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Antioxidant supplementation in disease prevention

Antioxidant supplementation in disease prevention

The Immunity strengthening exercises family of ROS-generating NADPH diseasd physiology and pathophysiology. Related Black cherry hydration drink Frontiers In Medicinal Chemistry. Moreover, it has been recently reported Giordano et al. No effect on cancer incidence, death from cancer, or the incidence of major cardiovascular events. Biomolecules, 9 11 Neural Regen.

Antioxidant supplementation in disease prevention -

Because most vitamins cannot be synthesized by humans, they need to be ingested in the diet to maintain health and prevent disease. The exceptions to this are pre-vitamin D 3 , which is synthesized in the skin following ultraviolet UV exposure, and vitamins K2 and B12, which can be synthesized by colonic microbes.

These should be distinguished from minerals such as calcium and iron , some of which are also essential micronutrients. To continue reading this article, you must sign in with your personal, hospital, or group practice subscription.

Subscribe Sign in. It does NOT include all information about conditions, treatments, medications, side effects, or risks that may apply to a specific patient. It is not intended to be medical advice or a substitute for the medical advice, diagnosis, or treatment of a health care provider based on the health care provider's examination and assessment of a patient's specific and unique circumstances.

Patients must speak with a health care provider for complete information about their health, medical questions, and treatment options, including any risks or benefits regarding use of medications. This information does not endorse any treatments or medications as safe, effective, or approved for treating a specific patient.

UpToDate, Inc. and its affiliates disclaim any warranty or liability relating to this information or the use thereof. All rights reserved. Topic Feedback. Diagnostic testing for suspected vitamin B12 or folate deficiency Treatment of vitamin B12 deficiency in adults.

Diagnostic testing for suspected vitamin B12 or folate deficiency. Treatment of vitamin B12 deficiency in adults. Vitamin deficiency syndromes and dietary sources of common vitamins[1] Clinical situations in which vitamin deficiency syndromes occur Dietary Reference Intakes DRIs : Recommended dietary allowances and adequate intakes of several vitamins in children Dietary reference intakes of trace elements Dietary reference intakes for fat-soluble vitamins Dietary reference intake DRI for water-soluble vitamins Examples of clinical guidelines for folic acid supplementation.

Vitamin deficiency syndromes and dietary sources of common vitamins[1]. Clinical situations in which vitamin deficiency syndromes occur.

Dietary Reference Intakes DRIs : Recommended dietary allowances and adequate intakes of several vitamins in children. Dietary reference intakes of trace elements. Dietary reference intakes for fat-soluble vitamins. Dietary reference intake DRI for water-soluble vitamins.

The Alpha-Tocopherol Beta-Carotene Cancer Prevention Study 24 measured the effects of vitamin E 50 IU per day and β-carotene 20 mg per day supplementation on lung cancer and CHD.

The incidence of nonfatal myocardial infarction was lower in all groups receiving supplementation and was significantly lower 32 percent in the group that received vitamin E.

Supplementation with vitamin E was associated with a nonsignificant increase in cerebral hemorrhage. Supplementation with β-carotene was associated with increased mortality rates for CHD 11 percent and lung cancer 18 percent , as well as an increase in overall mortality 8 percent.

The incidence of fatal CHD was significantly higher in the group that received β-carotene alone 75 percent and in the group receiving both vitamins 58 percent.

Vitamin E supplementation is supported by several studies Tables 2 17 — 21 and 3 22 — Increased vitamin E levels are associated with decreased CHD mortality and inversely correlated with risk of angina. Vitamin E significantly reduced the incidence of overall fatal and nonfatal CHD events by 47 percent and the incidence of nonfatal myocardial infarction by 77 percent; however, supplementation did not have a significant effect on overall mortality relative risk: 1.

Event reduction was better with supplementation at IU per day, but the study was not powered to assess dose-response significance. This clinical trial strongly supports evidence that vitamin E in dosages greater than IU per day reduces CHD events.

Vitamin C significantly improves arterial vasoreactivity and vitamin E regeneration. The National Health and Nutrition Examination Survey-I cohort study 29 found an inverse relationship between the highest vitamin C intake diet and supplements and CHD risk over 10 years in 11, U.

men and women 25 to 74 years of age. The only large primary prevention trial has been a study of 29, poorly nourished residents of Linixian, China. The patients who received vitamin C in a dosage of mg per day and molybdenum in a dosage of 30 μg per day demonstrated no significant reduction in total or cerebrovascular mortality.

Many studies have demonstrated the ability of vitamin C to improve arterial vasoreactivity. A single dose 2 g of vitamin C has been found to improve vasoreactivity in chronic smokers, 8 patients with hypercholesterolemia 10 and patients with CHD.

Research supports the benefit of a carotenoid-rich diet, but not β-carotene supplementation. The Beta-Carotene and Retinol Efficacy Trial 27 combined β-carotene and retinol supplementation in 18, smokers and patients with asbestos exposure.

However, the study was terminated prematurely because of a significant increase in lung cancer mortality and a non-significant increase in CHD mortality. In 12 years of β-carotene supplementation in 22, male physicians, no significant beneficial effects on CHD mortality, nonfatal MI or stroke were found.

A non-significant 20 to 30 percent reduction in CHD events occurred in the physicians who had clinical evidence of atherosclerosis. Vitamins C, E and β-carotene have few side effects. No significant toxicity has been noted for vitamin E in dosages of to 3, IU per day. Therefore, caution is recommended when vitamin E supplementation is used in patients receiving anticoagulant therapy.

In vitamin E clinical trials, no significant differences in bleeding rates were noted in supplemented and unsupplemented subjects. Vitamin C supplementation is usually non-toxic, although diarrhea, bloating and false-negative occult blood tests can occur at dosages greater than 2 g per day.

The intestinal absorptive capacity for vitamin C is approximately 3 g per day. However, confusion arises about excess vitamin C intake causing increased oxalic acid excretion and, thus, a possibly increased risk of oxalate kidney stones as urinary vitamin C is converted to oxalate with air exposure.

Given in dosages of 30 to mg per day, β-carotene has minimal side effects. Other antioxidants that may provide protection against CHD include selenium, bioflavonoids and ubiquinone.

One study 33 found that selenium levels are inversely associated with CHD mortality. One review 7 noted that conflicting results were reported in other studies.

Flavonoids are antioxidants found in tea, wine, fruits and vegetables. These antioxidants reduce platelet activation, but studies do not yet support an associated reduction in CHD. Ubiquinone, a reduced form of coenzyme Q 10 , decreases LDL oxidation, but no eventreduction data are available.

The results of studies of garlic supplements have been conflicting regarding lipoprotein and platelet effects. The B-complex vitamins, especially folate, pyridoxine vitamin B 6 and cyanocobalamin vitamin B 12 , may reduce CHD risk through a lowering of homocysteine levels.

Folic acid supplementation in a dosage greater than μg per day reduces the plasma homocysteine level. Use of a daily multivitamin supplement containing folate μg would reduce plasma homocysteine levels in most persons.

Oxidized LDL is atherogenic, and specific antioxidants can inhibit LDL oxidation. Epidemiologic studies report inverse relationships between CHD and supplementation with vitamins E, C and β-carotene. Clinical trials to reduce CHD events currently support vitamin E supplementation in dosages greater than IU per day.

Vitamin C promotes vitamin E regeneration and significantly improves vasoreactivity, but clinical event reduction has not been established. The results of β-carotene studies have generally been unfavorable, primarily for smokers. Folate reduces serum homocysteine levels, but trials focusing on CHD events have not been completed.

Ubiquinone, flavonoids, garlic and other supplements have not been adequately tested for CHD event reduction, appropriate dosing, reliability or long-term safety. Because of the benefits from dietary antioxidants and other micronutrients, physicians should recommend consumption of a diet containing five to seven servings of fruits and vegetables per day Table 4.

Based on current evidence, patients with CHD should probably take vitamin E in a dosage of IU per day; vitamin C supplementation in a dosage of to 1, mg per day should also be considered in these patients.

Patients receiving warfarin Coumadin therapy should limit vitamin E intake to IU per day and should avoid vitamin E if they are at high risk for bleeding.

Cohort studies suggest that patients with conditions in which LDL oxidation is common i. Supplementation of β-carotene is not recommended for CHD prevention because of the possible harm demonstrated in several studies.

A high-quality diet or a daily multivitamin may be a useful way to obtain important B vitamins, especially folate μg per day , which lowers homocysteine levels. Diaz MN, Frei B, Vita JA, Keaney JF. Antioxidants and atherosclerotic heart disease. N Engl J Med. Schwartz CJ, Valente AJ, Sprague EA.

A modern view of atherogenesis. Am J Cardiol. Jialal I, Grundy SM. Influence of antioxidant vitamins on LDL oxidation. Ann N Y Acad Sci. O'Keefe JH, Conn RD, Lavie CJ, Bateman TH.

The new paradigm for coronary artery disease: altering risk factors, atherosclerotic plaques, and clinical prognosis. Mayo Clin Proc. Jha P, Flather M, Lonn E, Farkouh M, Yusuf S. The antioxidant vitamins and cardiovascular disease. A critical review of epidemiologic and clinical trial data.

Ann Intern Med. Odeh RM, Cornish LA. Natural antioxidants for the prevention of atherosclerosis. Kwiterovich PO. The effect of dietary fat, antioxidants, and pro-oxidants on blood lipids, lipoproteins, and atherosclerosis.

J Am Diet Assoc. Heitzer T, Just H, Munzel T. Antioxidant vitamin C improves endothelial dysfunction in chronic smokers.

Reilly M, Delanty N, Lawson JA, FitzGerald GA. Modulation of oxidant stress in vivo in chronic cigarette smokers. Ting HH, Timimi FK, Haley EA, Roddy MA, Ganz P, Creager MA. Vitamin C improves endothelium-dependent vasodilation in forearm resistance vessels of humans with hypercholesterolemia.

Plotnick GD, Corretti MC, Vogel RA. Effect of antioxidant vitamins on the transient impairment of endothelium-dependent brachial artery vasoactivity following a single high-fat meal. Gaziano JM, Hatta A, Flynn M, Johnson EJ, Krinsky NI, Ridker PM, et al. Supplementation with beta-carotene in vivo and in vitro does not inhibit low-density lipoprotein oxidation.

Gey KF, Puska P, Jordan P, Moser UK. Inverse correlation between plasma vitamin E and mortality from ischemic heart disease in cross-cultural epidemiology. Am J Clin Nutr. Verlangieri AJ, Kapeghian JC, el-Dean S, Bush M. Fruit and vegetable consumption and cardiovascular mortality.

Med Hypotheses. Riemersma RA, Wood DA, Macintyre CC, Elton RA, Gey KF, Oliver MF. Risk of angina pectoris and plasma concentrations of vitamins A, C, and E and carotene.

Luoma PV, Nayha S, Sikkila K, Hassi J. High serum alphatocopherol, albumin, selenium and cholesterol, and low mortality from coronary heart disease in northern Finland. J Intern Med. Bolton-Smith C, Woodward M, Tunstall-Pedoe H. Dietary intake by food frequency questionnaire and odds ratios for coronary heart disease risk.

The antioxidant vitamins and fibre. Eur J Clin Nutr. Knekt P, Reunanen A, Jarvinen R, Seppanen R, Heliovaara M, Aromaa A. Antioxidant vitamin intake and coronary mortality in a longitudinal population study.

Am J Epidemiol. Stampfer MJ, Hennekens CH, Manson JE, Colditz GA, Rosner B, Willett WC. Vitamin E consumption and the risk of coronary disease in women. Rimm EB, Stampfer MJ, Ascherio A, Giovannucci E, Colditz GA, Willett WC.

Vitamin E consumption and the risk of coronary heart disease in men. Losonczy KG, Harris TB, Havlik RJ. Vitamin E and vitamin C supplement use and risk of all-cause and coronary heart disease mortality in older persons: the Established Populations for Epidemiologic Studies of the Elderly.

Hodis HN, Mack WJ, LaBree L, Cashin-Hemphill L, Sevanian A, Johnson R, et al. Serial coronary angiographic evidence that antioxidant vitamin intake reduces progression of coronary artery atherosclerosis. Blot WJ, Li JY, Taylor PR, Guo W, Dawsey S, Wang GQ, et al. J Natl Cancer Inst.

Virtamo J, Rapola JM, Ripatti S, Heinonen OP, Taylor PR, Albanes D, et al. Effect of vitamin E and beta carotene on the incidence of primary nonfatal myocardial infarction and fatal coronary heart disease. Arch Intern Med.

Rapola JM, Virtamo J, Ripatti S, Huttunen JK, Albanes D, Taylor PR, et al. Randomised trial of alpha-tocopherol and beta-carotene supplements on incidence of major coronary events in men with previous myocardial infraction.

Stephens NG, Parsons A, Schofield PM, Kelly F, Cheeseman K, Mitchinson MJ. Randomised controlled trial of vitamin E in patients with coronary disease: Cambridge Heart Antioxidant Study CHAOS. Omenn GS, Goodman GE, Thornquist MD, Balmes J, Cullen MR, Glass A, et al.

Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease. Hennekens CH, Buring JE, Manson JE, Stampfer M, Rosner B, Cook NR, et al. Lack of effect of long-term supplementation with beta-carotene on the incidence of malignant neoplasms and cardiovascular disease.

Enstrom JE, Kanim LE, Klein MA. Vitamin C intake and mortality among a sample of the United States population.

Editor-in-Chief: Dimitra Immunity strengthening exercises Diswase of Pharmaceutical Chemistry, School of Pharmacy Aristotle University Anttioxidant Thessaloniki Thessaloniki Greece. ISSN Ulcer prevention through exercise : ISSN Rpevention : dizease DOI: Excessive and uncontrolled oxidative stress can damage biomacromolecules, such as lipids, proteins, carbohydrates, and DNA, by free radical and oxidant overproduction. In this review, we critically discuss the main properties of free radicals, their implications in oxidative stress, and specific pathological conditions. In clinical medicine, oxidative stress can play a role in several chronic noncommunicable diseases, such as diabetes mellitus, cardiovascular, inflammatory, neurodegenerative diseases, and tumours. Antioxidant supplementation in disease prevention


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