Natural antioxidants for heart health -
Height was measured to the nearest 0. Waist circumference WC was measured with a non-flexible tape meter without any pressure to the body surface at the level of the umbilicus 24 and was taken at the end of a normal expiration over light clothing. Measurements were recorded to the nearest 0.
Blood samples were drawn into vacutainer tubes between and a. All biochemical analyses were performed using a Selectra 2 auto-analyzer at the TLGS research laboratory on the blood collection day. Fasting blood glucose FBG concentration was measured on the blood collection day using the colorimetric glucose oxidase procedure.
The standard 2-h post-challenge blood glucose test was performed by oral administration of High-density lipoprotein cholesterol HDL-C concentration was assessed after precipitation of the apolipoprotein B-containing lipoproteins by phosphotungstic acid. Total cholesterol TC and triglyceride TG were measured using the enzymatic colorimetric method.
For TC assay, cholesteryl ester hydrolase was used to convert cholesteryl ester to cholesterol, which was then oxidized by cholesterol oxidase to cholesterolenone and H2O2. TG was broken down to glycerol and free- fatty acids using lipoprotein lipase and glycerol was then phosphorylated to glycerol phosphate by glycerol kinase.
Glycerol phosphate was then converted to dihydroxyacetone phosphate and H2O2 by glycerol phosphate oxidase.
Details of the collection of CVD outcome data have been described elsewhere. Coronary heart disease CHD events included definite myocardial infarction diagnostic electrocardiographic [ECG] results and biomarkers , probable myocardial infarction positive ECG findings plus cardiac symptoms or signs plus missing biomarkers or positive ECG findings plus equivocal biomarkers , proven CHD by angiography, unstable angina pectoris new cardiac symptoms or changing symptom patterns and positive ECG findings with normal biomarkers , and CHD mortality.
CVD was defined as stroke a new neurological deficit that lasted more than 24 h , CHD events, or CVD death a fatal stroke or fatal CHD Statistical analyses were carried out using the Statistical Package for Social Sciences version For non-normal nutritional and biochemical variables TG concentration , log-transformed values were used for statistical analysis.
Antioxidant intakes with respect to quartiles of food group intakes were assessed using ANOVA test. P for trend was obtained by the linear regression analysis using the median of each quartile as a continuous variable for each food group.
Person-years of the follow-up were calculated for each individual from the date inclusion in the study and the exact date of CVD diagnosis, death, or end of the follow-up, whichever came first.
Survival time for censored individuals was calculated as the interval between the first and the last observation dates.
The event date was considered as the exact date of CVD events, and survival time was computed as the time between baseline examination and the event date for event cases or the last follow-up for censored cases.
Participants were censored due to loss to follow-up, death from a cause other than CVD, or the end of the study without the event appearing. Rates of CVD-free survival in participants across quartiles of vitamins E, C, and A and zinc intakes were compared using a Kaplan—Meier analysis and the log-rank test method was used for significance test.
The dietary intakes of vitamins E, C, and A, and zinc were adjusted for energy intake using gram per kcal for each nutrient. Energy adjusted of vitamins E, C, and A, and zinc intakes were categorized into quartiles, given the first quartile as the reference.
The median of each quartile was used as a continuous variable to assess the overall trends of HRs across quartiles of dietary intakes of vitamins E, C, and A and zinc in the Cox proportional hazard regression models.
Trend test was applied for evaluating dose—response effects in association studies. The confounders were selected based on previous studies and included in the univariable Cox regression model.
The mean age of subjects at baseline was Table 1 represents the baseline characteristics of men and women.
Men were older, had worse smoking habits, greater levels of physical activity, lower body mass index, and higher WC than women. Men had greater amounts of energy and carbohydrate intakes than women. Intakes of total fat, saturated fatty acid, monounsaturated fatty acid, polyunsaturated fatty acid, fiber, and vitamins A and C were higher in women than in men.
The association between dietary intakes of vitamins E, C, and A and zinc across quartiles of food groups are presented in Table 2. Higher consumption of fruit, vegetable, legumes, refined grains, vegetable oils, fish, and poultry was associated with higher intake of vitamin E.
Vitamin C intake was positively associated with all food groups, except for refined grains and red meat that showed a negative association with vitamin C intake. There was a positive association between vitamin A and quartiles of all food groups, except for red meat.
Compared with those in the lower quartiles, zinc intake was significantly higher among individuals in the upper quartiles of fruit, vegetable, legumes, whole grains, refined grains, dairy, fish, and poultry intake. Kaplan—Meier survival curves for CVD according to quartiles of vitamins A, C, and E and zinc intakes during follow-up periods are shown in Figs.
Significant differences were found in the risk of CVD between quartiles of zinc intake. Kaplan—Meier estimates of CVD-free survival according to quartiles of vitamin E intake. P values by log-rank test and number of CVD outcomes recorded in the groups categorized by vitamin E intake.
Kaplan—Meier estimates of CVD-free survival according to quartiles of vitamin C intake. P values by log-rank test and number of CVD outcomes recorded in the groups categorized by vitamin C intake.
Kaplan—Meier estimates of CVD-free survival according to quartiles of vitamin A intake. P values by log-rank test and number of CVD outcomes recorded in the groups categorized by vitamin A intake.
Kaplan—Meier estimates of CVD-free survival according to quartiles of zinc intake. P values by log-rank test and number of CVD outcomes recorded in the groups categorized by zinc intake.
After adjustment for potential confounders, the risk of CVD decreased from quartile 1 to quartile 4 for vitamin E intake [HR 1. The association between the risk of CVD and quartiles of vitamins A and C, and zinc intake were not statistically significant. The current investigation was a prospective cohort study, evaluating the association between dietary antioxidant vitamins A, E, and C and zinc intakes and risk of CVD.
Our results suggested that a higher intake of vitamin E was inversely associated with CVD incidence. Previous studies have found an association between dietary vitamin E intake and decreased risk of CVD in observational epidemiologic studies 28 , 30 , 31 , Several biological functions of vitamin E are due to its antioxidant properties to inhibit the oxidation of LDL-C and to scavenge lipid radicals In contrast, several large randomized controlled trials have failed to corroborate the benefits of vitamin E in CVD prevention 34 , which can be due to several factors, such as the time of intervention, gene polymorphisms, or inherent confounding, and pathophysiological conditions in study populations.
In addition, an intervention study suggested that in addition to prescribed medicine, supplemental doses of vitamin E should be given to ameliorate therapeutic strategies However, vitamin E supplements have not been recommended by the American heart association to prevent CVD due to the lack of approved results; however, it recommends eating foods rich in antioxidant vitamins, especially fruit and vegetable In our study, vitamin E was available in several food groups, which may be due to the connection between food groups, such as consuming oil olive oil and mayonnaise and vegetable that are mixed in salads or using oil for cooking.
Also, no association was found between nut intake and vitamin E, which may be due to the small quantities of nut consumption in our population. Anti-CVD properties of vitamin C have not yet been fully confirmed. No significant association was found between total vitamin C intake estimated by summing the vitamin C contribution of food items and supplements and CVD in a cohort of Spanish university graduates.
Therefore, it is concluded that the absence of significant results can be due to the low variability in the exposure. However, vitamin C is a single nutrient and may not represent the synergistic effect of the whole dietary pattern In contrast to our results, observational studies on the relationship between vitamin C and CVD risk have demonstrated an inverse association between vitamin C and CVD outcomes, especially heart failure 7 and hypertension 8.
The contradiction in results can be due to differences in the definition of CVD. Vitamin C increases the nitric oxide bioactivity of the endothelium, which causes a decrease in blood pressure Moreover, vitamin C reduces monocyte adhesion and inhibits LDL oxidation 39 , which plays an important role in decreasing the risk of atherosclerosis.
In addition, vitamin C keeps atheromatous plaques stable by preventing vascular smooth muscle cell apoptosis Consistent with our results, in a meta-analysis 41 , neither dietary nor supplemental vitamin A was associated with CVD risk. A large prospective study 10 indicated that among patients with stable angina pectoris in the upper tertile of serum vitamin A concentration, serum apolipoprotein B a predictor of CVD was associated with the CVD risk.
However, dietary intake of vitamin A did not correlate with serum concentration, which seems that another mechanism, other than vitamin A intake, regulates the serum vitamin A concentration Accordingly, in the current study, no association was observed between dietary vitamin A and CVD risk.
In the present study, no significant difference was found between dietary zinc intake and CVD incidence, which is consistent with a systematic review of prospective cohort studies on the association between dietary zinc intake or serum zinc levels and the incidence of CVD In contrast with our result, higher dietary zinc intake estimated by summing the zinc contribution of food items was associated with a greater incidence of CVD in a large longitudinal study on Australian women.
Therefore, more investigations are needed to investigate the association between zinc intake from meat and other major sources because dietary guidelines recommend reducing red meat intake and encouraging consuming other sources of zinc Also, more studies are needed to investigate the mechanisms of zinc function on the pathogenesis of CVD to provide dietary zinc recommendations for preventing CVD.
The prospective design of the present study was one of its major strengths that facilitated the estimation of disease incidence without concern about reverse causality between nutrients and outcomes. Considering the observational design of the current research, some confounders e.
supplement intake and socioeconomic levels and comorbidities during follow-up were not considered. Dietary assessment was considered at baseline only, and changes in dietary intakes were not recorded during the follow-up.
One of the limitations of this study was the use of an FFQ for collecting dietary data due to recall bias; however, expert dietitians interviewed the participants to reduce this bias. Also, the validity of the FFQ was acceptable among this population.
Moreover, some cases lost the follow-up; for example, those with a high risk of CVD were selectively excluded due to their poor mental or physical health. We did not split the analysis by gender due to the low number of cases and power reduction.
This study suggested an inverse association between vitamin E intake and the risk of CVD, which emphasized the potentially protective role of its dietary sources in the prevention of CVD events.
Jacob, R. Vitamin C nutriture and risk of atherosclerotic heart disease. Article CAS PubMed Google Scholar. Ceconi, C. Oxidative stress in cardiovascular disease: Myth or fact?. Mangge, H. Antioxidants, inflammation and cardiovascular disease. World J. Article PubMed PubMed Central Google Scholar.
Jain, A. Role of antioxidants for the treatment of cardiovascular diseases: Challenges and opportunities. Griffiths, K. et al. Food antioxidants and their anti-inflammatory properties: A potential role in cardiovascular diseases and cancer prevention. Diseases 4 , 28 Article PubMed Central Google Scholar.
Jayedi, A. Dietary and circulating vitamin C, vitamin E, beta-carotene and risk of total cardiovascular mortality: A systematic review and dose-response meta-analysis of prospective observational studies. Public Health Nutr. Article PubMed Google Scholar.
Pfister, R. Plasma vitamin C predicts incident heart failure in men and women in European Prospective Investigation into Cancer and Nutrition-Norfolk prospective study. Heart J. Buijsse, B. Plasma ascorbic acid, a priori diet quality score, and incident hypertension: A prospective cohort study.
PLoS ONE 10 , e Monaghan, B. The effects of carotene and of vitamin A on the oxidation of linoleic acid. Article CAS Google Scholar. Olsen, T. Cardiovascular disease risk associated with serum apolipoprotein B is modified by serum vitamin A.
Atherosclerosis , — Lourenco, B. Nutritional status and adequacy of energy and nutrient intakes among heart failure patients.
PubMed Google Scholar. Tan, C. The prediction of cardiovascular disease based on trace element contents in hair and a classifier of boosting decision stumps. Trace Elem.
de Oliveira Otto, M. Dietary intakes of zinc and heme iron from red meat, but not from other sources, are associated with greater risk of metabolic syndrome and cardiovascular disease.
Kubota, Y. Dietary intakes of antioxidant vitamins and mortality from cardiovascular disease: The Japan Collaborative Cohort Study JACC study. Stroke 42 , — Azizi, F. Prevention of non-communicable disease in a population in nutrition transition: Tehran Lipid and Glucose Study phase II.
Trials 10 , 5 Hosseini-Esfahani, F. Nutrition and cardio-metabolic risk factors: Findings from 20 years of the tehran lipid and glucose study. Sun, Q. White rice, brown rice, and risk of type 2 diabetes in US men and women. Mirmiran, P.
Reliability and relative validity of an FFQ for nutrients in the Tehran lipid and glucose study. Esfahani, F. Reproducibility and relative validity of food group intake in a food frequency questionnaire developed for the Tehran Lipid and Glucose Study.
J Epidemiol 20 , — Azar, M. Food Composition Table of Iran National Nutrition and Food Research Institute, Shahid Beheshti University Press, Google Scholar. United States Department of Agriculture. Food Composition Table. Momenan, A. Reliability and validity of the Modifiable Activity Questionnaire MAQ in an Iranian urban adult population.
Ainsworth, B. Compendium of physical activities: An update of activity codes and MET intensities. Sports Exerc. Klein, S. Friedewald, W.
Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Hadaegh, F. Association of total cholesterol versus other serum lipid parameters with the short-term prediction of cardiovascular outcomes: Tehran Lipid and Glucose Study.
General cardiovascular risk profile for use in primary care: The Framingham Heart Study. Circulation , — Williams, B. The Task Force for the management of arterial hypertension of the European Society of Cardiology ESC and the European Society of Hypertension ESH.
G Ital Cardiol. Rome 19 , 3—73 Lee, P. Identification of confounder in epidemiologic data contaminated by measurement error in covariates. BMC Med. Rimm, E. Vitamin E consumption and the risk of coronary heart disease in men. Stampfer, M. Vitamin E consumption and the risk of coronary disease in women.
Buring, J. Antioxidant vitamins and cardiovascular disease. Nutr Rev 55 , S53—S58 discussion S Mathur, P. Tocopherols in the prevention and treatment of atherosclerosis and related cardiovascular disease. Vardi, M. Vitamin E in the prevention of cardiovascular disease: The importance of proper patient selection.
Lipid Res. Article CAS PubMed PubMed Central Google Scholar. Sozen, E. Vitamin E: Regulatory role in the cardiovascular system. Good sources of beta carotene include:. Good sources of lycopene include:.
Research also shows that lycopene is better absorbed by our bodies when heated and combined with healthy fats such as olive and coconut oil. Some great ways to get the best absorption of these lycopene-rich foods are through recipes like:.
Resveratrol, which is found in red wine, is an antioxidant that may help prevent CHD. The potential heart-healthy benefits of red wine and other alcoholic drinks look promising. Those who drink moderate amounts of alcohol, including red wine, seem to have a lower risk of heart disease.
Alcohol can be addictive and cause other health problems. Astaxanthin antioxidant properties include being linked to improved blood flow and lowering oxidative stress in smokers and overweight people. A comparison study of astaxanthin and other carotenoids showed that it displayed the highest antioxidant activity against free radicals.
Astaxanthin is most commonly found in:. Are High Fat Foods Good for Your Heart? Sign up to receive Baptist Health emails to learn more about your health from our blog, e-newsletter, and Flourish. Or follow one of our social media accounts. April 09, Antioxidants for Heart Health.
Types of Antioxidants for Heart Health Antioxidants work to deactivate free radicals by binding to oxidants, which prevents damage from free radicals. Vitamin C Vitamin C is the predominant plasma antioxidant. Good sources of vitamin C include: Citrus fruits and their juices Berries Dark green vegetables Red and yellow peppers Tomatoes and tomato juice Pineapple Cantaloupe Mangos Papaya Guava Vitamin E Vitamin E prevents the peroxidation of polyunsaturated fatty acid in membranes.
Vitamin E is found in: Vegetable and seed oils Nuts and nut butters Seeds Whole grains Wheat germ Wheat Brown rice Oatmeal Soybeans Sweet potatoes Legumes Dark leafy green vegetables Selenium Selenium may provide protection against CHD and selenium levels are inversely associated with CHD mortality.
Bilirubin, Hezrt yellow-orange pigment, is formed Brown rice diet the breakdown of red ehart cells and is eliminated by Vegan nutrition facts liver. A recent analysis of health data from hexlthveterans, Natural antioxidants for heart health with and without Antioxidatns infection, antioxidqnts that within Ac and weight loss ranges, higher levels of bilirubin in the blood were associated with lower rates of heart failure, heart attack and stroke. The results are published in the Journal of the American Heart Association. Several studies have suggested that bilirubin may have beneficial effects, by acting as an antioxidant or interfering with atherosclerosis. The data from the veterans adds to this evidence, and specifically looks at people living with HIV and at an anti-HIV drug, atazanavir, known to elevate bilirubin. The researchers did not see an independent effect of atazanavir on cardiovascular risk.Video
5 Supplements for Heart Health \u0026 Prediabetes Magazines, news Brown rice diet, and food labels are Preventing dryness and flakiness to Natural antioxidants for heart health on dor heart-healthy bandwagon, touting the heary of certain nutrients, like antioxidants. Antioxidantw, veggies, nuts and whole grains are teeming with these heart-healthy nutrients. Highly processed foods, not so much. Supercharge your heart health with these A-list antioxidants. A growing body of research proposes these antioxidants can protect your body from the risk of cardiovascular diseases, thanks to them supporting blood flow and reducing the build up of plaque in arteries i. These fellas have a positive impact on your cholesterol, too.
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