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  1. #11
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    Lightbulb Iodide, antioxidant function and omega-6 and omega-3 fatty acids

    Iodide, antioxidant function and omega-6 and omega-3 fatty acids:
    a new hypothesis of a biochemical cooperation?

    Cocchi M. and Venturi S.
    Progress in Nutrition. 2000;2, 1:15-19

    Introduction.

    There is evidence in the most recent scientific literature (1,2,3) that iodide plays two different roles:

    1. antioxidant
    2. hormonal

    Both biological functions seem to coexist in the superior animal cells.

    Iodide is, also, strictly connected with two of the most important polyunsaturated fatty acids, Arachidonic Acid (AA, omega-6) and Docosahexaenoic Acid (DHA, omega-3), to forms specific iodolipids. Iodide, AA and DHA are determinant factors in brain development (4,5,6), having common metabolic pathways to guarantee brain growth and function. Those substances find a common denominator in the biochemical process which protect brain and nervous cells from peroxidative damage (7,8).

    In order to explain the biochemical hypothesis we must consider the phylogenetic and embryogenetic role of iodide and the modern explanation of AA and DHA during brain development and chemical maturation (9,10,11). Iodine is the richest in electrons among the element required in the diet. In nature, iodine exists as iodide ions (I-) and in this form is taken into the cells. Inorganic iodides are necessary for all living vegetal and animal cells, but only the Vertebrates have thyroid gland and its iodinated hormones.

    In humans, total amount of iodine is about 30.000 -50.000 mcg, and less than 20% are present in thyroid hormones and gland. About 60-80% og total iodine is non-hormonal and it is contentrated in non-thyroid tissues. The biological role of non-thyroid inorganic iodine is still unknown. Recently it has been hypothesized (2,12,13) that iodide might have, phylogenetically and evolutionistically, an ancient antioxidant role in all iodide-concentrating cells. Into these cells iodide acts as an electron donor in the presence of H2O2 and peroxidase (14). The remaining iodine readily iodinates the tyrosine and (more slowly) the histidine or some specific lipid, and so, neutralizes its owv high oxidant power.

    In fact, three billion years ago, Algae, which contain a high amount of iodine, were the first living cells to produce oxygen (which was toxic at that time) in terrestrial atmosphere. So, algal cells required a protective antioxidant action in which iodides might have had a specific role. Our hypothesis has now been confirmed experimentally in Algae by a recent study carried uot by Kupper et al. (15), and we....

    Reag more / les mer... (PDF redirect Sites.google.com)

  2. #12
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    Lightbulb Selenium and iodide: ancient antioxidants of cellular membrane lipids?

    Selenium and iodide: ancient antioxidants of cellular membrane lipids?
    Venturi S. M. Cocchi
    7th International Symposium on Selenium in Biology and Medicine. Venezia (Italy) Oct.1-5, 2000 Abstract Book, P-88 :134

    Over three billion years ago, blue-green algae (Cyanobacteria) ancestors of eukaryotic algae which contain high amount of iodine and selenium, were the first living cells to produce oxygen in the terrestrial atmosphere. So, algal membrane lipids and polyunsaturated fatty acids (PUFAs) required a protective antioxidant action in which iodide and selenium might have had this specific role. In fact, iodides and selenium are greatly available in seawater, where algal phytoplankton, the basis of marine food-chain, which is rich in PUFAs, acts as a biological accumulator of both of these trace elements (1). PUFAs and in particular Arachidonic Acid (AA, omega-6) and Docosahexaenoic Acid (DHA, omega-3) are essential for animal development and for cell membrane structure and function. DHA itself stimulates in cells the activites of catalase, glutatione-peroxidase and GSH.

    Recently, we have hypothesised that iodide might have an ancestral antioxidant function in all iodide-concentrating cells from primitive algae to more recent vertebrates (2). There is an interesting chemical gradient of electronegativity, according to Pauling-scale units, among Oxygen (3.44), Iodide (2.66), Selenium (2.55), which may explain their role in electron tranfert into oxygen of H2O2 via peroxidase enzymes. In the cells iodide acts as an electron donor in the presence of H2O2 and peroxidase, and the remaining iodine atom readily iodinates the tyrosine or the histidine or some specific PUFA, and so, it neutralizes its oxidant power. Iodine can add to double bonds of PUFAs, making them less reactive to free oxygen radicals. These iodolidips (iodo-lactone, iodo-AA, iodo-DHA) have structural and probably metabolic functions in vegetable and animal cells.

    In our current research we are studying iodide, selenium and PUFAs in different conditions during chick embryo development (3).

    References
    1. Cann SA et al. 2000. Hypothesis: iodine, selenium and the development of breast cancer.
      Cancer Causes Control; 11(2):121-7
    2. Venturi S et al. 2000. Role of iodine in evolution and carcinogenesis of thyroid, breast and stomach.
      Advances in Clinical Pathology; 4, 1:11-17
    3. Cocchi M and Venturi S. 2000. Iodide, antioxidant function and omega-6 and omega-3 fatty acids.
      Progress in Nutrition; 2, 1:15-19


    Source: Sites.google.com/site/iodinestudies/selenium

  3. #13
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    Lightbulb Iodine, PUFAs and iodolipids in health and diseases: an evolutionary perspective.

    Iodine, PUFAs and iodolipids in health and diseases: an evolutionary perspective. (PUFAs = Polyunsaturated fatty acids)
    S Venturi, CA Castellano, SC Cunnane
    Human Evolution: Past, Present & Future: Anthropological, Medical & Nutritional Considerations. London, 8-10th May 2013

    Iodine and polyunsaturates (PUFA)
    • Crucial for the evolution of life
    • “Membrane lipid language“ of cells (2) (Figures 1, 2)
    • Structurally and metabolically synergic

    Iodide (I-) – an antioxidant
    • Electron donor through peroxidase enzymes.
    • Most ancient inorganic antioxidant in all iodide concentrating cells from primitive marine algae to vertebrates (4,5).

    Evolution of the thyroid and brain
    • Origin in the primitive vertebrate foregut
    • About 500 million years ago, thyroid cells specialized in the uptake and storage of iodo-compounds in the thyroid, a new follicular organ.
    • At the same time, ectodermic cells differentiated into neuronal cells and became the primitive nervous system (2, 3).

    Iodo-lipids
    • Synthesized by thyroid cells, neurons
    • Novel “words” of the chemical “lipid language”
    • Membrane adaptation to the terrestrial environment.
    • Implicated in apoptosis, carcinogenesis, degenerative diseases as well as "(semi)aquatic theory" of human evolution.

    PUFA susceptible to peroxidation
    • Primitive oxygenic and photosynthetic algae, the basis of the marine food chain, accumulated trace-elements such as I and Se to protect the fragile PUFAs in their cell membranes against peroxidation (~3.5 billion years ago).
    • In chemistry, the amount of unsaturation (double bonds) in PUFA is the iodine value or iodine number.
    • Fish do not synthesize omega-3 fatty acids but only accumulate them by eating algae.

    Hypothyroidism in humans
    • Thyroidectomy or iodine deficient hypothyroidism - metabolic and phylogenetic regression to antecedent reptile stage.
    • Many symptoms of the hypothyroid humans seem to be like in reptiles: dry, hairless, scaly and cold skin with a general slowdown of metabolism, digestion, heart rate, nervous reflexes, lethargy and hypothermia (6).

    Amphibian metamorphosis
    • Iodine and T4 stimulate the spectacular apoptosis (programmed cell death) of the cells of the larval gills, tail and fins
    • Transforming the aquatic, vegetarian tadpole into the terrestrial, carnivorous frog with better neurological, visuospatial, olfactory and cognitive abilities for hunting (6).
    • Contrasts with neotenic amphibian salamanders, which, without introducing iodine, don’t transform in terrestrial adults and live and reproduce in the larval form of aquatic axolotl.

    Read more in PowerPoint Download from Sites.google.com, one page, 1,2 MB (big file)


    Iodine, PUFAs and iodolipids in health and diseases: an evolutionary perspective. (2) (PUFAs = Polyunsaturated fatty acids)

    The structural, metabolic and synergic actions of iodine and polyunsaturated fatty acids (PUFAs) are of crucial importance for the evolution of life on earth and for the "membrane lipid language“ of the cells (2) (Fig. 8).

    Iodide (I-), acts in marine and terrestrial organisms as an electrondonor through peroxidase enzymes and it is the most primitive inorganic antioxidant in all iodide-concentrating cells from primitive marine algae to more recent vertebrates.

    About 500 million years ago, thyroid cells (which had their origin in the primitive vertebrate foregut) migrated and they specialized in the uptake and storage of iodo-compounds in the thyroid, a new follicular organ. At the same time, ectodermic cells differentiated into neuronal cells and became the primitive nervous system and brain. (2, 3).

    Both these cells types synthesize iodo-lipids, as a novel “words” of the chemical “lipid language” that developed among cell membranes as an adaptation to the terrestrial environment. The study of iodo-lipids might be a new study area for research on apoptosis, carcinogenesis and degenerative diseases as well as on the "(semi)aquatic theory" of human evolution.

    Read more in PDF-file attached below...
    Vedlagte filer Vedlagte filer

  4. #14
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    Lightbulb Is there a role for iodine in breast diseases?

    Is there a role for iodine in breast diseases?
    Venturi S., 2001.
    Breast. 2001 Oct;10(5):379-82.

    "It is hypothesized that dietary iodine deficiency is associated with the development of mammary pathology and cancer. A review of the literature on this correlation and of the author's own work on the antioxidant function of iodide in iodide-concentrating extrathyroidal cells is reported.

    Mammary gland is embryogenetically derived from primitive iodide-concentrating ectoderm, and alveolar and ductular cells of the breast specialize in uptake and secretion of iodine in milk in order to supply offspring with this important trace-element.

    Breast and thyroid share an important iodide-concentrating ability and an efficient peroxidase activity, which transfers electrons from iodide to the oxygen of hydrogen peroxide, forming iodoproteins and iodolipids, and so protects the cells from peroxidative damage. The mammary gland has only a temporary ability to concentrate iodides, almost exclusively during pregnancy and lactation, which are considered protective conditions against breast cancer."

    Read more / les mer... (Sites.google.com)

  5. #15
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    Lightbulb Does iodide in the gastric mucosa have an ancient antioxidant role?

    Does iodide in the gastric mucosa have an ancient antioxidant role?
    by Sebastiano Venturi and Marta Venturi, Pennabilli, Italy,
    IDD Newsletter Volume 14 Number 4 November 1998

    The thyroid is derived both embryogenetically and phylogenetically from the primitive gut. As such, we may consider thyroid cells to be primitive gastroenteric cells that during evolution migrated and specialized in iodide uptake, storage, and elaboration of iodinated compounds. The stomach and thyroid share an iodine concentrating ability and many morphological and functional features, such as apical microvilli, secretion of glycoproteins (thyroglobulin and mucin) and amino-acid hormones, the ability to digest and reabsorb, and the ability to form iodotyrosines by peroxidase activity (1).

    However, the gastric iodide pump is phylogenetically more primitive than that of the thyroid, has a lower affinity for iodide, and does not respond to TSH.

    What is the role of iodide in stomach pathophysiology? Iodide reduces H2O2 in normal thyroid hormonogenesis and defends cells
    from lipid peroxidation in rats (2). In previous work (3) we have reported that iodine deficiency or excess might constitute a risk factor for stomach cancer and atrophic gastritis, both by regulating gastric response and by antagonizing the action of inhibitors such as nitrates, thiocyanates, and salt, well known risk factors for gastric carcinogenesis. Recently we have hypothesized that iodide might have an antioxidant role in more ancient organs, particularly in the stomach (4). In fact, three billion years ago, iodine-rich algae were the first living cells to produce oxygen, which was toxic at that time, in the terrestrial atmosphere. Therefore, algae cells required a protective antioxidant action, in which iodides might have a specific role.

    The thyroid gland is phylogenetically a modern organ. It first appeared in a primitive chordate and evolved more recently in
    mammals. T3 nuclear receptors are evolutionarily recent in comparison with those for T4. In fact, T4 is present in fibrous
    exoskeletal tissues of invertebrates without any hormonal action. When primitive marine animals started to emerge from the iodine-rich sea and transferred to the iodine-deficient land, their terrestrial diet became iodine deficient and also harbored iodine competitors, such as nitrates, nitrites, thiocyanates and some glycosides.

    From these considerations, we suggest that these animals learned to use T4 to transport antioxidant iodide into the cells, utilizing the remaining T3 for metamorphosis and thermogenesis, with new hormonal action made possible by the formation of modern T3 receptors.

    References:
    1. Banerjee RK, Bose AK, Chakraborty TK, et al. (1985) Peroxidase-catalyzed iodotyrosine formation in dispersed cells of mouse extrathyroidal tissues. J Endocrinol 106:159-65.
    2. Katamine S, Hoshino N, Totsuka K, Suzuki M 1985 Effects of the long-term feeding of high-iodine eggs on lipid metabolism and thyroid function in rats. J Nutr Sci Vitaminol 31:339-53.
    3. Venturi S, Venturi A, Cimini D, Arduini C, Venturi M, Guidi A 1993 A new hypothesis: iodine and gastric cancer. Eur J Cancer Prevention 2:17-23.
    4. Venturi S, Guidi A, Venturi M 1996 I disordini extra-tiroideida carenza iodica. Qual it reale fabbisogno di iodio? Le Basi Razionali della Terapia 16:267-75.



    Source: IDD Newsletter Volume 14 Number 4 November 1998 (Web.Archive.org)

  6. #16
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    Lightbulb Role of iodine in evolution and carcinogenesis of thyroid, breast and stomach.

    Role of iodine in evolution and carcinogenesis of thyroid, breast and stomach.
    Venturi S, Donati FM, Venturi A, Venturi M, Grossi L, Guidi A.
    Adv Clin Path. 2000 Jan;4(1):11-7. Review.

    “The authors have hypothesized that dietary iodine (deficiency or excess) is associated with the development of some gastric and mammary cancers, as it is well-known for thyroid cancer. They report a short review of their own work and of the general literature on this correlation and on the antioxidant function of iodide in stomach, breast and thyroid.

    Thyroid cells phylogenetically derived from primitive iodide-concentrating gastroenteric cells which, during evolution, migrated and specialized in uptake and storage of iodine, also in order to adapt the organisms from iodine-rich sea to iodine-deficient land. Mammary cells also derived from primitive iodide-concentrating ectoderm. Stomach, breast and thyroid share an important iodide-concentrating ability and an efficient peroxidase activity, which transfers electrons from iodides to the oxygen of hydrogen peroxide and so protects the cells from damage caused by lipid peroxidation.

    The authors suggest that iodide might have an ancestral antioxidant function in all iodide-concentrating cells from primitive Algae to more recent Vertebrates. In Italy, gastric cancer is more frequent in farmers and in iodine-deficient populations, living in mountainous and hilly areas, than in fishermen. In the last two decades, Italian decrease of gastric cancer seems to be correlated more to the higher dietary consumption of iodine-rich fish rather than to consumption of fruit and vegetables, which indeed has decreased in Italy."

    Read more / les mer... (PDF Sites.google.com/site/iodinestudies)

  7. #17
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    Lightbulb Dietary Iodine and Gastric Cancer

    Sitat Opprinnelig skrevet av Mod Vis post
    Dietary Iodine and Gastric cancer 1994-96
    S. Venturi - Coll.: M. Venturi, A. Guidi, F.M. Donati
    iProject of study published in "Directory of on-going research in cancer epidemiology" 1994 and 1996, IARC books, Lyon
    Eur. J. Cancer Prev., 2:17-23, 1993

    Project of study published in "Directory of on-going research in cancer epidemiology" 1994 and 1996, IARC books, Lyon

    The aim of this study is to test the hypothesis that iodine deficiency, or, in some cases, iodine excess is a risk factor for gastric cancer. Recent regional and district data on the epidemiology of endemic goitre and gastric cancer in Italy will be correlatad. Gastric cancer trends (until 1997) will be monitored in the populations (district of Montefeltro, Bolzano and Garfagnana) where iodine prophilaxis have been introduced only in recent years (1981-1985). Atrophic gastritis prevalence in Montefeltro district will be reconsidered, and gastric cancer mortality trends in the province of Aosta, where the iodine prophilaxis was interrupted in 1975, will be analysed. The iodide-trapping ability of the stomach and the thyroid gland is inhibited by goitrogens, such as nitrate, thiocyanate and salt, previously studied as risk factors for gastric cancer. Previous studies have shown that iodine deficient individuals have more gastric cancer and atrophic gastritis than non deficient subjects; it is believed that iodine is able to regulate gastric trophism and antagonise the action of the above mentioned iodine inhibitors.

    Source: https://sites.google.com/site/iodinestudies/dietary

  8. #18
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    Lightbulb Iodide, thyroid and stomach carcinogenesis: evolutionary story of a ....

    Iodide, thyroid and stomach carcinogenesis: evolutionary story of a primitive antioxidant?
    Sebastiano Venturi, Marta Venturi
    Letter to Editor
    European Journal of Endocrinology (1999) 140 371–372
    Eur J Endocinol. 1999 Apr;140(4):371-2


    The thyroid gland is, embryogenetically and phylogenetically, derived from primitive gut, and we may consider the thyroid cells such as primitive gastroenteric cells which, during evolution, migrated and specialized in uptake of iodide, and in storage and elaboration of iodine compounds.

    Stomach and thyroid share iodine-concentranting ability, and many morphological and functional similarities, such as cell polarity and apical microvilli, similar organ-specific antigens and associated autoimmune diseases (1), secretion of glycoproteins (thyroglobulin and mucin) and peptide hormones, the digesting and readsorbing ability and, lastly, similar ability to form iodotyrosines by peroxidase activity, where iodide acts as electron donor in the presence of H2O2 (2).

    However, gastric iodide-pump, phylogenetically more primitive than the thyroidal one, has lower affinity for iodide and do not respond to more recent TSH. So, in pregnant mouse, fetal gastric mucosa shows iodine-concentranting ability earlier than fetal thyroid (3). During human total-body 131I-scintiscans, the radioiodine remains on the stomach more than 72 hours. Similar finding has been reported in bovine abomasum, since cows have an efficient iodine recycling system via the gastrointestinal tract which conserves iodine and can protect them against low dietary iodine (4). In primitive reptilian stomach of lizard radioiodine remains more than 8 days (5).

    But which is the role of iodide in the pathophysiology of the stomach? Dietary iodides are able to defend brain cells from lipid peroxidation in rats (6). In normal thyroid hormonogenesis iodide, giving its electron to oxygen, reduce H2O2 by peroxidase activity. The remaining iodine readily iodinates the tyrosine and so neutralizes its own high oxidant power. The antioxidant action of iodide was described also in isolated rabbit eyes (7).

    In old works, Stocks (8) and Spencer (9), reported that iodine-deficient goitre constitute a risk for gastric cancer. Recently, we reported (10) that iodine-deficiency (or excess) might represent a risk factor for gastric cancer and atrophic gastritis, by regulating gastric trophism and by antagonizing (in thyroid cells and in gastric mucosa) the action of several iodine-inhibitors, such as nitrates, thiocyanates and salt (11), which are well-known risk-factors for gastric carcinogenesis.

    Furthermore, mammary gland has high ability to concentrate iodide and to form iodoproteins by mammary peroxidase, exclusively during pregnancy and lactation, which are considered protective conditions against breast cancer (12). Recently, we have hypothesized that iodide might have, since primitive Algae and primitive gastral cavity of Porifera, an antioxidant role in iodine-concentranting organs, and particularly in the stomach of the Vertebrates (13)(14). And now this role is experimentally confirmed in Algae by a study carried out by F.C. Kupper et al.(15).

    In fact, three billion years ago, Algae, which contain a high amount of iodine, were the first living cells to produce oxygen, toxic at that time, in terrestrial atmosphere. So, algae cells required a protective antioxidant action in which iodides might have had a specific role.

    The thyroid gland is, phylogenetically a modern organ and its function started and was improved from primitive Chordates to more recent Mammalia. Also evolutionistically recent are the T3-receptors in comparison with primitive Thyroxine (T4). In fact T4 is present in fibrous exoskeletal tissues of the lowest animals (Invertebrates)without showing any hormonal action (16). When the primitive marine-animals started to emerge from the sea, rich of iodine, and transfered in iodine-deficient mainland, their terrestrial diet became deficient of iodine and rich of iodine-competitors (nitrates, nitrites, thiocyanates, some glycosides, etc.).

    Therefore, we believe that, during the evolution to adapt to terrestrial life, these animals learned to use the primitive T4, in the place of the competitivized iodide, in order to transport into the cells this antioxidant trace-element, utilizing the remaining T3, the real active hormone of modern Vertebrates, for metamorphosis and thermogenesis with a new hormonal action through the formation of T3-receptors (16). As inhibitors of lipid peroxidation, by 5’-monodeiodinase activity, T4 and reverse T3 were found to be more effective in this antioxidant activity than vitamin E, glutathione and ascorbic acid (17).

    In conclusion, we believe that the evolutionary story of iodide and thyroid might suggest and explain a primitive antioxidant activity of this trace-element. We should point out that extrathyroidal action of iodide might be an important new area for investigation.

    REFERENCES

    1. Roitt I, Brostoff J & Male DK. The autoimmunity. In Immunologia, pp 231-7 (Eds Roitt I, Brostoff J & Male DK). Italian Ed USES ,1988.
    2. Banerjee RK, Bose AK, Chakraborty TK, De SK & Datta AG. Peroxidase-catalysed iodotyrosine formation in dispersed cells of mouse extrathyroidal tissues. J Endocrinol 1985 106 2, 159-65
    3. Ullberg S & Ewaldsson B. Distribution of radio-iodine studied by whole-body autoradiography. Acta Radiologica Therapy Physics Biology 1964 2 24-32
    4. Miller JK, Swanson EW & Spalding GE. Iodine absorption, excretion, recycling, and tissue distribution in the dairy cow. J Dairy Sci. 1975 58 1578-1593
    5. Shaham Y & Lewitus Z. Radioiodine metabolism in the thyroid gland of the lizard (Agama Stellio). General and Comparative Endocrinol.1971 17 142-8
    6. Katamine S, Hoshino N, Totsuka K & Suzuki M. Effects of the long-term feeding of high-iodine eggs on lipid metabolism and thyroid function in rats. J Nutr Sci Vitaminol 1985 31 339-53
    7. Elstner EF, Adamczyk R, Kromer R & Furch A. The uptake of potassium iodide and its effects as an antioxidant in isolated rabbit eyes. Ophthalmologica 1985 191 122-6
    8. Stocks P. Cancer and goitre. Biometrika 1924 16 364-401
    9. Spencer JGC. The influence of the thyroid gland in malignant disease. Br J Cancer 1954 8 393-411
    10. Venturi S, Venturi A, Cimini D, Arduini C, Venturi M & Guidi A. A new hypothesis: iodine and gastric cancer. Europ J Cancer Prevention 1993 2 17-23
    11. Wolff J. Transport of iodide and other anions in the thyroid gland. Physiol Rev 1964 44 45-90
    12. Eskin BA. Iodine metabolisme and breast cancer. NY Acad Sci 1970 32 911-947
    13. Venturi S, Guidi A & Venturi M. I disordini extra-tiroidei da carenza iodica. Qual è il reale fabbisogno di iodio? Le Basi Razionali della Terapia 1996 16 267-75
    14. Venturi S, Stanghellini V, Donati FM, Barbara B, Salvioli R & Corinaldesi R. Does dietary iodine prevent gastric cancer? Ital J Gastroenterol Hepatol 1998 30 238
    15. Kupper FC, Schweigert N, Ar Gall E, Legendre J-M, Vilter H & Kloareg B. Iodine uptake in Laminariales involves extracellular, haloperoxidase-mediated oxidation of iodide. Plancta 1998 207 :163-171
    16. Venturi S. Letter to the Editor. The Thyroid Gland, Clinical and Experimental 1998 1 23
    17. Tseng YL & Latham KR. Iodothyronines: oxidative deiodination by hemoglobin and inhibition of lipid peroxidation. Lipids 1984 19 96-102



    Read more / Les mer... (PDF Eje-online.org)

  9. #19
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    Lightbulb Syndrome thyro-gastric. Study on the relation between alimentary iodine deficiency...

    Syndrome thyro-gastric. Study on the relation between alimentary iodine deficiency and gastric cancer
    Venturi S, Marani L, Magni MA
    Epidemiology Prevention and Early Detection of Gastric Cancer.
    In: Ghironzi G, Jackson CE, Schuman BM, Editors. Editor CIC Intern. Rome, . (Chapter of book) 1987


    Update of content later...

  10. #20
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    Lightbulb A new hypothesis: iodine and gastric cancer.

    A new hypothesis: iodine and gastric cancer
    S. Venturi, A. Venturi, D. Cimini, C. Arduini, M. Venturi, A. Guidi
    European Journal of Cancer Prevention. Vol 2. 1993
    Eur J Cancer Prev. 1993 Jan;2(1):17-23.


    The authors have hypothesized that iodine-deficiency (I-def) or in some cases iodine-excess (I-excess) is associated with the development of gastric cancer. They report a short review of their own work and general literature on this subject in three fields: (1) epidemiology, where geographical and temporal correlations between territories with I-def (or I-excess) endemic goitre and high GC-death rate are reported; (2) immunology, where the possible correlations between I-def, immune-deficiency and GC are reported; and (3) thyroid gland and stomach correlations, both being embryologically derived from primitive gut and able to concentrate iodine. This ability is impaired by nitrates, thiocyanate, salt and by I-excess, which in fact can cause goitre. In our study I-def goitrous people have shown more atrophic gastritis than normal subjects. These data enable us to hypothesize that I-def or I-excess might constitute a new risk factor for gastric cancer, both by regulating gastric trophism and by antagonizing the action of those I-inhibitors (such as nitrates, thiocyanate and salt) previously studied as risk factors for gastric cancer.

    Read more / Les mer... (PDF redirect Sites.google.com/site/iodinestudies)
    Read more / Les mer... (PDF online Researchgate.net)
    Til alle norske og danske stoffskifte-pasienter, anbefaler vi boken STOP stofskiftevanviddet, skrevet av verdens ledende pasient-aktivist Janie Bowthorpe, som i 2005 grunnla nettstedet Stop The Thyroid Madness. Boken er utgitt på dansk i 2014. För alla svenska hypotyreos-patienter, rekommenderar vi samma bok, översatt till svenska med titeln Stoppa sköldkörtelskandalen (2012). Til alle gode leger, og pasienter som ønsker å lære mer av "the right stuff", anbefaler vi boken Stop The Thyroid Madness II (2014) med bidrag fra 10 leger MD. I Skandinavia, definitivt de to beste og mest nyttige bøker for hypotyreose-pasienter, for deres familier og venner, og for deres leger.

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