Heart Protection Study vitamin

Heart Protection Study Collaborative Group, MRC/BHF Heart Protection Smdy of antioxidant vitamin supplementation in 20,536 high-risk individuals a randomised placebo-controlled trial. Lancet, 360, 23, 2002. 

Heart Protection Study Collaborative Group (2002) MRC/BHF Heart Protection Study of Antioxidant Vitamin Supplementation in 20,536 High-Risk Individuals A Randomized Placebo-ControUed Trial, Lancet 360,23 33. 

ATBC, Alpha Tocopherol Beta Carotene Prevention Study CARET, Beta Carotene and Retinol Efficacy Trial HPS, Heart Protection Study LCPS, Linxian Cancer Prevention Study NSCPT, Nambour Skin Cancer Prevention Trial PHS, Physicians Health Study VACP, Vitamin A and Cancer Preventbn WHS, Women s Health Study CVD, Cardio Vascular disease. 

There are no published RCTs of vitamin C alone in primary prevention, but data from the small number of trials of vitamin C in combination with other nutrients have not provided any support for a role for high-dose vitamin C supplementation in cancer prevention (Table 3). The Linxian trial found no significant effect of supplementing Chinese men and women with 120 mg vitamin C and 30 pg molybdenum daily for 5 years on the risk of cancers of the oesophagus or stomach. The Polyp Prevention Study, a trial of 864 patients with previous adenoma, found no effect of either /3-carotene or a combination of vitamins E and C (1000 mg) on the incidence of subsequent colorectal adenomas. The Heart Protection Study also found no beneficial effects of supplementation with these three vitamins on cancer mortality. However, trials have generally... 

An average of 4 years of supplementation with 400 lU of vitamin E per day was found to exert no beneficial or harmful effect on CVD outcomes or on nephropathy. The Primary Prevention Project trial found no effect of vitamin E (300mg/day) supplementation for 3 or 4 years in diabetic subjects, and the Heart Protection Study, which included a number of people with diabetes, also reported no benefit of a combination of antioxidant vitamins on mortality or incidence of vascular disease. 

The Medical Research Council/British Heart Foundation study controlled the activity of antioxidants in the protection of a large group of patients (10,629) suffering from coronary disease who were treated daily with vitamin supplementation (vitamin E 600 mg, vitamin C 250 mg, and /3-carotene 20 mg). Similar high dosages were used in Age-Related Eye Disease Study (vitamin E 400 Ul, vitamin C 500mg, and /3-carotene 15 mg). In both studies the results were not positive. In these last two studies as in any of the studies reported in Table 9 the OS was measured to determine the real need of an antioxidant therapy. 

This mechanism is now considered to be of importance for the protection of LDL against oxidation stress, Chapter 25.) The antioxidant effect of ubiquinones on lipid peroxidation was first shown in 1980 [237]. In 1987 Solaini et al. [238] showed that the depletion of beef heart mitochondria from ubiquinone enhanced the iron adriamycin-initiated lipid peroxidation whereas the reincorporation of ubiquinone in mitochondria depressed lipid peroxidation. It was concluded that ubiquinone is able to protect mitochondria against the prooxidant effect of adriamycin. Inhibition of in vitro and in vivo liposomal, microsomal, and mitochondrial lipid peroxidation has also been shown in studies by Beyer [239] and Frei et al. [240]. Later on, it was suggested that ubihydroquinones inhibit lipid peroxidation only in cooperation with vitamin E [241]. However, simultaneous presence of ubihydroquinone and vitamin E apparently is not always necessary [242], although the synergistic interaction of these antioxidants may take place (see below). It has been shown that the enzymatic reduction of ubiquinones to ubihydroquinones is catalyzed by NADH-dependent plasma membrane reductase and NADPH-dependent cytosolic ubiquinone reductase [243,244]. 

The vitamin has been shown to be able to protect animals from the lethal effects of anoxia and hypoxia. Rats [189] and rabbits [190] fed on vitamin-E-supple-mented diets survived longer in hypoxia than non-supplemented animals. A similar protective effect has been demonstrated in vitro with cardiac muscle [ 167]. In hypoxic Langendorff-perfused rabbit heart, the presence of vitamin E protected the muscle from the deleterious effects of hypoxia, possibly by improving mitochondrial function [168]. However, in clinical studies, the use of vitamin E in ischaemic heart disease has met with little success [191, 192], although the results have been controversial [193]. 

Cardiovascular Pre-atherosclerotic blood vessels have increased levels of ROS. Vitamin E protects against development of atherosclerosis Disruption of SOD leads to heart failure and overexpression protects against injury PHSI no overall benefit of beta-carotene on CVD Benefit in high-risk subgroup. CHAOS trail vitamin E reduces rate of non-fatal myocaidial infaict. ATBC study no overall benefit on CVD rate with Vitamin E or beta-carotene Increase in CVD deaths with beta-caiotene. 

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