Gluten-Free Cereal Products and Beverages

Elke Arendt,Fabio Dal Bello

• Editorial: Academic Press
• Año: 2011
• ISBN:
  9780080557762
• Categoría: Tecnologia e ingegneria
• Categoría: Scienze dell'alimentazione

Gluten-Free Cereal Products and Beverages is the only book to address gluten-free foods and beverages from a food science perspective. It presents the latest work in the development of gluten-free products, including description of the disease, the detection of gluten, and the labeling of gluten-free products as well as exploring the raw materials and ingredients used to produce gluten-free products.

Identifying alternatives to the unique properties of gluten has proven a significant challenge for food scientists and for the 1% of the world's population suffering from the immune-mediated entropathy reaction to the ingestion of gluten and related proteins, commonly known as Celiac Disease. This book includes information on the advances in working with those alternatives to create gluten free products including gluten-free beer, malt and functional drinks.

Food scientists developing gluten-free foods and beverages, cereal scientists researching the area, and nutritionists working with celiac patients will find this book particularly valuable.

• Written by leading experts, presenting the latest developments in gluten-free products
• Addresses Coeliac Disease from a food science perspective
• Presents each topic from both a scientific and industrial point of view

1

Celiac disease

Carlo Catassi and Alessio Fasano

Publisher Summary

Celiac disease is an immune-mediated enteropathy triggered by the ingestion of gluten in genetically susceptible individuals. The major predisposing genes are located on the HLA system on chromosome 6, namely the HLA-DQ2 and DQ8 genes found in at least 95% of patients. Gluten is a complex mixture of storage proteins of wheat, a staple food for most populations in the world, and other cereals. Celiac disease is one of the most common lifelong disorders on a worldwide basis. The condition can manifest with a previously unsuspected range of clinical presentations, including the typical malabsorption syndrome (chronic diarrhea, weight loss, abdominal distention) and a spectrum of symptoms potentially affecting any organ or body system. It is a common disorder in children as well as in adults. The spectrum of clinical presentations is wide, and currently extraintestinal manifestations (e.g. anemia or short stature) are more common than the classical malabsorption symptoms. A high degree of awareness among healthcare professionals and a “liberal” use of serological celiac disease tests can help to identify many of the non-classic cases. The primary care doctor has therefore a central role in this process of case finding. Many key questions about this unique autoimmune condition remain unanswered. The answer to some of these questions may provide a better understanding of the pathophysiological mechanisms involved in the pathogenesis of celiac disease and, possibly of other autoimmune diseases, so paving the way to innovative treatment strategies.

Chapter Outline

Introduction

Epidemiology

The iceberg model

Pathogenesis

Clinical spectrum

Complications

Diagnosis

Management

Novel strategies for disease prevention and treatment

Wheat allergy

Conclusions

References

Introduction

Celiac disease is an immune-mediated enteropathy triggered by the ingestion of gluten in genetically susceptible individuals. The major predisposing genes are located on the HLA system on chromosome 6, namely the HLA-DQ2 and DQ8 genes found in at least 95% of patients. Gluten is a complex mixture of storage proteins of wheat, a staple food for most populations in the world, and other cereals (rye and barley). Gluten proteins have several unique features that contribute to their immunogenic properties. They are extremely rich in the amino acids proline and glutamine. Due to the high proline content, gluten is highly resistant to proteolytic degradation within the gastrointestinal tract because gastric and pancreatic enzymes lack post-proline cleaving activity. Moreover, the high glutamine content makes gluten a good substrate for the enzyme tissue transglutaminase (tTG). Gluten proteins are now known to encode many peptides that are capable of stimulating both a T cell-mediated and an innate response. The 33-mer is a gliadin peptide of 33 residues (α2-gliadin 56–88) produced by normal gastrointestinal proteolysis, containing six partly overlapping copies of three T cell epitopes. The 33-mer is an immunodominant peptide that is a remarkably potent T cell stimulator after deamidation by tTG (Shan et al., 2002).

Celiac disease is one of the most common lifelong disorders on a worldwide basis. The condition can manifest with a previously unsuspected range of clinical presentations, including the typical malabsorption syndrome (chronic diarrhea, weight loss, abdominal distention) and a spectrum of symptoms potentially affecting any organ or body system. Since celiac disease is often atypical or even silent on clinical grounds, many cases remain undiagnosed, leading to the risk of long-term complications, such as osteoporosis, infertility or cancer (Fasano and Catassi, 2001). There is a growing interest in the social dimension of celiac disease, since the burden of illness related to this condition is doubtless higher than previously thought (American Gastroenterological Association, 2001). Although celiac disease can present at any age, including the elderly, typical cases often manifest in early childhood. In 1888, Samuel Gee, having drawn attention to the disorder in a lecture delivered on October 5, 1887 at the Hospital for Sick Children, Great Ormond Street, London, produced his classical paper, On the Coeliac Affection (Gee, 1890). Dr. Gee described celiac disease as follows:

There is a kind of chronic indigestion which is met with in persons of all ages, yet is especially apt to affect children between one and five years old…. Signs of the disease are yielded by the faeces; being loose, not formed, but not watery; more bulky than the food taken would seem to account for ….

Remarkably, he already hypothesized that foodstuff could be the trigger of the disease:

The causes of the disease are obscure. Children who suffer from it are not all weak in constitution. Errors in diet may perhaps be a cause, but what error? Why, out of a family of children all brought up in much the same way, should one alone suffer? To regulate the food is the main part of treatment…. The allowance of farinaceous food must be small; highly starchy food, rice, sago, corn-flour are unfit.

Despite his great clinical acumen, Dr. Gee was not able to make the final link between gluten ingestion and celiac disease, since he concluded:

“Malted food is better, also rusks or bread cut thin and well toasted on both sides ….”

Epidemiology

In the general population

In the past, celiac disease was considered a rare disorder, mostly affecting children of European origin. Indeed, this idea is still widespread, so much that in many European countries celiac disease continues to be included in the list of rare disorders protected by specific regulations of the healthcare system. On the other hand, a huge number of studies have recently shown that celiac disease is one of the commonest lifelong disorders affecting humans in many areas of the world. Currently most cases remain undiagnosed, due to the lack of typical symptoms, and can be recognized only through serological screening by sensitive tools (e.g. serum IgA class anti-transglutaminase and anti-endomysial antibodies determination) (Catassi et al., 1996; Catassi, 2005). Serological screenings performed on general population samples have confirmed that the prevalence of celiac disease in Europe is very high (Catassi et al., 1994; Csizmadia et al., 1999; Catassi, 2005), ranging between 0.75 and 0.4% of the general population, with a trend toward higher figures (1% or more) in younger subjects and among groups that have been more isolated genetically (e.g. in Northern Ireland, Finland, and Sardinia) (Johnston et al., 1998; Meloni et al., 1999; Mäki et al., 2003). Until recently, celiac disease was generally perceived to be less common in North America than in Europe (Green et al., 2001). Should the frequency of celiac disease be lower in the USA, the existence of a protective environmental factor in that country should be postulated, since Americans and Europeans largely share a common genetic background. This epidemiological “dilemma” has recently been answered by our large US prevalence study including 4126 subjects sampled from the general population (Fasano et al., 2003). The overall prevalence of celiac disease in this US population sample was 1:133, actually overlapping the European figures. Similar disease frequencies have been reported from countries mostly populated by individuals of European origin (e.g. Australia, New Zealand, and Argentina) (Cook et al., 2000; Hovell et al., 2001; Gomez et al., 2001).

Celiac disease is not only frequent in developed countries, but it is increasingly found in areas of the developing world, such as North Africa (Bdioui et al., 2006), Middle East (Shahbazkhani et al., 2003), and India (Sood et al., 2006). This disorder can contribute substantially to childhood morbidity and mortality in many developing countries. The highest celiac disease prevalence in the world...