Dietary antioxidants and the risk of Parkinson Disease

Neurology ◽  
2021 ◽  
pp. 10.1212/WNL.0000000000011373
Author(s):  
Essi Hantikainen ◽  
Ylva Trolle Lagerros ◽  
Weimin Ye ◽  
Mauro Serafini ◽  
Hans-Olov Adami ◽  
...  
Keyword(s):  
Vitamin E ◽  
Parkinson Disease ◽  
Beta Carotene ◽  
Dietary Vitamin ◽  
Class Iii ◽  
Dietary Antioxidants ◽  
Men And Women ◽  
Hazard Ratios ◽  
Cox Proportional Hazard Regression ◽  
Vitamin E And C

ObjectiveTo determine whether high baseline dietary antioxidants and total non-enzymatic antioxidant capacity (NEAC) is associated with a lower risk of Parkinson disease in men and women, we prospectively studied 43,865 men and women from a large Swedish cohort.MethodsIn 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, 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 Parkinson disease.ResultsAfter a mean follow-up time of 17.6 years we detected 465 incidence cases of Parkinson disease. In the multivariable adjusted model, dietary vitamin E (HR: 0.68: 95% CI: 0.52–0.90; p for trend: 0.005) and C (HR: 0.68; 95% CI: 0.52–0.89; p for trend: 0.004) were inversely associated with the risk of Parkinson disease, when comparing subjects in the highest to the lowest tertiles of the exposure. No association was found with estimated intake of dietary beta-carotene or NEAC.ConclusionOur findings suggest that dietary vitamin E and C intake might be inversely associated with the risk of Parkinson disease. No association was found with dietary beta-carotene or NEAC.Classification of evidenceThis study provides Class III evidence that dietary vitamin E and C intake are inversely associated with the risk of Parkinson disease.

scholarly journals Dietary Vitamin B6 Intake Associated with a Decreased Risk of Cardiovascular Disease: A Prospective Cohort Study

Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1484 ◽  
Author(s):  
Jimin Jeon ◽  
Kyong Park
Keyword(s):  
Cardiovascular Disease ◽  
Vitamin B6 ◽  
Epidemiological Studies ◽  
Dietary Vitamin ◽  
Response Analysis ◽  
Cvd Risk ◽  
Beneficial Effects ◽  
Cox Proportional Hazard ◽  
Hazard Ratios ◽  
Cox Proportional Hazard Regression

Although the biological mechanisms underlying the beneficial effects of vitamin B6 on cardiovascular disease (CVD) have been reported on, epidemiological studies have yielded controversial results, and data on the Korean population are limited. This study examined the association between dietary vitamin B6 intake and CVD incidence in Koreans. A total of 9142 participants of the Korean Genome and Epidemiology Study, aged 40–69 years, who did not have CVD or cancer at the baseline were included in the analysis. Dietary data were assessed using a validated semi-quantitative food frequency questionnaire. CVD incidence was assessed using biennial questionnaires and confirmed through repeated personal interviews. Multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazard regression models. After multivariate adjustment, a higher vitamin B6 intake was significantly associated with a decreased CVD risk in men (HR: 0.44; 95% CI: 0.25–0.78); no such association was observed in women. Dose-response analysis confirmed the presence of inverse linearity between vitamin B6 intake and CVD incidence in men (p for nonlinearity = 0.3). A higher dietary intake level of vitamin B6 was associated with a reduced CVD risk in Korean men. These observations require further verification in other populations.

Use of Vitamin E and C Supplements for the Prevention of Cognitive Decline

2016 ◽  
Vol 51 (2) ◽  
pp. 118-124 ◽  
Author(s):  
Luta Luse Basambombo ◽  
Pierre-Hugues Carmichael ◽  
Sharlène Côté ◽  
Danielle Laurin
Keyword(s):  
Vitamin E ◽  
Cognitive Decline ◽  
Antioxidant Vitamin ◽  
Vitamin Supplements ◽  
Data Set ◽  
Hazard Ratios ◽  
Vitamins E And C ◽  
Primary Prevention Strategy ◽  
Vitamin E And C ◽  
The Continuum

Background: There are few studies of the association between the use of antioxidant vitamin supplements and the risk of Alzheimer’s disease (AD). Cognitive decline is generally viewed as part of the continuum between normal aging and AD. Objective: To evaluate whether the use of vitamin E and C supplements is associated with reduced risks of cognitive impairment, not dementia (CIND), AD, or all-cause dementia in a representative sample of older persons ≥65 years old. Methods: Data from the Canadian Study of Health and Aging (1991-2002), a cohort study of dementia including 3 evaluation waves at 5-yearly intervals, were used. Exposure to vitamins E and C was self-reported at baseline in a risk factor questionnaire and/or in a clinical examination. Results: The data set included 5269 individuals. Compared with those not taking vitamin supplements, the age-, sex-, and education-adjusted hazard ratios of CIND, AD, and all-cause dementia were, respectively, 0.77 (95% CI = 0.60-0.98), 0.60 (95% CI = 0.42-0.86), and 0.62 (95% CI = 0.46-0.83) for those taking vitamin E and/or C supplements. Results remained significant in fully adjusted models except for CIND. Similar results were observed when vitamins were analyzed separately. Conclusions: This analysis suggests that the use of vitamin E and C supplements is associated with a reduced risk of cognitive decline. Further investigations are needed to determine their value as a primary prevention strategy.

Dietary vitamin E and C intake is inversely associated with the severity of nonalcoholic fatty liver disease

2019 ◽  
Vol 51 (12) ◽  
pp. 1698-1705 ◽  
Author(s):  
Dana Ivancovsky-Wajcman ◽  
Naomi Fliss-Isakov ◽  
Federico Salomone ◽  
Muriel Webb ◽  
Oren Shibolet ◽  
...  
Keyword(s):  
Liver Disease ◽  
Vitamin E ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Dietary Vitamin ◽  
Nonalcoholic Fatty Liver ◽  
Vitamin E And C

scholarly journals Vitamin E supplementation may transiently increase tuberculosis risk in males who smoke heavily and have high dietary vitamin C intake – comments by Hernández-Garduño

2008 ◽  
Vol 101 (1) ◽  
pp. 145-145 ◽  
Author(s):  
Eduardo Hernández-Garduño
Keyword(s):  
Vitamin E ◽  
Vitamin C ◽  
Cancer Prevention ◽  
Beta Carotene ◽  
Alpha Tocopherol ◽  
Dietary Vitamin ◽  
Prevention Study ◽  
Tuberculosis Risk ◽  
Heavy Smokers ◽  
Vitamin E Supplementation

Hemilä & Kaprio(1) found a 72 % increase in the risk of tuberculosis (TB) in males taking vitamin E supplements and having high dietary vitamin C intake; the effect was restricted to heavy smokers as part of the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study.

Dietary supplementation with vitamin E and C attenuates dexamethasone-induced glucose intolerance in rats

2012 ◽  
Vol 302 (1) ◽  
pp. R49-R58 ◽  
Author(s):  
Deon B. Williams ◽  
Zhongxiao Wan ◽  
Bruce C. Frier ◽  
Rhonda C. Bell ◽  
Catherine J. Field ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Vitamin E ◽  
Glucose Tolerance ◽  
Glucose Intolerance ◽  
Alpha Tocopherol ◽  
Dietary Vitamin ◽  
Acid Oxidation ◽  
Mitochondrial Enzymes ◽  
Ampk Signaling ◽  
Vitamin E And C

Glucocorticoid excess induces marked insulin resistance and glucose intolerance. A recent study has shown that antioxidants prevent dexamethasone (DEX)-induced insulin resistance in cultured adipocytes. The purpose of this investigation was to examine the effects of dietary vitamin E and C (Vit E/C) supplementation on DEX-induced glucose intolerance in rats. We hypothesized that feeding rats a diet supplemented with Vit E/C would improve glucose tolerance and restore insulin signaling in skeletal muscle, adipose, and liver and prevent alterations in AMPK signaling in these tissues. Male Wistar rats received either a control or Vit E/C-supplemented diet (0.5 g/kg diet each of l-ascorbate and dl-all rac-alpha-tocopherol) for 9 days prior to, and during, 5 days of daily DEX treatment (subcutaneous injections 0.8 mg/g body wt). DEX treatment resulted in increases in the glucose and insulin area under the curve (AUC) during an intraperitoneal glucose tolerance test. The glucose, but not insulin, AUC was lowered with Vit E/C supplementation. Improvements in glucose tolerance occurred independent of a restoration of PKB phosphorylation in tissues of rats stimulated with an intraperitoneal injection of insulin but were associated with increases in AMPK signaling in muscle and reductions in AMPK signaling and the expression of fatty acid oxidation enzymes in liver. There were no differences in mitochondrial enzymes in triceps muscles between groups. This study is the first to report that dietary Vit E/C supplementation can partially prevent DEX-induced glucose intolerance in rats.

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