Search 
 
 
 
ANTI-AGING DRUGS AND SUPPLEMENTS
 
 5.1 DRUGS THAT ARE HIGHLY RECOMMENDED (for inclusion in your supplementation anti-aging program) 
   
 
  VITAMIN E  
   
Relationship between aging and vitamin E.
The role of vitamin E in T-cell differentiation and the decrease of cellular immunity with aging.
Significance of vitamin E in aging.
Vitamin E as an antioxidant of the lung: mechanisms of vitamin E delivery to alveolar type II cells.
Antioxidant vitamins--significance for preventing cardiovascular diseases. Part 1. Oxidized low-density lipoproteins and atherosclerosis; antioxidant dietary supplementation--vitamin E.
Oxidant and antioxidant systems in niddm patients: influence of vitamin E supplementation.
Vitamin E as a universal antioxidant and stabilizer of biological membranes.
Vitamin E: beyond antioxidant function.
Effect of dietary antioxidant combinations in humans. Protection of LDL by vitamin E but not by beta-carotene.
Does vitamin E supplementation prevent cardiovascular events?
Effects of vitamin E supplementation on blood antioxidants levels in patients with Behcet's disease.
Effect of daily vitamin E and multivitamin-mineral supplementation on acute respiratory tract infections in elderly persons: a randomized controlled trial.
A short-term dietary supplementation of high doses of vitamin E increases T helper 1 cytokine production in patients with advanced colorectal cancer.
Vitamin E supplementation in the prevention of coronary heart disease.
Effects of long-term supplementation with moderate pharmacologic doses of vitamin E are saturable and reversible in patients with type 1 diabetes.
Vitamin E supplementation increases the resistance of both LDL and HDL to oxidation and increases cholesteryl ester transfer activity.
 


INTRODUCTION


Vitamin E is a very important antioxidant nutrient - it helps to protect fatty cell membranes from oxidization through the action of highly reactive free radicals. The vitamin is needed for proper functioning of the immune system and healthy red blood cells. It occurs in a wide range of foods, although in very small amounts, and its deficiency is not. However, recent research has shown that higher than normal intakes of vitamin E result in a protective effect against certain diseases associated with aging- particularly cancer and heart disease.Vitamin E may be used to help improve blood circulation and treat premenstrual syndrome and menopausal symptoms. Vitamin E is also commonly used as a supplement to improve and moisturize dry skin, which makes it an ingredient of many beauty and anti-wrinkle creams.

   
   
Nippon Ronen Igakkai Zasshi. 2002 Sep;39(5):494-500.
Relationship between aging and vitamin E.
Takasaki M, Yanagawa K, Shinozaki K, Fujii H, Shibuya T, Takeda H, Matsumiya T, Egashira T.
Department of Geriatrics, Tokyo Medical University.

We investigated the pathophysiological significance in biomembranes of the redox dynamics of Vitamin E (alpha-tocopherol) which is lipophilic radical scavenger related to aging or pathologic status such as non-insulin-dependent diabetes mellitus or primary hyperlipidemia. Vitamin E eliminates lipid peroxyl radicals by the peroxidation chain reaction of the membrane lipid, and it becomes Vitamin E radical. Furthermore, the Vitamin E radical becomes Vitamin E quinone which is an oxidic metabolite of Vitamin E. Therefore, it was needed to determine the alpha-tocopherol and alpha-tocopherolquinone simultaneously to evaluate the antioxidative status of alpha-tocopherol in biomembranes exactly. For this purpose, we developed the assay method for the simultaneous determination of the two substances using HPLC system. Then we applied this method to basic and clinical research. 1) For the simultaneous determination of alpha-tocopherol and alpha-tocopherolquinone, highly-sensitive measurement system by HPLC-multiple coulometric ECD was developed. This system is useful to estimate the redox dynamics of alpha-tocopherol in biomembranes. 2) The utilization rate of alpha-tocopherol in the erythrocyte membrane of 10- to 120-week-old rats was significantly increased, whereas alpha-tocopherol uptake in the erythrocyte membrane decreased age-dependently. Furthermore, a significant increase in lipid hydroperoxide content and a marked decrease in the fluidity of the erythrocyte membrane were seen with age. 3) There was a strongly significant positive correlation between age and the utilization rate of alpha-tocopherol in the erythrocyte membrane of healthy volunteers aged between 23 and 103. 4) The alpha-tocopherol uptake in erythrocyte membrane was significantly lower in elderly non-insulin-dependent diabetes mellitus patients (average 68.1 years old) than in healthy subjects (average 71.8 years old). 5) The utilization rate of alpha-tocopherol in erythrocyte membrane and the alpha-tocopherol uptake in erythrocyte membrane were significant lower in elderly patients with primary hyperlipidemia (average 74.1 years old) compared to healthy subjects (average 71.2 years old). These findings suggest that the redox dynamics of alpha-tocopherol in biomembranes should be investigated with special regard to the onset, aggravation and complications of several diseases or aging as a result of oxidative stress. In addition redox dynamics were suggested to be useful to evaluate the grade of aging.

   
   
Biofactors. 1998;7(1-2):77-86.
The role of vitamin E in T-cell differentiation and the decrease of cellular immunity with aging.
Moriguchi S.
Department of Nutrition, School of Medicine, University of Tokushima, Japan.

The purpose of this study is to investigate the effects of vitamin E on both the decrease of cellular immunity with aging (Section 2) and the differentiation of T-cells in thymus (Section 3). In Section 2, spontaneously hypertensive rats (SHR) as a model for aging were used in this experiment and fed regular (50 IU/kg diet) or a high vitamin E (500 IU/kg diet) diet for 6 weeks. At 12 weeks old, they were killed and assayed. Although proliferation of thymic lymphocytes was significantly decreased in SHR fed the regular diet compared to that of Wistar Kyoto rats (WKY) fed the same diet, the high vitamin E diet induced higher proliferation of thymic lymphocytes in SHR, which was almost the same as that of WKY fed the regular diet. In addition, the expressions of both CD4 and CD8 antigens on CD4+ CD8+ T-cells were also decreased in SHR, which was significantly improved by a high vitamin E diet. These results suggest that a high vitamin E diet enhances thymic lymphocyte proliferation through increased T-cell differentiation in the thymus. Then, the effect of vitamin E on T-cell differentiation in the thymus was investigated by using male Fisher rats. Rats were divided into three groups; vitamin E-free, regular and high vitamin E groups and fed a diet containing various levels of vitamin E (0, 50 and 500 IU/kg diet) for 7 weeks. Although the proportions of CD4+ CD8- and CD4- CD8+ T-cells in thymocytes were significantly greater in the high vitamin E group, the proportion of CD4+ CD8- T-cells inversely decreased in the vitamin E-free group compared to that of the regular group. We have tried to investigate the mechanism on the increased T-cell differentiation in the thymus of rats fed the high vitamin E diet through cytokine production, thymic epithelial cell (TEC) and macrophage functions. As their results, we have found that vitamin E enhances T-cell differentiation through the increase of not macrophage but TEC function in the thymus, which is associated with the increased binding capacity of TEC to immature T-cells via increased expression of the adhesion molecule, ICAM-1. These results suggest that vitamin E is a potent nutrient for promoting health in the aged via the improvement of cellular immunity decreased with aging.

   
   
Z Gerontol. 1986 May-Jun;19(3):206-14.
Significance of vitamin E in aging.
Elmadfa I, Both-Bedenbender N, Sierakowski B, Steinhagen-Thiessen E.

In order to understand and investigate the phenomenon of aging and its related characteristics various hypotheses have been put forward. Among these the free radical hypothesis is the best known and the most often discussed. Considering the biological function of vitamin E as an important preventive factor, for lipid peroxidation, and on the basis of existing parallelisms between some characteristics of aging and different symptoms of tocopherol deficiency, a possible influence of this vitamin on the aging process was postulated. Many authors showed that high doses of vitamin E decrease synthesis and accumulation of aging-accompanied lipofuscin pigments. Nevertheless, no reasonable additional influence of such vitamin dosage is known for the aging process, especially on the elongation of the maximal life span in mammals. While high tocopherol concentrations inhibit the aggregation of thrombocytes induced in vitro, under in vivo conditions the supposed benefit of therapeutic use of vitamin E to diminish the high platelet aggregation rate noticed in patients with cardiovascular diseases is still not confirmed. Investigations of the vitamin E status in the elderly showed that the plasma tocopherol concentration is increased age-dependent. Considering this parameter the vitamin E status of healthy persons examined (n = 41; age 62-98 years of both sexes) was satisfactory.

   
   

Am J Respir Crit Care Med. 2002 Dec 15;166(12 Pt 2):S62-6.
Vitamin E as an antioxidant of the lung: mechanisms of vitamin E delivery to alveolar type II cells.
Kolleck I, Sinha P, Rustow B.
Department of Neonatology and Institute of Pathobiochemistry and Laboratory Medicine, Charite Hospital, Humboldt University Berlin, Berlin, Germany.

Oxidants play an important role in the development of acute and chronic lung injuries. Alveolar surfactant is the first target of air-borne oxidants. Surfactant contains, besides dipalmitoyl phosphatidylcholine, cholesterol and polyunsaturated phospholipids that play an important functional role. Therefore, vitamin E could be important for protecting surfactant lipids against oxidation and subsequent lung injury. Alveolar type II cells play a central role in synthesis and secretion of surfactant lipids and also supplement the surfactant with vitamin E during intracellular assembly. High density lipoprotein (HDL) is the primary source of vitamin E for type II cells. The uptake of vitamin E by specific lipid transfer is mediated by at least three HDL-specific receptors (scavenger receptor BI, membrane dipeptidase, and HDL-binding protein-2). In addition, cubilin and megalin mediate in a cooperative manner HDL-holoparticle uptake by alveolar type II cells. A temporary vitamin E deficiency induces a reversible change of the expression of pro- and antiinflammatory markers and of markers defining apoptosis, and reduces surfactant lipid synthesis in alveolar type II cells. These metabolic changes of type II cells may prime the lung to develop clinically manifest injury in response to an additional insult, e.g., hyperoxia.

   
   
Vutr Boles. 2000;32(3):11-8.
Antioxidant vitamins--significance for preventing cardiovascular diseases. Part 1. Oxidized low-density lipoproteins and atherosclerosis; antioxidant dietary supplementation--vitamin E.
Andreeva-Gateva P.

The knowledge that an oxidizing of LDL is necessary for the foam cell formation is in the basis of the so called oxidative hypothesis of atherosclerosis. The role of LDL-oxidation for the atherosclerotic plaque formation, as well as its association with inflammatory processes in the vascular wall, are well established. The important conclusion of this hypothesis is the possible role of the antioxidants attenuating atherosclerotic mechanisms. The advances in studying the principal antioxidant vitamins E, C and beta-carotene effects, revealed a great part of their molecular mechanisms, which are not necessarily antioxidative. The important aspects of the cooperative antioxidant action are revealed too, including the so called tocopherol-mediated peroxidation, suggesting the need of the co-antioxidants for effective antioxidant defense. In the recent years many vitamin antioxidant supplementations are used. The epidemiological results of such supplementation do not always reveal the same beneficial effects as expected theoretically or based on the observations made with diet rich in fruits and vegetables. The present paper generalizes the thought concerning the impact of oxidized LDL in atherosclerosis, as well as mechanisms of action and pharmacokinetics of the most widely used antioxidant vitamins--E, C and beta-carotene, and the perspectives of their usage in cardio-vascular prophylaxy based upon the recent experience in antioxidant vitamin supplementation.

   
   
Endocr Res. 2001 Aug;27(3):377-86.
Oxidant and antioxidant systems in niddm patients: influence of vitamin E supplementation.
Gokkusu C, Palanduz S, Ademoglu E, Tamer S.
Department of Biochemistry, Istanbul Faculty of Medicine, University of Istanbul, Capa, Turkey.

Free radical-mediated oxidative stress has been implicated in adverse tissue changes in a number of diseases. In view of the role of oxidative processes in non-insulin dependent diabetes mellitus (NIDDM), in this study, we investigated the oxidant and antioxidant status of plasma in patients with NIDDM and the effect of vitamin E (800 lU/day) supplementation on oxidative stress, antioxidant defense system, fructosamine levels and insulin action. Thirty controls and 40 NIDDM patients were studied. In controls and patients, plasma lipids, vitamin E, lipid peroxide, total thiols (t-SH), superoxide peroxidase (SOD) and glutathione peroxidase (GPx) were measured in the basal state and after vitamin E (800 IU/d) supplementation for a month. All lipids and lipid fractions in plasma were significantly decreased, whereas the HDL-C level was changed in diabetic patients supplemented with vitamin E when compared with baseline values. Vitamin E administration also significantly reduced fasting glucose and fructosamine levels, whereas increased significantly reduced fasting glucose and fructosamine levels, whereas increased significantly plasma C-peptide and insulin levels (p < 0.01, p < 0.001, respectively). Following vitamin E supplementation, TBARs levels were found to be significantly lower (p < 0.001) than the baseline value NIDDM patients are. On the other hand, activities of GPx and SOD were significantly higher (p < 0.001) than baseline values. A similar trend was observed for total thiols contents, but in this case, the increase was not significant. In conclusion, this study demonstrates that vitamin E improved beta-cell function and increased plasma insulin and C-peptide levels, possibly by inducing the antioxidant capacity of the organism and/or reducing the peripheral resistance in NIDDM. Long-term studies are needed to demonstrate the beneficial effects of vitamin E on treatment/prevention of NIDDM.

   
   
Membr Cell Biol. 1998;12(2):151-72.
Vitamin E as a universal antioxidant and stabilizer of biological membranes.
Evstigneeva RP, Volkov IM, Chudinova VV.
Lomonosov Moscow State Academy of Fine Chemical Technology.

The known literature data concerning the mechanisms of molecular action of vitamin E in biological membrane systems are reviewed. The role of vitamin E, possessing a broad range of biological activities, as a universal stabilizer of biological membranes in normal oxygen metabolism and peroxidation, and also in disorders of normal metabolism resulting in pathological alterations, has been discussed. The participation of vitamin E in redox reactions taking place in lipid media, its interaction with singlet oxygen, free fatty acids and enzyme systems are considered. Physiological effects of vitamin E and its ability to prevent numerous pathologies are also considered. Vitamin E was concluded to be a universal participant of antioxidant defence reactions in biological membranes, since it acts at all stages of membrane oxidative damage.

   
   
Am J Clin Nutr. 1995 Dec;62(6 Suppl):1501S-1509S.
Vitamin E: beyond antioxidant function.
Traber MG, Packer L.
Department of Molecular and Cell Biology, University of California, Berkeley 94720-3200, USA.

Vitamin E, a potent peroxyl radical scavenger, is a chain-breaking antioxidant that prevents the propagation of free radical damage in biological membranes. We consider the evidence for potential sites in cellular metabolism and signal transduction where vitamin E may have a structure-specific role in addition to its antioxidant function. The roles of tocopherol-binding proteins in cellular trafficking of vitamin E, especially the incorporation of RRR-alpha-tocopherol into nascent lipoproteins, and the delivery of RRR-alpha-tocopherol to the nucleus are considered. We discuss the functions of vitamin E both in the inhibition and potentiation of arachidonic acid metabolism. The interactions of vitamin E during cell proliferation and differentiation are also evaluated. These functions of vitamin E raise new questions and represent new and exciting areas for research in cell regulation with physiologic implications.

   
   
Arterioscler Thromb. 1993 Apr;13(4):590-600.
Effect of dietary antioxidant combinations in humans. Protection of LDL by vitamin E but not by beta-carotene.
Reaven PD, Khouw A, Beltz WF, Parthasarathy S, Witztum JL.
Department of Medicine, University of California, San Diego, La Jolla 92093-0682.

Experimental and epidemiological evidence supports the hypothesis that oxidation of low density lipoprotein (LDL) appears to be important in mediating the atherogenicity of LDL. To test this hypothesis in humans, it will be necessary to perform intervention studies in large populations. We performed two studies to assess the effectiveness of supplementation with beta-carotene and vitamin E, used alone and in combination with each other, and with vitamin C, to protect LDL from oxidation. In phase 1, after a placebo period, eight subjects were given beta-carotene (60 mg/day) for 3 months, then beta-carotene plus vitamin E (1,600 mg/day) for another 3 months, and then beta-carotene plus vitamin E plus vitamin C (2 g/day) for 3 months. During phase 2, beta-carotene and vitamin C were discontinued, and subjects took only vitamin E for 5 months. During each period, LDL samples were isolated, and measurements of susceptibility to oxidation were performed. beta-Carotene levels in LDL increased nearly 20-fold, but LDL susceptibility to oxidation did not change. Addition of vitamin E increased LDL vitamin E levels nearly 2.5-fold, and this decreased LDL oxidation 30-40%. During the vitamin C supplementation period, plasma levels of beta-carotene and vitamin E rose, but only beta-carotene increased in LDL. However, the susceptibility of LDL to oxidation in this period was not decreased further. During phase 2, when subjects took only vitamin E, LDL susceptibility to oxidation was decreased by 50% as measured by thiobarbituric acid-reactive substances, conjugated dienes, and lipid peroxide formation as well as by macrophage degradation. Thus, long-term supplementation with large doses of vitamin E alone, but not beta-carotene, conferred increased protection to LDL in in vitro assays of oxidation. These data should be useful in planning therapeutic strategies to test the antioxidant hypothesis in humans.

   
   
J Womens Health (Larchmt). 2003 Mar;12(2):123-36.
Does vitamin E supplementation prevent cardiovascular events?
Manson JE, Bassuk SS, Stampfer MJ.
Division of Preventive Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA.

In recent years, vitamin E has been investigated as a cardioprotective agent. Experimental studies have identified potential mechanisms by which vitamin E may inhibit the development of atherosclerosis, and observational studies of individuals without coronary disease suggest that vitamin E intake may prevent future cardiovascular events. Secondary prevention trials to date have demonstrated little benefit from vitamin E supplementation. It remains possible, however, that supplementation may be useful among certain high-risk groups, including those with nutritional deficiencies. Limited data from completed primary prevention trials also indicate minimal cardioprotection from vitamin E, but large-scale trials now in progress may yet show benefit. Results from ongoing trials will contribute powerfully to the totality of evidence on which to formulate both appropriate clinical recommendations for individual patients and a rational public health policy for the population as a whole. At this time, there is insufficient evidence for issuing a public health recommendation to use vitamin E supplements to prevent cardiovascular disease (CVD). Rather, increased intake of fruits, vegetables, and other antioxidant-rich foods should be promoted as part of a healthy diet because they provide nutritional benefits beyond any potential antioxidant effect. Moreover, even if found to reduce CVD risk, vitamin supplement use should be considered an adjunct, not an alternative, to established cardioprotective measures, such as smoking abstention, avoidance of obesity, adequate physical activity, and control of high blood pressure and hyperlipidemia.

   
   
Clin Biochem. 2002 Nov;35(8):633-9.
Effects of vitamin E supplementation on blood antioxidants levels in patients with Behcet's disease.
Kokcam I, Naziroglu M.
Department of Dermatology, Medical Faculty, Firat University, TR-23119, Elazig, Turkey.

Behcet's disease (BD) is known for many years, yet its etiology remains unknown. In BD, the increased production of reactive oxygen species from activated neutrophils may reduce concentrations of antioxidant vitamins and enzymes in plasma and red blood cells (RBC). Vitamin E is an important fat soluble antioxidant and its role on antioxidant parameters of BD is unclear. The study was undertaken to evaluate the role of vitamin E on lipid peroxidation (MDA) levels, antioxidant vitamin and enzyme concentrations in plasma and RBC in patients with BD. There were three groups i.e., control, patient and treatment groups with twenty-five subjects in each. Nonsmoking patients with BD, patient group, was compared with an equal number of healthy control subjects (control group). Blood samples were taken from both control and patient groups and then oral vitamin E was daily supplemented to the patients with BD for six weeks (treated group). At the end of six weeks, blood was taken from the treated group once more. RBC and plasma MDA levels, serum neopterin, complement system (C(3) and C(4)), ASO, CRP, rheumatoid factor, plasma lipoprotein (a), total cholesterol concentrations and erythrocyte sedimentation rate were higher in the patient group than in the control group, but they were lower in the treatment group than in the patient group. While vitamins A, E and beta-carotene concentrations in plasma, catalase, glutathione peroxidase activities and reduced glutathione levels in RBC and plasma were lower in patient group than in the controls, they were found to be higher in the treatment group than in the patient group. These results provide some evidence for a potential role of increased lipid peroxidation and decreased enzymatic and non enzymatic antioxidants in BD by its inflammatory character and vitamin E which may strengthen the antioxidant defense system, and may contribute to the treatment of BD.

   
   
JAMA. 2002 Aug 14;288(6):715-21.
Effect of daily vitamin E and multivitamin-mineral supplementation on acute respiratory tract infections in elderly persons: a randomized controlled trial.
Graat JM, Schouten EG, Kok FJ.
Division of Human Nutrition and Epidemiology, Wageningen University, PO Box 8129, 6700 EV Wageningen, The Netherlands.

CONTEXT: Immune response in elderly individuals has been reported to improve after micronutrient supplementation. However, efficacy trials evaluating infectious diseases as outcomes are scarce and inconclusive. OBJECTIVE: To investigate the effect of daily multivitamin-mineral and vitamin E supplementation on incidence and severity of acute respiratory tract infections in elderly individuals. DESIGN: A randomized, double blind, placebo-controlled, 2 x 2 factorial trial. SETTING AND PARTICIPANTS: A total of 652 noninstitutionalized individuals aged 60 years or older enrolled from 2 community-based sampling strategies in the Wageningen area of the Netherlands, conducted from 1998 to 2000. At baseline, 6% of participants had suboptimal ascorbic acid and 1.3% had suboptimal alpha-tocopherol plasma concentration. INTERVENTION: Physiological doses of multivitamin-minerals, 200 mg of vitamin E, both, or placebo. MAIN OUTCOME MEASURES: Incidence and severity of self-reported acute respiratory tract infections at 15 months, as assessed by a nurse (telephone contact), home visits, and microbiological and serological testing in subsets of patients. RESULTS: During a median observation period of 441 days, 443 (68%) of 652 participants recorded 1024 respiratory tract infection episodes. The incidence rate ratio of acute respiratory tract infection for multivitamin-mineral supplementation was 0.95 (95% confidence interval, 0.75-1.15; P =.58) and for vitamin E supplementation, 1.12 (95% confidence interval, 0.88-1.25; P =.21). Severity of infections was not influenced by multivitamin-mineral supplementation. For vitamin E vs no vitamin E, severity was worse: median (interquartile range) for illness-duration was 19 (9-37) vs 14 (6-29) days, P =.02; number of symptoms, 6 (3-8) vs 4 (3-8), P =.03; presence of fever, 36.7% vs 25.2%, P =.009; and restriction of activity, 52.3% vs 41.1%, P =.02. CONCLUSIONS: Neither daily multivitamin-mineral supplementation at physiological dose nor 200 mg of vitamin E showed a favorable effect on incidence and severity of acute respiratory tract infections in well-nourished noninstitutionalized elderly individuals. Instead we observed adverse effects of vitamin E on illness severity.

   
   
Clin Cancer Res. 2002 Jun;8(6):1772-8.
A short-term dietary supplementation of high doses of vitamin E increases T helper 1 cytokine production in patients with advanced colorectal cancer.
Malmberg KJ, Lenkei R, Petersson M, Ohlum T, Ichihara F, Glimelius B, Frodin JE, Masucci G, Kiessling R.
Cancer Center Karolinska, Immune and Gene Therapy Laboratory, Department of Oncology and Pathology, Karolinska Institutet, S-17176 Stockholm, Sweden.

PURPOSE: Patients with advanced cancer exhibit multifaceted defects in their immune capacity, which are likely to contribute to an increased susceptibility to infections and disease progression and to constitute a barrier to immunotherapeutic interventions. A chronic inflammatory condition associated with increased oxidative stress has been suggested as one of the responsible mechanisms behind the tumor-induced immune suppression. We, therefore, speculated that supplementation with the antioxidant vitamin E could enhance the immune functions in patients with advanced cancer. EXPERIMENTAL DESIGN: This hypothesis was here tested in twelve patients with colorectal cancer (Dukes' C and D) who, prior to intervention with chemo- or radiotherapy, received a daily dose of 750 mg of vitamin E during a period of 2 weeks. RESULTS: Short-term supplementation with high doses of dietary vitamin E leads to increased CD4:CD8 ratios and to enhanced capacity by their T cells to produce the T helper 1 cytokines interleukin 2 and IFN-gamma. In 10 of 12 patients, an increase of 10% or more (average, 22%) in the number of T cells producing interleukin 2 was seen after 2 weeks of vitamin E supplementation, as compared with peripheral blood monocyte samples taken before treatment (P = 0.02). Interestingly, there seemed to be a more pronounced stimulatory effect by vitamin E on naive (CD45RA(+)) T helper cells as compared with T cells with a memory/activated phenotype. CONCLUSIONS: Dietary vitamin E may be used to improve the immune functions in patients with advanced cancer, as a supplement to more specific immune interventions.

   
   
Mayo Clin Proc. 2001 Nov;76(11):1131-6.
Vitamin E supplementation in the prevention of coronary heart disease.
Pruthi S, Allison TG, Hensrud DD.
Division of General Internal Medicine, Mayo Clinic, Rochester, Minn 55905, USA.

Vitamin E consists of a number of compounds, tocopherols and tocotrienols, that function as lipid-soluble antioxidants. A hypothesis is that vitamin E may slow the progression of atherosclerosis by blocking the oxidative modification of low-density lipoprotein cholesterol and thus decrease its uptake into the arterial lumen. Basic science and animal studies have generally supported this hypothesis. Observational studies have primarily assessed patients with no established coronary heart disease (CHD), and results have generally supported a protective role of vitamin E in CHD. Early primary and secondary prevention clinical trials (Alpha-Tocopherol, Beta-Carotene Cancer Protection study and Cambridge Heart Antioxidant Study) showed mixed results. Despite years of encouraging evidence from basic science and observational studies, 3 large randomized clinical trials (Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto miocardico, Heart Outcomes Prevention Evaluation, and Primary Prevention Project) with a combined total of more than 25,000 patients failed to show a significant benefit with vitamin E taken as a dietary supplement for the prevention of CHD. Four large randomized primary prevention trials currently under way should add to our knowledge. The American Heart Association has recommended consumption of a balanced diet with emphasis on antioxidant-rich fruits and vegetables but has made no recommendations regarding vitamin E supplementation for the general population. Although vitamin E supplementation seems to be safe for most people, recommendations from health care professionals should reflect the uncertainty of established benefit as demonstrated in clinical trials.

   
   
Am J Clin Nutr. 2000 Nov;72(5):1142-9.
Effects of long-term supplementation with moderate pharmacologic doses of vitamin E are saturable and reversible in patients with type 1 diabetes.
Engelen W, Keenoy BM, Vertommen J, De Leeuw I.
Laboratory of Endocrinology, the University of Antwerp, Antwerp, Belgium.

BACKGROUND: Vitamin E supplementation has been proposed as adjunctive therapy to counteract the increased LDL oxidation in diabetes and thus prevent or delay cardiovascular complications. OBJECTIVE: The objective of this study was to investigate the effect of a moderate pharmacologic dose of vitamin E for </=1 y in patients with type 1 diabetes. DESIGN: The study was double blind and the subjects were randomly assigned to 2 groups: the supplemented group (group S; n = 22) received 250 IU (168 mg) RRR-alpha-tocopherol 3 times/d for 1 y and the placebo group (group P; n = 22) received a placebo for 6 mo followed by 250 IU (168 mg) RRR-alpha-tocopherol 3 times/d for an additional 6 mo. RESULTS: Serum vitamin E doubled after 3 mo of supplementation, from a mean (+/-SD) of 36.9 +/- 10.9 to 66.4 +/- 18.3 micromol/L (P: < 0.0005). Although lipid profiles, glycated hemoglobin, and blood biochemistry values did not change significantly, copper-induced in vitro peroxidizability of LDL and VLDL decreased after 3 mo of supplementation: the production of thiobarbituric acid-reactive substances decreased by 30-60% (P: < 0. 005) and the lag time for the appearance of fluorescent products increased from 107 +/- 25 to 123 +/- 30 min in group S (P: = 0.002 compared with group P). Vitamin E supplementation for an additional 3-9 mo resulted in no further changes in serum vitamin E and lipoprotein peroxidizability. Values returned to baseline after supplementation ended. CONCLUSIONS: Because the improvement in lipoprotein peroxidizability is saturable and reversible, life-long supplementation with vitamin E should be considered in patients with type 1 diabetes.

   
   
Atherosclerosis. 2000 May;150(1):129-34.
Vitamin E supplementation increases the resistance of both LDL and HDL to oxidation and increases cholesteryl ester transfer activity.
Arrol S, Mackness MI, Durrington PN.
University Department of Medicine, Manchester Royal Infirmary, Oxford Road, Manchester, UK.

There is increasing evidence that lipid peroxidation and oxidative modification of low density lipoprotein (LDL) is important in atherogenesis. Evidence that antioxidant therapy decreases mortality is, however, inconclusive. We have examined the effects of vitamin E on the susceptibility of LDL and high density lipoprotein (HDL) to oxidation, and on cholesteryl ester heteroexchange in an in vitro system using autologous serum lipoproteins. Vitamin E in doses of 200 and 400 mg/day were administered orally to 21 healthy volunteers (12 females and nine males) aged between 23 and 50 years, and to 16 healthy volunteers (eight females and eight males) aged between 22 and 51 years for 50 days, respectively. Fasting serum lipoproteins, susceptibility of lipoproteins to oxidation and cholesteryl ester transfer activity (CETA) were measured before and after vitamin E supplementation. Serum lipoprotein and lipid concentrations did not change significantly in either group. The LDL-conjugated diene (CD) lag phase during incubation with Cu(2+) was increased by 157% (110-232%) (median (interquartile range)) (P<0.05) on vitamin E (200 mg/day) and by 235% (185-259%) (P<0.0001) on 400 mg/day. The lag phases for LDL-lipid peroxide (LPO) generation were also significantly increased by 146% (122-192%) (P<0.005) and 177% (101-267%) (P<0.005), respectively. The HDL-CD lag phase also increased on both doses 140% (115-169%) (P<0.005) and 171% (122-192%) (P<0.005), as did the HDL-LPO lag phase by 123% (104-153%) (P<0.05) on 200 mg/day and 240% (97-360%) (P<0.005) on 400 mg daily. Cholesteryl ester transfer activity from HDL to very low and low density lipoproteins significantly increased from 12. 7+/-2.6 (mean+/-SEM) to 16+/-3.4 nmol/ml/h (P<0.05) on 200 mg/daily and 10.4+/-2.0 to 19.2+/-3.3 nmol/ml/h (P<0.005) on vitamin E, 400mg day. Thus, vitamin E (200 and 400mg daily) significantly decreased the susceptibility of LDL and HDL to oxidation in vitro. However, the increase in CETA resembled that reported with another antioxidant, probucol. Some evidence has suggested that increased CETA is potentially deleterious and it might therefore counteract beneficial effects of vitamin E or probucol on the susceptibility of lipoproteins to oxidation.

 
home
top
   
FASTING / LOW CALORIE PROGRAMS
on the Adriatic Coast
The Anti-Aging Fasting Program consists of a 7-28 days program (including 3 - 14 fasting days). 7-28-day low-calorie diet program is also available .
More information
    The anti-aging story (summary)
Introduction. Statistical review. Your personal aging curve
  Aging and Anti-aging. Why do we age?
    2.1  Aging forces (forces that cause aging
     
Internal (free radicals, glycosylation, chelation etc.) 
External (Unhealthy diet, lifestyle, wrong habits, environmental pollution, stress, poverty-change "poverty zones", or take it easy. etc.) 
    2.2 Anti-aging forces
     
Internal (apoptosis, boosting your immune system, DNA repair, longevity genes) 
External (wellness, changing your environment; achieving comfortable social atmosphere in your life, regular intake of anti-aging drugs, use of replacement organs, high-tech medicine, exercise)
    2.3 Aging versus anti-aging: how to tip the balance in your favour!
 
    3.1 Caloric restriction and fasting extend lifespan and decrease all-cause mortality (Evidence)
      Human studies
Monkey studies
Mouse and rat studies
Other animal studies
    3.2 Fasting and caloric restriction prevent and cure diseases (Evidence)
        Obesity
Diabetes
Hypertension and Stroke
Skin disorders
Mental disorders
Neurogical disorders
Asthmatic bronchitis, Bronchial asthma
Bones (osteoporosis) and fasting
Arteriosclerosis and Heart Disease
Cancer and caloric restriction
Cancer and fasting - a matter of controversy
Eye diseases
Chronic fatigue syndrome
Sleeping disorders
Allergies
Rheumatoid arthritis
Gastrointestinal diseases
Infertility
Presbyacusis
    3.3 Fasting and caloric restriction produce various
      biological effects. Effects on:
        Energy metabolism
Lipids metabolism
Protein metabolism and protein quality
Neuroendocrine and hormonal system
Immune system
Physiological functions
Reproductive function
Radio-sensitivity
Apoptosis
Cognitive and behavioral functions
Biomarkers of aging
    3.4 Mechanisms: how does calorie restriction retard aging and boost health?
        Diminishing of aging forces
  Lowering of the rate of gene damage
  Reduction of free-radical production
  Reduction of metabolic rate (i.e. rate of aging)
  Lowering of body temperature
  Lowering of protein glycation
Increase of anti-aging forces
  Enhancement of gene reparation
  Enhancement of free radical neutralisation
  Enhancement of protein turnover (protein regeneration)
  Enhancement of immune response
  Activation of mono-oxygenase systems
  Enhance elimination of damaged cells
  Optimisation of neuroendocrine functions
    3.5 Practical implementation: your anti-aging dieting
        Fasting period.
Re-feeding period.
Safety of fasting and low-calorie dieting. Precautions.
      3.6 What can help you make the transition to the low-calorie life style?
        Social, psychological and religious support - crucial factors for a successful transition.
Drugs to ease the transition to caloric restriction and to overcome food cravings (use of adaptogenic herbs)
Food composition
Finding the right physician
    3.7Fasting centers and fasting programs.
  Food to eat. Dishes and menus.
    What to eat on non-fasting days. Dishes and menus. Healthy nutrition. Relation between foodstuffs and diseases. Functional foods. Glycemic index. Diet plan: practical summary. "Dr. Atkins", "Hollywood" and other fad diets versus medical science
     

Vegetables
Fruits
Bread, cereals, pasta, fiber
Glycemic index
Fish
Meat and poultry
Sugar and sweet
Legumes
Fats and oils
Dairy and eggs
Mushrooms
Nuts and seeds
Alcohol
Coffee
Water
Food composition

  Anti-aging drugs and supplements
    5.1 Drugs that are highly recommended
      (for inclusion in your supplementation anti-aging program)
        Vitamin E
Vitamin C
Co-enzyme Q10
Lipoic acid
Folic acid
Selenium
Flavonoids, carotenes
DHEA
Vitamin B
Carnitin
SAM
Vinpocetine (Cavinton)
Deprenyl (Eldepryl)
    5.2 Drugs with controversial or unproven anti-aging effect, or awaiting other evaluation (side-effects)
        Phyto-medicines, Herbs
HGH
Gerovital
Melatonin
      5.3 Drugs for treatment and prevention of specific diseases of aging. High-tech modern pharmacology.
        Alzheimer's disease and Dementia
Arthritis
Cancer
Depression
Diabetes
Hyperlipidemia
Hypertension
Immune decline
Infections, bacterial
Infections, fungal
Memory loss
Menopause
Muscle weakness
Osteoporosis
Parkinson's disease
Prostate hyperplasia
Sexual disorders
Stroke risk
Weight gaining
    5.4 The place of anti-aging drugs in the whole
      program - a realistic evaluation
 
    6.1 Early diagnosis of disease - key factor to successful treatment.
      Alzheimer's disease and Dementia
Arthritis
Cancer
Depression
Diabetes
Cataracts and Glaucoma
Genetic disorders
Heart attacks
Hyperlipidemia
Hypertension
Immune decline
Infectious diseases
Memory loss
Muscle weakness
Osteoporosis
Parkinson's disease
Prostate hyperplasia
Stroke risk
Weight gaining
    6.2 Biomarkers of aging and specific diseases
    6.3 Stem cell therapy and therapeutic cloning
    6.4 Gene manipulation
    6.5 Prosthetic body-parts, artificial organs
        Blood
Bones, limbs, joints etc.
Brain
Heart & heart devices
Kidney
Liver
Lung
Pancreas
Spleen
    6.6 Obesity reduction by ultrasonic treatment
  Physical activity and aging. Experimental and clinical data.
        Aerobic exercises
Stretching
Weight-lifting - body-building
Professional sport: negative aspects
 
  Conclusion: the whole anti-aging program
    9.1 Modifying your personal aging curve
      Average life span increment. Expert evaluation.
     
Periodic fasting and caloric restriction can add 40 - 50 years to your lifespan
Regular intake of anti-aging drugs can add 20-30 years to your lifespan
Good nutrition (well balanced, healthy food, individually tailord diet) can add 15-25 years to your lifespan
High-tech bio-medicine service can add 15-25 years to your lifespan
Quality of life (prosperity, relaxation, regular vocations) can add 15-25 years to your lifespan
Regular exercise and moderate physical activity can add 10-20 years to your lifespan
These approaches taken together can add 60-80 years to your lifespan, if you start young (say at age 20). But even if you only start later (say at 45-50), you can still gain 30-40 years


Click image
to view
    9.2 The whole anti-aging life style - brief summary 
    References eXTReMe Tracker
        The whole anti-aging program: overview
         
       

       
     
Home Contact Us ANTI-AGING GUIDE 2003