Association of Coffee and Caffeine Consumption with Brain Lewy Pathology in the Honolulu-Asia Aging Study (S42.005)

Abstract

Objective: To examine the association of mid-life coffee and caffeine consumption with brain Lewy pathology (LP) in Honolulu-Asia Aging Study (HAAS) decedents. Background Coffee drinking is related to lower risk of Parkinson9s disease (PD). The mechanism is unknown. Demonstrating an inverse association between coffee drinking and LP in the brain would provide evidence that the relationship is biologically based. Design/Methods: Sensitive alpha-synuclein staining performed on 519 brains from HAAS participants was used to identify LP (Lewy bodies and Lewy neurites). Braak PD staging was performed. Information on coffee consumption and smoking was obtained from 1965 to 1968 when participants were aged 46 to 67 years (mean = 54). Percentage of brains with LP was determined within common coffee consumption strata (oz/d) and across quintiles of caffeine (mg/d) intake. Results: Average age at death was 85 years (range 73-102) and average time from dietary assessment to death was 31.3 years (range 24-38). There were 76 brains with LP. Percent of brains with LP was 20.2 for noncoffee drinkers, and 14.8, 17.2, 11.4 and 4.7 for those drinking >0-8, >8-16, >16-24, and >24 oz/d (p=0.013 in test for trend). Findings were similar across quintiles of caffeine consumption (p=0.048 in test for trend). Although the association with caffeine was weakened after adjustment for age, smoking, constipation, and physical activity (p=0.112), the association with coffee intake persisted (p=0.023). After removing cases of PD (N=29), the age and risk factor adjusted percentage of brains with LP continued to be lowest in those whose coffee consumption was>16 oz/d versus intakes that were lower (p=0.024). Conclusions: A significant inverse relationship was noted between coffee consumption and presence of LP. This is consistent with findings based on clinical PD and with the hypothesis of a primary protective effect of coffee consumption against PD that may be related to prevention of LP. Supported by: United States Department of the Army (DAMD17-98-1-8621), National Institute of Neurological Disorders and Stroke (R01-NS41265), National Institute on Aging (U01-AG019349, U01-AG17155), and by the Office of Research and Development, Medical Research Service, Department of Veterans Affairs. Disclosure: Dr. Ross has received research support from the Michael J. Fox Foundation. Dr. Duda has received personal compensation for activities with Delaware Media Group and Teva Pharmaceuticals, LTD.Dr. Duda holds stock and/or stock options in Celgene Corporation. Dr. Abbott has nothing to disclose. Dr. Petrovitch has nothing to disclose. Dr. Tanner has received personal compensation for activities with Impax Pharmaceuticals, Allergan, Inc. & Genentech, Inc. as a consultant. Dr. Tanner has received research support from Michael J. Fox Foundation, Department of Defense, Parkinson9s Disease Foundation, Parkinson9s Institute, Unity Walk and Brin Foundation. Dr. Masaki has nothing to disclose. Dr. Uyehara-Lock has nothing to disclose. Dr. Launer has nothing to disclose. Dr. White has nothing to disclose.