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  • Jefferson Adams
    Jefferson Adams

    How a Miracle Cure for Celiac Disease Backfired

    Reviewed and edited by a celiac disease expert.

    Bananas were once seen as a miracle cure for celiac disease. What happened?

    How a Miracle Cure for Celiac Disease Backfired - Why were bananas once regarded as a cure for celiac disease? Image: CC--jster
    Caption: Why were bananas once regarded as a cure for celiac disease? Image: CC--jster

    Celiac.com 06/22/2017 - Once upon a time, bananas were thought by many doctors to possess tremendous healing properties. Bananas were used to help diabetics to use weight. Doctors told mothers to feed bananas to their infants starting at 4 weeks. And for a long time, the diet seemed to help people "recover" from celiac disease.

    Invented by Dr. Sidney Haas in 1924, the high-calorie, banana-based diet excluded starches, but included bananas, milk, cottage cheese, meat and vegetables.

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    The diet was so effective in celiac disease patients that it was adopted by numerous doctors, and endorsed in the 1930s by the University of Maryland, according to pediatric gastroenterologist Alessio Fasano, chair of pediatrics at Harvard Medical School and a specialist in celiac disease.

    The general public picked up the trend, and embraced bananas as one of the great health foods. But, whatever the medical and public perception about bananas may have been, Dr. Haas was wrong about the curative powers of bananas, and that seemingly honest mistake had long-term consequences for numerous patients with celiac disease.

    That's because the bananas did not cure the condition, as was commonly thought. The bodies of the patients involved did not become tolerant to wheat. So, when they reintroduced wheat into their diets, as many did, assuming they were cured, they suffered physical consequences.

    One such patient was Lindy Redmond, whose celiac disease was “cured” with the banana diet as a child. "All my life I have told doctors I had celiac as a child," says Lindy Redmond, "and that I grew out of it. And all my life I have eaten wheat."

    Thinking she was cured, but suffering years of symptoms, Redmond, at 66 years old, finally underwent a gluten-antibody test and and received an intestinal biopsy.

    "My intestine was very damaged," she reports. "My doctor said she didn't know if it would ever recover." It was then that Redmond wondered about the possible connection between lifelong, untreated celiac disease and her two miscarriages, frequent bouts of colds and bronchitis, and interminable constipation. Now 74 and off gluten, Redmond says the colds and constipation are gone.

    It wasn't until 1952 that Dutch pediatrician, Willem Karel Dicke, and his colleagues identified gluten as the trigger for celiac disease, and the gluten-free diet was born.

    But Haas railed against the gluten-free diet and went on promoting his banana-based cure, claiming that only the banana diet could achieve "a cure which is permanent."

    The European medical community quickly adopted Dicke's gluten-free diet treatment, but in the United States, at least partly due to these erroneous medical beliefs, celiac disease remained under-diagnosed, and many patients suffered needlessly.

    Reda more at NPR.org

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    This article is misleading and to a large extent completely wrong about Dr. Haas' positions regarding gluten and other carbohydrates. Dr. Haas´ research led to the creation of the Specific Carbohydrate Diet - which forbids any grains and starch at all. It is a scientific diet used to treat ulcerative colitis, Crone's, Cystic Fibrosis, Celiac and other auto-immune and gastric disorders. He is one of the important contributors to our understanding of how food and the bodies processing of food contributes to the functioning of our bodies, including the brain. The author writes from a simplistic point of view better used to describe a baseball game. He does not understand the nature of the scientific process and how scientific knowledge is accumulated. Science is not a competition. Each scientist adds a little and knowledge builds. This is a very unfair article to all the scientists mentioned and to the continued understanding of the cellular biology of food´s interaction with our bodies. The tone of the article itself, as prefaced by the headline, is sensationalist and at heart mean. The writer clearly doesn't care about the truth of the subject at all.

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    The Specific Carbohydrate Diet is intended to remodel the community of flora and fauna in the gut by essentially feeding them by modifying what we eat in order to create a healthier gut microbiome. It is sad that this article ignores the re-emerging study of the human microbiome, which I feel is one of the most promising fields of study for all auto-immune mediation, and instead frames Dr. Haas' research as sort of a wacky fad diet. Dr. Haas was regarded as the world's foremost celiac expert.

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    This article is misleading and to a large extent completely wrong about Dr. Haas' positions regarding gluten and other carbohydrates. Dr. Haas´ research led to the creation of the Specific Carbohydrate Diet - which forbids any grains and starch at all. It is a scientific diet used to treat ulcerative colitis, Crone's, Cystic Fibrosis, Celiac and other auto-immune and gastric disorders. He is one of the important contributors to our understanding of how food and the bodies processing of food contributes to the functioning of our bodies, including the brain. The author writes from a simplistic point of view better used to describe a baseball game. He does not understand the nature of the scientific process and how scientific knowledge is accumulated. Science is not a competition. Each scientist adds a little and knowledge builds. This is a very unfair article to all the scientists mentioned and to the continued understanding of the cellular biology of food´s interaction with our bodies. The tone of the article itself, as prefaced by the headline, is sensationalist and at heart mean. The writer clearly doesn't care about the truth of the subject at all.

    No one is sought to minimize or mischaracterize Dr. Haas' contributions to medicine. At the time, the banana diet was not an unreasonable treatment for celiac disease. The condition can be controlled with such a diet. The Specific Carbohydrate Diet was also an important contribution to medicine. However, with respect to bananas curing celiac disease, Dr. Haas was simply wrong. His diet did not cure the condition, as he strongly maintained. The gluten-free diet was, in fact, a superior treatment for celiac disease. The fact is that Dr. Haas continued to advocate his banana-based diet, and continued to claim that it was the only diet that could achieve "a cure which is permanent" for people with celiac disease.

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    The Specific Carbohydrate Diet is intended to remodel the community of flora and fauna in the gut by essentially feeding them by modifying what we eat in order to create a healthier gut microbiome. It is sad that this article ignores the re-emerging study of the human microbiome, which I feel is one of the most promising fields of study for all auto-immune mediation, and instead frames Dr. Haas' research as sort of a wacky fad diet. Dr. Haas was regarded as the world's foremost celiac expert.

    This article does not address Dr. Haas' research in general. It focuses only on the fact that the banana diet was once seen as a cure for celiac disease. That was not true, as Dicke's research later showed. Even in the face of Dicke's claims to the contrary, Dr. Haas continued to suggest that with his diet “There is complete recovery with no relapses, no deaths, no crisis, no pulmonary involvement and no stunting of growth†after these patients were on the diet for at least a year. " Whatever merits Dr. Haas' diet may have, even for celiacs, these claims for total cure are not borne out by science.

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    Dr. Haas apparently ignored the basis of science...evidence and repeatability. He came up with something that had apparent effect, failed to pursue further research, and proceeded to trash a better solution that was found...at the cost of his patients. In the long run, that is the only metric that matters.

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  • About Me

    Jefferson Adams

    Jefferson Adams is Celiac.com's senior writer and Digital Content Director. He earned his B.A. and M.F.A. at Arizona State University, and has authored more than 2,500 articles on celiac disease. His coursework includes studies in science, scientific methodology, biology, anatomy, medicine, logic, and advanced research. He previously served as SF Health News Examiner for Examiner.com, and devised health and medical content for Sharecare.com. Jefferson has spoken about celiac disease to the media, including an appearance on the KQED radio show Forum, and is the editor of the book "Cereal Killers" by Scott Adams and Ron Hoggan, Ed.D.

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    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.

    Scott Adams
    By R.A. Gibbons, MD., M.R.C.P., Physician to The Grosvenor Hospital for Women and Children, Physician for the Diseases of Women and Children at the St. George's and St. James's Dispensary.

    Footnote: (1) This title is adopted by Dr. Gee, who was the first to direct my attention to the disease, at the Hospital for Sick Children, Great Ormond Street, and I have therefore thought it best to retain it.
    The subject of this paper is one which has not been described, to my knowledge, in any of the text-books, either on general medicine or on the diseases of children. As it is one of great importance, and one which is readily overlooked, even by excellent physicians, I have thought that it would be of interest to publish a few of the cases which have come under my own observation of this somewhat uncommon disease. These cases are very similar, and it is therefore unnecessary to burden my paper with more than four, which will serve as examples of all.
    The name "coeliac" is derived from the Greek Koilia, which means belly. The "coeliac flux" is a well-known and o1d expression signifying diarrhea, in which the undigested food is passed from the bowel. The name of the affection under consideration does not necessarily imply diarrhea, and is taken for want of a better one; it means merely that the disease pertains to the abdomen. It has, however, the merit of not conveying anything actually erroneous. The disease is not distinctly a diarrhea although undoubtedly children suffering from this affection are liable to attacks of diarrhea. In the latter affection, if the larger bowel is affected, we get dysenteric symptoms; if the smaller bowel is the seat of the trouble, it is generally considered that we have three different conditions affecting it, namely, increased movement, increased secretions, or a diseased condition of the mucous membrane. The coeliac affection corresponds with neither of these conditions, as will presently be shown.
    The following cases are epitomized from notes taken of some of the patients who have been under my care in private practice:
    Case I -- J.F., a boy, aged 2 years, was first seen on the 26th of April 1883 (1)
    He was lying in his nurse's lap, looking flushed, and complaining of pain over the abdomen. He had been languid and vomiting during the morning. I ascertained that the motions had been copious, frothy, and offensive. He had been latterly losing flesh. As to the previous history, I learned that the child had been brought up by hand, and there was nothing of importance to relate until last December, since which time he had been out of health, and seemed to be gradually getting worse. In that month they had sought advice, and he had caused his parents anxiety ever since, sometimes being a little better, at other times worse. On examination I found that the temperature was over 99, the pulse 108; but no definite disease could be made out. The examination of the chest yielded nothing. The abdomen was soft and doughy, but painful to the touch, and he cried out when any attempt was made to palpate. The spleen and liver were not enlarged, and I could detect no enlarged lymphatic glands. The flesh was soft and flabby. As he was having rather frequent actions of the bowels, a mixture of bismuth and compound tincture of camphor was ordered.
    His diet consisted of cream, with two or three times as much water or scalded whey. For a drink at breakfast, at 11 o'clock in the morning, and at bedtime, whey made wit essence of rennet; if mixed with cream, it was to be scalded. Pounded raw meat prepared in the ordinary way, and rubbed through a sieve; of this one, two, or three tablespoonfuls to be taken for dinner, with a little sifted sugar or fruit jelly. A tablespoonful of mashed floury potato. Rusks, plain biscuits, or toast with fresh butter; Savory & Moore's food made with whey, and a teaspoonful of cream added. Half a pint of asses' milk in the morning, and the same quantity- in the evening. One or two teaspoonfuls of raw meat in the after part of the day. The following day I carefully examined some motion microscopically, and could detect no pus and nothing extraordinary.
    Family History:-- The mother was a healthy woman. She had had no miscarriage.
    She had no history of any important disease. There was no trace of tubercle on her side. Her mother suffered occasionally from gout. The child's father appeared a healthy man; he occasionally passed free uric acid, and had symptoms rather like those of renal calculus. There was no history of syphilis obtainable, and no reason to suspect it. There were two other children, a boy and girl, older than this patient. The girl had suffered from suppuration of the submaxillary glands.
    The child improved considerably until 5th July, when he had an attack of watery- diarrhea, which prostrated him. The motions were extremely offensive. Dr. Gee saw him with me, and suggested, instead of the compound kino powder, which he was taking, that he should have minute doses of mercury and chalk every two hours; forty-eight hours later the diarrhea had stopped. Without going further into detail, it may be stated that this attack nearly proved fatal. He, however, gradually recovered, the first favorable sign being that the motion contained some solid material. There was no change in the diet, except that the meat was omitted and Brand's essence substituted.
    The following month left London for the seaside. He occasionally had attacks of diarrhea there. Six months afterwards I again saw him, when he seemed in excellent spirits, looked fat, and, although flabby, ran about and played with the other children with apparent enjoyment.
    This boy died of acute purpura haemorrhagica, the details of which illness I have already published in the Medical Times and Gazette for 1885.
    Case II -- S.H., aged 2 years and 8 months. First seen on 10th May 1885
    Her condition is as follows:-- She is very anaemic in appearance. She is not thin or wasted, but her flesh is flabby, and her legs and arms, though apparently well covered with flesh, are soft to the touch. Nothing is to be discovered on examination of the chest, the heart sounds being normal, and the lungs acting well. On palpation of the abdomen, it is found to be doughy, blown out with flatulence, and looking very large. The liver can be felt about one finger's breadth below the edge of the ribs, and the spleen is slightly enlarged. No enlarged lymphatic glands can be made out anywhere. She walks with difficulty, and has a great disinclination to go upstairs. A very little exertion makes her tired, and break out into a profuse perspiration, especially about the head. Her appetite is poor, and it is with great difficulty that she can be coaxed to eat. Her motions are light in color, frothy, and intensely offensive. Microscopically they contain nothing abnormal. Sometimes the actions vary from one to three in the twenty-four hours. The urine contains no albumen, sugar, or bile.
    Previous History:-- With the exception of an acute attack of laryngitis, there is nothing to report about her former health. She was nursed as a baby by her mother. She first began to complain in July last, but as the weather was very hot, it was thought that she was suffering merely from the effects of the heat. At that time her motions were clay colored, and she was very pale and languid, with occasional attacks of diarrhea; but in the beginning not much attention was paid to these symptoms. Soon after, becoming worse, advice was sought concerning her; and in a letter to me from her medical attendant, it was stated that the saw her for what he considered were symptoms of mesenteric disease, but that she greatly improved under treatment. She soon afterwards relapsed, and owing to the extreme
    debility and pallor, her case was considered hopeless.
    Family History:-- Her mother is perfectly healthy, with no history of any importance. Her father is at present healthy; he suffered some years ago from abscess of the hip joint. From this he perfectly recovered, and is in excellent health. The other children, three sisters, are all healthy.

    Treatment:-- She was placed upon a diet exactly similar to the other cases related, but in her case it seemed necessary, on account of exhaustion, to give as an addition brandy once or twice a day. Attacks of diarrhea were treated as they arose, but the medicine she principally took was iron in some form. Cod-liver oil could never be borne; it invariably caused looseness of the bowels. At one time she developed purpuric patches all over the lower part of the abdomen, which, however gradually disappeared; and she also had an attack of stomatitis, which lasted for about ten days. She was under observation for a considerable time during each year, and I constantly heard about her when she was not in London. The diet and general treatment were carefully attended to, and she was allowed to have chicken, eggs, tapioca, milk, and everything of a plain description. when I last heard, her condition was most satisfactory, and she had gained considerably in weight.
    Case III -- E.H.W., aged 2 years and 1 month. Her mother came to consult me about her on the 10th of May, 1887, complaining that the child's digestion was out of order, and the first thing she noticed was that the motions were offensive and copious.
    Previous History:-- The mother declared that she considered the child had not been thoroughly well ever since she was born. She was only suckled a fortnight, after which she had cows' milk and water, then donkeys' milk for a time, and then again cows' milk.
    Family History:-- The patient is an only child. The mother is a healthy woman; has never suffered from any miscarriage; there is no history of tubercle. There is no history of syphilis obtainable, and no reason to suspect it.

    The child has always been nervous and easily frightened. For several months past she has been dieted by the mother. Sometimes she would give her a little meat, and sometimes not. She often has attacks of sickness; the least thing causes her to vomit, and the food is very easily brought back in an undigested state. The motions are very large in quantity, pale in colour, and extremely offensive. On examination the child is found to be generally flabby, and does not look strong; she is pallid, but not thin, and there is no yellow tint of the skin. On examination of the chest, the right side is seen to be slightly flattened anteriorly, and the percussion note is of a higher pitch as compared with the left, probably from thickened pleura. The breath sounds are natural; the heart seems normal. The liver is one finger's breadth below the ribs. The spleen is not enlarged, and there are no enlarged lymphatic glands to be discovered. On examination of the blood, there is observed to be an excess of white cells. The red are less colored than is natural, and there are numerous lymphoid particles present. It is spanaemic, the number of cells being greatly diminished. The tongue is white and coated. She was ordered some perchloride of iron and cod-liver oil, with occasionally some decoction of aloes, and the diet was to consist of cream, whey, also asses' milk, raw meat, and potato.

    A week later, I saw her on account of pain in the abdomen. Her legs were drawn up and she complained of great pain all over the abdomen. Her medicines were stopped, and I substituted for them a mixture containing bismuth and compound tincture of camphor, under which she improved. On the 11th of June she had an attack of sickness. She vomited frequently, and had three copious loose motions, the last being watery. This attack was probably because there had been some mistake about the milk, the child having had cows' milk instead of asses' milk during the morning.
    When I last heard of her from the country, I was told that she seemed very much better and improved in every way. She had, however, to be extremely careful about food, and could not make any change with impugnity, -- in fact, the diet had had to be altered to an ordinary one with the greatest of care.
    Case IV -- D.G., aged 2 years and 8 months. First seen on 9th September 1886. Her mother brought her to me, complaining of her not passing water for many hours, sometimes as many as 10 or 12 elapsing without any inclination on the part of the child to relieve herself.
    Previous history:-- The child had been brought up by hand, and there is nothing of consequence to report concerning her, with the exception of a severe attack of laryngitis, from which she suffered a year previously. Family History.-- The mother is a delicate-looking woman, thin, and by no means strong. There is no distinct history of phthisis on either side, and there is no syphilitic history obtainable, and no reason to suspect it. There is one other child, older than the patient and perfectly healthy. She also had a severe attack of laryngitis when a baby, but nothing else of consequence.
    On examination, she was seen to be a rather delicate-looking child, but apparently well developed, although her flesh was soft and flabby. No signs of rickets could be detected. The abdomen seemed large and doughy. The heart and lungs appeared to be normal. The spleen and liver were not enlarged, and no enlarged lymphatic glands could be felt. The urine proved to be distinctly albuminous and to contain crystals of uric acid. The mother, who had come with her from the country, had not brought the nurse, and could tell me nothing about the motions, or whether the bowels were regular or not. She was given a mixture containing some sulphate of soda and citte of potash. I soon afterwards received a letter telling me that the motions were copious, frothy, whitish, and intensely offensive, and that the bowels acted once or twice daily. On the 26th October I again saw her, and then heard from the mother that the child had been very poorly a fortnight previously, owing to what was considered due to a chill. She told me that the child was seized with what she termed "spasms of the abdomen," that she drew her legs up, and seemed in great pain. This attack of pain apparently lasted of several hours, and the mother states that she was not feverish. At that time the motions were too light in colour; they were very large and extremely offensive. She passed a slight amount of blood with the motion, but the mother is not quite sure whether this was merely from straining at the first, or whether it was mixed with the motion; probably the former would account for it, for I never again heard of the presence of blood. The nurse said the motions were so large in quantity that they quite astonished her, considering the amount of food eaten; that they were intensely offensive, and that there were never more than two in the twenty-four hours, although usually there was but one.
    There being no doubt as to the diagnosis in this case, I ordered the same diet as in the previous cases, viz., cream and whey, pounded raw meat with sifted sugar and floury potato, and to have some compound decoction of aloes and cod-liver oil. On the 4th of November I saw her in what her mother described as her "stomach attacks," and I then found that she appeared to have considerable abdominal pain, with the legs drawn up. I therefore omitted the compound decoction of aloe sand the cod-liver oil, and gave a mixture containing some compound tincture of camphor. On a microscopical examination of the motions, it was found that they contained no pus. There were many long, rod-like virbios, and very numerous spores, like the penicilium glaucum.
    It may be briefly stated that she was kept upon this diet for many months; that the attacks of pain from which she originally suffered gradually diminished in intensity until they entirely ceased, and that her general condition was greatly improved. The albumen disappeared form the urine; she became more muscular and walked without fatigue, and the motions gradually assumed a natural colour. This improvement, however, did not take place rapidly, but occurred during a period of about two and a half years. When I last heard of her, her condition was satisfactory, and although she could not be considered to be a perfectly robust child, there seemed to be nothing amiss with her. She ran about and played like other children, and seemed well. Her motions have always been natural for months past, an she has gradually returned to ordinary every day diet; but the nurse has been extremely careful in giving her only what has been ordered for her, and she has at all times been cautious not to give her anything which she feared would din the least disagree with her. The child has, therefore, had every possible care regarding her treatment.
    The coeliac disease, amongst hospital patients, is popularly called "consumption of the bowels," meaning by this one the several affections to which they apply this term. This disease is characterized by the passage of large, loose, white or whitish, frothy, intensely foetid motions; by pallor of the skin; wasting; loss of muscular strength, and by the fact that it is most frequently met with in children between 1 and 5 years of age. The youngest child I have seen attacked by it was between 10 and 11 months old. I have seen it in children with perfectly healthy parents, and, indeed, with sisters and brothers in every way healthy. In only one family can I trace any history of struma on the side of the father. No history of tubercle can be traced in the family of any of the patients whose cases are related, except one, and in that, consumption occurred in a paternal uncle of the patient, and in all there is no history of syphilis obtainable, and no reason to suspect it. In most cases there is a history to be obtained of gout, either on the side of the father or mother, or in distant relations. The examination of the faeces themselves throws no light upon the matter. In those I have submitted to careful microscopical examination I have never been able to discover anything abnormal, and I have failed to detect any tubercle bacilli although carefully searched for.
    Pathology:-- Under this head there is really nothing to be detailed. Examination of the bowel after death has led to the discovery of nothing. There is no sign of wasting of the mucous membrane, of engorgement, or of ulceration, and this statement refers to the whole of the intestinal tract. I am not aware that any wasting of Lieberkuhn's follicles has been detected. The liver and the spleen are not remarkable for anything abnormal. The spleen, however, is occasionally enlarged. The blood usually has signs of anaemia and except for the excess of small lymphoid particles, might pass of ordinary anaemic blood. As, however, these small particles are not peculiar to this affection, they really need hardly to be noticed, for I have myself found them, on many occasions, especially in children suffering empyema. Therefore, taking all the facts into consideration, it is quite clear that up to the present moment nothing has occurred to throw any light upon the pathology of this extraordinary affection.

    Diagnosis:-- About this there can be no difficulty whatever, for the signs and symptoms are so clear that they cannot be mistaken. It is, however, of the greatest importance to examine the motions for one's self, for I am certain that if this had been done in several of the cases which have come under my notice, I should not have been the first to discover the child was suffering from anything beyond a little general debility. About this point one cannot be too strong, for, as there are usually no signs of ordinary diarrhea, and possibly but one action a day, the nurse, if not alarmed by the foetor, is apt to think nothing of the bowel, but to be more struck with the pallor and the generally increasing weakness of the child. The signs are so clearly indicative of this one affection, that there is no other with which it could be confounded.

    Prognosis:-- Unfortunately this is usually grave, and the majority of children suffering from this disease die. I have, however, with the exception of one, in the cases that have come under my observation, had the good fortune to witness their improvement; and I think it was partly due to the careful nursing that they had in their own homes, and to the fact that they have been the children of people who have been well off, and who have been able to give them everything that has been ordered, regardless of expense. I feel certain that this has a great deal to do with the well-being of the children, for, in one case, the second on the list, I am sure that without the most constant care and watching on the part of the mother and nurse, she would have died. As to the time at which death will take place, it is impossible to say, for, however bad these little patients are, they frequently have extraordinary rallies, and seem better for a time; but, without any warning, relapses take place, and after apparently progressing most favorably, they suddenly become exhausted, and rapidly fade away, usually from attacks of watery diarrhea.

    Symptoms and Progress:-- The onset is usually gradual, and there is nothing definite to call attention to the disease. The nurse or the mother generally states that the child has been a little out of health for some weeks, or possibly months, and yet there has been nothing special to cause alarm, with the result that no treatment has been adopted. The child becomes pale and anaemic, the blood evidently being affected, and sometimes there is a puffiness about the face. Possibly amongst the first indications, the motions have been marked by the nurse, and this has generally been owing to the colour being different, but above all, on account of their intensely foetid odor. This mal-odor is sometimes overpowering, and those who have not encountered can hardly realize it. The motions themselves, as already pointed out, are very large, soft, whitish in colour, and frothy. They resemble very much ordinary oatmeal porridge. The actions may be two or three in a day, but usually there is only one large one, and that may take place at a time to which the child is accustomed. Now and then there are attacks of so called diarrhea, that is to say, the child may have frequent evacuations of the bowels, that they may be very loose, and that they may be occasionally watery if the attack is severe, but these attacks of diarrhea are not an essential part of the disease, except in the cases of some children who have these constant attacks of diarrhea throughout the whole of the illness. The appetite is poor, usually capricious, sometimes large. The tongue is frequently coated with a whitish fur, at other times perfectly clean. In some cases there are attacks of crampy abdominal pain, possibly due to ordinary colic. These attacks were well marked in case 4. The abdomen is generally soft and doughy, although occasionally distended and hard. The liver is generally unaffected: now and then the spleen is found to be enlarged: no enlarged lymphatic glands can be detected. As a rule, the urine has nothing remarkable about it; occasionally it contains a trace of albumen. The temper of the child seems variable, most frequently he is extremely irritable, fretful, capricious, or peevish. Nothing seems to please him, and altogether he is quite unlike himself. Sometimes he is heavy and languid, complaining of headache, and wishing to lie down a good deal. The special senses seem to be normal. In all the cases that I have examined the various tendon reflexes were unaffected.
    The most remarkable sign about these children is that of loss of muscular power, with apparently no great loss of flesh; that is to say, to look at, the children do not seem to have wasted much, but on feeling the legs or arms, it is at once evident how soft and flabby and out of condition they are. A curious point is that they have a great objection to going upstairs, and in one case, on of the first symptoms which struck the nurse as being extraordinary was that the child did not care to mount the staircase, and that she had invariably to be carried up. The progress of this affection is as a rule slow. The children seem to gradually become more feeble, to waste away, and to lose power. Occasionally an attack of watery diarrhea, in those children who have been accustomed to suffer from diarrhea, may carry off the patient. In the case of colicky attacks I have seen a child in imminent danger from collapse. In non-fatal cases recovery is extremely gradual. An important point to note in this connection, is the tendency to relapses, each relapse taking a considerable time to make up for lost ground. When improvement begins to take place, it is usually shown in the healthier condition of the evacuations. The colour becomes better, the motions are more formed, and above all, less copious and less offensive. The child gains in strength, but is a long time gaining in colour. The muscular strength is the last to return, and mounting the stairs, or jumping, are amongst the very last things that can be done. The appetite generally improves but slowly, and is always capricious, or nearly so. Another important point concerning these patients is that the least thing apparently upsets them, and the smallest error in diet will bring on copious actions of the bowels, cause vomiting, or make the child quite ill again.

    Jefferson Adams
    Celiac.com 05/15/2010 - Willem-Karel Dicke was born in 1905, in Dordrecht, Holland, and died Utrecht in 1962.  Dicke was a Dutch pediatrician, the first clinician to develop the gluten-free diet, and to prove that certain types of flour cause relapses in celiac disease patients.
    From 1922 until 1929, Dicke studied medicine in Leiden.  He then specialized in pediatrics in Juliana Children’s Hospital in The Hague from 1929 until 1933.  In 1936, at just 31 years of age, he was named medical director of the hospital. 
    In the 1940s and 1950s he went on to formally establish the gluten-free diet, forever changing treatment methods and clinical outcomes of children suffering from celiac disease.  By 1952, Dicke recognized that the disease is caused by the ingestion of wheat proteins, not carbohydrates. 
    From the late 1880s into the 1920s and 30s, doctors like R. A. Gibbons, Sidney Haas and others pioneered the use of specialty diets to treat celiac disease.  Diets such as the banana diet, the fruit diet, the carbohydrate diet (fruit, puree of potatoes or tomatoes), the beefsteak diet, the milk diet had all been tried, with some success.
    In his now seminal 1950 thesis on celiac disease and wheat-free diet, Dicke lays out the results of the detailed dietary study he conducted over several years at the Juliana Children’s Hospital on a patient with celiac disease.
    The study likely had its earliest beginnings at the advent of Dicke’s promotion to medical director, if not slightly before.  From the testimony of Dicke’s wife in 1991, we know that Dicke was convinced of the beneficial effect of wheat free diet even before 1940.  She confirmed that between 1934 and 1936, Dicke began to conduct experiments with wheat free diets confirming Christopher Booth’s comments in The Lancet, Feb 25, 1989:
    “It was a young mother’s statement of her celiac child’s rash improving rapidly if she removed bread from the diet that alerted his interest,” when Dicke was a pediatrician in The Hague in 1936.
    Dicke published his first report on a wheat-free diet in Het Nederlands Tijdschrift voor Geneeskunde in 1941.  (W. K. Dicke: A simple diet for Gee-Herter’s Syndrome).  At the time, celiac was still called Gee-Herter’s syndrome.  It reads, in part:
    “In recent literature it is stated that the diet of Haas (Banana-diet) and Fanconi (fruit and vegetables) gives the best results in the treatment of patients suffering from coeliac disease.  At present (World War II) these items are not available.  Therefore, I give a simple diet, which is helping these children at this time of rationing.  The diet should not contain any bread or rusks.  A hot meal twice a day is also well tolerated.  The third meal can be sweet or sour porridge (without any wheat flour).”
    In the Netherlands, the last winter of World War II, the winter of 1944/45 became known as the ‘Winter of Hunger.’ 
    Delivery of regular food staples, such as bread, was largely disrupted, especially in the western part of the country.  This meant that people had to turn to uncommon foods, such as tulip bulbs, for sustenance.  It was during this time that Dicke became even more convinced that eating less grain, along with unusual foods, such as tulip bulbs, improved the clinical condition of his patients. 
    Dicke’s next major confirmation came when Allied planes started dropping bread in the Netherlands, and these same children began to deteriorate rapidly. 
    After World War II, Dicke conducted a series of experiments with standardized diets were performed on four children in the Wilhelmina Children’s Hospital in Utrecht and in one child in the Juliana Children’s Hospital in The Hague.  These experiments involved excluding or adding wheat or rye flour over long periods in the diets of these children with coeliac disease. 
    In Dicke’s post-war experiments, children were challenged with different cereals under a strict dietary protocol with measurement of total fecal output, fecal fat content, and the fat absorption coefficient was calculated.
    Dicke worked closely with biochemist J. H. van de Kamer of the Netherlands Central Institute for Nutritional Research TNO in Utrecht, who developed the first accurate and easily available method for measure fecal fat content in wet feces.  Dicke also worked closely with H. A. Weyers, a pediatrician from the Wilhelmina Children’s Hospital in Utrecht, who developed a method that used the coefficient of fat absorption to analyze fecal fat excretion in children with celiac disease.
    Based on these findings Dicke concluded in his 1950 thesis that wheat flour, but not well-purified wheat starch (amylum), and also rye flour, triggered the anorexia, the increased fecal output, and the streatorrhea common in celiac patients.  Dicke presented his doctoral thesis on the subject at the University of Utrecht in 1950.
    Dicke’s 1950 thesis refers to a celiac disease patient he treated in 1936.  The patient’s symptoms disappeared and he returned to normal weight and growth patterns after following a strict wheat free diet in the hospital.  However, each time the boy went home and was unable to maintain a wheat free diet, he suffered a decline in his growth curve. 
    Dicke charted these advances and reversals over four long-term admissions.  Each time the trend towards normal growth was restored.  In his thesis, Dicke presents several growth curves of children treated with a wheat free diet.  In long term studies over several years he shows that, with a wheat free diet, these children gain weight, reaching normal growth patterns when compared with age matched controls.  At the end of chapter 3 of his thesis he concludes that:
    “- if certain types of meal, such as wheat and rye are replaced in the daily diet, the patient improves;
    - acute attacks of diarrhea, do not occur, provided these types of meal are not given;
    - after a latent period which can vary in length, deterioration and acute attacks of diarrhea re-occur, if the objectionable types of meal are added to the diet too soon....”
    In 1953, together with van de Kamer and Weyers, he subsequently published Coeliac disease IV “An investigation into the injurious constituents of wheat in connection with their action on patients with coeliac disease.”
    They wrote that the alcohol soluble or the gliadin component of the water insoluble protein of wheat was responsible for the fat malabsorption in patients with celiac disease. 
    Although these findings were quickly confirmed by researchers in Britain, Scandinavia, and Germany, some researchers, especially in America, questioned the wisdom of a gluten free diet.
    After the establishment of the intestinal biopsy technique for the diagnosis of celiac disease, it became apparent that a wheat free diet should be maintained for long periods before an adequate response occurred, as Dicke had predicted. 
    In 1954, Dr. Dicke, Charlotte Anderson, and a number of their colleagues, confirmed these findings, and described the damage to the lining of the small intestine as being directly related to celiac disease.
    In 1957 he was appointed a professor of Utrecht University and became a medical director of Wilhelmina Children’s Hospital.
    To honor Willem Karel Dicke, Netherland’s Society of Gastroenterology established a gold medal in his name, to be presented to pioneering researchers in the field.  Willem Dicke himself was named as the recipient of the first gold Dicke Medal.
    Dr. Dicke died in 1962 of cerebrovascular disease.  He was just 57 years old.
    Willem Dicke.  Brilliant Clinical Observer and Translational Investigator.  Discoverer of the Toxic Cause of Celiac Disease, by David Yan and Peter R.  Holt , M.D. DOI: 10.1111/j.1752-8062.2009.00167.x GUT 1993; 34:1473-1475 Mulder, C.  “Pioneer in Glutenfree diet: Willem Karel Dicke 1905-1962 Over 50 Years of Gluten Free Diet.”  appended to: English translation by C.  Mulder June 1, 1993 of  Dicke, W.K.  “Coeliac Disease  Investigation of Harmful Effects of Certain Types of Cereal on Patients Suffering from Coeliac Disease.” Ph.  D.  Thesis, State University of Utrecht, 1950

    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.

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