Forskning i jod av dr. Sebastiano Venturi

(Introduksjon til denne tråden er skrevet av Anisa.)

"Kjertelen monterer 4 stk. Jodatomer på Thyrosinet og så har vi et T4 molekyl. Dette T4 bruker ikke kroppen til noe, men det er utgangspunktet til T3. Alle friske som har et fungerende kjertelsystem MÅ ha Jod til denne prosessen. Dette er imidlertid det eneste i kroppen som bruker jod.

Det vil si at hvis du IKKE har et fungerende kjertelsystem og spiser ferdig konstruerte T4 thyroxiner, så den Jod som evetuellt finnes i ditt legeme vil ikke bli brukt til noe som helst og bare hoper seg opp til inga nytte og skaper problemer istedenfor."

Lad os høre, hvad "videnskaben" siger til påstanden om at jod er kun for de friske, med sunde og velfungerende skjoldbruskkirtler, mens alle vi andre skal undgå jod, så det ikke "hoper seg opp til inga nytte og skaper problemer istedenfor".

Mere "videnskabeligt" end tidsskriftet Current Chemical Biology kan det næsten ikke blive, og netop i indledningen til Volume 5, Number 3, September 211 læser vi bl.a. følgende (her maskinoversat til norsk):

"De fleste studier av jod-metabolisme hos mennesker og dyr har fokusert på dets rolle i skjoldbruskkjertelens funksjon. Offentlig folkehelsepolitikk ble etablert for å forsyne jod-mangelfulle populasjoner med den nødvendige mengden av dette elementet for å utrydde jodmangelsykdommer, primært kretinismen. Imidlertid indikerer betydelige beviser på at jod kan også være innblandet i fysiologien av andre organer.

Hos mennesker er den totale mengden av jod i kroppen mellom 30 til 50 mg, og mindre enn 30% av det er til stede i skjoldbruskkjertelen og dens hormoner. Omtrent 60% av total jod er ikke-hormonelt og konsentreres i de øvrige vev og organer"...

... til hvad nytte mon, snupper resten af kroppen hele 60% af det daglige jod, mens skjoldbruskkirtlen og thyreoidea-hormoner i kirtlen og i blodbanen nøjes med kun 40%? Så er det godt, at vi har en jod-klog italiener til at besvare det spørgsmål.


Forskning i jod av dr. Sebastiano Venturi

https://www.stofskifteforum.dk/image...rs/Venturi.PNG
Source: https://sites.google.com/site/iodinestudies/

Ikke mange ved, at den italienske læge Sebastiano Venturi er en af verdens førende forskere i jod, blandt medicinsk-videnskabelige jod-kapaciteter som dr. Guy E. Abraham MD, farmaceuten J. Charles Hakala RPh, dr. Jorge Flechas MD, dr. David Brownstein MD (The Iodine Project [PDF]).

Ingen andre, som dr. Venturi, er rejst så langt tilbage i Jordens fortid i søgen efter spor jod har afsat i evolutionen af liv. Han er også den første videnskabsmand, der observeret overraskende ligheder mellem krybdyrenes stofskifte og sygdommen hypothyreose (lavt stofskifte), relateret til, og ubrydeligt forbundet med jod.

For alle der er blevet følelsesmæssigt, mentalt og intellektuelt udmarvet af den "moderne" reality-kultur, overfyldt til randen med tanketomme ansigter fulde af "mascara, blekede tenner, sillikon i pupper eller lepper, hold-in og push-up", tillige rigeligt krydret med tidens hipsters skønheds-karikaturer.... kan interessen for dr. Venturis jod-forskning - for det rette sind og intellekt - blive en ganske overraskende interessant, opbyggende og til tider også overvældende oplevelse...

Dr. Sebastiano Venturi er født d. 2. maj 1947 i Italien, i byen Pennabilli beliggende tæt på den gamle republik San Marino, i provinsen Pesaro e Urbino. Efter almindelig skolegang i fødebyen Pennabilli flyttede han til Bologna. I 1972 dimitterede han med udmærkelse i medicin og kirurgi fra Bologna Universitet. Fra 1972 til 1987 arbejdede dr. Venturi som læge ved flere hospitaler i Italien, herunder i National Health Service i Institut for Hygiejne & Sygdomsforebyggelse, og i Afrika.

Fra 1989 til 2002 arbejdede dr. Venturi indenfor medicinsk forskning ved Endokrinologisk Fakultet på Pisa University hos prof. Aldo Pinchera. I årene 2004-2007 var dr. Venturi lektor ved "Thyroid Club" årsmøder på Bologna og Urbino og Perugia Universiteter. Dr. Venturi er forfatter til over 70 internationale og nationale videnskabelige publikationer, to monografier (1978 og 2012), fem bog-kapitler (1987, 1990, 2006, 2010, 2011), og to bøger (1978, 1985). Dr. Venturis Curriculum Vitae kan læses her.

Dr. Venturis ekspertområder:

• Jod som antioxidant;
• Struma;
• Neuropsykologiske patologier;
• Kretinisme;
• Jodmetabolisme;
• Immunitet;
• Forebyggelse af jodmangel;
• Autoimmun Atrofisk Gasrtritis;
• Mavekræft;
• Brystkræft;
• Spytkirtler;
• Oral sundhed;
• Biokemisk evolution af liv på Jorden.

Indenfor disse emner, inviteres dr. Venturi til at reviewe artikler publiceret i følgende tidsskrifter:

• Clinical Chemistry and Laboratory Medicin,
• International Journal of Cancer,
• Acta oncologica,
• Tumor Biology, Thyroid,
• Surgery Today,
• European Journal of Nutrition,
• Endocrine-Related Cancer,
• Nature,
• Aquacultur,
• Journal of Pediatric Biochemistry,
• Clinical Nutrition.

Ressources:

• Dr. Sebastiano Venturi. Iodinestudies
• Sebastiano Venturi - Academia.edu
• Sebastiano Venturi - Publications - ResearchGate
• Sebastiano Venturi - Google Scholar Citations
• Sebastiano Venturi - YouTube
• Sebastiano Venturi - Slideshare.net

Dr. Venturi er sandsynligvis den nulevende forsker der ved mest om betydningen af mineralet Jod. Hans ekspertområde spænder vidt fra viden om betydningen af jod for opståen af liv på vores planet - til rollen som jod og jodmangel har spillet, og fortsat spiller både medicinsk, socialt og økonomisk i generationerne siden 1950-erne på planeten Jorden. Dr. Venturi er medlem af The Italian Thyroid Association (AIT).

Dr. Venturis hjemmeside er enkel, nogen vil endda driste sig til at kalde den "primitiv" eller "lavteknologisk". Den er i hvert fald ikke "moderne". Hvis man ønsker at nyde det sidste nye indenfor det ypperligste webdesign, skal man styre udenom dr. Venturis hjemmeside. Ønsker man derimod at få indblik i jod, jod-historie og jod-kundskab på højeste niveau - kommer man ikke til at surfe forgæves på dr. Venturis hjemmeside. Den er så afgjort værd at løsrive sig fra sin IPhone og sætte sig foran PCen igen.

Er man på rejse med sin IPhone i lommen, kan man besøge dr. Venturis Sebastiano_Venturi2/publications og Sebastiano_Venturi3/publications på den mobile responsive Researchgate.net

Herunder følger en "klikbar" liste med links til dr. Venturis vigtigste artikler oversat til engelsk. Foreløbig tæller listen 28 henvisninger. Den bliver opdateret efterhånden der evt. publiceres/oversættes flere. Enjoy.

1. Indledning
2. Iodine and Evolution (Iodo ed Evoluzione)
3. Evolutionary significance of iodine.
4. Environmental iodine deficiency: a challenge to the evolution of terrestial life?
5. Evolution of dietary antioxidants: role of iodine.
6. Evolution of dietary antioxidant defences.
7. Iodine, thymus and immunity.
8. Role of iodine in delayed immune response.
9. Iodine in evolution of salivary glands and in oral health. (1)
   Iodine in evolution of salivary glands and in oral health. (2)
10. Thyroid hormone, iodine and human brain evolution.
11. Iodide, antioxidant function and omega-6 and omega-3 fatty acids: a new hypothesis of a biochemical cooperation?
12. Selenium and iodide: ancient antioxidants of cellular membrane lipids?
13. Iodine, PUFAs and iodolipids in health and diseases: an evolutionary perspective. (1)
    Iodine, PUFAs and iodolipids in health and diseases: an evolutionary perspective. (2)
14. Is there a role for iodine in breast diseases?
15. Does iodide in the gastric mucosa have an ancient antioxidant role? 1998
16. Role of iodine in evolution and carcinogenesis of thyroid, breast and stomach.
17. Dietary Iodine and Gastric Cancer
18. Iodide, thyroid and stomach carcinogenesis: evolutionary story of a primitive antioxidant?
19. Syndrome thyro-gastric. Study on the relation between alimentary iodine deficiency and gastric cancer
20. A new hypothesis: iodine and gastric cancer
21. Iodine, Helicobacter Pylori, Stomach Cancer & Evolution.
22. Iodine, Evolution and Gastric Carcinogenesis.
23. Clinical picture of endemic cretinism in central Apennines .
    Iodine Deficiency in the Population of Montefeltro, A Territory in Central Italy Inside the Regions of Emilia-Romagna, Tuscany and Marche.
24. Audiological and neuropsychological development study in a sample of school children from a low-iodine area of the Central Apennines that is endemic for cretinism.
    An iodine-deficient area with endemic cretinism in the Central Apennines: studies of neuropsychological development in schoolchildren.
25. Humoral thyroid autoimmunity is not involved in the pathogenesis of myxedematous endemic cretinism.
26. Extrathyroid Iodine Deficiency Disorders. What is the real iodine requirement?
27. Enigma of the function of iodide in primitive algae and in animal extrathyroidal organs: is it an ancient antioxidant?
    The enigma of the function of thyroxine in animal extrathyroidal organs and in primitive stomach.
28. Preliminary study on the relation between alimentary iodine deficiency and gastric cancer: specific prevention prospects (1985 Book in Italian)

Dagens slogan: "Jod er ikke helse, men helse uden jod varer ikke længe!"

Today's slogan: Iodine is not health, but health without iodine does not last long!

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Opprinnelig skrevet av Mod

Iodine and Evolution.

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Iodine and Evolution
Venturi S
Published in Italian online: February 8, 2004

SUMMARY
The authors report their hypothesis on the antioxidant role of iodine in the evolution of life on the earth. Iodine is the most electron rich of the essential elements in the animal diet, and as iodide (I-) enters in the cells by an iodide transporter. Iodide, which acts as primitive electron donor by peroxidase enzymes, seems to have an ancestral antioxidant function in all iodide-concentrating cells from primitive marine algae to more recent terrestrial vertebrates.

Thyroxine and iodothyronines seem also to have an antioxidant activity, by deiodinase enzymes, which are donors of iodides and indirectly of electrons. Thyroid cells phylogenetically derived from primitive gastroenteric cells, which during evolution, migrated and specialized in uptake and storage iodine-compounds in the new follicle, as reservoir of iodine, for a better adaptation of modern vertebrates to iodine deficient terrestrial environment.

INTRODUCTION
Iodine (I) is the most electron rich of the essential elements in the animal diet, and as iodide (I-) enters in the cells. Inorganic iodide is necessary for all living cells, but only the vertebrates have a thyroid gland and its iodinated hormones. In humans, the total amount of iodine is about 25-50 mg and about 60-70 % of total iodine is non-hormonal which is concentrated in non-follicular extrathyroidal tissues, where its biological role is still unknown. Sodium iodide symporter (NIS) of iodide pump, which was in 1996 genetically characterised and cloned (1, 2), is a transmembrane protein which actively transports iodide into the cells.

Extrathyroidal NIS, more primitive than the thyroidal one, have a lower affinity for iodide and does not respond to more evolute TSH (Thyrotropin). We believe that the mechanism of iodide-pump (and NIS) is very ancient in the cells, and for this reason, there is a rather surprising lack of specificity for the anions. The pump is not able to distinguish iodide from other anions of similar atomic or molecular size, which may act as pseudo-iodides: thiocyanate, cyanate, nitrate, pertechnetate, perchlorate, [fluoride/red.]etc. On the contrary, this pump is partially able to defend itself and the cell from toxic I-excess (Wolff-Chaikoff effect) (3, 4).

IODINE AND EVOLUTION
Over three billion years ago, blue-green algae (Cyanobacteria), which are the most primitive oxygenic photosynthetic organisms, ancestors of multicellular eukaryotic algae that contain the highest amount of iodine (1-4 % of dry weight) and peroxidase enzymes, were the first living cells to produce poisonous oxygen in the atmosphere (5, 6, 7). Therefore algal cells required a protective antioxidant action in which iodides with peroxidase seem to have had this specific role (8, 9, 10).

In fact iodides are greatly present and available in sea-waters, where algal phytoplankton, the basis of marine food-chain, acts as a biological accumulator of iodides, selenium (and n-3 fatty acids). The sea is rich in iodine, about 60 micrograms (ug) per litre, since this is where most of the iodine removed and washed away from the soil accumulated by the glaciations ages.


Read more / les mer... (Sites.google.com The link is to the English summary, as well as the Italian article complete with pictures and diagrams.)

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Evolutionary significance of iodine.

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Evolutionary significance of iodine.
Chapter of book published in Current Chemical Biology: Volume 5, 3 Issues, 2011

Abstract: The significance of inorganic and organic forms of iodine in the evolution of plants and animals is reviewed. Iodine is one of the most electron-rich atoms in the diet of marine and terrestrial organisms, and it enters cells via iodide transporters. Iodide, which acts as a primitive electron donor through peroxidase enzymes, has an ancestral antioxidant function in all iodide-concentrating cells from primitive marine algae to more recent terrestrial vertebrates. Similarly, thyroxine and iodothyronines show antioxidant activities through deiodinase enzymes.

About 500-600 million years ago, in parallel with the evolution of the primitive brain in marine animals, thyroid cells originated from the primitive gut in vertebrates, migrated, and specialized in the uptake and storage of iodo-compounds in a novel follicular “thyroidal” structure, an adaptation that enabled the transition from the iodine-rich ocean to the iodine-deficient terrestrial environment.

Keywords: Antioxidants, evolution, iodine, iodide, thyroxine.


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Read more / les mer... (PDF Researchgate.net)

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Environmental iodine deficiency: a challenge to the evolution of terrestial life?

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Environmental iodine deficiency: a challenge to the evolution of terrestial life?
Sebastiano Venturi, Francesco M. Donati, Alessandro Venturi and Mattia Venturi
Published in "Thyroid", 2000 Aug;10 (8):727-9.

Iodine is the heaviest and richest in electrons among essential elements required in the diet. Inorganic iodides are necessary for all living vegetal and animal cells, but only the Vertebrates have the thyroid gland and its iodinated hormones. In humans the total amount of iodine is about 30-50 mg and less than 30 % is present in thyroid gland and in its hormones. About 60-80 % of total iodine is non-hormonal and it is concentrated in extrathyroidal tissues, but its biological role is still unknown. Recently we have hypothesized that iodide might have an ancestral antioxidant function in all iodide-concentrating cells from primitive Algae to more recent Vertebrates (1-7). Into these cells iodide acts as an electron donor in the presence of H2O2 and peroxidase (8), the remaining iodine readily iodinates the tyrosine and (more slowly) the histidine or some specific lipid (9), and so, neutralizes its own high oxidant power.

IODINE, THYROXINE AND THYROID EVOLUTION

Over three billion years ago, blue-green algae (Cyanobacteria), which are the most primitive oxygenic photosynthetic organisms, ancestors of multicellular eukaryotic algae, that contain the highest amount of iodine, were the first living cells to produce oxygen, which was toxic at that time, in the terrestrial atmosphere. So, algal cells required a protective antioxidant action in which iodides might have had this specific role. In fact iodides are greatly present and available in sea-waters, where algal phytoplankton acts as a biological accumulator of iodides. Recently our hypothesis of the ancestral antioxidant action of iodides has experimentally been confirmed in some algae by an important study carried out by Kupper et al.(10). Since about 700 million years ago thyroxine (T4) is present in fibrous exoskeletal scleroproteins of the lowest invertebrates (Porifera and Anthozoa)(11), without showing any hormonal action. When some primitive marine vertebrates started to emerge from the iodine-rich sea and transferred to iodine-deficient fresh water and finally land, their diet became iodine deficient and also harboured vegetal iodide-competitors such as nitrates, nitrites, thiocyanates and some glycosides (12). Hence these animals needed an efficient thyroid gland as reservoir of iodine. Therefore....

Keywords: antioxidant, evolution, iodide, iodine deficiency, selenium, thyroid

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Evolution of dietary antioxidants: role of iodine.

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Evolution of dietary antioxidants: role of iodine.
Venturi S, Venturi M
Lecture. Feb 6, 2007


The authors review the role of inorganic and organic forms of iodine as an antioxidant in evolution of plants and animals.

Iodine is one of the most abundant electron-rich essential element in the diet of marine and terrestrial organisms. It is transported from the diet to the cells via iodide transporters. Iodide, which acts as a primitive electron-donor through peroxidase enzymes, seems to have an ancestral antioxidant function in all iodide-concentrating cells from primitive marine algae to more recent terrestrial vertebrates. Thyroxine and iodothyronines have an antioxidant activity too and, through deiodinase enzymes, are donors of iodides and indirectly of electrons.

Thyroid cells phylogenetically derived from primitive gastroenteric cells, which during evolution of vertebrates migrated and specialized in uptake and storage of iodo-compounds in a new follicular “thyroidal” structure, for a better adaptation to iodine-deficient terrestrial environment. Finally, some animal and human chronic diseases, such as cancer and cardiovascular diseases, favored by dietary antioxidant deficiency, are briefly discussed.

Keywords: antioxidants, antioxidant evolution, evolution, iodine, iodide, thyroxine

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Read more / les mer... (Word.doc from Iodineresearch.com)

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Evolution of dietary antioxidant defences.

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Evolution of dietary antioxidant defences.
Venturi S. and Venturi M.
European Epi-Marker, 2007 Vol.11, 3 :1-12

SUMMARY. The evolution of oxygen-producing cells was probably one of the most significant events in the history of life. Protective endogenous antioxidant enzymes and exogenous dietary antioxidants (as Selenium, Iodine, etc.) helped to prevent oxidative stress. Iodide, which acts as a primitive electron-donor through peroxidase enzymes, seems to have an ancestral antioxidant function in all iodide-concentrating cells from primitive marine algae to more recent terrestrial vertebrates. When about 500 million years ago plants and animals began to transfer from the sea to rivers and land, environmental iodine-deficiency was a challenge to the evolution of terrestrial life. New endogenous antioxidants appeared in plants as ascorbic acid, polyfenols, carotenoids, flavonoids. A few of these appeared recently, about 200-50 million years ago in fruits and flowers of angiosperm plants. In the wide range of antioxidants, we hypothesise an “evolutionary hierarchy”, where the most ancient antioxidants might be more essential than the modern ones in the developing stages of animal and human organisms.

Keywords: antioxidants, ascorbic acid, carotenoids, flavonoids, evolution, iodine, selenium

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Iodine, thymus and immunity.

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Iodine, thymus and immunity.
Venturi S, Venturi M
Nutrition, 2009; 25 (9) : 977-9

The United Nations nutrition policy papers [1,2], Food and Nutrition Board and Institute of Medicine [3], Dunn [4], Dunn and Delange [5] of the International Council for the Control of Iodine Deficiency Disorders reported that extrathyroidal iodine has an important action on the immune system. The high iodide concentration of thymus provides the anatomic rationale for this role of iodine in the immune system [6,7] (Fig. 1)

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Role of iodine in delayed immune response.

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In this letter to the Israel Journal of Medical Sciences, the authors explain that in order to study the relationship between iodine intake and immune response they studied a population of 607 children, aged 6 to 10 years, living in an area where goitre was endemic. 48% of these children had a goitre. 215 of the children took Lugol’s solution (2 drops per week) for 8 months, and the remaining 392 did not. Immune response was assessed by means of skin testing with tetanus toxoid. If the diameter of the induration was at least 5 mm the response was classed as positive. Diameter of induration was significantly larger among those who had taken iodine than in those who did not. The authors conclude that adequate iodine intake is necessary for a normal delayed immune response.


Role of iodine in delayed immune response. [Iodine and delayed immunity].
[Article in Italian]
Marani L, Venturi S.
Minerva Med. 1986 May 7;77(19):805-9.

Abstract. Iodine was and is sometimes used therapeutically in various pathologies where the immune mechanism is known to play a dominant role. It has in fact been administered to patients with tubercular granulomatous, lepromatous, syphilitic and mycotic lesions where it facilitates cure. This effect does not depend on iodine's action on the micro-organism responsible. Iodine may also be used in Villanova-Panol Panniculitis, in erythema nodosum, in nodular vasculitis, erythema multiforme and Sweet's syndrome.

Oral iodine is also very effective in the lymphatic-cutaneous form of sporotrichosis. In order to establish a relationship between dietary iodine and immune response, 607 infants residing in an area of endemic goitre were studied: 215 were given Lugol solution (2 drops a week for about 8 months) and 392 not.

The immune response was assessed by the skin test method using tetanic toxoid and a clear correlation was shown between this and lymphocyte stimulation and monocytic chemotaxis tests. The test was considered positive when an infiltration of at least 5 mm in diameter was shown after 48 hours (in the U.S. 80% of paediatric cases aged 2-10 years old were positive).

A significant difference was noted in the average diameter of the infiltrations after the tetanic toxoid skin test in the two groups considered (P less than 0.001). The results appear to indicate that an adequate iodine intake is necessary for normal retarded immune response. The molecular mechanism by which iodine increases immune response is still to be decided.

Source: Pubmed (Full text article not yet found)

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Iodine in evolution of salivary glands and in oral health.
Iodine in evolution of salivary glands and in oral health. (2)

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Iodine in evolution of salivary glands and in oral health. (2005)
S. Venturi and M. Venturi
Lecture held at the “Thyroid Club” Annual Meeting of Bologna University, Febr.16, 2005

INTRODUCTION. Iodine (I) is the richest in electrons of the required elements in the animal diet, and as iodide (I-) enters into the cells. Inorganic iodide is necessary for all living animal cells, but only the vertebrates have the thyroid gland and its iodinated hormones.

In humans, the total amount of iodine is about 25-50 mg. About 50-70 % of total iodine is non-hormonal and it is concentrated in extra-thyroidal tissues, where its biological role is still unknown. In 1985, Venturi has hypothesized that iodide might have an ancestral antioxidant function in all I-concentrating cells from primitive marine algae to more recent terrestrial vertebrates [1-5 ]. In these cells iodide acts as an electron donor in the presence of H2O2 and peroxidases. The remaining iodine atom readily iodinates tyrosine, histidine or certain specific lipids, and so, neutralizes its own oxidant power.

Keywords: evolution, iodine, antioxidant, apoptosis, oral pathology, salivary glands

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Iodine in evolution of salivary glands and in oral health. (2) (2009)
S. Venturi and M. Venturi
Nutr Health. 2009;20(2):119-34.

ABSTRACT. The authors hypothesized that dietary deficiency or excess of iodine (I) has an important role in oral mucosa and in salivary glands physiology. Salivary glands derived from primitive Iodine-concentrating oral cells which, during embryogenesis, migrated and specialized in secretion of saliva and iodine.

Gastro-salivary clearance and secretions of iodides are a considerable part of “gastro-intestinal cycle of iodides”, which constitutes about 23% of iodides pool in the human body. Salivary glands, stomach and thyroid share I-concentrating ability by sodium iodide symporter (NIS) and peroxidase activity, which transfers electrons from iodides to the oxygen of hydrogen peroxide and so protects the cells from peroxidation.

Iodide seems to have an ancestral antioxidant function in all Iodine-concentrating organisms from primitive marine algae to more recent terrestrial vertebrates. The high Iodine-concentration of thymus supports the important role of iodine in the immune system and in the oral immune defence.

In Europe and in the world, Iodine-deficiency is present in a large part of the population. The authors suggest that the trophic, antioxidant and apoptosis-inductor actions and the presumed anti-tumour activity of iodides might be important for prevention of oral and salivary glands diseases, as for some other extrathyroidal pathologies.

FOREWORD. In the 1930s a correlation between malnutrition and oral health was reported, and, as cited by Weston A. Price (1939), some researchers have also hypothesized the specific correlation between Iodine-deficient goitre and dental caries (Hardgrove, 1939).

Price, in his famous world investigation "Nutrition and Physical Degeneration: A Comparison of Primitive and Modern Diets and Their Effects" (1939), mentioned that "in fish and sea food were essential trace-elements such as iodine, copper, manganese and special vitamins, which were very important for the prevention of health problems and tooth decay" in many coastal populations.

The aim of our study is to search for the pathophysiological correlation between these early nutritional studies and more recent (biochemical, autoradiographical and epidemiological) data regarding the correlation between dietary iodine and oral and salivary glands health.

Keywords: antioxidants; evolution; iodine; oral, dental and salivary pathologies

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Thyroid hormone, iodine and human brain evolution.

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Thyroid hormone, iodine and human brain evolution.
Venturi S. and Bégin M. E.
Chapter of book: "Environmental Influences on Human Brain Evolution"
by: Cunnane S. and Stewart K. Publisher: John Wiley, 2010. ISBN: 9780470452684

INTRODUCTION: Evolution of the hominin lineage is marked by progressive brain expansion and complexity concomitant with coordinated changes in other morphological and behavioral traits that characterize speciation events. In addition to gene variation, changes in climate, habitat, and diet are well-recognized environmental stimuli for evolutionary change. Iodine is an
environmental stimulus to which living organisms react, a point particularly evident in amphibian metamorphosis and potentially also in hominin evolution.

In toto, selection pressures effecting evolutionary change involve biological mechanisms permitting adaptation and evolution under changing environmental conditions. A common biological control mechanism could potentially coordinate a suite of physiological, morphological, and behavioral changes as important as brain evolution. We contend here that such a mechanism was hormonal and that thyroid hormone and iodine were pivotal components of such a mechanism.

The principal fossil sites of hominins correlated in space and time with volcanic and fissural local or nearby iodine sources (Borensztejn, 2005). In vertebrates, iodine is incorporated into thyroid hormone in the thyroid gland. Crockford (2003, 2008) provided solid evidence that changing thyroid function, specifically rhythms of thyroid hormone secretion, is crucial for speciation events taking place over decades.

The same thyroid hormone mechanism can be applied to the process of humanizing australopithecines. Here, we postulate a link between thyroid function, iodine, and evolutionary changes as they apply to the evolution of hominins and, more specifically, the large brain of Homo sapiens.

We emphasize changes in habitat and the connection between enhanced dietary availability of iodine, selenium, and polyunsaturated fatty acids (ikke flerumættede vegetabilske olier man spiser, men dem kroppen selv syntetiserer af fortrinsvis kostens animalske - æg, fuldfede mælkeprodukter, fisk m.v. - Omega-3'er/red.) as brain-selective nutrients necessary for thyroid function and hominin brain expansion.

Source: Environmental Influences on Human Brain Evolution (Book)

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

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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....

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Selenium and iodide: ancient antioxidants of cellular membrane lipids?

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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

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

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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.

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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.

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Is there a role for iodine in breast diseases?

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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."

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Does iodide in the gastric mucosa have an ancient antioxidant role? 1998

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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)

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Role of iodine in evolution and carcinogenesis of thyroid, breast and stomach.

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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."

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Dietary Iodine and Gastric cancer

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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

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Iodide, thyroid and stomach carcinogenesis: evolutionary story of a primitive antioxidant?

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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

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Syndrome thyro-gastric. Study on the relation between alimentary iodine deficiency and gastric cancer.

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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


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A new hypothesis: iodine and gastric cancer.

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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.

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Iodine, Helicobacter Pylori, stomach cancer & evolution.

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Iodine, Helicobacter Pylori, stomach cancer & evolution.
Venturi S, Grossi L, Marra GA, Venturi A, Venturi M
The Newsletter of the International Center for Studies and Research in Biomedicine, Luxembourg, Vol. 7, No. 2, April 2003, pp 1-7.


The authors have hypothesized that dietary iodine (I) deficiency or excess are associated with the development of atrophic gastritis and gastric cancer (GC). They report a short review of their own work and general literature on this correlation in three fields: (1) epidemiology, where geographical and temporal correlations between territories with I-deficiency, endemic goitre and high gastric cancer-death rate are reported; (2) iodine and atrophic gastritis correlations, and (3) immunology, where the correlations between I-deficiency, immune-deficiency and gastric cancer are reported.

Thyroid cells phylogenetically and embryologically, derived from primitive Iodine-concentrating gastric cells which, during evolution, migrated and specialized in uptake and storage of iodine, in order to adapt the organisms from Iodine-rich sea to Iodine-deficient land.

Stomach 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 peroxidations. Iodide seems to have an ancestral antioxidant function in all iodide-concentrating organisms 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 with the higher dietary consumption of Iodine-rich fish rather than with consumption of fruit and vegetables, which indeed has decreased in Italy.

In conclusion, iodine deficiency or excess seem to constitute an important risk factors for atrophic gastritis and gastric cancer, both by antioxidant activity and regulating gastric trophism and by antagonizing the actions of both Helicobacter pylori and of Iodine-inhibitors, such as nitrates, thiocyanate and salt, well-known risk factors for gastric cancer.

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[U]Iodine, Evolution and Gastric Carcinogenesis

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Iodine, Evolution and Gastric Carcinogenesis
Venturi S, Venturi M.
The 2nd Esophageal & Cardiac Cancer Summit, October 18-20 2007, Beijng, China

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Clinical picture of endemic cretinism in central Apennines (Montefeltro).

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Clinical Picture of Endemic Cretinism in Central Apennines (Montefeltro)
Donati L; Venturi S; Andreani M; Antonelli A; Gori E; Bertoni F; Pruneti CA; Berrettini S; Bruschini P; Baschieri L
Università di Pisa, Pisa, Tuscany, Italy
Thyroid. 10/1992; 2(4):283-290. DOI: 10.1089/thy.1992.2.283

ABSTRACT. Endemic cretinism is still present in an endemic goiter area of the central Apennines (Montefeltro) (goiter prevalence 55%; mean urinary iodine level 39 mug/g creatinine). Clinical and biochemical features of patients with myxedematous, neurologic, and mixed cretinism were studied. Also, in this area, as in most other, neurologic cretinism is more prevalent than myxedematous and mixed forms.

The hormonal profiles of the three types of cretinism were clearly different. Nevertheless, all myxedematous cretins had some neurologic disorders (hyperreflexia, increased muscle tone, disorder of gait, Babinski sign, hypoacusia) that were similar to those present in neurologic cretins. These findings suggest that neurologic damage is very similar in all forms of endemic cretinism, reflecting a diffuse insult to the developing fetal nervous system.

Furthermore, these data support the hypothesis that the primary pathophysiologic event in the different types of endemic cretinism is represented by maternal and fetal hypothyroidism, while differences may be explained by the extent and duration of postnatal hypothyroidism. All the cretins were over 35 of age, suggesting a severe iodine deficiency in the past decades, and a progressive improvement of nutritional status resulted in ''silent iodine prophylaxis.''

However, recent studies have revealed the persistence of a moderate iodine deficiency, a high prevalence of neurologic hypoacusia, and reduction of mental performance in normal schoolchildren of this area. These findings constitute strong evidence in favor of adequate iodine prophylaxis.

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https://www.stofskifteforum.dk/image...uri_1994_2.JPG

Goitrous cretins in valleys of Apennines in the Emilia-Romagna and Tuscany regions between prof. A. Pinchera of Pisa University and prof. J.T. Dunn of Virginia University. (Photographs by Venturi, 1994)
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Iodine Deficiency in the Population of Montefeltro, A Territory in Central Italy Inside the Regions of Emilia-Romagna, Tuscany and Marche
Venturi S.
International Journal of Anthropology Vol. 29 - n. 1-2 (1-12) - 2014

Introduction. Goiter (the abnormal enlargement of the thyroid gland) is the most specific clinical marker of iodine deficiency in the human body. According to WHO, iodine deficiency is the most common cause of preventable brain damage, causing impaired cognitive development in children, and in many countries it is still a major health problem. During pregnancy, severe iodine deficiency may impair fetal development, resulting in cretinism, with irreversible mental retardation and developmental abnormalities, as well as miscarriage and stillbirth.

This is a review of the endocrinological and neuropsychological studies conducted on the iodine deficient population of Montefeltro, a territory in central Italy, where the use of iodized table salt has only recently eradicated endemic malnutrition in its young population. However, in adults and the elderly scars still remain with some neuropsychiatric disorders and the last surviving cases of cretinism. I would also like to point out that research into the biochemical compounds of iodine is a new area of investigation and one which may provide insights into apoptosis, carcinogenesis and many cardiovascular and degenerative diseases.

Key words: iodine deficiency, iodolipids, goiter, cretinism, brain, evolution

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Audiological and neuropsychological development study in a sample of school children from a low-iodine area of the Central Apennines that is endemic for cretinism.

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Audiological and neuropsychological development study in a sample of school children from a low-iodine area of the Central Apennines that is endemic for cretinism
Donati L, Venturi S, Andreani M, Antonelli A, Gori E, Bertoni F, Pruneti CA, Berrettini S, Bruschini P, Baschieri L.
Minerva Endocrinologica Aprile-Giugno 1989, pagina 99-103
Article in Italian

Abstract. Neuropsychological and audiological study in "normal" schoolchildren in an iodine deficiency area with endemic cretinism in Central Apennines.

We have evaluated neuropsychic development in 70 normal schoolchildren in an area of severe endemic goitre and cretinism in Central Apennines (Montefeltro). In each subject we have studied auxological, psychometric and audiometric parameters, togehther with tympanogram and stapedial reflexogram. Auxological data were in the normal range, as stapedial reflexogram and tympanogram.

On the contrary, 54,8% of the sample performed below the 25th percentile in psychometric tests (Raven test PM-47), being also 22,8% below the 5th percentile. Audiometric data showed a neurological hearing impairment in 3,1% of the children tested, as compared with 0,28% in the area of Pisa. These data point out that an impairment of central nervous system function still persist in this area of severe endemic goitre. [Min Endocr 1989;14:99-103].

Key words: Endemic goitre, Neurological hypoacisua, Neuropsychic deficiency

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An iodine-deficient area with endemic cretinism in the Central Apennines: studies of neuropsychological development in schoolchildren.
Donati L, Venturi S, Andreani M, et al.
Journal of Endocrinological Investigation, 1988, 4 :11-12. nad IDD Newsletter, 1988

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Humoral thyroid autoimmunity is not involved in the pathogenesis of myxedematous endemic cretinism.

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Humoral thyroid autoimmunity is not involved in the pathogenesis of myxedematous endemic cretinism.
L Chiovato, P Vitti, G Bendinelli, F Santini, E Fiore, M Tonacchera, C Mammoli, A Capaccioli, S Venturi, and E Pretell
J Clin Endocrinol Metab. 1995 May;80(5):1509-14.
DOI: http://dx.doi.org/10.1210/jcem.80.5.7744994

Abstract. A role of thyroid autoimmunity in the pathogenesis of myxedematous endemic cretinism was suggested by reports indicating the presence of thyroid growth-blocking antibodies in the sera of these patients. To check this hypothesis, we searched for TSH receptor antibodies with thyroid growth-blocking or adenylate cyclase (AC)-inhibiting (TSH-blocking) activity in immunoglobulin G (IgG) from 18 euthyroid and 21 hypothyroid endemic cretins living in Italy and Peru. Among hypothyroid cretins, 12 had no palpable goiter.

Stages I-III goiters were present in 12 of 18 euthyroid cretins. Controls included 25 euthyroid nongoitrous subjects living in the same endemic regions as cretins, and 10 normal subjects from an iodine-sufficient area. IgG from 4 selected patients with autoimmune atrophic thyroiditis and from 2 neonates with sporadic transient congenital hypothyroidism due to maternal TSH-blocking antibodies were included in the study.

The blocking effect of the IgG was assessed in FRTL-5 cells by measuring TSH-stimulated [3H]thymidine incorporation, DNA accumulation, and AC activation. A radioreceptor assay was used to detect TSH-binding inhibiting antibodies (TBIAb). No IgG from hypothyroid endemic cretins without goiter contained TBIAb or inhibited TSH-stimulated cell growth or AC activation. The effect of IgG from hypothyroid nongoitrous cretins did not differ from that produced by IgG from hypothyroid cretins with goiter, euthyroid cretins with or without goiter, or normal controls.

In contrast to these results, IgG from patients with autoimmune atrophic thyroiditis and from neonates with sporadic transient congenital hypothyroidism contained TBIAb that inhibited both TSH-stimulated cell growth and AC activation. In conclusion, our results indicate that, similar to other types of endemic cretinism, hypothyroid endemic cretins without goiter do not have TSH receptor antibodies able to inhibit TSH-stimulated thyroid cell growth or function.

These observations argue against a role of humoral thyroid autoimmunity in the development of myxedematous endemic cretinism.

Source: Press.endocrine.org

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Extrathyroid Iodine Deficiency Disorders. What is the real iodine requirement?

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I disordini extra-tiroidei da carenza iodica. Qual e il real fabbisogno di iodio?
(Extrathyroid Iodine Deficiency Disorders. What is the real iodine requirement?):

The authors report a recent review of the most important extrathyroid iodine deficiency disorders in relation to: stomach, immune system, mammary glands, ovaries, arterial and articular system, epidermis and nervous system. All these organs concentrate about 80% of total body iodine in humans and animals, but the role of this extrathyroid iodine is not known.

The hypothesis is that this iodine might have a specific antioxydant role, from primitive algae, which contain the highest level of iodine, and which were the first living cells to produce oxygen. So we believe that this phylogenetically ancient antioxydant role is important also in animals and humans. In fact, the thyroid gland is only a phylogenetically modern organ, which was improved from primitive Chordates to more recent Mammalia. In the references are reported different studies on the antioxydant ability of iodine in rates and in humans.

By Venturi S, Guidi A, Venturi M. in the Journal of Italian Society of Pharmacology (Le Basi Razioneali Della Terapia), 1996; 16: 267-75. (Source: Tulane University)

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Enigma of the function of iodide in primitive algae and in animal extrathyroidal organs: is it an ancient antioxidant?

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Enigma of the function of iodide in primitive algae and in animal extrathyroidal organs: is it an ancient antioxidant?

Letter to the Editor

Dear Sir,
in relation to the functional role of inorganic iodide in metabolism of algal and animal cells, we have hypothesized, in previous (1) and recent works (2)(3) that iodide might have a (phylogenetically and evolutionistically) ancient antioxidant role in extrathyroidal iodide-concentrating cells.

Into these cells iodide may act as an electron donor in the presence of H2O2 and peroxidase, and the remaining iodine readily iodinates the tyrosine (and more slowly, the histidine (4)(5) or some protein and lipid), and so, neutralizes its own high oxidant power (3). 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.

Now this hypothesis of the antioxidant role of iodide is experimentally confirmed in Algae by a recent study carried out by Kupper et al. (6).

We believe that this work, which convalidates our hypothesis, may constitute a fundamental experimental milestone in the study of the extrathyroidal nonhormonal action of iodine-iodide in biology and physiology of the cells.

Several extrathyroidal organs in animals, many of which share the same gene expression of sodium-iodide symporter of thyroidal iodide-pump (7), particularly stomach mucosa and lactanting mammary gland, but also salivary glands, thymus, epidermis, choroid plexus, articular and arterial sistems, have a iodide-concentrating ability without showing any hormonal or biological action (8), and so, Algae, Porifera, Anthozoa (9) and several marine Invertebrates. In human organism extrathyroidal nonhormonal inorganic iodide is about 50-80% of the total amount of iodine and its role is not known. Besides, direct uptake of inorganic iodine by tumor shows experimentally a suppressive effect on DMBA-induced breast tumors growth in the rat (10). The antioxidant action of iodide may give a satisfactory explanation of the function of this trace-element and might be a very important knowledge for preventive purpose.

We should point out that extrathyroidal action of iodide might be an important new area for investigation.

REFERENCES

1. Venturi S et al (1993) A new hypothesis: iodine and gastric cancer. European Journal of Cancer Prevention. 2 :17-23
2. Venturi S & Venturi M (1998) Does iodine in the gastric mucosa have an ancient antioxidant role? IDD-Newsletter 14, 4 :61-2
3. Venturi S & Venturi M (1999). Iodide, thyroid and stomach carcinogenesis: evolutionary story of a primitive antioxidant? European Journal of Endocrinology 140, 4 :371-2
4. Li CH (1945) J Am Chem Soc 67 :1065
5. Mayberry WE & Hockert TJ (1970). Endocrinology 86 :225..
6. Kupper FC, Schweigert N, Ar Gall E, Legendre J-M, Vilter H & Kloareg B (1998). Iodine uptake in Laminariales involves extracellular, haloperoxidase-mediated oxidation of iodide. PLANCTA 207 :163-171
7. Spitzweg C, Joba W, Eisenmenger W & Heufelder AE (1998). Analysis of human sodium iodide symporter gene expression in extrathyroidal tissues and cloning of its complementary deoxyribonucleic acid from salivary gland, mammary gland, and gastric mucosa. J Clin Endocrinol Metab 83, 5 :1746-51
8. Venturi S, Guidi A & Venturi M (1996). I disordini extra-tiroidei da carenza iodica. Qual è il reale fabbisogno di iodio? Le Basi Razionali della Terapia 16 :267-75
9. Roche J (1952) Biochimie comparée des scléroprotéines iodées des Anthozoaires et des Spongiaires. Experientia 8 :45-56
10. Funahashi H, Imai T, Tanaka Y, Tobinaga J, Wada M, Morita T & al. (1996) Suppressive effect of iodine on DMBA-induced breast tumor growth in the rat. J Surg Oncol 61, 3 :209-13

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Preliminary study on the relation between alimentary iodine deficiency and gastric cancer: specific prevention prospects

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Preliminary study on the relation between alimentary iodine deficiency and gastric cancer: specific prevention prospects
Book in Italian with summary in English
By S. VENTURI, Pennabilli, Italy. 1-9-1985.

This book has the following stated objective: "correlation between alimentary iodine deficiency and gastric cancer".
The 3 methods employed are:

1) Epidemiological Studies
2) Study of the relation between iodine deficiency and lack of immune defense, by Skin-test
3) Relation between gastric and Thyroid diseases
Summary
Competitors anions contents: Specific prevention prospects.

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