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.
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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.
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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.
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