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Celiac.com 06/16/2016 - Do you realize that metabolic and emotional stress, hormonal imbalance and food sensitivities all impact digestion? Many individuals believe that once they stop eating gluten, digestive disorders will disappear. Nothing could be further from the truth as we take a closer look at gastroenterology and the link between the gut and brain. The adult gut has between 10 trillion and 100 trillion bacteria that make up the microbiome or surface of the intestines. The goal for digestive wellness is to be sure that there are more GOOD bacteria than BAD bacteria in the microbiome. Food choices, antibiotic use and lifestyle play an important part in creating that balance. Endocrine disrupting chemicals in plastics, along with artificial sweeteners all influence the bacteria or microbiome levels. The bacteria content of the gut begins at birth. A vaginal delivery results in a microbiome from the mother while a cesarean section produces a microbiome from everyone who handles the infant. Gut bacteria levels are also influenced by breast feeding versus the use of infant formula. Diets deficient in fruits and vegetables mean less antioxidants are consumed so free radicals can destroy digestive and immune function. In addition, fruits and vegetables provide fiber for bacteria to grow on. Current research from the Journal of Clinical Nutrition indicates high fiber diets yield more bacteroides bacteria growth that helps control body weight. Low fiber diets result in more firmicute bacteria which produces weight gain and can lead to obesity. Microbiological safety in fresh produce continues to gain prominence in the media. Fresh cut, RTE (ready to eat) produce in convenient packages leads the way in food safety recalls. Fruits and vegetables are prone to microbial contamination from irrigation water, soil, fertilizers, insects, animal feces and field workers during pre-harvest processing. After harvest, the washing and sanitation procedures lack oversight. Remember to wash all raw fruits and vegetables to minimize food poisoning potential. Listeria monocytogenes is one of the leading causes of death from food borne illness. It is found in raw milk, cheese, and packaged deli meats. Flu-like symptoms can last days to weeks, and in pregnant women listeria infection can lead to miscarriage. Noroviruses make the news regularly, especially on cruise ships. Common food sources include raw produce and shellfish such as clams, mussels, scallops and oysters. Symptoms begin as early s 12 hours after ingestion and the malaise disappears 3 to 4 days later. Salmonella continues to plague many with chills, nausea, joint pain and headaches beginning 12 hours post ingestion. Eggs, poultry and raw produce are major sources of salmonella. Probiotics are an important addition to the celiac diet for balancing the bacteria levels in the GI tract. They should be taken WITH food to reduce the degradation in an acid stomach. Research has shown that urinary tract and vaginal infections have an improved management rate when lactobacillus and bifidobacterium multi-species probiotics are used. Probiotics are live bacteria which have been shown to reduce inflammation in the gastrointestinal tract. They also reduce intestinal permeability and influence serotonin and melatonin production in the gut. So since the human gut contains 10 times more bacteria than all the human cells in our body, keeping a healthy balance of bacteria in the gut is critical for digestive wellness.

Celiac.com 05/08/2009 - In 1996-1997, in an effort to test a hypothesis by scientist Karl Ludvig Reichelt, Norwegian researchers began a long-term study of 23 children aged 4 to 11 from the southwestern Norwegian town of Stavanger. All of the children suffered from hyperactive disorders including ADHD. All children showed abnormal levels of peptides in their urine. Dr. Reichelt believed that metabolic disorders impair the effective breakdown of certain proteins in children and thereby cause mental problem, such as hyperactive disorders. Related international research has established links between protein disorder and the conditions of autism and schizophrenia. A growing number of studies also hint that some cases of ADHD are tied to digestive disorders. Data from this Norwegian study supports the idea that ADHD may also arise from a digestive disorder. This study indicates that consumption of certain foods, such as milk and gluten, may contribute to ADHD in children who lack the enzyme that breaks down proteins like casein, a component of milk--which also helps in the formation of cheese. Interestingly, when children who lack this enzyme eat foods that require the enzyme to properly digest proteins like casein, their brains experience an opium-like effect, which might explain at least some of the spaciness and impaired attention these kids exhibit. According to Reichalt's theory, hyperactivity can be controlled by reducing the intake of foods that require the presence of this missing enzyme to properly break down the offending proteins. In the study, 22 of the 23 children were placed on strict milk-free and/or gluten-free diets. They were taken off milk products and other foods containing casein. All exhibited a rapid improvement in general well-being, including improved mental health and general behavior, improved attention-span and better learning abilities. After a year, 22 of the 23 families reported clear improvements in their child's behaviour and attention-span. When the kids were taken off their diets, their symptoms returned nearly immediately. Before changing their diets, most of the children were taking medications, like Ritalin, to treat their symptoms. After their diets were established, their medications were discontinued. By 2004, a number of the children had ceased their diets for various reasons and some have returned to medication. Still, six children remained milk-free and several had also cut out gluten, which is found in wheat, rye, barley and to some extent oats. Due in part to the small sample size, and limited amounts of data from comprehensive studies on the number of ADHD children who suffer from peptide-breakdown abnormalities, the study has been met with a certain resistance among the medical community, where most doctors still believe that the evidence best supports medications like Ritalin as the best way to treat the ADHD. Still, the results carry weight among the parents, and among the Norwegians, as hundreds of other Norwegian children with ADHD, mainly in and around Stavanger, have in recent years been put on milk-free and/or gluten-free diets to help control ADHD and related disorders. Agence France Presse 2008. Yahoo! News 2008

The following report was prepared by Ann Whalen, celiac, and editor/publisher of Gluten-Free Living , which is a bimonthly newsletter for celiacs - Gluten-Free Living, PO Box 105, Hastings-on-Hudson, NY 10706. On March 10th, more than 20 members of the celiac community and celiac disease specialists (see list at end) attended a meeting of the Digestive Diseases Intra-agency Coordinating Committee, a part of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). The meeting, held to update the current status of Celiac Disease, was chaired by Jay Hoofnagle, M.D., Director of the Division of Digestive Diseases and Nutrition at the NIDDK. At the meeting, presentations were made by Martin Kagnoff, M.D., Joseph Murray, M.D., Alessio Fasano, M.D., and Frank Hamilton, M.D. Dr. Kagnoff is a gastroenterologist and Professor of Medicine at the University of California, San Diego. He spoke about his research into the genetics of Celiac Disease, focusing on the pathogenesis. Dr. Kagnoff is well known for his research into the genetics of Celiac Disease, and several of his studies have been funded by the NIH. Dr. Murray, Associate Professor of Medicine and clinician at the University of Iowa Hospitals and Clinics, described his experience with Celiac Disease both in Iowa and in Ireland, noting that his interest in celiac disease is clinical. He emphasized what he called the Classic II symptoms, meaning the actual symptoms patients have today and not the Classic symptoms many doctors may be familiar with. He said the rate of diagnosis is proportional to suspicion. Dr. Murray described the celiac disease experience at the University of Iowa from 1985 to 1997, presenting statistics that indicated a steep increase in diagnosis. At our institution, Celiac Disease is an adult disease, he said, and is now seen as frequently as Crohns Disease. Anticipating the question, Why look for Celiac Disease?, Dr. Murray gave his reasons: preventing lymphoma and osteoporosis, as well as resolving fatigue and nonspecific symptoms and shortening the current significant delays in diagnosis. Dr. Fasanos presentation was called Where Have All the American Celiacs Gone? He described what has happened in the field of celiac disease in various parts of the world, including some parts of the United States, but emphasized the European experience. Dr. Fasano noted that plans are already underway in Italy to screen all seven-year-olds in 1999. Dr. Fasano explained why an epidemiology study is critically needed in this country. He pointed out the benefits of such a study for four groups: The American health care community: lower health care costs, increased awareness of celiac disease and more knowledge of its protein manifestations in the US Participating physicians: publications, more patients and increased credibility. The American people: the prevalence will be established and celiac disease will be diagnosed more quickly. Celiac Patients: free screening of first-degree relatives, federal support for dietary and drug regulations, an improved food supply, stronger local support groups and more funding for celiac research. Dr. Fasano added that such a study, whatever its findings, would end in a win-win situation for everyone. If the study shows that celiac disease is underestimated in this country, patients will benefit as physicians begin looking for the problem with the knowledge that they might well find it. If the study shows celiac disease is indeed rare in the United States, its even more exciting because we will be able to figure out why. Dr. Hamilton, chief of the Digestive Diseases Program Branch at the NIDDK, briefly described the celiac disease research, to date, that has already been funded by the NIH. He said $1.4 million has been granted for such research, adding that over the last five years, we have seen growth in the funding of Celiac Disease. He said he was pleased funding has increased, and felt a lot of work has to be done. Dr. Hamilton ended by saying, Todays meeting will serve as an impetus for a partnership between the National Institutes of Health, academe, and the lay groups to foster more research. He added that it was important for the investigators and support group representatives present at the meeting to get the word out, referring to information about Celiac Disease. These talks were followed by a round table discussion, between the members of the committee and the presenters. Later, audience comment was invited. The committee showed an interest in the current adult nature of the disease, the changing symptoms, current testing methods, and identification of the most critical research needs. Patients who spoke were anxious to let the committee know what they felt were the important concerns in the real world. At the end of the meeting, Dr. Hoofnagle said his division will prepare a short, pithy plan, then present it to Drs. Kagnoff, Murray and Fasano. He noted that the important issues are pathogenesis, delivering the message to physicians, clinical research issues and pediatric health concern. Some Quotes from the Meeting Elaine Monarch: There is a general lack of knowledge, awareness and interest in Celiac Disease among the medical profession. We celiacs can go for years with substantial symptoms but not diagnosis...The cost to the medical community is enormous. Joseph Murray, M.D.: There is more than one gene involved in Celiac Disease. Most Europeans are homogenous. Here we have a mongrelized population. What happens when you mix? How much does it change? Our mongrelized population may be at risk at a later age. Martin Kagnoff, M.D.: The issue of other genes is not at all clear. Like Joe (Dr. Murray), I see adult celiacs. Their time delay to diagnosis is not exaggerated, but what is striking is the lack of knowledge of doctors, even at the University of California. They really are not aware of this disease. Alessio Fasano, M.D.: We receive 10-15 calls a day. The vast majority are self diagnosed. They say, I know more than my gastroenterologist. Peter Green, M.D.: We need to emphasize education of gastroenterologists. At my institution (Columbia-Presbyterian Medical Center in New York City), doctors are not used to looking at the duodenum...We need to educate many levels of the medical community and tell them, If you dont recognize something, take a biopsy. Sue Goldstein: Im concerned about the people who have not yet been diagnosed and the reasons why a physician wont consider Celiac Disease. It all boils down to, its rare and you cant have it. In addition to the speakers, the following were among those who attended: Phyllis Brogden, celiac, founder and chairperson of the Greater Philadelphia Celiac Sprue Support Group. Winnie Feldman, celiac, Celiac Disease Foundation Kenneth Fine, M.D., gastroenterologist/ researcher at Baylor University Medical Center in Dallas. Al Fornace, M.D., celiac, National Cancer Institute Sue Goldstein, celiac, founder and advisor, Westchester Celiac Sprue Support Group Peter Green, M.D., clinician/researcher at Columbia-Presbyterian Medical Center in New York City. Joanne Hameister, celiac, former chairperson, Western New York Gluten-Free Support Group Ivor Hill, M.D., clinician/researcher at Bowman Gray School of Medicine, Winston-Salem, North Carolina. Beth Hillson, celiac and proprietor of the Gluten-Free Pantry. Karoly Horvath, M.D., clinician/researcher at the University of Maryland School of Medicine in Baltimore. Marge Johanamen, celiac, CSA Kentucky state coordinator Pam King, University of Maryland Bob Levy, Celiac Research Foundation Ruth Levy, spouse Jax Lowell, celiac and author of Against the Grain Elaine Monarch, celiac, founder and Executive Director of the Celiac Disease Foundation Selwyn J. Monarch, Board of Directors, CDF Diane Paley, celiac, governing board CSA/USA Michelle Pietzak, M.D., pediatric gastroenterologist at Childrens Hospital, Los Angeles Connie Tur, celiac, president Greater Louisville Celiac Sprue Support Group

AU- Baudon JJ; Mougenot JF; Didry JR CS- Unite de Gastroenterologie Pediatrique, Hopital Trousseau, Paris, France. JN- J Pediatr Gastroenterol Nutr; 6 (2) p244-51 PY- Mar-Apr 1987 AB- The lymphoblastic stimulation test (LST) with cows milk proteins was performed in 114 infants. In 42 infants, digestive intolerance to cows milk proteins (CMI) was suspected; withdrawal/re-challenge test confirmed intolerance in 34, and disproved it in the other eight patients. Of the other patients, 17 had acute gastroenteritis, 11 had postgastroenteritis sub-acute diarrhea, 12 had gluten intolerance, 14 had intractable diarrhea, and 18 had no digestive disorders. Of the 34 infants with CMI, 27 (79%) had a positive LST to one or more cows milk proteins. Of the 34 positive LST patients, 12 also had Soya intolerance; nine of these 12 infants (75%) had positive LST to Soya. Of the eight infants who had a negative cows milk re-challenge test, five (62%) had a positive LST. In the other groups, results were also positive in 12-27% of those having diarrhea of infectious origin or gluten intolerance, and in none of the infants without digestive disorders. Of the 14 cases of severe intractable diarrhea, 12 (86%) were also LST-positive, but CMI could not be excluded. LST was positive, particularly in diarrhea of neonatal origin. Lymphoblastic stimulation was induced more frequently by casein than by beta lactoglobulin, and least frequently by alpha lactalbumin. In conclusion, LST is frequently positive in CMI, but is not sufficiently specific to be a reliable diagnostic examination.

Dr. Kelly, who is a refractory sprue specialist, had interesting insights into Celiac Disease. He first described once having a patient say to him that eating at a restaurant or food take out is the gastronomic equivalent of promiscuous and unprotected sex because (you) dont know where food has been, who else its been with, and what you might get from it. Dr. Kelly explained that his job when seeing a patient with possible Refractory Sprue is to first confirm that the patient really has Celiac Disease and is adhering to a gluten-free (gluten-free) diet. He explained that some patients would rather prefer an iron shot than adhere to a gluten-free diet and that sensitivities vary which removes another drive to say gluten-free; however, if symptomatic, he has found that the patient has the motivation to adhere. Hes even had to recruit and train dieticians to take an interest in Celiac Disease. He said that Celiac Disease or Gluten Sensitive Enteropathy is driven by activated lamina propria T-cells to whom gliadin is being presented through their T-cell receptors. In Refractory Sprue, he said that the cells are evident at intraepithelial lymphocytes rather than lamina propria lymphocytes and they no longer require gluten in order to be driven. So, theyre on auto-pilot. He emphasized that this is a rare disease and advised that doctors get a competent dietician to help patient adhere to diet. If the concern is that the patient is adhering but is not responding, Dr. Kelly advised doctors to think of other disorders masquerading as Celiac Disease, especially if patient is IgA, EmA (anti-endomysial) negative or if not HLA DQ2 or DQ8 (common Celiac genes) positive. He added that not every flat mucosa consistent with Celiac Sprue is Gluten Sensitive Enteropathy but that there can be a differential diagnosis such as cow protein intolerance. He said that there are unusual immunologic disorders that can be mistaken for sprue or refractory sprue. He said that doctors should consider these if the patient was not IgA endomysial or human tTg (transglutaminase) antibody positive at diagnosis. He explained that the positive predictive value of those tests are so strong that really its in some ways has a higher positive predictive value than even biopsy that you dont get very, very if any false positives at least by the immunofluorescence assay. So, if theyre negative at diagnosis considering other possibilities and this is one instance where HLA typing actually may be clinically useful if you have a patient you think has Celiac Sprue but isnt behaving or responding as you would expect with a gluten free diet and you ask do they really have Sprue. If they are HLA DQ2/DQ8 negative, then the likelihood of them having gluten sensitive disease is much, much lower. He said that serology (blood tests) were helpful but not be relied upon. He said that IG antibody levels against gliadin, or tissue transglutaminase tend to drop fairly quickly usually within 2 to 3 months provided they (patient) were positive to begin with. ...The IgG takes much longer so it tends to be less useful and of course, if they are IgA deficient, they wont be IgA positive to begin with and you cant use then. Even if their antibody levels are high to begin with, and remain high, that to me means that theyre still exposed to the antigen and they still have T-cells. Their lamina propia T-cells are still being driven by the antigen. But if theyre negative, Im afraid that its not particularly sensitive and low levels of gluten exposure may result in symptoms and poor response would not necessarily be identifiable by antibody.... Dr. Kelly said that patients with subtle manifestations of Celiac Sprue who have been previously diagnosed with irritable bowel or host of other disorders are now being more frequently seen. He said that there has been a lot of discussion in the past year about Celiac Sprue being misdiagnosed as Irritable Bowel Syndrome. Dr. Kelly also described the circumstance that patients with Celiac Sprue show improvement both serologically (blood) and histologically (biopsy) but their symptoms persist. He said that doctors need to be aware that just because a patient has gluten sensitive enteropathy doesnt mean they cant get another gastrointestinal disorder. He gave examples such as microscopic colitis and what he called a classical association, hyperthyroidism, or something else which could also cause diarrhea and weight loss. Dr. MacDonald, a celiac specialist, discussed new insights into the pathogenesis of Celiac Disease. Dr. MacDonald discussed primarily the role that other factors besides the DQ2 (gene) molecule, control the T-cells in the gut mucosa which produce the lesion or flat mucosa. In the genesis of the lesion, he explained how the T-cell immune response in the gut wall results in a gut shape of tall villi and short crypts which results in an increase in mucosa volume with flat mucosa and an increase in mucosa thickness. My husband, a PhD immunologist, interpreted this for me; He said that imagine the villi are the hill and the crypts are the valley. The valley is where things grow. The oldest cells are at the tip of the hill and as cells mature, they get transported up the hill. As damage occurs, the hill gets chopped down, valleys get deeper making more area for cells to replicate. Dr. MacDonald assumed that because the epithelium is turning over so fast in Celiac Disease that the lamina propria, the shape of the gut itself would be turning over, but actually the data says otherwise. The flat mucosa isnt turning over at all, ... a rather stable shape, its not really dynamic, its remodeled. He said that putting Celiacs on a gluten free diet may take them a long time to get better, because it takes a long time for this to go back because this is actually stable, its remodeled.... Dr. MacDonald explained that gliadin peptides associate with DQ2 and DQ8 molecules putting themselves into the grooves to be seen by T cells. However, he gave an instance where a particular gliadin peptide doesnt fit well into the pockets of DQ2 to be seen by T cells. Tissue Transglutaminase or Ttg deamidates (removes chemical groups on certain amino acids and allows peptide to bind to DQ2) this peptide in terms of glutamine into glutamic acid, gives a negative charge, fits very well into pocket, and binding increases 100 fold. Tightness of the binding ... controls the specificity and strength of the T-cell response. Dr. MacDonald also described the case of a woman with cancer who was treated with interferon. He said that she had the endomysial antibodies, was DQ2 positive, and had Celiac Disease; however, he cited that the reason why the Celiac Disease was not found earlier was that interferon alpha/gamma used to treat the cancer may have precipitated clinical Celiac Disease. He added that her son was later diagnosed with Celiac Disease as well. It was also eluded to that a viral infection like a gastrointestinal flu would stimulate or produce interferon alpha. Dr. Alessio Fasano from the Center for Celiac Research at the Univ. of Maryland also explained that its not just the gluten antigen and genes (i.e., HLA DQ2 or DQ8) but an added element like that alluded to by Dr. MacDonald such as a viral infection which can result in Celiac Disease. Dr. Fasano described a study performed on North African children who were thought to have symptoms resembling infectious disease with symptoms like anemia and diarrhea were found to have Celiac Disease at the rate of 1 in 18. He said because they have a high consumption of grains and seem to carry a high frequency of the genetic elements, he felt that non-profit organizations may intervene to help institute a gluten-free diet in this Celiac population. Dr. Fasano mentioned a study performed in Southern California which found Celiac Disease in 2 to 4% of people with symptoms or associated diseases and 5% in family members of Celiacs. Dr. Fasano stated that the overall prevalence is 1 in 266 which he said on a global scale, by far this is the most frequently genetic disease of human kind. Fasano said that in the 1970s, it was thought Celiac Disease was confined to the pediatric population but that since 1998 there has been a surge in adult versus child cases. He believes that the disease may have been overlooked in adults because adults have more atypical symptoms like anemia, osteoporosis, abortion that would NOT see a Gastroenterologist but would see an internist, reproductive OBGyn, endocrinologist, etc. Dr. Fasano said that if the iceberg idea is diarrhea, weight loss, abdominal symptoms, you will surely crash into the iceberg, but he proposed, what about the people who have joint pain, constipation, fatigue, and so on. He said that if you are willing to see the monument of the problems, you have to get down under the water because in the vast majority of cases, Celiacs will not see a Gastroenterologist and that doctors must be aware of those under the water. Dr. Fasano during the question and answer session listened to a doctor in the audience describe a patient with diarrhea and schizophrenia whose diarrhea and schizophrenia resolved when put on a gluten-free diet. The doctor didnt know what to do with the patient but explained that the patients background, being of Irish descent, gave him a red flag into the possibility of Celiac Disease. Dr. Fasano in response described how there can be a change in behavior such as attention deficit disorder, depression, and schizophrenia. He described a theory that the epitopes of gluten could cross the intestinal barrier, cut into the bloodstream, and cross the blood brain barrier. He believes that there is a clear association between Celiac Disease and change in behavior.