Celiac disease is an autoimmune disorder triggered by the ingestion of gluten, which is found in wheat, barley, and rye. The only treatment for celiac disease is a strict gluten-free diet (GFD), which eliminates common gluten-containing foods found in many cultures and cuisines. This research examined how families experienced celiac disease and the GFD in their households, focusing on the ripple effect of celiac disease for all members of the family and how families promoted adherence and quality of life (QOL). A mixed-methods approach used questionnaires, photographs, and semi-structured interviews with families recruited from the Celiac Disease Center at Columbia University Medical Center. Participants were 16 families with children ages 8-18 living at home who had physician-confirmed diagnoses of celiac disease. A total of 71 in-depth semi-structured interviews were conducted (n =16 reference children with celiac disease, 16 mothers, 15 fathers, 24 siblings). Results showed that the reference children with celiac disease had high GFD adherence (mean CDAT = 9) and QOL (mean CDPQOL 81 of 100). Mothers’ and fathers’ ratings of how their child’s celiac disease diagnosis affected their lifestyle, social life, and level of burden in caring for child’s dietary needs differed significantly (all p-values < 0.05), with mothers reporting more change and burden. Emerging themes related to a negative ripple effect included the burden of assuming the majority of food tasks related to GFD (mothers), the limited restaurant choices for the family (fathers), and feeling annoyed by having to limit certain foods at home (siblings). Emerging themes related to a positive ripple effect, included becoming more creative cooks (mothers), incorporating new family traditions (fathers), and developing empathy for others (siblings). Overall, there was substantial evidence of a ripple-effect of a child’s celiac disease diagnosis on other family members, including how mothers and fathers may experience the change in lifestyle and added responsibilities of maintaining the GFD differently. Including parents and siblings in research provides insight into the entire family experience and can help inform family-centered interventions on how to maximize QOL for everyone impacted by a child’s celiac disease diagnosis.

Els Departaments de Salut Laboral proporcionen prevenció i tractament de patologies relacionades amb l’entorn laboral, però alhora també ajuden a detectar patologies freqüents de les que se’n pot realitzar prevenció. La incorporació d’autoanticossos específics de la malaltia celíaca (MC) al perfil analític dels Departaments de Salut Laboral és útil per detectar la malaltia celíaca i per revertir les complicacions associades a aquesta. La prevalença de MC a Catalunya no ha estat mai avaluada i no hi ha dades a la literatura mèdica que demostrin de manera inequívoca si hi ha diferències en la prevalença relacionades amb l’edat. La MC de l’adult és més prevalent del que es pensava prèviament i les seves característiques clíniques i histològiques difereixen de les del nen. Aquesta tesi conté dos estudis diferenciats, els objectius dels quals són: A) Objectius de l’estudi 1 1) Avaluar la freqüència i la rellavància clínica de l’ESG (tant de Marsh I com de Marsh III) detectada per serologia en un programa de cribratge poblacional sistemàtic de població en edat laboral. 2) Comparar la sensibilitat dels tTGA i EmA per detectar tot l’espectre de l’ESG (de Marsh I a Marsh III) 3) Avaluar el grau d’adherència al programa de cribratge sistemàtic i l’efectivitat de la instauració de DSG en els individus detectats per cribratge. B) Objetius de l’estudi 2 1) Avaluar la prevalença global de la MC en la població general de Catalunya. 2) Avaluar si existeixen diferències en la prevalença de la MC relacionades amb l’edat i el sexe.

Background: Celiac disease occurs worldwide in approximately 1% of the population, whereof the majority of cases are undiagnosed. Sweden experienced an epidemic (1984-1996) of clinically detected celiac disease in children below 2 years of age, partly attributed to changes in infant feeding. Whether the epidemic constituted a change in disease occurrence and/or a shift in the proportion of diagnosed cases remains unknown. Moreover, the cause of the epidemic is not fully understood. Objective: To increase the knowledge regarding the occurrence of celiac disease in Sweden, with focus on the epidemic period and thereafter, as well as the etiology of celiac disease in general, by investigating the Swedish epidemic and its potential causes. Methods: We performed a two-phased cross-sectional multicenter screening study investigating the total prevalence, including both clinically- and screening-detected cases, of celiac disease in 2 birth cohorts of 12-year-olds (n=13 279): 1 of the epidemic period (1993) and 1 of the post-epidemic period (1997). The screening strategy entailed serological markers analyses, with subsequent small intestinal biopsy when values were positive. Diagnosis was ascertained in clinical cases detected prior to screening. Infant feeding practices in the cohorts were ascertained via questionnaires. An ecological approach combined with an incident case-referent study (475 cases, 950 referents) performed during the epidemic were used for investigating environmental- and lifestyle factors other than infant feeding. Exposure information was obtained via register data, a questionnaire, and child health clinic records. All studies utilized the National Swedish Childhood Celiac Disease Register. Results: The total prevalences of celiac disease were 2.9% and 2.2% for the 1993 and 1997 cohorts, respectively, with 2/3 cases unrecognized prior to screening. Children born in 1997 had a significantly lower celiac disease prevalence compared to those born in 1993 (prevalence ratio, 0.75; 95% confidence interval [CI], 0.60-0.93). The cohorts differed in infant feeding; more specifically in the proportion of infants introduced to dietary gluten in small amounts during ongoing breastfeeding. Of the environmental and lifestyle factors investigated, no additional changes over time coincided with the epidemic. Early vaccinations within the Swedish program were not risk factors for celiac disease. Early infections (≥3 parental-reported episodes) were associated with increased risk for celiac disease (adjusted odds ratio [OR] 1.5; 95% CI, 1.1-2.0), a risk that increased synergistically if, in addition to having ≥3 infectious episodes, the child was introduced to gluten in large amounts, compared to small or medium amounts, after breastfeeding was discontinued (OR 5.6; 95% CI, 3.1-10). Early infections probably made a minor contribution to the Swedish epidemic through the synergistic effect with gluten, which changed concurrently. In total, approximately 48% of the epidemic could be explained by infant feeding and early infections. Conclusion: Celiac disease is both unexpectedly prevalent and mainly undiagnosed in Swedish children. Although the cause of the epidemic is still not fully understood, the significant difference in prevalence between the 2 cohorts indicates that the epidemic constituted a change in disease occurrence, and importantly, corroborates that celiac disease can be avoided in some children, at least up to 12 years of age. Our findings suggest that infant feeding and early infections, but not early vaccinations, have a causal role in the celiac disease etiology and that the infant feeding practice – gradually introducing gluten-containing foods from 4 months of age, preferably during ongoing breastfeeding – is favorable.

Diss. (sammanfattning) Göteborg : Göteborgs universitet , 2007. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karol. inst., 2005. / Härtill 4 uppsatser.

Diss. (sammanfattning) Uppsala : Uppsala universitet, 2005. / Härtill 4 uppsatser.

Diss. (sammanfattning) Linköping : Univ., 2006. / Härtill 5 uppsatser.

Thesis (Ph.D.)--Duquesne University, 2009. / Title from document title page. Abstract included in electronic submission form. Includes bibliographical references (p. 129-140) and index.

abstract: Celiac Disease (CD) is now widespread as one in 133 people are currently diagnosed, while there were only one in 150 in 2006. Much of the research concerning CD is still in the early stages, as formal epidemiological studies are relatively recent. CD is aggravated by the consumption of gluten, which is found mainly in wheat, rye, oats, and barley. Not surprisingly, the rising prevalence of CD has created a significant business opportunity for food manufacturers in developing products that are tailored to CD sufferers. While the entire Gluten-Free (GF) industry has been experiencing double digit growth rates, the expansion in available snack foods has outstripped all others. Observation of GF snack food prices suggests that food manufacturers are responding to high retail prices associated with GF foods. However, GF foods are often also advertised with other attributes that generally sell for a premium over conventional foods. Therefore, whether the high retail price for GF snack foods can be attributed specifically to the GF attribute is an empirical question. The objective of this research is to determine whether there is a retail-price premium for GF snack foods and, if there is, to estimate its magnitude. A hedonic pricing model is used to answer this question. Specifically, a hedonic pricing model was applied to a unique dataset of snack food products in order to estimate the marginal value for the GF attribute, while controlling for a number of other important attributes. Results show that the GF attribute is both economically and statistically significant, implying a premium of nearly $1.86 above gluten-containing products. Production costs for smaller manufacturers can be two to three times higher for GF foods relative to non-GF foods, but this still implies an excess premium of over $0.50 (assuming 40% margins). However, high premiums may not last as large retailers are utilizing their influence over suppliers to keep retail margins low. Therefore, the primary implication of the research is that the rapid growth in recent years can easily be explained on economic grounds for large agribusinesses, as this implies a major profit opportunity. / Dissertation/Thesis / M.S. Agribusiness 2010

INTRODUCTION: Foods enter the oral cavity and mix with saliva. Some foods are not well tolerated, for instance, gluten proteins in individuals suffering from celiac disease (CD). Celiac disease is a chronic immune-mediated inflammation of the duodenum, triggered by gliadin component of gluten contained in wheat, barley and rye. In previous studies we showed that oral Rothia bacteria can degrade gliadin in vitro. The objective of this study was to gain more insights into the role of Rothia bacteria and subtilisin-A enzyme on gliadin digestion in vivo, with the ultimate goal to find new therapeutic options for CD. MATERIALS AND METHODS: Part I: Rothia bacterial proteins were analyzed for enzyme activity and subjected to LC-ESI-MS/MS. For in vivo, mice chow was prepared with and without R. aeria. Gliadin epitope abolishment was assessed in the mice stomach contents (n=9/group) by ELISA. Part II: Subtilisin-A was dissolved in various solutions, temperatures and incubation time to assess enzyme activity by using enzyme substrate (Suc-AAPF-pNA). Part III: PEGylation of subtilisin-A (Sub-A) was performed by mixing Sub-A with methoxy-polyethylene glycol (mPEG) and further encapsulated by polylactic-glycolic acid (PLGA). The activity of the modified enzyme to detoxify the immunogenic gliadin epitopes was evaluated at pH3.0. RESULTS: Part I: R. aeria gliadin-degrading enzyme was found to be a member of the subtilisin family. In vivo, gliadins immunogenic epitopes were reduced by 32.6%. Part II: Sub-A dissolved at pH1.5 showed a band of 27kDa, while it only showed bands below 10kDa when dissolved at pH7.0, suggesting auto-proteolysis. The enzyme activity was completely lost at temperatures exceeding 60°C and also reduced 4-fold after 6hr incubation at 37°C. Part III: PEGylation protected Sub-A from autolysis. The microencapsulated Sub-A-mPEG-PLGA showed significantly increased protection against acid exposure in vitro. In vivo, gliadin immunogenic epitopes were decreased by 60% in the stomach of the mice fed with chow containing Sub-A-mPEG-PLGA. CONCLUSION: The results provide proof for the contribution of oral Rothia bacteria to gliadin digestion and pharmaceutical modification can protect Sub-A from auto-digestion as well as from acidic insults, thus rendering the usefulness of coated subtilisins as a digestive aid for gluten degradation. / 2019-01-13T00:00:00Z