Pioneer in the gluten free diet: Willem-Karel Dicke 1905-1962, over 50 years of gluten free diet.

Berge‐Henegouwen, G. P. Van; Mulder, Cjj

doi:10.1136/gut.34.11.1473

Cited by 95 publications

(55 citation statements)

References 9 publications

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“…His findings were published in Dutch in 1950 and 1953 in English (Dicke WK, 1950; Van de Kamer et al, 1953;Pena, 1991;Van Berge-Henegouwen & Mulder, 1993). A few years later the oral small bowel biopsy technique made it possible to demonstrate the celiac enteropathy in live patients.…”

Section: Historical Perspectivesmentioning

confidence: 99%

Gut Microflora Associated Characteristics in Children with Celiac Disease

Tjellström

Stenhammar

Högberg

et al. 2005

Am J Gastroenterology

120

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All previously published papers were reproduced with permission from the publisher. ABSTRACT AimThe over-arching aim of this thesis was to study some metabolic functions of the gut microflora in children with known or screening detected celiac disease (CD) and their first-degree relatives. Materials Study I. A number of 36 untreated CD children, 47 after at least 3 months on glutenfree diet (GFD) and 42 healthy controls (HC). Study II. A number of 76 first-degree relatives to CD children and 93 healthy controls (HC). Study III. A number of 17 screening detected CD children were included to be compared with the untreated children and controls from study I; with exchange of one child in the untreated group, due to low age. Study IV. A comparative study regarding correlation between iso-forms of short chain fatty acids (SCFAs) in humans as well as in animals. Methods Faecal short chain fatty acids were measured in all four studies. Additionally faecal tryptic activity (FTA) was measured in study II. Major findingsAll groups of CD children demonstrated a similar SCFAs profile, i.e. significantly more total SCFAs and acetic acid and a strong tendency to more iso-butyric and iso-valeric acids compared with HC. The first-degree relatives demonstrated another SCFAs profile, i.e. significantly less total SCFAs and acetic acid and significantly more FTA than HC. Conclusions and future outlookBased upon the strong similarities between all groups of CD children we are allowing ourselves hypothesising that CD children have a "celiacogenic" flora compared with healthy controls. In a similar way it can be said that the first-degree relatives are harbouring a "celiacprotective" microflora. Our findings open up for challenging new diagnostic, therapeutic and prognostic possibilities.

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Section: Historical Perspectivesmentioning

confidence: 99%

Gut Microflora Associated Characteristics in Children with Celiac Disease

Tjellström

Stenhammar

Högberg

et al. 2005

Am J Gastroenterology

120

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“…Subsequently, Dicke and his colleagues documented evidence for glutenfree diet treatment. Studies included long-term growth measurements of affected Dutch children during periods of starvation and re-feeding as well as measured endpoints of intestinal absorption, specifically calculated coefficients of fecal fat absorption [27].…”

Section: The Post-aretaeus Periodmentioning

confidence: 99%

The Neolithic Revolution and Subsequent Emergence of the Celiac Affection

Freeman¹

2016

IJCD

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Evidence suggests that celiac disease initially emerged as a distinct intestinal disorder sometime after organization of hunter-gatherers into human workforces capable of agriculture, especially wheat cultivation. This Neolithic revolution possibly developed to permit competitive survival over other hunter-gatherer groups. Recent archeological data suggests that wheat cultivation may have occurred in eastern Turkey, near the Gobleki Tepe, a recently discovered archeological site in the Fertile Crescent, about 10,000 to 12,000 years ago. DNA fingerprinting data suggests that diploid Einkorn wheat from this region was domesticated through hybridization into other more modern hexaploid grains with a higher more immunogenic gliadin content. Clinical features suggestive of celiac disease and recommendations for treatment are believed to have been first described by Aretaeus from Cappadocia about 250 AD, and later, by other clinicians from Europe and North America. In recent decades, celiac disease has become further defined as a clinical and pathological disorder developing in genetically predisposed individuals as a result of an immune-mediated reaction to specific peptides in wheat and other grains. Data largely from screening studies also suggests that the disorder is not uncommon, occurring in up to 2% of most populations studied. Detection is also increasing, possibly due to better clinical recognition, wider use of screening methods and, possibly, a true increase in celiac disease occurrence.

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“…Thus, it was discovered that CD was caused by the consumption of cereal gluten proteins from wheat, barley and rye and it was proposed to treat patients with a lifelong gluten-free diet (GFD) [42](Rewieved in [40,43]. In the 1950´s it was found that the fingerlike projections of the small bowel mucosa, the intestinal villi, were absent in patients with CD who consume gluten (Rewieved in [40,44]).…”

Section: Historymentioning

confidence: 99%

Studies of Mucosal Immune Regulation in Celiac Disease and Type 1 Diabetes

Lahdenperä¹

2014

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Pioneer in the gluten free diet: Willem-Karel Dicke 1905-1962, over 50 years of gluten free diet.

Cited by 95 publications

References 9 publications

Gut Microflora Associated Characteristics in Children with Celiac Disease

Gut Microflora Associated Characteristics in Children with Celiac Disease

The Neolithic Revolution and Subsequent Emergence of the Celiac Affection

Studies of Mucosal Immune Regulation in Celiac Disease and Type 1 Diabetes

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