Symptoms of Wheat Allergy - Articles - Zimbio

Stop Allergy Symptoms Now!

Sat, 16 Nov 2008 00:59:36 GMT

posted by csp052002

Sometimes our bodies decide that they just don’t like something. When this happens, they let us know in a variety of ways. When we come into contact with an irritating substance, our bodies sometimes complain by itching, sneezing, coughing, and breaking out in rash. This lovely collection of symptoms is called ‘allergies’. The above-mentioned symptoms aren’t the only signs of allergies. Sufferers frequently experience irritated, watery eyes and runny noses. Others, particularly children, might get dark circles under their eyes.

Think you might have allergies? If you do, you’re not alone. Over 50 million people suffer from allergies in the U.S. alone. With so many symptomatic individuals running around, it’s no surprise that a number of treatments have sprung up.

If your allergies are persistent, talk to your doctor about prescription or over-the-counter medications. They’ll be able to recommend the best drug for you. Popular anti-allergy medications include nasal sprays and antihistamines. Nasal sprays, such as Flonase and Nasonex, contain mild corticosteroids to fight inflammation. Antihistamines fight the body’s production of reactionary chemicals called histamines. Histamines cause allergy symptoms. An antihistamine, like Claritin or Benadryl, can be used in place of or in addition to nasal sprays. Some antihistamines cause drowsiness, so be sure to consult with your doctor to see which one is right for you.

Would you rather avoid drugs and treat your allergies the natural way? Natural treatments are great for mild to moderate allergies. Here are a few ways that you can cut down on your exposure to allergens each day.

First, educate yourself about allergies. If you have food allergies, make sure that you know how to read food labels and decipher their information. Improve the air quality in your home or office with a dehumidifier or air filtration system. Avoid prolonged trips outside and close doors and windows during high pollen days and in the mornings. Don’t keep pets that trigger allergies. Many allergy sufferers find it helpful to wash all their sleeping linens thoroughly each week.

Allergies tend to be hereditary. But before you blame Mom and Dad for your sniffles, take a look at the things you encounter every day that trigger your allergies. Do you have dust and mold around your house? Do you come into contact with animals that make you allergic? There are many factors that you can eliminate from your daily life to reduce your allergy symptoms. Take the necessary steps to ensure that you’ll enjoy an allergy-free existence - no matter the season!

Gluten Free Products-Follow The Crowd

Fri, 15 Nov 2008 05:00:00 GMT

posted by mjesales
If you suddenly find your life more complicated with disease related to gluten intolerant that stops you from following your normal diet then relax you are not only the one but there are many people in the list and the most important news is that it is not so difficult to maintain diet because there are so many gluten free products available in the market to choose from. Diet is an important part for the people suffering from celiac disease as they have to follow gluten-free products to replace all those foods containing wheat, rye, barley and oats that we loved to eat--like bread, cookies, cakes and pastas. Such diet is completely a new diet that includes food that we have never tasted and till then until we are diagnosed with such disease. And our common sense will never put a second thought to the diet that is specially meant for celiac patients because it is a patientâs diet and we are not patient. Among the various gluten-free products that are available in the market some products are good, some are only okay and many are reported to be bad in taste. As soon as you are diagnose with gluten intolerant disease a gluten-free diet is said to strictly follow and initially it starts with âYukâ, and the many of the foods that you have purchased will ultimately end up in your garbage pail and will leave you frustrated and that is really saddening.** End Summary** Click to read the rest of the story

Corissa & the wonder bread

Sun, 20 Oct 2008 06:44:08 GMT

posted by YvesKlein

I started to make the amazing wonder bread which one can eat almost every one, all the healthy people, but on top of that 100 % people with allergy to yeast, wheat and milk, close to 100 % people with Gluten Intolerance and around 95% people with Celiac Disease. This bread is made from wheat flour with high protein gluten contains based on old recipes. No one believed me at the beginning because the scientist and doctors stating that gluten is toxic. My education (I have two Masters in Scientism chemistry) helped me to find a new explanation how the allergy and disease is generated, end helped for me to develop the Wonder Bread. Because no one scientist and no one government believed me I started to collect Certificates from my customers (see Web: http://picasaweb.google.com/Firebird432/Certificate#) all of them with medical record regarding their illness. Most of my customers have no medical record that is why limited number of certificates.

Duration : 0:0:25

Technorati Tags: environment

Gluten Intolerance-What Your Doctor May Not Tell You

Sat, 31 Aug 2008 19:10:06 GMT

posted by dmkashen
The associated health issues related to gluten intolerance (GI), have a wide range, with Celiac Disease being the defining and best known aspect of that problem. However, GI can often go undiagnosed, because it does not always present with the more obvious symptoms seen in Celiac Disease (CD). GI and even CD can be cryptic, or a hidden problem, in many individuals. Gastrointestinal symptoms, such as diarrhea, abdominal pain, bloating, fatty stools, nausea or vomiting, and distention are at times part of the clinical presentation of GI and CD, however these symptoms may be mild or absent altogether. Cryptic or hidden GI, is commonly referred to as sub-clinical gluten intolerance or sensitivity, and bears distinguishing it’s clinical features from CD. Sub-clinical gluten intolerance is often confused with celiac disease, also referred to as celiac sprue or non-tropical sprue, or gluten enteropathy. In essence, CD is a diagnosis that is confirmed by biopsy of intestinal tissue. If the damage is apparent upon biopsy and there is other supportive evidence, such as elevated antibodies, then the diagnosis of CD is given. The reaction to gluten in sub-clinical gluten intolerance, commonly referred to as gluten “sensitivity”, may be similar to the gluten intolerance in celiac disease, except for the actual degree of presenting symptoms and the damage to the small intestine-if any exists. In many cases there is not any typical presenting symptoms and absence of any apparent intestinal damage, but there will be other health issues, such as anemia, fatigue due to malabsorption of nutrients, mood disorders, elevated thyroid antibodies, rheumatic pains or other related autoimmune diseases. Other medical references to forms of CD, include “silent” CD, which does not present with any symptoms that normally characterizes a GI, but upon a biopsy, there will be damage to the tissues of the small intestine. Silent CD, may present as one of many other celiac disease related disorders. “Latent CD”, refers to a finding of positive blood antibody tests, but there are is minimal or no appearance of damage to the intestinal tissues upon examination. It is thought that these latent cases reflect gluten sensitive individuals, or perhaps a relatively gluten free diet, albeit also having a high probability for eventual damage to the intestinal tract with any significant exposure to gluten. These references to GI and classifications of CD are not concrete definitions. They are at times used interchangeably and are used more so to categorize atypical CD. Gluten Intolerance-Celiac Disease The exact mechanisms in Celiac disease (CD), are complex and not completely known. What is generally accepted to be the primary course of CD, involves the effects of gluten on the intestinal structures and immune system. There is perhaps no other such complex biological disease that has such a simple answer-the avoidance of gluten. Nevertheless, the understanding of the inter-related processes of gluten intolerance and CD, gifts us with insights into the dynamics of the intestinal milieu and subsequently a better grasp as to the workings of an amazing universe within-our digestive tracts. The gluten/celiac disease theory proposes that CD is caused by an exaggerated (hyper) immune response to the gluten found in wheat, and wheat related and hybrid grains-spelt, kamut, and triticale, as well as barley, and rye. There are many other wheat strains, such as couscous and bulghur that are in the family of prime gluten offenders as well. Other grains like oats are considered by some to potentially have negative health effects related to gluten Intolerance (GI), albeit in most studies, they do not promote the same immune/gluten intolerance reactions. The issue of oats is somewhat confounding. Oats have the similar toxic peptide sequences (avenin) as gliadin in wheat, yet in studies, there are conflicting results indicating that oats are very harmful to some individuals with CD, while not very harmful to others. It may be that the load of the gluten in oats is such that it may take more long term exposure, or greater amounts of oats ingested, to elicit the gut immune responses typical of gluten sensitivity or celiac disease. The issue of oats in some individuals, may also be one of cross contamination by wheat, in processing facilities that handles both grains. In any case, oats and other grains may contribute to inflammatory reactions (allergies) in sensitive individuals and contribute to, or converge with the cascade of immune responses and leaky gut issues that occurs in CD, regardless of their gluten profile. A distinction to note here is that intolerances to foods, is not an allergy response. There are several food intolerances, such as lactose intolerance, that are primarily due to a lack of specific enzymes that break down either sugars or proteins. Gluten intolerance is the only intolerance that involves an immune system reaction, albeit not the same as in a true allergy or delayed food sensitivity. The predominant theory with respect to GI, is that there is an inherent lack in ability to break down gluten, a generic term for a type of protein in grains. More specifically, gliadin (i.e. alpha-gliadin), a polypeptide in wheat gluten, and other prolamins in grains are the offending protein. Prolamins (a group of proteins-prolamines, with similar protein structures), namely gliadin from wheat, hordeins from barley and secalins from rye, have been identified as the trigger for celiac disease. These polypeptides (strings of amino acids) are the residual from incompletely broken down pieces of protein from gluten that are potentially toxic to the intestinal tissues. Gluten and prolamins, are in other grains like rice and corn, but these do not contain the toxic peptide(s) sequence that can provoke an immune response and that are toxic to, and damage the intestinal tissues in gluten intolerant or sensitive individuals. Nevertheless, as noted above, some grains like corn and soy, are common allergens that can problematic in people with food sensitivites and intolerances and should be carefully assessed as to any possible role they may be playing in ramping up inflammation in the gut. The toxic peptides from select prolamins eventually trigger a specific immune response that is part of the immune cascade associated with CD. However, a proinflammatory condition in the digestive tract may be a requisite intestinal environment before gluten can exert it’s influence.(1,2) Food allergies and sensitivities as well as some common gut infections, can potentially contribute to “breaking tolerance” (see below), and opening the gate to immune/inflammatory reactions characteristic of CD. In GI and CD, chronic exposure to these gliadin containing grains, leads to an inflammatory condition of the small intestine. The repeated immune reactivity to gluten/gliadin, in some individuals, eventually manifests in an “autoimmune” condition, in which immune system antibodies attack the intestine and cause severe damage over time. The immune/inflammatory reaction in the small intestine, damages the villi of the small intestine, and causes changes to the structure (hyperplasia) of the tissues deep between and at the base of the villi, the crypts. The villi are finger-like projections on the intestinal wall where nutrient absorption occurs. This damage impairs the absorption of nutrients from digested food. With repeated exposure to gliadin in gluten, these villi can become shortened or completely flattened, with the subsequent loss of nutrient absorptive surface area. The immune reaction and intestinal intolerance to gluten, can cause diarrhea, abdominal pain, bloating, nausea, malabsorption of nutrients (iron, calcium, zinc, folate, fat soluble vitamins), and other gastrointestinal problems. However, the typical symptom picture of sub-clinical or silent CD, may not have much or any of the digestive distress symptoms that characterizes CD. Often GI and CD may be written off as an irritable bowel syndrome problem, or a spastic colon. More severe intestinal/bowel disorders related to gluten intolerance reactions are inflammatory bowel diseases such as Crohn’s disease. Other symptoms that may indicate an intolerance to gluten include, bone pain, muscle cramps, migraine headaches, tingling, numbness and nerve pain of the extremities (neuropathy), miscarriage and infertility problems, menstrual irregularities, depression, gall bladder disease, vitiligo (discoloration of skin), and developmental and growth problems in children. Enzyme Therapy Enyzyme deficiency (peptidase) in gluten intolerance was once theorized to play a role in the development of CD. Peptidases, are protein digesting enzymes secreted by the intestinal tissues (brush border), and are distinguishable from pancreatic enzymes that also break down proteins for absorption. More recent research in enzyme therapy and CD, reveals that enzyme therapy with newer enzyme products demonstrate a promising role, in at the very least, ameliorating gluten intolerance (GI) reactions and perhaps buffering the margin of error in a gluten free diet. In numerous studies, pancreatic insufficiency (enzyme production) has been noted in a considerable percentage of celiac patients, and could in part explain why a population of celiac patients do not do as well despite eliminating gluten from the diet.(3) Enzyme therapy in part protects patients with CD with amelioration of symptoms related to gluten intake.(4) Enzyme therapy can provide important digestive support, and offer some protection for all CD patients where the gluten status of the meal is uncertain, as when eating out, or for those who are especially sensitive to gluten. Specific enzyme derivatives, demonstrate enhanced gluten digest, and shows promise in management of GI. Enzyme products that contain Aspergillus niger (fungal) derived enzymes, survive stomach acid and pepsin degradation, and effectively break down gluten proteins.(5) However, to date Aspergillus niger derivatives specific for gluten digest are not commercially available. Several peptidase enzymes also have demonstrated resistance to stomach acid, effective break down of gliadin peptides, and thus promise in the treatment and management of celiac disease.(6) An additional benefit to enzyme therapy is the enhanced digest of other proteins, particularly those in dairy products, as well as the sugar lactose. A secondary feature of GI is lactose intolerance, that is a consequence of the damage to the intestinal tissues and the enzyme secreting cells. Lactose intolerance and bacterial overgrowth of the small intestine, the latter a common condition that follows the inadequate digest of foods, are suspected as underlying factors that contributes to the unresponsiveness to a gluten free diet in some individuals.(7,8) The autoimmune profile of CD may also result in hydrochloric acid deficiency (HCL). HCL deficiency has been associated with dermatitis herpetiformis (9), a skin disorder that is linked to CD. I consider enzyme and HCL supplementation a must for the management and support GI and CD. The Lectin Connection According to another theory, a component in wheat gluten, wheat germ agglutinin (WGA), may act as a lectin with toxic properties to the intestinal cells. Lectins, are specialized proteins that bind specifically to sugars or other carbohydrates, usually on other proteins, which are located on the membranes of cells. They are thus often referred to as carbohydrate-binding proteins. Lectins causes cells to agglutinate, or stick to each other, compromising their function. In the digestive tract, lectins bind to specialized intestinal cells (crypt cells).(10) If they enter the blood stream, they also bind to red blood cells causing agglutination or clumping. High levels of lectins may be found in grains, the legume family (beans, peanuts), dairy and plants in the nightshade family. While lectins are present in most foods, their higher levels in some, are problematic for many individulas that are genetically vulnerable to their potentially toxic effects. “Lectins are (a) toxic, inflammatory, or both; (b) resistant to cooking and digestive enzymes; and (c) present in much of our food.”(11) Among the effects observed in the small intestine of lectin fed rodents is stripping away of the mucous coat lining the intestinal tract, increased intestinal permeability (leaky gut), and the overgrowth of toxic bacteria and.(12,13,14). The characteristic damage from gluten intolerance (crypt hyperplasia), to the intestinal tissue, is also caused by WGA.(15) Breaking Tolerance In examining the details of a food intolerance like gluten, it is a logical course to look at the known pathways of the immune reactions, intestinal anatomy and function, the genetic characteristics of predisposed individuals, and the unique construct of gluten containing grains. Nevertheless, all of that examination does not entirely reveal why some genetically gluten intolerant individuals never develop celiac disease (CD), why some celiac disease patients do not recover even after eliminating gluten from the diet, or why a few (rare) without the genetic blueprint, manage to become “intolerant”. The answers to these questions, may come from a deeper examination as to the factors that may “break” a gluten tolerant individual, into an intolerant pattern - it is the proverbial straw that broke the camel’s back. Normally, the intake of food does not elicit an immune reaction as the body is able to modify the immune response to proteins in the diet. As we ingest proteins growing up, our immune system adapts, and suppresses immune reactions to many of the more allergenic foods we are exposed to. This phenomenon is known as “oral tolerance”. Oral tolerance of foods that potentially can provoke an immune response is acquired as our digestive tracts are exposed to foods, and our immune systems accomodate during childhood. That is familiar to many families as they slowly introduce a variety of foods, particularly proteins, to a growing and developing child. In a large study, the second by the same investigators, of 1560 children with a genetic predisposition (diabetes type 1 genotypes-HLA-DR3 or DR4 gene variations)* for celiac disease, those exposed to gluten before month 3, had a 5-fold increased risk in developing CD, compared with children exposed to gluten-containing foods at 4 to 6 months.(17) An interesting timing aspect of this study, was that children exposed to gluten after 7 months, had a significantly increased risk of CD compared with exposure at 4 to 6 months. While the age times of exposure raises some questions that hopefully will be answered by other studies, the real takeaway, is that exposing genetically susceptible children to gluten at a young age increases their risk for CD. I would not recommend exposing at-risk infants to gluten at age 4 to 6 months to hopefully lessen the probability of incurring CD. Why raise the probability of breaking tolerance! Especially if there is a family history of type 1 diabetes or CD. The immune system of the digestive tract is constantly in a state of tolerance to it’s own population of microorganisms (bacteria) and to food allergens as it attempts to maintain a steady immune response-one that is not reacting to just any potential insult, and subsequently moderating inflammatory responses. So what is it that skews an immune response in one individual that results in an allergy response or perhaps a gluten intolerance response, and yet in another individual there is a tolerance to that allergen? The answers are complex and specific to types of foods or proteins. Gluten intolerance (GI) is predicated on a number of factors. Yes genetics plays a role, but it may be more limited than is currently accepted, or there are a number of other genes that are yet not understood as to specific influences. As detailed below, some interesting research is percolating, that implicates leaky gut genes as part of the holism of gluten intolerance. It is largely accepted that genetics plays a primary role in various food intolerances. This certainly could fully explain the intolerance to gluten as we well know that gliadin and other prolamins stimulate immune-inflammatory reactions in susceptible individuals. Nevertheless, we also have evidence that in tolerant individuals, regardless of genetics, certain triggers will turn that tolerance into an intolerant profile. Viruses (rotavirus), gut infections (bacteria & candida) and even pregnancy may act as triggers in a apparently gluten tolerant individual, and stimulate inflammatory responses that promotes the cascade of events that results in intolerance. The preganacy link indicates that hormones may exert some influence as well. There may be degrees of intolerance as evidenced by cases that manifest into full blown celiac disease, down to the less “sensitive” individual that seems to have a tolerance predicated on the amount of gluten ingested, the timeline involved or “triggers” that may push one over the edge. Two recent scientific publications have now shown that a rotavirus (common gut viral infection) protein may be linked to celiac disease through a “molecular mimicry” mechanism. “Molecular Mimicry” describes a phenomena whereby some pathogens like viruses, yeast or bacteria, can evoke an immune response because they have enough similarity to the body’s own proteins to cause an autoimmune reaction. This is evident in a number of autoimmune disorders associated with certain HLA genotypes (susceptibilty genes) such as in rheumatoid arthritis (RA) or Ankylosing Spondylitis (AS). In some cases of AS or RA, gut bacteria that passes through the gut barrier and is recognized by the immune system as “similar” to joint tissues. As the immune system reacts to the bacteria to eliminate it, it actually attacks the joint isssue. In the case of a rotavirus infection, a common cause of gastrointestinal infection and inflammation (gastroenteritis), it is seen as a similar to the gialdin molecule and the body is triggered into the same intolerance, or immune reaction as stimulated by gliadin in susceptible individuals. Antibodies to this celiac peptide also recognize and bind to the rotavirus protein (VP-7) and cause the same leaky gut/intestinal permeability that is a key step in the immune activation associated with CD.(19) Thus, viral infection and/or tissue damage in the intestine may cause inflammation and immune reactivity, leading to loss of tolerance for gluten. These recent studies on the link of a viral trigger in CD, provide the first indication that a high frequency of rotavirus infections may increase the risk of celiac disease autoimmunity in childhood in genetically predisposed individuals.(18) “Our findings show that in active celiac disease, a subset of anti-transglutaminase IgA antibodies recognize the viral protein VP-7, suggesting a possible involvement of rotavirus infection in the pathogenesis of the disease, through a mechanism of molecular mimicry.”(19) Bacterial (dysbiosis) and yeast (i.e. candida albicans) overgrowth are common patterns in digestive disorders-either as a primary infection causing digestive or systemic health problems, a concommitant or byproduct of various intestinal disease processes, or as a residual of other causative factors like antibiotics. In the case of Candida albicans, a fascinating dynamic occurs between Candida and the reactive antibody tTG (tissue Transglutaminase) IgA. Apparently Candida contains proteins-peptide sequences, that are identical and very similar to those found in gluten, including gliadin. Candida infections or overgrowth, in individuals that are genetically inclined to be GI, can trigger the same tissue transglutaminase and endomysial enzyme antibodies involved in celiac disease.(20) This study and several others illustrate that Candida albicans can “mimic” gliadin, and that under certain conditions, may result in the reactive immune response typical of GI. There is not enough research yet, to unequivocally establish the candida link to CD as a trigger. However, the lack of sufficient evidence, to draw firm conclusions does not rule it out either. Based on my own clinical observations, gluten sensitive individuals that address “overgrowth” of unhealthy gut bacteria and yeast, wind up with better tolerance and reduced titers of gut SIgA gliadin. Bacterial overgrowth of the small intestine may also inhibit the success of a gluten free diet and recovery from CD.(21) This posting, Gluten Intolerance-What Your Doctor May Not Tell You, is posted by Ralph S. at Wellsphere.com

What is the atopic march?

Sat, 7 Sep 2008 13:31:00 GMT

posted by maracow2
The atopic march refers to the natural history of atopic diseases. They include eczema (or atopic dermatitis), food allergies, allergic rhinitis (or hay fever), and asthma. There is a typical progression when you look at the prevalence of these diseases over time in a large population. (Photo from reference 4.) In genetically predisposed infants, usually eczema is the first manifestation of allergic diseases. Food allergies may also be present. Both peak by age 2 years of age and then fall off. Respiratory diseases rise and persist. 2/3 of patients with atopic dermatitis develop allergic rhinitis later in life. 1/2 of patients with atopic dermatitis develop asthma later in life. The stronger the family history of allergic diseases, particularly in the parents and grandparents, the greater likelihood one of their offspring will be affected. It's chance. The stronger one parent is affected by allergic diseases, any or all of atopic dermatitis, food allergies, allergic rhinitis, and asthma, the greater chance that each offspring will be affected similarly. Finally, to see yours or your child's future, look into the crystal ball, our own parents and grandparents health. If they have had severe or lifelong allergies and the same allergic genes have been passed on, the odds favor history repeating itself. If you can forsee this happening to yourself or your children, take preventative action now!!! Do whatever you can to reduce your or your children's allergic reactions. Consider avoidance and allergen immunotherapy. Regretably, at this point in time, medications have not been shown to alter the natural history of allergic diseases. Medications can very effectively minimize the signs and symptoms, but the underlying fire of atopy still burns on.

References:
1. Saarinen UM, Kajosaari M. Lancet 1995; 346:1065–1069.
2. Spergel JM, Paller AS. J Allergy Clin Immunol 2003; 112 (suppl 6): S118-S127.
3. Homburger HA. Arch Pathol Lab Med 2004; 128: 1028-1031.
4. Wahn U. What drives the allergic march? Allergy 2000 Jul;55(7):591-9 or http://www.worldallergy.org/professional/allergic_diseases_center/allergic_march/