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Movement disorders
Original research
Flavonoid intake and risk of Parkinson’s disease
  1. Helena Sandoval-Insausti1,
  2. Mario H Flores-Torres1,
  3. Kjetil Bjornevik1,2,
  4. Marianna Cortese1,2,
  5. Albert Y Hung3,
  6. Michael Schwarzschild3,
  7. Tian-Shin Yeh1,2,4,5,6,
  8. Alberto Ascherio1,2,7
  1. 1 Department of Nutrition, Harvard University T H Chan School of Public Health, Boston, Massachusetts, USA
  2. 2 Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA
  3. 3 Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA
  4. 4 Department of Physical Medicine and Rehabilitation, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
  5. 5 Department of Physical Medicine and Rehabilitation, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan
  6. 6 Nuffield Department of Population Health, University of Oxford, Oxford, UK
  7. 7 Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA
  1. Correspondence to Dr Helena Sandoval-Insausti, Department of Nutrition, Harvard University T H Chan School of Public Health, Boston, Massachusetts, USA; hsandov{at}hsph.harvard.edu

Abstract

Background Flavonoids have been proposed to reduce the risk of Parkinson’s disease (PD). However, results from epidemiological studies have been inconclusive.

Objective To prospectively examine the association between the intake of flavonoids and their subclasses and the risk of PD and how pesticides may confound or modify that association.

Methods The study population comprised 80 701 women (1984–2016) and 48 782 men (1986–2016) from two large US cohorts. Flavonoid intake was ascertained at baseline and every 4 years thereafter using a semiquantitative Food Frequency Questionnaire. We conducted multivariable-adjusted Cox regression models to estimate HRs and 95% CIs of PD according to quintiles of baseline and cumulative average intakes of flavonoids and subclasses. We repeated the analyses, adjusting for intakes of high-pesticide-residue fruits and vegetables (FVs) and stratifying by servings/day of high-pesticide-residue FV intake.

Results We identified 676 incident PD cases in women and 714 in men after 30–32 years of follow-up. Higher total flavonoid intake at baseline was not associated with a lower PD risk, neither in men (HR comparing highest to lowest quintile: 0.89, 95% CI: 0.69 to 1.14) nor in women (HR comparing highest to lowest quintile: 1.27, 95% CI: 0.98 to 1.64). Similar results were observed for cumulative average intakes and flavonoid subclasses. Results remained similar after adjustment for and stratification by high-pesticide-residue FV and when analyses were restricted to younger PD cases.

Conclusion These results do not support a protective effect of flavonoid intake on PD risk. Pesticide residues do not confound or modify the association.

  • PARKINSON'S DISEASE
  • NEUROEPIDEMIOLOGY

Data availability statement

Data are available on reasonable request. ‘Further information including the procedures to obtain and access data from the Nurses’ Health Studies and Health Professionals Follow-up Study is described at https://www.nurseshealthstudy.org/researchers (contact email: nhsaccess@channing.harvard.edu) and https://sites.sph.harvard.edu/hpfs/for-collaborators/.’

https://doi.org/10.1136/jnnp-2023-332672

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    Data availability statement

    Data are available on reasonable request. ‘Further information including the procedures to obtain and access data from the Nurses’ Health Studies and Health Professionals Follow-up Study is described at https://www.nurseshealthstudy.org/researchers (contact email: nhsaccess@channing.harvard.edu) and https://sites.sph.harvard.edu/hpfs/for-collaborators/.’

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    Footnotes

    • Correction notice Since this paper first published, affiliations 4 and 5 have been updated.

    • Contributors AA and HSI contributed to the conception and design of the study; HSI and MHF-T contributed to the acquisition and analysis of data; HSI, MHF-T and KB contributed to drafting the text or preparing the figures, MC, MS, T-SY and AYH revised the manuscript.

      HSI is the guarantor.

    • Funding This study was supported by the NIH grant R01 NS126260. The NHS cohort is funded by NIH grant UM1 CA186107. The HPFS cohort is funded by NIH grant U01 167552.

    • Competing interests None declared.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.