NLM database Documents

Record 1 from database: MEDLINE
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Title

Antioxidant potentials of vitamin A and carotenoids and their relevance to heart disease.

Author

Palace VP; Khaper N; Qin Q; Singal PK

Address

Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Center, Winnipeg, Manitoba, Canada.

Source

Free Radic Biol Med, 1999 Mar, 26:5-6, 746-61

Abstract

Despite being one of the first vitamins to be discovered, the full range of biological activities for vitamin A remains to be defined. Structurally similar to vitamin A, carotenoids are a group of nearly 600 compounds. Only about 50 of these have provitamin A activity. Recent evidence has shown vitamin A, carotenoids and provitamin A carotenoids can be effective antioxidants for inhibiting the development of heart disease. Vitamin A must be obtained from the diet: green and yellow vegetables, dairy products, fruits and organ meats are some of the richest sources. Within the body, vitamin A can be found as retinol, retinal and retinoic acid. Because all of these forms are toxic at high concentrations, they are bound to proteins in the extracellular fluids and inside cells. Vitamin A is stored primarily as long chain fatty esters and as provitamin carotenoids in the liver, kidney and adipose tissue. The antioxidant activity of vitamin A and carotenoids is conferred by the hydrophobic chain of polyene units that can quench singlet oxygen , neutralize thiyl radicals and combine with and stabilize peroxyl radicals. In general, the longer the polyene chain, the greater the peroxyl radical stabilizing ability. Because of their structures, vitamin A and carotenoids can autoxidize when O2 tension increases, and thus are most effective antioxidants at low oxygen tensions that are typical of physiological levels found in tissues. Overall, the epidemiological evidence suggests that vitamin A and carotenoids are important dietary factors for reducing the incidence of heart disease. Although there is considerable discrepancy in the results from studies in humans regarding this relationship, carefully controlled experimental studies continue to indicate that these compounds are effective for mitigating and defending against many forms of cardiovascular disease. More work, especially concerning the relevance of how tissue concentrations, rather than plasma levels, relate to the progression of tissue damage in heart disease is required. This review assembles information regarding the basic structure and metabolism of vitamin A and carotenoids as related to their antioxidant activities. Epidemiological, intervention trials and experimental evidence about the effectiveness of vitamin A and carotenoids for reducing cardiovascular disease is also reviewed.

Language of Publication

English

Unique Identifier

99233033

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MeSH Heading (Major)

Carotenoids|*PD/*TU; Heart Diseases|*PC/PP/TH; Vitamin A|*PD/*TU

MeSH Heading

Animal; Antioxidants|PD/TU; Diet; Fruit; Human; Support, Non-U.S. Gov't; Vegetables

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC

ISSN

0891-5849

Country of Publication

UNITED STATES

Record 2 from database: MEDLINE
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Title

The synergistic effects of vitamin E and selenium in iron-overloaded mouse hearts.

Author

Bartfay WJ; Hou D; Brittenham GM; Bartfay E; Sole MJ; Lehotay D; Liu PP

Address

Centre For Cardiovascular Research, Toronto Hospital, Ontario.

Source

Can J Cardiol, 1998 Jul, 14:7, 937-41

Abstract

OBJECTIVES: To determine whether supplementation with vitamin E and selenium can improve myocardial antioxidant defenses in iron-overloaded mouse hearts. INTERVENTIONS: Iron-overload state was created in B6D2F1 mice (n = 20) by daily injection of iron dextran (5 mg intraperitoneally/mouse) for four weeks. The mice were also simultaneously randomly assigned to receive vitamin E (alpha-tocopherol acetate, 40 mg intraperitoneally, n = 5), selenium (sodium selenite, 1 part/million orally, n = 5), both (vitamin E + selenium, n = 5) or iron-only treatment (n = 5). The hearts were harvested for determination of selenium concentration and glutathione peroxidase activity. In a subsequent study, 15 B6D2F1 mice were randomly assigned to receive daily injections of iron (n = 5) or iron and combined antioxidant treatment (vitamin E + selenium, n = 5), or to serve as controls (n = 5) for four weeks. The hearts were harvested for determination of total iron concentrations. MAIN RESULTS: Significantly greater concentrations of heart selenium and glutathione peroxidase activity were observed in groups supplemented with both agents, as opposed to iron-only treated or single supplemented mice. Significantly lower concentrations of iron were found in controls and in those receiving combined iron and antioxidant treatment (vitamin E + selenium) than in iron-only treated mice. CONCLUSIONS: Vitamin E and selenium function synergistically in the myocardium to provide important antioxidant defenses in iron-overload states, including increased concentrations of selenium, increased glutathione peroxidase activity and decreased concentrations of iron.

Language of Publication

English

Unique Identifier

98371553

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MeSH Heading (Major)

Iron|*AD/AE; Myocardial Diseases|CI/*DT; Selenium|*AD/PD; Vitamin E|*AD/PD

MeSH Heading

Animal; Disease Models, Animal; Dose-Response Relationship, Drug; Drug Synergism; Heart|DE; Human; Mice; Overdose; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW LITERATURE

ISSN

0828-282X

Country of Publication

CANADA

Record 3 from database: MEDLINE
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Title

Vitamin C and cardiovascular disease: a systematic review.

Author

Ness AR; Powles JW; Khaw KT

Address

Institute of Public Health, University Forvie Site, Cambridge, UK.

Source

J Cardiovasc Risk, 1996 Dec, 3:6, 513-21

Abstract

BACKGROUND: Laboratory studies suggest that antioxidants, such as Vitamin C, are important inhibitors of atherosclerotic lesions. Most epidemiological reviews have considered all antioxidants together. This review seeks to clarify the current state of knowledge specifically concerned with vitamin C. METHODS: All ecological studies, case-control studies, prospective studies and trials in humans that examined the association between vitamin C intake or blood levels of vitamin C and cardiovascular disease were included. Relevant references were located by MEDLINE search for articles published from 1966 to 1996, by an EMBASE search for articles published from 1980 to 1996, by searching personal bibliographies, books and reviews and from citations in located articles. RESULTS: For coronary heart disease four of seven ecological studies, one of four case-control studies and three of 12 cohort studies found a significant protective association with vitamin C intake or status. For strokes two of two ecological studies, none of one case-control study and two of seven cohort studies found a significant protective association. For total circulatory disease, two of three cohort studies reported a significant protective association. CONCLUSIONS: The evidence, albeit limited, is consistent with vitamin C having protective effect against stroke whereas the evidence that vitamin C is protective against coronary heart disease is less consistent. The lack of an association for coronary heart disease could be explained in terms of there being a true lack of effect, dietary measurement error, a threshold effect, and effect of seasonal variations in intake, an interaction with other dietary constituents or a relatively short duration of follow-up.

Language of Publication

English

Unique Identifier

97254677

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MeSH Heading (Major)

Ascorbic Acid|*AD; Cardiovascular Diseases|*PC; Diet|*

MeSH Heading

Case-Control Studies; Cohort Studies; Epidemiologic Factors; Female; Food, Fortified; Human; Male; Prospective Studies; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

1350-6277

Country of Publication

ENGLAND

Record 4 from database: MEDLINE
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Title

Most free-radical injury is iron-related: it is promoted by iron, hemin, holoferritin and vitamin C, and inhibited by desferoxamine and apoferritin.

Author

Herbert V; Shaw S; Jayatilleke E; Stopler Kasdan T

Address

Nutrition Center, Mount Sinai, Bronx, New York.

Source

Stem Cells (Dayt), 1994 May, 12:3, 289-303

Abstract

Iron is a double-edged sword. In moderate quantities and leashed to protein, it is an essential element in all cell metabolism and growth, but it is toxic when unleashed. Because of its ability to switch back and forth between ferrous and ferric oxidation states, iron is both a strong biological oxidant and reductant. The human diet contains a multitude of natural chemicals which are carcinogens and anticarcinogens, many of which act by generating oxygen radicals, which initiate degenerative processes related to cancer, heart disease and aging (the "oxygen radical hypothesis of aging"). Among these many dietary chemicals are many redox agents, including vitamin C and beta carotene. Free radical damage is produced primarily by the hydroxyl radical (.OH). Most of the .OH generated in vivo comes from iron-dependent reduction of H2O2. Supporting too much iron as a free radical-generating culprit in the risk of cancer, NHANES I data indicated that high body iron stores, manifested by increased transferrin saturation, are associated with an increased cancer risk. Other data shows an increased heart attack risk.

Language of Publication

English

Unique Identifier

94355914

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MeSH Heading (Major)

Apoferritin|*PD; Ascorbic Acid|*PD; Deferoxamine|*PD; Diet|*; Ferritin|*PD; Hemin|*PD; Iron|*TO; Neoplasms|CI/*ET; Superoxides|*

MeSH Heading

Animal; Anticarcinogenic Agents; Carcinogens; Free Radicals; Heart Diseases|ET; Human; Oxidation-Reduction; Support, Non-U.S. Gov't; Support, U.S. Gov't, Non-P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC

ISSN

1066-5099

Country of Publication

UNITED STATES

Record 5 from database: MEDLINE
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Title

Interacting nutritional and infectious etiologies of Keshan disease. Insights from coxsackie virus B-induced myocarditis in mice deficient in selenium or vitamin E.

Author

Levander OA; Beck MA

Address

Nutrient Requirements and Functions Laboratory, Beltsville Human Nutrition Research Center, U.S. Department of Agriculture, ARS, MD 20705-2350, USA.

Source

Biol Trace Elem Res, 1997 Jan, 56:1, 5-21

Abstract

In 1979, Chinese scientists reported that selenium had been linked to Keshan disease, an endemic juvenile cardiomyopathy found in China. However, certain epidemiological features of the disease could not be explained solely on the basis of inadequate selenium nutrition. Fluctuations in the seasonal incidence of the disease suggested involvement of an infectious agent. Indeed, a coxsackievirus B4 isolated from a Keshan disease victim caused more heart muscle damage when inoculated into selenium-deficient mice than when given to selenium-adequate mice. Those results led us to study the relationship of nutritional status to viral virulence. Coxsackievirus B3/0 (CVB3/0), did not cause disease when inoculated into mice fed adequate levels of Se and vitamin E. However, mice fed diets deficient in either Se or vitamin E developed heart lesions when infected with CVB3/0. To determine if the change in viral phenotype was maintained, we passaged virus isolated from Se-deficient hosts, designated as CVB3/0 Se-, back into Se-adequate hosts. The CVB3/0 Se- virus caused disease in Se-adequate mice. To determine if the phenotype change was due to changes in the viral genome, we sequenced viruses isolated from Se-deficient mice and compared them with the input CVB3/0 virus. Six point mutations differed between the parent strain and the recovered CVB3/0 Se- isolates. When the experiment was repeated using vitamin E-deficient mice, the same 6 point mutations were found. This is the first report of a specific host nutritional deficiency altering viral genotype. Keshan disease may be the result of several interacting causes including a dominant nutritional deficiency (selenium), other nutritional factors (vitamin E, polyunsaturated fatty acids), and an infectious agent (virus).

Language of Publication

English

Unique Identifier

97297039

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MeSH Heading (Major)

Coxsackieviruses B|GE/*PY; Myocardial Diseases|*ET; Selenium|*DF; Vitamin E Deficiency|*CO

MeSH Heading

Animal; Disease Models, Animal; Human; Mice; Myocarditis|ET; Nutritional Status; Oxidative Stress; Virulence

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0163-4984

Country of Publication

UNITED STATES

Record 6 from database: MEDLINE
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Title

Vitamin C and cardiovascular disease: a review.

Author

Simon JA

Address

Prevention Sciences Group of the University of California, San Francisco, School of Medicine.

Source

J Am Coll Nutr, 1992 Apr, 11:2, 107-25

Abstract

Vitamin C functions as a regulator of the catabolism of cholesterol to bile acids in the guinea pig and has been demonstrated to be an important factor in lipid regulation of the guinea pig, rabbit and rat. Correlation studies in humans have shown an inverse relationship between vitamin C intake and cardiovascular disease mortality. Observational and experimental studies in humans have yielded inconsistent results, but taken together indicate that for individuals with high total cholesterol concentrations, greater than or equal to 5.20 mmol/L (200 mg/dl) and less than full tissue saturation, increasing the concentration of vitamin C may have a salutary effect on total cholesterol. Vitamin C's effect on promoting the production and inhibiting the degradation of prostacyclin is reviewed, as are implications of these findings regarding thrombosis and atherogenesis. Evidence indicative of a protective effect on lipid peroxidation by vitamin C is examined. Analysis of the literature regarding groups at high risk for coronary heart disease reveals that men, the elderly, smokers, diabetics, hypertensives and perhaps oral estrogen-containing contraceptive users have lowered plasma vitamin C levels. Evidence linking vitamin C to human cardiovascular disease is largely circumstantial, but taken in total, is suggestive of an association. Further examination of the relationship between vitamin C and cardiovascular disease is warranted.

Language of Publication

English

Unique Identifier

92251056

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MeSH Heading (Major)

Ascorbic Acid|*PH/TU; Cardiovascular Diseases|ET/*PC; Cholesterol|*ME

MeSH Heading

Animal; Blood Pressure; Hemostasis; Human; Lipid Peroxidation; Risk Factors

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC

ISSN

0731-5724

Country of Publication

UNITED STATES

Record 7 from database: MEDLINE
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Title

Will the 'good fairies' please prove to us that vitamin E lessens human degenerative disease? [corrected and republished in Free Radic Res 1997 Nov;27(5):511-32]

Author

Diplock AT

Address

International Antioxidant Research Centre, United Medical and Dental School (University of London) Guy's Hospital, United Kingdom.

Source

Free Radic Res, 1997 Jun, 26:6, 565-83

Abstract

Recent research about the role of free radical derivatives of oxygen and nitrogen in biological systems has highlighted the possibility that antioxidants, such as vitamin E, that prevent these processes in vitro may be capable of carrying out a similar function in living organisms in vivo. There is increasing evidence that free radical reactions are involved in the early stages, or sometimes later on, in the development of human diseases, and it is therefore of particular interest to inquire whether vitamin E and other antioxidants, which are found in the human diets, may be capable of lowering the incidence of these diseases. Put simply, the proposition is that by improving human diets by increasing the quantity in them of antioxidants, it might be possible to reduce the incidence of a number of degenerative diseases. Of particular significance to these considerations is the likely role of the primary fat-soluble dietary antioxidant vitamin E in the prevention of degenerative diseases such as arteriosclerosis, which is frequently the cause of consequent heart attacks or stroke, and prevention of certain forms of cancer, as well as several other diseases. Substantial evidence for this proposition now exists, and this review is an attempt to give a brief account of the present position. Two kinds of evidence exist; on the one hand there is very substantial basic science evidence which indicates an involvement of free radical events, and a preventive role for vitamin E, in the development of human disease processes. On the other hand, there is also a large body of human epidemiological evidence which suggests that incidence of these diseases is lowered in populations having a high level of antioxidants, such as vitamin E, in their diet, or who have taken steps to enhance their level of intake of the vitamin by taking dietary supplements. There is also some evidence which suggests that intervention with dietary supplements of vitamin E can result in a lowered risk of disease, in particular of cardiovascular disease, which is a major killer disease among the developed nations of the world. The intense interest in this subject recently has as its objective the possibility that, by making some simple alterations to dietary lifestyle, or by enhancing the intake of vitamin E by fortification of foods, or by dietary supplements, it may be possible to reduce substantially the risk of a large amount of common, highly disabling human disease. By this simple means, therefore it may be possible to improve substantially the quality of human life, in particular for people of advancing years.

Language of Publication

English

Unique Identifier

97355869

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MeSH Heading (Major)

Antioxidants|*ME; Vitamin E|*PH

MeSH Heading

Atherosclerosis|ET; Cardiovascular Diseases|PC; DNA|ME; Fatty Acids, Unsaturated|ME; Free Radicals; Human; Lipid Peroxides|ME; Lipoproteins|BL; Membrane Lipids|ME; Neoplasms|ET/PC

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC

ISSN

1071-5762

Country of Publication

SWITZERLAND

Record 8 from database: MEDLINE
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Title

Will the 'good fairies' please prove to us that vitamin E lessens human degenerative disease? [corrected and republished article originally printed in Free Radic Res 1997 Jun;26(6):565-83]

Author

Diplock AT

Address

Division of Biochemistry and Molecular Biology, United Medical and Dental School (University of London), Guy's Hospital, United Kingdom.

Source

Free Radic Res, 1997 Nov, 27:5, 511-32

Abstract

Recent research about the role of free radical derivatives of oxygen and nitrogen in biological systems has highlighted the possibility that antioxidants, such as vitamin E, that prevent these processes in vitro may be capable of carrying out a similar function in living organisms in vivo. There is increasing evidence that free radical reactions are involved in the early stages, or sometimes later on, in the development of human diseases, and it is therefore of particular interest to inquire whether vitamin E and other antioxidants, which are found in the human diets, may be capable of lowering the incidence of these diseases. Put simply, the proposition is that by improving human diets by increasing the quantity in them of antioxidants, it might be possible to reduce the incidence of a number of degenerative diseases. Of particular significance to these considerations is the likely role of the primary fat-soluble dietary antioxidant vitamin E in the prevention of degenerative diseases such as arteriosclerosis, which is frequently the cause of consequent heart attacks or stroke, and prevention of certain forms of cancer, as well as several other diseases. Substantial evidence for this proposition now exists, and this review is an attempt to give a brief account of the present position. Two kinds of evidence exist; on the one hand there is very substantial basic science evidence which indicates an involvement of free radical events, and a preventive role for vitamin E, in the development of human disease processes. On the other hand, there is also a large body of human epidemiological evidence which suggests that incidence of these diseases is lowered in populations having a high level of antioxidants, such as vitamin E, in their diet, or who have taken steps to enhance their level of intake of the vitamin by taking dietary supplements. There is also some evidence which suggests that intervention with dietary supplements of vitamin E can result in a lowered risk of disease, in particular of cardiovascular disease, which is a major killer disease among the developed nations of the world. The intense interest in this subject recently has as its objective the possibility that, by making some simple alterations to dietary lifestyle, or by enhancing the intake of vitamin E by fortification of foods, or by dietary supplements, it may be possible to reduce substantially the risk of a large amount of common, highly disabling human disease. By this simple means, therefore it may be possible to improve substantially the quality of human life, in particular for people of advancing years.

Language of Publication

English

Unique Identifier

98139362

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MeSH Heading (Major)

Aging, Premature|*PC; Antioxidants|*TU; Atherosclerosis|*PC; Cardiovascular Diseases|*PC; Neoplasms|*PC; Vitamin E|*TU

MeSH Heading

Animal; Human

Publication Type

CORRECTED AND REPUBLISHED ARTICLE; JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

1071-5762

Country of Publication

SWITZERLAND

Record 9 from database: MEDLINE
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Title

Clinical uses of vitamin E.

Author

Machlin LJ

Address

 

Source

Acta Vitaminol Enzymol, 1985, 7 Suppl:, 33-43

Abstract

Early administration of vitamin E to low birth weight (less than 1500 g) infants results in alleviation of the symptoms of retinopathy of prematurity and a lowered incidence of intraventricular hemorrhage. If vitamin E is given to children with cholestatic liver disease (orally or parenterally) before 3 years of age, neurological symptoms such as areflexia, ataxia, and sensory neuropathy are prevented or reversed. Restitution of neurological function is more limited in children ages 5-17 years even after prolonged therapy. Vitamin E is also useful in prevention of neuropathy and retinopathy associated with abetalipoproteinemia and cystic fibrosis. Blood levels of tocopherol are often low in subjects with hemolytic anemias. Administration of vitamin E to G-6-P-D-deficient subjects increased hemoglobin levels, and decreased the number of irreversibly sickled cells in sickle-cell anemia subjects. Most trials have indicated that administration of vitamin E for 6 months or more to subjects with intermittent claudication results in longer walking distance and improved blood flow. Vitamin E reduces platelet aggregation, platelet adhesion to collagen, and platelet thromboxane production. Prostacyclin production is generally enhanced. The significance of these effects to thrombotic diseases. Epidemiological studies have indicated that subjects with higher blood levels of vitamin E have lower risk of death from ischemic heart disease and cancer, a lower risk of breast cancer, and a lower incidence of infections.

Language of Publication

English

Unique Identifier

87045643

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MeSH Heading (Major)

Vitamin E|BL/*TU

MeSH Heading

Adolescence; Adult; Anemia, Hemolytic|BL; Blood Platelets|DE; Breast Neoplasms|BL; Child; Child, Preschool; Cholestasis, Intrahepatic|DT; Coronary Disease|BL; Glucosephosphate Dehydrogenase Deficiency|BL; Human; Infant; Infant, Low Birth Weight; Infant, Newborn; Infant, Premature; Retinal Diseases|PC

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0300-8924

Country of Publication

ITALY

Record 10 from database: MEDLINE
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Title

Therapeutic potential of vitamin E against myocardial ischemic-reperfusion injury.

Author

Janero DR

Address

Research Department, CIBA-GEIGY Corporation, Summit, NJ 07901.

Source

Free Radic Biol Med, 1991, 10:5, 315-24

Abstract

Myocardial ischemia is a disease process characterized by reduced coronary flow such that the supply of nutritive blood to heart muscle (myocardium) is insufficient for normal myocardial aerobic metabolism. Prompt reestablishment of coronary flow by invasive and noninvasive clinical procedures is the most direct and effective means of limiting myocardial damage in ischemic heart disease patients, although reperfusion carries with it an injury component which may reflect, at least to some degree, the toxic effects of partially reduced oxygen species and their participation in degenerative cellular processes such as membrane lipid peroxidation. Vitamin E, a lipophilic, chain-breaking antioxidant, is a prominent membrane constituent in heart muscle, where it modulates/regulates various aspects of heart muscle-cell metabolism and function. Vitamin E's beneficial effects against experimentally induced oxidative damage to the heart, along with inverse epidemiological correlations between plasma vitamin E level and either anginal pain or mortality due to ischemic heart disease, suggest that vitamin E might have protective and therapeutic roles against myocardial ischemic-reperfusion injury. Laboratory investigations aimed at addressing this possibility have demonstrated that vitamin E supplementation protects isolated hearts against ischemic-reperfusion injury, and relatively more inconsistent and limited data document cardioprotective effects of vitamin E in some animal models of myocardial ischemia-reperfusion, especially when administered prior to the ischemic period. Clinical attempts to establish whether vitamin E has therapeutic benefit in ischemic heart disease patients remain inconclusive, having relied upon a variety of nonuniformly controlled protocols and a single, rather subjective endpoint (anginal pain). Consequently, although laboratory data constitute a conceptual context for and indirect support of the idea that vitamin E could be a cardioprotectant against ischemic-reperfusion injury, compelling clinical evidence regarding vitamin E's therapeutic potential in the ischemic heart-disease patient is lacking. Elective coronary revascularization would appear to provide an attractive clinical setting for evaluating the therapeutic efficacy of vitamin E in the context of cardiac ischemia-reperfusion. Further biochemical work would still be required to define how vitamin E exerts any cardioprotective effect observed in these patients.

Language of Publication

English

Unique Identifier

91309902

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MeSH Heading (Major)

Myocardial Reperfusion Injury|*PC; Vitamin E|*TU

MeSH Heading

Animal; Antioxidants; Free Radicals; Human; Nutritional Status

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC

ISSN

0891-5849

Country of Publication

UNITED STATES

Record 11 from database: MEDLINE
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Title

Coronary heart disease: the significance of coronary pathology in infancy and the role of mitogens such as vitamin D.

Author

Davies H

Address

Papworth Hospital, Papworth Everard, Cambridge, UK.

Source

Med Hypotheses, 1989 Nov, 30:3, 179-85

Abstract

Intimal hyperplasia, damage to the internal elastic lamina, and proliferation of medial smooth muscle cells characterise the early response of an artery to damage. These changes are seen in the coronary arteries of the transplanted human heart, and are commonly seen in "normal" infants. Lipid incursion occurs only later, and the end-result is atheroma. These lesions of infancy are probably pathologic rather than physiologic, and are the precursors of later coronary heart disease. The early intimal and medial changes may be immune-engendered, encouraged by mitogens such as Vitamin D, and evolve in infancy as an aberration of the normal mechanisms controlling cellular proliferation.

Language of Publication

English

Unique Identifier

90097666

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MeSH Heading (Major)

Coronary Disease|ME/*PA/PP; Vitamin D|*ME/PH

MeSH Heading

Cell Division|DE; Human

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0306-9877

Country of Publication

ENGLAND

Record 12 from database: MEDLINE
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Title

Vitamin E and heart disease: a case study.

Author

Kushi LH

Address

Division of Epidemiology, the University of Minnesota School of Public Health, Minneapolis 55454-1015, USA. kushi@epi.umn.edu

Source

Am J Clin Nutr, 1999 Jun, 69:6, 1322S-1329S

Abstract

The role of nutritional epidemiology studies in the development of nutritional recommendations has been controversial, in part because individual studies supporting either side of a given issue can often be identified. Several sets of criteria for inference of a causal relation between a dietary factor and a disease from epidemiologic studies have been suggested. One such set is that of Sir Austin Bradford Hill, which includes criteria such as strength of association, dose-response relation, consistency of association, temporally correct association, specificity of association, and biological plausibility. Another set of criteria, used by the US Preventive Services Task Force, ranks evidence according to study design, designating evidence from randomized controlled trials as superior to evidence from cohort or case-control studies, which are in turn superior to evidence from ecologic studies or opinions of respected authorities. The application of these criteria to the question of whether vitamin E intake is associated with coronary heart disease is examined here. It is suggested that the epidemiologic evidence from prospective cohort studies generally supports an inverse association of vitamin E intake and risk of coronary heart disease. The information available from randomized trials is limited but suggestive of an inverse association with nonfatal, but not with fatal, coronary events. It is suggested that the application of criteria for causal inference to specific questions in nutritional epidemiology may provide clarity to seemingly contradictory information.

Language of Publication

English

Unique Identifier

99285765

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MeSH Heading (Major)

Coronary Disease|*PC; Vitamin E|AD/*TU

MeSH Heading

Causality; Dose-Response Relationship, Drug; Epidemiologic Studies; Female; Human; Male

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, MULTICASE

ISSN

0002-9165

Country of Publication

UNITED STATES

Record 13 from database: MEDLINE
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Title

Vitamin E as a universal antioxidant and stabilizer of biological membranes.

Author

Evstigneeva RP; Volkov IM; Chudinova VV

Address

Lomonosov Moscow State Academy of Fine Chemical Technology. rpe@httos.mitht.msk.ru

Source

Membr Cell Biol, 1998, 12:2, 151-72

Abstract

The known literature data concerning the mechanisms of molecular action of vitamin E in biological membrane systems are reviewed. The role of vitamin E, possessing a broad range of biological activities, as a universal stabilizer of biological membranes in normal oxygen metabolism and peroxidation, and also in disorders of normal metabolism resulting in pathological alterations, has been discussed. The participation of vitamin E in redox reactions taking place in lipid media, its interaction with singlet oxygen, free fatty acids and enzyme systems are considered. Physiological effects of vitamin E and its ability to prevent numerous pathologies are also considered. Vitamin E was concluded to be a universal participant of antioxidant defence reactions in biological membranes, since it acts at all stages of membrane oxidative damage.

Language of Publication

English

Unique Identifier

99095615

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MeSH Heading (Major)

Antioxidants|*PD; Free Radicals|*ME; Membranes|*PH; Vitamin E|CH/ME/*PH

MeSH Heading

Aging; Ascorbic Acid|ME; Fatty Acids, Unsaturated|ME; Glutathione|ME; Heart Diseases|ME; Human; Kidney Diseases|ME; Lipid Peroxidation; Liver Diseases|ME; Neoplasms|ME

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

1023-6597

Country of Publication

SWITZERLAND

Record 14 from database: MEDLINE
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Title

Vitamin E supplements and coronary heart disease.

Author

Byers T; Bowman B

Address

Chronic Disease Prevention Branch, Centers for Disease Control and Prevention, Atlanta, GA 30341.

Source

Nutr Rev, 1993 Nov, 51:11, 333-6

Abstract

Although two new epidemiologic studies on the association between vitamin E and heart disease do not resolve important issues related to dose-response, mechanisms of action, or specificity, they do provide important evidence that supports the development of new strategies for preventing heart disease.

Language of Publication

English

Unique Identifier

94150887

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MeSH Heading (Major)

Coronary Disease|EP/*PC; Vitamin E|AD/*TU

MeSH Heading

Adult; Aged; Female; Human; Male; Middle Age; Risk Factors

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0029-6643

Country of Publication

UNITED STATES

Record 15 from database: MEDLINE
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Title

Effect of supplementation with vitamin E on LDL oxidizability and prevention of atherosclerosis.

Author

Suzukawa M; Ayaori M; Shige H; Hisada T; Ishikawa T; Nakamura H

Address

First Department of Internal Medicine, National Defense Medical College, Saitama, Japan.

Source

Biofactors, 1998, 7:1-2, 51-4

Abstract

Supplementation of LDL with vitamin E is thought to protect LDL from oxidative modification and prevent the development of atherosclerosis. Large epidemiological studies have revealed that vitamin E levels in plasma are inversely correlated to the incidence of coronary heart disease. Double-blind placebo-controlled trials have reported that supplementation with vitamin E decreases the incidence of coronary events in coronary heart disease (CHD) patients. However, it is not clear how high a dose of vitamin E is needed to prevent formation of atherosclerosis. In animal studies, a diet containing 0.125% vitamin E increased its levels in plasma two-fold and prevented formation of early atherosclerotic lesions in the thoracic aorta of hypercholesterolemic rabbits. Dose-response studies in humans have reported that 400 IU/day vitamin E increased its levels in plasma two-fold and prolonged the lag time before LDL oxidation. It has been reported that oxidizability of LDL was correlated to the atherosclerotic score of coronary angiography in CHD patients. About 400 IU/day vitamin E, which increases its levels two-fold and prolongs sufficiently the lag time before LDL oxidation, might be beneficial in decreasing the individual risk of CHD.

Language of Publication

English

Unique Identifier

98183629

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MeSH Heading (Major)

Atherosclerosis|*PC; Lipid Peroxidation|*DE; Lipoproteins, LDL|*ME; Vitamin E|*AD/BL/TU

MeSH Heading

Animal; Coronary Disease|BL/MO/PC; Human; Rabbits; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0951-6433

Country of Publication

NETHERLANDS

Record 16 from database: MEDLINE
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Title

Inverse correlation of vitamin E and ischemic heart disease.

Author

Gey KF

Address

 

Source

Int J Vitam Nutr Res Suppl, 1989, 30:, 224-31

Abstract

According to animal experiments, deficiency in vitamin E may be related to arterial lesions. In current cross-cultural epidemiology of middle-aged men representing 11 European populations with different mortality from ischemic heart disease (IHD) all principal antioxidant vitamins and selenium were compared in plasma. The vitamin E concentration within lipoproteins (alpha-tocopherol/cholesterol ratio) showed the most prominent correlation with IHD. This highly significant correlation seemed to be independent of the risk of coronary mortality attributable to hypercholesterolemia. The levels of lipid-standardized vitamin E associated with a relatively higher IHD risk were still in a range which has hitherto been considered "normal." The differences between individuals of lipid-standardized plasma vitamin E were reflected by corresponding changes of vitamin E in the erythrocyte and buccal mucosa. On the other hand, membrane vitamin E varied independently from the level of polyunsaturated fatty acids (PUFAs) in the membrane. The present data suggest that the plasma level of lipid-standardized vitamin E is a hitherto underrated risk factor of IHD which may substantially complement previously known risk factors, such as hypercholesterolemia and a critical state of PUFAs. A conceivable preventive effect of (an enlarged RDA of) vitamin E remains to be elucidated by an intervention trial.

Language of Publication

English

Unique Identifier

90010356

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MeSH Heading (Major)

Coronary Disease|*ET; Vitamin E|*BL

MeSH Heading

Adult; Human; Male; Middle Age; Risk Factors

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW LITERATURE

ISSN

0373-0883

Country of Publication

CANADA

Record 17 from database: MEDLINE
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Title

Furosemide and vitamin E. Two problem drugs in neonatology.

Author

Aranda JV; Chemtob S; Laudignon N; Sasyniuk BI

Address

 

Source

Pediatr Clin North Am, 1986 Jun, 33:3, 583-602

Abstract

This article focuses on some of the problems encountered with two of the drugs currently given to newborns.

Language of Publication

English

Unique Identifier

86232257

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MeSH Heading (Major)

Furosemide|*AE/TU; Infant, Newborn, Diseases|*DT; Vitamin E|*AE/TU

MeSH Heading

Acid-Base Imbalance|CI; Anemia|DT; Bronchopulmonary Dysplasia|PC; Cerebral Hemorrhage|PC; Diuresis; Ductus Arteriosus, Patent|DT; Glomerular Filtration Rate|DE; Heart Failure, Congestive|DT; Human; Infant, Newborn; Infant, Premature, Diseases|DT; Kidney Tubules|DE; Pulmonary Edema|DT; Respiratory Distress Syndrome|DT; Retinal Diseases|PC; Support, Non-U.S. Gov't; Water-Electrolyte Imbalance|CI

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0031-3955

Country of Publication

UNITED STATES

Record 18 from database: MEDLINE
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Title

Vitamin E: hype or hope.

Author

Gray MA

Address

 

Source

Orthop Nurs, 1996 Jul, 15:4, 55-7

Abstract

Unlike other vitamins, Vitamin E probably has received less attention in the past because humans are not likely to suffer from deficiency disorders. This fat soluble vitamin is available in many foods, is easily stored, and is readily reused by the body. The original research carried out in the 1920s found that a Vitamin E deficiency in rats produced problems in their reproductive capacity. The name given to the substance at that time, "tocopherol," reflects this action as it is taken from the Greek word, "tocos," meaning "to give birth."

Language of Publication

English

Unique Identifier

97022429

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MeSH Heading (Major)

Vitamin E|*/PH/TU; Vitamin E Deficiency|CO/*DT

MeSH Heading

Adolescence; Adult; Animal; Child; Child, Preschool; Female; Heart Diseases|PC; Human; Infant; Infant, Newborn; Male; Neoplasms|PC; Nutritional Requirements; Rats

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0744-6020

Country of Publication

UNITED STATES

Record 19 from database: MEDLINE
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Title

Vitamin C-driven free radical generation from iron [published errata appear in J Nutr 1996 Jun;126(6):1746 and 1996 Jul;126(7):1902]

Author

Herbert V; Shaw S; Jayatilleke E

Address

The Mount Sinai and Bronx Veterans Affairs Medical Centers, New York City, NY, USA.

Source

J Nutr, 1996 Apr, 126:4 Suppl, 1213S-20S

Abstract

Circulating free iron is lethal. Humans have two circulating iron binding proteins to soak up free iron to prevent it from generating toxic quantities of free radicals. These proteins are transferrin, a high-affinity, low-capacity protein (2 atoms of iron per molecule of transferrin) for which there are receptors on the surface of every iron-requiring cell; and ferritin, a lower-affinity, high-capacity protein (maximum of 4500 atoms of iron per molecule of ferritin) for which there are receptors only on the surface of iron-storage cells such as RE (reticulo-endothelial) cells. Iron is trapped inside the ferritin protein shell as harmless Fe3. When there is a high serum level of reduced ascorbic acid, it drives through the pores of the ferritin protein shell to the inside surface, where it converts the Fe3 to catalytic Fe2, which then leaks out of the pores of the ferritin protein shell and generates billions of free radicals. In normal individuals, per milliliter of serum, there are approximately 300,000 molecules of transferrin per molecule of ferritin. Ferritin protein is an acute phase reactant that sharply rises in the presence of inflammation of any kind, whereas transferrin is a reverse acute phase reactant that falls in the presence of inflammation of any kind.

Language of Publication

English

Unique Identifier

96239424

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MeSH Heading (Major)

Ascorbic Acid|*PD; Iron|*ME/TO

MeSH Heading

Ferritin|ME; Free Radicals; Heart Diseases|TH; Human; Neoplasms|TH; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0022-3166

Country of Publication

UNITED STATES

Record 20 from database: MEDLINE
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Title

Epidemiologic evidence for vitamin E in prevention of cardiovascular disease.

Author

Stampfer MJ; Rimm EB

Address

Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115, USA.

Source

Am J Clin Nutr, 1995 Dec, 62:6 Suppl, 1365S-1369S

Abstract

Ecologic studies of vitamin E have shown that regions with relatively low dietary vitamin E tend to have higher rates of coronary heart disease (CHD), but it is difficult to adjust for other risk factors. Cross-sectional studies in individuals have yielded conflicting results, as have prospective studies based on stored blood samples. Two large prospective studies found that persons who had used vitamin E supplements for > or = 2 y had approximately 40% lower rates of CHD. Short durations and doses of < 100 IU/d had no significant effect. The effect of dietary vitamin E was modest and nonsignificant. Adjustment for a wide array of other coronary risk factors had little effect on the findings, which were specific for vitamin E and not other supplements. The only large, randomized trial found no material reduction in CHD risk for 50 IU vitamin E/d. The epidemiologic evidence suggests that high doses of vitamin E may reduce the risk of CHD.

Language of Publication

English

Unique Identifier

96094689

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MeSH Heading (Major)

Coronary Disease|*PC; Vitamin E|*AD

MeSH Heading

Animal; Diet; Human; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9165

Country of Publication

UNITED STATES

Record 21 from database: MEDLINE
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Title

Vitamin E, alpha- and gamma-tocopherol, and prostate cancer.

Author

Moyad MA; Brumfield SK; Pienta KJ

Address

Section of Urology, University of Michigan, Ann Arbor 48109-0330, USA.

Source

Semin Urol Oncol, 1999 May, 17:2, 85-90

Abstract

Vitamin E is one of the most researched compounds in medicine. Vitamin E is actually a general name for potentially eight different compounds, so supplements can contain several forms and vitamin E in the diet also differs from the form found over the counter. There has been a strong interest in this supplement in the prostate cancer arena primarily because of a Finnish study that demonstrated a lower morbidity and mortality from this disease in men taking 50 mg of synthetic (alpha-tocopherol) vitamin E daily. In addition, observations from laboratory and clinical studies dealing with heart disease have found that gamma-tocopherol may also play a significant role in prevention; therefore, we decided to test the ability of this compound (versus synthetic vitamin E) to control the growth of a human prostate cancer cell line. Gamma-tocopherol was found to be superior to alpha-tocopherol in terms of cell inhibition in vitro. Both forms of vitamin E (and others) should be thoroughly evaluated in the future to provide the most effective chemoprevention information to the patient.

Language of Publication

English

Unique Identifier

99263716

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MeSH Heading (Major)

Prostatic Neoplasms|EP/MO/*PC; Vitamin E|CH/PD/*TU

MeSH Heading

Dietary Fats; Disease Progression; Drug Screening Assays, Antitumor; Human; Incidence; Male; Morbidity; Tumor Cells, Cultured

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

1081-0943

Country of Publication

UNITED STATES

Record 22 from database: MEDLINE
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Title

Vitamin C nutriture and risk of atherosclerotic heart disease.

Author

Jacob RA

Address

USDA Agricultural Research Service, Presidio of San Francisco, CA 94129, USA.

Source

Nutr Rev, 1998 Nov, 56:11, 334-7

Abstract

There is substantial evidence for a role of dietary antioxidants in the prevention of cardiovascular disease, but evidence for a protective effect of vitamin C is inconclusive. Two recent reports add to the supporting evidence and provide some new observations. The first study, a 5-year prospective population study of Finnish men, suggests that vitamin C-deficient men may be at increased risk of myocardial infarction. The second study suggests that vitamin C may play a role in preventing manifestations of existing coronary artery disease, rather than in limiting disease progression. Although these results suffer from the limitations of observational studies, they provide impetus for further investigation.

Language of Publication

English

Unique Identifier

99056178

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MeSH Heading (Major)

Ascorbic Acid|*PH; Atherosclerosis|*/PC; Nutrition|*

MeSH Heading

Antioxidants; Ascorbic Acid Deficiency; Female; Human; Male; Prospective Studies; Risk Factors

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0029-6643

Country of Publication

UNITED STATES

Record 23 from database: MEDLINE
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Title

Vitamin E and atherosclerosis.

Author

Chan AC

Address

Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada K1H 8M5.

Source

J Nutr, 1998 Oct, 128:10, 1593-6

Abstract

Vitamin E was advocated as an effective treatment for heart disease by Dr. Even Shute of London, Ontario more than 50 years ago. His pioneering claims, which were unacceptable to the medical community at large, have been confirmed by recent findings from epidemiologic studies and clinical trials. This review integrates our current knowledge of atherogenesis with the biological functions of vitamin E. The response-to-injury hypothesis explains atherosclerosis as a chronic inflammatory response to injury of the endothelium, which leads to complex cellular and molecular interactions among cells derived from the endothelium, smooth muscle and several blood cell components. Inflammatory and other stimuli trigger an overproduction of free radicals, which promote peroxidation of lipids in LDL trapped in the subendothelial space. Products of LDL oxidation are bioactive, and they induce endothelial expression and secretion of cytokines, growth factors and several cell surface adhesion molecules. The last-mentioned are capable of recruiting circulating monocytes and T lymphocytes into the intima where monocytes are differentiated into macrophages, the precursor of foam cells. In response to the growth factors and cytokines, smooth muscle cells proliferate in the intima, resulting in the narrowing of the lumen. Oxidized LDL can also inhibit endothelial production of prostacyclin and nitric oxide, two potent autacoids that are vasodilators and inhibitors of platelet aggregation. Evidence is presented that vitamin E is protective against the development of atherosclerosis. Vitamin E enrichment has been shown to retard LDL oxidation, inhibit the proliferation of smooth muscle cells, inhibit platelet adhesion and aggregation, inhibit the expression and function of adhesion molecules, attenuate the synthesis of leukotrienes and potentiate the release of prostacyclin through up-regulating the expression of cytosolic phospholipase A2 and cyclooxygenase. Collectively, these biological functions of vitamin E may account for its protection against the development of atherosclerosis.

Language of Publication

English

Unique Identifier

98445484

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MeSH Heading (Major)

Atherosclerosis|ET/*PC; Muscle, Smooth|*DE/ME; Vitamin E|*PH/*TU

MeSH Heading

Animal; Arachidonic Acid|ME; Coronary Disease|DT; Endothelium|DE; Human; Lipid Peroxidation|DE; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0022-3166

Country of Publication

UNITED STATES

Record 24 from database: MEDLINE
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Title

Vitamin nutrition status and homocysteine: an atherogenic risk factor.

Author

Ubbink JB

Address

Department of Chemical Pathology, University of Pretoria, South Africa.

Source

Nutr Rev, 1994 Nov, 52:11, 383-7

Abstract

In an epidemiologic survey, a marginal status of folic acid, vitamin B12, and vitamin B6 was shown to be associated with hyperhomocysteinemia. In a case-control study, a low plasma folate concentration was associated with increased coronary heart disease risk. This phenomenon appears to be mediated by folate's effect on homocysteine metabolism. Both studies offer further perspectives on homocysteine as an atherogenic risk factor.

Language of Publication

English

Unique Identifier

95157879

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MeSH Heading (Major)

Atherosclerosis|*ET; Folic Acid|BL/*PH; Homocysteine|BL/*PH; Nutritional Status|*; Pyridoxine|BL/*PH; Vitamin B 12|BL/*PH

MeSH Heading

Case-Control Studies; Coronary Disease|ET; Human; Risk Factors

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0029-6643

Country of Publication

UNITED STATES

Record 25 from database: MEDLINE
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Title

Vitamin C and cardiovascular risk factors.

Author

Trout DL

Address

Carbohydrate Nutrition Laboratory, US Department of Agriculture, Beltsville, MD 20705.

Source

Am J Clin Nutr, 1991 Jan, 53:1 Suppl, 322S-325S

Abstract

The concept that ascorbic acid (vitamin C) supplementation protects against coronary heart disease developed in the late 1970s when vitamin C intakes in industrialized nations were lower than at present. Supplementation was then shown to lower plasma total cholesterol and, among some elderly men, to raise high-density lipoprotein cholesterol. However, among people in initially good vitamin C nutriture, these effects are usually not seen. In five populations of essentially healthy people, blood pressure has been found to correlate negatively with vitamin C status. Recently, in a placebo-controlled, doub