InteractionsGuide Index Page

Case Analysis Toolclose
Enter Each Substance:

Analysis Search Terms:

Vitamin E

Nutrient Name: Vitamin E.
Synonyms: Vitamin E; d-alpha-tocopherol.
Related Compounds: d-beta-tocopherol, d-gamma-tocopherol, d-delta-tocopherol; tocopheryl acetate, tocopheryl succinate.
Trade Names: Aqua Gem E, Aquasol E, E-Gems, Key-E, Key-E Kaps.

Summary Table
Drug/Class Interaction TypeMechanism and SignificanceManagement
Acetylsalicylic acid (ASA, aspirin)
Concomitant use of aspirin and vitamin E may provide an additive effect in reducing platelet aggregation and otherwise reducing cerebrovascular risk. Evidence mixed but suggesting positive trend for clinically significant supportive interaction; use of antioxidant could clarify findings and enhance preventive effect.Coadminister aspirin with multiple antioxidants, including mixed tocopherols and coenzyme Q10.

Combining topical application of vitamin E with anthralin can provide antioxidant protection against drug-induced lipid peroxidation and inflammation. Narrow but strong evidence indicating clinically significant supportive interaction.Compound and coadminister.
Bile acid sequestrants
Bile acid sequestrants may interfere with absorption of vitamin E, as well as of folic acid and other fat-soluble nutrients. Despite mixed evidence, reasonable probability of clinically significant adverse effect on status of nutrients relevant to cardiovascular health, particularly in at-risk individuals.Supplement with vitamin E and other affected nutrients away from medication.
Chemotherapy and radiotherapy
/ / / / /
Associated oral mucositis

Vitamin E and other antioxidants may provide protective activity against lipid peroxidation and other damaging forms of oxidative stress induced by conventional oncological therapies and may exert synergistic therapeutic activity when coadministered in a systematic and clinically appropriate manner. However, inappropriate or ill-timed usage may interfere with therapies relying on action of free radicals for therapeutic effect. Evidence of interference is lacking while evidence of synergy is mixed. Research into strategic coadministration and clinical guidelines is preliminary and evolving. Blanket declarations of risk, efficacy, or clinical significance are premature and unsupported.Avoid concomitant use outside appropriate care. Concurrent or alternating administration can be appropriate in certain clinical situations under close supervision and regular monitoring.
Cisplatin, oxaliplatin
Platinum chemotherapy
/ /
Coadministration of vitamin E may reduce the adverse effects of platinum-based chemotherapy due to free-radical damage, particularly neuropathies and nephrotoxicity, while compensating for nutrient depletion and potentially enhancing therapeutic efficacy. Growing body of evidence suggests a supportive interaction of clinical significance with appropriate clinical management.Avoid concomitant use outside appropriate care. Concurrent or alternating administration can be appropriate in certain clinical situations under close supervision and regular monitoring.
/ /
Vitamin E coadministration may reduce nephrotoxicity and other adverse effects of cyclosporine while enhancing its bioavailability and decreasing its clearance and steady-state volume of distribution.Coadministration may be beneficial unless otherwise indicated. Supervise and monitor.

The strong oxidative action of dapsone can cause hemolysis by damaging red cell membranes. Coadministration of vitamin E may partially protect against dapsone-induced hemolysis. Evidence supportive but mixed and inconclusive.Coadminister vitamin E, preferably as mixed tocopherols; effect may be enhanced by other antioxidants.

Oxidative damage contributes to the cardiomyopathy typical of anthracycline chemotherapy. Vitamin E coadministration may mitigate such adverse effects through its antioxidant activity and enhance tolerance of adverse effects; synergistic effects also possible. Evidence of benefit inadequate; possibility of interference with drug activity contentious but unproven.Coadministration of vitamin E, preferably as mixed tocopherols, may help prevent or treat cardiotoxicity. Consider coenzyme Q10 and other antioxidants, as well as L-carnitine, L-taurine, ginkgo, and fish oils. Concurrent or alternating administration can be appropriate in certain clinical situations under close supervision and regular monitoring.
/ / /
Gemfibrozil may reduce serum levels of alpha- and gamma-tocopherol, and other antioxidants. Evidence mixed and contradictory. Clinical significance uncertain.Patients with or at risk for cardiovascular disease likely to benefit from a diet rich in vitamin E and other antioxidant nutrients; role of supplementation contentious.

Vitamin E can reduce lipid peroxidation and may enhance glycemic control and improve insulin action. Evidence supportive but preliminary.Diet rich in vitamin E and allied nutrients and emphasizing low glycemic index advisable. Supplementation, preferably as mixed tocopherols, may be appropriate. Regular monitoring of blood glucose levels essential.
Free radical production and oxidative damage caused by haloperidol contribute to tardive dyskinesia and other adverse effects, and may be due, to some degree, to drug-induced vitamin E depletion. Research indicates that vitamin E coadministration may reduce adverse effects in certain patient subgroups with minimal risk of significant adverse effects or interference with drug activity.Coadminister vitamin E, preferably as mixed tocopherols; effect may be enhanced by other antioxidants. Supervise and monitor.
HMG-CoA reductase inhibitors (statins)
/ /
Vitamin E may support therapeutic action of statin agents and reduce their adverse effects, particularly on oxidative status; however, vitamin E may interfere with therapeutic action of statins, but concerns remain unclear and unsubstantiated. Antioxidant combinations, including vitamin E, may interfere with the HDL-elevating activity of statin-niacin combinations, most likely through their interaction with niacin. Vitamin E may also enhance clearance of statins by promoting detoxification processes. Coadministration may enhance antihyperlipidemic therapy and reduce cardiovascular risk. Evidence is preliminary but emerging. Efficacy controversial and clinical significance unclear.Statins (without niacin) may be compatible with administration of multiple antioxidant combinations emphasizing mixed tocopherols and coenzyme Q10. Supervise and monitor within an integrative strategy.
Proton pump inhibitors

Antioxidant activity of vitamin E may reduce esophagitis and support omeprazole therapy by increasing the mucosal resistance to oxidative damage from gastroesophageal reflux. Preliminary evidence indicates reasonable probability of clinically significant beneficial interaction from coadministration.Coadminister. Drug dose may be reduced.
/ /
Orlistat may decrease absorption of vitamin E and other fat-soluble nutrients. Preliminary evidence indicates vitamin E depletion pattern with reasonable probability of clinical significance over extended period.Supplement with vitamin E and other nutrients preventively or if indication of deficiency with extended orlistat therapy.
Oral vitamin K antagonist anticoagulants
/ /
Research involving individuals not taking anticoagulants as well as warfarin-related case reports indicate that high-dose vitamin E may enhance effect of coumadin-derivative anticoagulants by decreasing vitamin K levels and activity, reflected by PIVKA-II, an underactive form of prothrombin produced in presence of vitamin K insufficiency. Further research is warranted to determine nutrient interaction between vitamins K and E in patients using oral anticoagulants and appropriate clinical responses to coadministration.Closely monitor and titrate if coadministration is appropriate.
nutrient description

Chemistry and Forms

Alpha-tocopherol is either d-alpha (RRR) or dl- (all-racemic) alpha tocopherol.

Naturallly ocurring forms of vitamin E include tocopherols (d-alpha-tocopherol, d-beta-tocopherol, d-gamma-tocopherol, d-delta-tocopherol) and tocotrienols (alpha-tocotrienol, d-beta-tocotrienol, d-gamma-tocotrienol, d-delta-tocotrienol).

Physiology and Function

Vitamin E was discovered in the 1920s, but our comprehension of the full implications of this nutrient in health, dysfunction, and disease is only beginning to emerge. Alpha-tocopherol is the only recognized form of the lipid-soluble vitamin E in animal tissues and plasma. However, vitamin E antioxidants are a group of eight tocopherol and tocotrienol compounds, including four tocopherols and four additional tocotrienol (alpha, beta, gamma, delta), which occur naturally in foods. Research over the past decade has focused on this nutrient's role in antioxidant functions, but important discoveries have also emerged concerning the direct role of vitamin E in control of cell division, inflammatory processes, xenobiotic detoxification, blood cell regulation, and connective tissue growth.

Vitamin E absorption depends on the presence of bile and decreases as dosage increases. At normal levels of intake, about 50% of dietary vitamin E is absorbed. A diet high in unsaturated fat increases vitamin E requirements. Vitamin E is distributed to all body tissues but has a particular affinity for adipose tissue. Adipose tissue slowly accumulates vitamin E and then in time slowly releases it while the liver just briefly stores vitamin E, and does so continuously. Alpha-tocopherol transfer protein (TTP), present in the liver and cerebellum, is the lipophilic vitamin-binding protein responsible for the incorporation of alpha-tocopherol into lipoproteins and for the transport of alpha-tocopherol between membranes. Dietary intake of vitamin E is metabolized in the liver to CEHCs, which are then glucuronidated and excreted via the urine.

Vitamin E's principal physiological role is to act as an antioxidant to prevent free-radical damage (lipid peroxidation) and protect the stability and integrity of cellular tissues and membranes. Vitamin E's role in stabilizing cell membranes is especially important in the lungs and red blood cells (RBCs), which are particularly susceptible to oxidative damage because of their high oxygen tension. As a fat-soluble nutrient, this antioxidant activity occurs particularly in lipid media and protects fatty acids against oxidative damage caused by various pollutants, peroxides, and free radicals formed during metabolic processes. It also reduces formation of lipofuscin, an oxidized fat that has been implicated in the aging process. If insufficient vitamin E is present, polyunsaturated fatty acids (PUFAs) may become oxidized in the body, creating toxins that may lead to chromosomal damage and carcinogenesis. Alpha-tocopherol has been shown to inhibit platelet aggregation, enhance vasodilation, affect the expression and activity of immune and inflammatory cells, and inhibit the activity of protein kinase C, an important cell-signaling molecule. Researchers have recently determined that vitamin E, especially as d-alpha-tocopherol, can act as a ligand for, and thereby increase the metabolic activity of, pregnane X receptor (PXR), which regulates a constellation of genes involved in detoxification of xenobiotics. 1 Vitamin E also plays an important role in preventing neurological abnormalities such as peripheral neuropathies.

nutrient in clinical practice

Known or Potential Therapeutic Uses

Research into the role of vitamin E in health and disease has yet to mature and remains the subject of controversy and discovery. Within the conventional perspective on nutrition, the metabolic function of vitamin E is usually considered as still unidentified, although its major function as a nonspecific chain-breaking antioxidant is acknowledged and emphasized. In contrast, since the 1940s, health care professionals practicing nutritional therapeutics have often presented vitamin E as a primary component of health optimization, disease prevention, and therapeutic intervention. Although conventional medicine usually disclaims the value of antioxidant therapy via nutritional supplements in the primary prevention of cardiovascular disease and cancer, the lack of cohesive understanding of the role of vitamin E and other antioxidants in secondary prevention is also acknowledged. Clinical trials have typically investigated individual antioxidants, such as vitamin E, without considering that most health care professionals practicing nutritional therapeutics employ antioxidant formulations aimed at achieving synergistic action from multiple ingredients. Such factors may account for many of the recent inconsistencies and disappointments in outcomes of studies examining the efficacy of vitamin E supplementation for heart disease and other conditions. Further, research employing vitamin E, as with most other studies involving nutritional supplements, have often been designed without regard to the particular form of the nutrient(s) employed, dosage levels typical of informed clinical practice, or the underlying pathophysiological mechanisms.

This subject exemplifies the need for well-designed clinical trials focused on clearly defined health care goals and informed by an integrative approach utilizing the knowledge and experience of clinicians and researchers from a diverse range of perspectives. Furthermore, the conclusions of reviews and meta-analyses of vitamin E studies require a careful parsing of trial data based on form of the nutrient involved, design and time frame, concomitant therapies, and patient population characteristics if they are to be accurate and clinically useful. Fortunately, in the meantime, a broad consensus supports the primary value of a balanced and diverse diet rich in antioxidants as the foundation of health optimization and disease prevention.

Possible Uses

Acne, allergies, Alzheimer's disease, amyotrophic lateral sclerosis (risk reduction), anemia (sickle cell anemia and other types of hemolytic anemia), angina, anti-inflammatory, antioxidant, ataxia with isolated vitamin E deficiency (AVED), atherosclerosis, bronchitis, burns, cardiovascular effects, cataracts, cold sores, cystic fibrosis, dermatitis herpetiformis, diabetes mellitus, diabetic retinopathy (prevention), Down syndrome, Dupuytren's contracture, dysmenorrhea, epilepsy (pediatric), fibrocystic breast disease, fibromyalgia, hemolytic anemia (deficiency), hepatitis, herpetic lesions and postherpetic neuralgia, high-altitude exercise performance, human immunodeficiency virus and acquired immunodeficiency syndrome (HIV/AIDS) support, hypercholesterolemia, mild hypertension, hypoglycemia, immune support (especially for elderly), infertility, inflammatory thrombophlebitis, intermittent claudication, leukoplakia, lung cancer (risk reduction), macular degeneration, menopause (including hot flashes and atrophic vaginitis), menorrhagia (heavy menstruation), muscular dystrophy, myocardial infarction, nocturnal cramping, Osgood-Schlatter disease, osteoarthritis, pancreatic insufficiency, peripheral neuropathy (due to deficiency), photosensitivity, preeclampsia (risk reduction), premature infants, premenstrual syndrome, prostate cancer (risk reduction), psoriasis, Raynaud's syndrome, restless legs syndrome, retinopathy, retrolental fibroplasia, rheumatoid arthritis, scar tissue, seborrheic dermatitis, scleroderma, skin ulcers, spinocerebellar ataxia (due to deficiency), spontaneous abortion, sudden infant death syndrome (SIDS), sunburn, systemic lupus erythematosus (SLE), tardive dyskinesia, vaginal atrophy, vaginitis, wound healing, yellow nail syndrome.

Deficiency Symptoms

Frank vitamin E deficiency is rare in humans, but dietary intake in developed countries is often compromised by heavy reliance on processed foods. Very little vitamin E is transferred across the placenta, so premature infants, who are not breast-fed or supplemented, are susceptible to deficiency and subsequent damage of the retina (retrolental fibroplasia) if exposed to high oxygen tension from oxygen supplementation. Individuals with a genetic defect in alpha-tocopherol transfer protein (TTP) have an especially significant susceptibility to a severe vitamin E deficiency, characterized by low blood and tissue levels of vitamin E and progressive nerve abnormalities. Deficiency of vitamin E can cause a peripheral neuropathy, in which sensory neurons are particularly affected, such that the large-caliber axons die, ultimately resulting in a spinocerebellar ataxia.

Possible signs and symptoms of vitamin E deficiency include decreased integrity of RBC membranes, hemolytic anemia (with consequent elevated indirect bilirubin), peripheral neuropathy, spinocerebellar ataxia, elevated heavy metal levels, cataracts, cystic fibrosis, cholestatic liver disease, various lipid malabsorption syndromes, atrophy of reproductive organs, infertility, premenstrual syndrome, hot flashes, fibrocystic disease, benign prostatic hypertrophy, dry skin, eczema, psoriasis, poor wound healing, atrophy and weakness in skeletal and smooth muscles, and Osgood-Schlatter disease (also associated with selenium deficiency), as well as increased risk of cancer, atherosclerosis, rheumatoid arthritis, major depression, and preeclampsia. Sickle cell anemia and beta-thalassemia predispose to vitamin E insufficiency.

Dietary Sources

Unrefined, cold-pressed vegetable oils, particularly wheat germ oil, sunflower seed oil, and olive oil and all whole, raw, or sprouted seeds, nuts, and grains (especially whole wheat) are considered the best dietary sources of vitamin E. Asparagus, avocados, brussels sprouts, egg yolks, legumes, shrimp, spinach, sweet potatoes, and leafy green vegetables, generally, can be good sources. Although wheat germ can be an excellent source, it must be absolutely fresh (less than a week old) because the oil oxidizes rapidly, and rancid wheat germ does not contain active vitamin E.

Food sources can provide the recommended dietary allowance (RDA) level of 15 mg alpha-tocopherol per day, an appropriate intake for many conditions, while offering a rich diversity of gamma-tocopherol and other tocopherols. However, clinical research indicates that the maintenance dosage levels and especially the higher range of therapeutic dosage levels, typically hundreds of units per day, required for some conditions may be difficult to obtain through diet alone. This is particularly true for individuals who reduce their intake of dietary fats, because vitamin E tends be more abundant in diets richer in fats. Moreover, recent research on vitamin E bioavailability shows that absorption of vitamin E is higher if it is part of or closely associated with the digestion of a food that contains fat. For example, grain cereal fortified with vitamin E raised plasma levels of new vitamin E more consistently and to higher levels proportionately than did vitamin E as a supplement only, with liquids on an empty stomach, or even taken with milk. 2 On a broader level, there is a growing body of evidence that large doses of vitamin E, especially if used without an accompanying diverse antioxidant network, may be deleterious for some individuals.

Tocopherols are oily yellow liquids that are water insoluble, heat and acid stable, and deteriorate with exposure to alkali, light, oxygen, iron, or lead. Frying of foods as well as freezing also decreases the potency of vitamin E. In contrast, tocopheryl esters, which are most often found in fortified foods (particularly breakfast cereals), tend to be fairly resistant to both frying and freezing (as well as highly bioavailable).

Nutrient Preparations Available

Although alpha-tocopherol has long been the standard of vitamin E supplementation, research is evolving to a greater understanding of the importance of naturally occurring forms and the advantages of mixed tocopherols. RRR-alpha-tocopherol, more commonly known as d-alpha-tocopherol, is the only form of alpha-tocopherol that occurs naturally in foods, whereas synthetic dl-alpha-tocopherol (all-racemic alpha-tocopherol) is composed of equal amounts of all stereoisomers. The establishment of d-alpha as the “active” isomer was based on the rat fetus resorption assay developed in the 1940s, in which only the d-alpha isomer is active; in pregnant rats made vitamin E deficient, the fetuses die and are resorbed, which is prevented only by d-alpha-tocopherol. The other isomers may have superior in vivo biological antioxidant activity, and gamma appears to have greater prostate cancer–preventive activity than alpha. The tocotrienols are much superior in cellular membrane protection because of a greater ability to move within membrane structures. Naturally occurring d-alpha-tocopherol is significantly more bioavailable, perhaps 200%, and exerts greater physiological activity than synthetic dl–alpha-tocopherol. 3 Some clinicians have reported that water-soluble forms of vitamin E can be better absorbed and more effective with individuals experiencing fat malabsorption problems, especially middle-age and menopausal women. Vitamin E is sold in both esterified and nonesterified forms but is usually manufactured as acetate or succinate esters because pure vitamin E compounds are easily oxidized. A tocopherol form is appropriate in topical use; tocopheryl forms require an enzyme to split the vitamin E from the acid moiety to which it is attached by an ester linkage.

Dosage Forms Available

Capsule, gel capsule; emulsified liquid drops, mycelized liquid drops; injection; liquid; ointment; powder; solution, oral drops; spray; suppository; tablet; topical.


  • 1 mg d-alpha-tocopheryl acetate=1.49 IU
  • 1 IU all-racemic alpha-tocopherol=0.45 mg

The current RDA is given in milligrams of alpha-tocopherol.

Dosage Range


  • Dietary:   RDA based on RRR-alpha-tocopherol (d-alpha-tocopherol):
  • Adults, 19 years and older: 15 mg (22.5 IU)/day
  • Pregnancy (all ages): 15 mg (22.5 IU)/day
  • Breastfeeding (all ages): 19 mg (28.5 IU)/day

Supplemental/Maintenance: 15 mg/day, higher doses may not be more efficacious. 4,5

Pharmacologic/Therapeutic: 400 to 2500 IU/day (excluding pregnant or lactating women) in clinical practice; 100 to 1000 IU/day in the scientific literature.

Toxic: The safe upper intake level (UL) of vitamin E for adults as d-alpha-tocopheryl acetate is 1500 IU/day (1000 mg), or 1100 IU/day dl-alpha.

Pediatric (<18 years)

Dietary: RDA based on RRR-alpha-tocopherol (d-alpha-tocopherol)

  • Infants, birth to 6 months: 4 mg (6 IU)/day
  • Infants, 7 to 12 months: 5 mg (7.5 IU)/day
  • Children, 1 to 3 years: 6 mg (9 IU)/day
  • Children, 4 to 8 years: 7 mg (10.5 IU)/day
  • Children, 9 to 13 years: 11 mg (16.5 IU)/day
  • Adolescents, 14 to 18 years: 15 mg (22.5 IU)/day
Supplemental/Maintenance: Not established.

Laboratory Values

Plasma vitamin E: Less than 11.6 μmol/L indicates deficiency.

Plasma alpha-tocopherol (μmol/L)/plasma cholesterol (mmol/L): Ratio less than 2.2 indicates deficiency. Accurate measurement of vitamin E status inherently includes the ratio of vitamin E/total cholesterol because vitamin E level in the blood is directly correlated with the blood lipid level.

Plasma tocopherol: Less than 10 μmol/L generally indicates deficiency.

Note: Alpha-tocopherol normally constitutes more than 90% of total plasma vitamin E.

There is no correlation between plasma levels and vitamin E stores. A serum peroxide value can give an indirect status.

safety profile


Vitamin E supplements are widely considered to be safe and unlikely to cause adverse side effects in most individuals at typical dosage levels. At common therapeutic doses intended for long-term use, 800 IU per day, vitamin E, in its various forms, is considered nontoxic in most individuals. Daily doses of 2000 to 3500 IU have been used in clinical setting for extended periods without adverse effects. Nevertheless, there has been a recent trend in the scientific literature suggesting potential adverse effects of dosages significantly higher than the recently revised RDA. Warnings against use of dosage levels greater than 200 IU/day usually derive from trials using vitamin E as an isolated antioxidant, synthetic dl-alpha-tocopherol, and patients with pathologies, behaviors, diet, or other factors characterized by high oxidative stress. Meta-analyses and reviews encompassing such studies are limited by their failure to emphasize the clinical implications of such study factors and attendant mixing of findings from trials employing essentially different substances (e.g., natural vs. synthetic forms, multiple vs. single nutrient). Thus, a potentially dangerous pro-oxidant effect can be created when one or two antioxidants, especially in synthetic forms, are given in high dosages to individuals who are chronically antioxidant deficient and under increased oxidative stress. Even so, “higher circulating concentrations of alpha-tocopherol within the normal range are associated with significantly lower total and cause-specific mortality in older male smokers.” 6 Unfortunately, the mainstream of scientific research and medical practice has yet to consider, let alone investigate this concept.

Nutrient Adverse Effects

General Adverse Effects

The rare occasions of adverse effects from supplemental forms of vitamin E, typically in high dosages for extended durations, have been characterized by fatigue, headache, hemorrhage, double vision, nausea, flatulence, diarrhea, gastrointestinal distress, and muscular weakness. One study, published in 2005 and widely publicized in the popular press when initially released online in late 2004, was a meta-analysis suggesting that high dosages of vitamin E were associated with a small increase in risk for all-cause mortality at doses above 400 IU daily among individuals being treated for various health conditions, and this dose-dependent increase began to be seen above doses of 150 IU/day. These researchers also found that the meta-analysis of the vitamin E studies involving low doses (i.e., <200 IU/day) indicated a small decrease in all-cause mortality, although it did not reach statistical significance. These conclusions were based on meta-analysis from 19 randomized, placebo-controlled trials involving d-alpha-tocopherol and dl-alpha-tocopherol (synthetic form) in diverse populations, including high proportions of the elderly and high-risk individuals with chronic pathologies. 7 None of these studies included any of the other naturally occurring tocopherol or tocotrienol isomers of the vitamin E complex.

Pregnancy and Nursing

Note: With pregnant women, monitor plasma tocopherol concentrations (normal range, 6-14 μg/mL).

In one randomized, placebo-controlled trial involving 722 pregnant women at risk for preeclampsia, researchers observed a slightly elevated incidence of small-for-gestational-age neonates among women administered vitamin C (1000 mg) and vitamin E (RRR-alpha-tocopherol, 400 IU) versus placebo. 8

Infants and Children

Reports of infant deaths from vasculocentric hepatotoxicity in 1983 due to parenteral administration of vitamin E were found to be related to the solubilizing agent polysorbate instead of vitamin E. 9 This compound, E-Ferol, was subsequently banned. In a 1989 review article, Mino 10 summarized a cautious perspective: “In the course of therapy with elevated dosages of vitamin E, administered either orally, intramuscularly, or intravenously, many problems arose in the infants, such as unexpected death, increased frequency of necrotizing enterocolitis (NEC) and sepsis, and the development of unusual symptoms including hepatic injuries.”

Toxicity: Vitamin E toxicity is generally considered to be very rare. Increased risk of hemorrhage may result from vitamin E toxicity. A dose of 1800 IU/day has been shown to cause a prolonged bleeding time (an in vivo test of platelet function).


  • Chronic rheumatic heart disease: Avoid initial use of high doses; increase gradually.
  • Hypertension.
  • Congestive heart failure (CHF): Large doses of a single antioxidant supplement, such as vitamin E, in patients likely to be under oxidative stress who do not consume a diet rich in antioxidants, may contribute to further oxidative stress.

Precautions and Warnings

Hypersensitivity to vitamin E, source material, or any component of the formulation; intravenous (IV) route.

interactions review

Strategic Considerations

Vitamin E deficiency resulting from inadequate dietary intake is relatively uncommon in the developed world, but it may occur within certain populations, such as elderly persons and institutionalized individuals. Further, a wide range of common drugs deplete key nutrients, including vitamin E and other antioxidants, and the risk of drug-induced deficiency of vitamin E and consequent adverse effects is considered to be substantial.

Conversely, supplementation with naturally occurring forms of vitamin E may prevent or reverse adverse effects of many medications. However, controversy continues as to whether coadministration of vitamin E with drugs that deplete it offers superior therapeutic outcomes, or whether such polypharmacy simply obscures the outcome or even interferes with intended drug actions.

The role of vitamin E in conventional medicine has undergone many sharp turns, particularly at the start of the twenty-first century, as a number of interventional clinical trials, as well as several meta-analysis studies, were published. Perhaps most importantly, the issue of single versus multiple isomers of vitamin E, as well as natural versus synthetic sources, reveals deep divisions within the medical and scientific community as to nutritional therapeutics and underlying assumptions. This pivotal factor in clinical practice, research design, and scientific discourse was further exacerbated by the recent redefinition of “vitamin E” away from the previous functional definition based on physiological action to a narrower, more pharmaceutic definition exclusively specifying d-alpha-tocopherol.

Any discussion of “vitamin E” first requires a common understanding of meaning and context and should begin with questions as to forms and sources being applied. Thus, studies referring to “vitamin E” could indicate alpha-tocopherol more exactly (although often failing to differentiate isomer and source), supplements containing multiple tocopherol isomers, supplements containing multiple forms of naturally occurring vitamin E (i.e., mixed tocopherols and tocotrienols), or food sources. Many controversies and much confusion would be rapidly resolved if discourse was founded on such clear communication and consistent nomenclature. The clinical significance of such discriminations becomes apparent in the treatment of conditions such as congestive heart failure, in which the interaction between different forms of “vitamin E” may constitute one of the more significant physiological factors. The exclusive reliance on alpha-tocopherol in almost all clinical trials of vitamin E fails to acknowledge the inherent balance and synergistic interplay among alpha-, beta-, gamma-, and delta-tocopherol and thus limits both the immediate applicability of any resultant findings and their extrapolation.

Over the past 40 years the role of vitamin E in preventing heart disease has been the subject of often acrimonious debate and collegial miscommunication. The ongoing controversy regarding the role of vitamin E in the prevention and treatment of cardiovascular disease reveals a deep schism in the often opposing world views of the linear reductionistic philosophy that permeates much of conventional medicine, and the more holistic empirical approaches of “natural” medicine. This dynamic suggests an emerging paradigm that might offer novel approaches to research, prevention, and therapeutics that can transcend and yet be inclusive of previously conflicting viewpoints. Oxidative stress plays a central role in the physiopathology underlying many chronic degenerative diseases, particularly cardiovascular disease, but its clinical implications are not understood in a consistent and comprehensive way. The underlying assumption in the field was that if the antioxidant effect of vitamin E conclusively proved to be clinically significant, vitamin E would logically be confirmed as playing an integral role in the prevention and treatment of heart disease. The role of antioxidant nutrients has evolved through a cycle of ill-founded enthusiasm and premature expectations that verge on regarding them as a panacea, into a body of research using single antioxidants in high doses (and often synthetic forms), with mostly negative results, and toward an emerging reconceptualization of nutrients’ physiological nature and function, clinical uses, and effects. The interactions between antioxidants and statin drugs provide an important illustration of this dialogue and suggest ways in which both research and clinical practice can mature.

Thus, over the past two decades, the attitude toward vitamin E has gone from acceptance and often enthusiasm in some quarters, especially in relation to heart disease, to near-condemnation in more recent papers. However, the limitations of the research thus far clearly point to the need for further research into the differences between pharmaceutical and food sources of vitamin E, the physiological functions of and interplay among the various forms of naturally occurring tocopherol isomers, and the implications of such findings in formulating preparations for research and clinical practice. Furthermore, the emerging knowledge of physiological detoxification systems, such as hepatic phase I, II, and III enzyme systems, and the operative mechanisms of nuclear receptors, such as pregnane X receptor (PXR), offers significant prospects for understanding the clinical significance of drug metabolism and its stimulation by vitamin E and other nutrients. Further research, education, and communication will also be necessary to clarify the importance of using naturally occurring forms of vitamin E, preferably mixed tocopherols and tocotrienols, within the context of a comprehensive antioxidant strategy and with a respect for the particular needs and vulnerabilities of specific patient populations.

Some aspects of this controversy may derive from differences in the research questions being asked, trial design, observational studies versus randomized controlled clinical trials versus meta-analyses, characteristics of subject populations, nutrient forms and dosages, dietary sources versus supplemental intake, concomitant dietary and lifestyle factors, polypharmacy, and outcome measures. From early research into the possible beneficial nature of the interaction between the two, the ground shifted dramatically to claims that antioxidants diminish the effectiveness of statins, and finally to frank warnings that key antioxidants such as beta-carotene and alpha-tocopherol might actually increase risk of coronary artery disease and heart failure. 11,12Conversely, the unresolved concerns regarding the safety and ultimate efficacy of statin drugs increasingly suggest that the dominant paradigm of scientific knowledge of their nature and action (i.e., lowering of cholesterol) may provide an inadequate explanation of their preventive and therapeutic effects as observed in a wide range of conditions. Ultimately the key to resolving such apparent conflicts may reside in greater individualization of care, with reference to the emerging tools of pharmaco-/nutrigenomics, through titration of drug doses to effect and/or blood levels and close monitoring within a flexible, responsive, and evolving integrative approach.

Many of the issues that arise in clinical research regarding vitamin E reflect clinical experience with vitamin E in particular and nutritional therapies in general, and the role such interventions play in defining clinical options and shaping therapeutic strategy. For example, the HATS study published in fall 2001 (discussed later) was widely interpreted as a negative interaction between antioxidants and statins, but on closer analysis more likely shows a blunting effect of the antioxidants on the rise of high-density lipoprotein (HDL) cholesterol, more associated with niacin, rather than a direct effect on the statin therapy. Most statins have minimal if any positive effects on HDL, and often actually reduce HDL, along with low-density lipoprotein (LDL), which is why the statin-niacin combination has become widely used since that study. Even so, the accepted fact that simvastatin is metabolized by cytochrome P450 3A4 (CYP3A4) may be a potentially significant observation given the findings of a single in vitro experiment showing that alpha-tocopherol could theoretically stimulate drug metabolism, particularly through its effect on PXR, with subsequent increased expression of the CYP3A4 enzyme. Nevertheless, failure to include coenzyme Q10 and methyl donors in the nutrient mix may also have represented a significant limitation in the trial design. Such modification would have addressed underlying mechanisms at issue: the inhibitory activity of statins on endogenous synthesis of coenzyme Q10 and niacin's depletion of methyl donors, particularly in the liver. Correction of these two drug-nutrient interactions with supplementation might have led to a very different outcome.

Lastly, an important aspect of antioxidant function rarely factored into the design of clinical trials is a recognition of the pro-oxidant potential of antioxidants. One or two antioxidants, especially synthetic ones (e.g., all- trans beta carotene), given in high doses to individuals under high oxidative stress, who consume diets low in antioxidants (e.g., male Finnish smokers, alcohol/tobacco users), can create a situation in which the antioxidants are forced to act as pro-oxidants. The resultant deficit in the antioxidant network causes the carotene and/or tocopherol and/or ascorbate radicals to persist without being quenched, and thereby increase free-radical damage. The increased incidence of heart failure among high-risk individuals taking 400 mg/day of vitamin E (with ramipril), observed in the HOPE study, appears to reveal such an adverse effect of increased oxidative stress when a comprehensive antioxidant network is not available. 13 Subsequent meta-analyses will be limited by their indiscriminate inclusion of trials using varied agents in isolation with diverse populations. Similarly, the related findings of HOPE and HOPE-TOO trials emphasized the limitations and potential adverse response to use of vitamin E as a single antioxidant in individuals characterized by a state of oxidative stress. These researchers reported that natural-source vitamin E (400 IU alpha-tocopherol daily) failed to significantly reduce risk of cancer or cardiovascular events, the primary focus of the study, and appeared to be associated with an increased risk of heart failure. It is noteworthy that the subject group comprised older patients (average age, >70 years) with a history of heart disease, stroke, or diabetes, most of whom demonstrated very strong risk factors and were taking numerous medications. Furthermore, the authors of this study, as well as most commentators, do not appear to have considered the established relationship between alpha-tocopherol and gamma-tocopherol and its implications in such a patient population. High doses of alpha-tocopherol are known to deplete gamma-tocopherol, not only disrupting the natural balance among the various forms, but particularly influencing the production of natriuretic hormone, which plays a central role in regulating fluid and salt balance and for which gamma-tocopherol is a precursor. Any gamma-tocopherol deficiency induced by alpha-tocopherol could further stress the heart in this already-compromised population and thus contributed to an increased risk of heart failure. The authors conceded that the “unexpected” results “cannot be confirmed at this time by other trials” and “could be due to chance.” 11 Such findings reveal an emerging pattern, approaching consensus, confirming the lack of efficacy of an exclusively pharmacological approach to vitamin E therapeutics, narrowly defined as alpha-tocopherol, in achieving the successes attributed to “vitamin E,” particularly in individuals with heart disease, diabetes, or similarly compromised conditions. The findings point strongly toward the appropriate use of nutrient-rich food sources, or at least their closest approximation in the form of supplements, providing coordinated, multiple antioxidants, particularly mixed tocopherols and tocotrienols (which are up to 50 times more potent antioxidants than the tocopherols).

As knowledge of interactive complexity at molecular and cellular levels unfolds, so do prospects for more appropriately designed clinical trials. The French SuViMax study, which coadministered five antioxidants, showed a cancer prevention effect in likely dietarily antioxidant-deficient males. This exemplifies the hypothesis that the larger the number of antioxidant nutrients combined, that act in both aqueous and lipidic compartments, the better the clinical results should be. As collective knowledge of the mechanisms and nuances of integrative therapeutics matures, so do prospects for increasingly relevant, large-scale, well-designed clinical trials focusing on clinical outcomes. In the meantime, the role of vitamin E as a key antioxidant is undergoing a reassessment as clinicians and researchers obtain greater knowledge and deeper insight into antioxidant networks, the influences of dietary and supplemental sources, and their roles in health promotion, disease prevention, and therapeutic intervention.

nutrient-drug interactions
Acetylsalicylic Acid (ASA, aspirin)
Bile Acid Sequestrants
Chemotherapy (Various Agents)
Interaction Type and Significance
Interaction Type and Significance
Cisplatin and Oxaliplatin
Doxorubicin and Related Anthracycline Chemotherapy
HMG-CoA Reductase Inhibitors (Statins)
Warfarin and Related Oral Vitamin K Antagonist Anticoagulants
theoretical, speculative, and preliminary interactions research, including overstated interactions claims
Benzamycin and Benzoyl Peroxide
Cationic Amphiphilic Drugs
Cytochrome P450 3A4 Substrates
Hormone Replacement Therapy (HRT): Estrogen-Containing and Synthetic Estrogen and Progesterone Analog Medications
Isotretinoin and Related Retinoids
Mineral Oil
Oral Contraceptives: Monophasic, Biphasic, and Triphasic Estrogen Preparations (Synthetic Estrogen and Progesterone Analogs)
Phenobarbital, Phenytoin, Valproic Acid, and Related Anticonvulsant Medications
Ramipril and Other Angiotensin-Converting Enzyme (ACE) Inhibitors
Zidovudine (AZT)
nutrient-nutrient interactions
Polyunsaturated Fatty Acids; Omega-3 and Omega-6 Fatty Acids
Vitamin A
Vitamin C
Vitamin K
Citations and Reference Literature
  • 1.Traber MG. Vitamin E, nuclear receptors and xenobiotic metabolism. Arch Biochem Biophys 2004;423(1):6-11. (Review.)View Abstract
  • 2.Leonard SW, Good CK, Gugger ET, Traber MG. Vitamin E bioavailability from fortified breakfast cereal is greater than that from encapsulated supplements. Am J Clin Nutr 2004;79:86-92.View Abstract
  • 3.Acuff RV, Thedford SS, Hidiroglou NN et al. Relative bioavailability of RRR- and all-rac-alpha-tocopheryl acetate in humans: studies using deuterated compounds. Am J Clin Nutr 1994;60:397-402.View Abstract
  • 4.Rimm E. Micronutrients, coronary heart disease and cancer: should we all be on supplements? 60th Annual Biology Colloquium. Oregon State University, Corvallis; 1999.
  • 5.Panel on Dietary Antioxidants and Related Compounds, Food and Nutrition Board. Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. Washington, DC: National Academy Press: Institute of Medicine, National Academy of Sciences; 2000:249-259.
  • 6.Wright ME, Lawson KA, Weinstein SJ et al. Higher baseline serum concentrations of vitamin E are associated with lower total and cause-specific mortality in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study. Am J Clin Nutr 2006;84:1200-1207.View Abstract
  • 7.Miller ER 3rd, Pastor-Barriuso R, Dalal D et al. Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality. Ann Intern Med 2004;142(1):37-46.View Abstract
  • 8.Poston L, Briley AL, Seed PT et al. Vitamin C and vitamin E in pregnant women at risk for pre-eclampsia (VIP trial): randomized placebo-controlled trial. Lancet 2006;367:1145-1154.
  • 9.Bove KE, Kosmetatos N, Wedig KE et al. Vasculopathic hepatotoxicity associated with E-Ferol syndrome in low-birth-weight infants. JAMA 1985;254:2422-2430.View Abstract
  • 10.Mino M. Use and safety of elevated dosages of vitamin E in infants and children. Int J Vitam Nutr Res Suppl 1989;30:69-80.View Abstract
  • 11.Lonn E, Bosch J, Yusuf S et al. Effects of long-term vitamin E supplementation on cardiovascular events and cancer: a randomized controlled trial. JAMA 2005;293:1338-1347.View Abstract
  • 12.Brown BG, Crowley J. Is there any hope for vitamin E? JAMA 2005;293:1387-1390.
  • 13.Zoler ML. Supplemental vitamin E linked to heart failure. Fam Pract News 2003;33:28.
  • 14.Steiner M, Glantz M, Lekos A. Vitamin E plus aspirin compared with aspirin alone in patients with transient ischemic attacks. Am J Clin Nutr 1995;62:1381S-1384S.View Abstract
  • 15.Kim JM, White RH. Effect of vitamin E on the anticoagulant response to warfarin. Am J Cardiol 1996;77:545-546.View Abstract
  • 16.Liede KE, Haukka JK, Saxen LM, Heinonen OP. Increased tendency towards gingival bleeding caused by joint effect of alpha-tocopherol supplementation and acetylsalicylic acid. Ann Med 1998;30:542-546.View Abstract
  • 17.Celestini A, Pulcinelli FM, Pignatelli P et al. Vitamin E potentiates the antiplatelet activity of aspirin in collagen-stimulated platelets. Haematologica 2002;87:420-426.View Abstract
  • 18.Stampfer MJ, Hennekens CH, Manson JE et al. Vitamin E consumption and the risk of coronary disease in women. N Engl J Med 1993;328:1444-1449.View Abstract
  • 19.Rimm EB, Stampfer MJ, Ascherio A et al. Vitamin E consumption and the risk of coronary heart disease in men. N Engl J Med 1993;328:1450-1456.View Abstract
  • 20.Stephens NG, Parsons A, Schofield PM et al. Randomised controlled trial of vitamin E in patients with coronary disease: Cambridge Heart Antioxidant Study (CHAOS). Lancet 1996;347:781-786.View Abstract
  • 21.Boaz M, Smetana S, Weinstein T et al. Secondary prevention with antioxidants of cardiovascular disease in endstage renal disease (SPACE): randomised placebo-controlled trial. Lancet 2000;356:1213-1218.View Abstract
  • 22.Gum PA, Thamilarasan M, Watanabe J et al. Aspirin use and all-cause mortality among patients being evaluated for known or suspected coronary artery disease: a propensity analysis. JAMA 2001;286:1187-1194.
  • 23.Catella-Lawson F. Vascular biology of thrombosis: platelet-vessel wall interactions and aspirin effects. Neurology 2001;57:S5-S7.View Abstract
  • 24.Zebrack JS, Anderson JL. The role of inflammation and infection in the pathogenesis and evolution of coronary artery disease. Curr Cardiol Rep 2002;4:278-288.View Abstract
  • 25.Wald NJ, Law MR. A strategy to reduce cardiovascular disease by more than 80%. BMJ 2003;326:1419.View Abstract
  • 26.Finnen MJ, Lawrence CM, Shuster S. Inhibition of dithranol inflammation by free-radical scavengers. Lancet 1984;2:1129-1130.View Abstract
  • 27.West RJ, Lloyd JK. The effect of cholestyramine on intestinal absorption. Gut 1975;16:93-98.View Abstract
  • 28.Colestipol therapy and selected vitamin and mineral levels in children. Nutr Rev 1980;38:236-237.
  • 29.Knodel LC, Talbert RL. Adverse effects of hypolipidaemic drugs. Med Toxicol 1987;2:10-32.View Abstract
  • 30.Cardiovascular drugs, antihyperlipidemic agents, bile acid sequestrants. In: Threlkeld DS, ed. Facts and Comparisons Drug Information. St Louis: Facts and Comparisons; February 1999:171L.
  • 31.Werbach MR. Foundations of Nutritional Medicine. Tarzana, Calif: Third Line Press; 1997.
  • 32.Hodis HN, Mack WJ, LaBree L et al. Serial coronary angiographic evidence that antioxidant vitamin intake reduces progression of coronary artery atherosclerosis. JAMA 1995;273:1849-1854.View Abstract
  • 33.Schwarz KB, Goldstein PD, Witztum JL, Schonfeld G. Fat-soluble vitamin concentrations in hypercholesterolemic children treated with colestipol. Pediatrics 1980;65:243-250.View Abstract
  • 34.Schlierf G, Vogel G, Kohlmeier M et al. [Long-term therapy of familial hypercholesterolemia in young patients with colestipol: availability of minerals and vitamins]. Klin Wochenschr 1985;63:802-806.View Abstract
  • 35.Tonstad S, Sivertsen M, Aksnes L, Ose L. Low dose colestipol in adolescents with familial hypercholesterolaemia. Arch Dis Child 1996;74:157-160.View Abstract
  • 36.Kong Q, Lillehei KO. Antioxidant inhibitors for cancer therapy. Med Hypotheses 1998;51:405-409.View Abstract
  • 37.Weijl NI, Hopman GD, Wipkink-Bakker A et al. Cisplatin combination chemotherapy induces a fall in plasma antioxidants of cancer patients. Ann Oncol 1998;9:1331-1337.View Abstract
  • 38.Taper HS, de Gerlache J, Lans M, Roberfroid M. Non-toxic potentiation of cancer chemotherapy by combined C and K3 vitamin pre-treatment. Int J Cancer 1987;40:575-579.View Abstract
  • 39.Sacks PG, Harris D, Chou TC. Modulation of growth and proliferation in squamous cell carcinoma by retinoic acid: a rationale for combination therapy with chemotherapeutic agents. Int J Cancer 1995;61:409-415.View Abstract
  • 40.Albini A, D’Agostini F, Giunciuglio D et al. Inhibition of invasion, gelatinase activity, tumor take and metastasis of malignant cells by N-acetylcysteine. Int J Cancer 1995;61:121-129.
  • 41.Kurbacher CM, Wagner U, Kolster B et al. Ascorbic acid (vitamin C) improves the antineoplastic activity of doxorubicin, cisplatin, and paclitaxel in human breast carcinoma cells in vitro. Cancer Lett 1996;103:183-189.View Abstract
  • 42.Fujiwaki R, Iida K, Ohnishi Y et al. Intra-arterial neoadjuvant chemotherapy followed by radical surgery and radiotherapy for stage IIb cervical carcinoma. Anticancer Res 1997;17:3751-3755.View Abstract
  • 43.Gillissen A, Nowak D. Characterization of N-acetylcysteine and ambroxol in anti-oxidant therapy. Respir Med 1998;92:609-623.View Abstract
  • 44.Kodama J, Ikuhashi H, Hongo A et al. [Neoadjuvant chemotherapy for advanced cervical cancer]. Gan To Kagaku Ryoho 1999;26:89-92.View Abstract
  • 45.Wagdi P, Fluri M, Aeschbacher B et al. Cardioprotection in patients undergoing chemo- and/or radiotherapy for neoplastic disease: a pilot study. Jpn Heart J 1996;37:353-359.View Abstract
  • 46.Weijl NI, Cleton FJ, Osanto S. Free radicals and antioxidants in chemotherapy-induced toxicity. Cancer Treat Rev 1997;23:209-240.View Abstract
  • 47.Salignik R, et al. Avoiding vitamins A and E may improve cancer therapy. 39th Annual Meeting of the American Society for Cell Biology; 1999.
  • 48.Bairati I, Meyer F, Gelinas M et al. Randomized trial of antioxidant vitamins to prevent acute adverse effects of radiation therapy in head and neck cancer patients. J Clin Oncol 2005;23:5805-5813.View Abstract
  • 49.Kennedy DD, Tucker KL, Ladas ED et al. Low antioxidant vitamin intakes are associated with increases in adverse effects of chemotherapy in children with acute lymphoblastic leukemia. Am J Clin Nutr 2004;79:1029-1036.View Abstract
  • 50.Birdsall TC, Alschuler LN, Martin J et al. Effect of concomitant naturopathic therapies on clinical tumor response to external beam radiation therapy for prostate cancer. Society of Integrative Oncology’s Third International Conference. Boston; 2006.
  • 50a.Block KI, Koch AC, Mead MN, et al. Impact of antioxidant supplementation on chemotherapeutic efficacy: a systematic review of the evidence from randomized controlled trials. Cancer Treat Rev 2007;33(5):407-418. Epub 2007 March 23.
  • 51.Wadleigh RG, Redman RS, Graham ML et al. Vitamin E in the treatment of chemotherapy-induced mucositis. Am J Med 1992;92:481-484.View Abstract
  • 52.Lopez I, Goudou C, Ribrag V et al. [Treatment of mucositis with vitamin E during administration of neutropenic antineoplastic agents]. Ann Med Interne (Paris) 1994;145:405-408.
  • 53.Mills EE. The modifying effect of beta-carotene on radiation and chemotherapy induced oral mucositis. Br J Cancer 1988;57:416-417.View Abstract
  • 54.Biswal BM, Zakaria A, Ahmad NM. Topical application of honey in the management of radiation mucositis: a preliminary study. Support Care Cancer 2003;11:242-248.View Abstract
  • 55.Ferreira PR, Fleck JF, Diehl A et al. Protective effect of alpha-tocopherol in head and neck cancer radiation-induced mucositis: a double-blind randomized trial. Head Neck 2004;26:313-321.View Abstract
  • 56.Gregg RW, Molepo JM, Monpetit VJ et al. Cisplatin neurotoxicity: the relationship between dosage, time, and platinum concentration in neurologic tissues, and morphologic evidence of toxicity. J Clin Oncol 1992;10:795-803.
  • 57.Traber MG, Sokol RJ, Ringel SP et al. Lack of tocopherol in peripheral nerves of vitamin E–deficient patients with peripheral neuropathy. N Engl J Med 1987;317:262-265.View Abstract
  • 58.Leonetti C, Biroccio A, Gabellini C et al. Alpha-tocopherol protects against cisplatin-induced toxicity without interfering with antitumor efficacy. Int J Cancer 2003;104:243-250.
  • 59.McCarron MO, Russell AJ, Metcalfe RA, Deysilva R. Chronic vitamin E deficiency causing spinocerebellar degeneration, peripheral neuropathy, and centro-cecal scotomata. Nutrition 1999;15:217-219.View Abstract
  • 60.Pathak AK, Singh N, Khanna N et al. Potentiation of the effect of paclitaxel and carboplatin by antioxidant mixture on human lung cancer h520 cells. J Am Coll Nutr 2002;21:416-421.View Abstract
  • 61.Pace A, Savarese A, Picardo M et al. Neuroprotective effect of vitamin E supplementation in patients treated with cisplatin chemotherapy. J Clin Oncol 2003;21:927-931.View Abstract
  • 62.Argyriou AA, Chroni E, Koutras A et al. Vitamin E for prophylaxis against chemotherapy-induced neuropathy: a randomized controlled trial. Neurology 2005;64:26-31.View Abstract
  • 63.Chang T, Benet LZ, Hebert MF. The effect of water-soluble vitamin E on cyclosporine pharmacokinetics in healthy volunteers. Clin Pharmacol Ther 1996;59:297-303.View Abstract
  • 64.Pan SH, Lopez RR Jr, Sher LS et al. Enhanced oral cyclosporine absorption with water-soluble vitamin E early after liver transplantation. Pharmacotherapy 1996;16:59-65.View Abstract
  • 65.Van Rensburg CE, Joone G, Anderson R. Alpha-tocopherol antagonizes the multidrug-resistance-reversal activity of cyclosporin A, verapamil, GF120918, clofazimine and B669. Cancer Lett 1998;127:107-112.View Abstract
  • 66.Parra Cid T, Conejo Garcia JR, Carballo Alvarez F, de Arriba G. Antioxidant nutrients protect against cyclosporine A nephrotoxicity. Toxicology 2003;189:99-111.View Abstract
  • 67.Lake K. Antioxidant vitamins E and C may interact with cyclosporine in heart transplant recipients. Abstract P900. American Transplant Congress. Washington, DC; 2003.
  • 68.Kelly JW, Scott J, Sandland M et al. Vitamin E and dapsone-induced hemolysis. Arch Dermatol 1984;120:1582-1584.View Abstract
  • 69.Prussick R, Ali MA, Rosenthal D, Guyatt G. The protective effect of vitamin E on the hemolysis associated with dapsone treatment in patients with dermatitis herpetiformis. Arch Dermatol 1992;128:210-213.View Abstract
  • 70.Lardo MM, Diaz NB, Artaza JR et al. [Vitamin E as protective agent against hemolysis in leprosy patients under dapsone treatment]. Medicina (B Aires) 1997;57:150-154.View Abstract
  • 71.Quiles JL, Huertas JR, Battino M et al. Antioxidant nutrients and Adriamycin toxicity. Toxicology 2002;180:79-95.View Abstract
  • 72.Mortensen SA, Olsen HS, Baandrup U. Chronic anthracycline cardiotoxicity: haemodynamic and histopathological manifestations suggesting a restrictive endomyocardial disease. Br Heart J 1986;55:274-282.View Abstract
  • 73.Mortensen SA, Aabo K, Jonsson T, Baandrup U. Clinical and non-invasive assessment of anthracycline cardiotoxicity: perspectives on myocardial protection. Int J Clin Pharmacol Res 1986;6:137-150.View Abstract
  • 74.Steinherz LJ, Steinherz PG, Tan CT et al. Cardiac toxicity 4 to 20 years after completing anthracycline therapy. JAMA 1991;266:1672-1677.View Abstract
  • 75.Brouwer CA, Gietema JA, van den Berg MP et al. Long-term cardiac follow-up in survivors of a malignant bone tumour. Ann Oncol 2006;17(10):1586-1591.View Abstract
  • 76.Myers CE, McGuire W, Young R. Adriamycin: amelioration of toxicity by alpha-tocopherol. Cancer Treat Rep 1976;60:961-962.View Abstract
  • 77.Sonneveld P. Effect of alpha-tocopherol on the cardiotoxicity of Adriamycin in the rat. Cancer Treat Rep 1978;62:1033-1036.View Abstract
  • 78.Krivit W. Adriamycin cardiotoxicity amelioration by alpha-tocopherol. Am J Pediatr Hematol Oncol 1979;1:151-153.View Abstract
  • 79.Legha SS, Wang YM, Mackay B et al. Clinical and pharmacologic investigation of the effects of alpha-tocopherol on Adriamycin cardiotoxicity. Ann NY Acad Sci 1982;393:411-418.View Abstract
  • 80.Wood LA. Possible prevention of Adriamycin-induced alopecia by tocopherol. N Engl J Med 1985;312:1060.View Abstract
  • 81.Powis G, Kooistra KL. Doxorubicin-induced hair loss in the Angora rabbit: a study of treatments to protect against the hair loss. Cancer Chemother Pharmacol 1987;20:291-296.View Abstract
  • 82.Ripoll EA, Rama BN, Webber MM. Vitamin E enhances the chemotherapeutic effects of Adriamycin on human prostatic carcinoma cells in vitro. J Urol 1986;136:529-531.View Abstract
  • 83.Aberg F, Appelkvist EL, Broijersen A et al. Gemfibrozil-induced decrease in serum ubiquinone and alpha- and gamma-tocopherol levels in men with combined hyperlipidaemia. Eur J Clin Invest 1998;28:235-242.View Abstract
  • 84.Yoshida H, Ishikawa T, Ayaori M et al. Beneficial effect of gemfibrozil on the chemical composition and oxidative susceptibility of low density lipoprotein: a randomized, double-blind, placebo-controlled study. Atherosclerosis 1998;139:179-187.View Abstract
  • 85.Paolisso G, D’Amore A, Giugliano D et al. Pharmacologic doses of vitamin E improve insulin action in healthy subjects and non-insulin-dependent diabetic patients. Am J Clin Nutr 1993;57:650-656.
  • 86.Paolisso G, D’Amore A, Galzerano D et al. Daily vitamin E supplements improve metabolic control but not insulin secretion in elderly type II diabetic patients. Diabetes Care 1993;16:1433-1437.
  • 86a.Balabolkin MI, Mikhailova EV, Kniazeva AP, Pankova SS. [Effect of high doses of tocopherol on the processes of lipid peroxidation and insulin secretion in patients with non-insulin-dependent diabetes mellitus] Probl Endokrinol (Mosk) 1994;40(3):10-12. [Russian]
  • 87.Sharma A, Kharb S, Chugh SN et al. Effect of glycemic control and vitamin E supplementation on total glutathione content in non-insulin-dependent diabetes mellitus. Ann Nutr Metab 2000;44:11-13.View Abstract
  • 88.VonVoigtlander PF, Burian MA, Althaus JS, Williams LR. Effects of chronic haloperidol on vitamin E levels and monoamine metabolism in rats fed normal and vitamin E deficient diets. Res Commun Chem Pathol Pharmacol 1990;68:343-352.View Abstract
  • 89.Gattaz WF, Emrich A, Behrens S. Vitamin E attenuates the development of haloperidol-induced dopaminergic hypersensitivity in rats: possible implications for tardive dyskinesia. J Neural Transm Gen Sect 1993;92:197-201.View Abstract
  • 90.Adler LA, Peselow E, Duncan E et al. Vitamin E in tardive dyskinesia: time course of effect after placebo substitution. Psychopharmacol Bull 1993;29:371-374.View Abstract
  • 91.Adler LA, Peselow E, Rotrosen J et al. Vitamin E treatment of tardive dyskinesia. Am J Psychiatry 1993;150:1405-1407.View Abstract
  • 92.Adler LA, Edson R, Lavori P et al. Long-term treatment effects of vitamin E for tardive dyskinesia. Biol Psychiatry 1998;43:868-872.View Abstract
  • 93.Adler LA, Rotrosen J, Edson R et al. Vitamin E treatment for tardive dyskinesia. Veterans Affairs Cooperative Study #394 Study Group. Arch Gen Psychiatry 1999;56:836-841.View Abstract
  • 94.Barak Y, Swartz M, Shamir E et al. Vitamin E (alpha-tocopherol) in the treatment of tardive dyskinesia: a statistical meta-analysis. Ann Clin Psychiatry 1998;10:101-105.View Abstract
  • 95.Lohr JB, Kuczenski R, Niculescu AB. Oxidative mechanisms and tardive dyskinesia. CNS Drugs 2003;17:47-62.View Abstract
  • 96.Williams D, Feely J. Pharmacokinetic-pharmacodynamic drug interactions with HMG-CoA reductase inhibitors. Clin Pharmacokinet 2002;41:343-370.View Abstract
  • 97.Kliewer SA, Goodwin B, Willson TM. The nuclear pregnane X receptor: a key regulator of xenobiotic metabolism. Endocr Rev 2002;23:687-702.View Abstract
  • 98.Arad Y, Spadaro LA, Roth M et al. Treatment of asymptomatic adults with elevated coronary calcium scores with atorvastatin, vitamin C, and vitamin E: the St. Francis Heart Study randomized clinical trial. J Am Coll Cardiol 2005;46:166-172.View Abstract
  • 99.Sinatra ST. Is cholesterol lowering with statins the gold standard for treating patients with cardiovascular risk and disease? South Med J 2003;96:220-222.
  • 100.Chen L, Haught WH, Yang B et al. Preservation of endogenous antioxidant activity and inhibition of lipid peroxidation as common mechanisms of antiatherosclerotic effects of vitamin E, lovastatin and amlodipine. J Am Coll Cardiol 1997;30:569-575.View Abstract
  • 101.Palomaki A, Malminiemi K, Metsa-Ketela T. Enhanced oxidizability of ubiquinol and alpha-tocopherol during lovastatin treatment. FEBS Lett 1997;410:254-258.
  • 102.Palomaki A, Malminiemi K, Solakivi T, Malminiemi O. Ubiquinone supplementation during lovastatin treatment: effect on LDL oxidation ex vivo. J Lipid Res 1998;39:1430-1437.
  • 103.Palomaki A, Malminiemi K, Malminiemi O, Solakivi T. Effects of lovastatin therapy on susceptibility of LDL to oxidation during alpha-tocopherol supplementation. Arterioscler Thromb Vasc Biol 1999;19:1541-1548.
  • 104.Neunteufl T, Kostner K, Katzenschlager R et al. Additional benefit of vitamin E supplementation to simvastatin therapy on vasoreactivity of the brachial artery of hypercholesterolemic men. J Am Coll Cardiol 1998;32:711-716.View Abstract
  • 105.Horne BD, Muhlestein JB, Carlquist JF et al. Statin therapy, lipid levels, C-reactive protein and the survival of patients with angiographically severe coronary artery disease. J Am Coll Cardiol 2000;36:1774-1780.View Abstract
  • 106.Hunninghake DB, McGovern ME, Koren M et al. A dose-ranging study of a new, once-daily, dual-component drug product containing niacin extended-release and lovastatin. Clin Cardiol 2003;26:112-118.View Abstract
  • 107.Cheung MC, Zhao XQ, Chait A et al. Antioxidant supplements block the response of HDL to simvastatin-niacin therapy in patients with coronary artery disease and low HDL. Arterioscler Thromb Vasc Biol 2001;21:1320-1326.View Abstract
  • 108.Brown BG, Zhao XQ, Chait A et al. Simvastatin and niacin, antioxidant vitamins, or the combination for the prevention of coronary disease. N Engl J Med 2001;345:1583-1592.View Abstract
  • 109.Matthan NR, Giovanni A, Schaefer EJ et al. Impact of simvastatin, niacin, and/or antioxidants on cholesterol metabolism in CAD patients with low HDL. J Lipid Res 2003;44:800-806.View Abstract
  • 110.Brown BG, Cheung MC, Lee AC et al. Antioxidant vitamins and lipid therapy: end of a long romance? Arterioscler Thromb Vasc Biol 2002;22:1535-1546.
  • 111.Vivekananthan DP, Penn MS, Sapp SK et al. Use of antioxidant vitamins for the prevention of cardiovascular disease: meta-analysis of randomised trials. Lancet 2003;361:2017-2023.View Abstract
  • 112.Jacobson TA. Combination lipid-lowering therapy with statins: safety issues in the postcerivastatin era. Expert Opin Drug Saf 2003;2:269-286.View Abstract
  • 113.Hecht HS, Harman SM. Relation of aggressiveness of lipid-lowering treatment to changes in calcified plaque burden by electron beam tomography. Am J Cardiol 2003;92:334-336.View Abstract
  • 114.Zambon A, Deeb SS, Brown BG et al. Common hepatic lipase gene promoter variant determines clinical response to intensive lipid-lowering treatment. Circulation 2001;103:792-798.View Abstract
  • 115.Mirmomen S. Combination of omeprazole 20 mg every other day and vitamin E in preventing endoscopic relapse of erosive esophagitis: a placebo-controlled double-blind study. Abstract Wed-OP-G-228. 11th United European Gastroenterology Week. Madrid; 2003.
  • 116.Sifton DW, ed. Physicians’ Desk Reference. Montvale, NJ: Medical Economics Company; 2000.
  • 117.Xenical (orlistat): Product prescribing information. Nutley, NJ: Roche Laboratories; September 2000.
  • 118.Finer N, James WP, Kopelman PG et al. One-year treatment of obesity: a randomized, double-blind, placebo-controlled, multicentre study of orlistat, a gastrointestinal lipase inhibitor. Int J Obes Relat Metab Disord 2000;24:306-313.View Abstract
  • 119.McDuffie JR, Calis KA, Booth SL et al. Effects of orlistat on fat-soluble vitamins in obese adolescents. Pharmacotherapy 2002;22:814-822.View Abstract
  • 120.Melia AT, Koss-Twardy SG, Zhi J. The effect of orlistat, an inhibitor of dietary fat absorption, on the absorption of vitamins A and E in healthy volunteers. J Clin Pharmacol 1996;36:647-653.View Abstract
  • 121.Heck AM, Yanovski JA, Calis KA. Orlistat, a new lipase inhibitor for the management of obesity. Pharmacotherapy 2000;20:270-279.View Abstract
  • 122.Corrigan JJ Jr, Ulfers LL. Effect of vitamin E on prothrombin levels in warfarin-induced vitamin K deficiency. Am J Clin Nutr 1981;34:1701-1705.View Abstract
  • 123.Corrigan JJ Jr. The effect of vitamin E on warfarin-induced vitamin K deficiency. Ann NY Acad Sci 1982;393:361-368.View Abstract
  • 124.Booth SL, Golly I, Sacheck JM et al. Effect of vitamin E supplementation on vitamin K status in adults with normal coagulation status. Am J Clin Nutr 2004;80:143-148.View Abstract
  • 125.Corrigan JJ Jr, Marcus FI. Coagulopathy associated with vitamin E ingestion. JAMA 1974;230:1300-1301.View Abstract
  • 126.Kachel DL, Moyer TP, Martin WJ 2nd. Amiodarone-induced injury of human pulmonary artery endothelial cells: protection by alpha-tocopherol. J Pharmacol Exp Ther 1990;254:1107-1112.View Abstract
  • 127.Babich H, Zuckerbraun HL, Wurzburger BJ et al. Benzoyl peroxide cytotoxicity evaluated in vitro with the human keratinocyte cell line, RHEK-1. Toxicology 1996;106:187-196.View Abstract
  • 128.Weber SU, Thiele JJ, Han N et al. Topical alpha-tocotrienol supplementation inhibits lipid peroxidation but fails to mitigate increased transepidermal water loss after benzoyl peroxide treatment of human skin. Free Radic Biol Med 2003;34:170-176.View Abstract
  • 129.Scuntaro I, Kientsch U, Wiesmann UN, Honegger UE. Inhibition by vitamin E of drug accumulation and of phospholipidosis induced by desipramine and other cationic amphiphilic drugs in human cultured cells. Br J Pharmacol 1996;119:829-834.View Abstract
  • 130.Leonhardt ET. Effect of vitamin E on serum cholesterol and triglycerides in hyperlipidemic patients treated with diet and clofibrate. Am J Clin Nutr 1978;31:100-105.View Abstract
  • 131.Vitamin E Fact Book. VERIS Information Service (Vitamin E Research and Information Service) LaGrange, Ill;1994.
  • 132.Ghosh J, Das S. Role of vitamin A in prevention and treatment of sarcoma 180 in mice. Chemotherapy 1987;33:211-218.View Abstract
  • 133.Vinitha R, Thangaraju M, Sachdanandam P. Effect of administering cyclophosphamide and vitamin E on the levels of tumor-marker enzymes in rats with experimentally induced fibrosarcoma. Jpn J Med Sci Biol 1995;48:145-156.View Abstract
  • 134.Jaakkola K, Lahteenmaki P, Laakso J et al. Treatment with antioxidant and other nutrients in combination with chemotherapy and irradiation in patients with small-cell lung cancer. Anticancer Res 1992;12:599-606.View Abstract
  • 135.Traber MG. Vitamin E in human nutrition: concepts and controversies. American College of Nutrition 44th Annual Meeting. Nashville, Tenn; 2003.
  • 136.Synold TW, Dussault I, Forman BM. The orphan nuclear receptor SXR coordinately regulates drug metabolism and efflux. Nat Med 2001;7:584-590.View Abstract
  • 137.Eberlein-Konig B, Placzek M, Przybilla B. Phototoxic lysis of erythrocytes from humans is reduced after oral intake of ascorbic acid and d-alpha-tocopherol. Photodermatol Photoimmunol Photomed 1997;13:173-177.View Abstract
  • 138.Lores Arnaiz S, Travacio M, Monserrat AJ et al. Chemiluminescence and antioxidant levels during peroxisome proliferation by fenofibrate. Biochim Biophys Acta 1997;1360:222-228.
  • 139.Chaput E, Maubrou-Sanchez D, Bellamy FD, Edgar AD. Fenofibrate protects lipoproteins from lipid peroxidation: synergistic interaction with alpha-tocopherol. Lipids 1999;34:497-502.View Abstract
  • 140.Fetoni AR, Sergi B, Scarano E et al. Protective effects of alpha-tocopherol against gentamicin-induced oto-vestibulo toxicity: an experimental study. Acta Otolaryngol 2003;123:192-197.View Abstract
  • 141.Jin X, Sheng X. Methylcobalamin as antagonist to transient ototoxic action of gentamicin. Acta Otolaryngol 2001;121:351-354.View Abstract
  • 142.Casano RA, Johnson DF, Bykhovskaya Y et al. Inherited susceptibility to aminoglycoside ototoxicity: genetic heterogeneity and clinical implications. Am J Otolaryngol 1999;20:151-156.View Abstract
  • 143.Niedzielska G, Katska E. [Familial occurrence of hearing loss following streptomycin (SM) treatment]. Otolaryngol Pol 2001;55:313-315.View Abstract
  • 144.Tang HY, Hutcheson E, Neill S et al. Genetic susceptibility to aminoglycoside ototoxicity: how many are at risk? Genet Med 2002;4:336-345.
  • 145.Gallo-Teran J, Morales-Angulo C, del Castillo I et al. [Familial susceptibility to aminoglycoside ototoxicity due to the A1555G mutation in the mitochondrial DNA]. Med Clin (Barc) 2003;121:216-218.View Abstract
  • 146.Lashmanova AP, Omel’chenko OG, Akimov VG. [The dynamics of the griseofulvin levels in the blood and skin of guinea pigs during its combined use with alpha-tocopherol]. Vestn Dermatol Venerol 1990:15-16.
  • 147.Anonymous. Vitamin E boosts griseofulvin. Mycol Observer 1990:8.
  • 148.Clemente C, Caruso MG, Berloco P et al. Alpha-tocopherol and beta-carotene serum levels in post-menopausal women treated with transdermal estradiol and oral medroxyprogesterone acetate. Horm Metab Res 1996;28:558-561.View Abstract
  • 149.Inal M, Sunal E, Kanbak G, Zeytinoglu S. Effects of postmenopausal hormone replacement and alpha-tocopherol on the lipid profiles and antioxidant status. Clin Chim Acta 1997;268:21-29.View Abstract
  • 150.Waters DD, Alderman EL, Hsia J et al. Effects of hormone replacement therapy and antioxidant vitamin supplements on coronary atherosclerosis in postmenopausal women: a randomized controlled trial. JAMA 2002;288:2432-2440.View Abstract
  • 151.Schwartz JB. The influence of sex on pharmacokinetics. Clin Pharmacokinet 2003;42:107-121.View Abstract
  • 152.Lee AJ, Kosh JW, Conney AH, Zhu BT. Characterization of the NADPH-dependent metabolism of 17beta-estradiol to multiple metabolites by human liver microsomes and selectively expressed human cytochrome P450 3A4 and 3A5. J Pharmacol Exp Ther 2001;298:420-432.
  • 153.Kliewer SA, Moore JT, Wade L et al. An orphan nuclear receptor activated by pregnanes defines a novel steroid signaling pathway. Cell 1998;92:73-82.View Abstract
  • 153a.Skrha J, Sindelka G, Kvasnicka J, Hilgertova J. Insulin action and fibrinolysis influenced by vitamin E in obese Type 2 diabetes mellitus. Diabetes Res Clin Pract 1999;44(1):
  • 154.Dimery IW, Hong WK, Lee JJ et al. Phase I trial of alpha-tocopherol effects on 13-cis-retinoic acid toxicity. Ann Oncol 1997;8:85-89.View Abstract
  • 155.Salasche SJ, Lebwohl M. Clinical pearl: vitamin E (alpha-tocopherol), 800 IU daily, may reduce retinoid toxicity. J Am Acad Dermatol 1999;41:260.View Abstract
  • 156.Dich J, Zahm SH, Hanberg A, Adami HO. Pesticides and cancer. Cancer Causes Control 1997;8:420-443.View Abstract
  • 157.Podstawka U, Grabarczyk M, Kopec-Szlezak J. Vitamin E protects human leucocytes against toxic effects of lindan in vitro. Mater Med Pol 1991;23:285-289.View Abstract
  • 158.Clark JH, Russell GJ, Fitzgerald JF, Nagamori KE. Serum beta-carotene, retinol, and alpha-tocopherol levels during mineral oil therapy for constipation. Am J Dis Child 1987;141:1210-1212.
  • 159.Diarrhea and constipation. In: Berkow R, Fletcher AJ, Beers MH et al, eds. The Merck Manual of Diagnosis and Therapy. 16th ed. Rahway, NJ: Merck Research Laboratories; 1992:810.
  • 160.Holt GA. Food and Drug Interactions. Chicago: Precept Press; 1998.
  • 161.Tangney CC, Driskell JA. Vitamin E status of young women on combined-type oral contraceptives. Contraception 1978;17:499-512.View Abstract
  • 162.Ciavatti M, Renaud S. Oxidative status and oral contraceptive: its relevance to platelet abnormalities and cardiovascular risk. Free Radic Biol Med 1991;10:325-338.View Abstract
  • 163.Delanian S, Balla-Mekias S, Lefaix JL. Striking regression of chronic radiotherapy damage in a clinical trial of combined pentoxifylline and tocopherol. J Clin Oncol 1999;17:3283-3290.View Abstract
  • 164.Higashi A, Tamari H, Ikeda T et al. Serum vitamin E concentration in patients with severe multiple handicaps treated with anticonvulsants. Pediatr Pharmacol (NY) 1980;1:129-134.View Abstract
  • 165.Higashi A, Ikeda T, Matsukura M, Matsuda I. Serum zinc and vitamin E concentrations in handicapped children treated with anticonvulsants. Dev Pharmacol Ther 1982;5:109-113.View Abstract
  • 166.Birringer M, Drogan D, Brigelius-Flohe R. Tocopherols are metabolized in HepG2 cells by side chain omega-oxidation and consecutive beta-oxidation. Free Radic Biol Med 2001;31:226-232.
  • 167.Dursun SM, Oluboka OJ, Devarajan S, Kutcher SP. High-dose vitamin E plus vitamin B6 treatment of risperidone-related neuroleptic malignant syndrome. J Psychopharmacol 1998;12:220-221.View Abstract
  • 168.Gogu SR, Beckman BS, Rangan SR, Agrawal KC. Increased therapeutic efficacy of zidovudine in combination with vitamin E. Biochem Biophys Res Commun 1989;165:401-407.View Abstract
  • 169.Gogu SR, Lertora JJ, George WJ et al. Protection of zidovudine-induced toxicity against murine erythroid progenitor cells by vitamin E. Exp Hematol 1991;19:649-652.View Abstract
  • 170.Deuchi K, Kanauchi O, Shizukuishi M, Kobayashi E. Continuous and massive intake of chitosan affects mineral and fat-soluble vitamin status in rats fed on a high-fat diet. Biosci Biotechnol Biochem 1995;59:1211-1216.View Abstract
  • 171.Roob JM, Khoschsorur G, Tiran A et al. Vitamin E attenuates oxidative stress induced by intravenous iron in patients on hemodialysis. J Am Soc Nephrol 2000;11:539-549.View Abstract
  • 172.Melhorn DK, Gross S. Relationships between iron-dextran and vitamin E in iron deficiency anemia in children. J Lab Clin Med 1969;74:789-802.
  • 173.Weber P, Bendich A, Machlin LJ. Vitamin E and human health: rationale for determining recommended intake levels. Nutrition 1997;13:450-460.View Abstract
  • 174.Zandi PP, Anthony JC, Khachaturian AS et al. Reduced risk of Alzheimer disease in users of antioxidant vitamin supplements. Arch Neurol 2004;61:82-88.View Abstract
  • 175.Bruno RS, Ramakrishnan R, Montine TJ et al.α-Tocopherol disappearance is faster in cigarette smokers and is inversely related to their ascorbic acid status. Am J Clin Nutr 2005;81:95-103.View Abstract
  • 176.Bruno RS, Leonard SW, Atkinson J et al. Faster plasma vitamin E disappearance in smokers is normalized by vitamin C supplementation. Free Radic Biol Med 2006;40:689-697.View Abstract
  • .[No author listed.] Drug evaluations subscription. Vol II, Section 10. Chicago: American Medical Association; 1994.
  • .[No authors listed.] MRC/BHF Heart Protection Study of cholesterol-lowering therapy and of antioxidant vitamin supplementation in a wide range of patients at increased risk of coronary heart disease death: early safety and efficacy experience. Eur Heart J 1999;20(10):725-741.
  • .Ames BN. DNA damage from micronutrient deficiencies is likely to be a major cause of cancer. Mutat Res 2001;475(1-2):7-20. (Review)
  • .Ames BN. Low micronutrient intake may accelerate the degenerative diseases of aging through allocation of scarce micronutrients by triage. Proc Natl Acad Sci U S A 2006;103:17589-17594.
  • .Anonymous. Vitamin E and cell injury. Nutr Rev 1988;46:1367. (Review)
  • .Arvindakshan M, Ghate M, Ranjekar PK, et al. Supplementation with a combination of omega-3 fatty acids and antioxidants (vitamins E and C) improves the outcome of schizophrenia. Schizophr Res 2003;62(3):195-204.
  • .Ascherio A, Weisskopf MG, O’Reilly EJ, et al. Vitamin E intake and risk of amyotrophic lateral sclerosis. Ann Neurol 2005;57(1):104-110.
  • .Ayres S Jr, Mihan R. Nocturnal leg cramps (systremma): a progress report on response to vitamin E. South Med J 1974;67(11):1308-1312.
  • .Azen SP, Qian D, Mack WJ, et al. Effect of supplementary antioxidant vitamin intake on carotid arterial wall intima-media thickness in a controlled clinical trial of cholesterol lowering. Circulation 1996;94(10):2369-2372.
  • .Baigent C, Keech A, Kearney PM, et al. Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins. Lancet 2005;366(9493):1267-1278. Erratum in Lancet 2005;366(9494):1358.
  • .Bairati I, Meyer F, Gelinas M, et al. A randomized trial of antioxidant vitamins to prevent second primary cancers in head and neck cancer patients. J Natl Cancer Inst 2005;97(7):481-488.
  • .Bardia A, Tleyjeh IJ, Cerhan JR, et al. Does antioxidant supplementation reduce primary cancer incidence and mortality? Systematic review and meta analysis. Abstract A159. American Association for Cancer Research, Frontiers in Cancer Prevention Research meeting. Boston, Nov 13, 2006.
  • .Baum M, Cassetti L, Bonvehi P, et al. Inadequate dietary intake and altered nutrition status in early HIV-1 infection. Nutrition 1994;10(1):16-20.
  • .Bays HE, Dujovne CA. Drug interactions of lipid-altering drugs. Drug Saf 1998;19(5):355-371. (Review)
  • .Bays H, Stein EA. Pharmacotherapy for dyslipidaemia: current therapies and future agents. Expert Opin Pharmacother 2003;4(11):1901-1938.
  • .Behl C, Rupprecht R, Skutella T, et al. Haloperidol-induced cell death: mechanism and protection with vitamin E in vitro. Neuroreport 1995;7(1):360-364.
  • .Berthold HK, Unverdorben S, Ralf Degenhardt R, et al. Effect of policosanol on lipid levels among patients with hypercholesterolemia or combined hyperlipidemia: a randomized controlled trial. JAMA 2006;295:2262-2269.
  • .Beyer RE. The role of ascorbate in antioxidant protection of biomembranes: interaction with vitamin E and coenzyme Q. J Bioenerg Biomembr 1994;26(4):349-358. (Review)
  • .Beyrouty P, Chan HM. Co-consumption of selenium and vitamin E altered the reproductive and developmental toxicity of methylmercury in rats. Neurotoxicol Teratol 2006;28(1):49-58.
  • .Blatt DH, Leonard SW, Traber MG. Vitamin E kinetics and the function of tocopherol regulatory proteins. Nutrition 2001;17(10):799-805. (Review)
  • .Block KI. Why integrative therapies? Integr Cancer Ther 2006;5(1):53-56. (Editorial)
  • .Boshtam M. Vitamin E can reduce blood pressure in mild hypertensives. Abstract 1P-0292. 13th International Symposium on Atherosclerosis. Kyoto, Japan, Sep 29, 2003.
  • .Brown BG, Crowley J. Is there any hope for vitamin E? JAMA 2005;293(11):1387-1390. (Editorial)
  • .Bruno RS, Leonard SW, Atkinson J, et al. Faster plasma vitamin E disappearance in smokers is normalized by vitamin C supplementation. Free Radic Biol Med 2006;40(4):689-697.
  • .Bruno RS, Ramakrishnan R, Montine TJ, et al. alpha-Tocopherol disappearance is faster in cigarette smokers and is inversely related to their ascorbic acid status. Am J Clin Nutr 2005;81(1):95-103.
  • .Buchi KN, Gray PD, Rollins DE, et al. Protection against sodium valproate injury in isolated hepatocytes by alpha-tocopherol and N,N'-diphenyl-p-phenylenediamine. J Clin Pharmacol 1984;24(4):148-154.
  • .Butler EB, McKnight E. Vitamin E in the primary treatment of primary dysmenorrhea. Lancet 1955;268(6869):844-847.
  • .Canfield LM, Giuliano AR, Neilson EM, et al. beta-Carotene in breast milk and serum is increased after a single beta-carotene dose. Am J Clin Nutr 1997;66(1):52-61.
  • .Cao G, Alessio HM, Cutler RG. Oxygen-radical absorbance capacity assay for antioxidants. Free Radic Biol Med 1993;14(3):303-311.
  • .Cario WR. [The use of vitamin E in childhood.] Kinderarztl Prax 1990;58(10):511-7. [German] (Review)
  • .Castano G, Menendez R, Mas R, et al. Effects of policosanol and lovastatin on lipid profile and lipid peroxidation in patients with dyslipidemia associated with type 2 diabetes mellitus. Int J Clin Pharmacol Res 2002;22(3-4):89-99.
  • .Chen L, Haught WH, Yang B, et al. Preservation of endogenous antioxidant activity and inhibition of lipid peroxidation as common mechanisms of antiatherosclerotic effects of vitamin E, lovastatin and amlodipine. J Am Coll Cardiol. 1997;30(2):569-575.
  • .Christen S, Woodall AA, Shigenaga MK, et al. gamma-tocopherol traps mutagenic electrophiles such as NO(X) and complements alpha-tocopherol: physiological implications. Proc Natl Acad Sci U S A 1997;94(7):3217-3222.
  • .Coghlan A. Vitamin E could reduce heart risk. New Scientist 1991;1770:25.
  • .Collins R, Peto R, Armitage J. The MRC/BHF Heart Protection Study: preliminary results. Int J Clin Pract 2002;56(1):53-56.
  • .Corrigan JJ Jr. Coagulation problems relating to vitamin E. Am J Pediatr Hematol Oncol 1979;1(2):169-173.
  • .Coutinho AK, Rocha Lima CM. Metastatic colorectal cancer: systemic treatment in the new millennium. Cancer Control 2003;10(3):224-238. (Review)
  • .Di Cyan E. Vitamin E and aging. New York: Pyramid Books;1972.
  • .Doroshow JH. Redox modulation of chemotherapy-induced tumor cell killing and normal tissue toxicity. J Natl Cancer Inst 2006;98(4):223-225.
  • .Dostal M, Blahova S. Embryotoxicity of cortisone combined with vitamin E. Folia Morphol (Praha) 1986;34(2):132-140.
  • .Eichhorn JC, Lee R, Dunster C, et al. Alpha- and gamma-tocopherol plasma and urinary biokinetics following alpha-tocopherol supplementation. Ann N Y Acad Sci 2004;1031:339-340.
  • .Elinder LS, Hadell K, Johansson J, et al. Probucol treatment decreases serum concentrations of diet-derived antioxidants. Arterioscler Thromb Vasc Biol 1995;15(8):1057-1063.
  • .Ellison, NM. Relationship between vitamin E and cancer: facts, not fancy. Cancer Bull 1985;37(3):112-113.
  • .Ellison, NM, Londer H. Vitamin E and C and their relationship to cancer. In: Newell GR, Ellison NM, eds. Nutrition and cancer: etiology and treatment. New York: Raven Press; 1981.
  • .Engler MM, Engler MB, Malloy MJ, et al. Antioxidant vitamins C and E improve endothelial function in children with hyperlipidemia: Endothelial Assessment of Risk from Lipids in Youth (EARLY) Trial. Circulation 2003;108:1059-1063.
  • .Eranti VS, Gangadhar BN, Janakiramaiah N.  Haloperidol-induced extrapyramidal reaction: lack of protective effect by vitamin E. Psychopharmacology (Berl) 1998;140(4):418-420.
  • .Etminan M, Gill SS, Samii A, et al. Intake of vitamin E, vitamin C, and carotenoids and the risk of Parkinson’s disease: a meta-analysis. Lancet Neuro 2005;4(6):362-365. (Review)
  • .Faloon WW, Paes IC, Woolfolk D, et al. Effect of neomycin and kanamycin upon intestinal absortion. Ann N Y Acad Sci 1966;132(2):879-887.
  • .Faloon WW. Metabolic effects of nonabsorbable antibacterial agents. Am J Clin Nutr 1970;23(5):645-651.
  • .Farmer JA, Gotto AM Jr. Antihyperlipidaemic agents: drug interactions of clinical significance. Drug Saf 1994;11(5):301-309.
  • .Farmer JA, Gotto AM Jr. Choosing the right lipid-regulating agent: a guide to selection. Drugs 1996;52(5):649-661.
  • .Food and Nutrition Board, Institute of Medicine. Vitamin E: dietary reference intakes for vitamin C, vitamin E, selenium, and carotenoids. Washington, DC: National Academy Press; 2000:95-185.
  • .Ford ES, Ajani UA, Mokdad AH. Brief communication: the prevalence of high intake of vitamin E from the use of supplements among U.S. adults. Ann Intern Med 2005;143(2):116-120.
  • .Galan P, Favier A, Preziosi P, et al. [The bank of biological material in the SU.VI.MAX study.] Rev Epidemiol Sante Publique 2003;51(1 Pt 2):147-150. [French]
  • .Gaw A. A new reality: achieving cholesterol-lowering goals in clinical practice. Atheroscler Suppl 2002;2(4):5-11. (Review)
  • .Gent P, Massey K. An overview of chemotherapy-induced peripheral sensory neuropathy, focusing on oxaliplatin. Int J Palliat Nurs 2001;7(7):354-359. (Review)
  • .Getz L, Sigurdsson JA, Hetlevik I, et al. Estimating the high risk group for cardiovascular disease in the Norwegian HUNT 2 population according to the 2003 European guidelines: modelling study. BMJ 2005;331(7516):551.
  • .Gey KF. Vitamins E plus C and interacting conutrients required for optimal health: a critical and constructive review of epidemiology and supplementation data regarding cardiovascular disease and cancer. Biofactors 1998;7(1-2):113-174. (Review)
  • .Gohil K, Godzdanker R, O’Roark E, et al. Alpha-tocopherol transfer protein deficiency in mice causes multi-organ deregulation of gene networks and behavioral deficits with age. Ann N Y Acad Sci 2004;1031:109-126.
  • .Gohil K, Schock BC, Chakraborty AA, et al. Gene expression profile of oxidant stress and neurodegeneration in transgenic mice deficient in alpha-tocopherol transfer protein. Free Radic Biol Med 2003;35(11):1343-1354.
  • .Gouni-Berthold I, Berthold HK. Policosanol: clinical pharmacology and therapeutic significance of a new lipid-lowering agent. Am Heart J 2002;143(2):356-365. (Review)
  • .Graf WD, Oleinik OE, Glauser TA, et al. Altered antioxidant enzyme activities in children with a serious adverse experience related to valproic acid therapy. Neuropediatrics 1998;29(4):195-201.
  • .Greenberg ER. Vitamin E supplements: good in theory, but is the theory good? Ann Intern Med 2005;142(1):75-76. (Editorial)
  • .Guallar E, Hanley DF, Miller ER III. An editorial update: annus horribilis for vitamin E. Ann Intern Med 2005;143(2):143-145. (Editorial)
  • .Gueguen S, Leroy P, Gueguen R, et al. Genetic and environmental contributions to serum retinol and alpha-tocopherol concentrations: the Stanislas Family Study. Am J Clin Nutr 2005;81(5):1034-1044.
  • .Haeger K. Long-term study of alpha-tocopherol in intermittent claudication. Ann N Y Acad Sci 1982;393:369-375.
  • .Haeger K. Long-time treatment of intermittent claudication with vitamin E. Am J Clin Nutr 1974;27(10):1179-1181.
  • .Hahn T, Szabo L, Gold M, et al. Dietary administration of the proapoptotic vitamin E analogue alpha-tocopheryloxyacetic acid inhibits metastatic murine breast cancer. Cancer Res 2006;66(19):9374-9378.
  • .Hak AE, Stampfer MJ, Campos H, et al. Plasma carotenoids and tocopherols and risk of myocardial infarction in a low-risk population of US male physicians. Circulation 2003;108:802-807.
  • .Halvorsen BL, Carlsen MH, Phillips KM, et al. Content of redox-active compounds (ie, antioxidants) in foods consumed in the United States. Am J Clin Nutr 2006;84:95-135.
  • .Hathcock JN, Azzi A, Blumberg J, et al. Vitamins E and C are safe across a broad range of intakes. Am J Clin Nutr 2005;81(4):736-745. (Review)
  • .Hardison WG, Rosenberg IH.  The effect of neomycin on bile salt metabolism and fat digestion in man. J Lab Clin Med 1969;74(4):564-573.
  • .Hathcock JN. Metabolic mechanisms of drug-nutrient interactions. Fed Proc 1985;44(1 Pt 1):124-129. (Review)
  • .Helzlsouer KJ, Huang HY, Alberg AJ, et al. Association between alpha-tocopherol, gamma-tocopherol, selenium, and subsequent prostate cancer. J Natl Cancer Inst 2000;92(24):2018-2023.
  • .Henquin N, Havivi E, Reshef A, et al. Nutritional monitoring and counselling for cancer patients during chemotherapy. Oncology 1989;46(3):173-177.
  • .Hercberg S, Bertrais S, Czernichow S, et al. Alterations of the lipid profile after 7.5 years of low-dose antioxidant supplementation in the SU.VI.MAX Study. Lipids 2005;40(4):335-342.
  • .Hercberg S, Galan P, Preziosi P, et al. The SU.VI.MAX Study: a randomized, placebo-controlled trial of the health effects of antioxidant vitamins and minerals. Arch Intern Med 2004;164:2335-2342.
  • .Hercberg S, Preziosi P, Briancon S, et al. A primary prevention trial using nutritional doses of antioxidant vitamins and minerals in cardiovascular diseases and cancers in a general population: the SU.VI.MAX study: design, methods, and participant characteristics: SUpplementation en VItamines et Mineraux AntioXydants. Control Clin Trials 1998;19(4):336-351.
  • .Hercberg S, Preziosi P, Galan P, et al. “The SU.VI.MAX Study”: a primary prevention trial using nutritional doses of antioxidant vitamins and minerals in cardiovascular diseases and cancers: SUpplementation on VItamines et Mineraux AntioXydants. Food Chem Toxicol 1999;37(9-10):925-930.
  • .Hill FW. An investigation of the effects of oral neomycin on intestinal absorption and serum cholesterol levels in the dog. Br Vet J 1973;129(4):337-344.
  • .Hodkova M, Dusilova-Sulkova S, Kalousova M, et al. Influence of oral vitamin E therapy on micro-inflammation and cardiovascular disease markers in chronic hemodialysis patients. Ren Fail 2006;28(5):395-399.
  • .Hoffer A. The true cost of cynicism. J Orthomol Med 1992;7(4).
  • .Holbrook AM, Pereira JA, Labiris R, et al. Systematic overview of warfarin and its drug and food interactions. Arch Intern Med 2005;165;1095-1106.
  • .Horwitt MK, Harvey CC, Dahm CH Jr. Relationship between levels of blood lipids, vitamins C, A, and E, serum copper compounds, and urinary excretions of tryptophan metabolites in women taking oral contraceptive therapy. Am J Clin Nutr 1975;28(4):403-412.
  • .Jiang Q, Christen S, Shigenaga MK, et al. gamma-tocopherol, the major form of vitamin E in the US diet, deserves more attention. Am J Clin Nutr 2001;74(6):714-722.
  • .Jurima-Romet M, Abbott FS, Tang W, et al. Cytotoxicity of unsaturated metabolites of valproic acid and protection by vitamins C and E in glutathione-depleted rat hepatocytes. Toxicology 1996;112(1):69-85.
  • .Kaempf-Rotzoll DE, Traber MG, Arai H. Vitamin E and transfer proteins. Curr Opin Lipidol 2003;14(3):249-254. (Review)
  • .Kang JH, Cook N, Manson J, et al. A randomized trial of vitamin E supplementation and cognitive function in women. Arch Intern Med 2006;166:2462-2468.
  • .Kelly FJ, Lee R, Mudway IS. Inter- and intra-individual vitamin E uptake in healthy subjects is highly repeatable across a wide supplementation dose range. Ann N Y Acad Sci 2004;1031:22-39.
  • .Kelly G. The interaction of cigarette smoking and antioxidants: part II: alpha-tocopherol. Altern Med Rev 2002;7(6): 500-511. (Review)
  • .Kendall MJ, Chan K. Drug-induced malabsorption. Xenobiotica 1973;3(11):727-744. (Review)
  • .Kerwin RW, Mancama DT, Arranz MJ. Genetic strategies for the personalization of antipsychotic treatment. Expert Rev Mol Diagn 2001;1(3):275-280. (Review)
  • .Khanna S, Roy S, Slivka A, et al. Neuroprotective properties of the natural vitamin E alpha-tocotrienol. Stroke 2005;36(10):2258-2264.
  • .Khosla P, Patel V, Whinter JM, et al. Postprandial levels of the natural vitamin E tocotrienol in human circulation. Antioxid Redox Signal 2006;8(5-6):1059-1068.
  • .Kirsh VA, Hayes RB, Mayne ST, et al. Supplemental and dietary vitamin E, beta-carotene, and vitamin C intakes and prostate cancer risk. J Natl Cancer Inst 2006;98(4):245-524.
  • .Klein EA, Thompson IM, Lippman SM, et al. SELECT: the next prostate cancer prevention trial: Selenum and Vitamin E Cancer Prevention Trial. J Urol 2001;166(4):1311-1315.
  • .Kliewer SA. The nuclear pregnane X receptor regulates xenobiotic detoxification. J Nutr 2003;133(7 Suppl):2444S-2447S.
  • .Knekt P, Ritz J, Pereira MA, et al. Antioxidant vitamins and coronary heart disease risk: a pooled analysis of 9 cohorts. Am J Clin Nutr 2004;80(6):1508-1520.
  • .Koehler CM, Beverly KN, Leverich EP. Redox pathways of the mitochondrion. Antioxid Redox Signal 2006;8(5-6):813-822. (Review)
  • .Komiyama K, Iizuka K, Yamaoka M, et al. Studies on the biological activity of tocotrienols. Chem Pharm Bull (Tokyo) 1989;37(5):1369-1371.
  • .Kong Q, Lillehei KO. Antioxidant inhibitors for cancer therapy. Med Hypotheses 1998;51(5):405-409.
  • .Kryzhanovskii GN, Shandra AA. [Effect of diazepam, carbamazepine, sodium valproate and their combinations with vitamin preparations on epileptic activity.] Biull Eksp Biol Med 1985;100(11):545-547. [Russian]
  • .Labriola D, Livingston R. Possible interactions between dietary antioxidants and chemotherapy. Oncology (Huntingt) 1999;13(7):1003-1008; discussion 1008,1011-1012.
  • .Lamson DW, Brignall MS. Antioxidants in cancer therapy; their actions and interactions with oncologic therapies. Altern Med Rev 1999;4:304-329. (Review)
  • .Lee I-M, Cook NR, Gaziano Jl, et al. Vitamin E in the primary prevention of cardiovascular disease and cancer: The Women’s Health Study: a randomized controlled trial. JAMA 2005;294:56-65.
  • .Leichtle A, Teupser D, Thiery J. Alpha-tocopherol distribution in lipoproteins and anti-inflammatory effects differ between CHD-patients and healthy subjects. J Am Coll Nutr 2006;25(5):420-428.
  • .Leonard JP, Desager JP, Beckers C, et al. In vitro binding of various biological substances by two hypocholesterolaemic resins: cholestyramine and colestipol. Arzneimittelforschung 1979;29(7):979-981.
  • .Leonard SW, Good CK, Gugger ET, et al. Vitamin E bioavailability from fortified breakfast cereal is greater than that from encapsulated supplements. Am J Clin Nutr 2004;79(1):86-92.
  • .Leshchenko VM, Omel’chenko OG, Poliakova IIa, et al. [Treatment of patients with zooanthroponotic microsporosis with griseofulvin in combination with alpha-tocopherol.] Vestn Dermatol Venerol 1988;(12):24-26. [Russian]
  • .Levy AP, Friedenberg P, Lotan R, et al. The effect of vitamin therapy on the progression of coronary artery atherosclerosis varies by haptoglobin type in postmenopausal women. Diabetes Care 2004;27(4):925-930.
  • .Li D, Saldeen T, Mehta JL. Gamma-tocopherol decreases ox-LDL-mediated activation of nuclear factor-kappaB and apoptosis in human coronary artery endothelial cells. Biochem Biophys Res Commun 1999;259(1):157-161.
  • .Lindheimer MD, Sibai BM. Antioxidant supplementation in pre-eclampsia. Lancet. Published online March 30, 2006;367(9517):1119-1120. (Editorial)
  • .Lippman SM, Goodman PJ, Klein EA, et al. Designing the Selenium and Vitamin E Cancer Prevention Trial (SELECT). J Natl Cancer Inst 2005;97(2):94-102.
  • .Lodge JK. Vitamin E bioavailability in humans. J Plant Physiol 2005;162(7):790-796. (Review)
  • .Lonn E, Yusuf S, Hoogwerf B, et al. Effects of vitamin E on cardiovascular and microvascular outcomes in high-risk patients with diabetes: results of the HOPE study and MICRO-HOPE substudy. Diabetes Care 2002;25(11):1919-1927.
  • .Lonn E. Clinical trial update III: Extended follow-up of the vitamin E component of the Heart Outcomes Prevention Evaluation (HOPE-TOO). European Society of Cardiology Congress 2003. Vienna, Austria, Sep 4, 2003.
  • .Machtey I, Ouaknine L. Tocopherol in osteoarthritis: a controlled pilot study. J Am Geriatr Soc 1978;26(7):328-330.
  • .Malafa MP, Fokum FD, Andoh J, et al. Vitamin E succinate suppresses prostate tumor growth by inducing apoptosis. Int J Cancer 2005. [Epub ahead of print.]
  • .Mann JF, Yi QL, Sleight P, et al. New trial data on prevention: potassium and CV risk in hope. Pacing Clin Electrophysiol 2003;26(7 Pt 1):1565.
  • .Mantovani G, Maccio A, Madeddu C, et al. A phase II study with antioxidants, both in the diet and supplemented, pharmaconutritional support, progestagen, and anti-cyclooxygenase-2 showing efficacy and safety in patients with cancer-related anorexia/cachexia and oxidative stress. Cancer Epidemiol Biomarkers Prev 2006;15(5):1030-1034.
  • .Marz R. Medical nutrition from Marz. 2nd ed. Portland, OR: Omni Press; 1997. (Review)
  • .Meyer F, Galan P, Douville P, et al. Antioxidant vitamin and mineral supplementation and prostate cancer prevention in the SU.VI.MAX trial. Int J Cancer 2005;116(2):182-186.
  • .Miller ER III, Pastor-Barriuso R, Dalal D, et al. Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality. Ann Intern Med 2005;142(1):37-46. (Meta-analysis)
  • .Montonen J, Knekt P, Jarvinen R, et al. Dietary antioxidant intake and risk of type 2 diabetes. Diabetes CareĀ  2004;27(2):362-366.
  • .Montine TJ, Morrow J.D. Fatty acid oxidation in the pathogenesis of Alzheimer’s disease. Am J Pathol 2005;166(5):1283-1289.
  • .Morris MC, Evans DA, Tangney CC, et al. Associations of vegetable and fruit consumption with age-related cognitive change. Neurology 2006;67:1370-1376.
  • .Morris MC, Evans DA, Tangney CC, et al. Relation of the tocopherol forms to incident Alzheimer disease and to cognitive change. Am J Clin Nutr 2005;81(2):508-514.
  • .Moss RW. Should patients undergoing chemotherapy and radiotherapy be prescribed antioxidants? Integr Cancer Ther 2006;5(1):3-6.
  • .Nurge ME, Anderson CR, Bates E. Metabolic and nutritional implications of valproic acid. Nutr Res 1991;11:949-960.
  • .Odeleye OE, Watson RR. The potential role of vitamin E in the treatment of immunologic abnormalities during acquired immune deficiency syndrome. Prog Food Nutr Sci 1991;15(1-2):1-19. (Review)
  • .Okamoto K, Ogura R. Effects of vitamins on lipid peroxidation and suppression of DNA synthesis induced by adriamycin in Ehrlich cells. J Nutr Sci Vitaminol (Tokyo) 1985;31(2):129-137.
  • .Omel’chenko OG. [Dynamics of the concentration of griseofulvin in the blood and urine when used jointly with alpha-tocopherol.] Vestn Dermatol Venerol 1987;(8):12-15. [Russian]
  • .Ozdemir V, Basile VS, Masellis M, et al. Pharmacogenetic assessment of antipsychotic-induced movement disorders: contribution of the dopamine D3 receptor and cytochrome P450 1A2 genes. J Biochem Biophys Methods 2001;47(1-2):151-157.
  • .Packer L. Interactions among antioxidants in health and disease: vitamin E and its redox cycle. Proc Soc Exp Biol Med 1992;200(2):271-276. (Review)
  • .Palan PR, Magneson AT, Castillo M, et al. Effects of menstrual cycle and oral contraceptive use on serum levels of lipid-soluble antioxidants. Am J Obstet Gynecol 2006;194(5):e35-e38.
  • .Poston L, Briley AL, Seed PT, et al. Vitamin C and vitamin E in pregnant women at risk for pre-eclampsia (VIP trial): randomized placebo-controlled trial. Lancet 2006;367:1145-1154.
  • .Poston L, Raijmakers M, Kelly F. Vitamin E in preeclampsia. Ann N Y Acad Sci 2004;1031:242-248. (Review)
  • .Prasad KN, Edwards-Prasad J, Ramanujam S, et al. Vitamin E increases the growth inhibitory and differentiating effects of tumor therapeutic agents on neuroblastoma and glioma cells in culture. Proc Soc Exp Biol Med 1980;164(2):158-163.
  • .Raju GB, Behari M, Prasad K, et al. Randomized, double-blind, placebo-controlled, clinical trial of D-alpha-tocopherol (vitamin E) as add-on therapy in uncontrolled epilepsy. Epilepsia 1994;35(2):368-732.
  • .Rapola JM, Virtamo J, Ripatti S, et al. Randomised trial of alpha-tocopherol and beta-carotene supplements on incidence of major coronary events in men with previous myocardial infarction. Lancet 1997;349(9067):1715-1720.
  • .Ratnaike RN, Jones TE. Mechanisms of drug-induced diarrhoea in the elderly. Drugs Aging 1998;13(3):245-253.
  • .Ravnskov U, Rosch PJ, Sutter MC, et al. Should we lower cholesterol as much as possible? BMJ 2006;332(7553):1330-1332. (Letter)
  • .Reboul E, Richelle M, Perrot E, et al. Bioaccessibility of carotenoids and vitamin E from their main dietary sources. J Agric Food Chem 2006;54(23):8749-8755.
  • .Redberg RF. Vitamin E and cardiovascular health: does sex matter? JAMA 2005;294(1):107-109.
  • .Robinson C, Weigly E. Basic nutrition and diet therapy. New York: Macmillan; 1984.
  • .Roe DA. Diet and drug interactions. New York: Van Nostrand Reinhold; 1989.
  • .Roe DA. Drug-induced nutritional deficiencies. 2nd ed. Westport, CT: Avi Publishing; 1985:158-159.
  • .Roe DA. Essential hyperlipemia with xanthomatosis: effects of cholestyramine and clofibrate. Arch Dermatol 1968;97(4):436-445.
  • .Roe DA. Risk factors in drug-induced nutritional deficiencies. In: Roe DA, Campbell T, eds. Drugs and nutrients: the interactive effects. New York: Marcel Decker; 1984:505-523.
  • .Salignik R, et al. Avoiding vitamins A and E may improve cancer therapy. 39th Annual Meeting of the American Society for Cell Biology: Washington, DC, Dec 11, 1999.
  • .Samman S, Sivarajah G, Man JC, et al. A mixed fruit and vegetable concentrate increases plasma antioxidant vitamins and folate and lowers plasma homocysteine in men. J Nutr 2003;133(7):2188-2193.
  • .Scarmeas N, Stern Y, Mayeux R, et al. Mediterranean diet, Alzheimer disease, and vascular mediation. Arch Neurol 2006;10.1001/archneur.63.12.noc60109.
  • .Scarmeas N, Stern Y, Tang MX, et al. Mediterranean diet and risk for Alzheimer’s disease. Ann Neurol 2006;59(6):912-921.
  • .Sen CK, Khanna S, Roy S. Tocotrienols: vitamin E beyond tocopherols. Life Sci 2006;78(18):2088-2098. (Review)
  • .Shute W, Shute E. Alpha tocopherol in cardiovascular disease. London, Ontario: The Shute Institute; 1954.
  • .Shute W, Shute E. The heart and vitamin E. London, Ontario: The Shute Institute; 1956.
  • .Shute WE, Taub HJ. Vitamin E for ailing and healthy hearts. New York: Pyramid House; 1969.
  • .Simon E, Gariepy J, Cogny A, et al. Erythrocyte, but not plasma, vitamin E concentration is associated with carotid intima-media thickening in asymptomatic men at risk for cardiovascular disease. Atherosclerosis 2001;159(1):193-200.
  • .Sokol RI, et al. Improvement of cyclosporine absorption in children after liver transplantation by means of water-soluble vitamin E. Lancet 1991;338:212-215.
  • .Steffen LM. Eat your fruit and vegetables. Lancet 2006;367:278-279. (Editorial)
  • .Steffen LM, Folsom AR, Cushman M, et al. Greater fish, fruit, and vegetable intakes are related to lower incidence of venous thromboembolism. the longitudinal investigation of thromboembolism etiology. Circulation 2006. Epub. December 18, 2006. 10.1161/CIRCULATIONAHA.106.641688.
  • .Steffen LM, Kroenke CH, Yu X, et al. Associations of plant food, dairy product, and meat intakes with 15-y incidence of elevated blood pressure in young black and white adults: the Coronary Artery Risk Development in Young Adults (CARDIA) Study. Am J Clin Nutr 2005;82:1169-1177.
  • .Stephens NG, Parsons A, Schofield PM, et al. Randomised controlled trial of vitamin E in patients with coronary disease: Cambridge Heart Antioxidant Study (CHAOS). Lancet 1996;347(9004):781-786.
  • .Sullivan C, Capaldi N, Mack G, et al. Seizures and natural vitamin E. Med J Austr 1990;152(11):613-614 (Letter)
  • .Synold TW, Dussault I, Forman BM. The orphan nuclear receptor SXR coordinately regulates drug metabolism and efflux. Nat Med 2001;7(5):584-590.
  • .Tabatabaei AR, Abbott FS. Assessing the mechanism of metabolism-dependent valproic acid-induced in vitro cytotoxicity. Chem Res Toxicol 1999;12(4):323-330.
  • .Taylor PR, Qiao YL, Abnet CC, et al. Prospective study of serum vitamin E levels and esophageal and gastric cancers. J Natl Cancer Inst 2003;95(18):1414-1416.
  • .Teicher BA, et al. In vivo modulation of several anticancer agents by beta-carotene. Cancer Chemother Pharmacol 1994;34(3):235-241.
  • .Traber MG. Does vitamin E decrease heart attack risk? Summary and implications with respect to dietary recommendations. J Nutr 2001;131(2):395S-397S.
  • .Traber MG. The ABCs of vitamin E and beta-carotene absorption. Am J Clin Nutr 2004;80(1):3-4. (Review)
  • .Traber MG. Utilization of vitamin E. Biofactors 1999;10(2-3):115-120.
  • .Traber MG. Vitamin E, nuclear receptors and xenobiotic metabolism. Arch Biochem Biophys 2004;423(1):6-11. (Review)
  • .Traber MG, Elsner A, Brigelius-Flohe R. Synthetic as compared with natural vitamin E is preferentially excreted as alpha-CEHC in human urine: studies using deuterated alpha-tocopheryl acetates. FEBS Lett 1998;437(1-2):145-148.
  • .Traber MG, Winklhofer-Roob BM, Roob JM, et al. Vitamin E kinetics in smokers and nonsmokers. Free Radic Biol Med 2001;31(11):1368-1374.
  • .Trovato A, Nuhlicek DN, Midtling JE. Drug-nutrient interactions. Am Fam Physician 1991;44(5):1651-1658.(Review)
  • .Tsang RC, Roginsky MS, Mellies MJ, et al. Plasma 25-hydroxy-vitamin D in familial hypercholesterolemic children receiving colestipol resin. Pediatr Res 1978;12(10):980-982.
  • .Vazquez Martinez C, Galan P, Preziosi P, et al. [The SUVIMAX (France) study: the role of antioxidants in the prevention of cancer and cardiovascular disorders.] Rev Esp Salud Publica 1998;72(3):173-183. [Spanish]
  • .Veldink JH, Kalmijn S, Groeneveld G-J, et al. Intake of polyunsaturated fatty acids and vitamin E reduce the risk of developing ALS. J Neurol Neurosurg Psychiatry. Published online first. April 28, 2006. doi:10.1136/jnnp.2005.083378.
  • .VERIS. A comparison of natural and synthetic vitamin E: research summary. VERIS Research Information Service: 1999.
  • .Wang X, Thomas B, Sachdeva R, et al. Mechanism of arylating quinone toxicity involving Michael adduct formation and induction of endoplasmic reticulum stress. PNAS 2006;10.1073/pnas.0510962103.
  • .Watkins DW, Khalafi R, Cassidy MM, et al. Alterations in calcium, magnesium, iron, and zinc metabolism by dietary cholestyramine. Dig Dis Sci 1985;30(5):477-482.
  • .Weber T, Lu M, Andera L, et al. Vitamin E succinate is a potent novel antineoplastic agent with high selectivity and cooperativity with tumor necrosis factor-related apoptosis-inducing ligand (Apo2 ligand) in vivo. Clin Cancer Res 2002;8(3):863-869.
  • .Weijl NI, Hopman GD, Wipkink-Bakker A, et al. Cisplatin combination chemotherapy induces a fall in plasma antioxidants of cancer patients. Ann Oncol 1998;9(12):1331-1337.
  • .Weinstein SJ, Wright ME, Pietinen P, et al. Serum alpha-tocopherol and gamma-tocopherol in relation to prostate cancer risk in a prospective study. J Natl Cancer Inst 2005;97:396-399. 
  • .Werbach MR. Foundations of nutritional medicine. Tarzana, CA: Third Line Press; 1997. (Review)
  • .Whitworth A. Micronutrients: to supplement, or not to supplement? J Natl Cancer Inst 2006;98(4):230-232. (Editorial)
  • .Wiehl W, Hart LL. Vitamin E as an anticonvulsant. DICP 1991;25(4):362-363. (Review)
  • .Wood LA. Possible prevention of Adriamycin-induced alopecia by tocopherol. N Engl J Med 1985;312:1060. (Letter)
  • .Yoshikawa S, Morinobu T, Hamamura K, et al. The effect of gamma-tocopherol administration on alpha-tocopherol levels and metabolism in humans. Eur J Clin Nutr 2005;59(8):900-905.
  • .Yusuf S, Sleight P, Pogue J, et al. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients: the Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med 2000;342(3):145-153. Erratum in N Engl J Med 2000;342(18):1376; N Engl J Med 2000;342(10):748.
  • .Zhang XY, Zhou DF, Cao LY, et al. The effect of vitamin E treatment on tardive dyskinesia and blood superoxide dismutase: a double-blind placebo-controlled trial. J Clin Psychopharmacol 2004;24(1):83-86.
  • .Ziaei S, Zakeri M, Kazemnejad A. A randomised controlled trial of vitamin E in the treatment of primary dysmenorrhoea. BJOG 2005;112(4):466-469.
  • .Zoler ML. Supplemental vitamin E linked to heart failure. Fam Pract News 2003;33(19):28.