Gluten Free Low Glycemic Cookbook
Gluten Free Living Secrets
Are you sick and tired of trying every weight loss program out there and failing to see results? Or are you frustrated with not feeling as energetic as you used to despite what you eat? Perhaps you always seem to have a bit of a
Serological testing for autoantibodies relevant to CD includes measurement of antigliadin antibodies (AGA), serum endomysial antibodies (EMA), tissue transglutaminase antibodies (tTG), and total serum IgA. Antigliadin antibodies are antibodies against the proteins present in the ethanol-soluble fraction of wheat gluten and can be measured using IgA- or IgG-specific AGA ELISA assays. The AGA test is the least sensitive (IgA AGA 75-90 IgG AGA 69-85 ) and least specific (IgA AGA 82-95 IgG AGA 73-90 ) serological test for the diagnosis of CD.2 The lower sensitivity of AGA is illustrated in this patient's lab results, where AGA IgA and IgG were both negative, even though the other serological tests for CD were positive and the diagnosis of CD was confirmed by biopsy and response to a gluten-free diet. IgA EMA are detected by indirect immunofluorescence using monkey esophagus or human umbilical cord frozen sections as substrate, and results are expressed as titers. Traditionally EMA was the...
Coeliac disease is also known as gluten enteropathy because it is caused by immune reactivity triggered by glutamine- and proline-rich gluten proteins, found mainly in wheat, rye, barley and oats. The illness may become apparent at any age, from infancy to old age, may remain asymptomatic, and may be detected incidentally.
For some major diseases, such as inflammatory bowel disease, the aetiological agent has not been identified, despite rapidly advancing genetic and molecular research. Conversely, coeliac disease, another serious and common gastrointestinal inflammatory disease, is caused by a well-characterized immune response to wheat-derived proteins.
Hyperinflation as seen on chest x-ray. In addition, pancreatic insufficiency and failure to thrive are also common characteristics of the disease. In most cases, the diagnosis of CF involves elevated Na+ and Cl sweat concentrations as measured by quantitative pilocarpine iontophoresis. Elevated sweat tests can be seen in patients with other disorders such as fucosidosis, glycogen storage disease type 1 mucopolysaccharidosis, hypothyroidism, celiac disease, malnutrition, and asthma. These diseases are clinically distinguishable from CF, and an elevated sweat test ( 60 mmol L) is usually sufficient for CF diagnosis. However, atypical CF cases have been described in which the sweat chloride values were below 60 mmol L.2 The sensitivity of sweat chloride determined by quantitative pilocarpine iontophoresis using a cutoff of 60 mmol L is 98 with a specificity of 83 . One drawback of sweat analysis is that a minimum weight of sweat collected (75 mg) is required to ensure accurate results...
Dietary folate deficiency has been previously associated with poor socio-economic groups but now is thought to exist in 5-10 of the population of most communities. Intestinal absorption is impaired in those with coeliac disease or tropical sprue which if left untreated can lead to folate deficiency (Scott, 2000) (see also section 3.33). Pregnancy is associated with increased folate catabolism, particularly in the second and third trimesters, when it exceeds intake. Women who enter pregnancy with adequate stores or receive prophylaxis during pregnancy will avoid deficiency. Haemolytic anaemia, a condition with increased cell division, can also lead to folate deficiency (Scott, 2000). Anticonvulsant drug therapy is associated with folate deficiency but the mechanism is not known (Scott, 2000). It was suggested that the drugs cause folate malabsorption or excretion of folate through hepatic enzyme induction but this theory has now been discarded. Chronic alcoholics usually have folate...
Absorption of the fat-soluble vitamins A, D, E and K depends on adequate bile salt secretion and an intact small intestinal mucosa. Deficiencies therefore occur in liver disease, obstructive jaundice and pancreatic insufficiency, and with small intestinal pathology, such as coeliac disease.
Gastrointestinal disease inevitably interferes with nutrition. Reduced intake may be due to nausea and vomiting, poor dentition, or dysphagia secondary to oesophageal disease. Pancreatic, biliary and intestinal diseases cause malabsorption. Coeliac disease and Crohn's disease in particular are associated with multiple deficiencies, including calcium and vitamin D deficiency leading to osteoporosis.
In genetically susceptible individuals, immunological reaction to gluten-derived gliadin peptides develops upon dietary exposure. The exact genes causing coeliac disease have not been identified but certain major histocompatibility complex (MHC) class II gene alleles are strongly associated with the condition. Early dietary exposure to gluten, particularly after weaning from milk, may increase the risk of developing the disease. The concentration of dietary gluten is highest proximally in the intestine and therefore coeliac disease affects the duodenum and proximal jejunum most severely.
Coeliac disease can become apparent at any age, although most cases are diagnosed in early childhood or in middle age. Coeliac disease may remain clinically silent and people with circulating antibodies to tTG, but no overt pathology, may be considered to have latent disease. Nutrients that are mainly absorbed in the proximal small intestine, such as iron and calcium, are most affected by coeliac disease, while nutrients predominantly absorbed in thejejunum and ileum, such as folic acid, vitamin C and vitamin B12, are affected only in more advanced disease. Possibly as the result of chronic inflammation, people with uncontrolled coeliac disease are at increased risk of developing intestinal neoplasms, particularly intestinal lymphoma. This risk is substantially reduced by strict adherence to a gliadin-free diet (see Chapter 38).
Gastric and intestinal lymphomas are rare and are usually caused by chronic inflammation and activation of the local immune system, as with H. pylori infection, coeliac disease and immunoproliferative small intestinal disease (IPSID), which occurs with chronic intestinal infection (see Chapters 18, 31 & 35). Eradicating H. pylori infection, or prolonged antibiotic treatment of IPSID, may cure early cases. In coeliac disease, strict adherence to a gluten-free diet removes the antigenic stimulus to lymphocytes and reduces the risk of lymphoma.
Most patients with abetalipoproteinemia, however, initially come to medical attention as infants because of failure to thrive and diarrhea. Thus, they are often misdiagnosed as having celiac disease or cystic fibrosis. Abetalipoproteinemia can often be differentiated from these more common diseases by a careful medical history and the presence and or absence of the various clinical findings that are unique to these diseases. The finding of fat-laden but normal-size villi via endoscopic examination and a normal sweat chloride test can also be used to rule out celiac disease and cystic fibrosis, respectively.
Celiac disease (CD), also known as gluten-sensitive enteropathy, is an autoimmune disease of the small intestine that is triggered by the ingestion of gluten-containing grains such as wheat, rye, and barley in genetically susceptible individuals.1-5 In patients with CD, T-cell infiltration into the intestinal epithelium leads to immunity-mediated destruction of the microscopic villi of the small intestine and subsequent malabsorption of nutrients. The major known disease contributors include the environmental factor gluten, as well as a genetic susceptibility in people with HLA-DQ2 or HLA-DQ8 alleles. Other unknown environmental factors may contribute to disease occurrence. Chronic inflammation and immunity-mediated tissue damage in the small intestine, including villous atrophy of the small intestinal mucosa, are characteristic of CD. Epidemiological studies in the United States and Europe have shown the prevalence of CD to approach 1 .1,7 The widespread occurrence of the disease has...
CD has been shown to be closely associated with a number of other disorders. Dermatitis herpetiformis, a skin disease characterized by symmetric pruritic papulovesicular lesions and the presence of granular deposits of IgA in the skin, affects 10-20 of patients with CD and responds to withdrawal of gluten from the diet. CD is also strongly associated with type I diabetes and autoimmune thyroid disease, especially hypothyroidism. The prevalence of CD in type I diabetes patients is 3-8 .2 Patients with untreated CD have an increased risk of certain types of cancer, specifically non-Hodgkin lymphoma, enteropathy-associated T-cell lymphoma, small intestinal adenocarcinoma, and esophageal or oropharyngeal squamous carcinoma. Neurological disorders, including peripheral neuropathy, cerebellar ataxia, epilepsy, and migraine, have also been shown to be associated with CD. Women with untreated CD may present with infertility, and infertility secondary to impotence or abnormally low sperm count...
As part of a study on celiac disease. Transglutaminase is thought to be involved in the etiology of celiac disease.247 In the above study identifying transglutaminase substrates in human intestinal epithelial cells,247 more than 25 proteins were identified. The reader is directed to several recent publications248,249 for information on technical approaches to the study of transglutaminase substrates.
Coeliac disease Celiac disease (US) Gluten enteropathy atrophy of villi in small intestine leads to impaired absorption of nutrients. Caused by sensitivity to gluten (protein of wheat and rye). Sufferers have serum antibodies to gluten and show delayed hypersensitivity to gluten the risk factor is ten times greater in HLA-B8-positive individuals.
But glass transition is also observed in systems where no solvent is present the glass transition indeed occurs in every polymer material that is brittle for T Tg and rubbery for T Tg. Many foods contain biopolymers like amylose, amylopectin, gluten, etc. Therefore typical Tg shifts of the base line are found in the DSC traces of relatively dry food samples.
A 5-year-old girl was brought to her physician for worsening of diarrhea. She was having about six to seven bowel movements of foul-smelling stools per day. The diarrhea seemed to worsen with ingestion of fatty food. The mother described that since infancy, her daughter had failure to thrive, chronic diarrhea, and malabsorption. She was tentatively diagnosed with celiac disease at 18 months of age without a biopsy. A gluten-free diet was started but did not appear to relieve her diarrhea. There was no family history of celiac disease. Inconsistent with celiac disease, the duodenum was found by endoscopy to have normally formed villi, but it had an unusual white frosting appearance. On histologic examination, numerous Oil Red stain-positive vacuoles were observed in the villi consistent with the intracellular fat accumulation that occurs in abetalipoproteinemia. Because of the suspected diagnosis, the patient was referred to an ophthalmologist, who also observed pigmentary degeneration...
The laboratory results were consistent with iron deficiency anemia and were otherwise normal. The physician then ordered serological testing for celiac disease and gastroenterology (GI) consultation The diagnosis of celiac disease was made on the basis of the biopsy and serology findings, and the patient was placed on a gluten-free diet. She reported alleviation of symptoms and gained weight. Three months later, a follow-up biopsy of the small bowel was performed and histology appeared normal.
Celiac disease A condition in which the small intestine cannot absorb and digest food, caused by gluten sensitivity. Although an estimated one in 4,700 Americans have been diagnosed with this disease, a study from the Red Cross suggests it may be far more common one in every 250 Americans. For those who cannot tolerate gluten, the substance damages the lining of the intestines and flattens the villi small hair-like projections that normally protrude from the intestinal surfaces that help absorb nutrients. permanent intolerance to gluten that damages the small intestine can be reversed by avoiding gluten in the diet. As the villi become damaged, they are unable to absorb water and nutrients, which causes the child to be susceptible to a variety of other conditions related to malabsorption. Celiac disease is hereditary and primarily affects whites of northwestern European ancestry, rarely affecting blacks, jews, Asians, or people of Mediterranean ancestry. It affects twice as many girls...
Chronic immune stimulation, for example, by Helicobacter pylori or by coeliac disease, can lead to excess proliferation of immune cells, neoplastic change and intestinal lymphoma. Dysregulated immune responses are implicated in coeliac disease, where there is hypersensitivity to peptides derived from wheat and other cereals and in inflammatory bowel disease (IBD). Inflammation may normally be actively prevented by subsets of T lymphocytes, which might have regulatory functions that are defective in IBD.
While avoiding excessive investigation, which increases the patient's anxiety that 'something must be wrong and the doctors still can't find it', some simple tests are usually performed to exclude serious underlying pathology. These include a blood count, serum electrolyte determination, serological tests for coeliac disease, gastro-oesophageal endoscopy, sigmoidoscopy or colonoscopy, and stool culture.
Many studies of the nutritional effects of irradiation on proteins have been made with generally only small or insignificant changes found. For example, irradiation of fish and meat meal, eggs, wheat and wheat gluten (Kennedy and Ley, 1971) showed little change in nutritive value in feeding studies after irradiation at doses up to 10kGy. The biggest changes were in wheat gluten (7 ). At 50kGy larger losses occurred, but were largely reversed by supplementation of the diets with methionine.
The surface activity of MC and HPMC also improves the whippability of reduced-egg cake batters. The stabilization of the foam is further reinforced by the thermal gelation of these molecules during the baking stage. In addition, MC and HPMC aid in the production of low-gluten bread. There, they contribute to obtaining the body and texture normally associated with standard, full-gluten bread. Further benefits include increased tolerance to overmixing, longer holding times, and improved product yield.