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Vitamin A

36 Scientific Studies -- On This Page -- Below

These studies each include "Vitamin A" in the title of the study, and heart disease in the text. These would generally be studies showing any relationship between various dosages of Vitamin A and heart disease.      These are ALL the studies with these search words over a 30 year period.  Generally these studies do NOT show that Vitamin A in large doses is dangerous or causes heart disease.

Vitamin A and Carotenes

Vitamin A was the first recognized fat-soluble vitamin. Although identified as a necessary growth factor in 1913, it was not chemically characterized until 1930. Two groups of researcher, McCollum and Davis at the University of Wisconsin, and Osborne and Mendel at Yale University, make the initial discovery of vitamin A almost simultaneously. They found that young animals fed a diet deficient in natural fats became very unhealthy, as evidenced by their inability to grow and their poor immune function. These researchers also noted that the animals’ eyes became severely inflamed and infected on the restricted diet-conditions quickly relieved by the addition of butterfat or cad liver oil to the diet. Once known as the "anti-infective vitamin," vitamin A recently regained recognition as a major determinant of immune status., Carotenes, some of which can be converted into vitamin A, are also gaining a great deal of attention as immune system enhancers. Because of the vitamin A activity of some carotenes, this chapter explores both vitamin A and carotenes.

Beta Carotene  -- More Expensive -- Just As Effective -- Politically Correct

60-Page Report By The Institute Of Medicine -- January 2001 -- Setting Lower Limits For Vitamin A

Government Attack On "High Doses" Of Vitamin A  -- In Six Parts  -- Part 1

        Part 2

        Part 3

        Part 4

        Part 5

        Part 6

Ingredients In Super Life Glow, Including Vitamin A

Ingredients in Life Glow Plus, Including Vitamin A

The 3D Structure of Vitamin A

Vitamin A Toxicity  -- Deception From Merck

Vibrant Life Technical Information  Synthetic Versus Natural Forms Of  Vitamins


Results for your query on February 6, 2000
Search all fields for: heart disease
Words in title only: Vitamin A
Published in 1957 through 1999
Only select references with abstracts available
Show references published in English only
Show references pertaining to humans
With an article type of: REVIEW

Documents: 1 to 36 of 36
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1 Palace VP, et al; Antioxidant potentials of vitamin A and carotenoids and their relevance to heart disease. (Free Radic Biol Med, 1999 Mar, Abstract available) [MEDLINE]
2 Bartfay WJ, et al; The synergistic effects of vitamin E and selenium in iron-overloaded mouse hearts. (Can J Cardiol, 1998 Jul, Abstract available) [MEDLINE]
3 Ness AR, et al; Vitamin C and cardiovascular disease: a systematic review. (J Cardiovasc Risk, 1996 Dec, Abstract available) [MEDLINE]
4 Herbert V, et al; Most free-radical injury is iron-related: it is promoted by iron, hemin, holoferritin and vitamin C, and inhibited by desferoxamine and apoferritin. (Stem Cells (Dayt), 1994 May, Abstract available) [MEDLINE]
5 Levander OA, et al; Interacting nutritional and infectious etiologies of Keshan disease. Insights from coxsackie virus B-induced myocarditis in mice deficient in selenium or vitamin E. (Biol Trace Elem Res, 1997 Jan, Abstract available) [MEDLINE]
6 Simon JA; Vitamin C and cardiovascular disease: a review. (J Am Coll Nutr, 1992 Apr, Abstract available) [MEDLINE]
7 Diplock AT; 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] (Free Radic Res, 1997 Jun, Abstract available) [MEDLINE]
8 Diplock AT; 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] (Free Radic Res, 1997 Nov, Abstract available) [MEDLINE]
9 Machlin LJ; Clinical uses of vitamin E. (Acta Vitaminol Enzymol, 1985, Abstract available) [MEDLINE]
10 Janero DR; Therapeutic potential of vitamin E against myocardial ischemic-reperfusion injury. (Free Radic Biol Med, 1991, Abstract available) [MEDLINE]

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11 Davies H; Coronary heart disease: the significance of coronary pathology in infancy and the role of mitogens such as vitamin D. (Med Hypotheses, 1989 Nov, Abstract available) [MEDLINE]
12 Kushi LH; Vitamin E and heart disease: a case study. (Am J Clin Nutr, 1999 Jun, Abstract available) [MEDLINE]
13 Evstigneeva RP, et al; Vitamin E as a universal antioxidant and stabilizer of biological membranes. (Membr Cell Biol, 1998, Abstract available) [MEDLINE]
14 Byers T, et al; Vitamin E supplements and coronary heart disease. (Nutr Rev, 1993 Nov, Abstract available) [MEDLINE]
15 Suzukawa M, et al; Effect of supplementation with vitamin E on LDL oxidizability and prevention of atherosclerosis. (Biofactors, 1998, Abstract available) [MEDLINE]
16 Gey KF; Inverse correlation of vitamin E and ischemic heart disease. (Int J Vitam Nutr Res Suppl, 1989, Abstract available) [MEDLINE]
17 Aranda JV, et al; Furosemide and vitamin E. Two problem drugs in neonatology. (Pediatr Clin North Am, 1986 Jun, Abstract available) [MEDLINE]
18 Gray MA; Vitamin E: hype or hope. (Orthop Nurs, 1996 Jul, Abstract available) [MEDLINE]
19 Herbert V, et al; 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] (J Nutr, 1996 Apr, Abstract available) [MEDLINE]
20 Stampfer MJ, et al; Epidemiologic evidence for vitamin E in prevention of cardiovascular disease. (Am J Clin Nutr, 1995 Dec, Abstract available) [MEDLINE]

Menu Position #20

21 Moyad MA, et al; Vitamin E, alpha- and gamma-tocopherol, and prostate cancer. (Semin Urol Oncol, 1999 May, Abstract available) [MEDLINE]
22 Jacob RA; Vitamin C nutriture and risk of atherosclerotic heart disease. (Nutr Rev, 1998 Nov, Abstract available) [MEDLINE]
23 Chan AC; Vitamin E and atherosclerosis. (J Nutr, 1998 Oct, Abstract available) [MEDLINE]
24 Ubbink JB; Vitamin nutrition status and homocysteine: an atherogenic risk factor. (Nutr Rev, 1994 Nov, Abstract available) [MEDLINE]
25 Trout DL; Vitamin C and cardiovascular risk factors. (Am J Clin Nutr, 1991 Jan, Abstract available) [MEDLINE]
26 Rader DJ, et al; Abetalipoproteinemia. New insights into lipoprotein assembly and vitamin E metabolism from a rare genetic disease [clinical conference] (JAMA, 1993 Aug, Abstract available) [MEDLINE]
27 Traber MG, et al; Vitamin E in humans: demand and delivery. (Annu Rev Nutr, 1996, Abstract available) [MEDLINE]
28 Stocker R; The ambivalence of vitamin E in atherogenesis. (Trends Biochem Sci, 1999 Jun, Abstract available) [MEDLINE]
29 Sauberlich HE; Pharmacology of vitamin C. (Annu Rev Nutr, 1994, Abstract available) [MEDLINE]
30 Thurman JE, et al; Vitamin supplementation therapy in the elderly. (Drugs Aging, 1997 Dec, Abstract available) [MEDLINE]

Menu Position #30

31 Gey KF, et al; Increased risk of cardiovascular disease at suboptimal plasma concentrations of essential antioxidants: an epidemiological update with special attention to carotene and vitamin C. (Am J Clin Nutr, 1993 May, Abstract available) [MEDLINE]
32 Thurnham DI, et al; Optimal nutrition: vitamin A and the carotenoids. (Proc Nutr Soc, 1999 May, Abstract available) [MEDLINE]
33 Astedt B; Antenatal drugs affecting vitamin K status of the fetus and the newborn. (Semin Thromb Hemost, 1995, Abstract available) [MEDLINE]
34 Gerster H; High-dose vitamin C: a risk for persons with high iron stores? (Int J Vitam Nutr Res, 1999 Mar, Abstract available) [MEDLINE]
35 Upston JM, et al; Tocopherol-mediated peroxidation of lipoproteins: implications for vitamin E as a potential antiatherogenic supplement. (FASEB J, 1999 Jun, Abstract available) [MEDLINE]
36 Boucher BJ; Inadequate vitamin D status: does it contribute to the disorders comprising syndrome 'X'? (Br J Nutr, 1998 Apr, Abstract available) [MEDLINE]


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, double-blinded study, extra ascorbic acid for 6 wk was observed to lower systolic and pulse pressure in a small group of borderline hypertensive subjects.
Language of Publication
English
Unique Identifier
91090033

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MeSH Heading (Major)
Ascorbic Acid|BL/PD/*TU; Coronary Disease|*PC
MeSH Heading
Age Factors; Blood Pressure|DE; Cholesterol|BL; Diabetes Mellitus|ME; Human; Lipoproteins, HDL Cholesterol|BL; Risk Factors; Sex Factors; Smoking|AE

Publication Type
JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN
0002-9165
Country of Publication
UNITED STATES

 

Record 26 from database: MEDLINE
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Title
Abetalipoproteinemia. New insights into lipoprotein assembly and vitamin E metabolism from a rare genetic disease [clinical conference]
Author
Rader DJ; Brewer HB Jr
Address
Molecular Disease Branch, National Heart, Lung, and Blood Institute, Bethesda, Md. 20892.
Source
JAMA, 1993 Aug, 270:7, 865-9
Abstract
Abetalipoproteinemia is a rare genetic disease that has provided important new insights into the physiology of lipoprotein assembly and vitamin E metabolism. Forty-two years after its initial description, a molecular etiology of ABL has been reported to be a deficiency of a microsomal transfer protein, thus suggesting that this protein plays a key role in lipoprotein particle assembly and secretion both in the intestine and in the liver. Furthermore, studies in patients with ABL have established the critical role of hepatic secretion of VLDL in the delivery of vitamin E to peripheral tissues and the essential role of vitamin E in the maintenance of normal physiological function of multiple tissues. The systematic investigation of this rare genetic disease has provided insights that have substantially enhanced our understanding of human physiology.
Language of Publication
English
Unique Identifier
93341066

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MeSH Heading (Major)
Abetalipoproteinemia|*/DI/ET/ME/PP/TH
MeSH Heading
Adult; Case Report; Female; Human; Lipoproteins|ME; Vitamin E|ME

Publication Type
CLINICAL CONFERENCE; JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN
0098-7484
Country of Publication
UNITED STATES

 

Record 27 from database: MEDLINE
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Title
Vitamin E in humans: demand and delivery.
Author
Traber MG; Sies H
Address
Department of Molecular and Cell Biology, University of California, Berkeley 94720, USA.
Source
Annu Rev Nutr, 1996, 16:, 321-47
Abstract
How much vitamin E is enough? An established use of supplemental vitamin E in humans is in the prevention and therapy of deficiency symptoms. The cause of vitamin E deficiency, characterized by peripheral neuropathy and ataxia, is usually malabsorption-a result of fat malabsorption or genetic abnormalities in lipoprotein metabolism. Genetic abnormalities in the hepatic alpha-tocopherol transfer protein also cause vitamin E deficiency-defects in this protein cause an impairment in plasma vitamin E transport. Impaired delivery of vitamin E to tissues, thereby, results in deficiency symptoms. Also discussed is the use of supplemental vitamin E in chronic diseases such as ischemic heart disease, atherosclerosis, diabetes, cataracts, Parkinson's disease, Alzheimer's disease, and impared immune function, as well as in subjects receiving total parenterol nutrition. In healthy individuals, a daily intake of about 15-30 mg of alpha-tocopherol is recommended to obtain "optimal plasma alpha-tocopherol concentrations" (30 microM or greater).
Language of Publication
English
Unique Identifier
96437116

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MeSH Heading (Major)
Vitamin E|*AD/CH/ME/PD/PK/TU
MeSH Heading
Diet; Human; Vitamin E Deficiency|CO/PC

Publication Type
JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
ISSN
0199-9885
Country of Publication
UNITED STATES

 

Record 28 from database: MEDLINE
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Title
The ambivalence of vitamin E in atherogenesis.
Author
Stocker R
Address
Biochemistry Group, The Heart Research Institute, 145 Missenden Rd, Camperdown, NSW 2050, Australia. r.stocker@hri.org.au
Source
Trends Biochem Sci, 1999 Jun, 24:6, 219-23
Abstract
The early events in atherogenesis might be due to the oxidation of low- density lipoprotein. The antioxidant vitamin E, therefore, has received much attention as a potential anti-atherogenic agent. Recent mechanistic studies of the early stage of lipoprotein-lipid oxidation show that the role of vitamin E in this process is not simply that of a classical antioxidant. Unless additional compounds are present, vitamin E can have antioxidant, neutral or pro-oxidant activity. This more complex function is reflected in the results of vitamin-E-intervention studies of atherosclerosis in animals and of controlled prospective trials on the incidence of cardiovascular disease in humans, which, overall, are inconclusive.
Language of Publication
English
Unique Identifier
99296697

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MeSH Heading (Major)
Atherosclerosis|*ME; Vitamin E|*PH
MeSH Heading
Disease Models, Animal; Human; Lipid Peroxidation; Models, Biological; Support, Non-U.S. Gov't; Tissue Distribution

Publication Type
JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN
0167-7640
Country of Publication
ENGLAND

 

Record 29 from database: MEDLINE
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Title
Pharmacology of vitamin C.
Author
Sauberlich HE
Address
Department of Nutrition Sciences, University of Alabama at Birmingham 35294.
Source
Annu Rev Nutr, 1994, 14:, 371-91
Abstract
A better understanding of the functions of ascorbic acid would help clarify the magnitude of the influence of this vitamin on health-related conditions. Many of the purported benefits require confirmation as well as a knowledge of the mechanism of action. The majority of investigations of the association of vitamin C with various types of cancer, with cardiovascular risk, and with cataract formation were epidemiologic studies. Often it was not possible to discern whether the apparent protective effect was due to vitamin C, vitamin E, or carotene, or to a combined effect of these nutrients or of additional factors. Human intervention trials may provide definitive and quantitative assessments of the role of vitamin C in health maintenance. We need to gain a more thorough understanding of the interactions of vitamin C with other nutrients, such as vitamin E and carotenoids, in order to appreciate the role of vitamin C in disease prevention. Investigators are increasingly recognizing the diverse functions of vitamin C in the body in addition to its role in collagen synthesis. However, the functional consequences of these many important roles of vitamin C remain essentially unknown. Excluding scurvy, the health consequences of inadequate vitamin C status are not well characterized. Nonetheless, epidemiologic evidence suggests a role for vitamin C in cancer and heart disease as well as in a number of other diseases.
Language of Publication
English
Unique Identifier
95033453

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MeSH Heading (Major)
Ascorbic Acid|AD/AE/PH/*TU
MeSH Heading
Antioxidants; Ascorbic Acid Deficiency; Biological Availability; Human; Support, U.S. Gov't, P.H.S.

Publication Type
JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN
0199-9885
Country of Publication
UNITED STATES

 

Record 30 from database: MEDLINE
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Title
Vitamin supplementation therapy in the elderly.
Author
Thurman JE; Mooradian AD
Address
Department of Internal Medicine, St Louis University Medical School, Missouri, USA.
Source
Drugs Aging, 1997 Dec, 11:6, 433-49
Abstract
Vitamin supplementation in large dosages is increasingly common in the older population. Often, such supplementation is used in an attempt to improve an individual's health status. There have been claims that the effects of vitamins halt the normal aging process or prevent and cure disease. However, several recent studies have failed to demonstrate the efficacy of vitamin supplementation in preventing several types of cancer. In moderate dosages, supplementation with vitamin E (tocopherols) shows promise as a lipid antioxidant, and may reduce the risk of coronary heart disease. However, before vitamin E becomes an accepted medical therapy, further long term studies must be undertaken to examine the safety and efficacy of such therapy. An adequate intake of vitamins should be ensured by adherence to a well balanced diet. However, the elderly are prone to circumstances that may prevent them from eating a balanced diet. In addition, there are several age-related medical conditions that may predispose individuals to dietary and vitamin deficiencies. To prevent vitamin deficiency diseases and their associated morbidity, modest vitamin supplementation may be necessary. However, supplementation should be reserved for individuals with documented deficiency or who are at risk of developing such deficiencies, especially those who are homebound or institutionalised. Vitamins taken in large dosages should be considered as drugs. These medicines, which are obtainable over-the-counter, should be carefully regulated to prevent toxicity.
Language of Publication
English
Unique Identifier
98075622

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MeSH Heading (Major)
Dietary Supplements|*; Vitamins|AE/*TU
MeSH Heading
Adult; Aged; Aged, 80 and over; Aging|DE; Antioxidants|TU; Ascorbic Acid|TU; Avitaminosis|DT; Carotenoids|TU; Drug Interactions; Human; Middle Age; Retinoids|TU; Vitamin B Complex|TU; Vitamin D|TU; Vitamin E|TU; Vitamin K|TU

Publication Type
JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN
1170-229X
Country of Publication
NEW ZEALAND

 

Record 31 from database: MEDLINE
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Title
Increased risk of cardiovascular disease at suboptimal plasma concentrations of essential antioxidants: an epidemiological update with special attention to carotene and vitamin C.
Author
Gey KF; Moser UK; Jordan P; Stähelin HB; Eichholzer M; Lüdin E
Address
Vitamin Unit, University of Berne, Switzerland.
Source
Am J Clin Nutr, 1993 May, 57:5 Suppl, 787S-797S
Abstract
For the prolongation of life expectancy and reduction of ischemic heart disease (IHD) dietary guidelines generally recommend lowering saturated mammalian fat with partial replacement by vegetable oils and increasing generously vegetables, legumes, and fruits, which provide more essential antioxidants. Plasma antioxidants as assayed in epidemiological studies of complementary type (ie the cross-cultural MONICA Vitamin Substudy reevaluation considering the "Finland-Factor", the Edinburgh Angina-Control Study, and the Basel Prospective Study) consistently revealed an increased risk of IHD (and stroke) at low plasma concentrations of antioxidants, with the rank order as follows: lipid-standardized vitamin E >> carotene = vitamin C > vitamin A, independently of classical IHD risk factors. Decreasing IHD risk through nutrition may be possible when plasma concentrations have the following values: > 27.5-30.0 mumol vitamin E/L, 0.4-0.5 mumol carotene/L, 40-50 mumol vitamin C/L and 2.2-2.8 mumol vitamin A/L. Thus, previous prudent regimens may now be updated, aiming at an optimal status of all essential and synergistically linked antioxidants.
Language of Publication
English
Unique Identifier
93235821

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MeSH Heading (Major)
Ascorbic Acid|*BL; Carotene|*BL; Cholesterol|*BL; Myocardial Ischemia|*BL/EP/PC; Selenium|*BL; Vitamin E|*BL
MeSH Heading
Angina Pectoris|BL; Blood Pressure; Cerebrovascular Disorders|BL/EP/PC; Comparative Study; Cross-Cultural Comparison; Human; Male; Middle Age; Risk Factors; Support, Non-U.S. Gov't

Publication Type
JOURNAL ARTICLE; REVIEW; REVIEW LITERATURE
ISSN
0002-9165
Country of Publication
UNITED STATES

 

Record 32 from database: MEDLINE
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Title
Optimal nutrition: vitamin A and the carotenoids.
Author
Thurnham DI; Northrop Clewes CA
Address
Northern Ireland Centre for Diet and Health, University of Ulster, Coleraine, UK. di.thurnham@ulst.ac.uk
Source
Proc Nutr Soc, 1999 May, 58:2, 449-57
Abstract
There are two major dietary sources of vitamin A: easily absorbed retinyl palmitate in foods of animal origin, and poorly bioavailable carotenoids from plant foods. Plasma retinol is tightly controlled, probably by regulation of retinol-binding protein (RBP) formation in the liver, and only hormonal factors (e.g. oral contraceptives) and infection will alter the homeostasis. Delivery of retinol to the tissues is facilitated by the RBP-retinol complex; however, there is evidence that this mechanism can be bypassed when very high doses of vitamin A are given. Some retinyl ester may be released to tissues from chylomicrons when the latter bind to tissue lipoprotein receptors during their passage from the gut to the liver following a meal. High-dose vitamin A therapy is a means of rapidly improving vitamin A status in persons with sub-optimal vitamin A nutrition but there are dangers of toxic symptoms (e.g. teratogenicity) from excess vitamin A usage. Evidence is presented to suggest that the plasma retinol: RBP may be a guide to optimal vitamin A status, since values less than one frequently occur in less-developed countries and during infection. In contrast to plasma retinol, plasma carotenoids reflect the dietary intake of plant foods. However, absorption is limited by poor bioavailability and a saturable uptake mechanism in competition with other phytochemicals. Recent work on bioavailability suggests that the calculation of plant food vitamin A activity should be re-examined. Illness has little influence on plasma levels except by suppressing appetite. Carotenoids are generally regarded as non-toxic yet intervention studies with beta-carotene in smokers have been associated with increased lung cancer and heart disease. Some carotenoids are important as vitamin A precursors, but the physiological importance of their antioxidant properties is not known and consequently the amount needed for optimal nutrition is uncertain.
Language of Publication
English
Unique Identifier
99395684

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MeSH Heading (Major)
Nutrition|*; Vitamin A|*/AD/BL
MeSH Heading
Absorption; Biological Availability; Child, Preschool; Homeostasis; Human; Infant; Infant, Newborn; Infection|BL; Nutritional Requirements; Nutritional Status

Publication Type
JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN
0029-6651
Country of Publication
ENGLAND

 

Record 33 from database: MEDLINE
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Title
Antenatal drugs affecting vitamin K status of the fetus and the newborn.
Author
Astedt B
Address
Department of Obstetrics and Gynecology, University Hospital, Lund, Sweden.
Source
Semin Thromb Hemost, 1995, 21:4, 364-70
Abstract
Coumarin derivatives and anticonvulsants administered during pregnancy enter the fetal circulation, interfering with the action of vitamin K. Vitamin K plays a crucial part in the gamma-carboxylation of glutamic acid residues of the vitamin K-dependent coagulation factors prothrombin, FVII, FIX, and FX. Other vitamin K-dependent proteins in the coagulation cascade are protein C and protein S. Vitamin K-dependent bone proteins are osteocalcin and gamma-carboxyglutamate matrix protein. Administration of coumarol derivatives results in under carboxylation of the vitamin K-dependent proteins. Anticoagulation therapy with warfarin is followed by an increased risk of embryopathy, which has been shown to be greatest between gestational weeks 6 and 12. Administration of warfarin is also followed by an increased risk both of fetal intraventricular hemorrhage, and of cerebral microbleedings, which may result in microencephaly and mental retardation. Treatment with coumarol derivatives should therefore be avoided during pregnancy, even in pregnant women with artificial heart valves, and replaced by heparin. Hemorrhage in the newborn related to the use of anticonvulsant drugs during pregnancy occurs very early within the first 24 hours, probably due to increased degradation of vitamin K. Transplacental administration of vitamin K has been shown to prevent neonatal hemorrhage induced by maternal anticonvulsant therapy. Prophylactic administration of vitamin K, especially by intramuscular injection, has been reported to be associated with an increased risk of childhood cancer. However, subsequent extensive studies have yielded no evidence of any relationship between prophylactic vitamin K administration and the occurrence of childhood cancer.
Language of Publication
English
Unique Identifier
96357539

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MeSH Heading (Major)
Abnormalities, Drug-Induced|*ET; Anticoagulants|*AE/PK; Anticonvulsants|*AE/PK; Coumarins|*AE/PK; Fetal Diseases|*CI; Pregnancy Complications|*DT; Prenatal Exposure Delayed Effects|*; Vitamin K|AE/*PH/TU; Vitamin K Deficiency|*CI/EM/PC
MeSH Heading
Blood Coagulation Factors|ME; Child; Cohort Studies; Epilepsy|DT; Female; Great Britain|EP; Hemorrhage|CI; Human; Infant, Newborn; Maternal-Fetal Exchange; Neoplasms|CI/EP; Pregnancy; Protein Processing, Post-Translational; Support, Non-U.S. Gov't; Sweden|EP; Thrombosis|DT

Publication Type
JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
ISSN
0094-6176
Country of Publication
UNITED STATES

 

Record 34 from database: MEDLINE
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Title
High-dose vitamin C: a risk for persons with high iron stores?
Author
Gerster H
Address
Vitamin Research Department, F. Hoffmann-La Roche Ltd, Basel, Switzerland.
Source
Int J Vitam Nutr Res, 1999 Mar, 69:2, 67-82
Abstract
The contribution of vitamin C (ascorbic acid) to the prevention of iron deficiency anemia by promoting the absorption of dietary non-heme iron-especially in persons with low iron stores--is well established. But the question has been raised whether high-dose intakes of vitamin C might unduly enhance the absorption of dietary iron in persons with high iron stores or in patients with iron overload, possibly increasing the potential risk of iron toxicity. Extensive studies have shown that overall the uptake and storage of iron in humans is efficiently controlled by a network of regulatory mechanisms. Even high vitamin C intakes do not cause iron imbalance in healthy persons and probably in persons who are heterozygous for hemochromatosis. The uptake, renal tubular reabsorption and storage of vitamin C itself are also strictly limited after high-dose intake so that no excessive plasma and tissue concentrations of vitamin C are produced. The effect of high-dose vitamin C on iron absorption in patients with iron overload due to homozygous hemochromatosis has not been studied. Of special importance is the early identification of hemochromatosis patients, which is assisted by the newly developed PCR test for hereditary hemochromatosis. Specific treatment consists of regular phlebotomy and possibly iron-chelating therapy. These patients should moreover avoid any possibility of facilitated absorption of iron and need to limit their intake of iron. Patients with beta-thalassemia major and sickle cell anemia who suffer from iron overload due to regular blood transfusions or excessive destruction of red blood cells need specialized medical treatment with iron chelators and should also control their intake of iron. The serum of patients with pathological iron overload can contain non-transferrin-bound iron inducing lipid peroxidation with subsequent consumption of antioxidants such as vitamin E and vitamin C. The role of iron in coronary heart disease and cancer is controversial. Early suggestions that moderately elevated iron stores are associated with an increased risk of CHD have not been confirmed by later studies. In vitro, ascorbic acid can act as a prooxidant in the presence of transition metals such as iron or copper, but in the living organism its major functions are as an antioxidant. High intakes of vitamin C have thus not been found to increase oxidative damage in humans. Accordingly, the risk of CHD or cancer is not elevated. On the contrary, most studies have shown that diets rich in vitamin C are inversely related to the incidence of these diseases.
Language of Publication
English
Unique Identifier
99234766

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MeSH Heading (Major)
Anemia, Iron-Deficiency|*PC; Ascorbic Acid|*AD/*AE/PH; Iron, Dietary|*ME
MeSH Heading
Animal; Biological Availability; Human; Lipid Peroxidation; Risk Factors

Publication Type
JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
ISSN
0300-9831
Country of Publication
SWITZERLAND

 

Record 35 from database: MEDLINE
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Title
Tocopherol-mediated peroxidation of lipoproteins: implications for vitamin E as a potential antiatherogenic supplement.
Author
Upston JM; Terentis AC; Stocker R
Address
Biochemistry Group, The Heart Research Institute, Sydney, Australia.
Source
FASEB J, 1999 Jun, 13:9, 977-94
Abstract
The 'oxidation theory' of atherosclerosis proposes that oxidation of low density lipoprotein (LDL) contributes to atherogenesis. Although little direct evidence for a causative role of 'oxidized LDL' in atherogenesis exists, several studies show that, in vitro, oxidized LDL exhibits potentially proatherogenic activities and lipoproteins isolated from atherosclerotic lesions are oxidized. As a consequence, the molecular mechanisms of LDL oxidation and the actions of alpha-tocopherol (alpha-TOH, vitamin E), the major lipid-soluble lipoprotein antioxidant, have been studied in detail. Based on the known antioxidant action of alpha-TOH and epidemiological evidence, vitamin E is generally considered to be beneficial in coronary artery disease. However, intervention studies overall show a null effect of vitamin E on atherosclerosis. This confounding outcome can be rationalized by the recently discovered diverse role for alpha-TOH in lipoprotein oxidation; that is, alpha-TOH displays neutral, anti-, or, indeed, pro-oxidant activity under various conditions. This review describes the latter, novel action of alpha-TOH, termed tocopherol-mediated peroxidation, and discusses the benefits of vitamin E supplementation alone or together with other antioxidants that work in concert with alpha-TOH in ameliorating lipoprotein lipid peroxidation in the artery wall and, hence, atherosclerosis.
Language of Publication
English
Unique Identifier
99270893

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MeSH Heading (Major)
Atherosclerosis|*PC; Lipid Peroxidation|*; Lipoproteins, LDL|*ME; Vitamin E|*ME/*TU
MeSH Heading
Animal; Antioxidants|ME/TU; Arteries|ME; Human; Models, Chemical; Oxidants|ME/TU; Support, Non-U.S. Gov't

Publication Type
JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
ISSN
0892-6638
Country of Publication
UNITED STATES

 

Record 36 from database: MEDLINE
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Title
Inadequate vitamin D status: does it contribute to the disorders comprising syndrome 'X'?
Author
Boucher BJ
Address
Academic Medical Unit, St. Bartholomew's and the Royal London Hospital Medical & Dental School, UK.
Source
Br J Nutr, 1998 Apr, 79:4, 315-27
Abstract
Environmental factors are important in the aetiology of glucose intolerance, type II diabetes and IHD. The lack of vitamin D, which is necessary for adequate insulin secretion, relates demographically to increased risk of myocardial infarction. These disorders are connected, degenerative vascular disease increasing with glucose intolerance and diabetes and, with its risk factors, comprising syndrome 'X'. Evidence is presented suggesting that vitamin D deficiency may be an avoidable risk factor for syndrome 'X', adding another preventative measure to current recommendations which are aimed at reducing the worldwide epidemic of these disorders. Experimentally, vitamin D deficiency progressively reduces insulin secretion; glucose intolerance follows and becomes irreversible. Relationships between vitamin D status, glucose tolerance and 30 min insulin secretion during oral glucose tolerance tests are reported in British Asians; insulin secretion, but not glycaemia, improving with short-term supplementation. Studies showing reduction in blood pressure and in risk of heart attack and diabetes with exercise (usually outdoor), rarely consider the role of vitamin D status. Glycaemia and insulin secretion in elderly European men, however, relate to vitamin D status, independent of season or physical activity. Prolonged supplementation can improve glycaemia. Hypertension improves with vitamin D treatment with or without initial deficiency. Vitamin D status and climate are reviewed as risk factors for myocardial infarction; the risk reducing with altitude despite increasing cold. Glycaemia and fibrinogenaemia improve with insulin secretion increases in summer. Variation in vitamin D requirements could arise from genetic differences in vitamin D processing since bone density can vary with vitamin D-receptor genotype. Vitamin D receptors are present in islet beta cells and we report insulin secretion in healthy Asians differing profoundly with the Apa I genotype, being independent of vitamin D status. Those at risk of vitamin D deficiency include the elderly, those living indoors or having a covered-up style of dress, especially dark-skinned immigrants, and pregnant women, and these are groups recognized as being at increased risk of diabetes.
Language of Publication
English
Unique Identifier
98287286

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MeSH Heading (Major)
Insulin Resistance|*; Nutritional Status|*; Vitamin D Deficiency|*CO
MeSH Heading
Adult; Aged; Animal; Diabetes Mellitus, Non-Insulin-Dependent|ET; Female; Human; Male; Middle Age; Pregnancy; Seasons

Publication Type
JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
ISSN
0007-1145
Country of Publication
ENGLAND

 


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