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Coeliac disease and gluten intolerance

Coeliac disease is a chronic enteropathy produced by gluten intolerance, specifically prolamines, which cause an atrophy of an intestinal villi, lesions on the mucosa of the proximal small intestine and malabsorption. Gastrointestinal symptoms are frequent, although non-gastrointestinal features are equally as common.

There is limited knowledge about the natural history of coeliac disease. It is presumed that patients with the condition who continue to ingest gluten will (at some time) develop symptoms. Findings resulting from biopsies on suspected patients undergoing gluten challenge, however, have often indicated that many patients remain asymptomatic despite histologic evidence of the disease, with the severity of the intestinal lesion not correlating with the severity of clinical symptoms. Coeliac disease is considered a disease of the proximal small intestine, presumably on the basis of higher concentrations of gluten in this region of bowel. Genetic factors are believed to act with environmental factors in the generation of celiac disease. (1)   In fact, most individuals with celiac disease have celiac disease-associated antibodies and specific pairs of allelic variants in two HLA genes, HLA-DQA1 and HLA-DQB1, with 30% of the general population presenting with one of the celiac disease-associated HLA alleles. (2)

The persistence of the mucosal histologic lesion of celiac disease is important for the following reasons: the danger of malignancy, the presence of unsuspected nutritional deficiencies, and the occurrence of autoimmune disorders.One study of 93 patients presenting for evaluation of iron deficiency anemia found 11% with small bowel biopsy findings compatible with coeliac disease.(2) Megaloblastic anemia from vitamin B12 or folate malabsorption, pericarditis, menstrual disturbances, mood and mental changes, depression, ataxia, epilepsy, and autistic behavior and infertility have all been linked to celiac disease. Recurrent apthous ulcers, anorexia, glossitis, hypoplasia of dental enamel, and abdominal pain secondary to transient intussusception have also been reported. Furthermore, unexplained fractures of the hip, vertebrae, or upper extremities as the result of osteoporosis may be a subtle sign of coeliac disease and can occur without gastrointestinal symptoms. In one study, bone mineral density and the prevalence of osteopenia and osteoporosis in 77 patients with coeliac disease was compared with 157 controls. Patients with coeliac disease had significantly decreased bone mineral density in the lumbar spine and femoral neck compared with controls. (3)

The gluten-induced enteropathy that affects the small intestinal mucosa leads to symptoms of malabsorption. When they are diagnosed, some patients show a substantial weight loss, anemia and evidence of vitamin and mineral deficit. Reduced levels of iron, folate, vitamin B12, vitamin D, zinc, and magnesium are common in untreated coeliac disease patients likely due to loss of brush border proteins and enzymes needed for the absorption of these nutrients. In particular, magnesium levels has been shown to be depleted in Coeliacs. (4)

With over 300 enzymatic activity, the physiological role of magnesium is a major cation in the human body, magnesium ranks fourth in overall abundance, but intracellularly it is second only to potassium. A 70kg human contains about 35 grams of magnesium, of which approximately 55% to 60% is located in the bone, another 20% to 25% in soft tissues and bout 1% in extracellular fluids. (5)

Furthermore, intracellular free magnesium acts as an allosteric activator of enzyme action including critical enzyme systems such as adenylate cyclase, phospholipase C, and Na/K-ATPase. Transport of other ions such as potassium and calcium across the plasma membrane may also require the presence of magnesium. Magnesium is, therefore, critical for a number of cellular functions, including oxidative phosphorylation, glycolysis, DNA transcription, and protein synthesis. Magnesium depletion also profoundly affects potassium homeostasis. Magnesium absorption occurs throughout the small intestine, mainly in the distal jejunum and ileum. The colon also may play a role in the absorption of magnesium, especially if the disease has interfered with magnesium absorption in the small intestine. Although magnesium absorption may be influenced various factors, such as dietary intake, high levels of calcium and phosphorus, the inhibition is most apparent when magnesium consumption is low or impaired. (6) Since gluten-free cereal products have a lower magnesium content as compared with gluten-containing counterparts, a magnesium-enriched diet should be encouraged in individuals with coeliac disease, as the resolution of mucosal inflammation may not be sufficient to abrogate magnesium deficiency.

 Article written by:  Manuela Malaguti-Boyle PhDc. ND

References:

1. Rossi T. Celia disease. Adolescent Medicine Clinics; 2004; 15 (1): 91-103

2. Snyder L., MS, Young, DO., Green P. Celiac Disease. Gene Reviews 2008: 3

2. Zhu A., Kaneshiro M., D. Kaunitz D. Evaluation and Treatment of Iron Deficiency Anemia: A Gastroenterological Perspective. Digestive Diseases in Science. 2010; 55(3): 548–559.

3. Kemppainen T, Kroger H, Janatuinen E, et al. Osteoporosis in adult patients with celiac disease.Bone. 1999;24(3):249-55.

4. Caruso R, Pallone F, Stasi E, et al. Appropriate nutrient supplementation in celiac disease.Annals of Medicine. 2013 ;45(8):522-31

5. Gropper S., Smith J.Groff J. Advanced Nutrition and Human Metabolism. Cengage Learning. 2009; 447-451

6. Moe SM.Disorders Involving Calcium, Phosphorus, and Magnesium. Primary Care. 2008; 35(2): 215–vi.