Vitamin E is a natural antioxidant as it prevents other fat-soluble vitamins from being destroyed by oxygen and thus acts as a natural preservative in the Xtend-Life Cholest-Natural formula.
Vitamin E helps to prevent oxidative damage to cell membranes, vein degeneration and atherosclerosis. Vitamin E helps the body to use vitamin A, improves circulation and is needed for tissue repair and skin health. It modulates production of prostaglandins, reduces inflammation, and improves tension, pain, irritability and incoordination.
The amount of this oil used in Cholest-Natural is quite low so as to not 'overdose' when the formula is used in conjunction with other supplements.
Published Clinical Studiescl top
Vitamin E treatment in pediatric obesity-related liver disease: a randomized study.1
Vajro P, Mandato C, Franzese A, Ciccimarra E, Lucariello S, Savoia M, Capuano G, Migliaro F.
Department of Pediatrics, University of Naples Federico II, Italy. vajro@unina.it
OBJECTIVE: A beneficial role of antioxidants in hepatopathic obese individuals has hitherto been inferred only from uncontrolled pilot studies. The authors compared the effect of vitamin E and weight loss on transaminase values and on ultrasonographic bright liver in a controlled group of children with obesity-related liver dysfunction. METHODS: Twenty-eight children with obesity-related hypertransaminasemia and bright liver were randomly allocated to two single-blind groups: group 1 (n = 14) treated with a low-calorie diet associated with oral placebo for 5 months, and group 2 (n = 14) treated with a low-calorie diet associated with oral vitamin E (400 mg/d x 2 months, 100 mg/d x 3 months). Transaminase values and ultrasonographic liver brightness along with weight loss and vitamin E levels were monitored. RESULTS: Variations in transaminase levels and percentage of patients with normalized transaminase values were comparable in the two groups. The disappearance of bright liver was observed only in patients who lost weight and was twice as common in patients from group 1. Two subgroups of patients with complete normalization of transaminase values emerged as a consequence of controlled adherence to diet alone (n = 6; significant decrease of percent overweight: P = 0.0019 ) and to vitamin E alone (n = 7; unmodified percent overweight and significant increase of vitamin E/cholesterol ratio: P < 0.0001). Changes in treatment-induced alanine aminotransferase levels in these two subgroups were comparable at month 2, whereas values at month 5 were significantly lower in the subgroup adherent to diet alone (P = 0.04). In the subgroup adherent to vitamin E alone, after 2 months washout, transaminase remained stable in 5 patients and increased in 2; bright liver persisted in all. CONCLUSIONS: Oral vitamin E warrants consideration in obesity-related liver dysfunction for children unable to adhere to low-calorie diets.
PMID: 14676594 [PubMed - in process]
2
Effects of vitamin E and C supplementation either alone or in combination on exercise-induced lipid peroxidation in trained cyclists.
Bryant RJ, Ryder J, Martino P, Kim J, Craig BW.
Human Performance Laboratory, Ball State University, Munice, Indiana 47306, USA.
Seven trained male cyclists (ate 22.3 +/- 2 years) participated in 4 separate supplementation phases. They ingested 2 capsules per day containing the following treatments: placebo (placebo plus placebo); vitamin C (1 g per day vitamin C plus placebo); vitamin C and E (1 g per day vitamin C plus 200 IU per kg vitamin E); and vitamin E (400 IU per kg vitamin E plus placebo). The treatment order (placebo, vitamin C, vitamin C and E, and vitamin E) was the same for all subjects. Performance trials consisting of a 60-minute steady state ride (SSR) and a 30-minute performance ride (PR) on Cybex 100 Metabolic cycles were performed after each trial. Workloads of 70% of the VO2max were set for the SSR and PR rides, with pedal rate maintained at 90 rpm (SSR) or self determined (PR). Blood samples (5 ml) were drawn pre- and postexercise and analyzed for malonaldehyde (MDA) and lactic acid. The results indicate that vitamin E treatment was more effective than vitamin C alone or vitamin C and E. Pre-exercise plasma levels of MDA in the vitamin E trial was 39% below the pre-exercise MDA levels of the placebo: 2.94 +/- 0.54 and 4.81 +/- 0.65 micromol per ml, respectively. Plasma MDA following exercise in the vitamin E group was also lower than the placebo: 4.32 +/- 0.37 vs 7.89 +/- 1.0 micromol per ml, respectively. Vitamin C supplementation, on the other hand, elevated both the resting and exercise plasma levels of MDA. None of th supplemental phases had any significant effect on performance. In conclusion, the results indicate that 400 IU/day of vitamin E reduces membrane damage more effectively than vitamin C but does not enhance performance. Athletes are encouraged to include antioxidants, such as vitamin E and C, in their diet to counteract these detrimental effects of exercise. The data presented here suggests that 400 IU/day of vitamin E will provide adequate protection but supplementing the diet with 1 g per day of vitamin C may promote cellular damage. However neither of these vitamins, either alone or in combination, will enhance exercise performance.
PMID: 14666945 [PubMed - in process]
Dynamics of antioxidant action of vitamin E.3
Niki E, Noguchi N.
Human Stress Signal Research Center, National Institute of Advanced Industrial Science and Technology, Ikeda, Osaka 563-8577, Japan, and Research Center for Advanced Science and Technology, University of Tokyo, 4-6-1, Komaba, Tokyo 153-8904, Japan.
Vitamin E is the major lipophilic, radical-scavenging antioxidant in vivo and protects humans from the oxidative stress mediated by active oxygen and nitrogen species. The mechanisms of the inhibition of oxidation by vitamin E in vitro are now fairly well understood, but the dynamics of antioxidant action of vitamin E in vivo have not been well elucidated yet, primarily because of the inherent heterogeneity of biological systems. In this Account, the factors which determine the antioxidant capacity of vitamin E are discussed, and the importance of its localization and mobility in the membranes and lipoproteins is emphasized.
PMID: 14730993 [PubMed - in process]
4
Long-term combined beneficial effects of physical training and metabolic treatment on atherosclerosis in hypercholesterolemic mice.
Napoli C, Williams-Ignarro S, De Nigris F, Lerman LO, Rossi L, Guarino C, Mansueto G, Di Tuoro F, Pignalosa O, De Rosa G, Sica V, Ignarro LJ.
Department of General Pathology, Medicine, Clinical Pathology, and Human Pathology, University of Naples, 80131 Naples, Italy. claunap@tin.it
The pathogenic mechanisms by which physical exercise influences atherosclerotic lesion formation remain poorly understood. Because vigorous physical training increases oxidative stress, this study tested the hypothesis that graduated and moderate physical exercise together with metabolic intervention (l-arginine and antioxidants) may contribute to increased vascular protection. Exercise training in mice was induced by graduated swimming. In hypercholesterolemic male mice on an atherogenic high-cholesterol diet, graduated and moderate exercise lowered plasma cholesterol and decreased atherosclerotic lesions compared with sedentary control mice. Antioxidants (1.0% vitamin E added to the chow and 0.05% vitamin C added to the drinking water) and l-arginine (6% in drinking water) supplementation to exercising hypercholesterolemic mice further and synergistically reduced atherosclerosis compared with untreated exercised mice. Arterial oxidation-specific epitopes and systemic oxidative stress were reduced by metabolic intervention. Graduated chronic exercise elicited an increase in production of nitric oxide through increased endothelial nitric oxide synthase expression and ameliorated scavenger activities. Thus, metabolic intervention with l-arginine and antioxidants together with graduated and moderate exercise training reduce atherosclerotic lesion formation.
PMID: 15169957 [PubMed - in process]
The impact of vitamin and/or mineral supplementation on lipid profiles in type 2 diabetes.5
Farvid MS, Siassi F, Jalali M, Hosseini M, Saadat N.
Department of Nutrition and Biochemistry, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Objective: The purpose of the present study was to assess the impact of [Formula: see text], Vitamins [Formula: see text], and combination of these micronutrients on serum lipid and lipoprotein profiles in type 2 diabetic patients. Materials and methods: In a randomized, double-blind, placebo controlled clinical trial, 69 type 2 diabetic patients were randomly divided into four groups, each group receiving one of the following daily supplement for 3 months; group M: 200mg Mg and 30mg Zn ( [Formula: see text] ), group V: 200mg Vitamin C and 150mg Vitamin E ( [Formula: see text] ), group MV: minerals plus vitamins ( [Formula: see text] ), group P: placebo ( [Formula: see text] ). Fasting blood and urine samples were collected at the beginning and at the end of the trial. Serum triglyceride, total cholesterol, high density lipoprotein cholesterol (HDL-c) and low density lipoprotein cholesterol (LDL-c) were measured enzymatically. Apolipoproteins (apo) A1 and B were measured by immunoturbidimetric method. Adjustment for differences in baselines covariates and changes in variables during study were performed by analysis of covariance using general linear models. Results: Results indicate that after 3 months of supplementation mean serum levels of HDL-c and apo A1 increased significantly in the MV group by 24% ( [Formula: see text] mg/dl versus [Formula: see text] mg/dl) and 8.8% ( [Formula: see text] mg/dl versus [Formula: see text] mg/dl), respectively ( [Formula: see text] ). There were no significant changes in the levels of these parameters in the other three groups. Serum levels of total cholesterol, LDL-c, triglyceride, and apo B were not altered after supplementation in all four groups. Conclusion: It is concluded that since co-supplementation of Mg, Zn, Vitamins C and E significantly increases HDL-c and apo A1, supplementation of these micronutrients could be recommended for the type 2 diabetic patients based on their daily requirements.
PMID: 15163474 [PubMed - in process]
Anti-atherosclerotic effects of vitamin E--myth or reality?6
Munteanu A, Zingg JM, Azzi A.
Institute of Biochemistry and Molecular Biology, University of Bern, Bern, Switzerland.
Atherosclerosis and its complications such as coronary heart disease, myocardial infarction and stroke are the leading causes of death in the developed world. High blood pressure, diabetes, smoking and a diet high in cholesterol and lipids clearly increase the likelihood of premature atherosclerosis, albeit other factors, such as the individual genetic makeup, may play an additional role. Several epidemiological studies and intervention trials have been performed with vitamin E, and some of them showed that it prevents atherosclerosis. For a long time, vitamin E was assumed to act by decreasing the oxidation of LDL, a key step in atherosclerosis initiation. However, at the cellular level, vitamin E acts by inhibition of smooth muscle cell proliferation, platelet aggregation, monocyte adhesion, oxLDL uptake and cytokine production, all reactions implied in the progression of atherosclerosis. Recent research revealed that these effects are not the result of the antioxidant activity of vitamin E, but rather of precise molecular actions of this compound. It is assumed that specific interactions of vitamin E with enzymes and proteins are at the basis of its non-antioxidant effects. Vitamin E influences the activity of several enzymes (e.g. PKC, PP2A, COX-2, 5-lipooxygenase, nitric oxide synthase, NADPH-oxidase, superoxide dismutase, phopholipase A2) and modulates the expression of genes that are involved in atherosclerosis (e.g. scavenger receptors, integrins, selectins, cytokines, cyclins). These interactions promise to reveal the biological properties of vitamin E and allow designing better strategies for the protection against atherosclerosis progression.
PMID: 15090261 [PubMed - in process]
7
Molecular mechanisms of cholesterol or homocysteine effect in the development of atherosclerosis: Role of vitamin E.
Kartal Ozer N, Negis Y, Aytan N.
Department of Biochemistry, Faculty of Medicine, Marmara University, 81326 Haydarpasa, Istanbul, Turkey. nkozer@escortnet.com
The development of atherosclerosis is a multifactorial process in which both elevated plasma cholesterol levels and proliferation of smooth muscle cells play a central role. Numerous studies have suggested the involvement of oxidative processes in the pathogenesis of atherosclerosis and especially of oxidized low density lipoprotein. Some epidemiological studies have shown an association between high dietary intake and high serum concentrations of vitamin E and lower rates of ischemic heart disease. Cell culture studies have shown that alpha-tocopherol brings about inhibition of smooth muscle cell proliferation. This takes place via inhibition of protein kinase C activity. alpha-Tocopherol also inhibits low density lipoprotein induced smooth muscle cell proliferation and protein kinase C activity. The following animal studies showed that vitamin E protects development of cholesterol induced atherosclerosis by inhibiting protein kinase C activity in smooth muscle cells in vivo. Elevated plasma levels of homocysteine have been identified as an important and independent risk factor for cerebral, coronary and peripheral atherosclerosis. However the mechanisms by which homocysteine promotes atherosclerotic plaque formation are not clearly defined. Earlier reports have been suggested that homocysteine exert its effect via H2O2 produced during its metabolism. To evaluate the contribution of homocysteine in the pathogenesis of vascular diseases, we examined whether the homocysteine effect on vascular smooth muscle cell growth is mediated by H2O2. We show that homocysteine induces DNA synthesis and proliferation of vascular smooth muscle cells in the presence of peroxide scavenging enzyme, catalase. Our data suggest that homocysteine induces smooth muscle cell growth through the activation of an H2O2 independent pathway and accelerate the progression of atherosclerosis. The results indicate a cellular mechanism for the atherogenicity of cholesterol or homocysteine and protective role of vitamin E in the development of atherosclerosis.
PMID: 14757978 [PubMed - indexed for MEDLINE]
8
[Lipid peroxidation and plasma vitamin E concentration in hypercholesterolemic children from Medellin (Colombia)]
Velasquez Rodriguez CM, Uscategui Penuela RM, Burgos Herrera LC.
Centro de Investigacion en Alimentacion y Nutricion. Escuela de Nutricion y Dietetica. Universidad de Antioquia. Colombia.
Background: Serum lipid abnormalities in early childhood are risk factors for atherosclerosis. Lipid peroxidation might play an important role in this process, along with hypercholesterolemia.Objective: To compare plasma concentrations of malondialdehyde (MDA) and vitamin E in two groups of children: one group with low density lipoproteins (LDL) concentrations ? 130 mg/dL and another group with LDL concentrations < 130 mg/dL.Methods: Cross-sectional study.Healthy schoolchildren from the city of Medellin selected by probabilistic sampling performed by staff at the Universidad de Antioquia in Colombia.Sample: There were 134 subjects, aged 6 to 9 years old, divided into two groups: a group of 67 hypercholesterolemic children (LDL ? 130 mg/dL) and a control group of 67 normocholesterolemic children (LDL < 130 mg/dL).Results: Hypercholesterolemic children with a mean serum LDL concentration of 147.7 6 15.5 mg/dL and a total cholesterol concentration of 212 6 17 mg/dL had higher MDA plasma concentrations than the control group (0.18 6 0.1 6 ?M; 0.08 6 0.06 ?M, p < 0,0001, respectively). A negative correlation was observed between a -tocopherol/total lipids ratio and MDA values in children with hypercholesterolemia (r 5 0.337 p < 0.01).Conclusion: Lipid peroxidation was higher in hypercholesterolemic children than in the control group and was even higher when there was a deficit in the a -tocopherol/total lipids ratio. Hypercholesterolemia and lipid peroxidation are co-existing risk factors that are established during school age.
PMID: 15228929 [PubMed - as supplied by publisher]
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