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In response to beckxx's previous post about food allergies, here are some research abstracts that discuss the effects of not avoiding foods that one is intolerant of, or allergic to. This is just the first few I came across, there are endless articles out there. A major thing that I noticed came up multiple times was the high incidence of eosinophilic esophagitis in untreated food allergies. Obviously with severe food allergies such as those with anaphylactic responses, "untreated" food allergies often cause death, so I didn't focus on finding research on those. Hope this helps the original poster and anyone who might be interested. If you are a student you may be able to access the full text of these studies through your university's library.

Rev Clin Esp. 2006 May;206(5):236-8.

[Eosinophilic esophagogastroenteritis within the spectrum of food allergies]

[Article in Spanish]

* Sanchez-Fayos Calabuig P,
* Martin Relloso MJ,
* Porres Cubero JC.

Servicio de Aparato Digestivo, Fundacion Jimenez Diaz, Universidad Autonoma, Madrid. palomasanchezfayos@wanadoo.es

Under normal conditions, the digestive tube immune system is capable of establishing an effective plan of tolerance to food that is eaten daily by the human beings. However, this tolerance plan sometimes fails and in the final steps of this immunological dysreaction, other cellular elements, usual residents of the digestive mucous, such as eosinophil granulocytes, generally participate, together with the main cells of this system. This is the case, among others, of the so-called EGE-Eos. The authors summarize the spectrum of pathogenic options of these immunological food intolerances that range from those in which "all" depend on a specific IgE (GI food anaphylaxis) and those others in which "nothing" depends on this reagin (celiac sprue). An intermediate position would be occupied by the EGE-Eos in which there seems to be overlapping of immune reactions of cellular character together with a certain role of the IgE. These pathogenic pathways frequently cross a tangle of cellular and molecular events that cannot be untangled with either an image or one thousand words.

PMID: 16750107 [PubMed - indexed for MEDLINE]

1: Am J Gastroenterol. 1999 Mar;94(3):839-43. Links

Depression in adult untreated celiac subjects: diagnosis by the pediatrician.

* Corvaglia L,
* Catamo R,
* Pepe G,
* Lazzari R,
* Corvaglia E.

Department of Pediatric Gastroenterology, St. Orsola Hospital, University of Bologna, Italy.

Untreated celiac disease can lead to serious behavioral disorders. We describe three adult patients with undiagnosed or untreated celiac disease without particular intestinal signs, causing persistent depressive symptoms in three of the parents of our pediatric patients. In two of the three cases, the pediatrician suspected the diagnosis when taking the family history of the children. In fact, a diagnosis of celiac disease was made during childhood, when they had intestinal symptoms, but the gluten-free diet was spontaneously interrupted during the teenage period because of the disappearance of the typical intestinal signs. In the third case the mother was tested for antiendomysium antibodies (EmA), as she had a diagnosed celiac child. In all three patients, the depressive symptoms improved quickly with a gluten-free diet. In conclusion, celiac disease should be taken into consideration in the presence of behavioral and depressive disorders, particularly if they are not responsive to the usual antidepressive therapy.

PMID: 10086676 [PubMed - indexed for MEDLINE]


J Pediatr Gastroenterol Nutr. 2003 Jul;37(1):27-34.Click here to read Links

Cytokines and adhesion molecules in duodenal mucosa of children with delayed-type food allergy.

* Veres G,
* Westerholm-Ormio M,
* Kokkonen J,
* Arato A,
* Savilahti E.

Hospital for Children and Adolescents, University of Helsinki, Finland.

OBJECTIVES: The aim was to investigate the expression of cytokines, adhesion molecules, and activation and proliferation markers in duodenal biopsies from children with delayed-type food allergy (FA). METHODS: Seven children with untreated FA (uFA), seven children with treated FA (tFA) to cow milk and/or cereals, and five normal controls furnished duodenal biopsy specimens. Additionally, five pediatric patients with celiac disease were included, serving exclusively as positive controls for in situ hybridization. Interferon-gamma (IFN-gamma), interleukin-4 (IL-4), adhesion molecules, and activation markers were detected by immunohistochemistry, and expression of IFN-gamma and IL-4 messenger RNA was revealed by in situ hybridization. RESULTS: uFA patients had a higher density of IFN-gamma positive cells in the lamina propria than did tFA patients and controls (P = 0.053 and P = 0.018). Moreover, the uFA patients exhibited a higher proportion of crypt cells in mitosis than did tFA patients (P = 0.026), and stronger staining of HLA-DR in the crypts and increased density of gammadelta-T cell receptor-positive intraepithelial lymphocytes than did controls (P = 0.048 and P = 0.010). The densities of alpha(4)beta(7) positive cells in the lamina propria tended to be higher in controls than in uFA or tFA patients (P = 0.106, P = 0.073). Expression of IL-4 mRNA was significantly higher in celiac patients than in the other study groups (uFA P = 0.006, tFA P = 0.010; controls P = 0.029), and celiac patients showed higher expression of IFN-gamma mRNA than did tFA patients or controls (P = 0.017 and P = 0.016). CONCLUSIONS: As expected, Th1 dominance was present in the lamina propria of children with delayed-type FA. It may cause activation of epithelial cells and increase their turnover.

PMID: 12827002 [PubMed - indexed for MEDLINE]


Scand J Gastroenterol. 2000 Nov;35(11):1137-42. Links

Children with untreated food allergy express a relative increment in the density of duodenal gammadelta+ T cells.

* Kokkonen J,
* Holm K,
* Karttunen TJ,
* Maki M.

Dept. of Pediatrics, University of Oulu, Finland.

BACKGROUND: We investigated whether children with food allergy (FA) express increased densities of intraepithelial gammadelta+ T cells similarly to subjects with celiac disease. METHODS: The duodenal specimens taken by gastroduodenoscopy from 20 children with untreated FA, 17 with treated FA, 12 with celiac disease (CD) and 12 controls were studied with monoclonal antibodies and a three-layer peroxidase staining method. RESULTS: The subjects with untreated FA expressed equal densities of total intraepithelial CD3+ and alpha/beta+ T cells, but significantly higher densities of gammadelta+ cells than the subjects currently on an elimination diet for FA or the controls. Accordingly, their gammadelta+/CD3+ ratio was higher. On the other hand, the results differed clearly from CD, where all the three cell populations showed high densities. Another finding that discriminated the subjects with FA from the CD patients was endoscopic examination. Lymphonodular hyperplasia (LNH) of the duodenal bulb with a normal villous pattern was demonstrated in 14 (70%) of the 20 subjects with untreated FA and in 8 (47%) of the 17 with treated FA, but in none of the celiac patients or controls. Surprisingly, the biopsy samples from the subjects with FA showed quite normal histological findings. CONCLUSIONS: According to this preliminary observation, high densities of intraepithelial gammadelta+ T cells and a significantly elevated gammadelta+/CD3+ ratio are associated with untreated FA. If seen LNH in a gastroduodenoscopy and/or increased densities of gammadelta+ T cells in the biopsy specimen, the possibility of gastrointestinal FA should be reliably assessed by a food challenge.

PMID: 11145283 [PubMed - indexed for MEDLINE]


J Pediatr Gastroenterol Nutr. 1995 Jan;20(1):44-8. Links

Quantitative analysis and immunohistochemical studies on small intestinal mucosa of food-sensitive enteropathy.

* Nagata S,
* Yamashiro Y,
* Ohtsuka Y,
* Shioya T,
* Oguchi S,
* Shimizu T,
* Maeda M.

Department of Pediatrics, Juntendo University, School of Medicine, Tokyo, Japan.

Quantitative analysis and immunohistochemical studies of small intestinal mucosa were performed to investigate the mechanism of mucosal damage in 10 patients with food-sensitive enteropathy. Jejunal biopsy specimens were taken before and after treatment and after clinical relapse following a challenge test. The low villous height of untreated patients normalized after introduction of an elimination diet but declined again to subnormal level after a challenge test. Several other types of cells were significantly increased in the untreated patients in comparison to controls. These included HLA-DR+ (DR+) CD4+ cells in the lamina propria and intraepithelial CD8+ cells. Moreover, those cell patterns, such as increased DR+ CD4+ cells and CD8+ cells, normalized with treatment but regressed to pretreatment levels when the patients were challenged. These findings suggest that activated CD4+ cells in the lamina propria of the small intestinal mucosa, probably by releasing cytokines, may play an important role in contributing to mucosal damage in patients with food-sensitive enteropathy.

PMID: 7884618 [PubMed - indexed for MEDLINE]


[Antibodies against milk and soy proteins in specific intolerances and celiac disease]

[Article in Italian]

* Martelossi S,
* Ventura A,
* Perticarari S,
* Not T,
* Anibal J.

Clinica Pediatrica, IRCCS Burlo Garofolo, Trieste, Italia.

It has been suggested that high serum level of food proteins antibodies (especially cow's milk protein antibodies) may have a specific meaning in the diagnosis of food allergy, especially presenting with gastrointestinal complaints. In our study we tested with enzyme-linked immunoabsorbent assay test (ELISA) the antibody serum level to cow's milk and soy proteins in 123 children. The following patients were included in the study: 30 children with cow's milk enteropathy (CME), 27 children with soy proteins intolerance (SI), 19 coeliac children on gluten containing diet (CD), 9 coeliac children on gluten free diet (GFD) and 50 healthy sex and age matched control children. All coeliac patients had assumed cow's milk and soy proteins at the moment of the test or a few days before. Higher antibody serum level was found in coeliac disease to both cow's milk and soy proteins and in cases with cow's and soy allergy, than in control cases. The highest mean value of cow's milk and soy proteins antibodies have been found in the untreated coeliac children (CD), also higher than in the two groups of specific allergy. In treated coeliac children (GFD) with normalized jejunal mucosa cow's milk and soy proteins antibodies was normal. None of the 19 CD with high cow's milk and soy proteins antibodies level showed clinical intolerance to cow's milk and soy proteins.(ABSTRACT TRUNCATED AT 250 WORDS)

PMID: 8488125 [PubMed - indexed for MEDLINE]


Gut. 1989 Nov;30(11):1574-80. Links

Raised number of jejunal IgG2-producing cells in untreated adult coeliac disease compared with food allergy.

* Rognum TO,
* Kett K,
* Fausa O,
* Bengtsson U,
* Kilander A,
* Scott H,
* Gaarder PI,
* Brandtzaeg P.

Institute of Forensic Medicine, University of Oslo, Norway.

The subclass distribution of IgG-producing immunocytes was studied by two colour immunohistochemistry with monoclonal antibodies in jejunal biopsy specimens from 10 adults with untreated coeliac disease, 11 coeliac disease patients on a gluten free diet, and seven patients with established food allergy. Paired immunofluorescence staining was performed with subclass specific murine monoclonal antibodies in combination with polyclonal rabbit antibody reagent to total IgG; the proportion of cells belonging to each subclass could thereby be determined. The ratio of IgG2 immunocytes was significantly higher (p less than 0.05) in untreated coeliac disease patients (median, 35.2%; range, 26.7-65.2%) than in those on a gluten free diet (median, 7.3%; range, 0-31.9%) or those having food allergy (median, 12.5%; range, 0-36.5%). The disparity in the local IgG2 response between patients with untreated coeliac disease and those with food allergy might be due to differences in the nature of the antigenic stimuli, dissimilar genetic 'make-up' of the subjects, or both.

PMID: 2599444 [PubMed - indexed for MEDLINE]

Eur Rev Med Pharmacol Sci. 2004 Jul-Aug;8(4):153-64. Links

Natural history of cow's milk allergy. An eight-year follow-up study in 115 atopic children.

* Cantani A,
* Micera M.

Department of Pediatrics, University La Sapienza - Rome (Italy).

BACKGROUND: Cow's milk allergy (CMA) is a disease of infancy and usually appears in the first few months of life. The evaluation of infants for possible CMA is one of the more common problems shared by pediatricians. The role of foods in determining and/or aggravating the clinical features of atopic dermatitis (AD) has been stressed in the last decades. OBJECTIVE: The aim of the present study was to investigate, in children with food related AD, the development of tolerance to the offending food(s), clinical or laboratory data to predict the development of food tolerance, and whether there are clinical or laboratory data to predict the onset of respiratory allergy. MATERIALS AND METHODS: In this prospective study we report on 115 babies, first examined at a median age of 6 months, and followed-up for 8 years. We have investigated several factors as predictive of the outcome, as follows: early onset; widespread or not-typical (reverse pattern) skin lesions, family history positive for atopy; persisting FA, high levels of total and specific IgE antibodies, association with CMA and asthma. RESULTS: All these parameters were significantly predictive of a long-term morbidity of AD children with CMA. The median age for tolerance to cow's milk was 7 years + 11 months, to egg 6 years + 6 months, and to wheat 7 years + 2 months. However a great number of both tolerant and intolerant children developed multiple sensitizations. Only 66 children (57%) acquired food tolerance, but there was the onset of asthma in 54% of cases. CONCLUSION: The natural history of CMA is not well-known, since not many related studies have been done in children. The several predictive factors, all in a negative sense, may be the norm in atopic children. We suggest possible areas of intervention in children at risk due to parental atopy. Preventive measures may induce a dramatic improvement in children with food allergy, but we stress that the long-term prognosis is challenging, since asthma prevalence may increase up to 54% during a long follow-up. Therefore, the natural history of IgE-mediated AD in atopic children sensitized to several allergens may be less optimistic than generally reported.

PMID: 15636401 [PubMed - indexed for MEDLINE]

1: Med Hypotheses. 1997 Sep;49(3):285-8.Click here to read Links

Considering wheat, rye, and barley proteins as aids to carcinogens.

* Hoggan R.

The increased incidence of lymphoma in celiac sprue (CS) is well documented, and the risk of developing this malignancy is 40-100-fold greater than in the general population. The author believes that gluten may also be at the root of lymphomas in asymptomatic and latent celiac sprue, as well. Among the 20-30% of the population which has the HLA factors most common in celiac, increased intestinal permeability leads to absorption of macromolecular peptides with opioid activity, which derive from pepsin digests of wheat. The presence, in the bloodstream, of these peptides may increase the risk of lymphomas for the entire hereditary group, which includes CS. Several processes contribute to the effect that is herein hypothesized, including opioid attachment at the hypothalamic-pituitary-adrenal axis (HPA), and subsequent downregulation of production of natural killer cells. This may offer an explanation for our longstanding awareness that there is an 'impaired lymphocyte reactivity against tumor cells in patients with coeliac disease' which may also apply to first-degree relatives with the same HLA markers.

PMID: 9293475 [PubMed - indexed for MEDLINE]

Scand J Gastroenterol. 2000 Oct;35(10):1048-52. Links

Fructose- and sorbitol-reduced diet improves mood and gastrointestinal disturbances in fructose malabsorbers.

* Ledochowski M,
* Widner B,
* Bair H,
* Probst T,
* Fuchs D.

Dept. of Clinical Nutrition, Institute of Medical Chemistry and Biochemistry, University of Innsbruck, Austria.

BACKGROUND: Fructose malabsorption is characterized by the inability to absorb fructose efficiently. As a consequence fructose reaches the colon where it is broken down by bacteria to short fatty acids, CO2 and H2. Bloating, cramps, osmotic diarrhea and other symptoms of irritable bowel syndrome are the consequences and can be seen in about 50% of fructose malabsorbers. We have previously shown that fructose malabsorption is associated with early signs of mental depression and low serum tryptophan concentrations. It was therefore of interest whether a fructose-reduced diet could not only improve gastrointestinal complaints but also depressive signs seen in fructose malabsorbers. METHODS: Fifty-three adults (12 males, 41 females), who were identified as fructose malabsorbers according to their breath-H2 concentrations, filled out a Beck's depression inventory-questionnaire, and a questionnaire with arbitrary scales for measurement of meteorism, stool frequency and quality of life for a 4-week period before dietary intervention and 4 weeks after dietary change as for fructose- and sorbitol-reduced diet. RESULTS: Depression scores were reduced by 65.2% after 4 weeks of diet (P < 0.0001), and there was a significant reduction of meteorism (P < 0.0001) and stool frequency (P < 0.01). Improvement of signs of depression and of meteorism was more pronounced in females than in males. CONCLUSION: Fructose- and sorbitol-reduced diet in subjects with fructose malabsorption does not only reduce gastrointestinal symptoms but also improves mood and early signs of depression.

PMID: 11099057 [PubMed - indexed for MEDLINE]

World J Gastroenterol. 2007 Jan 7;13(1):146-51.Click here to read Links

Malignancy and mortality in a population-based cohort of patients with coeliac disease or 'gluten sensitivity'.

* Anderson LA,
* McMillan SA,
* Watson RG,
* Monaghan P,
* Gavin AT,
* Fox C,
* Murray LJ.

Centre for Clinical and Population Sciences, Mulhouse Building, Grosvenor Road, Belfast, BT12 6BJ, United Kingdom, l.anderson@qub.ac.uk.

AIM: To determine the risk of malignancy and mortality in patients with a positive endomysial or anti-gliadin antibody test in Northern Ireland. METHODS: A population-based retrospective cohort study design was used. Laboratory test results used in the diagnosis of coeliac disease were obtained from the Regional Immunology Laboratory, cancer statistics from the Northern Ireland Cancer Registry and mortality statistics from the General Registrar Office, Northern Ireland. Age standardized incidence ratios of malignant neoplasms and standardized mortality ratios of all-cause and cause-specific mortality were calculated. RESULTS: A total of 13 338 people had an endomysial antibody and/or an anti-gliadin antibody test in Northern Ireland between 1993 and 1996. There were 490 patients who tested positive for endomysial antibodies and they were assumed to have coeliac disease. There were 1133 patients who tested positive for anti-gliadin antibodies and they were defined as gluten sensitive. Malignant neoplasms were not significantly associated with coeliac disease; however, all-cause mortality was significantly increased following diagnosis. The standardized incidence and mortality ratios for non-Hodgkin's lymphoma were increased in coeliac disease patients but did not reach statistical significance. Lung and breast cancer incidence were significantly lower and all-cause mortality, mortality from malignant neoplasms, non-Hodgkin's lymphoma and digestive system disorders were significantly higher in gluten sensitive patients compared to the Northern Ireland population. CONCLUSION: Patients with coeliac disease or gluten sensitivity had higher mortality rates than the Northern Ireland population. This association persists more than one year after diagnosis in patients testing positive for anti-gliadin antibodies. Breast cancer is significantly reduced in the cohort of patients with gluten sensitivity.

PMID: 17206762 [PubMed - in process]

Best Pract Res Clin Gastroenterol. 2006;20(3):467-83.Click here to read Links

Food allergies and food intolerances.

* Ortolani C,
* Pastorello EA.

Istituto Allergologico Lombardo, Piazza Monsignor Moneta 1, 20090 Cesano Boscone, Milan, Italy. all@ambrosianacdc.it

Adverse reactions to foods, aside from those considered toxic, are caused by a particular individual intolerance towards commonly tolerated foods. Intolerance derived from an immunological mechanism is referred to as Food Allergy, the non-immunological form is called Food Intolerance. IgE-mediated food allergy is the most common and dangerous type of adverse food reaction. It is initiated by an impairment of normal Oral Tolerance to food in predisposed individuals (atopic). Food allergy produces respiratory, gastrointestinal, cutaneous and cardiovascular symptoms but often generalized, life-threatening symptoms manifest at a rapid rate-anaphylactic shock. Diagnosis is made using medical history and cutaneous and serological tests but to obtain final confirmation a Double Blind Controlled Food Challenge must be performed. Food intolerances are principally caused by enzymatic defects in the digestive system, as is the case with lactose intolerance, but may also result from pharmacological effects of vasoactive amines present in foods (e.g. Histamine). Prevention and treatment are based on the avoidance of the culprit food.

PMID: 16782524 [PubMed - indexed for MEDLINE]

Proc Nutr Soc. 2005 Nov;64(4):434-50.Click here to read Links

Coeliac disease: a diverse clinical syndrome caused by intolerance of wheat, barley and rye.

* McGough N,
* Cummings JH.

Coeliac UK, Octagon Court, High Wycombe, Bucks.

Coeliac disease is a lifelong intolerance to the gluten found in wheat, barley and rye, and some patients are also sensitive to oats. The disease is genetically determined, with 10% of the first-degree relatives affected and 75% of monozygotic twins being concordant. Of the patients with coeliac disease 95% are human leucocyte antigen (HLA)-DQ2 or HLA-DQ8 positive. Characteristically, the jejunal mucosa becomes damaged by a T-cell-mediated autoimmune response that is thought to be initiated by a 33-mer peptide fragment in A2 gliadin, and patients with this disorder have raised levels of anti-endomysium and tissue transglutaminase antibodies in their blood. Coeliac disease is the major diagnosable food intolerance and, with the advent of a simple blood test for case finding, prevalence rates are thought to be approximately 1:100. Classically, the condition presented with malabsorption and failure to thrive in infancy, but this picture has now been overtaken by the much more common presentation in adults, usually with non-specific symptoms such as tiredness and anaemia, disturbance in bowel habit or following low-impact bone fractures. Small intestinal biopsy is necessary for diagnosis and shows a characteristically flat appearance with crypt hypoplasia and infiltration of the epithelium with lymphocytes. Diet is the key to management and a gluten-free diet effectively cures the condition. However, this commitment is lifelong and many aisles in the supermarket are effectively closed to individuals with coeliac disease. Compliance can be monitored by measuring antibodies in blood, which revert to negative after 6-9 months. Patients with minor symptoms, who are found incidentally to have coeliac disease, often ask whether it is necessary to adhere to the diet. Current advice is that dietary adherence is necessary to avoid the long-term complications, which are, principally, osteoporosis and small bowel lymphoma. However, risk of these complications diminishes very considerably in patients who are on a gluten-free diet.

PMID: 16313685 [PubMed - indexed for MEDLINE]

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