Karen M. Powers

A reduced risk for Parkinson's disease (PD) among cigarette smokers has been observed consistently during the past 30 years. Recent evidence suggests that caffeine may also be protective. Findings are presented regarding associations of PD with smoking, caffeine intake, and alcohol consumption from a case-control study conducted in western Washington State in 1992-2000. Incident PD cases (n = 210) and controls (n = 347), frequency matched on gender and age were identified from enrollees of the Group Health Cooperative health maintenance organization. Exposure data were obtained by in-person questionnaires. Ever having smoked cigarettes was associated with a reduced risk of PD (odds ratio (OR) = 0.5, 95% confidence interval (CI): 0.4, 0.8). A stronger relation was found among current smokers (OR = 0.3, 95% CI: 0.1, 0.7) than among ex-smokers (OR = 0.6, 95% CI: 0.4, 0.9), and there was an inverse gradient with pack-years smoked (trend p < 0.001). No associations were detected for coffee consumption or total caffeine intake or for alcohol consumption. However, reduced risks were observed for consumption of 2 cups/day or more of tea (OR = 0.4, 95% CI: 0.2, 0.9) and two or more cola drinks/day (OR = 0.6, 95% CI: 0.3, 1.4). The associations for tea and cola drinks were not confounded by smoking or coffee consumption.

BACKGROUND: Dietary influences on oxidative stress have been thought to play important role in the etiology of PD. OBJECTIVE: To examine associations of PD with dietary nutrients, including minerals, vitamins, and fats. METHODS: A population-based case-control study was conducted among newly diagnosed case (n = 250) and control subjects (n = 388) identified between 1992 and 2002 from enrollees of the Group Health Cooperative health maintenance organization in western Washington state. Controls were frequency matched to cases on sex and age. In-person interviews elicited data on food frequency habits during most of adult life. Nutrient intakes were calculated and analyzed by adjusting each person's nutrient intake by their total energy intake (the nutrient density technique). RESULTS: Subjects with an iron intake in the highest quartile compared with those in the lowest quartile had an increased risk of PD (odds ratio = 1.7, 95% CI: 1.0, 2.7, trend p = 0.016). There was an apparent joint effect of iron and manganese; dietary intake above median levels of both together conferred a nearly doubled risk compared with lower intakes of each nutrient (odds ratio = 1.9, 95% CI: 1.2, 2.9). No strong associations were found for either antioxidants or fats. CONCLUSION: A high intake of iron, especially in combination with high manganese intake, may be related to risk for PD.

Inverse associations of Parkinson's disease (PD) with cigarette smoking, coffee drinking, and nonsteroidal anti-inflammatory drug (NSAID) use have been reported individually, but their joint effects have not been examined. To quantify associations with PD for the individual, two-way and three-way combinations of these factors, a case-control association study with 1,186 PD patients and 928 controls was conducted. The study setting was the NeuroGenetics Research Consortium. Subjects completed a structured questionnaire regarding smoking, coffee, and NSAID consumption. Odds ratios were calculated using unconditional logistic regression. Smoking, coffee, and over the counter NSAID use as individual factors exhibited significantly reduced risks of 20% to 30%. The two-way and three-way combinations were associated with risk reduction of 37% to 49%, and 62%, respectively. Smoking and coffee exhibited significant inverse risk trends with increasing cumulative exposures, suggesting dose-response relations. With respect to the combination of all three exposures, persons who were at the highest exposure strata for smoking and coffee and used NSAIDs had an estimated 87% reduction in risk (OR = 0.13, 95% CI = 0.06-0.29). Whether this finding reflects true biologic protection needs to be investigated.

BACKGROUND: Parkinson's disease (PD) has been associated with various workplace factors, but the evidence is inconsistent. OBJECTIVE: To estimate the risk of PD associated with various jobs and workplace exposures. METHODS: We conducted a population-based, case-control study of 404 incident PD cases and 526 age and sex-matched controls, collecting self-reported work histories including job titles and exposures to various industrial toxicants. Relative risks of PD from these exposures were estimated with odds ratios (OR) and 95% confidence intervals (CI) using logistic regression. RESULTS: Risk was not significantly affected by farming work, by metal work, or by exposure to pesticides, metals, or solvents. CONCLUSIONS: These findings do not provide support for the hypothesis that workplace factors affect the risk of PD.

Mannitol is used widely to decrease intracranial pressure (ICP); however, the mechanism by which this effect occurs is unclear. This study was designed to examine the effects of mannitol on cerebrospinal fluid (CSF) formation rate (Vf), resistance to reabsorption of CSF (Ra), and brain tissue water content (BTWC). Eighteen New Zealand White rabbits were allocated into one of three groups and studied at baseline and at two sequential doses of 20% mannitol: 0.75 g/kg followed by 4.4 mg.kg-1.min-1, and 2.0 g/kg (1.25 g/kg added to the initial dose of 0.75 g/kg) followed by 8.6 mg.kg-1.min-1. In Group 1, closed ventriculocisternal perfusion (VCP) was performed to determine changes in ICP due to mannitol. In Group 2, the increase in CSF osmolality due to mannitol was determined. In Group 3, mock CSF was used for open VCP to determine Vf and Ra. At the conclusion of each study, brain tissue samples were taken for determination of BTWC. Mannitol increased CSF and plasma osmolality. Ra was increased by 104% with the low dose of mannitol and not significantly changed by the high dose. Mannitol decreased BTWC, Vf (by 49% with the high dose), ICP, and hematocrit. The authors conclude that two of the mechanisms contributing to decreased ICP with mannitol are: 1) decreased CSF volume as indicated by decreased Vf, and 2) decreased brain tissue volume as indicated by decreased BTWC.