Vitamin E (Natural) 18IU's

Clinical Studies
References


Vitamin E is an antioxidant needed for protection against the oxidation of fatty acids and cholesterol, helping to prevent oxidative damage to cell membranes and atherosclerosis. It prevents vein degeneration.

Vitamin E 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. Vitamin E prevents other fat-soluble vitamins from being destroyed by oxygen and it helps the body to use vitamin A.

Vitamin E may be beneficial in epilepsy, immune function, intermittent claudication, osteoarthritis, rheumatoid arthritis, impotence, Alzheimer's disease, angina, atherosclerosis, athletic performance, bronchitis, cold sores, dermatitis herpetiformis, diabetes, heart attacks, cancer (reduces risks of), pancreatic insufficiency, premenstrual syndrome, skin ulcers, wound healing and yellow nail syndrome.

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Published Clinical Studiesclin
Vitamin E (Natural) 18IU's

Effect of Vitamins C and E on cognitive function in mouse.1

Arzi A, Hemmati AA, Razian A.

 

Department of Pharmacology and Toxicology, School of Pharmacy, Ahwaz University of Medical Sciences, Ahwaz, Iran.

The aim of this study was to verify the role of Vitamins C and E on the cognitive function of young and aged mice. First and second groups of young animals (aged 3 months) received either Vitamin E (250mg/kg per day) or Vitamin C (300mg/kg per day) for 60 days. Third group was treated with the combination of Vitamin E (250mg/kg per day) and Vitamin C (300mg/kg per day) for 60 days. The control group received only vehicle. The aged animal group (aged 15 months) were treated as the young group. Passive avoidance method was used for the assessment of cognitive function in both young and aged animals. The results indicated a significant improvement in the cognitive function of aged mice while there were no significant changes in young animals.

PMID: 14726220 [PubMed - in process]

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Dynamics of antioxidant action of vitamin E.2

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]

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3
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]

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Vitamin E treatment in pediatric obesity-related liver disease: a randomized study.4

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]

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The effect of vitamin e treatment on tardive dyskinesia and blood superoxide dismutase: a double-blind placebo-controlled trial.

Zhang XY, Zhou DF, Cao LY, Xu CQ, Chen da C, Wu GY.

 

Institute of Mental Health, Peking University, 100083 Beijing, China; dagger Beijing Hui-Long-Guan Hospital, 100096 Beijing, China.

SUMMARY: Free radicals may be involved in the pathogenesis of tardive dyskinesia (TD). Vitamin E, a free radical scavenger, has been reported to improve symptoms of TD. The present study was designed to replicate this finding in a group of Chinese patients with TD, and to examine the effect of vitamin E treatment on blood superoxide dismutase (SOD), a critical enzyme in the detoxification of free radicals. Forty-one inpatients with TD completed a double-blind, placebo-controlled, parallel-group study of vitamin E. Twenty-two of the patients were randomly assigned to receive a fixed dose of 1200 IU/d vitamin E, and 19 were assigned to a placebo for 12 weeks. Patients were assessed primarily using the Abnormal Involuntary Movement Scale (AIMS) at baseline, weeks 6 and 12. Blood SOD levels were measured by radioimmunometric assay before and after treatment. The results showed that the reduction in AIMS score from baseline was significantly higher with vitamin E treatment compared with placebo (45.9% vs. 4.3%). Blood SOD levels were significantly increased after treatment with vitamin E (P = 0.001), but no change with placebo treatment (P < 0.05). These results support earlier findings of the efficacy of vitamin E in the treatment of TD. Moreover, the efficacy of vitamin E may be due to its ability to increase SOD level, which may reduce oxidative injure in tardive dyskinesia.

PMID: 14709952 [PubMed - in process]

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Role of dietary vitamin E in cadmium-induced oxidative damage in rabbit's blood, liver and kidneys.

Beytut E, Yuce A, Kamiloglu NN, Aksakal M.

 

Department of Physiology, Veterinary Faculty of Kaskas University, Kars/Turkey. ebrubeytut@hotmail.com

The aim of this work was to determine the effect of dietary vitamin E intake on lipid peroxidation (LPO) by measuring thiobarbituric acid reactive substances (TBARS), vitamin E and reduced glutathione (GSH) levels, and glutathione peroxidase (GSH-Px: EC 1.11.1.9) activity in plasma, red blood cells (RBC), livers, and kidneys of rabbits dosed with cadmium (Cd). Six-month-old clinically healthy New Zealand White rabbits (8 in each group) were given tap water only, containing 1 g CdCl2/L, or tap water with CdCl2 plus vitamin E (100 mg dl-alpha-tocopheryl acetate in 0.2 mL corn oil) daily for 30 days. The vitamin E level in the plasma, liver, and kidneys was significantly higher in the control than in the Cd-only group, and TBARS levels were significantly lower. There were no statistical differences between the control and Cd-only groups GSH-Px activities and GSH levels in RBC, liver, and kidneys. Vitamin E levels in plasma, liver, and kidneys and GSH-Px activity in RBC were higher in the vitamin E group than in both control and Cd-only groups. However, the TBARS levels of RBC, liver, and kidneys in vitamin E administered group were decreased. Therefore, the present study demonstrates the effectiveness of vitamin E in reducing oxidative stress in Cd-treated rabbits and suggests that reductions in increased TBARS due to Cd toxicity may be an important factor in the action of vitamin E.

PMID: 14639799 [PubMed - in process]

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Referencesref

  1. Corrigan JJ Jr. The effect of vitamin E on warfarin-induced vitamin K deficiency. Ann N Y Acad Sci 1982;393:361-8.
  2. Newall CA, Anderson LA, Philpson JD. Herbal Medicine: A Guide for Healthcare Professionals. London, UK: The Pharmaceutical Press, 1996.
  3. Meydani M. Effect of functional food ingredients: vitamin E modulation of cardiovascular diseases and immune status in the elderly. Am J Clin Nutr 2000;71:1665S-8S.
  4. Surai PF, MacPherson A, Speake BK, Sparks NH. Designer egg evaluation in a controlled trial. Eur J Clin Nutr 2000;54:298-305.
  5. Devaraj S, Jialal I. Low-density lipoprotein postsecretory modification, monocyte function, and circulating adhesion molecules in type 2 diabetic patients with and without macrovascular complications: the effect of alpha-tocopherol supplementation. Circulation 2000;102:191-6.
  6. Skyrme-Jones RA, O'Brien RC, Berry KL, Meredith IT. Vitamin E supplementation improves endothelial function in type I diabetes mellitus: a randomized, placebo-controlled study. J Am Coll Cardiol 2000;36:94-102.
  7. McKevoy GK, ed. AHFS Drug Information. Bethesda, MD: American Society of Health-System Pharmacists, 1998.
  8. Corrigan JJ Jr. Coagulation problems relating to vitamin E. Am J Pediatr Hematol Oncol 1979;1:169-73.
  9. Kim JM, White RH. Effect of vitamin E on the anticoagulant response to warfarin. Am J Cardiol 1996;77:545-6.
  10. Berson EL, Rosner B, Sandberg MA, et al. A randomized trial of vitamin A and vitamin E supplementation for retinitis pigmentosa. Arch Ophthalmol 1993;111:761-72.
  11. Brinker F. Herb Contraindications and Drug Interactions. 2nd ed. Sandy, OR: Eclectic Medical Publications, 1998.
  12. Corrigan JJ Jr, Marcus FI. Coagulopathy associated with vitamin E ingestion. JAMA 1974;230:1300-1.
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  14. Lavine JE. Vitamin E treatment of nonalcoholic steatohepatitis in children: a pilot study. J Pediatr 2000;136:734-8.
  15. Gamel JW, Barr CC. A randomized trial of vitamin A and vitamin E supplementation for retinitis pigmentosa. Arch Ophthalmol 1993;111:1462-3.
  16. Fielder AR. A randomized trial of vitamin A and vitamin E supplementation for retinitis pigmentosa. Arch Ophthalmol 1993;111:1463;discussion 1463-6.
  17. Clowes DD. A randomized trial of vitamin A and vitamin E supplementation for retinitis pigmentosa. Arch Ophthalmol 1993;111:1461-2.
  18. Norton EW. A randomized trial of vitamin A and vitamin E supplementation for retinitis pigmentosa. Arch Ophthalmol 1993;111:1460.
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