Flavonoids Not Tied to Reduced Parkinson's Risk 2024 medscape.com/viewarticle/fl...
TOPLINE:
Higher intake of flavonoids shows no association with a later reduced risk for Parkinson's disease (PD), in a new study. The findings, which contradict earlier reports suggesting an association between flavonoids and PD risk, were not modified by the presence or absence of pesticide residues in fruits and vegetables, researchers reported.
METHODOLOGY:
• Investigators used data from the Nurses' Health Study and the Health Professionals Follow-Up Study, which included 80,701 women and 47,782 men who entered the study in 1984 and 1986, respectively, and were free of PD at baseline.
• Flavonoid intake was ascertained at baseline and every 4 years thereafter until 2016 using a Food Frequency Questionnaire.
• Investigators accounted for a range of confounders, including ethnicity, physical activity, body mass index, family history of PD, smoking, alcohol intake, and current use of multivitamins.
• The research updates a previous study by the same researchers that showed men with higher flavonoid intake had significantly lower PD risk and that anthocyanin (a flavonoid subclass) was inversely associated with PD risk. The current study included 10 more years of follow-up and 583 additional PD cases.
TAKEAWAY:
• During the 30- to 32-year follow-up, 1390 incident PD cases were identified (676 in females and 714 in males).
• Higher total flavonoid intake at baseline was not associated with a lower PD risk in either men or women (adjusted hazard ratio comparing highest to lowest quintile, 0.89 [95% CI, 0.69-1.14] and 1.27 [95% CI, 0.98-1.64], respectively).
• The researchers obtained similar findings for the various flavonoid subclasses including anthocyanin.
• Results remained similar, even after adjustment for and stratification by high-pesticide residue fruits and vegetables and even after the researchers restricted analyses to younger PD cases.
IN PRACTICE:
"These findings are in contrast with previously reported beneficial associations of dietary flavonoids among participants in these cohorts," the authors wrote. While this discrepancy could theoretically be explained if high flavonoid intake slowed the pathologic process of preclinical PD, investigators note the lack of association between flavonoid consumption and PD risk was consistent, even after adjusting for age at the time of diagnosis. This reduced the likelihood that the "aging of the cohort is a plausible explanation for the discrepancy with our previous report."
SOURCE:
Helena Sandoval-Insausti, of the Department of Nutrition, Harvard University T.H. Chan School of Public Health, Boston, Massachusetts, was the lead and corresponding author of the study. It was published online on January 24, 2024, in the Journal of Neurology, Neurosurgery and Psychiatry.
LIMITATIONS:
The study was observational and relied on participants' self-reported intake of flavonoids. Pesticide exposure was measured only indirectly by linking self-reported fruit and vegetable intake to pesticides, which could lead to misclassification.
DISCLOSURES:
The study was supported by the National Institutes of Health. The authors declared no competing relationships.