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Vitamin atherosclerosis

Antioxidants protect the body from damage cansed by harmful molecules called free radicals this damage is a factor in the development of atherosclerosis. Vitamin C captnres the free radical and nentralizes it before it causes damage. [Pg.375]

Low levels of vitamin Bg may cause hyperhomocysteinaemia since vitamin Bg acts as a cofactor for tra .s-sulfation of cysteine (Siri et al. 1998). There is evidence that an elevated homocysteine level is a risk factor for heart disease and stroke. Endo et al. (2006) reported that vitamin Bg deficiency induced the oxidant stress which accelerates atherosclerosis. They also highlighted that the antioxidant activity of vitamin Bg may suppress the homo-cysteine-induced atherosclerosis. Vitamin Bg levels may be important in the prevention of coronary heart disease intake of vitamin Bg above the current recommended dietary allowance has been shown to be instrumental in the primary prevention of coronary heart disease among women (Rimm et al. 1998). [Pg.171]

Also see ATHEROSCLEROSIS VITAMIN [S] VITAMIN B-COMPEEX and VITAMIN B-6.)... [Pg.548]

Cinter, L., "Vitamin C in Lipid Metabolism and Atherosclerosis," Vitamin C, edited by G. G. Birch and K. J. Parker, Applied Science Publishers, Ltd., Essex England, 1974, p. 179. [Pg.549]

Homocysteine arises from dietary methionine. High levels of homocysteiae (hyperhomocysteinemia) are a risk factor for occlusive vascular diseases including atherosclerosis and thrombosis (81—84). In a controlled study, semm folate concentrations of <9.2 nmol/L were linked with elevated levels of plasma homocysteiae. Elevated homocysteine levels have beea associated also with ischemic stroke (9). The mechanism by which high levels of homocysteine produce vascular damage are, as of yet, aot completely uaderstood. lateractioa of homocysteiae with platelets or eadothehal cells has beea proposed as a possible mechanism. Clinically, homocysteine levels can be lowered by administration of vitamin B, vitamin B 2> foHc acid. [Pg.42]

Methyl-tetrahydro folic acid is furthermore, together with vitamin B12 and B6, required to regenerate homocysteine (see Vitamin B12, Fig. 1). Homocysteine results when methionine is used as a substrate for methyl group transfer. During the last few years, homocysteine has been acknowledged as an independent risk factor in atherosclerosis etiology. Folic acid supplementation can help reduce elevated homocysteine plasma levels and is therefore supposed to reduce the risk of atherosclerosis as well [2]. [Pg.509]

Vitamin C status is supposed to play a role in immune function and to influence the progression of some chronic degenerative diseases like atherosclerosis, cancer, cataracts, and osteoporosis. The role of vitamin C in immune function, especially during common cold and upper respiratory tract infection, is the subject of lively debate. The exact mechanisms of action have not yet been fully elucidated, but the results of several trials point to a reduced duration and intensity of infections in subjects consuming high amounts of vitamin C (200-1000 mg/d). However, the incidence of common cold was not influenced significantly (24). [Pg.1294]

One major prerequisite for the maintenance of health is that there be optimal dietary intake of a number of chemicals the chief of these are vitamins, certain amino acids, certain fatty acids, various minerals, and water. Because much of the subject matter of both biochemistry and nutrition is concerned with the smdy of various aspects of these chemicals, there is a close relationship between these two sciences. Moreover, more emphasis is being placed on systematic attempts to maintain health and forestall disease, ie, on preventive medicine. Thus, nutritional approaches to—for example—the prevention of atherosclerosis and cancer are receiving increased emphasis. Understanding nutrition depends to a great extent on a knowledge of biochemistry. [Pg.2]

Cholesterol is probably the best known steroid because of its association with atherosclerosis. However, biochemically it is also of significance because it is the precursor of a large number of equally important steroids that include the bile acids, adrenocortical hormones, sex hormones, D vitamins, cardiac glycosides, sitosterols of the plant kingdom, and some alkaloids. [Pg.117]

LDL when oxidized is recognized to play a crucial role in the development of atherosclerosis. It was thought that flavonoids could also protect LDL against oxidation, especially by limiting the degradation of vitamin E, the main antioxidant in LDL. Other beneficial effects of flavonoids have been reported inhibition of platelet... [Pg.137]

Iribarren, C. et al.. Association of serum vitamin levels, LDL susceptibility to oxidation, and autoantibodies against MDA-LDL with carotid atherosclerosis a case-control %Vady, Arterioscler. Thromb. Vase. Biol, 17, 1171, 1997. [Pg.142]

There have been more than 20 studies relating to the prevention of atherosclerosis by antioxidants. In vitro, several studies have shown that antioxidant treatment (e.g. vitamin E) inhibits both oxidation and the formation of cytotoxic LDL (Steinbrecher etal., 1984 Par-thasarathy etal., 1986 Esterbauer etal., 1987). In vivo, vitamin E supplementation prevents LDL oxidation in... [Pg.192]

Epileptiform fits associated with degenerative changes in the myelin sheath of peripheral nerves and spinal cord occur in B6-deficient animals. Lesions in the arteries, resembling those of human atherosclerosis, have been observed in Be-deficient monkeys. Recently, a state of Be deficiency in human infants, characterized by loss of ability to convert tryptophan to nicotinic acid, by impaired growth, convulsions, and hypochromic anemia, has been described, following omission of vitamin B6 from the diet. [Pg.212]

Dl. Dalderup, L. M, Atherosclerosis and toxemia of pregnancy in relation to nutrition and other physiological factors. Vitamins and Hormones 17, 223-306 (1959). [Pg.241]

The standard diet used in our experiments is a semipurified, cholesterol-free preparation that is composed of 25% protein, 40% sucrose, 13% coconut oil, 1% corn oil, 15% cellulose, 5% mineral mix, and 1% vitamin mix. This diet has been shown to induce an endogenous hypercholesterolemia and lead to atherosclerosis in rabbits and monkeys (4, 5). The specific question addressed by our series of investigations is whether the type of dietary protein, when all other dietary components are constant, can influence the development of hyperlipoproteinemia and atherosclerosis. More specifically, we have examined the effects of the individual amino acids, lysine and arginine, and their ratios in the diet on plasma and hepatic lipids as well as the development of arterial plaques. [Pg.155]

Thomas, S.R., and Stocker, R., 2000, Molecular action of vitamin E in lipoprotein oxidation impheations for atherosclerosis. Free Radio. Biol. Med. 28 1795-1805. [Pg.149]

Vitamin deficiencies may produce a more mild form of homocystinemia. Mild homocystinemia is associated with increased risk for atherosclerosis, deep vein thrombosis, and stroke. The vitamin deficiencies causing homocystinemia include ... [Pg.249]

Figure 22.6 How various factors increase the risk of atherosclerosis, thrombosis and myocardial infarction. The diagram provides suggestions as to how various factors increase the risk of development of the trio of cardiovascular problems. The factors include an excessive intake of total fat, which increases activity of clotting factors, especially factor VIII an excessive intake of saturated or trans fatty acids that change the structure of the plasma membrane of cells, such as endothelial cells, which increases the risk of platelet aggregation or susceptibility of the membrane to injury excessive intake of salt - which increases blood pressure, as does smoking and low physical activity a high intake of fat or cholesterol or a low intake of antioxidants, vitamin 6 2 and folic acid, which can lead either to direct chemical damage (e.g. oxidation) to the structure of LDL or an increase in the serum level of LDL, which also increases the risk of chemical damage to LDL. A low intake of folate and vitamin B12 also decreases metabolism of homocysteine, so that the plasma concentration increases, which can damage the endothelial membrane due to formation of thiolactone. Figure 22.6 How various factors increase the risk of atherosclerosis, thrombosis and myocardial infarction. The diagram provides suggestions as to how various factors increase the risk of development of the trio of cardiovascular problems. The factors include an excessive intake of total fat, which increases activity of clotting factors, especially factor VIII an excessive intake of saturated or trans fatty acids that change the structure of the plasma membrane of cells, such as endothelial cells, which increases the risk of platelet aggregation or susceptibility of the membrane to injury excessive intake of salt - which increases blood pressure, as does smoking and low physical activity a high intake of fat or cholesterol or a low intake of antioxidants, vitamin 6 2 and folic acid, which can lead either to direct chemical damage (e.g. oxidation) to the structure of LDL or an increase in the serum level of LDL, which also increases the risk of chemical damage to LDL. A low intake of folate and vitamin B12 also decreases metabolism of homocysteine, so that the plasma concentration increases, which can damage the endothelial membrane due to formation of thiolactone.
The role of the antioxidant properties of vitamins C, E, and p-carotene in the prevention of cardiovascular disease has been the focus of several recent studies. Antioxidants reduce the oxidation of low-density lipoproteins, which may play a role in the prevention of atherosclerosis. However, an inverse relationship between the intake or plasma levels of these vitamins and the incidence of coronary heart disease has been found in only a few epidemiological studies. One study showed that antioxidants lowered the level of high-density lipoprotein 2 and interfered with the effects of lipid-altering therapies given at the same time. While many groups recommend a varied diet rich in fruits and vegetables for the prevention of coronary artery disease, empirical data do not exist to recommend antioxidant supplementation for the prevention of coronary disease. [Pg.781]

Vitamin K antagonists, such as dicoumarol (8.61, a natural product) and warfarin (8.62), are used as anticoagulants in human therapy (thrombosis, atherosclerosis) and as rat poisons that lead to internal bleeding and death in rodents. Heparin, a polysaccharide consisting of 2-0-sulfonated glucuronic acid and 2-N,6-0-disulfonated glucosamine, is also a widely used anticoagulant, but its effect is connected not with Vitamin K but with enzyme inhibition. [Pg.512]

Wu, Y. J., C. Y. Hong, S. J. Lin, P. Wu, and M. S. Shiao. 1998. Increase of vitamin E content in LDL and reduction of atherosclerosis in cholesterol-fed rabbits by a water-soluble antioxidant-rich fraction of Salvia miltiorrhiza. Arterioscler. Thromb. Vase. Biol. 18 481-486. [Pg.331]


See other pages where Vitamin atherosclerosis is mentioned: [Pg.128]    [Pg.132]    [Pg.128]    [Pg.132]    [Pg.253]    [Pg.162]    [Pg.939]    [Pg.1294]    [Pg.111]    [Pg.219]    [Pg.481]    [Pg.486]    [Pg.374]    [Pg.47]    [Pg.132]    [Pg.243]    [Pg.791]    [Pg.920]    [Pg.946]    [Pg.614]    [Pg.300]    [Pg.336]    [Pg.272]    [Pg.12]    [Pg.792]    [Pg.921]   
See also in sourсe #XX -- [ Pg.97 ]

See also in sourсe #XX -- [ Pg.97 ]

See also in sourсe #XX -- [ Pg.97 ]




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