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OK, amid my recent neverending research, I bumped into this article. This is important for those that have PCOS or perhaps a subtype (SAHA, HAIR-AN) along with a myriad of other's with "mysteriously" developed diseases.

Hidden Gluten Sensitivity a Leading Cause of Infertility

That bagel you had for breakfast just might be one of the reasons you haven’t been able to get pregnant. A hidden sensitivity to a protein in grain can cause infertility, depression, diarrhea, constipation, anemia and fatigue. This protein, called gluten, is present in wheat, rye, oats, triticale, spelt, kamut, and other grains. Gluten sensitivity is related to celiac disease, but it is much more common.

While celiac disease affects approximately 1 in 133 people, hidden gluten sensitivity may affect as many as 1 person out of every 2. Celiac disease has dramatic symptoms including rapid weight loss and severe anemia. Hidden celiac disease or gluten sensitivity can remain hidden precisely because the symptoms are not apparent. Gluten sensitivity can be determined with a blood test, but if it is still in the early stages it may not show on a blood test.

Melissa Diane Smith is a nutritionist and health educator. She is also the author of Going Against the Grain, an explanation of how a sensitivty to gluten can ruin your health and what you can do about it. Smith spoke at the After the Diet PCOS conference in April 2006 where she talked about the infertility and gluten sensitivity. She stated that gluten sensitivity is a leading cause of recurrent miscarriage.

Symptoms of gluten sensitivity can include anemia, abdominal pain, bloating and gas, depression, fatigue, diahrrea and constipation. Gluten sensitivity is associated with a variety of other disease including infertility, autism, autoimmune diseases, frequent headaches, psoriasis and skin conditions as well as other problems. Women with celiac disease who do not follow a gluten-free diet have been found to enter menopause 4-5 years earlier than other women.

In addition, up to 39% of women with celiac disease have been shown to have periods of amenorhea (no periods). Clearly, if you are sensitive to gluten it can negatively impact your reproduction. Men with celiac disease have also been shown to have reduced fertility. While gluten sensitivity is not different than celiac disease, it only makes sense to investigate gluten sensitivity while battling unexplained infertility.

Smith said that 85% of her PCOS clients test positive for a sensitivity to gluten. When these women remove gluten from their diets they often see a marked improvement in their PCOS symptoms. She has also seen dramatic improvement in cholesterol levels, thyroid function and weight loss in women who have changed their diets to avoid gluten.

Smith recommends that women who suffer from gluten sensitivity avoid gluten containing foods including hidden gluten such foods as soy sauce, teas and foods containging barley malt, vegetable protein made from wheat gluten, and beer. Don't just replace the high glutne grains with more starchy or sugary foods though or you run the risk of developing insulin resistance. Instead, focus on fresh vegetables.

For more information about gluten sensitivity read Going Against the Grain: How Reducing and Avoiding Grains Can Revitalize Your Health. You can find gluten-free living information at http://www.bellaonline.com/articles/art1507.asp

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Protein in Wheat Plays A Role in Promoting Type 1 Diabetes

posted 04/16/03

Researchers have identified a protein in wheat called Glb1 which may play a role in the development of type 1 diabetes.

Researchers investigating type 1 diabetes agree that the disease develops through the interaction of genes and one or more environment triggers. Although many theories have been proposed suggesting that exposure to dietary proteins may trigger the immune system attack leading to type 1 diabetes, studies attempting to establish such links until now have produced negative or contradictory results.

The research, funded partly by JDRF, sheds light on autoimmune responses set into motion by certain dietary components. It also raises the possibility that exposing children to Glb1 at a young age could teach the immune system not to overreact when exposed to the protein at a later time.

The gastrointestinal tract is lined with large numbers of immune cells that defend against potentially harmful microbes. In animal models of type 1 diabetes, researchers have found inflammation in this tissue that resembles inflammation found in the pancreas of animals (and people) developing type 1 diabetes. In addition, patients with type 1 diabetes are at an increased risk for another autoimmune affliction involving the gastrointestinal tract:

Celiac disease occurs when immune cells in the gut react to a certain protein, called gluten, proteins found in wheat, rye, and barley. Once aroused, the immune cells attack and damage the lining of the intestine making it difficult to absorb nutrients from foods. Although rare in the general population, celiac disease occurs more frequently in people with type 1 diabetes (with estimates ranging from 2 – 16 percent). The fact that people with type 1 diabetes have celiac disease at a much higher rate than the general population suggests that some people that share common risk genes may be particularly sensitive to wheat and could develop a misguided immune response to certain foods.

Dr. Scott began testing various diets in diabetes-prone rodents. His goal was to identify specific food proteins that promoted development of diabetes and to understand the mechanisms by which this occurs. Dr. Scott identified wheat proteins as a prime candidate because wheat-based diets resulted in high diabetes incidence in animal models of diabetes. Scott and his colleagues proposed that one or more wheat proteins were spurring the gastrointestinal immune cells into action, and once aroused, the cells were targeting pancreatic islets and causing type 1 diabetes.

Dr. Scott and his colleagues scanned through one million candidate proteins from wheat, eventually narrowing the field to three that cause reaction in the immune system, and then finally to Glb1, which is associated with damage in the pancreatic islets. The researchers took blood from people with type 1 diabetes and a rat model for the disease and exposed it to Glb1. Antibodies in the blood reacted strongly to Glb1, suggesting it plays some role in triggering the autoimmune attack that causes diabetes. The results from the study were selected as the cover illustration for the January 3 issue of the Journal of Biological Chemistry.

The researchers have also shown that exposing diabetes-prone animals to wheat proteins in infancy can delay and protect some diabetes-prone animals from the disease possibly by teaching the developing immune system not to overreact if it encounters these proteins later in life. This work was published in the January 2002 issue of Diabetes. It is not clear yet whether such an approach would be beneficial in people at high risk for type 1 diabetes.

Source: Diabetes In Control Dot Com. http://www.defeatdiabetes.org/Articles/type1030416.htm

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hidden gluten sensitivity may affect as many as 1 person out of every 2.

I think that's important. You might not be a full-fledged celiac, but that doesn't necessarily mean that gluten doesn't affect you.

Also, people with gluten sensitivity might not have any symptoms at all. I've read one figure that says that 50% of gluten-intolerantettes exhibit no symptoms of gluten sensitivity.

Of course I think it's pretty systematic for people here to test themselves for gluten sensitivity so I'm not worried about anybody who browses this forum.

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I keep reading in studies that either you're celiac or either you're not.

The idea of hidden gluten sensitivity and some of the means used to diagnose it (like feces tests) are not considered realiable. Blood tests and if needed gastroscopy should be enough to detect any sort of adverse reaction to gluten. If nothing is detected there's no sort of gluten adversion. The higher figures have been questioned by celiac experts and the figure of 1 out of 2 person having an harmful and yet subclinical form of gluten intolerance is imo way over the lines.

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I keep reading in stupids that either you're celiac or either you're not.

The idea of hidden gluten sensitivity and some of the means used to diagnose it (like feces tests) are not considered realiable. Blood tests and if needed gastroscopy should be enough to detect any sort of adverse reaction to gluten. If nothing is detected there's no sort of gluten adversion. The higher figures have been questioned by celiac experts and the figure of 1 out of 2 person have an harmful and yet subclinical form of gluten intolerance is imo over the lines.

Actually Danny, even when Celiac Disease runs in the family....some children will still test negative.

Even when they get an endoscopic exam...they will still test negative.

Yet....these children usually have some sort of health condition, be it gastrointestinal, ADHD, or Autism and upon going on the diet...usually the signs/symptoms cease.

Therefore, as with the case of any sort of concern of there being a food/chemical hypersensitivity...the Gold Standard is still avoidance and observation or rather...an Elimination & Provocation Diet.

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hidden gluten sensitivity may affect as many as 1 person out of every 2.

I think that's important. You might not be a full-fledged celiac, but that doesn't necessarily mean that gluten doesn't affect you.

You're still celiac just like 127 mg/dl glycemia is still diabetes only of a small entities.

Most diseases are divided by their magnitude but they're still the same pathology.

If there's no celiac morb there's nothing else.

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I keep reading in stupids that either you're celiac or either you're not.

The idea of hidden gluten sensitivity and some of the means used to diagnose it (like feces tests) are not considered realiable. Blood tests and if needed gastroscopy should be enough to detect any sort of adverse reaction to gluten. If nothing is detected there's no sort of gluten adversion. The higher figures have been questioned by celiac experts and the figure of 1 out of 2 person have an harmful and yet subclinical form of gluten intolerance is imo over the lines.

Actually Danny, even when Celiac Disease runs in the family....some children will still test negative.

Even when they get an endoscopic exam...they will still test negative.

Yet....these children usually have some sort of health condition, be it gasterointestinal, ADHD, or Autism and upon going on the diet...usually the signs/symptoms cease

This is a bit suspect.

It is like burning your organs before burning your skin.

How can the celiac be so strong to cause autism and even gastrointestinal conditions and yet a gastroscopy found no trace of this in the villis? The effect on the gastrointestinal system are required for the other effects to even approach let alone develop into full invalidating diseases.

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I keep reading in stupids that either you're celiac or either you're not.

The idea of hidden gluten sensitivity and some of the means used to diagnose it (like feces tests) are not considered realiable. Blood tests and if needed gastroscopy should be enough to detect any sort of adverse reaction to gluten. If nothing is detected there's no sort of gluten adversion. The higher figures have been questioned by celiac experts and the figure of 1 out of 2 person have an harmful and yet subclinical form of gluten intolerance is imo over the lines.

Actually Danny, even when Celiac Disease runs in the family....some children will still test negative.

Even when they get an endoscopic exam...they will still test negative.

Yet....these children usually have some sort of health condition, be it gasterointestinal, ADHD, or Autism and upon going on the diet...usually the signs/symptoms cease

This is a bit suspect.

It is like burning your organs before burning your skin.

How can the celiac be so strong to cause autism and even gastrointestinal conditions and yet a gastroscopy found no trace of this in the villis? The effect on the gastrointestinal system are required for the other effects to even approach let alone develop into full invalidating diseases.

Honestly, I don't know. What I do know from reading various Celiac forums and Peer-Reviewed journal articles is that this is the case.

What I do know is that Celiac Disease is linked to a few other diseases that are considered "hormonal disorders" that can have acne as a symptom. With these disorders a percentage of the people do end up being dx as having Celiac Disease. I don't know what causes it for others....maybe it's sub-clinical or maybe it's something else.

For those that have family members that have the gene, but aren't displaying any "typical" signs...I guess it's a matter of time....or maybe...they are expressing signs...just atypical ones.

Maybe....scientists and doctors are not ready to believe that our prime food source could be causing some major issues or that other seemingly harmless foods might not be the right fit for certain people...based on their gene-environmentinteractions.

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For those that have family members that have the gene, but aren't displaying any "typical" signs...I guess it's a matter of time....or maybe...they are expressing signs...just atypical ones.

But when someone in the family as a celiac gene the chances that the children won't have the gene and the disease are as many as the chances that they will have it. Often in a family where the celiac gene is running and there are let's say three children, one of the children have the gene and the diseases and the other two have neither of them.

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For those that have family members that have the gene, but aren't displaying any "typical" signs...I guess it's a matter of time....or maybe...they are expressing signs...just atypical ones.

But when someone in the family as a celiac gene the chances that the children won't have the gene and the disease are as many as the chances that they will have it. Often in a family where the celiac gene is running and there are let's say three children, one of the children have the gene and the diseases and the other two have neither of them.

LOL...why are you even debating this Danny. I'm just reporting what the studies have found and what Celiacs and their family members have experienced. Despite the genetic punnett square, apparently you can be:

  • Allergic to wheat/gluten
  • Sensitive to wheat/gluten
  • Gluten intolerant (CD)

Thus, there are varying levels of sensitivity. :angel:

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Celiac Disease and Gluten Sensitivity

By Carol E. Semrad, M. D.

Celiac disease, also referred to as celiac sprue, is an inflammatory condition of the small intestine precipitated by the ingestion of wheat in individuals with certain genetic makeups. The onset of illness most commonly occurs around age two, after wheat has been introduced into the diet, and in early adult life (third and fourth decades). However celiac disease can begin anytime in life. In susceptible individuals, the wheat protein gluten triggers an inflammatory reaction in the small bowel which results in a decrease in the amount of surface area available for nutrient and fluid and electrolyte absorption. The extent of loss of intestinal absorptive surface area generally dictates whether an individual with celiac disease will develop symptoms. Individuals with celiac disease may experience severe symptoms such as diarrhea, weakness, and weight loss indicating a marked decrease in intestinal absorptive surface area involving much of the small intestine. On the other hand, some individuals present with anemia related fatigue and have no symptoms referable to the gastrointestinal tract. Such individuals likely have disease limited to the proximal small bowel where iron is normally absorbed, with the remainder of bowel adequate for nutrient and fluid absorption. Other extraintestinal manifestations of celiac disease include osteopenic bone disease, tetany and rarely neurologic disorders. Gluten sensitivity can also manifest itself as a blistering, burning, itchy rash on the extensor surfaces of the body (dermatitis herpetiformis). Most of these individuals have intestinal biopsies characteristic of celiac disease regardless of gastrointestinal symptomatology. Recently, with the discovery of antibodies which are specific for celiac disease, screening of families of celiacs and select populations have identified a growing number of asymptomatic individuals who have circulating antibodies and changes on intestinal biopsies characteristic of celiac disease. These individuals clearly have a gluten sensitivity but it is unclear whether they will develop the clinical features of celiac disease over time. Removal of wheat (gluten) from the diet of individuals with celiac disease or gluten sensitivity results in regeneration of the intestinal mucosal absorptive surface area and resolution of symptoms in most patients.

Cause of celiac disease

There are two important factors that contribute to the development of celiac disease:

The ingestion of wheat

The "Coeliac Affection" was first reported by Gee in 1888, however it was not until 1950 that wheat was proposed to be the cause of celiac disease. The evidence was based on the observation of a Dutch physician named Dicke who noted during World War II, a time when wheat grains were scarce in Holland, that children with celiac disease who had otherwise failed to thrive improved on a wheat-poor diet. Since then the large water-insoluble protein, gluten, present in wheat has been identified as the offending substance. Extraction of gluten with alcohol has further narrowed activity to smaller proline-rich proteins called gliadins which are capable of precipitating disease in previously asymptomatic celiacs. Analogous proteins exist in other grains such as rye, barley and oats and therefore these grains are also capable of exacerbating celiac disease. The specific peptide sequence of the gliadins responsible for triggering intestinal inflammation has not yet been identified.

The genetic background of the individual

Celiac disease runs in families. First degree relatives of individuals with celiac disease may or may not manifest symptoms of the disease. Predisposition to gluten sensitivity has been mapped to the major histocompatibility (MHC) D region on chromosome 6. The most important HLA haplotype is DQw2 which is often in linkage with DR3. Other important HLA haplotypes identified are DR7 and DPB 1, 3, 4.1 and 4.2. The sites on these MHC class 2 expressed proteins responsible for interacting with gliadin and host T cell receptors thereby sensitizing the intestine to gluten have not been identified.

Intestinal response to inflammation

The main function of the small intestine is to absorb nutrients and fluid and electrolytes, a process dependent on adequate surface area. In this regard, the absorptive epithelium (villus) of the small intestine is pleated in the intestinal lumen to increase its surface area. Intestinal inflammation of any etiology, if severe enough, is associated with flattening of the villus epithelium which results in a decrease in intestinal absorptive surface area. How activated inflammatory cells in the lamina propria beneath the surface epithelium and interspersed between epithelial cells bring about villus flattening remains a mystery. Intestinal biopsies taken from individuals with celiac disease and gluten sensitivity show a spectrum of these mucosal abnormalities. Three distinct patterns have clinical relevance:

Infiltration of the villus epithelium with lymphocytes and a normal villusand crypt architecture

This pattern is found in 40% of individuals with Dermatitis Herpetiformis and a portion of first degree relatives of celiacs who have no gastrointestinal symptomatology.

A flat mucosa characterized by villus flattening and crypt elongation with inflammatory cells in the lamina propria

This pattern is classically found in individuals with celiac disease who have gastrointestinal symptoms, but has also been reported in asymptomatic celiac relatives and individuals with Dermatitis Herpetiformis. It is important to keep in mind that intestinal biopsies are most commonly obtained endoscopically from the duodenum and therefore do not provide information as to the extent of disease along the length of jejunum. Since the duodenum is the first segment of small intestine exposed to gluten, villus flattening might be most severe in this location while much of the jejunal villi remain relatively normal, accounting for an asymptomatic state. In most of these individuals, treatment with a gluten-free diet results in the return of villus and crypt architecture to normal or near normal.

A hypoplastic mucosa characterized by villus flattening and small crypts

This biopsy is found in the small group of patients with presumed severe celiac disease refractory to a gluten-free diet. These individuals have persistent ill-health due to intestinal malabsorption and sometimes require nutritional support parenterally. This intestinal lesion is irreversible.

Diagnosis of celiac disease

There is no test yet which is definitively diagnostic of celiac disease. Relief of symptoms or reversion of an abnormal intestinal biopsy to normal on a gluten-free diet is the most convincing evidence that an individual has celiac disease or gluten sensitivity. Intestinal biopsies as discussed above show characteristic findings compatible with celiac disease but are obtained just as often to exclude other intestinal conditions, most importantly infection, which can have a clinical presentation similar to celiac disease.

The first serologic marker reported to be of use in the diagnosis of celiac disease was the IgG class antigliadin antibody (AGA). Though sensitive, this antibody is also found in other diseases and is therefore not specific for celiac disease. IgA class AGA is more specific, however about 2 % of patients with celiac disease have selective IgA deficiency. A positive IgG and IgA AGA gives a reported sensitivity of 96 % to100 % and specificity of 96 % to 97 %. If only the IgG AGA is positive an evaluation for selective IgA deficiency should be undertaken. Antireticulin antibodies (ARA) have also been reported in individuals with celiac disease, but are nonspecific. IgG ARA is relatively useless, but IgA ARA has a high sensitivity and specificity in adults (97 % and 98 % respectively). In children these values are much lower. Recently two antibodies, IgA class antiendomysial antibody (EMA) and human jejunal antibody (JAB), have been identified which are highly sensitive and specific for active celiac disease (100 % sensitivity and specificity reported in one study). The one best characterized is the EMA, an antibody against endomysium reticulin fibers. In adult studies, EMA was only found in patients with active celiac disease and not other diseases. The test is less powerful in children as EMAs have been detected in other childhood diseases. The more important limitation of EMAs in children is the reported fall in sensitivity observed in children with celiac disease less than 2 years old. Even the EMA and JAB antibody tests in adults are not fool proof as they may not be positive in individuals with celiac disease and IgA deficiency.

A panel of these antibodies seems to be most useful in the diagnosis of celiac disease. A combination of IgG AGA, IgA AGA and EMA have a reported positive predictive value of 99.3 % when all were positive and a negative predictive value of 99.6 % when all were negative. These antibodies tend to lessen or disappear when individuals are maintained on a gluten-free diet. Antibody testing is important in screening individuals who are at risk for having celiac disease but have no symptomatology, in individuals with atypical symptoms or extraintestinal manifestations of celiac disease, and in individuals with presumed celiac disease who fail to respond to a gluten-free diet. Patients with postive antibody tests must undergo small intestinal biopsy to confirm the diagnosis and assess the degree of mucosal involvement.

Treatment of celiac disease

Unlike autoimmune diseases in which the precipitating antigen either is not identified or if identified can not be removed, the antigen precipitating celiac disease i.e. gluten can be removed from the diet. This sounds easier than done as wheat is used as a filler and thickener in a number of store bought and restaurant prepared foods. Avoidance of gluten in the diet requires careful scrutiny of food labels for the presence of wheat and other offending grains such as rye, oats and barley. Products labelled wheat-free are not necessarily gluten-free. Common food items that can not be eaten include breads, bagels, pastries, pasta and pizza. There are companies throughout the United States which produce gluten-free products made predominantly from rice flour. Most patients treated with a gluten-free diet will note a lessening of symptoms within 2 weeks and no follow up intestinal biopsy is required. A small group of patients have partial or no response to a gluten-free diet. One important cause of a poor dietary response is the continued ingestion of gluten in foods thought to be gluten-free or just plain dietary cheating. Antibody testing while such patients are on a "strict" gluten-free diet may be useful in this situation. A kit which utilizes the Elisa assay has been developed to test food products for the presence of the gluten antigen. In individuals who have a poor response to a gluten-free diet, a repeat intestinal biopsy is mandatory after 3 months treatment to assure that other intestinal lesions such as infection or intestinal lymphoma was not missed.

Why treat celiac disease?

In symptomatic patients the obvious answer is to relieve debilitating symptoms. What about individuals who have minimal symptoms or who are asymptomatic? There are two reasons to treat such individuals with a gluten-free diet: 1) a subgroup of these patients will progress to more severe disease and hence develop symptoms and 2) there is an increased incidence of small intestinal lymphomas and adenocarcinomas in individuals with celiac disease. The increased incidence of cancer seems to correlate with the degree of intestinal inflammation (activity) present, as individuals whose disease responded to a gluten-free diet and who remained compliant with the diet had a lower incidence of such cancers. Whether individuals who are found to have elevated antibodies specific for celiac disease but are asymptomatic and have normal intestinal biopsies should be treated with a gluten-free diet is unclear.

The following patient organizations provide information on celiac disease, gluten sensitivity and dietairy treatment:

American Celiac Society-Dietary Support Coalition

58 Musano Court

West Orange, NJ 07052

(201) 325-8837

Celiac Disease Foundation (CDF)

13251 Ventura Blvd. #3

Studio City, CA 91604

(818) 990-2354

Celiac Sprue Association/USA, Inc.

P.O. Box 31700

Omaha, NE 68131-0700

(402) 558-0600

Gluten Intolerance Group of North America

Cynthai Kupper, Exectutive Director

15110 10 Ave SW Suite A

Seattle WA 98166-1820

206-246-6652

FAX 206-246-6531

[email protected]

www.gluten.net http://www.cumc.columbia.edu/dept/gi/celiac.html

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I wonder if there's any good way to quicken the healing of the villus after going on a gluten-free diet? Any particular foods that are helpful?

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