Celiac disease

Hyperthyroidism, also called Grave’s Disease, is an immunologically mediated thyroid disease.  That basically means it is brought on by the action of specific abnormal autoantibodies, called thyroid receptor antibodies (TRAb), that stimulate excessive release of normal thyroid hormones into the blood.  Thyroid hormones control body metabolism.

Features of hyperthyroidism are diffuse non-tender goiter (enlarged thyroid gland), elevated blood levels of thyroxine hormone, suppressed blood levels of thyrotropin hormone (TSH), and the presence of thyroid receptor antibodies in the blood.

Symptoms include various degrees of bulging eyeballs, staring, firm areas of edema or swellings of the lower legs in most patients, rapid pulse, increased blood pressure, palpitations, nervousness, depression, anxiety, heat intolerance, weight loss, thigh and upper arm weakness, brisk tendon reflexes, cardiac abnormalities and oligomenorrhea in females – infrequent or scanty menstruation. 

According to a recent medical study of 111 people with hyperthyroidism, 4.5% had positive celiac disease antibodies, 14% had anti-gliadin antibodies and 3% had IgA deficiency. Anti-gliadin antibodies demonstrate a normal reaction to the abnormal presence of gluten in the blood. The high presence of anti-gliadin antibodies in thyroid disorders is likely related to gluten entering the bloodstream through the small intestine via “leaky gut.”  Leaky gut can result from poorly digested gluten with or without celiac disease. 

An immune-linked reason for the co-existence of hyperthyroidism and celiac disease revolves around the fact that both disorders (and several other diseases) share the immune system genetic markers HLA B-8 and HLA DR3. Individuals having these genetic markers can develop one or more of a certain cluster of diseases associated with these genes.1

The good news is that a strict gluten free diet can successfully treat hyperthyroidism in celiac disease.

Thyroid function should be assessed in all celiac disease patients at diagnosis and follow-up if clinically indicated. Screening of high-risk groups such as those with autoimmune thyroid disease is a reasonable strategy.2

If you have hyperthyroidism, be sure your doctor tests you for celiac disease and gluten sensitivity. Anti-gliadin antibody (AGA-IgA and AGA-IgG) tests for gluten sensitivity while EMA-IgA and EMA-IgG or tTG-IgA and tTG-IgG  are specific tests for celiac disease.  Testing that is based on IgA only would give a false negative result for individuals who are unable to produce IgA antibodies, that is, in IgA deficiency.

If your physician refuses or dismisses the idea of testing for celiac disease, please get a second opinion from a medical provider who is knowledgeable about celiac disease.  The longer gluten is consumed, the greater will be its damaging effects on your body.

(This Health Alert was taken from information found in Issue #11 – “Gluten and the Thyroid” of the Gluten Free Gazette.)

Celiac disease is a hereditary, auto-immune disorder estimated to affect 1% of the human population (3 million in the US). Less than 3 % are estimated to be medically diagnosed, but numbers are expected to rapidly increase as diagnosis improves. Celiac disease is caused by the ingestion of wheat, barley, rye and oats and treated by removing these items from the diet. Signs, symptoms, associated disorders and complications can affect any part of the body and removal of the offending foods can result in complete recovery.  Visit Glutenfreeworks.com for more information.
Grave’s Disease and Gluten Sensitivity Enteropathy (GSE). Elaine Moore. http://www.suite101.com/article.cfm/graves_disease/54749
Ch’ng CL, Keston Jones M, Kingham JGC. Celiac disease and autoimmune thyroid disease. Clinical Medicine & Research. May 2007; 5(3)184-192.

The brain is a delicate organ, where billions of cells, electrical and chemical reactions have to interact correctly to function optimally.  When something unbalances brain chemistry, interrupts reactions or damages the cells, brain dysfunction results. Gluten does all these things – whether or not you have celiac disease.

Neurological disorders from gluten can arise in either, or both, of the following ways.  Gluten can penetrate the intestinal lining and enter the bloodstream, by its own mechanism, travel to the brain where it can damage or disrupt cells or cause inflammation.  This is the direct effect of gluten on the brain.  Gluten can also lead to malabsorption of nutrients in celiac disease.  In this case, the body does not absorb the nutrients it needs. Nutrients are chemicals. The brain, therefore, does not receive the chemicals it needs to function correctly and problems develop.

Nervous system disorders have been found in over 50% of newly diagnosed celiacs.  The list of nervous disorders is long: autism, gait ataxia, gluten ataxia, progressive myoclonic ataxia, chorea, tremors, brain atrophy, cerebral perfusion abnormalities, cortical calcifying angiomatosis (cerebral calcifications), dementia, headaches, epilepsy, chronic fatigue and chronic fatigue syndrome, migraines, multiple sclerosis, vasculitis of the central nervous system, chronic maladaptive anxiety, apathy, depression, inability to concentrate, insomnia, irritability, schizophrenia spectrum disorders, and peripheral neuropathy.  New disorders are being added as the link between

These nervous disorders can include either hard or soft disorders.

Examples of hard disorders would be epilepsy, ataxia (motor abnormalities), myoclonus, internuclear ophthalmoplegia, multifocal leukoencephlopathy, dementia and peripheral neuropathies.  Hard disorders, besides peripheral neuropathies, do not respond to gluten restriction – so identifying gluten sensitivity and/or celiac disease early is critical.

Soft disorders in celiac disease include a broad range of what are considered common neurological disorders.  Hypotonia (flaccid muscles in babies), developmental delay, learning disorders and ADHD, headaches and cerebellar ataxia are examples.  Importantly, there does not seem to be a difference in whether people with infantile-onset gastrointestinal symptoms, those with late onset symptoms or are asymptomatic (have no symptoms at all) develop soft disorders.

This means you may never experience a gastrointestinal symptom, yet still suffer from neurological disorder due to celiac disease.

Recovery from these neurological disorders usually depends on length of time gluten has been digested. The gluten-free diet can result in complete recovery, improvement or no recovery depending on the amount of damage incurred. This means the earlier gluten is removed from the diet, the greater the likelihood of successful recovery.

For these reasons, anyone with an unexplained neurological disorder that does or does not respond to traditional treatment should be screened for celiac disease and gluten sensitivity.

(This Health Alert was taken from information found in Issue #10 – “How Gluten Perturbs the Brain” of the Gluten Free Gazette.)

Celiac disease is a hereditary, auto-immune disorder estimated to affect 1% of the human population (3 million in the US). Less than 3 % are estimated to be medically diagnosed, but numbers are expected to rapidly increase as diagnosis improves. Celiac disease is caused by the ingestion of wheat, barley, rye and oats and treated by removing these items from the diet. Signs, symptoms, associated disorders and complications can affect any part of the body and removal of the offending foods can result in complete recovery.

Visit Glutenfreeworks.com for more information.

You can definitely die from celiac disease, in a variety of ways:

1. Dehydration – Extreme damage to the intestinal lining can lead to death through dehydration.  In this case, the lining that is supposed to hold water in your body no longer functions.  The gut actually pulls water from your body.

2. Malignancies – Malabsorption of nutrients or consistent damage to cellular structures leads to cancers: lymphoma, leukemia, intestinal, esophageal, etc.

3. Pregnancy complications – Nutrient deficiencies can lead to cardiomyopathy in the mother or birth defects in the fetus from folic acid deficiency, protein deficiency, etc.

4. Immunodeficiency – A weakened immune system can allow common illnesses to become deadly – the flu for example.  Other illnesses normally fought off, are not.

5. Autoimmune diseases – Celiac disease, if not diagnosed and treated early, causes the body to react to other things in the body.  As the body tries to unsuccessfully attack and remove gluten (because the person keeps eating it), the immune system stays on a heightened alert and starts attacking other things.

6. Malnutrition – Any health problem that comes from malnutrition of any one or more nutrient that can lead to death can be caused by celiac disease.

Here are just 6 examples of how celiac disease can kill you.  It is a deadly serious condition caused by eating what is essentially a poison to susceptible people – people with celiac disease.

The gluten-free diet is the elimination of gluten from the diet.  That is only the first step.  The next step is determining any health problems that have arisen and treating them.  The final step is ongoing identification of health problems that arise in the future to determine how to treat yourself.

-John Libonati

John Libonati is Vice President and co-Founder of Gluten Free Works, Inc. He can be reached at john.libonati@glutenfreeworks.com.

Contact: Sally Webster
s.webster@qmul.ac.uk
44-207-882-5404
Queen Mary, University of London

Scientists who last year identified a new genetic risk factor for coeliac disease, have, following continued research, discovered an additional seven gene regions implicated in causing the condition. The team, lead by David van Heel, Professor of Gastrointestinal Genetics at Barts and The London School of Medicine and Dentistry, have further demonstrated that of the nine coeliac gene regions now know, four of these are also predisposing factors for type 1 diabetes. Their research sheds light not only on the nature of coeliac disease, but on the common origins of both diseases. It is published online today (2 March 2008) in Nature Genetics.

Professor van Heel and his team, including collaborators from Ireland, the Netherlands, and the Wellcome Trust Sanger Institute, first performed a genome wide association study in coeliac disease. Genetic markers across the genome were compared in coeliac disease subjects versus healthy controls. They then assessed around 1,000 of the strongest markers in a further ~ 5,000 samples. Their results identified seven new risk regions, six of which harbour important genes critical in the control of immune responses, highlighting their significance in the development of the disease.

Coeliac disease is common in the West, afflicting around 1 per cent of the population. It is an immune-mediated disease, triggered by intolerance to gluten (a protein found in wheat, barley and rye containing foods), that prevents normal digestion and absorption of nutrients. If undetected it can lead to a number of often severe problems among them anaemia, poor bone health, fatigue and weight loss. Currently only a restricted diet can diminish symptoms.

Professor van Heel said: “So far our findings explain nearly half of the heritability of coeliac disease – now studies with many more samples from individuals with coeliac disease are needed to identify the precise causal genetic variants from each region, and understand how these influence biological processes.”

###

The research was funded by Coeliac UK and The Wellcome Trust. Coeliac disease case studies are available for interview from Coeliac UK upon request.

The paper, ‘Newly identified genetic risk variant for celiac disease related to the immune response’ is published online, on 2 March 2008, in Nature Genetics.

For case studies contact:
Kate Newman
Press Office
Coeliac UK
Tel: 020 8399 7478
Mobile: 07952 071014

Notes to editors:

Barts and The London School of Medicine and Dentistry offers international levels of excellence in research and teaching while serving a population of unrivalled diversity amongst which cases of diabetes, hypertension, heart disease, TB, oral disease and cancers are prevalent, within east London and the wider Thames Gateway. Through partnership with our linked trusts, notably Barts and The London NHS Trust, and our associated University Hospital trusts – Homerton, Newham, Whipps Cross and Queen’s – the School’s research and teaching is informed by an exceptionally wide ranging and stimulating clinical environment.

At the heart of the School’s mission lies world class research, the result of a focused programme of recruitment of leading research groups from the UK and abroad and a £100 million investment in state-of-the-art facilities. Research is focused on translational research, cancer, cardiology, clinical pharmacology, inflammation, infectious diseases, stem cells, dermatology, gastroenterology, haematology, diabetes, neuroscience, surgery and dentistry.

The School is nationally and internationally recognised for research in these areas, reflected in the £40 million it attracts annually in research income. Its fundamental mission, with its partner NHS Trusts, and other partner organisations such as CRUK, is to ensure that that the best possible clinical service is underpinned by the very latest developments in scientific and clinical teaching, training and research.

Websites
www.coeliac.org.uk
www.coeliac.co.uk/about_us/press_office/writing_about_coeliac_disease/118.asp
http://www.wellcome.ac.uk
http://www.icms.qmul.ac.uk/
http://www.icms.qmul.ac.uk/Profiles/Gastro/van%20Heel%20David.htm
http://www.nature.com/ng/index.html

The article below describes a study showing if a woman enters menopause with a low bone mineral density, the risk is 25% to develop fractures compared to 9% who had normal bone mineral density. This is a significant and important reason for women with celiac disease to: 

1) Keep a strict gluten-free diet to be able to absorb calcium, vitamin D and other nutrients vital to bone health,  

2) Influence disinterested relatives to get tested, and 

3) Get a baseline bone mineral density (BMD) test with follow-up for the appropriate supplementation.

Bone Density Tests Do Predict Women’s Fracture Risk
Largest, longest study ever supports screening and prevention of osteoporosis

By Amanda GardnerPosted 12/18/07

TUESDAY, Dec. 18 (HealthDay News) — One bone mineral density test can accurately predict a woman’s chance of spinal fractures 15 years down the line, new research shows.

And, according to the largest and longest prospective study of osteoporosis ever, women who had a spinal fracture at the beginning of the study had four times the risk of sustaining another fracture later on.

The bottom line: “Women need to talk to their doctors about the risk of osteoporosis,” according to Jane Cauley, lead author of the study and professor of epidemiology at the University of Pittsburgh Graduate School of Public Health.

Her team published the findings in the Dec. 19 issue of the Journal of the American Medical Association.

“I agree with the guidelines that all women after the age of 65 have bone density tests, and Medicare will pay for that,” Cauley said. “Women who are postmenopausal, 50 to 64 years of age, should consider having a bone density test if they have other risk factors for osteoporosis or if they want to know what their bone density is before they consider any other treatment.”

The findings don’t change current standard practice, experts said, and they don’t change the basic message to women: Don’t ignore bone health, especially in middle and old age.

“The only really major advance here is that it’s a longer term study. Mostly studies are five years typically. This one went out 15 years,” said Paul Brandt, associate professor of neuroscience and experimental therapeutics at Texas A&M Health Science Center College of Medicine in College Station. “Women need to get their bone mineral density tested after they start menopause and if they stay on hormone replacement therapy or an anti-osteoporotic treatment.” he said.

Postmenopausal women are particularly vulnerable to fractures resulting from osteoporosis, a degenerative weakening of the bones. Some 10 million Americans, including one in five American women over the age of 50, suffer from osteoporosis, which is the most common type of bone disease.

Spinal fractures are the most common type of fracture resulting from osteoporosis, affecting 35 percent to 50 percent of women over 50 (about 700,000 vertebral fractures annually in the

United States).
But many, if not most, of these fractures go undetected. “Osteoporosis is sometimes called the silent thief,” Cauley said. “It basically robs the skeleton of strength and resources, and women don’t really know about it. About 75 percent of all spine fractures actually occur silently.”

“Identifying risk factors for spine fractures is less well developed. You have to systematically look for them by repeated X-rays,” Cauley continued.

The findings from this study are based on bone mineral density data from 2,300 women over the age of 65 who enrolled in the Study of Osteoporotic Fractures (SOF), initiated in 1986.

After 15 years of follow-up, it was evident that 25 percent of women who had low BMD at the beginning of the study developed fractures of the spine, compared with only 9 percent of women with normal BMD.

“It was pretty much a strong gradient of risk,” Cauley explained. “If you had normal bone density when you entered and did not have an [existing] fracture, the risk of having a new spine fracture was about 9 percent, compared to a risk of 56 percent in women who had osteoporosis and who had an existing fracture. So, the range of risk varied dramatically depending on bone density and previous spine fractures.”

According to Brandt, one interesting finding from the study is that a previous vertebral fracture topped even bone mineral density as a predictor for future fracture.

This indicates that women with an existing vertebral fracture should be treated for osteoporosis regardless of their BMD, the authors reported.

“People think osteoporosis is an inevitable consequence of aging, but it is preventable and treatable,” she said.

More information There’s more on age-linked bone loss at the U.S. National Library of Medicine. Copyright © 2007 ScoutNews, LLC. All rights reserved.