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Dietary Antioxidants and the Risk of Parkinson Disease: The Swedish National March Cohort.
Neurology. 2021 02 09; 96(6):e895-e903.Neur

Abstract

OBJECTIVE

To determine whether high baseline dietary antioxidants and total nonenzymatic antioxidant capacity (NEAC) is associated with a lower risk of Parkinson disease (PD) in men and women, we prospectively studied 43,865 men and women from a large Swedish cohort.

METHODS

In the Swedish National March Cohort, 43,865 men and women aged 18-94 years were followed through record linkages to National Health Registries from 1997 until 2016. Baseline dietary vitamin E, vitamin C, and beta-carotene intake, as well as NEAC, were assessed by a validated food frequency questionnaire collected at baseline. All exposure variables were adjusted for energy intake and categorized into tertiles. Multivariable Cox proportional hazard regression models were fitted to estimate hazard ratios (HRs) with 95% confidence intervals (CIs) for PD.

RESULTS

After a mean follow-up time of 17.6 years, we detected 465 incidence cases of PD. In the multivariable adjusted model, dietary vitamin E (HR 0.68, 95% CI 0.52-0.90; p for trend 0.005) and vitamin C (HR 0.68, 95% CI 0.52-0.89; p for trend 0.004) were inversely associated with the risk of PD when comparing participants in the highest vs the lowest tertiles of exposure. No association was found with estimated intake of dietary beta-carotene or NEAC.

CONCLUSION

Our findings suggest that dietary vitamin E and C intake might be inversely associated with the risk of PD. No association was found with dietary beta-carotene or NEAC.

CLASSIFICATION OF EVIDENCE

This study provides Class III evidence that dietary vitamin E and C intake are inversely associated with the risk of PD.

Authors+Show Affiliations

From the Department of Statistics and Quantitative Methods (E.H., R.B.), University of Milano-Bicocca, Milan; Institute for Biomedicine, Eurac Research (E.H.), Affiliated Institute of the University of Lübeck, Bolzano, Italy; Clinical Epidemiology Division, Department of Medicine (Solna) (Y.T.L., S.B.), and Department of Medical Epidemiology and Biostatistics (W.Y., H.-O.A., R.B.), Karolinska Institutet, Stockholm; Obesity Center, Academic Specialist Center (Y.T.L.), Stockholm Health Services, Sweden; Functional Food and Metabolic Stress Prevention Laboratory, Faculty of BioSciences and Technology for Food, Agriculture and Environment (M.S.), University of Teramo, Italy; and Clinical Effectiveness Research Group, Institute of Health (H.-O.A.), University of Oslo, Norway. essimarjatta.hantikainen@eurac.edu.From the Department of Statistics and Quantitative Methods (E.H., R.B.), University of Milano-Bicocca, Milan; Institute for Biomedicine, Eurac Research (E.H.), Affiliated Institute of the University of Lübeck, Bolzano, Italy; Clinical Epidemiology Division, Department of Medicine (Solna) (Y.T.L., S.B.), and Department of Medical Epidemiology and Biostatistics (W.Y., H.-O.A., R.B.), Karolinska Institutet, Stockholm; Obesity Center, Academic Specialist Center (Y.T.L.), Stockholm Health Services, Sweden; Functional Food and Metabolic Stress Prevention Laboratory, Faculty of BioSciences and Technology for Food, Agriculture and Environment (M.S.), University of Teramo, Italy; and Clinical Effectiveness Research Group, Institute of Health (H.-O.A.), University of Oslo, Norway.From the Department of Statistics and Quantitative Methods (E.H., R.B.), University of Milano-Bicocca, Milan; Institute for Biomedicine, Eurac Research (E.H.), Affiliated Institute of the University of Lübeck, Bolzano, Italy; Clinical Epidemiology Division, Department of Medicine (Solna) (Y.T.L., S.B.), and Department of Medical Epidemiology and Biostatistics (W.Y., H.-O.A., R.B.), Karolinska Institutet, Stockholm; Obesity Center, Academic Specialist Center (Y.T.L.), Stockholm Health Services, Sweden; Functional Food and Metabolic Stress Prevention Laboratory, Faculty of BioSciences and Technology for Food, Agriculture and Environment (M.S.), University of Teramo, Italy; and Clinical Effectiveness Research Group, Institute of Health (H.-O.A.), University of Oslo, Norway.From the Department of Statistics and Quantitative Methods (E.H., R.B.), University of Milano-Bicocca, Milan; Institute for Biomedicine, Eurac Research (E.H.), Affiliated Institute of the University of Lübeck, Bolzano, Italy; Clinical Epidemiology Division, Department of Medicine (Solna) (Y.T.L., S.B.), and Department of Medical Epidemiology and Biostatistics (W.Y., H.-O.A., R.B.), Karolinska Institutet, Stockholm; Obesity Center, Academic Specialist Center (Y.T.L.), Stockholm Health Services, Sweden; Functional Food and Metabolic Stress Prevention Laboratory, Faculty of BioSciences and Technology for Food, Agriculture and Environment (M.S.), University of Teramo, Italy; and Clinical Effectiveness Research Group, Institute of Health (H.-O.A.), University of Oslo, Norway.From the Department of Statistics and Quantitative Methods (E.H., R.B.), University of Milano-Bicocca, Milan; Institute for Biomedicine, Eurac Research (E.H.), Affiliated Institute of the University of Lübeck, Bolzano, Italy; Clinical Epidemiology Division, Department of Medicine (Solna) (Y.T.L., S.B.), and Department of Medical Epidemiology and Biostatistics (W.Y., H.-O.A., R.B.), Karolinska Institutet, Stockholm; Obesity Center, Academic Specialist Center (Y.T.L.), Stockholm Health Services, Sweden; Functional Food and Metabolic Stress Prevention Laboratory, Faculty of BioSciences and Technology for Food, Agriculture and Environment (M.S.), University of Teramo, Italy; and Clinical Effectiveness Research Group, Institute of Health (H.-O.A.), University of Oslo, Norway.From the Department of Statistics and Quantitative Methods (E.H., R.B.), University of Milano-Bicocca, Milan; Institute for Biomedicine, Eurac Research (E.H.), Affiliated Institute of the University of Lübeck, Bolzano, Italy; Clinical Epidemiology Division, Department of Medicine (Solna) (Y.T.L., S.B.), and Department of Medical Epidemiology and Biostatistics (W.Y., H.-O.A., R.B.), Karolinska Institutet, Stockholm; Obesity Center, Academic Specialist Center (Y.T.L.), Stockholm Health Services, Sweden; Functional Food and Metabolic Stress Prevention Laboratory, Faculty of BioSciences and Technology for Food, Agriculture and Environment (M.S.), University of Teramo, Italy; and Clinical Effectiveness Research Group, Institute of Health (H.-O.A.), University of Oslo, Norway.From the Department of Statistics and Quantitative Methods (E.H., R.B.), University of Milano-Bicocca, Milan; Institute for Biomedicine, Eurac Research (E.H.), Affiliated Institute of the University of Lübeck, Bolzano, Italy; Clinical Epidemiology Division, Department of Medicine (Solna) (Y.T.L., S.B.), and Department of Medical Epidemiology and Biostatistics (W.Y., H.-O.A., R.B.), Karolinska Institutet, Stockholm; Obesity Center, Academic Specialist Center (Y.T.L.), Stockholm Health Services, Sweden; Functional Food and Metabolic Stress Prevention Laboratory, Faculty of BioSciences and Technology for Food, Agriculture and Environment (M.S.), University of Teramo, Italy; and Clinical Effectiveness Research Group, Institute of Health (H.-O.A.), University of Oslo, Norway.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

33408141

Citation

Hantikainen, Essi, et al. "Dietary Antioxidants and the Risk of Parkinson Disease: the Swedish National March Cohort." Neurology, vol. 96, no. 6, 2021, pp. e895-e903.
Hantikainen E, Trolle Lagerros Y, Ye W, et al. Dietary Antioxidants and the Risk of Parkinson Disease: The Swedish National March Cohort. Neurology. 2021;96(6):e895-e903.
Hantikainen, E., Trolle Lagerros, Y., Ye, W., Serafini, M., Adami, H. O., Bellocco, R., & Bonn, S. (2021). Dietary Antioxidants and the Risk of Parkinson Disease: The Swedish National March Cohort. Neurology, 96(6), e895-e903. https://doi.org/10.1212/WNL.0000000000011373
Hantikainen E, et al. Dietary Antioxidants and the Risk of Parkinson Disease: the Swedish National March Cohort. Neurology. 2021 02 9;96(6):e895-e903. PubMed PMID: 33408141.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dietary Antioxidants and the Risk of Parkinson Disease: The Swedish National March Cohort. AU - Hantikainen,Essi, AU - Trolle Lagerros,Ylva, AU - Ye,Weimin, AU - Serafini,Mauro, AU - Adami,Hans-Olov, AU - Bellocco,Rino, AU - Bonn,Stephanie, Y1 - 2021/01/06/ PY - 2020/06/22/received PY - 2020/10/05/accepted PY - 2021/1/8/pubmed PY - 2021/2/24/medline PY - 2021/1/7/entrez SP - e895 EP - e903 JF - Neurology JO - Neurology VL - 96 IS - 6 N2 - OBJECTIVE: To determine whether high baseline dietary antioxidants and total nonenzymatic antioxidant capacity (NEAC) is associated with a lower risk of Parkinson disease (PD) in men and women, we prospectively studied 43,865 men and women from a large Swedish cohort. METHODS: In the Swedish National March Cohort, 43,865 men and women aged 18-94 years were followed through record linkages to National Health Registries from 1997 until 2016. Baseline dietary vitamin E, vitamin C, and beta-carotene intake, as well as NEAC, were assessed by a validated food frequency questionnaire collected at baseline. All exposure variables were adjusted for energy intake and categorized into tertiles. Multivariable Cox proportional hazard regression models were fitted to estimate hazard ratios (HRs) with 95% confidence intervals (CIs) for PD. RESULTS: After a mean follow-up time of 17.6 years, we detected 465 incidence cases of PD. In the multivariable adjusted model, dietary vitamin E (HR 0.68, 95% CI 0.52-0.90; p for trend 0.005) and vitamin C (HR 0.68, 95% CI 0.52-0.89; p for trend 0.004) were inversely associated with the risk of PD when comparing participants in the highest vs the lowest tertiles of exposure. No association was found with estimated intake of dietary beta-carotene or NEAC. CONCLUSION: Our findings suggest that dietary vitamin E and C intake might be inversely associated with the risk of PD. No association was found with dietary beta-carotene or NEAC. CLASSIFICATION OF EVIDENCE: This study provides Class III evidence that dietary vitamin E and C intake are inversely associated with the risk of PD. SN - 1526-632X UR - https://www.unboundmedicine.com/medline/citation/33408141/Dietary_Antioxidants_and_the_Risk_of_Parkinson_Disease:_The_Swedish_National_March_Cohort_ L2 - http://www.neurology.org/cgi/pmidlookup?view=long&pmid=33408141 DB - PRIME DP - Unbound Medicine ER -