Atherosclerosis supplementation

Muller PJ, Miserez AR. Mutations in the gene encoding sterol-regulatory element-binding protein-2 in hypercholes-terolaemic subjects. Atherosclerosis Supplements 2001 2 69. 

Willett, W. C. (2006). Trans fatty acids and cardiovascular disease-epidemiological data. Atherosclerosis Supplements, 7(2), 5-8. 

Mortensen, A., Breinholt, V., Frandsen, H., Lund, C.O., Ottesen, B., and Larsen, J.J. 2003. Dietary soy supplement reduces aortic atherosclerosis in ovariectomized Watanabe heritable hyperlip-idemic rabbits. Atherosclerosis Supplements 4, 276. 

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]. 

Supplements of 400 Ig/d of folate begun before conception result in a significant reduction in the incidence of neural mbe defects as found in spina bifida. Elevated blood homocysteine is an associated risk factor for atherosclerosis, thrombosis, and hypertension. The condition is due to impaired abihty to form methyl-tetrahydrofolate by methylene-tetrahydrofolate reductase, causing functional folate deficiency and resulting in failure to remethylate homocysteine to methionine. People with the causative abnormal variant of methylene-tetrahydrofolate reductase do not develop hyperhomocysteinemia if they have a relatively high intake of folate, but it is not yet known whether this affects the incidence of cardiovascular disease. 

CHOPRA M, MCLOONE u L, o neill m, WILLIAMS N and THURNHAM DI (1996) Fruit and vegetable supplementation - effect on ex vivo LDL oxidation in hiunans , in Kumpulainen, J T and Saonen, J T (eds), Natural Antioxidants and Food Quality in Atherosclerosis and Cancer Prevention, Cambridge, Royal Society of Chemistry, 150-55. 

Zhao, C. et al.. Effects of commercial anthocyanin-rich extracts on colonic cancer and nontumorigenic colonic cell growth, J. Agric. Food Chem., 52, 6122, 2004. Kaplan, M. et al.. Pomegranate juice supplementation to atherosclerotic mice reduces macrophage lipid peroxidation, cellular cholesterol accumulation and development of atherosclerosis, J. Nutr, 131, 2082, 2001. 

Kim, H.S. and Lee, B.M., Protective effects of antioxidant supplementation on plasma lipid peroxidation in smokers, J. Toxicol. Environ. Health A, 63, 583, 2001. Gaziano, J.M. et al.. Supplementation with beta-carotene in vivo and in vitro does not inhibit low density lipoprotein oxidation. Atherosclerosis, 112, 187, 1995. Sutherland, W.H.F. et al.. Supplementation with tomato juice increases plasma lycopene but does not alter susceptibility to oxidation of low-density lipoproteins from renal transplant recipients, Clin. Nephrol, 52, 30, 1999. 

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... 

Oxidized low-density lipoprotein (LDL) may play a key role in the initiation and progression of atherosclerosis. Risk factors for elevated levels of oxidized LDL are not well established and may be important in identifying individuals who may benefit from antioxidant supplementation or interventions to reduce oxidant stress. 

Howes, J.B., Sullivan, D., Lai, N., Nestel, P., Pomeroy, S., West, L., Eden, J.A. and Howes, L.G. (2000). The effects of dietary supplementation with isoflavones from red clover on the lipoprotein profiles of post menopausal women with mild to moderate h5q)ercholesterolaemia, Atherosclerosis, 152, 143-147. 

Homocysteine blood levels (>15 jtmol/L) promote atherosclerosis, perhaps by stimulating proliferation of arterial wall smooth muscle cells. Supplementing the diet with folic acid can reduce high levels. Lpa is a mod-ihed LDL particle that is both atherogenic and pro-thrombic. 

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. 

Samman S, Lyons-Wall PM, Chan GS, Smith SJ, Petocz P. The effect of supplementation with isoflavones on plasma lipids and oxidisability of low density lipoprotein in premenopausal women. Atherosclerosis 147, 277-283, 1999. 

The effects of wine and its polyphenol constituents on early indicators of coronary heart disease such as elevated levels of plasma lipids, platelets and serum antioxidant activity were discussed in a review by Cooper et al. (2004). This review also addressed whether the polyphenols or alcohol are responsible for the beneficial effects of wine on cardio-vascular health. The authors conclude that red wine polyphenols have little effect on plasma lipid concentrations, but that wine consumption reduces the susceptibility of low-density lipoprotein (LDL) cholesterol to oxidation and increase serum antioxidant capacity. These effects, however, do depend on the amount of wine that is consumed and the period of supplementation. It was suggested that specific polyphenols appear to have endothelium-dependent vaso-relaxing abilities. Red wine phenolics also have an inhibitory effect on platelet aggregation. Evidence suggests that alcohol has a positive synergistic effect with wine polyphenols on some atherosclerosis risk factors. Thus, evidence that wine drinking is beneficial for cardiac health appears positive. 

People with severe hypertriglyceridemia associated with Type V hyperlipoproteinemia may be at increased risk of hypervitaminosis A, even with moderate degrees of vitamin A supplementation (1199). Long-term vitamin A administration is associated with an increase in serum cholesterol and serum triglyceride concentrations (1200) and consequently might be linked with atherosclerosis (SEDA-8, 345) (1201,1202). 

Elevated serum cholesterol levels are invariably associated with the etiology of atherosclerosis and coronary artery disease, and it has been shown by several investigators that pectin from a variety of sources when supplemented in the diet of a number of laboratory animals, as well as human volunteers, causes lowering... 

Finally, creatine supplements may be useful in the treatment of heart problems. Creatine has improved exercise capacity in patients suffering from congestive heart failure, and lowered blood cholesterol in animal studies. Limited study of creatine s effect on blood cholesterol levels in healthy humans has had mixed results, with one study reporting a positive impact and another reporting no effect at all. Further research is needed to determine if creatine is beneficial in improving blood cholesterol and preventing atherosclerosis. 

Aviram, M. et al., Pomegranate juice polyphenols decrease oxidative stress, low-density lipoprotein atherogenic modifications and atherosclerosis, Free Radic. Res., 36 (Supplement 1), 72, 2002. 

Kaplan, M. et al., Pomegranate juice supplementation to atherosclerotic mice reduces macrophages lipid peroxidation, cellular cholesterol accumulation and development of atherosclerosis, J. Nutr., 131, 2082, 2001. 

Homocysteine is a nonprotein-building amino acid formed as a metabolite in the methionine cycle. It was first associated with disease in 1962 (1,2). Individuals with a mutation in cystathionine-(3-synthase (CBS) develop classical homocystin-uria with extremely elevated plasma tHcy (> 100 xmol/L) (3). Homocystinuria is characterized by early atherosclerosis and thromboembolism as well as mental retardation and osteoporosis and is ameliorated by vitamin supplementation aimed at reducing the blood concentration of homocysteine (4). 

Increases in plasma S-AA levels have previously been reported in patients with coronary disease (57). S-AA and plasma intracellular adhesion molecule-1 were elevated in patients with CAD and hyperhomocysteinemia, but only S-AA decreased after vitamin supplementation (35). Homocysteine activates nuclear factor- in endothelial cells, possibly via oxidative stress (58), and increases monocyte chemoattractant protein-1 expression in vascular smooth muscle cells (59). Additionally, it stimulates interleukin-8 expression in human endothelial cultures (60). These inflammatory factors are known to participate in the development of atherosclerosis. Taken together, these reports suggest an association of elevated tHcy and low-grade inflammation in CAD. 

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