• Join our community!

    Do you have questions about celiac disease or the gluten-free diet?

  • Ads by Google:
     




    Get email alerts Subscribe to Celiac.com's FREE weekly eNewsletter

    Ads by Google:



       Get email alertsSubscribe to Celiac.com's FREE weekly eNewsletter

  • Member Statistics

    77,936
    Total Members
    3,093
    Most Online
    Bushet
    Newest Member
    Bushet
    Joined
  • 0

    Push-back Against Report Linking GMOs to Celiac Disease, Gluten Sensitivity


    Jefferson Adams

    Celiac.com 01/08/2014 - Push-back mounts against a controversial new report alleging that genetically engineered foods may trigger gluten sensitivity and celiac disease.


    Ads by Google:




    ARTICLE CONTINUES BELOW ADS
    Ads by Google:



    Photo: CC--MDGLillehammerIn the first salvo, Celiac Disease Foundation CEO Marilyn Geller derided the report, published last week by the Institute for Responsible Technology (IRT), as merely "speculative."

    Then followed comments by leading plant geneticist, Dr. Wayne Parrott, professor of crop science at the University of Georgia, that the report relied on "a handful of deeply flawed"studies and ignored "more than 1,000 studies that have been published in refereed journals and which show that GM crops are as safe as their counterparts."

    According to Geller, no one has offered scientific evidence "for a GMO/celiac disease link that is supported by the CDF Medical Advisory Board.

    For their part, the authors of the IRT report admit that there is no data to prove that GMO consumption causes gluten sensitivity.

    However, they try to hedge slightly by claiming that more and more research shows that GMO consumption may worsen celiac symptoms or lead to gluten sensitivity. Here again, they offer no good data to support their claims.

    Source:

    0


    User Feedback

    Recommended Comments

    I was diagnosed with celiac and went totally gluten free in 2004. I suffered with serious symptoms for years, before that. I always have, and still do, get severe stomach pains and other symptoms, if I eat anything that is likely to be GMO. Since GM foods are not truthfully labeled, there is no proof that they are genetically modified. I have to totally avoid foods likely to be GMO, so I do think that there could be leaky gut or other gut damage caused by them, in some of us. They have never been proven to be safe, there is no test for any harm to human health, no tracking of any harm they may cause, and no labels to show we ever even ate them. 64 other countries in the world require labels on GMO and products that contain them, but not in the USA. Why not label GM foods, if they are as safe as claimed. What do they know, that they don't want us to know?

    Share this comment


    Link to comment
    Share on other sites
    I was diagnosed with celiac and went totally gluten free in 2004. I suffered with serious symptoms for years, before that. I always have, and still do, get severe stomach pains and other symptoms, if I eat anything that is likely to be GMO. Since GM foods are not truthfully labeled, there is no proof that they are genetically modified. I have to totally avoid foods likely to be GMO, so I do think that there could be leaky gut or other gut damage caused by them, in some of us. They have never been proven to be safe, there is no test for any harm to human health, no tracking of any harm they may cause, and no labels to show we ever even ate them. 64 other countries in the world require labels on GMO and products that contain them, but not in the USA. Why not label GM foods, if they are as safe as claimed. What do they know, that they don't want us to know?

    Re Donnie's comment that "What do they know, that they don't want us to know." It is not hiding. I am an agricultural producer with celiac. I have no employees except for occasional help from son and spouse. I am already inundated with paperwork. Having to spend many hours a week find out GMO status of every seed in my pasture might be a full time job in itself. It would put many small producers out of business. For large businesses that have a hundred employees, having one employee only handling GMO/organic paperwork is a much smaller total cost than for a small producer. And don't forget we have to compete pricewise with foods produced in countries with little or no regulation. When California ag is driven out, do you want to import your food from China?

     

    I just don't think the general public realizes the amount of time consuming paperwork now required. Things like trying to put a creek crossing in so livestock are not walking through the creek. Everyone may agree that this is a good practice, but getting permits, (engineering the permits require is usually much more costly than the actual permits) takes years. It often costs more than the actual work and prevents the project from happening. Environmentalists who want more regulation are doing a disservice to the environment.

    Share this comment


    Link to comment
    Share on other sites

    The possible problems for humans eating GMO food cannot be established at this time, because the use in humans has not been tracked due to the fact that the GMOs aren't labeled. My opinion would be that arguments from both sides of this controversy are merely speculative. I am much like another person who commented, and sometimes have issues when eating GMO foods. Possible cross contamination could be the issue, but it also could be that a foreign protein in the GMO food closely resembles that of gliadin or, for me, avenin, since I am one of those unlucky celiacs who cannot tolerate oats. I also have some issue with Quinoa, so who knows what it is that is causing the problems for me. I just wish that, because there are foreign proteins in GMOs, other than those which would normally be found in the food substance we think we are buying, that it would be very helpful for people such as myself to know exactly what it is that I am eating before I eat it. No studies have been done on humans with regard specifically to GMOs and Celiac Disease, so I don't see how either side can claim any sort of proof as to whether or not GMOs are safe for people with food intolerances.

    Share this comment


    Link to comment
    Share on other sites
    Re Donnie's comment that "What do they know, that they don't want us to know." It is not hiding. I am an agricultural producer with celiac. I have no employees except for occasional help from son and spouse. I am already inundated with paperwork. Having to spend many hours a week find out GMO status of every seed in my pasture might be a full time job in itself. It would put many small producers out of business. For large businesses that have a hundred employees, having one employee only handling GMO/organic paperwork is a much smaller total cost than for a small producer. And don't forget we have to compete pricewise with foods produced in countries with little or no regulation. When California ag is driven out, do you want to import your food from China?

     

    I just don't think the general public realizes the amount of time consuming paperwork now required. Things like trying to put a creek crossing in so livestock are not walking through the creek. Everyone may agree that this is a good practice, but getting permits, (engineering the permits require is usually much more costly than the actual permits) takes years. It often costs more than the actual work and prevents the project from happening. Environmentalists who want more regulation are doing a disservice to the environment.

    I also agree with Donnie.

    Share this comment


    Link to comment
    Share on other sites
    Guest Somhairle1314

    Posted

    Re Donnie's comment that "What do they know, that they don't want us to know." It is not hiding. I am an agricultural producer with celiac. I have no employees except for occasional help from son and spouse. I am already inundated with paperwork. Having to spend many hours a week find out GMO status of every seed in my pasture might be a full time job in itself. It would put many small producers out of business. For large businesses that have a hundred employees, having one employee only handling GMO/organic paperwork is a much smaller total cost than for a small producer. And don't forget we have to compete pricewise with foods produced in countries with little or no regulation. When California ag is driven out, do you want to import your food from China?

     

    I just don't think the general public realizes the amount of time consuming paperwork now required. Things like trying to put a creek crossing in so livestock are not walking through the creek. Everyone may agree that this is a good practice, but getting permits, (engineering the permits require is usually much more costly than the actual permits) takes years. It often costs more than the actual work and prevents the project from happening. Environmentalists who want more regulation are doing a disservice to the environment.

    Sharon, they are required in Europe to label for GMO, maybe study how they do it there. Has food production in Europe suffered import competition from China or have you bought into the fear mongering from the big agricultural-pac's? Also, wouldn't our laws requiring labeling affect imports as well?

    Tracking might be easier if the labeling requirements started with seeds, then you would know which seeds you plant are GMO or not; all you would need then, is a spreadsheet. Also, I do not believe that the sustainability of your or any other business is more important than our right to know what we are putting in our bodies.

    Share this comment


    Link to comment
    Share on other sites


    Your content will need to be approved by a moderator

    Guest
    You are commenting as a guest. If you have an account, please sign in.
    Add a comment...

    ×   Pasted as rich text.   Paste as plain text instead

      Only 75 emoji are allowed.

    ×   Your link has been automatically embedded.   Display as a link instead

    ×   Your previous content has been restored.   Clear editor

    ×   You cannot paste images directly. Upload or insert images from URL.


  • Ads by Google:

  • About Me

    Jefferson Adams is a freelance writer living in San Francisco. He has covered Health News for Examiner.com, and provided health and medical content for Sharecare.com. His work has appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate, among others.

  • Popular Contributors

  • Ads by Google:

  • Who's Online   9 Members, 0 Anonymous, 430 Guests (See full list)

  • Related Articles

    Scott Adams
    We have recently reported on Lancet (1) a consistent cohort of patients affected by drug-resistant epilepsy with cerebral calcifications, half of which were cured by a gluten-free diet. All had an atrophic jejunal mucosa, which recovered on a gluten free diet. Gluten intolerance is now a recognized cause of brain calcifications and epilepsy, of dementia, of psychiatric disturbances: many researchers believe that, in genetically predisposed subjects, gluten is not healthy for the brain function (2).
    This is just too much.
    Having had over 25 years of variegated experience with gluten intolerance I find hard to imagine that the single most common food intolerance to the single most diffuse staple food in our environment might provoke such a complexity of severe adverse immune-mediated reactions in any part of the human body and function. The list is endless, but malignancies, adverse pregnancy outcome and impaired brain function are indeed complications above the tolerable threshold of this food intolerance.
    On the other end today we know very well that the majority (as many as 9 to 1) of gluten intolerant subjects, identified by familial or population screening, do not manifest any complaint, although they do have a flat intestinal mucosa (3).
    In conclusion a sizable proportion of our population (from 0.3 to 1%) is gluten intolerant and reacts with a wide spectrum of symptoms from no apparent reaction to severe life-threatening diseases.
    This intolerance is strongly linked to specific genetic markers which have indeed required thousands years to develop and be selected: the 'population genetic' time is of this dimension, while the changes in the environment and in the food we eat, require centuries or less.
    Where did they come from?
    Hunters, Fishers and Gatherers
    Human beings have been on Earth for over 3 millions year, but Homo Sapiens Sapiens, our nearest parent, is only 100,000 years old. For ninety thousand years he conducted a nomadic life getting food by hunting, fishing and collecting fruits, seeds, herbs and vegetables from nature. Only quite recently (about 10.000 years ago) did some nomadic tribes start to have stable settlements because they developed the ability to gather enough food to be stored. The cultivation of wild seeds begun.
    Ten thousand years ago the last glaciation came to an end: a Neo-thermal period ensued which marked the passage from the Paleolithic to the Neolithic age. Ices melted gradually from the equator to the poles over several thousands years when new fertile and humid lands were uncovered in South East Asia all of Europe was still covered with ice and Northern Countries had to wait up to 4000 years more to get out from a frozen environment.
    The Great Revolution: The First Farmers
    The discovery in the Neolithic age of ways to produce and store food has been the greatest revolution mankind ever experienced. Passage from collection to production originates the first system in which human labor is transferred onto activities which produced income for long periods of time. The principle of property was consolidated and fortifications to protect the land and food stores were developed.
    Archeological findings suggest that this revolution was not initiated by the man hunter and warrior, but by the intelligent observations made by the woman. The woman carried the daily burden of collecting seeds, herbs, roots and tubers. Most probably she used a stick to excavate roots and tubers: during this activity she observed the fall of grain seeds on the ground and their penetration into the soil with rain. She may have been surprised to find new plants in the places which she herself dug with a stick, and made the final connection between fallen seeds and new 'cultivated' plants.
    She was, for thousands years, the sole leader of the farming practices and provided a more and more consistent integration to the scanty products of the man hunter (6).
    To our actual knowledge, the origin of farming practices should be located in the 'Fertile Crescent': the wide belt of South East Asia which includes Southern Turkey, Palestine, Lebanon and North Iraq. In the highlands of this area abundant rainfall was caused by the neo-thermal switch. In all of this area existed, and still exists, a wide variety of wild cereals, sometimes in natural extended fields, induced by the rainfalls. Triticum Dicoccoides (wheat) and Hordeum Spontaneum (barley) were common and routinely collected by the local dwellers. The wild cereals had very few seeds (2-4) which fell easily on the ground on maturation.
    The people from the Uadi el-Natuf Tell of South East Asia (7800 B.C.) provided the first traces of the gradual shift from hunters to grain cultivators. Their economy was based on the hunt of the gazelle, but their diet also included collected grain seeds. These gradually came to form a substantial proportion of their energy input, as cultivation practices ensued. There were no grinding stones or mills and it was most probable that gathering prevailed on cultivation. But during the Proto-Neolithic superior a cuneiform mortar appeared. 1000-2000 years later (5000 B.C.) wild animals, more rare due to incoming drought, formed only 5% of the daily diet, while cereals and farmed animals become a sizable part of it (4).
    Stable settlements were founded: the village of Catal-Huyuk in Southern Turkey had a population of 5000 inhabitants 9000 years B.C. In that area a collection of sickles was found with inserted oxidian blades, smoothed by the routine contact with the siliceous stalk of cereals. The sickles indicate that it was possible to collect seeds not only by picking on the ground, but also by cutting stems of plants which were capable of retaining the seed in an ear (5). 'Mesopotamic' populations, originated in the first farmers, developed a great civilization with large cities and powerful armies to defend their land property and food stores. In Egypt a civilization based on farming practices developed in the 5th millennium: they became specialists in the cultivation of wheat, barley (to produce beer) and flax.
    The Expansion Of The Farmers
    While in South East Asia the progressive drought made hunting difficult and encouraged farming, in Europe the Paleolithic culture of hunters and gatherers persisted for 5000 years more, gradually transforming into the Mesolithic age.
    In the 'Fertile Crescent' the availability of food stores and the gradual development of animal farming stimulated an unprecedented demographic explosion. The nuclear family had had a small dimension for hundreds thousands of years: the birth rate had been limited by nomadic life. In transmigrations the mother had been able to carry one infant, while the others had been obliged to walk and move on their own. Small babies in between had less chances of surviving. Thus mankind remained of approximately the same size during entire ages.
    Farmers, on the contrary, were settlers, possessed food stores and most probably took advantages in the farming practices of more hands in the family. In this manner the family size exploded and, as a result, a progressive continuous need to gain more lands ensued.
    The farmer's expansion lasted from 9000 B.C. up to the 4000 B.C. when they reached Ireland, Denmark and Sweden covering most cultivable lands in Europe. The expansions followed the waterways of Mediterranean and of Danube across the time of Egyptians, Phoenicians, Greeks and Romans (7).
    The farmers' expansion was not limited to the diffusion of the agricultural practices, but was a 'demic' expansion: that is a substantial replacement of the local dwellers, the Mesolithic populations of Europe, by the Neolithic from South East Asia. More than 2/3 of our actual genetic inheritance originated in this new population, while the native genetic background has been progressively lost or confined to isolated geographical areas.
    The genetic replacement of the native European population is marked by the B8 specificity of the HLA system. Cavalli Sforza and coworkers showed that the migration of farmers is paralleled by the diffusion of B8. The frequency of B8 is inversely proportional to the time length of wheat cultivation. In practice B8 appears to be less frequent in populations which have lived on wheat for a longer time, as it is caused by a negative genetic selection in wheat cultivators (7). We are aware that in Ireland, where the wheat cultivation came only 3000 years B.C., a very high frequency of gluten intolerance has been reported.
    The Evolution Of Cereals
    The early wild cereals, of the Triticum (wheat) and Hordeum (barley) species were genetically diploid and carried few seeds, which usually fell on the ground at maturation, making any harvest very difficult. A chromosomes in single couples (diploidicity) allowed for a wide genetic and phenotypic heterogeneity with remarkable variations in the content of protein and starches. Poliploid plants occasionally originated in nature, but they had few chances to survive, without artificial (cultivation) practices and were usually lost (8).
    The beginning of farming, with the use of irrigation, allowed the survival, and the expansion, of poliploid grains. But the new poliploid grains had substantially reduced genetic variations (since each gene is represented in several copies) and more frequently autoimpollinate themselves, causing remarkable increase of the genetic uniformity.
    The first stable formation of poliploid grains is dated around 6000 years B.C.: the genetic uniformity caused a considerable rise in stability and yield, convincing the early farmer to induce a progressive and rapid replacement of the wild species.
    Genetic variability of grains was essential in order to adapt the plant to the very different environmental conditions of different areas, but the yield was generally low (9).
    Triticum Turgide Dicoccoides was crossed with Triticum Fanschii to originate the Triticum Aestivum, which is the progenitor of all our actual wheat. The Aestivum is an esaploid wheat with 42 chromosomes, versus the 14 of the T. Monococcum. Such powerful grain replaced all existing varieties to the point where genetic variability nowadays is lost: over the world we have 20,000 cultivated species of the same unique T. Aestivum wheat. The Triticum Turgidum Dicoccoides, progenitor of the actual 'durum' wheat with which pasta is made, had just few seeds encapsulated into a pointed and twilled kernel: at maturation the seeds fell on the soil and penetrated into it with rain, eased by the arrow-shaped structure of the kernel.
    Ten thousand years ago it was difficult to pick them up: hence the attempt, made by the Neolithics, to select varieties which could retain the seed longer, in order to allow for an harvest.
    Genetic variability was already substantially reduced in Roman times: 'farrum', i.e. spelt, (T. Dicoccoides) and 'Siligo' (T. Vulgaris) were the common grains. Siligo was used for bread making and contained a certain amount of gluten, while spelt, used mainly for soups, was poorer in gluten content (10).
    But cultivation of wheat and barley was not started or diffused in the whole world: only a small geographic area (South East Asia) developed gluten-containing cereals. In Asia rice was the cultivated species, while in America maize prevailed and in Africa sorghum and millet. All these plants were present in nature and were gradually cultivated in the places of origin (7).
    In our part of the world grains had for centuries been selected in order to improve their homogeneity and productivity, but soon (Roman times or before?) another desirable quality was preferred: the ability to stick, to glue up a dough to improve bread making. Early bread making activities pushed towards grains that contained greater amounts of a structural protein which greatly facilitated the bread making: the gluten. Gluten was not chosen because of its, at the time unknown, nutritional value (which is not absolutely special, since it is a protein with relatively low nutritional value), but for its commercial qualities.
    Rice, maize, sorghum, millet do not contain gluten: no leavened bread was prepared with them: the majority of mankind never lived on bread, as we do know it.
    Over the last 200 years of our modern age active genetic selection, and actual genetic manipulation, have changed the aspect of the original Triticacee enormously: from few grains and little gluten to great wheat harvests very enriched in gluten (50% of the protein content), well adapted to cultivation practices and ready to be handled by monstrous machinery.
    The Rise Of The Intolerance To Gluten
    Did everybody adapt to such profound changes in the basic nutrition over such a short period of time? South Eastern populations, presumably well adapted to the new foods, grossly replaced the existing Mesolithic European dwellers who still lived on hunting and gathering. But a proportion of the local populations (or, rather, of their inheritance ) persisted beside the invaders. The feeding changes were not well tolerated by everybody.
    The best similar example is lactose intolerance: populations that have more recently adapted to milk consumption, still lack the genetic ability to digest lactose over the infancy period. Environment has changed centuries before any change in the inheritance may have been possible.
    Similarly a considerable proportion of the hunters and gatherers of the pre-Neolithic ages have not fully adapted to the great feed changes induced by the cultivation of wheat. These people could not recognize gluten as a 'tolerable' protein available for digestion and absorption: they may have not have any problem or complaint for centuries, since the content of gluten in the grains was very low, but when 'industrial' quantities of gluten were induced by selection of wheat in order to improve bread making, they were exposed to unbearable quantities of an 'intolerable' protein or peptide.
    This population, genetically identifiable today by their specific HLA pattern, did not recognized, through their HLA system, the gluten peptide as a tolerable item, but, because of the similarity of some sequences of gliadin peptides with several pathogenic viruses, they generate a complex defense mechanism (an immune response) which does not eventually find the pathogen to destroy, and most probably activate an auto-immune response which ultimately is the origin of the damage to their intestine and other organs.
    These fierce descendants of hunters and fishers, exposed to this subtle enemy, could not develop the defense of tolerance and, in the attempt to fight the unknown, they ultimately develop a disease due to excess defense. For centuries they underwent a negative selective pressure, with less chances to survive, and then to be manifest (11).
    In the last millennium gluten-intolerant children mostly had a harsh time behind them: after weaning, malabsorption and malnutrition were the underlying causes of poor defense to infections during infancy and early childhood. Acute infectious diarrhea was the main killer of infants up to 50 years ago in Europe and up to 15 babies every thousand died for this condition. In the suburbs of Naples, only 25 years ago, infectious diarrhea was the main killer (25% on an infant mortality rate of 100 per thousands live births) (12).
    The vast majority of gluten intolerance occurred among these poor infants. In my own clinical experience 25 years ago I observed several fatal gastrointestinal infections in babies with the 'celiac crisis', which has now disappeared from our wards.
    Few chances to survive, few intolerant children that reached the reproductive age, and become capable of transmitting the intolerance, few adult cases. Then gluten intolerance may have become extinct, as was in fact the case with several other pathogenic conditions? Not at all.
    The intolerance most probably had some selective advantage which counterbalanced the gluten intolerance: it is possible to suggest that it was their very effective HLA Class II system that gave them a selective advantage against infections, which compensated the disadvantage due to gluten intolerance.
    When, in the last 50 years, infantile infections greatly diminished, the descendants of the hunters and gatherers with very active immune-defense, 'over reacted' more frequently to the gluten than to their ordinary enemy. Hence the rise of the cohort that now appears to manifest, in different manners, a gluten intolerance.
    However, not all populations of the world were ever exposed to such a nasty protein: the vast majority of mankind, after the development of agriculture, lived on maize, rice, sorghum and millet, tubers: all gluten free. All of them did not underwent the selective pressure of gluten intolerance and they may in fact have been the reservoir of wild genes.
    Finally, breast feeding most probably played a major role in preserving some children from the fatal infection of infancy (13). The capacities of breast milk to protect against viral and bacterial attack, the protection given by maternal antibodies and the delaying effect on the manifestation of symptoms of gluten intolerance (in the predisposed subjects) may all have protected the hunters and gatherers, who in this manner avoided to develop fatal symptoms and managed to survive and transmit their genes to our population.
    Hints On The Epidemiology Of Gluten Intolerance
    The epidemiology of gluten intolerance, as we know it today, is the complex result of the apparition of the population of hunters and gatherers in our modern world.
    As the cohort of those born before the World War II had few chances to survive infancy, we nowadays have few adult cases and few long term complications. Where the intolerance is still manifested mainly in the classical way (infants and small children, malabsorption, diarrhea, often switched on by an infection) we do not frequent encounter 'atypical' presentations and adult cases or long term complications. In this case the epidemiological calculations on observed cases made by gastroenterologist may be in great contrast with those made by pediatricians. On the contrary the rarity of 'classical' cases, which has been used as the proof of the 'disappearance' of gluten intolerance, is counterbalanced by the presence of atypical and late diagnosis, where actively searched for.
    Finally nutritional attitudes have played a major role with regard to the chances for hunters to manifest themselves in different age groups: the example of Sweden as compared to the nearest Denmark or Finland is paradigmatic (14).
    As shown by Maki et al, the ability to identify atypical cases may completely change the observed epidemiological pattern in a given region. Hence the reason for the 'iceberg': most cases still to be discovered (15). Similarly, population-based screening programs uncover more 'silent' than overt cases (3).
    Nevertheless, the 'cohort effect', regional differences and so on, have up to now failed to overcome the limits of numbers: when local incidence rates are compared with other regions' rates, the 95% Confidence Intervals of the rates are very often so wide to contain the all lot of observed rates. No clear-cut statistical difference has really been shown in the incidence of gluten intolerance in Europe (16).
    Wherever extensive studies on symptomatic cases have been run an incidence of 1 case per each 1000 live births has been reached, but very often the incidence has been much lower: up to 1 cases every 250 live births. Population screening studies invariably come to an incidence rate of 1 every 250. This is very close to the rate predicted by age-adjusted incidence density studies (17). Recent reports indicate an incidence close to 1 case per every 100 live births, but this finding needs confirmation.
    Gluten Sensitive Versus Gluten Intolerant
    But the epidemiology of gluten intolerance, which entails the tracing of a group of our ancestors, may completely change once we consider the increasing knowledge about the 'gluten-sensitive' individuals. 6 to 10% of first degree relatives of known cases themselves are gluten intolerant and have a flat intestinal mucosa (these are silent cases), but up to 30% of sibs of cases, when challenged with a dose of gluten (or its digest) activates a specific mucosal immune-response (with increase in intraepithelial infiltration and activation of T-Cells), without having any sign of mucosal damage (potential cases?) (18).
    We may, in the near future, have a substantial group of individuals who do not activate, in presence of gluten, a 'pathogenic' immune response (auto-immunity), but who recognize gluten as a 'suspect' protein in the same way as their peers really intolerant.
    Finally gluten intolerance is indeed linked to a specific genetic predisposition: most probably at least two genetic loci are involved in running the risk of intolerance.
    How many possess these specific genetic risk at a 'carrier' state? Certainly more than 5% of the actual population. In conclusion we have a wide population of 'gluten-reactants' in Europe (EC): at least 1 million cases of total intolerance to gluten - an estimated similar amount of 'gluten sensitive' people - 10-15 times more 'carriers' of the risk of becoming gluten intolerant.
    So we have found our ancestral hunters and gatherers: they are a substantial proportion of our actual community and do deserve a 'gluten-free' alternative not only as a therapeutic mean, but as an option of our daily life.
    References Gobbi G, Bouquet F, Greco L, Lambertini A, Tassinari CA, Ventura A, Zaniboni MG: "Coeliac Disease, epilepsy and cerebral calcifications" Lancet, 340, Nx 8817, 439-443, 1992 Epilepsy and other neurological disorders in Coeliac Disease. Republic of S. Marino Meeting, April 10-12 1995, G. Gobbi edt., Raven Press, in preparation. Catassi C, Ratsch IM, Fabiani E, Rossini M, Bordicchia F, Candela F, Coppa GV, Giorgi PL: Coeliac Disease in the year 2000: exploring the iceberg. Lancet, 1994, 343: 200-203. Furon R. Manuel de Prehistorie Generale., 1958, Payor, Paris. Cambel H, Braidwood RJ. An old farmer's village in Turkey. Le Scienze, 1970, 22: 96-103. Heichelheim F. An Ancient Economic History. A.W. Sijthoff edt., Leiden, 1970. Cavalli-Sforza L. Chi Siamo (Who are we). 1993 Mondadori, Milano. Raven PH, Evert RF, Eichorn S Biology of plants. 4th ed. Worth Publ. Inc, New York, 1986. Feldman M, Sears ER The wild gene resources of wheat. Scientific American, 1981: 98-109. Lucio Giunio Moderato Columella " Libri rei rusticae" Anni 60-65 dopo Cristo. Ed. Einaudi,1977. Simoons FJ: Coeliac Disease as a Geographic Problem. Food, Nutrition and Evolution, 1982, 179-199. Greco,L.: " Malnutrizione di classe a Napoli" Inchiesta, 24, 53-63, 1976. Greco,L., Mayer,M., Grimaldi,M., Follo,D., De Ritis,G., Auricchio,S.: "The effect of Early Feeding on the onset of Sympthoms in Coeliac Disease" J.Pediat. Gastroenterology Nutrition, 4:52-55, 1985. Maki M, Holm K, Ascher H, Greco L.: Factors affecting clinical presentation of coeliac disease: role of type and amount of gluten containing cereals in the diet. In "Common Food Intolerances 1: Epidemiology of Coeliac Disease", Auricchio S, Visakorpi JK, editors, Karger, Basel, 1992, pp 76-83. Maki M, Kallonen K, Landeaho ML, Visakorpi JK.:Changing pattern of childhood coeliac disease in Finland. Acta Paediatr Scand 1988; 77:408-412. Greco L, Maki M, Di Donato F, Visakorpi JK. Epidemiology of Coeliac Disease in Europe and the Mediterranean area. A summary report on the Multicentric study by the European Society of Paediatric Gastroenterology and Nutrition. In "Common Food Intolerances 1: Epidemiology of Coeliac Disease", Auricchio S, Visakorpi JK, editors, Karger, Basel, 1992, pp 14-24. Magazzu, Bottaro G, Cataldo F, Iacono G, Di Donato F, Patane R, Cavataio F, Maltese I, Romano C, Arco A, Totolo N, Bragion E, Traverso G, and Greco L: "Increasing Incidence of childhood celiac disease in Sicily: results of a multicentric study" Acta Paediatr, 83:1065-1069, 1994. Troncone R, Greco L, Mayer M, Mazzarella G, Maiuri L, Congia M, Frau F, De Virgiliis S, Auricchio S.: "In half of Siblings of Coeliac Children rectal gluten challenge reveals gluten sensitivity not restricted to coeliac HLA.

    Roy Jamron
    This article appeared in the Summer 2008 edition of Celiac.com's Scott-Free Newsletter.
    Celiac.com 06/16/2008 - Do vitamin D deficiency, gut bacteria, and timing of gluten introduction during infancy all combine to initiate the onset of celiac disease? Two recent papers raise the potential that this indeed may be the case. One paper finds that when transgenic mice expressing the human DQ8 heterodimer (a mouse model of celiac disease) are mucosally immunized with gluten co-administered with Lactobacillus casei bacteria, the mice exhibit an enhanced and increased immune response to gluten compared to the administration of gluten alone.[1] A second paper finds that vitamin D receptors expressed by intestinal epithelial cells are involved in the suppression of bacteria-induced intestinal inflammation in a study which involved use of germ-free mice and knockout mice lacking vitamin D receptors exposed to both friendly and pathogenic strains of gut bacteria.[2] Pathogenic bacteria caused increased expression of vitamin D receptors in epithelial cells. Friendly bacteria did not.
    If one considers these two papers together, one notices: (1) Certain species of gut bacteria may work in conjunction with gluten to cause an increased immune response which initiates celiac disease; (2) The presence of an adequate level of vitamin D may suppress the immune response to those same gut bacteria in such a way as to reduce or eliminate the enhanced immune response to gluten caused by those gut bacteria, thus preventing the onset of celiac disease.
    Vitamin D has recently been demonstrated to play a role in preserving the intestinal mucosal barrier. A Swedish study found children born in the summer, likely introduced to gluten during winter months with minimal sunlight, have a higher incidence of celiac disease strongly suggesting a relationship to vitamin D deficiency.[3] Recent studies found vitamin D supplementation in infancy and living in world regions with high ultraviolet B irradiance both result in a lower incidence of type 1 diabetes, an autoimmune disease closely linked to celiac disease.[4][5]
    Gut bacteria have long been suspected as having some role in the pathogenesis of celiac disease. In 2004, a study found rod-shaped bacteria attached to the small intestinal epithelium of some untreated and treated children with celiac disease, but not to the epithelium of healthy controls.[6][7] Prior to that, a paper published on Celiac.com[8] first proposed that celiac disease might be initiated by a T cell immune response to "undigested" gluten peptides found inside of pathogenic gut bacteria which have "ingested" short chains of gluten peptides resistant to breakdown. The immune system would have no way of determining that the "ingested" gluten peptides were not a part of the pathogenic bacteria and, thus, gluten would be treated as though it were a pathogenic bacteria. The new paper cited above[1] certainly gives credence to this theory.
    Celiac disease begins in infancy. Studies consistently find the incidence of celiac disease in children is the same (approximately 1%) as in adults. The incidence does not increase throughout life, meaning, celiac disease starts early in life. Further, in identical twins, one twin may get celiac disease, and the other twin may never experience celiac disease during an entire lifetime. Something other than genetics differs early on in the childhood development of the twins which initiates celiac disease. Differences in vitamin D levels and the makeup of gut bacteria in the twins offers a reasonable explanation as to why one twin gets celiac disease and the other does not. Early childhood illnesses and antibiotics could also affect vitamin D level and gut bacteria makeup. Pregnant and nursing mothers also need to maintain high levels of vitamin D for healthy babies.
    Sources:
    [1] Immunol Lett. 2008 May 22.
    Adjuvant effect of Lactobacillus casei in a mouse model of gluten sensitivity.
    D'Arienzo R, Maurano F, Luongo D, Mazzarella G, Stefanile R, Troncone R, Auricchio S, Ricca E, David C, Rossi M.
    http://dx.doi.org/10.1016/j.imlet.2008.04.006
    [2] The FASEB Journal. 2008;22:320.10. Meeting Abstracts - April 2008.
    Bacterial Regulation of Vitamin D Receptor in Intestinal Epithelial Inflammation
    Jun Sun, Anne P. Liao, Rick Y. Xia, Juan Kong, Yan Chun Li and Balfour Sartor
    http://www.fasebj.org/cgi/content/meeting_abstract/22/1_MeetingAbstracts/320.10
    [3] Vitamin D Preserves the Intestinal Mucosal Barrier
    Roy S. Jamron
    https://www.celiac.com/articles/21476/
    [4] Arch Dis Child. 2008 Jun;93(6):512-7. Epub 2008 Mar 13.
    Vitamin D supplementation in early childhood and risk of type 1 diabetes: a systematic review and meta-analysis.
    Zipitis CS, Akobeng AK.
    http://adc.bmj.com/cgi/content/full/93/6/512
    [5] Diabetologia. 2008 Jun 12. [Epub ahead of print]
    The association between ultraviolet B irradiance, vitamin D status and incidence rates of type 1 diabetes in 51 regions worldwide.
    Mohr SB, Garland CF, Gorham ED, Garland FC.
    http://www.springerlink.com/content/32jx3635884xt112/
    [6] Am J Gastroenterol. 2004 May;99(5):905-6.
    A role for bacteria in celiac disease?
    Sollid LM, Gray GM.
    http://dx.doi.org/10.1111/j.1572-0241.2004.04158.x
    [7] Am J Gastroenterol. 2004 May;99(5):894-904.
    Presence of bacteria and innate immunity of intestinal epithelium in childhood celiac disease.
    Forsberg G, Fahlgren A, Hörstedt P, Hammarström S, Hernell O, Hammarström ML.
    http://dx.doi.org/10.1111/j.1572-0241.2004.04157.x
    [8] Are Commensal Bacteria with a Taste for Gluten the Missing Link in the Pathogenesis of Celiac Disease?
    Roy S. Jamron
    https://www.celiac.com/articles/779/


    Jefferson Adams
    Celiac.com 06/24/2013 - Researchers don't know much about the genetic history of celiac disease. They know especially little about the age of specific gene sequences that leave people at risk for developing celiac disease.
    A recent case study provides a small bit of information about that question. The information was gathered by a team of researchers looking into the case of a young, first century AD woman, found in the archaeological site of Cosa. The woman's skeleton showed clinical signs of malnutrition, such as short height, osteoporosis, dental enamel hypoplasia and cribra orbitalia, indirect sign of anemia, all strongly suggestive for celiac disease.
    The research team included G. Gasbarrini, O. Rickards, C. Martínez-Labarga, E. Pacciani, F. Chilleri, L. Laterza, G. Marangi, F. Scaldaferri, and A. Gasbarrini. They are affiliated with the Ricerca in Medicina Foundation NGO, Falcone and Borsellino Gallery, in Bologna, Italy.
    However, initial inspection of the woman's bones did not provide answers about the genetics that might confirm that these traits were, in fact, associated directly with celiac disease.
    To do that, the team needed to examine her human leukocyte antigen (HLA) class II polymorphism. That required extracting DNA from a bone sample and a tooth and genotyping HLA using three HLA-tagging single nucleotide polymorphisms for DQ8, DQ2.2 and DQ2.5, specifically associated to celiac disease.
    The results showed that the woman did in fact carry HLA DQ 2.5, the haplotype associated to the highest risk of celiac disease. This is the first time that researcher have documented the presence of a celiac-associated HLA haplotype in an archaeological specimen.
    The results show that the genetic markers associated with high risk of celiac disease are at least a couple of thousand years old.
    Source:
    World J Gastroenterol. 2012 Oct 7;18(37):5300-4. doi: 10.3748/wjg.v18.i37.5300.

    Jefferson Adams
    Celiac.com 11/06/2013 - Some researchers have questioned whether celiac disease may have arisen as a side effect of recent genetic adaptations since the domestication of wheat about 10,000 years ago.
    In his keynote address at the 2013 International Celiac Disease Symposium in Chicago, John Hawks spoke about the history of celiac disease and how he is using that history to explore the responses of complex gene networks to environmental changes during recent human evolution.
    Specifically, Hawks is "looking at how human genes evolved in the recent past to get an idea of how those genes work, especially in complex phenotypes."
    The risk of developing celiac disease has strong genetic factors, many are a function of immune system molecules called human leukocyte antigens, or HLAs.
    HLAs are one of the most variable gene systems in the human genome, with more genetic variants in the modern human population than any other type of gene.
    These molecules dot cell surfaces and help the immune system distinguish friendly particles from potentially dangerous pathogens.
    According to Hawks, as populations grew more dense after the rise of agriculture, infectious diseases likely became a more serious issue, which led to a situation where the positive effects of a strong immune system outweigh any negative effects such as autoimmune reactions.
    Hawks and former graduate student Aaron Sams recently published evidence of changes in other, non-HLA genes related to celiac disease risk.
    However, recent data suggest that the genetics of celiac disease may not be the result of recent evolutionary pressures and changes, but more likely, Hawks says is "characteristic of much more ancient humans."
    Hawks and others continue to explore how functional networks of different genes respond to environmental changes.
    Hawks hopes to look bring this approach to other autoimmune disorders, such as type 1 diabetes.
    Source:
    http://www.news.wisc.edu/22157

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/23/2018 - If you’re looking for a great gluten-free Mexican-style favorite that is sure to be a big hit at dinner or at your next potluck, try these green chili enchiladas with roasted cauliflower. The recipe calls for chicken, but they are just as delicious when made vegetarian using just the roasted cauliflower. Either way, these enchiladas will disappear fast. Roasted cauliflower gives these green chili chicken enchiladas a deep, smokey flavor that diners are sure to love.
    Ingredients:
    2 cans gluten-free green chili enchilada sauce (I use Hatch brand) 1 small head cauliflower, roasted and chopped 6 ounces chicken meat, browned ½ cup cotija cheese, crumbled ½ cup queso fresco, diced 1 medium onion, diced ⅓ cup green onions, minced ¼ cup radishes, sliced 1 tablespoon cooking oil 1 cup chopped cabbage, for serving ½ cup sliced cherry or grape tomatoes, for serving ¼ cup cilantro, chopped 1 dozen fresh corn tortillas  ⅔ cup oil, for softening tortillas 1 large avocado, cut into small chunks Note: For a tasty vegetarian version, just omit the chicken, double the roasted cauliflower, and prepare according to directions.
    Directions:
    Heat 1 tablespoon oil in a cast iron or ovenproof pan until hot.
    Add chicken and brown lightly on both sides. 
    Remove chicken to paper towels to cool.
     
    Cut cauliflower into small pieces and place in the oiled pan.
    Roast in oven at 350F until browned on both sides.
    Remove from the oven when tender. 
    Allow roasted cauliflower to cool.
    Chop cauliflower, or break into small pieces and set aside.
    Chop cooled chicken and set aside.
    Heat 1 inch of cooking oil in a small frying pan.
    When oil is hot, use a spatula to submerge a tortilla in the oil and leave only long enough to soften, about 10 seconds or so. 
    Remove soft tortilla to a paper towel and repeat with remaining tortillas.
    Pour enough enchilada sauce to coat the bottom of a large casserole pan.
    Dunk a tortilla into the sauce and cover both sides. Add more sauce as needed.
    Fill each tortilla with bits of chicken, cauliflower, onion, and queso fresco, and roll into shape.
    When pan is full of rolled enchiladas, top with remaining sauce.
    Cook at 350F until sauce bubbles.
    Remove and top with fresh cotija cheese and scallions.
    Serve with rice, beans, and cabbage, and garnish with avocado, cilantro, and sliced grape tomatoes.

     

    Roxanne Bracknell
    Celiac.com 06/22/2018 - The rise of food allergies means that many people are avoiding gluten in recent times. In fact, the number of Americans who have stopped eating gluten has tripled in eight years between 2009 and 2017.
    Whatever your rationale for avoiding gluten, whether its celiac disease, a sensitivity to the protein, or any other reason, it can be really hard to find suitable places to eat out. When you’re on holiday in a new and unknown environment, this can be near impossible. As awareness of celiac disease grows around the world, however, more and more cities are opening their doors to gluten-free lifestyles, none more so than the 10 locations on the list below.
    Perhaps unsurprisingly, the U.S is a hotbed of gluten-free options, with four cities making the top 10, as well as the Hawaiian island of Maui. Chicago, in particular, is a real haven of gluten-free fare, with 240 coeliac-safe eateries throughout this huge city. The super hip city of Portland also ranks highly on this list, with the capital of counterculture rich in gluten-free cuisine, with San Francisco and Denver also included. Outside of the states, several prominent European capitals also rank very highly on the list, including Prague, the picturesque and historic capital of the Czech Republic, which boasts the best-reviewed restaurants on this list.
    The Irish capital of Dublin, meanwhile, has the most gluten-free establishments, with a huge 330 to choose from, while Amsterdam and Barcelona also feature prominently thanks to their variety of top-notch gluten-free fodder.
    Finally, a special mention must go to Auckland, the sole representative of Australasia in this list, with the largest city in New Zealand rounding out the top 10 thanks to its 180 coeliacsafe eateries.
    The full top ten gluten-free cities are shown in the graphic below:
     

    Jefferson Adams
    Celiac.com 06/21/2018 - Would you buy a house advertised as ‘gluten-free’? Yes, there really is such a house for sale. 
    It seems a Phoenix realtor Mike D’Elena is hoping that his trendy claim will catch the eye of a buyer hungry to avoid gluten, or, at least one with a sense of humor. D’Elena said he crafted the ads as a way to “be funny and to draw attention.” The idea, D’Elena said, is to “make it memorable.” 
    Though D’Elena’s marketing seeks to capitalizes on the gluten-free trend, he knows Celiac disease is a serious health issue for some people. “[W]e’re not here to offend anybody….this is just something we're just trying to do to draw attention and do what's best for our clients," he said. 
    Still, the signs seem to be working. D'elena had fielded six offers within a few days of listing the west Phoenix home.
    "Buying can sometimes be the most stressful thing you do in your entire life so why not have some fun with it," he said. 
    What do you think? Clever? Funny?
    Read more at Arizonafamily.com.

    Advertising Banner-Ads
    Bakery On Main started in the small bakery of a natural foods market on Main Street in Glastonbury, Connecticut. Founder Michael Smulders listened when his customers with Celiac Disease would mention the lack of good tasting, gluten-free options available to them. Upon learning this, he believed that nobody should have to suffer due to any kind of food allergy or dietary need. From then on, his mission became creating delicious and fearlessly unique gluten-free products that were clean and great tasting, while still being safe for his Celiac customers!
    Premium ingredients, bakeshop delicious recipes, and happy customers were our inspiration from the beginning— and are still the cornerstones of Bakery On Main today. We are a fiercely ethical company that believes in integrity and feels that happiness and wholesome, great tasting food should be harmonious. We strive for that in everything we bake in our dedicated gluten-free facility that is GFCO Certified and SQF Level 3 Certified. We use only natural, NON-GMO Project Verified ingredients and all of our products are certified Kosher Parve, dairy and casein free, and we have recently introduced certified Organic items as well! 
    Our passion is to bake the very best products while bringing happiness to our customers, each other, and all those we meet!
    We are available during normal business hours at: 1-888-533-8118 EST.
    To learn more about us at: visit our site.

    Jefferson Adams
    Celiac.com 06/20/2018 - Currently, the only way to manage celiac disease is to eliminate gluten from the diet. That could be set to change as clinical trials begin in Australia for a new vaccine that aims to switch off the immune response to gluten. 
    The trials are set to begin at Australia’s University of the Sunshine Coast Clinical Trials Centre. The vaccine is designed to allow people with celiac disease to consume gluten with no adverse effects. A successful vaccine could be the beginning of the end for the gluten-free diet as the only currently viable treatment for celiac disease. That could be a massive breakthrough for people with celiac disease.
    USC’s Clinical Trials Centre Director Lucas Litewka said trial participants would receive an injection of the vaccine twice a week for seven weeks. The trials will be conducted alongside gastroenterologist Dr. James Daveson, who called the vaccine “a very exciting potential new therapy that has been undergoing clinical trials for several years now.”
    Dr. Daveson said the investigational vaccine might potentially restore gluten tolerance to people with celiac disease.The trial is open to adults between the ages of 18 and 70 who have clinically diagnosed celiac disease, and have followed a strict gluten-free diet for at least 12 months. Anyone interested in participating can go to www.joinourtrials.com.
    Read more at the website for Australia’s University of the Sunshine Coast Clinical Trials Centre.

    Source:
    FoodProcessing.com.au