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Vitamin E -- Main Page

Jump To Misleading Article About Vitamin E used for heart patients

Jump to Article showing Vitamin E reduced artery blockage

Jump to another article about Vitamin E

Vitamin E --- How Much Is Enough

There is 705 International Units of Vitamin E in the Life Glow formula.  There is a similar quantity when you take the full 30 capsule dose of Super Life Glow.

There have been claims that much more than this can be toxic.  I disagree with those who say that.  There is plenty of evidence that doses up to 100,000 IU per day have been very effective in preventing heart disease.

Claims of toxicity often trace back to liquid Vitamin E injections -- often in babies.

I've listed, below, a series of 20 scientific studies on this general subject. These studies were the first 20 out of several hundred when I used the search phrase:  "vitamin E toxicity."  So, I was NOT looking for articles that were likely to be favorable to Vitamin E.  See how much criticism you can find here of large doses of Vitamin  E!  In fact, most of the studies which mention Vitamin E are very favorable as to its treatment to prevent cancer.  There are even studies which comment on the low toxicity of Vitamin E.  The two studies which follow the party line claim that you can get all the Vitamins you need from food.  If you believe that you are on the wrong web site!

Here is a good explanation of Vitamin E, on a different page.

Below, still on this page are various articles and studies concerning Vitamin E.

Let me know what YOU think.

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HealthGate Documents

Record 1 from database: MEDLINE
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Title

Safety of antioxidant vitamins and beta-carotene.

Author

Diplock AT

Address

Division of Biochemistry and Molecular Biology, United Medical School, Guy's Hospital, University of London, United Kingdom.

Source

Am J Clin Nutr, 1995 Dec, 62:6 Suppl, 1510S-1516S

Abstract

Epidemiologic evidence links high antioxidant status with low risk of degenerative disease. Optimal intakes of antioxidants may not be achievable by diet alone; supplements may be taken, particularly in subgroups of the population at high risk. It is thus necessary to ensure that antioxidant supplements are safe and free from side effects. The toxicity of vitamin E is low; no mutagenic, teratogenic, or carcinogenic effects are known and in double-blind studies in which large amounts of vitamin E were used in humans, no side effects occurred. High concentrations are contraindicated in subjects with vitamin K-associated blood coagulation disorders, and the toxicity in normal subjects ingesting large amounts of vitamin E over long periods requires additional investigation. Toxicity of beta-carotene also is low. Evidence from human toxicity trials is not available but there is much circumstantial evidence that 15-50 mg/d is without side effects except for hypercarotenemia in some subjects at high intakes. The findings of more lung cancer in subjects who smoked and who were given 20 mg beta-carotene/d than in those given a placebo could be influenced by the cancer being well advanced before beta-carotene administration. Massive anecdotal evidence exists that vitamin C (at > or = 1 g/d) is safe. Exhaustive literature searches have failed to reveal a controlled study of vitamin C toxicity in human subjects. Anxiety exists about oxalate stone formation, uricosuria, vitamin B-12 destruction, mutagenicity, and iron overload, but the consensus is that adverse effects do not occur in healthy subjects ingesting large amounts of vitamin C.

Language of Publication

English

Unique Identifier

96094709

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MeSH Heading (Major)

Antioxidants|*AE; Ascorbic Acid|*AE; Carotene|*AE; Vitamin E|*AE

MeSH Heading

Human

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9165

Country of Publication

UNITED STATES

Record 2 from database: MEDLINE
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Title

Chemoprevention of oral cancer: beta-carotene and vitamin E in leukoplakia.

Author

Garewal H

Address

Section of Hematology-Oncology, University of Arizona, Tucson.

Source

Eur J Cancer Prev, 1994 Mar, 3:2, 101-7

Abstract

The most definitive and direct way to show that a putative chemoprevention agent actually prevents cancer would be to demonstrate a reduction in cancer incidence in a clinical trial. From a practical standpoint this approach is not feasible for most cancers. Therefore, it becomes necessary to draw conclusions on chemopreventive activity through consideration of indirect lines of evidence, one of which is activity in premalignant lesions such as leukoplakia. As a corollary, it must be emphasized that the goal of undertaking chemoprevention trials in oral leukoplakia is to develop approaches for the prevention of oral cancer. Because the risk of cancer in the usual leukoplakia lesion is low, only non-toxic agents should be tested in this setting and they should be suited for eventual use in a prevention setting. Beta-carotene and vitamin E, unlike the retinoids, fulfill the criteria for a suitable chemopreventive agent and several lines of evidence point to a preventive role for them against oral cancer. These include laboratory in vitro and animal model findings, but the strongest evidence comes from epidemiologic studies which uniformly suggest protection by beta-carotene against head and neck cancer. Much like the retinoids, but without toxicity, beta-carotene and vitamin E can produce regression of oral leukoplakia, a premalignant lesion for oral cancer, as has now been shown in eight clinical trials, five with beta-carotene alone, one with vitamin E alone and two that used these agents as part of combinations.(ABSTRACT TRUNCATED AT 250 WORDS)

Language of Publication

English

Unique Identifier

94290282

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MeSH Heading (Major)

Carotene|AD/*TU; Leukoplakia, Oral|*PC; Mouth Neoplasms|*PC; Vitamin E|AD/*TU

MeSH Heading

Animal; Clinical Trials; Drug Combinations; Human; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0959-8278

Country of Publication

ENGLAND

Record 3 from database: MEDLINE
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Title

Vitamin E in the genesis and prevention of cancer. A review.

Author

Das S

Address

Department of Experimental Leukaemia, Chittaranjan National Cancer Institute, Calcutta, India.

Source

Acta Oncol, 1994, 33:6, 615-9

Abstract

A review of current literature reveals that the relationships between vitamin E and cancer is not yet fully understood though many experimental and clinical studies have shown that vitamin E can protect against carcinogenesis and tumour growth. This vitamin also appears to reduce toxicity of several anticancer therapies. Such effects are probably due to the antioxidant property and immunomodulatory function of vitamin E. The findings of different groups suggest that this vitamin may be helpful as a cancer chemopreventive agent.

Language of Publication

English

Unique Identifier

95033327

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MeSH Heading (Major)

Anticarcinogenic Agents|*PD; Neoplasms|*PC; Vitamin E|*PD

MeSH Heading

Animal; Antioxidants; Human; Immunity|DE

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0284-186X

Country of Publication

NORWAY

Record 4 from database: MEDLINE
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Title

Antioxidants in oral cancer prevention.

Author

Garewal H

Address

University of Arizona Medical Center, Tucson, USA.

Source

Am J Clin Nutr, 1995 Dec, 62:6 Suppl, 1410S-1416S

Abstract

I present evidence in support of a chemopreventive role for the so-called antioxidant nutrients, beta-carotene and vitamin E, against oral cavity cancer. This evidence is from laboratory studies, animal model systems, epidemiologic surveys, intervention trials involving reversal of premalignant changes, and prevention of malignancies in particularly high-risk subjects. Because agents proposed for disease prevention are meant to be used widely without close medical supervision, almost any toxicity is unacceptable. beta-Carotene and vitamin E fulfill this criterion for a suitable chemopreventive agent. In several epidemiologic studies, low intakes of vitamin E, carotenoids, or both have been associated with a higher cancer risk. Smoking, a major risk factor, results in lower beta-carotene concentrations in plasma and oral mucosal cells. In several laboratory and animal model systems, beta-carotene and other antioxidant nutrients are inhibitors of oral cavity carcinogenesis. beta-Carotene and vitamin E can produce clinical regression of oral leukoplakia, a premalignant lesion for oral cancer. The design and limitations of such studies in oral leukoplakia are discussed. Cancer incidence reduction trials in high-risk groups have targeted prevention of second malignancies in patients cured of a primary oral cancer. These trials are in progress. The data thus far are supportive of a significant preventive role for these nutrients in oral cancer.

Language of Publication

English

Unique Identifier

96094696

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MeSH Heading (Major)

Antioxidants|*AD; Carotene|*AD; Mouth Neoplasms|*PC; Vitamin E|*AD

MeSH Heading

Animal; Human; Leukoplakia, Oral|PC

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0002-9165

Country of Publication

UNITED STATES

Record 5 from database: MEDLINE
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Title

Small bowel intussusception and brown bowel syndrome in association with severe malnutrition.

Author

Drake WM; Winter TA; Price SK; OKeefe SJ

Address

Department of Gasiroenterology, Groote Schuur Hospital, University of Cape Town, Observatory, South Africa.

Source

Am J Gastroenterol, 1996 Jul, 91:7, 1450-2

Abstract

Brown bowel syndrome is a rare condition characterized by deposition of lipofuscin in the smooth muscle cells of the gastrointestinal tract. The number of reported cases is small, but all are associated with malabsorptive states. Despite these small numbers, there is considerable evidence that vitamin E deficiency is important etiologically. We report here the case of a severely malnourished [body mass index 11.7 kg/m (2): normal range 20-25 kg/m (2)] 31-yr-old black male with a longstanding history of alcohol abuse, who was on anti-tuberculosis therapy. The patient presented with an acute abdomen and was found, at operation, to have a mid-ileal intussusception. Histological examination of the resected specimen demonstrated lipofuscin accumulation consistent with brown bowel syndrome, but no tumor. Subsequent investigations revealed no significant quantities of vitamin E in the blood and pancreatic steatorrhea. However, deficiency of other fat-soluble (vitamin A and D) and water-soluble vitamins (vitamin C and thiamine) also were detected. This report supports the association of brown bowel syndrome with vitamin E deficiency but cannot exclude the compounding effects of protein calorie malnutrition, multiple vitamin deficiencies, and chronic alcohol toxicity.

Language of Publication

English

Unique Identifier

96280524

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MeSH Heading (Major)

Ileal Diseases|DI/*ET/SU; Intussusception|DI/*ET/SU; Lipofuscin|*ME; Malabsorption Syndromes|*CO/DI; Nutrition Disorders|*CO/DI

MeSH Heading

Abdomen, Acute|DI/ET/SU; Adult; Alcoholism|CO; Case Report; Human; Male; Vitamin E Deficiency|CO/DI

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW OF REPORTED CASES

ISSN

0002-9270

Country of Publication

UNITED STATES

Record 6 from database: MEDLINE
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Title

Vitamin supplementation therapy in the elderly.

Author

Thurman JE; Mooradian AD

Address

Department of Internal Medicine, St Louis University Medical School, Missouri, USA.

Source

Drugs Aging, 1997 Dec, 11:6, 433-49

Abstract

Vitamin supplementation in large dosages is increasingly common in the older population. Often, such supplementation is used in an attempt to improve an individual's health status. There have been claims that the effects of vitamins halt the normal aging process or prevent and cure disease. However, several recent studies have failed to demonstrate the efficacy of vitamin supplementation in preventing several types of cancer. In moderate dosages, supplementation with vitamin E (tocopherols) shows promise as a lipid antioxidant, and may reduce the risk of coronary heart disease. However, before vitamin E becomes an accepted medical therapy, further long term studies must be undertaken to examine the safety and efficacy of such therapy. An adequate intake of vitamins should be ensured by adherence to a well balanced diet. However, the elderly are prone to circumstances that may prevent them from eating a balanced diet. In addition, there are several age-related medical conditions that may predispose individuals to dietary and vitamin deficiencies. To prevent vitamin deficiency diseases and their associated morbidity, modest vitamin supplementation may be necessary. However, supplementation should be reserved for individuals with documented deficiency or who are at risk of developing such deficiencies, especially those who are homebound or institutionalised. Vitamins taken in large dosages should be considered as drugs. These medicines, which are obtainable over-the-counter, should be carefully regulated to prevent toxicity.

Language of Publication

English

Unique Identifier

98075622

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MeSH Heading (Major)

Dietary Supplements|*; Vitamins|AE/*TU

MeSH Heading

Adult; Aged; Aged, 80 and over; Aging|DE; Antioxidants|TU; Ascorbic Acid|TU; Avitaminosis|DT; Carotenoids|TU; Drug Interactions; Human; Middle Age; Retinoids|TU; Vitamin B Complex|TU; Vitamin D|TU; Vitamin E|TU; Vitamin K|TU

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

1170-229X

Country of Publication

NEW ZEALAND

Record 7 from database: MEDLINE
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Title

Mechanistic considerations in chemopreventive drug development.

Author

Kelloff GJ; Boone CW; Steele VE; Fay JR; Lubet RA; Crowell JA; Sigman CC

Address

Chemoprevention Branch, Division of Cancer Prevention and Control (DCPC), National Cancer Institute (NCI), Bethesda, MD 20892, USA.

Source

J Cell Biochem Suppl, 1994, 20:, 1-24

Abstract

This overview of the potential mechanisms of chemopreventive activity will provide the conceptual groundwork for chemopreventive drug discovery, leading to structure-activity and mechanistic studies that identify and evaluate new agents. Possible mechanisms of chemopreventive activity with examples of promising agents include carcinogen blocking activities such as inhibition of carcinogen uptake (calcium), inhibition of formation or activation of carcinogen (arylalkyl isothiocyanates, DHEA, NSAIDs, polyphenols), deactivation or detoxification of carcinogen (oltipraz, other GSH-enhancing agents), preventing carcinogen binding to DNA (oltipraz, polyphenols), and enhancing the level or fidelity of DNA repair (NAC, protease inhibitors). Chemopreventive antioxidant activities include scavenging reactive electrophiles (GSH-enhancing agents), scavenging oxygen radicals (polyphenols, vitamin E), and inhibiting arachidonic acid metabolism (glycyrrhetinic acid, NAC, NSAIDs, polyphenols, tamoxifen). Antiproliferation/antiprogression activities include modulation of signal transduction (glycyrrhetinic acid, NSAIDs, polyphenols, retinoids, tamoxifen), modulation of hormonal and growth factor activity (NSAIDs, retinoids, tamoxifen), inhibition of aberrant oncogene activity (genistein, NSAIDs, monoterpenes), inhibition of polyamine metabolism (DFMO, retinoids, tamoxifen), induction of terminal differentiation (calcium, retinoids, vitamin D3), restoration of immune response (NSAIDs, selenium, vitamin E), enhancing intercellular communication (carotenoids, retinoids), restoration of tumor suppressor function, induction of programmed cell death (apoptosis) (butyric acid, genistein, retinoids, tamoxifen), correction of DNA methylation imbalances (folic acid), inhibition of angiogenesis (genistein, retinoids, tamoxifen), inhibition of basement membrane degradation (protease inhibitors), and activation of antimetastasis genes. A systematic drug development program for chemopreventive agents is only possible with continuing research into mechanisms of action and thoughtful application of the mechanisms to new drug design and discovery. One approach is to construct pharmacological activity profiles for promising agents. These profiles are compared among the promising agents and with untested compounds to identify similarities. Classical structure-activity studies are used to find optimal agents (high efficacy with low toxicity) based on good lead agents. Studies evaluating tissue-specific and pharmacokinetic parameters are very important. A final approach is design of mechanism-based assays and identification of mechanism-based intermediate biomarkers for evaluation of chemopreventive efficacy.

Language of Publication

English

Unique Identifier

95341856

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MeSH Heading (Major)

Anticarcinogenic Agents|ME/*PD/*TU; Neoplasms|ME/*PC; Neoplasms, Experimental|ME/*PC

MeSH Heading

Animal; Human; Mice; Rats

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0733-1959

Country of Publication

UNITED STATES

Record 8 from database: MEDLINE
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Title

Susceptibility to alcohol-related liver injury.

Author

Lieber CS

Address

Alcohol Research and Treatment Center, Bronx Veterans Affairs Medical Center, New York, USA.

Source

Alcohol Alcohol Suppl, 1994, 2:, 315-26

Abstract

Alcohol affects the liver through metabolic disturbances associated with its oxidation. Redox changes produced by the hepatic alcohol dehydrogenase pathway affect lipid, carbohydrate and protein metabolism. Ethanol is also oxidized in liver microsomes by the ethanol-inducible cytochrome P4502E1, resulting in ethanol tolerance and selective hepatic perivenular damage. Furthermore, P4502E1 activates various xenobiotics, explaining the increased susceptibility of the heavy drinker to the toxicity of anesthetics, commonly used medications (i.e. isoniazid), analgesics (i.e. acetaminophen), and chemical carcinogens. Induction of microsomal enzymes also contributes to vitamin A depletion, enhances its hepatotoxicity and results in increased acetaldehyde generation from ethanol, with formation of protein adducts, glutathione depletion, free-radical-mediated toxicity, and lipid peroxidation. Chronic ethanol consumption strikingly enhances the number of hepatic collagen-producing activated lipocytes. Both in vivo (in our baboon model of alcoholic cirrhosis) and in vitro (in cultured myofibroblasts and activated lipocytes) ethanol and/or its metabolite acetaldehyde increase collagen accumulation and mRNA for collagen. Gender differences are related, in part, to lower gastric ADH activity (with consequent reduction of first pass ethanol metabolism) in young women, decreased hepatic fatty acid binding protein and increased free-fatty acid levels as well as lesser omega-hydroxylation, all of which result in increased vulnerability to ethanol. Elucidation of the biochemical effects of ethanol are now resulting in improved therapy: in baboons, S-adenosyl-L-methionine attenuates the ethanol-induced glutathione depletion and associated mitochondrial lesions, and polyenylphosphatidylcholine opposes the ethanol-induced hepatic phospholipid depletion, the decrease in phosphatidylethanolamine methyltransferase activity and the activation of hepatic lipocytes, with full prevention of ethanol-induced septal fibrosis and cirrhosis; its dilinoleoyl species also increases collagenase activity in lipocytes. The efficacy of this compound in man is now being studied in randomized multicenter clinical trials.

Language of Publication

English

Unique Identifier

97129894

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MeSH Heading (Major)

Ethanol|ME/*TO; Liver|*DE/*IN/ME

MeSH Heading

Acetaldehyde|ME; Age Factors; Alcohol Dehydrogenase|ME; Aldehyde Dehydrogenase|ME; Animal; Catalase|ME; Cytokines|PH; Female; Hepatitis, Viral, Human|CO; Human; In Vitro; Liver Diseases, Alcoholic|ET/GE/ME; Male; Microsomes, Liver|ME; Nutrition; Oxidation-Reduction; Papio; Sex Factors; Support, U.S. Gov't, Non-P.H.S.; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC

ISSN

1358-6173

Country of Publication

ENGLAND

Record 9 from database: MEDLINE
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Title

Deciphering the cause of Friedreich ataxia.

Author

Koenig M; Mandel JL

Address

Institut de GÆenÆetique et Biologie MolÆeculaire et Cellulaire (IGBMC), INSERM, CNRS, UniversitÆe Louis Pasteur, Strasbourg, France. mkoenig@igbmc.u-strasbg.fr

Source

Curr Opin Neurobiol, 1997 Oct, 7:5, 689-94

Abstract

Friedreich ataxia (FA), the most frequent cause of recessive ataxia, is attributable, in most cases, to a large expansion of an intronic GAA repeat, resulting in decreased expression of the target frataxin gene. This gene encodes a novel mitochondrial protein that has homologues of unknown function in yeast and even in gram-negative bacteria. Yeast deficient in the frataxin homologue accumulate iron in their mitochondria and show increased sensitivity to oxidative stress. This finding suggests that FA patients suffer from a mitochondrial dysfunction that causes free-radical toxicity, reminiscent of the clinically similar ataxia caused by inherited isolated vitamin E deficiency.

Language of Publication

English

Unique Identifier

98045996

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MeSH Heading (Major)

Friedreich's Ataxia|*GE/ME/PP

MeSH Heading

Animal; Human; Phosphotransferases (Alcohol Group Acceptor)|GE/ME/PH; Support, Non-U.S. Gov't; Vitamin E Deficiency|PP

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0959-4388

Country of Publication

ENGLAND

Record 10 from database: MEDLINE
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Title

Magnesium and therapeutics.

Author

Durlach J; Durlach V; Bac P; Bara M; Guiet Bara A

Address

SDRM, HÈopital St. Vincent-de-Paul, Paris, France.

Source

Magnes Res, 1994 Dec, 7:3-4, 313-28

Abstract

Two different types of therapy with magnesium are used: physiological oral magnesium supplementation which is totally atoxic since it palliates magnesium deficiencies by simply normalizing the magnesium intake and pharmacological magnesium therapy which may induce toxicity since it creates iatrogenic magnesium overload. Primary and secondary magnesium deficiencies constitute the sole indication of physiological oral magnesium therapy. It is therefore necessary to be well acquainted with the clinical and paraclinical pattern of magnesium deficit and to discriminate between magnesium deficiency due to an insufficient magnesium intake which only requires oral physiological supplementation and magnesium depletion related to a dysregulation of the control mechanisms of magnesium status which requires more or less specific regulation of its causal dysregulation. Physiological oral magnesium load constitutes the best tool for diagnosis of magnesium deficiency and the first step of its treatment. Physiological oral magnesium supplementation (5 mg/kg/day) is easy and can be carried out in the diet or with magnesium salts, with practically only one contra-indication: overt renal failure. Specific and aspecific treatments of magnesium depletion are tricky using for example magnesium sparing diuretics, pharmacological doses of vitamin B6, physiological doses of vitamin D and of selenium. In order to use the pharmacological properties of induced therapeutic hypermagnesaemia, high oral doses of magnesium (> 10 mg/kg/day) are advisable for chronic indications and the parenteral route is suitable for acute indications. There are 3 types of indications: specific (for the treatment of some forms of magnesium deficit i.e. acute), pharmacological (i.e. without alterations of magnesium status) and mixed--pharmacological and aetiopathogenic--(for example complications of chronic alcoholism). Today pharmacological magnesium therapy mainly concerns the obstetrical, cardiological and anaesthesiological fields. The main indications are eclampsia, some dysrhythmias (torsades de pointe particularly) and myocardial ischaemias. But it is now difficult to situate the exact place of the pharmacological indications of magnesium. Magnesium infusions can only be envisaged in intensive care units with careful monitoring of pulse, arterial pressure, deep tendon reflexes, hourly diuresis, electrocardiogram and respiratory recordings. High oral magnesium doses besides their laxative action may bring latent complications which may reduce lifespan. There may remain some indications of the laxative and antacid properties of non soluble magnesium, particularly during intermittent haemodialysis. Lastly local use of the mucocutaneous and cytoprotective properties of magnesium is still valid, in cardioplegic solutions and for preservation of transplants particularly.

Language of Publication

English

Unique Identifier

95306269

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MeSH Heading (Major)

Magnesium|AD/AE/CT/*TU

MeSH Heading

Administration, Oral; Clinical Trials; Diagnosis, Differential; Diet; Drug Interactions; Female; Gastrointestinal Diseases|DT; Human; Kidney Failure; Magnesium Deficiency|DI/DT; Pregnancy; Pregnancy Complications|DT

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC

ISSN

0953-1424

Country of Publication

ENGLAND

Record 11 from database: MEDLINE
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Title

The toxicity of air pollution in experimental animals and humans: the role of oxidative stress.

Author

Menzel DB

Address

Department of Community and Environmental Medicine, University of California, Irvine 92717.

Source

Toxicol Lett, 1994 Jun, 72:1-3, 269-77

Abstract

Nitrogen dioxide (NO2) and ozone (O3) occur throughout the world as the primary pollutants of urban air. NO2 and O3 oxidize cell membrane lipids and proteins. Inflammatory agents are elaborated from the lung either as a direct result of oxidation or as a consequence of leukocytes recruited into the lung by injury. My hypothesis is that NO2 and O3 initiate or exacerbate chronic lung disease through an inflammatory mechanism which can be reduced by supplementation with greater amounts than those required to alleviate vitamin deficiency symptoms of vitamins C (ascorbic acid) and E (alpha-tocopherol). Children, whose lungs are developing, are the most likely group to benefit from supplementation with vitamins C and E because the adverse effects of inflammation on the developing lung are likely to be greater and the time of exposure is longer than in adults. This hypothesis is in accord with current human and experimental animal data and the chemistry of O3 and NO2 toxicity, and is supported by recent ecological epidemiological studies of persons supplementing their intake of vitamins C and E.

Language of Publication

English

Unique Identifier

94262080

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MeSH Heading (Major)

Air Pollutants, Environmental|AE/*TO; Lung Diseases|*CI/ME; Nitrogen Dioxide|AE/*TO; Ozone|AE/*TO; Stress|*CI/ME/*PP

MeSH Heading

Animal; Chronic Disease; Human; Oxidation-Reduction

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0378-4274

Country of Publication

NETHERLANDS

Record 12 from database: MEDLINE
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Title

Tretinoin tocoferil as a possible differentiation-inducing agent against myelomonocytic leukemia.

Author

Makishima M; Honma Y

Address

Department of Chemotherapy, Saitama Cancer Center Research Institute, Ina-machi, Japan.

Source

Leuk Lymphoma, 1997 Jun, 26:1-2, 43-8

Abstract

Tretinoin tocoferil is an alpha-tocopherol ester of all-trans retinoic acid (ATRA) and safely used to treat skin ulcers. Tretinoin tocoferil stimulates the formation of granulation tissue in the ulcer, and enhances the migration of guinea pig macrophages and stimulates the proliferation of human skin fibroblasts. These effects are different from those of either ATRA or alpha-tocopherol. Tretinoin tocoferil induces the granulocytic differentiation of human promyelocytic leukemia HL-60 cells, and more than additively enhances cellular differentiation induced by sub-optimal concentrations of ATRA. Tretinoin tocoferil and ATRA synergistically inhibit the proliferation of HL-60 cells, suggesting that tretinoin tocoferil acts differently than ATRA on leukemia cells. Tretinoin tocoferil also enhances the differentiation of HL-60 cells induced by dimethyl sulfoxide, phorbol ester and 1alpha,25-dihydroxyvitamin D3(VD3). Tretinoin tocoferil and VD3 synergistically inhibit the proliferation and induce the differentiation of other myelomonocytic leukemia cells. Toxicity tests in animal models have shown that tretinoin tocoferil is at least 150 times less toxic than ATRA and does not induce teratogenesis. Therefore, the combination of tretinoin tocoferil and VD3 may be useful for treating myelomonocytic leukemia.

Language of Publication

English

Unique Identifier

97392572

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MeSH Heading (Major)

Antineoplastic Agents|*TU; Leukemia, Myelomonocytic, Acute|*DT; Tretinoin|*AA/TU; Vitamin E|*AA/TU

MeSH Heading

Cell Differentiation|DE; Drug Combinations; Human; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

1042-8194

Country of Publication

SWITZERLAND

Record 13 from database: MEDLINE
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Title

Hepatic side-effects of antibiotics.

Author

Westphal JF; Vetter D; Brogard JM

Address

Internal Medicine Service, Medical B Clinic, 1 place de l'HÈopital, CHRU, Strasbourg, France.

Source

J Antimicrob Chemother, 1994 Mar, 33:3, 387-401

Abstract

Although the liver is particularly exposed to drugs and their metabolites, hepatic side-effects of antibiotics are far less frequent than other adverse effects such as gastrointestinal disorders or cutaneous reactions. However, the potential severity of hepatic side-effects for some drugs is stressed. Antibiotic related liver injuries cover most of the clinical and pathological expressions of hepatic dysfunction, including cytotoxic hepatitis (isoniazid), intrahepatic cholestasis (macrolides, penicillins, clavulanic acid), mixed hepatitis (sulphonamides), chronic active hepatitis (nitrofurantoin), or microvesicular steatosis (tetracycline). In most cases, toxicity is idiosyncratic, reactions occurring only in some susceptible individuals. The mechanisms underlying toxicity may be primarily metabolite-dependent (isoniazid), hypersensitivity-mediated (beta-lactams), or result from both processes (sulphonamides, erythromycin derivatives). In some cases, the liver is not the primary target organ for toxicity but appears to mediate the clinical expression of some adverse effects induced by antibiotics. The most significant example of this is hypoprothrombinaemia due to the inhibition of hepatic gamma-carboxylation of vitamin K-dependent clotting factors by sulphydryl group-containing cephalosporins. Inhibition of bilirubin conjugation or transport by rifampicin or fusidic acid may also be viewed as hepatic side-effects of antibiotics. Ascertaining the casual relationship of a given drug to an hepatic adverse effect may prove particularly difficult, because of the potential contribution of host status and concurrent medications. Diagnosis is based mainly on circumstantial evidence, i.e. the temporal relationship between drug administration (or withdrawal) and the time-course of liver dysfunction. Improving morbidity related to drug hepatotoxicity relies on a free flow of information between manufacturers and practitioners in order to optimize detection of potentially serious liver damage, and advances in pharmacogenetics toward a better identification of those at particular risk for developing drug-related liver toxicity.

Language of Publication

English

Unique Identifier

94314687

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MeSH Heading (Major)

Antibiotics|*AE/TO; Liver|*DE

MeSH Heading

Animal; Antibiotics, Lactam|AE; Antitubercular Agents|AE; Human; Sulfonamides|AE

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0305-7453

Country of Publication

ENGLAND

Record 14 from database: MEDLINE
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Title

Cancer of the prostate: a nutritional disease?

Author

Fair WR; Fleshner NE; Heston W

Address

Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, NY 10021, USA.

Source

Urology, 1997 Dec, 50:6, 840-8

Abstract

In summary, epidemiologic and laboratory evidence increasingly demonstrate that nutritional factors, especially reduced fat intake, soy proteins, vitamin E derivatives, and selenium, may have a protective effect against prostate cancer. The experimental observation that low-fat diets and soy protein extracts may influence the progression of established tumors, rather than inhibiting etiologic factors, is particularly intriguing because it may serve to help explain the paradox whereby the incidence of clinical prostate cancer shows wide geographic variation, yet the evidence persists that the incidence of microfocal tumors is essentially the same worldwide. These observations, plus the likelihood that nutrition trials are likely to have little in the way of toxicity that would preclude their completion, argue that such trials should be performed. It is estimated that 30% to 50% of human malignancies may be related to dietary factors, and although the feasibility of trials involving low-fat diets has been proved in ongoing trials for colon and breast cancer, no similar study exists for prostate malignancy. Critics of epidemiologic research argue that data derived from case-control studies are subject to recall bias and are thus artifactual. Indeed, many researchers now believe that the breast cancer-dietary fat hypothesis has been discredited. The major difference between the prostate cancer and breast cancer literature is the remarkable consistency of the cohort studies. In these studies, exposure is determined prospectively and is therefore free from recall bias. In this sense they more closely resemble a clinical trial. The majority of cohort studies involving dietary fat and breast cancer have been negative. We believe that these data justify large-scale trials in the area of prevention of prostate cancer. One such proposed study already submitted for National Institutes of Health funding from a consortium of centers is the Prostate Interventional Nutrition Study (PINS), modeled after the Women's Interventional Nutrition Study, which investigates the effect of low-fat diets in women receiving therapy for node-positive breast cancer. The PINS study will be limited to men who have detectable serum PSA levels but no other clinical evidence of disease after radical prostatectomy. All subjects will receive nutritional guidance, with randomization between a control arm receiving the currently recommended 30% fat diet and an interventional arm in which a 15% fat diet is supplemented with soy protein, vitamin E, and selenium. The end points for evaluation will be compared with progression based on changes in PSA and the time of onset of clinical, as opposed to biochemical, disease. Single-institution trials involving groups thought to be at high risk of developing clinical cancer--including men with persistently elevated PSA levels, two negative prostate biopsies, high-grade prostatic intraepithelial neoplasia on biopsy, and a strong family history of prostate cancer--are being initiated at MSKCC and other institutions. CONCLUSIONS: We have reviewed the evidence that nutritional factors play a role in the progression rate of prostate cancer and may help to explain the geographic variation in the incidence observed. However, without well-controlled prospective trials, the attractive hypothesis that nutrition plays a role in tumor progression remains simply an attractive hypothesis. To date, no definite proof of a preventive effect has been shown in a study that will withstand rigid scientific scrutiny. The opportunity exists, however, for the urologic community, working together with experts in the area of nutrition, not only to advance our understanding of prostate tumorigenesis, but to rebut those critics of modern medical technology who claim that we have ignored the total or holistic approach to healing. (ABSTRACT TRUNCATED)

Language of Publication

English

Unique Identifier

98088117

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MeSH Heading (Major)

Carcinoma|ET/*ME; Nutrition Disorders|CO/*ME; Prostatic Neoplasms|ET/*ME

MeSH Heading

Animal; Animal Nutrition; Comparative Study; Diet|AE; Human; Male; Nutrition

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0090-4295

Country of Publication

UNITED STATES

Record 15 from database: MEDLINE
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Title

Effect of calcium channel blockers on intracellular calcium accumulation.

Author

Haag Weber M; Hörl WH

Address

Department of Medicine, University of Vienna, Austria.

Source

Nephrol Dial Transplant, 1994, 9 Suppl 3:, 24-7

Abstract

Protection against acute renal failure by calcium channel blockers include radiocontrast agent, cyclosporin, aminoglycosides, amphotericin B, cisplatin nephrotoxicity, and ischaemia-induced toxicity. Calcium overload occurs in ischaemic cells. The type of calcium channel blocker influences the potential effect on protection against nephrotoxicity. A number of growth factors and hormones induce cellular activation by increasing calcium concentrations. Calcium channel blockers interfere with activation of different cell types, e.g. decrease platelet aggregation, macrophage activation, platelet-activating factor release and also proliferative response of vascular smooth muscle and mesangial cells. Uraemia is also a state of calcium accumulation. Increase of intracellular calcium [Ca2+]i in PMNLs is associated with deactivation. Treatment with calcium channel blockers normalizes elevated PMNL [Ca2+]i and improves functional parameters of PMNLs. Normalization of enhanced [Ca2+]i of PMNLs can also be achieved with effective 1,25(OH)2 vitamin D3 therapy by lowering PTH. Uraemia is also a state of insulin resistance. Elevated levels of [Ca2+]i in insulin target cells diminish sensitivity to insulin at the postbinding site. Therapeutic manoeuvres preventing the increase of cytosolic calcium may improve insulin resistance.

Language of Publication

English

Unique Identifier

94352613

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MeSH Heading (Major)

Calcium|*ME/PO; Calcium Channel Blockers|*PD; Intracellular Membranes|DE/*ME

MeSH Heading

Animal; Human; Kidney Failure, Acute|PC; Uremia|ME

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0931-0509

Country of Publication

ENGLAND

Record 16 from database: MEDLINE
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Title

Effectiveness of beta-carotene in cancer chemoprevention.

Author

Toma S; Losardo PL; Vincent M; Palumbo R

Address

National Institute for Cancer Research-IST, Genova, Italy.

Source

Eur J Cancer Prev, 1995 Jun, 4:3, 213-24

Abstract

This article reviews the current knowledge on the cancer-preventive potential of beta-carotene, a precursor of vitamin A, and plentiful in fruits and vegetables, which has been studied widely as a promising chemopreventive agent in reducing the risk of cancer in humans. Several retrospective and prospective epidemiological investigations have demonstrated that a diet rich in micronutrients such as vitamins, carotenoids and selenium, could prevent the arising, in 'high-risk' patients, of precancerous and neoplastic lesions of specific sites, particularly of the upper aerodigestive tract. Numerous in vitro expressions have been performed in order to verify the true role played by this agent on cell proliferation and differentiation; until now, findings have been very encouraging, uniformly showing the beta-carotene can affect carcinogenesis, particularly in early stages, through an antigenotoxic action. Antioxidant functions, immunomodulatory effects and control of intercellular messages via gap junctions are possible action mechanisms of the ability of beta-carotene to block the carcinogenetic process. In vivo animal studies partially confirm the results obtained in vitro showing that beta-carotene is able to reduce the induce cancer development; moreover, the association of the carotenoid with other microelements, such as vitamins E, C and glutathione often appears to be more effective than each agent used alone. From a clinical point of view, beta-carotene appears an 'ideal' agent to be used in chemoprevention trials in humans, although optimal doses and intake methods need to be better defined; its almost zero toxicity permits the long-term administration of the drug, a vital condition for its anti-cancer activity, with good patient compliance. Human intervention studies performed so far, both randomized and uncontrolled clinical trials, have showed positive findings in specific cancer sites such as oral cavity, head and neck and colon; less consistent or negative are results on skin, lung and oesophagus cancer. The ongoing studies will provide more answer on these issues. A definitive evaluation of the ability of beta-carotene to prevent cancer in human requires further controlled trials; studies on a larger spectrum of cancer sites and different stages of disease must be encouraged. In addition, further investigation on biomarkers related to cancer risk and cancer incidence are necessary, particularly focused on the measurements for genotoxic damage, eg micronuclei, that may provide a valid and 'easy' marker for early stage carcinogenesis.

Language of Publication

English

Unique Identifier

95375669

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MeSH Heading (Major)

Antineoplastic Agents|*TU; Carotene|*TU; Neoplasms|ET/*PC

MeSH Heading

Animal; Diet; Human; Neoplasms, Experimental|PC; Risk Factors

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0959-8278

Country of Publication

ENGLAND

Record 17 from database: MEDLINE
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Title

Treatment of refractory cutaneous lupus erythematosus.

Author

Duna GF; Cash JM

Address

Cleveland Clinic Foundation, Ohio, USA.

Source

Rheum Dis Clin North Am, 1995 Feb, 21:1, 99-115

Abstract

Photoprotection, topical steroids, and hydroxychloroquine are the mainstays of therapy of cutaneous LE. In severe and/or refractory disease, antimalarials remain the drugs of choice, and multiple induction and combination strategies can be employed to achieve optimal results with minimal toxicity. Retinoids, dapsone, clofazimine, and thalidomide are effective but more toxic alternatives. Their use dictates frequent and careful monitoring. Retinoids and thalidomide are teratogenic, and thalidomide is not available in the United States. Results with vitamin E are controversial. Gold and IFN-alpha have unacceptably high risk to benefit ratios. Cytotoxic agents are generally restricted to the patients with concomitant organ-threatening systemic disease.

Language of Publication

English

Unique Identifier

95249764

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MeSH Heading (Major)

Lupus Erythematosus, Cutaneous|*TH

MeSH Heading

Human

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0889-857X

Country of Publication

UNITED STATES

Record 18 from database: MEDLINE
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Title

P-glycoprotein functions and substrates: possible roles of MDR1 gene in the kidney.

Author

Ernest S; Bello Reuss E

Address

Department of Internal Medicine, University of Texas Medical Branch, Galveston, USA.

Source

Kidney Int Suppl, 1998 Apr, 65:, S11-7

Abstract

There is a renewed attention on the multidrug resistance genes and their products, P-glycoproteins, since recent molecular and functional studies revealed unexpected functions in normal tissues. There are two types of human P-glycoprotein: Type I, encoded by the MDR1 gene, present in excretory organs and in non-polarized cells; and Type II, encoded by MDR2, present in the canalicular membrane of hepatocytes. MDR1 Pgp transports xenobiotics, peptides, steroids, and phospholipids, and is also a regulator of swelling-activated chloride channels. MDR2 Pgp is exclusively a phosphatidylcholine translocase. In the kidney, the MDR1 gene and protein are expressed in mesangial, proximal tubule, thick loop of Henle, and collecting duct cells. In mesangial and proximal tubule cells Pgp transports xenobiotics. Concomitant exposure of kidney cells to two Pgp substrates results in increased cell toxicity. Extracts from supernatants of mesangial cell cultures inhibit Pgp-mediated transport, suggesting that a mesangial-cell metabolite could be a substrate of Pgp. Active vitamin D3 and platelet activating factor inhibit Pgp transport and are possible endogenous substrates in proximal tubule and mesangial cells, respectively. Pgp could be also a regulator of swelling-activated chloride channels present in the kidney.

Language of Publication

English

Unique Identifier

98212790

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MeSH Heading (Major)

Kidney|*ME; P-Glycoprotein|*GE/*PH

MeSH Heading

Animal; Biological Transport; Human; Interleukin-2|ME; Steroids|ME; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.; Xenobiotics|PK

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0098-6577

Country of Publication

UNITED STATES

Record 19 from database: MEDLINE
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Title

Bioactivities of N-(4-hydroxyphenyl) retinamide and retinoyl beta-glucuronide.

Author

Formelli F; Barua AB; Olson JA

Address

Istituto Nazionale per lo Studio e la Cura dei Tumori, Division of Experimental Oncology, Milan, Italy.

Source

FASEB J, 1996 Jul, 10:9, 1014-24

Abstract

N-(4-Hydroxyphenyl) retinamide (4HPR) and retinoyl beta-glucuronide (RAG) are two derivatives of all-trans retinoic acid (RA) that show properties both similar to as well as different from their parent compound, RA. Both retinoids possess the important property of showing much-reduced toxicity relative to RA while maintaining significant biological activity. 4HPR, a synthetic derivative, is active in the prevention and treatment of a variety of neoplasms in animals, and by inducing apoptosis, shows growth inhibitory activity against many human tumor cell types in vitro. In humans, 4HPR reduces the incidence of new occurrences of leukoplakia and is currently being tested as a preventive agent for breast cancer. RAG, a naturally occurring metabolite of RA, effectively stimulates the growth of vitamin A-deficient animals, induces the differentiation of epithelial cells in vivo and in vitro, and is effective in the topical treatment of acne in humans. Unlike RA, RAG is nontoxic when applied to the skin and is nonteratogenic when given orally to rats. Possible mechanisms of action of both compounds are discussed. These two derivatives of retinoids show interesting physiologic effects and potentially beneficial pharmacologic actions.

Language of Publication

English

Unique Identifier

96388956

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MeSH Heading (Major)

Fenretinide|*PD; Tretinoin|*AA/PD

MeSH Heading

Animal; Antineoplastic Agents|PD; Cell Differentiation|DE; Human; Rats; Support, Non-U.S. Gov't; Support, U.S. Gov't, Non-P.H.S.; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0892-6638

Country of Publication

UNITED STATES

Record 20 from database: MEDLINE
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Title

Safety of megavitamin therapy.

Author

Omaye ST

Address

Source

Adv Exp Med Biol, 1984, 177:, 169-203

Abstract

Carbon compounds that are needed in small amounts in the diet because they are not made in the body of vertebrates are defined as vitamins. Excluded from this definition are vitamins D, K, and niacin which can be synthesized by the organism or, as in the case of vitamin K, by the host's intestinal bacteria. Lack of such vitamins can result in characteristic deficiency diseases. The therapeutic use of such compounds (megavitamin intake) is based on the spectacular effect of vitamins on deficiency diseases; however, evidence that the ingestion of large amounts of vitamins beyond the "Recommended Daily Allowances" (RDA) is beneficial is not within the basic concept of nutrition. Vitamins, like many substances, may be toxic when taken in large quantities, especially the fat-soluble vitamins, and the concept of "more is better" is a common misconception. Vitamin supplements can be suggested only in the unusual cases of patients having inadequate intake, disturbed absorption (genetic or otherwise), or increased tissue requirements. A well-balanced diet that includes a wide variety of foods from each of the four food groups is adequate for the supply of vitamins, as well as other nutrients, in healthy people. This paper will review some of the recent findings regarding vitamin toxicity and the mechanisms of toxicity.

Language of Publication

English

Unique Identifier

85043289

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MeSH Heading (Major)

Orthomolecular Therapy|AE/*ST

MeSH Heading

Ascorbic Acid|TO/TU; Drug Interactions; Human; Vitamin A|TO/TU; Vitamin B Complex|TO/TU; Vitamin D|TO/TU; Vitamin E|TO/TU; Vitamin K|TO/TU

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0065-2598

Country of Publication

UNITED STATES

CAS Registry/EC Number

11103-57-4 (Vitamin A); 12001-76-2 (Vitamin B Complex); 12001-79-5 (Vitamin K); 1406-16-2 (Vitamin D); 1406-18-4 (Vitamin E); 50-81-7 (Ascorbic Acid)

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