In a case-control study, we investigated the possible etiologic relevance to Parkinson's disease (PD) of rural factors such as farming activity, pesticide exposures, well-water drinking, and animal contacts; toxicologic exposures such as wood preservatives, heavy metals, and solvents; general anesthesia; head trauma; and differences in the intrauterine environment. We recruited 380 patients in nine German clinics, 379 neighborhood control subjects, and 376 regional control subjects in the largest case-control study investigating such factors and collected data in structured personal interviews using conditional logistic regression to control for educational status and cigarette smoking. The latter was strongly inversely associated with PD. There were significantly elevated odds ratios (OR) for pesticide use, in particular, for organochlorines and alkylated phosphates, but no association was present between PD and other rural factors. A significantly elevated OR was present for exposure to wood preservatives. Subjective assessment by the probands indicated that exposure to some heavy metals, solvents, exhaust fumes, and carbon monoxide was significantly more frequent among patients than control subjects, but this was not confirmed by a parallel assessment of job histories according to a job exposure matrix. Patients had undergone general anesthesia and suffered severe head trauma more often than control subjects, but a dose-response gradient was not present. Patients reported a significantly larger number of amalgam-filled teeth before their illness than control subjects. The frequency of premature births and birth order did not differ between patients and control subjects. Patients reported significantly more relatives affected with PD than control subjects. These results support a role for environmental and genetic factors in the etiology of PD.

In a case-control study, we compared the past dietary habits of 342 Parkinson's disease (PD) patients recruited from nine German clinics with those of 342 controls from the same neighborhood or region. Data were gathered with a structured interview and a self-administered food-frequency questionnaire. Nutrient intakes were calculated from the reported food intakes through linkage with the German Federal Food Code and analyzed using multivariate conditional logistic regression to control for total energy intake, educational status, and cigarette smoking. At the macronutrient level, patients reported higher carbohydrate intake than controls after adjustment for total energy intake, smoking, and educational status (OR = 2.74, 95% confidence interval [CI]: 1.30-6.07, for the highest versus lowest quartile, p trend = 0.02). This was reflected in higher monosaccharide and disaccharide intakes at the nutrient level. There was no difference between patients and controls in protein and fat intake after adjustment for energy intake. We found an inverse association between the intakes of beta-carotene (OR = 0.67, 95% CI: 0.37-1.19, p trend = 0.06) and ascorbic acid (OR = 0.60, 95% CI: 0.33-1.09, p trend = 0.04) by patients, although only the trend for ascorbic acid intake reached statistical significance. There was no difference between groups for alpha-tocopherol intake after adjustment for energy intake. We also found that patients reported a significantly lower intake of niacin than controls (OR = 0.15, 95% CI: 0.07-0.33, p trend< 0.00005). Our results suggest that if antioxidants play a protective role in this disease, the amounts provided by diet alone are insufficient. Although the interpretation of the inverse association between niacin intake and PD is complicated by the high niacin content in coffee and alcoholic beverages, which were also inversely associated with PD in this study, the strength of this association and its biologic plausibility warrant further investigation.

In a case-control study, we compared the past dietary habits of 342 Parkinson's disease (PD) patients recruited from nine German clinics with those of 342 controls from the same neighborhood or region. Data were gathered with a structured interview and a self-administered food-frequency questionnaire, and analyzed using multivariate conditional logistic regression to control for educational status and cigarette smoking. There was no significant difference between cases and controls in the consumption of fruits and vegetables, although there was a negative trend for the consumption of raw vegetables. Controls reported a higher potato consumption than patients (OR = 0.43, 95% confidence interval [CI]: 0.24-0.74, highest versus lowest quartile). Patients reported eating significantly larger quantities of sweet foods as well as having more snacks than controls. This may, however, be the result of an illness-related change in dietary habits leading to a selective recall effect, since sweet foods may enhance the transport of L-dopa across the blood-brain barrier. We also found that patients consumed less beer (OR = 0.26, 95% CI: 0.14-0.49) and spirits (OR = 0.56, 95% CI: 0.36-0.86), but not wine, and they consumed less coffee (OR = 0.27, 95% CI: 0.14-0.52, highest versus lowest quartile), but not tea, than controls. This may relate to a possible interaction between dopaminergic activity and the intake of ethanol or caffeine. Significantly more patients than controls reported ever consuming raw meat (OR = 1.78, 95% CI: 1.21-2.63). These results suggest that the intake of certain foods may be associated with the development of PD.

The objective of this case-control study was to identify the main risk factors for community-acquired pneumonia (CAP) in a German adult population. A self-administered questionnaire was given to CAP cases provided by the German competence network CAPNETZ and population-based, randomly selected controls (sex- and age-matched). Multivariate analysis showed that in addition to known risk factors such as previous CAP [odds ratio (OR) 1.6, 95% confidence interval (CI) 1.3-2.1], more than one respiratory infection during the previous year (OR 3.6, 95% CI 2.9-4.5), chronic pulmonary diseases (OR 2.3, 95% CI 1.7-3.0), number of comorbidities (OR 1.6, 95% CI 1.4-1.9), and number of children in the household (2 children: OR 2.2, 95% CI 1.5-3.4; > or = 3 children: OR 3.2, 95% CI 1.5-7.0) were independent risk factors for CAP. This was pronounced in particular in people aged < or = 65 years. The most likely explanation for this finding is higher exposure to infectious agents.

The results are considered in terms of criteria for causality. Plausible explanations for the observed inverse association between smoking and PD include: 1. A genetic predisposition that increases the risk for PD (such as defective detoxification enzymes) simultaneously decreases the likelihood of smoking. 2. Inherently lower dopamine levels in predestined PD patients cause them to be less prone to addiction. 3. Smoking is neuroprotective.