. The absence of adjustment for, or at least discussion of, these interactions represent a substantial clinical limitation, given that mortality in PD may be mediated by complications related to falls, dysphagia, or drug interactions rather than a direct effect of alcohol.

In terms of originality, the study stands out for focusing specifically on Parkinson’s patients and exploring mortality as an outcome, a relatively understudied area compared to the general population. The initial distinction between former drinkers and never-drinkers also adds a novel perspective within Parkinson’s epidemiological research. Nevertheless, the clinical and methodological originality is limited because the study does not analyse alcohol type, consider medication interactions, or evaluate disease-specific outcomes such as falls, dysphagia, or neurological complications. Overall, the study provides interesting descriptive evidence and hypothesis-generating suggestions but lacks sufficient innovation to support definitive conclusions or clinical recommendations.”

Forum member McIntosh suggests that “Park et al. (2025) attempt to examine the effect of alcohol use on Parkinson’s disease in an all-cause mortality model. Their only result is shown in the first two columns of Table 1 below, in which hazard rates for various types of drinkers are displayed.

Table 1.

Drinker Type          Hazard Ratio     CI                 Hazard Ratio      CI

                                 Park et al.  (2024)                 Kim et al. (2024)

Non-Drinker          1.0                                 1.0

Mild                      0.78     [0.71, 0.84]         0.83        [0.81, 0.84]

Moderate              0.69     [0,58, 0.82]         0.93        [0.91, 0.94]

Heavy                   0.84     [0.69, 1.02]         1.11        [1.08, 1.12]

This has the commonly observed J shape, indicating that all levels of alcohol consumption are associated with longer lifespans, with the moderate drinking category providing the greatest longevity benefit for Koreans who have suffered from PD. 

Unfortunately, this result provides no information about the connection between alcohol consumption and lifespan for those who have PD. A procedure which determines whether alcohol has any effect on PD must distinguish between the effect on those who have it as opposed to those who don’t.

One way to address this issue is to run this model on matched subsamples of Koreans who do not have PD and compare the two sets of hazard ratios. This is what the authors of this study could have done. However, other researchers have also investigated the impact of alcohol consumption on longevity. The second two columns in Table 1 are from a very recent study of Korean all-cause mortality for a large representative sample of the population for the same year, Kim et al. (2024). The hazard ratios are significantly higher than those in the first two columns, indicating some beneficial effect of alcohol use on lifespan for all causes of death among those suffering from Parkinson’s disease.

However, the best way of analysing this problem is to run a competing risk model of all the important causes of death to see whether alcohol use has any effect on these durations. It is important to allow other diseases to censor PD’s durations because this disease in not in the top 10 causes of death in Korea and many of the more prominent diseases also have durations which depend on alcohol use.”

Forum member Harding’s only comment is on the way alcohol consumption was assessed in the cohort. “The question posed was, How much do you usually drink a day (cups)?  This is because in Korea, different standard-sized cups are customarily used to consume different types of alcoholic beverages, beer being consumed in 220 ml cups and soju (a distilled spirit usually made from rice, but sometimes from sweet potatoes, wheat or tapioca) in 50 ml cups.  These two drinks comprise over 99% by volume of all alcoholic beverages consumed in Korea (beer 67% and soju 32%), so it is reasonable to base this study on just those two.

But then the paper states, Although beverages (i.e., beer and soju) may have different alcohol percentages, previous studies have shown that the alcohol content per cup is similar in Korea regardless of the type of cup (Kim et al. 2020b, Yoo et al. 2021). An examination of these two papers reveals that this assertion is based on the assumption that beer contains 4.5% alcohol and soju contains 21% alcohol, without any supporting evidence. The Wikipedia entry on beer in South Korea suggests that 4.5% might be on the low side. A Google search on the nature of soju has revealed that the strength can vary in the range of 21% to 34%, or in the range of 12.5% to 53%, with low alcohol soju (below 20%) now being the most common type. Thus, it is not clear how robust the assumption of 21% actually is.”

Forum member Waterhouse has two concerns. “First, the use of these diagnostic codes was implemented only two years before the study started, so I am concerned that the use of these codes might not have been very consistent or reliable.  Second, as previously noted, the association between PD and the observed effect on mortality may be irrelevant.  I think they should have had a control population of similar subjects who had not had a PD diagnosis.  Without that comparison, I don’t see how they could have observed any interaction between alcohol consumption and PD. “

Forum member Goldfinger further suggests that “cultural differences, including both the predominant types of alcohol consumed and the patterns of consumption, make direct comparisons with Western populations difficult, at best. The findings do not establish causality.”

Forum member Ellison thought this paper “was interesting, but may have limited applicability to most other populations, especially in developed Western cultures. Among the Koreans in this study, the percentage of subjects who consumed alcohol was much lower than in North American and European populations, and the types of alcoholic beverages were different, with the pattern of drinking not well known. The rates of alcohol consumption among women were particularly low, with almost 93% being abstainers. Furthermore, the Koreans who did consume alcohol appeared to differ significantly from abstaining subjects in many ways, especially regarding smoking habits, obesity, physical activity, rural living, and some laboratory factors such as dyslipidaemia. While attempts were made to ‘control’ for these differences in the multivariable analysis, such control seldom completely adjusts for disparities. I believe that the results of this study require replication among Western populations, with longer-term follow-up, before the findings can be applied to those cultures.

Interpreting the finding that total mortality rates among subjects with PD were lower for drinkers might be clearer if the causes of death were reported. Deaths among PD subjects arise from a number of conditions, not always directly related to the disease itself. A similar pattern has been observed in breast cancer in women. For example, the incidence of breast cancer is usually slightly higher among moderate drinkers than among abstaining women, yet the overall mortality risk in such groups is generally reduced in most studies. When cardiovascular disease is the primary cause of death, differences in risk factors for such disease may help explain these findings.”

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Comments on this critique by the International Scientific Forum on Alcohol Research were provided by the following members:

Henk Hendriks, PhD, Independent consultant and partner of the Nutrition Consultants Cooperative, Netherlands

Creina Stockley, PhD, MBA, Independent consultant and Adjunct Senior Lecturer in the School of Agriculture, Food and Wine at the University of Adelaide, Australia

Raquel Romano, PhD, Independent consultant and Professor of Applied Technology at the University of Aconcagua, Argentina

James McIntosh, PhD, Retired Professor of Economics, Concordia University, Montreal, Canada

Richard Harding, PhD, Formerly Head of Consumer Choice, Food Standards and Special Projects Division, Food Standards Agency, UK

Andrew Waterhouse, PhD, Department of Viticulture and Enology, University of California, Davis, CA, USA

Tedd Goldfinger, DO, FACC, Desert Cardiology of Tucson Heart Center, University of Arizona School of Medicine, Tucson, AZ, USA

R. Curtis Ellison, MD, Section of Preventive Medicine/Epidemiology, Boston University School of Medicine, Boston, MA, USA