Smoking, Caffeine Consumption Inversely Related to Parkinson's Disease Risk

April 18, 2007 — A study of families affected by Parkinson's disease (PD) has shown again a possible lower risk for the disease associated with increased cigarette smoking or caffeine consumption. These findings, published in the April issue of the Archives of Neurology, underline that environmental factors such as these must be taken into account when studying the genetics of PD, the authors write.

"Given the complexity of PD, these environmental factors likely do not exert their effects in isolation, thus highlighting the importance of gene-environment interactions in determining PD susceptibility," corresponding author William K. Scott, PhD, from the Miami Institute for Human Genomics at the University of Miami in Florida, and colleagues write. "Smoking and caffeine possibly modify genetic effects in families with PD and should be considered as effect modifiers in candidate gene studies for PD."

Inverse Association
In the current study, the authors used a family-based case-control design, which commonly is used in genetic association studies because it reduces confounding by ethic background as well as confounding by familial influences on exposure. Case patients and control subjects tend to be well matched on unmeasured genetic and environmental factors that could predispose to exposure behaviors and to disease, the authors point out.

The authors examined the associations between PD and 3 factors that had been shown in previous studies to have a putative protective effect: smoking; caffeine intake through coffee, tea, and soft drink consumption; and the use of nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin, ibuprofen, and naproxen.

The study included 356 case patients and 317 family control subjects; environmental exposures were self-reported.

After controlling for age and sex, the authors found that subjects with PD were significantly less likely than unaffected family members to report ever smoking or current smoking.

Similarly, caffeine consumption was inversely associated with PD risk. Increasing dosage, intensity, and total caffeine consumption all were associated with lower risk for PD. High-dose caffeine showed a significant inverse association with PD, with an odds ratio (OR) of 0.58 (95% confidence interval [CI], 0.34 - 0.99).

No relationship was seen in this moderate-sized sample between NSAID use and PD risk, the authors note. They point out though that small- to moderate-sized case-control samples may be underpowered to detect an NSAID effect.

Despite epidemiologic support for these environmental factors in neuroprotection, the biological mechanisms, "if existent, have eluded investigators," the authors write. Some investigators have proposed that the inverse associations with smoking and caffeine may alternatively reflect a preclinical PD state of aversion, when smoking and consuming caffeine may be less rewarding.

However, the authors write, "We detected significant associations for smoking and caffeine when truncating exposures at the reference age, at 10 years before the reference age, and at 20 years before the reference age, suggesting that the preclinical aversion hypothesis does not adequately explain these data."

In a statement from Duke University Medical Center in Durham, North Carolina, where several of the authors are based, the researchers emphasized that smoking and caffeine consumption "carry their own risks, and should not be taken up in an attempt to avoid developing Parkinson's disease."

The study was supported by grants from the National Institute of Neurological Disorders and Stroke. The authors have disclosed no relevant financial relationships.

Arch Neurol. 2007;64:576-580.

Source: http://www.medscape.com/viewarticle/555353?src=mp