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Vibrant Life Technical Information  Synthetic Versus Natural Forms Of  Vitamins

The age-old debate about whether there is such a thing as "natural" forms of vitamins, and then whether these "natural" forms are "better" than synthetic forms of the same vitamins -- that is the subject of this page.

This debate came to me, Karl Loren, in the form of a letter from a customer, Dr. Robert S, asking me to review a lengthy article he enclosed.  The article by Dr. West, of Standard Brands vitamins, claimed that "natural" forms of vitamins were far superior to the "synthetic forms."  Click Here to read the initial correspondence on this published in the FAQ (Frequently Asked Questions) section of this web site.

In a complete search of the 7,000,000 scientific studies available through the premium search service, MedLine, I entered "synthetic vitamins" and "synthetic vitamins" and got exactly 13 references. 

This page includes ALL 13 of these references, even if, upon reading, they don't seem to be very helpful in answering the basic question.

After review of these studies I find that there are several references to the fact that synthetic and natural forms of vitamins are of equal value in preventing cancer.  In some studies there are differences recognized between the natural and synthetic, but no conclusions yet drawn about which might be better.  In a few cases the synthetic form of the vitamin is shown to be more beneficial than the natural form.

I conclude that those vitamin companies which claim that "natural forms" of vitamins are superior make that claim without reference to standard clinical studies.

I conclude that Standard Brands, supposedly one of the highest quality vitamin products, supposedly ONLY sold THROUGH doctors, has not backed up their suspect claim with references to any scientific studies.

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HealthGate Documents

Record 1 from database: MEDLINE
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Title

Iron and vitamins.

Author

Hallberg L

Address

Department of Internal Medicine, University of GÂoteborg, Sweden.

Source

Bibl Nutr Dieta, 1995, :52, 20-9

Abstract

(1) Ascorbic acid has a key role in the absorption of dietary nonheme iron. (2) Natural and synthetic ascorbic acid have the same effect. (3) Ascorbic acid has a log/log dose-effect relationship in iron absorption. (4) The absorption is not reduced by prolonged intake of higher amounts of ascorbic acid. (5) There is a very efficient regulatory system for the absorption of iron preventing the development of dietary iron overload in normal subjects. (6) Each main meal should contain at least 50 mg ascorbic acid--more if a meal contains much phytate, and more if energy expenditure is low.

Language of Publication

English

Unique Identifier

96245676

MeSH Heading (Major)

Iron|*PH; Vitamins|*PH

MeSH Heading

Ascorbic Acid|PH; Erythropoiesis; Human; Nutritional Requirements; Support, Non-U.S. Gov't; Vitamin A|PH

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0067-8198

Country of Publication

SWITZERLAND

Record 2 from database: MEDLINE
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Title

Morphological structure of the mucous membrane and submucosa of rumen in calves receiving synthetic or natural beta-carotene and vitamins AD3E.

Author

Szarek J; Iwa ska S; Bomba G; Pysera B; Strusi ska D

Address

Department of Forensic Veterinary Medicine, University of Agriculture and Technology, Olsztyn, Poland.

Source

Acta Vet Hung, 1992, 40:4, 303-9

Abstract

In an experiment conducted on 20 calves from 1 day to 12 weeks old, supplements of beta-carotene were fed in the form of Rovimix beta-carotene 10%, artificially dehydrated carrot or vitamins AD3E. Postmortem examination carried out at 12 weeks showed that supplementation of beta-carotene or vitamins AD3E resulted in a better structural development of the ruminal papillae as compared to the control group. In addition, beta-carotene reduced the keratinization of the stratified squamous epithelial cell layer of the rumen and increased the glycosaminoglycan level of that organ wall.

Language of Publication

English

Unique Identifier

93297452

MeSH Heading (Major)

Carotene|*PD; Cattle|*AH; Gastric Mucosa|AH/*DE; Rumen|AH/*DE; Vitamins|*PD

MeSH Heading

Animal; Cholecalciferol|PD; Male; Vitamin A|PD; Vitamin E|PD

Publication Type

JOURNAL ARTICLE

ISSN

0236-6290

Country of Publication

HUNGARY

CAS Registry/EC Number

0 (Vitamins); 11103-57-4 (Vitamin A); 1406-18-4 (Vitamin E); 36-88-4 (Carotene); 67-97-0 (Cholecalciferol); 7235-40-7 (Beta Carotene)

Record 3 from database: MEDLINE
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Title

Free radicals and antioxidants in cardiovascular disease.

Author

Maxwell SR; Lip GY

Address

Department of Clinical Pharmacology, Clinical Sciences Building, Leicester Royal Infirmary, England.

Source

Br J Clin Pharmacol, 1997 Oct, 44:4, 307-17

Abstract

Several lines of evidence suggest that free radical-mediated oxidative damage to lipoproteins may be an important factor predisposing them to uptake into the vascular wall. This has led to interest in the factors that determine the susceptibility of lipoproteins to oxidation and their relationship to the development of coronary heart disease. Of these factors, the lipoprotein content of natural antioxidant vitamins such as vitamin E, and beta-carotene have aroused particular interest. Studies in animal models of atherosclerosis suggest that natural and synthetic antioxidants can retard the development of atheroma. Epidemiological comparisons between populations and studies within populations also support the contention that high plasma levels or dietary intake of natural antioxidant vitamins may protect against the development of coronary disease in man. Prospective randomized controlled trials of antioxidants in high risk groups are underway to test whether the theoretical promise of a beneficial role for antioxidants in coronary heart disease prevention will be fufilled.

Language of Publication

English

Unique Identifier

98014395

MeSH Heading (Major)

Antioxidants|CH/*TU; Atherosclerosis|*PC/PP; Coronary Disease|*PC/PP; Free Radicals|CH/*ME; Lipoproteins|CH/*PH; Vitamin E|*TU

MeSH Heading

Animal; Arteries|PP; Clinical Trials; Diet; Human; Lipid Peroxidation

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0306-5251

Country of Publication

ENGLAND

Record 4 from database: MEDLINE
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Title

Prospects for the use of antioxidant therapies.

Author

Maxwell SR

Address

Department of Medicine, Queen Elizabeth Hospital, Birmingham, England.

Source

Drugs, 1995 Mar, 49:3, 345-61

Abstract

Free radical oxidative stress has been implicated in the pathogenesis of a variety of human diseases. Natural antioxidant defences have been found to be defective in many of the same diseases. This has led to suggestions that oxidative damage and therefore disease progression may be retarded by supplementing natural antioxidant defences. Potential antioxidant therapy includes natural antioxidant enzymes and vitamins or synthetic agents with antioxidant activity. Diseases where antioxidant therapy may be beneficial include diabetes mellitus, reperfusion injury, inflammatory diseases and the prevention of chronic processes such as atherosclerosis and carcinogenesis. Further well controlled prospective clinical trials of antioxidants are required to establish the efficacy and tolerability of antioxidant therapy in the treatment of human diseases.

Language of Publication

English

Unique Identifier

95292865

MeSH Heading (Major)

Antioxidants|AD/PD/*TU

MeSH Heading

Acquired Immunodeficiency Syndrome|DT/PC; Atherosclerosis|DT/PC; Central Nervous System Diseases|DT/PC; Diabetes Mellitus|DT/PC; Enzymes|AD/PD/TU; Exercise; Free Radical Scavengers|AD/PD/TU; Free Radicals; Graft Rejection|PC; Human; Hypertension|DT/PC; Inflammation|DT/PC; Neoplasms|DT/PC; Reperfusion Injury|DT/PC

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC

ISSN

0012-6667

Country of Publication

NEW ZEALAND

Record 5 from database: MEDLINE
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Title

Experience from clinical trials in cancer prevention.

Author

Greenwald P

Address

Division of Cancer Prevention and Control, National Cancer Institute, National Institutes of Health, Bethesda, Maryland.

Source

Ann Med, 1994 Feb, 26:1, 73-80

Abstract

Conduct of randomized, controlled, large-scale prevention trials is fundamental to the full assessment of the efficacy of interventions to prevent cancer. Clinical trials in cancer prevention, which include dietary modification and chemoprevention, are based on leads from epidemiological and laboratory studies. Dietary intervention trials involve the modification of overall eating patterns, whereas chemoprevention trials involve the administration of natural or synthetic substances reported to have anticarcinogenic properties, e.g. vitamins, minerals, and pharmaceuticals. Clinical/metabolic studies can help advance knowledge of the role of diet in the etiology and prevention of cancer by investigating the metabolism of factors thought to influence cancer risk; thus, these studies have the potential to provide a stronger scientific base for progression to randomized, controlled clinical trials. Cancer prevention trials supported by the National Cancer Institute include the Polyp Prevention Trial, which is testing a low-fat, high-fibre, and vegetable- and fruit-enriched eating pattern on the prevention of polyp recurrence, and the Nutrition Intervention Trials of Oesophageal Cancer in Linxian, China, which are testing the efficacy of vitamin-mineral supplements in the prevention of oesophageal cancer in high-risk populations. Results from clinical cancer prevention trials will enable investigators to establish more firmly the relationships between diet and cancer and to translate the information effectively into significant reductions in cancer incidence and mortality.

Language of Publication

English

Unique Identifier

94220297

MeSH Heading (Major)

Neoplasms|*PC

MeSH Heading

Clinical Trials; Diet; Female; Human; Male; Randomized Controlled Trials

Publication Type

JOURNAL ARTICLE

ISSN

0785-3890

Country of Publication

ENGLAND

Record 6 from database: MEDLINE
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Title

Bionutrition and oral cancer in humans.

Author

Enwonwu CO; Meeks VI

Address

Department of Biochemistry, College of Dental Surgery, University of Maryland, Baltimore 21201, USA.

Source

Crit Rev Oral Biol Med, 1995, 6:1, 5-17

Abstract

Tobacco (smoking and smokeless) use and excessive consumption of alcohol are considered the main risk factors for oral cancer (ICD9 140-149). Conspicuous national and international variations in oral cancer incidence and mortality rates, as well as observations in migrant populations, raise the possibility that diet and nutritional status could be an important etiologic factor in oral carcinogenesis. As shown in this report, abuse of alcohol and tobacco has serious nutritional implications for the host, and generates increased production of reactive free radicals as well as eliciting immunosuppression. Maintenance of optimal competence of the immune system is critical for cancer surveillance. Active oxygen species and other reactive free radicals mediate phenotypic and genotypic alterations that lead from mutation to neoplasia. Consequently, the most widely used chemopreventive agents against oral cancer (e.g., vitamins A, E, C, and beta-carotene) are anti-oxidants/free radical scavengers. These anti-oxidants, both natural and synthetic, neutralize metabolic products (including reactive oxygen species), interfere with activation of procarcinogens, prevent binding of carcinogens to DNA, inhibit chromosome aberrations, restrain replication of the transformed cell, suppress actions of cancer promoters, and may even induce regression of precancerous oral lesions such as leukoplakia and erythroplakia. Malnutrition is characterized by marked tissue depletion of anti-oxidant nutrients, including GSH (gamma-glutamyl-cysteinyl-glycine), a key cellular anti-oxidant as well as a modulator of T-cell activation. GSH or its precursor cysteine inhibits activation of the nuclear transcription factor kB(NFkB), and has been shown to be protective against chemically induced oral cancer and leukoplakia. Alcohol-, tobacco-, and/or malnutrition-induced immunosuppression promotes impaired salivary gland function and oral mucosal immunity, a prominent reduction in the number of helper CD4 cells with less marked changes in number of suppressor T-cells, and depressed NK cell activity, among others. These suggest a breakdown in capacity or the malnourished to mount effective tumor surveillance. This review article underscores the compounding but important roles of nutritional/dietary factors in the long-established causal link between abuse of alcohol and tobacco (smoking and smokeless) and oral cancer.

Language of Publication

English

Unique Identifier

95359352

MeSH Heading (Major)

Cocarcinogenesis|*; Mouth Neoplasms|*ET/IM/ME/PC; Nutrition Disorders|*CO/ME

MeSH Heading

Alcohol Drinking|AE; Anticarcinogenic Agents|TU; Antioxidants|TU; Free Radicals|AE; Human; Immunologic Surveillance; Oxidative Stress; Risk Factors; Support, U.S. Gov't, P.H.S.; Tobacco Use Disorder|CO

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

1045-4411

Country of Publication

UNITED STATES

Record 7 from database: MEDLINE
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Title

The effect of carotene and vitamins A and E supplementation on reproduction of sows.

Author

Preø J; Fuchs B; Schleicher A

Address

Department of Animal Nutrition and Fodder Management, Agricultural University, Wroc…aw, Poland.

Source

Arch Vet Pol, 1993, 33:1-2, 55-64

Abstract

The effects of synthetic and natural beta-carotene as well as vitamins A and E supplementation on the fertility of sows and number of piglets in a litter were the subject of our studies. The sows fed beta-carotene had from 2 to 4 more piglets in a litter. Vitamin E had a harmful influence on beta-carotene action. It was found that synthetic beta-carotene and vitamin A increased the number of viable embryos and yellow bodies in the sows slaughtered on the 28th day of gestation, moreover beta-carotene subsequently improved the fertility of sows in the next reproductive cycle.

Language of Publication

English

Unique Identifier

94332231

MeSH Heading (Major)

Carotene|*PD; Reproduction|*PH; Swine|*PH; Vitamin A|*PD; Vitamin E|*PD

MeSH Heading

Animal; Animal Feed; Comparative Study; Female; Fertility|DE; Ovulation|PH; Random Allocation

Publication Type

JOURNAL ARTICLE

ISSN

1230-5359

Country of Publication

POLAND

CAS Registry/EC Number

11103-57-4 (Vitamin A); 1406-18-4 (Vitamin E); 36-88-4 (Carotene)

Record 8 from database: MEDLINE
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Title

Comparative assessment of the toxicology of vitamin A and retinoids in man.

Author

Biesalski HK

Address

Institut für Physiologische Chemie II, Universität Mainz, F.R.G.

Source

Toxicology, 1989 Jul 17, 57:2, 117-61

Abstract

As the title implies, any assessment of the toxic effects of vitamin A derivatives must distinguish between vitamin A in the truest sense, i.e. retinol, and retinoic acid and its synthetic derivatives. Just as no single description is universally applicable to the mode of action of vitamin A derivatives, so too do their toxic effects defy generalization. The recommendation made in 1982 by IUPAC [Eur. J. Biochem., 129 (1989) 1] to designate all derivatives with the typical structure of the vitamin as being retinoids may be chemically logical and correct but, when it comes to describing the effects and side-effects of vitamin A derivatives, it leads to misunderstandings. Retinol, which is frequently used as synonym for vitamin A, can eliminate all symptoms of vitamin A deficiency if it is taken in sufficient quantity with the diet. The term retinol will therefore be used here as a synonym for vitamin A whereas retinoic acid and its derivatives--including the synthetic ones--will be referred to as retinoids because they do not cover the whole spectrum of effects exerted by retinol and because they also vary markedly in their side-effects. In contrast to the nomenclature proposed by IUPAC, this system provides a clear and logical distinction for describing biological processes. Other authors have favoured it in recent times [Chytil, F., J. Am. Acad. Dermatol., 15 (1986) 741; Olson, J.A., Semin. Oncol., x (3) (1983) 290; Olson, J.A., Am. J. Clin. Nutr., 45 (1987) 704; Zbinden, G., Acta Dermatovener., 74 (1975) 36]. By vitamin A, therefore, is meant all derivatives that can possibly originate from retinol in the organism. This also covers the small quantities of retinoic acid formed from retinol. On the other hand, by retinoids is meant the natural retinoic acid derivatives and their synthetic forms in their special modes of action. Since retinoic acid cannot be reduced to retinol in the organism, this nomenclature provides a clear demarcation within the biological system. Vitamin A is essential to the growth and development of higher life forms and functions in many different ways within the organism. Although vitamin A was one of the first vitamins to be described, even today there is still some uncertainty as to its mode of action, with the exception of that of retinal (vitamin A aldehyde) in vision.(ABSTRACT TRUNCATED AT 400 WORDS)

Language of Publication

English

Unique Identifier

89318226

MeSH Heading (Major)

Retinoids|AE/PK/*TO; Vitamin A|AE/PK/*TO

MeSH Heading

Animal; Human; Structure-Activity Relationship

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC

ISSN

0300-483X

Country of Publication

NETHERLANDS

CAS Registry/EC Number

0 (Retinoids); 11103-57-4 (Vitamin A)

Record 9 from database: MEDLINE
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Title

Chemoprevention of bladder cancer.

Author

Malone WF; Kelloff GJ; Pierson H; Greenwald P

Address

 

Source

Cancer, 1987 Aug 1, 60:3 Suppl, 650-7

Abstract

There is a growing body of basic science and epidemiologic evidence to support a research thrust to determine whether several natural or synthetic agents, given alone or together, can lower cancer incidence. Candidate agents include analogs of vitamin A and the vitamin A precursor, beta-carotene, vitamins C and E, and the trace metal selenium. Other agents now being studied in the laboratory include phenolic antioxidants, protease inhibitors, prostaglandin synthesis inhibitors, and indoles. Research in chemoprevention involves identifying and characterizing agents with reported activity, efficacy and toxicologic testing to select the most promising agents, and clinical trials to test those with the most potential in humans. Activities are underway in all the above areas, including 24 clinical trials, to evaluate selected compounds in preventing cancer at various cancer sites. Included are studies of individuals at high risk, individuals with precancerous lesions and individuals free of cancer but at risk to second cancers. A number of agents have shown activity in reducing bladder cancer incidence in animal models. The potential applicability of these agents for studies in human cancer risk reduction intervention studies is discussed. Cancer induction is postulated to be a multistage process involving initiation and promotion. Progress in cancer prevention may result from not only reducing exposures to initiators, but also suppressing promotional activity in initiated cells. Newly developed research technologies including cellular, animal, and epidemiologic procedures are being used for identifying, refining, and testing cancer prevention strategies.

Language of Publication

English

Unique Identifier

87243931

MeSH Heading (Major)

Bladder Neoplasms|EP/PA/*PC

MeSH Heading

Animal; Ascorbic Acid|TU; Carotene|TU; Clinical Trials; Disease Models, Animal; Drug Evaluation; Epidemiologic Methods; Female; Human; Male; Mice; Rats; Selenium|TU; United States; Vitamin A|TU; Vitamin E|TU

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE

ISSN

0008-543X

Country of Publication

UNITED STATES

CAS Registry/EC Number

11103-57-4 (Vitamin A); 1406-18-4 (Vitamin E); 36-88-4 (Carotene); 50-81-7 (Ascorbic Acid); 7235-40-7 (Beta Carotene); 7782-49-2 (Selenium)

Record 10 from database: MEDLINE
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Title

Diet and carcinogenesis.

Author

Rogers AE; Zeisel SH; Groopman J

Address

Boston University School of Medicine, Department of Pathology, MA 02116.

Source

Carcinogenesis, 1993 Nov, 14:11, 2205-17

Abstract

In summary there is a wealth of information on dietary and nutritional effects on carcinogenesis in laboratory rodents. Experimental studies based on epidemiological evidence, earlier experimental studies and known or predicted cellular, biochemical and molecular effects of nutrients have produced clear evidence that carcinogenesis in laboratory rodents is influenced by dietary intake of calories, fat, lipotropes (choline, methionine), vitamin A and related retinoids, Se, calcium, zinc, fiber, ethanol and a large number of non-nutrient components of foods. For these substances or groups of substances mechanistic hypotheses supported by experimental data and are leading to further research. The information provided will contribute to understanding of basic processes in carcinogenesis as well as of the specific interactions studied, and should contribute to significant advances in preventive medicine. Restriction of caloric intake of rodents by amounts > 10% over a significant portion of their lifetime reduces tumorigenesis. That level of restriction reduces the rate of growth and maturation, and most experiments in this area employ greater restrictions that virtually abolish growth from a young age. Therefore, the observations are of interest in mechanistic studies, but their applicability to preventive medicine requires better definition of the degree and duration of restriction required for a significant effect and the age at which it must be imposed. Restriction of total fat intake and modifications to increase the intake of omega-3 fats have a reasonably consistent effect on tumorigenesis in rodents but a much less consistently demonstrable effect in humans. Again, the observations in rodents are providing a major stimulus to mechanistic studies. The lipotropes are extremely valuable as tools for investigating mechanisms of carcinogenesis in rodents. Their importance in the epidemiology of human cancer has yet to be demonstrated clearly and is a subject of research at present. The naturally occurring vitamins and minerals, as well as fiber, derive their importance in this context from investigations to explain the consistent epidemiological demonstrations of reduction of tumor risk with increased consumption of fruits and vegetables. The activity of the isolated nutrients as anticarcinogens in rodents has generally not matched the activity expected from epidemiological studies. The anticarcinogenic activity of many of the non-nutrient components of fruits and vegetables is remarkable in particular models, however, as is the activity of natural and synthetic retinoids. At present the results must be interpreted to indicate an important effect of combinations of the whole foods with identification of particular nutrients or non-nutrients in specific cases.(ABSTRACT TRUNCATED AT 400 WORDS)

Language of Publication

English

Unique Identifier

94062099

MeSH Heading (Major)

Carcinogens|*; Diet|*; Neoplasms|EP/*ET/PC; Neoplasms, Experimental|CI/*PP

MeSH Heading

Alcohol Drinking; Animal; Calcium; Dietary Fats; Dietary Fiber; Energy Intake; Fruit; Human; Minerals; Risk Factors; Vegetables

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC

ISSN

0143-3334

Country of Publication

ENGLAND

CAS Registry/EC Number

0 (Carcinogens); 0 (Dietary Fats); 0 (Minerals); 7440-70-2 (Calcium)

Record 11 from database: MEDLINE
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Title

1 alpha,25-Dihydroxyvitamin D3 and a novel vitamin D analogue MC 903 are potent inhibitors of human interleukin 1 in vitro.

Author

Muller K; Svenson M; Bendtzen K

Address

Laboratory of Medical Immunology, Rigshospitalet, Copenhagen, Denmark.

Source

Immunol Lett, 1988 Apr, 17:4, 361-5

Abstract

1 alpha,25-dihydroxycholecalciferol (1,25(OH)2D3) inhibits the lymphocyte growth hormone, interleukin 2. Since its production is dependent upon interleukin 1 (IL-1) produced by antigen-presenting cells, we tested five vitamin D3 analogues for effects on the production and function of human natural and recombinant IL-1. The production was not affected, but 1,25(OH)2D3 (greater than 10(-11) M) and a synthetic derivative MC 903 (greater than = 10(-10) M) inhibited the proliferation of mouse thymocytes to IL-1. The vitamins failed to affect the cytotoxic activity of tumor necrosis factor. 1,25(OH)2D3 may play a physiological immunomodulatory role as a selective inhibitor of the function of IL-1, and MC 903 may prove clinically useful in this regard because of its limited calcium metabolic activity.

Language of Publication

English

Unique Identifier

88226767

MeSH Heading (Major)

Calcitriol|*AA/*PD; Interleukin-1|*IM/PD

MeSH Heading

Animal; Human; In Vitro; Lymphocyte Transformation|DE; Mice; Support, Non-U.S. Gov't; T-Lymphocytes|DE/IM

Publication Type

JOURNAL ARTICLE

ISSN

0165-2478

Country of Publication

NETHERLANDS

CAS Registry/EC Number

0 (Interleukin-1); 112965-21-6 (calcipotriene); 32222-06-3 (Calcitriol)

Record 12 from database: MEDLINE
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Title

Alteration of human granulocyte functional responses by menadione.

Author

Shakarjian MP; Carchman RA

Address

Department of Pharmacology and Toxicology, Medical College of Virginia, Virginia Commonwealth University, Richmond 23261.

Source

Arch Biochem Biophys, 1990 Nov 15, 283:1, 1-11

Abstract

Menadione is a synthetic derivative of the natural vitamins K with antiinflammatory activity among its potentially significant clinical properties. We have found this agent to stimulate the production of superoxide anion (O2-) in human polymorphonuclear leukocytes (PMN) and dimethylsulfoxide-differentiated HL-60 cells in a time-, cell number-, and drug concentration-dependent manner. Conversely, menadione attenuates both O2- production and lysozyme release in cells stimulated by phorbol myristate acetate (PMA), fMet-Leu-Phe, or Ca2+ ionophore. 4-Acetamido-4'-isothiocyano-2-2'-disulfonic acid stilbene and 4,4'-diisothiocyano-2-2'disulfonic acid stilbene, agents which inhibit transmembrane O2-) flux, do not alter menadione's effects on superoxide dismutase (SOD) inhibitable cytochrome c reduction in resting or PMA-stimulated PMN. Likewise, quinone reductase inhibitors, warfarin and dicumarol, known to attenuate vitamin K-dependent responses and enhance quinone-mediated oxidative stress, have no effect upon menadione-stimulated O2- production. Furthermore, menadione-induced suppression of stimulus-mediated lysozyme release is not reversed by cotreatment with oxygen metabolite scavenging enzymes SOD and catalase. Nevertheless, under conditions of restricted oxygen supply, the suppressive effect of menadione on stimulant-induced lysozyme release is greatly diminished. Thus, although pharmacological manipulation suggests otherwise, there appears to exist at least a component of the inhibitory activity of menadione that is oxygen dependent, and may be oxidative stress-related.

Language of Publication

English

Unique Identifier

91053167

MeSH Heading (Major)

Neutrophils|CY/DE/*PH; Superoxides|*BL; Vitamin K|*PD

MeSH Heading

Anaerobiosis; Cell Survival|DE; Cells, Cultured; Dicumarol|PD; Human; Kinetics; Lactate Dehydrogenase|BL; Muramidase|BL; Support, U.S. Gov't, P.H.S.; SITS|AA/PD; Tetradecanoylphorbol Acetate|PD; Time Factors; Warfarin|PD

Publication Type

JOURNAL ARTICLE

ISSN

0003-9861

Country of Publication

UNITED STATES

CAS Registry/EC Number

EC 1.1.1.27 (Lactate Dehydrogenase); EC 3.2.1.17 (Muramidase); 11062-77-4 (Superoxides); 12001-79-5 (Vitamin K); 16561-29-8 (Tetradecanoylphorbol Acetate); 27816-59-7 (SITS); 53005-05-3 (DIDS); 66-76-2 (Dicumarol); 81-81-2 (Warfarin)

Record 13 from database: MEDLINE
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Title

The effects of elemental diet and subsequent food reintroduction on rheumatoid arthritis.

Author

Kavanaghi R; Workman E; Nash P; Smith M; Hazleman BL; Hunter JO

Address

Department of Rheumatology, Addenbrooke's Hospital, Cambridge.

Source

Br J Rheumatol, 1995 Mar, 34:3, 270-3

Abstract

The role of diet in rheumatoid arthritis (RA) remains controversial and there have been no controlled studies on the use of elemental diet in the treatment of RA. Elemental diet is an hypoallergenic protein-free artificial diet consisting of essential amino acids, glucose, trace elements and vitamins. This study was carried out to assess the role of elemental diet and subsequent food reintroduction in RA. Elemental diet (E028) (and a small number of foods) was given to 24 patients with definite RA in order to induce a remission and then foods were gradually introduced. Where a food was suspected of causing symptoms it was removed from the diet. Twenty-three control patients supplemented their usual diet with E028. After the elemental diet there was a statistically significant improvement in the diet group in grip strength (P = 0.008) and Ritchie score (P = 0.006) but not in ESR, CRP, thermographic joint score or functional score. The diet group lost more weight than the control group and this correlated with the improvement in grip strength. This improvement was not present following food reintroduction. As the improvements took place in more subjective disease parameters and because of the difficulties in adequately blinding studies of diet in arthritis, a placebo effect must be considered. There was a high default rate, only 38% of those patients originally enrolled completed the study. In conclusion, this study shows that elemental diet can cause an improvement in a number of disease parameters in RA but this is not sustained by an individualized diet. It also illustrates some of the difficulties involved in the study of diet in arthritis.

Language of Publication

English

Unique Identifier

95245622

MeSH Heading (Major)

Arthritis, Rheumatoid|CO/*DH/PP

MeSH Heading

Adult; Female; Food, Formulated; Hand Strength; Human; Male; Pilot Projects; Severity of Illness Index; Support, Non-U.S. Gov't; Weight Loss

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL

ISSN

0263-7103

Country of Publication

ENGLAND

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SUBSCRIBE:  The Wednesday Letter is a free electronic monthly newsletter written and published by Karl Loren.  You can view more than 50 back issues of this publication by clicking here.  The Wednesday Letter subscription list is maintained on a secure server, no name is ever given or sold to anyone, and it is never used except for this Newsletter.  It is automatically published on the Tuesday night just before the first Wednesday of every month.  You can subscribe to this free monthly electronic letter by entering your eMail address and name below.  You will then automatically receive a request for confirmation, sent to whatever address you have entered.  If you do NOT receive this confirmation request, then you will not be subscribed.  There may have been an error with your address and you should resubmit.  The letter is never sent twice to the same address -- so you do not have to worry about a duplicate subscription.  When you receive this confirmation request you must reply to it, or your subscription will not become active.  No one can subscribe your name, and address, without you being notified, and if you get an unwanted notice of subscription you only need to DO NOTHING and the subscription will NOT be active.

REMOVAL:  You can remove yourself from the subscription list in several different ways.  Click here to read about this entire newsletter system.  Every edition of The Wednesday Letter is delivered to your address with YOUR name and address in view on the letter, with a link that allows you to remove THAT name from the subscription list.  If you try to send this removal message from an address different from the one you used to send in your original confirmation, then you will get a warning notice first, sent to the subscription address, asking you to confirm that you want to be removed from the list -- by replying to THAT request for confirmation, you will then be automatically removed.  Thus, no one else can unsubscribe you, from some other computer, without your knowledge.  But, if you send in the unsubscribe notice from the same machine used to receive the Letter, then the removal from the subscription list is automatic.

Personal Message:  When you send a personal message to Karl Loren, you will receive a personal reply as per his instructions.  Karl pledges that every personal message will get a personal answer. When you provide your mail address, we will send you free information including our free catalog and a cassette tape lecture by Karl Loren about heart disease, no charge, by mail, even if outside the US.  You can select particular information you would like to receive, along with the free cassette tape and catalog.

You can reach Vibrant Life in many ways, including by mail to Vibrant Life, 2808 N. Naomi St., Burbank, CA 91504.  Within the US and Canada, use the toll free number:  (800) 523-4521, the local number:  (818) 558-1799, the FAX:  (818) 558-7299, eMail to kimberly@oralchelation.com or any one of the hundreds of message forms throughout the 50 web sites.  Vibrant Life normally ships the same day we get an order.  There are message forms on each of the 100,000+ pages on this and other sites where you can communicate with Vibrant Life.  Check out our companion site, at:  http://www.oralchelation.net where Karl's 2000 page book is published.  Karl Loren is the author and webmaster for this BOOK, as well as for another web site about ORAL CHELATION.  His personal philosophical articles are at PHILOSOPHY. 

Copyright © May 20, 2008 6:24 AM by Karl Loren on behalf of Vibrant Life, ALL RIGHTS RESERVED.  Permission is granted for non-commercial downloading, copying, distribution or redistribution on two conditions:  One, that some form of copyright notice is included in every copy distributed or copied, showing the copyright belonging to Vibrant Life, Burbank, CA, at www.oralchelation.com . The second condition is that the material is not to be used for any purpose contrary to the purposes and objectives of this site.  This permission does not extend to materials on this site which are copyrighted by others.