Mid-life smoking and late-life dementia: the Honolulu-Asia Aging Study.

We studied the association between mid-life smoking and late-life dementia in the Honolulu Heart Program (1965-1971) and follow-up assessment for dementia (1991-1996) of 3734 Japanese-American men (80% of survivors). Neuropathologic data were available for 218 men. Adjusting for age, education and apolipoprotein E (APOE) genotype, the risk of Alzheimer's disease (AD) in smokers increased with pack-years of smoking at medium (odds ratio (OR)=2.18, 95% confidence interval (CI)=1.07-4.69) and heavy (OR=2.40; 95% CI=1.16-5.17) smoking levels. Very heavy smoking was not associated with AD (OR=1.08; 95% CI=0.43-2.63). Findings were similar when AD cases included those with cerebrovascular disease and for all dementias combined. Adjustment for cardiovascular and respiratory factors or stratification by apolipoprotein E genotype did not change these associations. In an autopsied subsample, the number of neuritic plaques increased with amount smoked. This study suggests that amount smoked is associated with an increasing risk of AD and Alzheimer-type neuropathology up to heavy smoking levels. The lack of association in very heavy smokers may be due to a hardy survivor effect.

Dietary fat intake, pesticide use, and Parkinson's disease.

BACKGROUND: Dietary fat intake may modify Parkinson's disease (PD) risk directly or by altering the response to environmental neurotoxicants including pesticides. METHODS: We conducted a case-control study of PD nested in the Agricultural Health Study (AHS), a cohort of pesticide applicators and spouses. We evaluated diet and pesticide use before diagnosis in 89 PD cases, confirmed by movement disorder specialists, or a corresponding date in 336 frequency-matched controls. Associations were evaluated using multivariate logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: In the AHS, PD was inversely associated with N-3 polyunsaturated fatty acids (PUFAs) (OR 0.4, 95% CI 0.2-0.8 for highest vs. lowest tertile) and the N-3 precursor α-linolenic acid (0.4, 0.2-0.8). In a meta-analysis of nine studies, including the present one, PD was inversely associated with α-linolenic acid (0.81, 0.68-0.96). In the AHS, associations of PD with the pesticides paraquat and rotenone were modified by fat intake. The OR for paraquat was 4.2 (1.5-12) in individuals with PUFA intake below the median but 1.2 (0.4-3.4) in those with higher intake (p-interaction = 0.10). The OR for rotenone was 5.8 (2.3-15) in those with saturated fat intake above the median but 1.5 (0.5-4.2) in those with lower intake (p-interaction = 0.02). CONCLUSIONS: PUFA intake was consistently associated with lower PD risk, and dietary fats modified the association of PD risk with pesticide exposure. If confirmed, these findings suggest that a diet high in PUFAs and low in saturated fats might reduce risk of PD.