Lifestyle, Family History, and Risk of Parkinson Disease
Lifestyle, Family History, and Risk of Parkinson Disease
The relationship between Parkinson disease (PD) and smoking has been examined in several studies, but little is known about smoking in conjunction with other behaviors and a family history of PD. Using unconditional logistic regression analysis, we studied individual and joint associations of these factors with idiopathic PD among 1,808 Danish patients who were diagnosed in 1996–2009 and matched to 1,876 randomly selected population controls. Although there was a downward trend in duration of smoking, this was not observed for daily tobacco consumption. A moderate intake of caffeine (3.1–5 cups/day) was associated with a lower odds ratio for PD (0.45, 95% confidence interval: 0.34, 0.62), as was a moderate intake of alcohol (3.1–7 units/week) (odds ratio = 0.60, 95% confidence interval: 0.58, 0.84); a higher daily intake did not reduce the odds further. When these behaviors were studied in combination with smoking, the odds ratios were lower than those for each one alone. Compared with never smokers with no family history of PD, never smokers who did have a family history had an odds ratio of 2.81 (95% confidence interval: 1.91, 4.13); for smokers with a family history, the odds ratio was 1.60 (95% confidence interval: 1.15, 2.23). In conclusion, duration of smoking seems to be more important than intensity in the relationship between smoking and idiopathic PD. The finding of lower risk estimates for smoking in combination with caffeine or alcohol requires further confirmation.
After the first report of a lower mortality rate from Parkinson disease (PD) among smokers in 1959, many studies confirmed that inverse association, noting a duration-dependent reduction in risk. A lower risk of PD among coffee drinkers has also been demonstrated, although the association is not as consistent and strong as that for cigarette smoking. An inverse relationship between alcohol consumption and PD has been suggested; although multiple large prospective cohort studies failed to demonstrate an association, a lower risk among alcohol drinkers was found in a recent meta-analysis. These behaviors are often concurrent, but little is known about the association of PD with smoking in the context of regular intakes of caffeine-containing coffee and alcohol. Because cigarette smoking can accelerate the metabolism and clearance of caffeine in humans and alcohol affects nicotinic acetylcholine receptors in the brain, it is conceivable that smoking modifies the associations of caffeine and alcohol consumption with PD.
An inherited predisposition is considered to play an etiological role in PD, and several studies have shown a strong familial aggregation of the disease. In 2 small case-control studies of the interaction between smoking and a family history of PD, however, divergent results were obtained. In the present case-control study, we assessed the individual and combined associations of cigarette smoking, caffeine intake, and alcohol consumption with a family history of PD in a large group of patients with idiopathic Parkinson disease (IPD).
Abstract and Introduction
Abstract
The relationship between Parkinson disease (PD) and smoking has been examined in several studies, but little is known about smoking in conjunction with other behaviors and a family history of PD. Using unconditional logistic regression analysis, we studied individual and joint associations of these factors with idiopathic PD among 1,808 Danish patients who were diagnosed in 1996–2009 and matched to 1,876 randomly selected population controls. Although there was a downward trend in duration of smoking, this was not observed for daily tobacco consumption. A moderate intake of caffeine (3.1–5 cups/day) was associated with a lower odds ratio for PD (0.45, 95% confidence interval: 0.34, 0.62), as was a moderate intake of alcohol (3.1–7 units/week) (odds ratio = 0.60, 95% confidence interval: 0.58, 0.84); a higher daily intake did not reduce the odds further. When these behaviors were studied in combination with smoking, the odds ratios were lower than those for each one alone. Compared with never smokers with no family history of PD, never smokers who did have a family history had an odds ratio of 2.81 (95% confidence interval: 1.91, 4.13); for smokers with a family history, the odds ratio was 1.60 (95% confidence interval: 1.15, 2.23). In conclusion, duration of smoking seems to be more important than intensity in the relationship between smoking and idiopathic PD. The finding of lower risk estimates for smoking in combination with caffeine or alcohol requires further confirmation.
Introduction
After the first report of a lower mortality rate from Parkinson disease (PD) among smokers in 1959, many studies confirmed that inverse association, noting a duration-dependent reduction in risk. A lower risk of PD among coffee drinkers has also been demonstrated, although the association is not as consistent and strong as that for cigarette smoking. An inverse relationship between alcohol consumption and PD has been suggested; although multiple large prospective cohort studies failed to demonstrate an association, a lower risk among alcohol drinkers was found in a recent meta-analysis. These behaviors are often concurrent, but little is known about the association of PD with smoking in the context of regular intakes of caffeine-containing coffee and alcohol. Because cigarette smoking can accelerate the metabolism and clearance of caffeine in humans and alcohol affects nicotinic acetylcholine receptors in the brain, it is conceivable that smoking modifies the associations of caffeine and alcohol consumption with PD.
An inherited predisposition is considered to play an etiological role in PD, and several studies have shown a strong familial aggregation of the disease. In 2 small case-control studies of the interaction between smoking and a family history of PD, however, divergent results were obtained. In the present case-control study, we assessed the individual and combined associations of cigarette smoking, caffeine intake, and alcohol consumption with a family history of PD in a large group of patients with idiopathic Parkinson disease (IPD).
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