Study: Alcohol, Tobacco Use May Reduce Parkinson’s Risk
Drinking alcohol and smoking tobacco may reduce a person’s risk of developing Parkinson’s disease, according to a new study that found evidence of a cause-and-effect relationship.
“It is crucial to be aware that smoking and drinking pose serious health risks to individuals,” the researchers wrote, noting there was “no clear association between [Parkinson’s] risk and smoking initiation (ever vs. never being a regular smoker), smoking heaviness (number of cigarettes per day), or the age at smoking initiation.”
Instead, their findings regarding tobacco use “support the role of smoking as a protective factor against [Parkinson’s] … only when comparing current vs. former smokers,” they wrote.
Nonetheless, the researchers called for further study into the mechanisms behind these causative effects, with a goal toward tapping into any potential benefits.
“A better understanding of the underlying biology and their relationship with [Parkinson’s] risk could ultimately help delineate novel targets for prevention or treatment without the adverse health effects of smoking and drinking,” the team wrote.
The findings were published in Scientific Reports, in a study titled “Understanding the effect of smoking and drinking behavior on Parkinson’s disease risk: a Mendelian randomization study.”
Prior research has revealed inverse correlations between Parkinson’s risk and drinking or smoking — in other words, it’s known that people who drink or smoke are less likely to develop the disease. However, it hasn’t been clear whether this is a cause-and-effect relationship, or is due to other factors at play.
In medical science, the gold standard for determining cause-and-effect relationships is a randomized controlled clinical trial, in which participants are randomly assigned and “doses” are regulated. Doing such a study using alcohol or tobacco, however, given their numerous well-established health risks, would be ethically dubious.
Now, instead, a team led by researchers at Harvard Medical School, in Massachusetts, used a method to test causality based on genetics, called Mendelian randomization or MR.
The underlying principle of MR is that some genetic variations have known links with behavior — for instance, certain mutations are associated with a tendency to drink more alcohol. While it’s not feasible to make inferences about any single person’s behavior based on these genes, in a very large population, researchers can use these genetic variations as a proxy for the behavior in question.
Given a large population and the requisite genetic data, therefore, researchers can look for those individuals who, based on their genetics, are most likely to perform a certain behavior, like heavy drinking. Then, the risk of Parkinson’s for those individuals can be compared with the risk among people predisposed against the behavior.
If there is a statistically significant difference in Parkinson’s risk, then that difference is likely attributable to the differences in behavior.
In MR, researchers also perform analyses to make sure that the genes associated with a given behavior do not directly affect the risk of developing the disease. That way scientists can make sure that what’s being assessed is the effect of the behavior itself.
In this study, the researchers used prior data on approximately 1.2 million people to identify genetic links between alcohol-drinking and tobacco-smoking behaviors. Then, they employed MR to assess whether these behaviors affected Parkinson’s risk, using a separate dataset comprising 37,688 patients and 18,618 people without the disease.
These datasets comprise “substantially larger and better-powered samples” than those used in prior studies that attempted similar analyses, according to the researchers.
The new analysis revealed a statistically significant inverse correlation between Parkinson’s risk and number of drinks per week. This means that the MR supports a cause-and-effect relationship between drinking alcohol and a decreased risk of Parkinson’s.
“In the present study, we provide genetic evidence to support a protective role of moderate alcohol intake against [Parkinson’s disease] risk,” the team wrote.
People who were current smokers also were found to be at significantly lower risk of Parkinson’s than former smokers. However, there was not a significant difference in risk between “ever-smokers” and “never-smokers,” nor were there significant associations between Parkinson’s risk and how much people smoked.
The team noted that most people who start smoking will, at some point, try to quit.
“Therefore, being a current smoker could simply be interpreted as individuals being less likely to quit because they have a stronger genetic predisposition to smoking, whereas former smokers have a comparatively weaker predisposition and can quit successfully,” the researchers wrote. “Thus, our results support the hypothesis of smoking being a protective factor against PD.”
More specifically, they said that the finding “suggests that prolonged smoking confers the protective effect against [Parkinson’s] risk compared to shorter-term smoking,” though they noted a need for further research to better understand this relationship.
A noted limitation of the study is that the researchers could not perform subgroup analyses — for example, to test whether the effects of drinking or smoking were similar in people of different sexes.
These analyses also did not account for the effects of drinking and smoking themselves on survival: “Heavy smoking increases mortality, so heavy smokers may be underrepresented among [Parkinson’s] patients,” the researchers wrote.