Category Archives: Research

CeliAction Study Extension

I sincerely hope to be back to blogging soon. In the meantime I wanted to let you all know that the CeliAction Study has been extended through September 2014, so it is not too late to participate. All questions and comments on this post will receive responses from a CeliAction Study representative. I hope you are all having a great summer!  -Jess

celiactionaugust

Did you know there isn’t a single drug approved to treat celiac disease? Currently, attempting a gluten-free diet is the only option recommended by doctors, but a clinical research study called the CeliAction Study is researching if an investigational drug improves any symptoms of the disease.

You may qualify for the CeliAction Study if you:

  • Have been diagnosed with celiac disease by a healthcare professional
  • Are attempting to be on a gluten-free diet
  • Have experienced at least one moderate or severe symptom of celiac disease in the past month

If you participate in the CeliAction Study, you:

  • Will be able to maintain your current diet restrictions
  • Will be provided with study-related care at no cost
  • Do not need medical insurance to take part
  • May be compensated for time and travel
  • Will help advance medical research for celiac disease

To learn more about this research study and see if you qualify, visit www.CeliActionStudy.com
or call 1-855-3333-ACT.

Email This Page
doctorpatient

Celiac Disease: 10 Things for Doctors and Patients to Know

I came across this list on PubMed the other day, and although I posted it on Facebook, I thought it might be worth sharing on here for everyone else. It comes from an abstract titled “Celiac Disease: Ten Things that Every Gastroenterologist Should Know.” It was written by Drs. A. Oxentenko and J. Murray (from the Mayo Clinic) and published online in the journal “Clinical Gastroenterology and Hepatology” on July 19, 2014. I usually don’t like “Top 10″ lists, but it has some good information for both gastroenterologists and their patients. Just for clarification, the quoted statements come directly from the publication and the words in italics are mine.

  1. “The IgA TTG is the single best serologic test to use for the detection of celiac disease (CD).” Most celiac antibody panels (blood tests) include the TTG IgA. However, it is possible for a person to have a negative TTG IgA and still have celiac disease. False negatives can occur in small children, people with a condition called selective IgA deficiency, and in people who are tested after already starting on the gluten free diet.
  2. “Celiac disease can be recognized endoscopically, and water immersion enhances villi detection, although a normal endoscopic appearance does not preclude the diagnosis.” If an endoscopy is done to look for celiac disease, biopsies also need to be done.  The damage from celiac disease is often microscopic. I have met people whose GI doctors did endoscopies and told them they did not have celiac without doing any biopsies!
  3. “It is recommended that four biopsies be taken from the second part of the duodenum, and two bulb biopsies taken at the 9 and 12-o’clock positions to maximize the sensitivity for histologic confirmation of CD.” The intestinal damage from celiac disease can be patchy, so if not enough biopsies are done, it can be missed.
  4. “Consider serologic testing of first-degree relatives, patients with type 1 diabetes, Down’s, Turner’s and William’s syndromes, as well as those with premature osteoporosis, iron deficiency, abnormal liver biochemistries and other manifestations of CD.” First degree relatives are parents, siblings, and children of those with celiac disease.  Screening in high-risk people also needs to be repeated periodically, as celiac disease can develop at any time during one’s life.
  5. “Patients already on a prolonged gluten-free diet (GFD) should be tested for the presence of HLA DQ2 or DQ8, thereby avoiding the need for further evaluation of CD in non-allelic carriers.”This can be very helpful in people who go GF prior to being tested for celiac disease. If one does not carry the 2 main genes, the chances of having celiac disease are very low (between 1-2% of celiacs are DQ2 and DQ8 negative) and non-celiac gluten sensitivity is much more likely than celiac. 
  6. “The basic treatment of CD is a strict, life-long GFD, enabled by an expert dietitian.” Don’t think I need to explain this one!
  7. “Newly-diagnosed adults with CD should be assessed for micronutrient deficiencies (iron, B12, folate, zinc, copper), fat soluble vitamins deficiencies (vitamin D) and bone densitometry.” Osteopenia (low bone mineral density) is rather common. Vitamin and mineral levels should be assessed at follow-up appointments, as well, to make sure there has been improvement.
  8. “All patients diagnosed with CD should have clinical follow-up to ensure response and adherence to a GFD.” From what I have read, this should happen between 6 and 12 months after going on the gluten-free diet.
  9. “In those with persistent or relapsing symptoms, the robustness of the original diagnosis should be reviewed, gluten exposure sought, and a systematic evaluation for alternative and associated diseases.” I was given the opportunity to write about this problem, which is called nonresponsive celiac disease, in Gluten-Free Living magazine. You can find my article here. Although the most common cause of continued symptoms is accidental gluten exposure, In some cases people do not get better because they were misdiagnosed with celiac disease in the first place!
  10. “Evaluate those with refractory disease for malignant transformation.”  People with refractory celiac disease are at risk for lymphoma. This is why it is important to get medical follow-up if you do not get better on the gluten-free diet.

Thanks for reading! I hope you are all having a nice summer and I really appreciate your comments, emails, questions, etc. Please keep them coming!

Email This Page
DNA

Celiac Disease Autoimmunity

I first came across the term “celiac disease autoimmunity” a few weeks ago as I read summaries of the article “Risk of Pediatric Celiac Disease According to HLA Haplotype and Country” that was published in the July 3, 2014 issue of the New England Journal of Medicine (NEJM).

Based on my reading and interpretation of the article, it seems that celiac disease autoimmunity is interchangeable with the more commonly used term “potential celiac disease.” Both are used to describe cases in which people have abnormally high levels of celiac antibodies (TTG IgA)  in their blood but their small intestinal biopsies do not show changes consistent with celiac disease. In other words, there is an autoimmune response to gluten that has yet to cause destruction to the villi of the small intestine. For the sake of this study, the subjects had to have abnormally high TTG IgA levels on 2 separate occasions, at least 3 months apart, to be labeled as having celiac disease autoimmunity.

The results published in NEJM come from the multinational TEDDY study, which is prospectively following a large cohort of children who are at genetically at risk of developing Type 1 (juvenile) diabetes mellitus.  Since some children with both Type 1 diabetes and celiac disease share the same “at-risk” genes, HLA-DQ2 and DQ8, the researchers have also been able to follow a large group of genetically-susceptible children for the development of celiac disease. The study is ongoing and subjects are being followed for the development of both diabetes and celiac disease from infancy until age 15. This is one of many papers that have already come from the TEDDY study.

Thus far, 6403 study subjects have been found to have genes that predispose to celiac disease.  Subjects have been placed into 4 risk groups:

-HLA DQ2/HLA DQ2 (homozygous for DQ2)

-HLA DQ2/HLA DQ8

-HLA DQ8/HLA DQ8 (homozygous for DQ8)

-HLA DQ8/HLA DQ4

As you can see, the first 3 groups of kids all have 2 copies of celiac-risk genes, and the 4th group has only one copy of DQ8, so only one gene associated with celiac disease. Subjects’ testing for celiac disease autoimmunity started at age 24 months and has been repeated every year. In all, 786 of the 6403 (11%) at risk subjects were found to have celiac disease autoimmunity (elevated blood TTG IgA antibodies at least twice) at time of data analysis Overall, 25% of the children with celiac disease autoimmunity had a diagnosis of celiac disease by age 3.

The researchers broke down the risk of both celiac disease autoimmunity and celiac disease by genes and found the following risks by age 5:

Celiac Disease Autoimmunity Risk in Children with Celiac Genes by Age 5:

HLA DQ2/HLA DQ2 (homozygous for DQ2): 26%

HLA DQ2/HLA DQ8: 11%

HLA DQ8/HLA DQ8 (homozygous for DQ8): 8%

HLA DQ8/HLA DQ4: 3%

Celiac Disease Risk in Children with Celiac Genes by Age 5:

HLA DQ2/HLA DQ2 (homozygous for DQ2): 11%

HLA DQ2/HLA DQ8: 3%

HLA DQ8/HLA DQ8 (homozygous for DQ8): 3%

HLA DQ8/HLA DQ4: less than 1%

Children with both celiac disease and celiac disease autoimmunity were found to be at a higher risk of having diabetes than the general population (1% for celiac disease autoimmunity and 2% for celiac disease v. 0.3% risk for general U.S. population).

In summary, in this large study, over 25% of children with the DQ2/DQ2 genotype were found to have celiac disease autoimmunity by age 5 and greater than 10% with DQ2/DQ2 were diagnosed with celiac disease by age 5.  Over half of these children had no symptoms of celiac disease, therefore, there is a good chance that many of these diagnoses would have been missed if these children had not been subjects in this study.

After reading this article I am a much stronger proponent of genetic testing of children at risk for celiac disease, if possible. And, as my husband and I both carry genes associated with celiac disease, I feel much less guilty for making my own kids get screened for celiac disease, via TTG IgA blood testing, every 2 years (you can see my post from May 2014 for more details). Lastly, I feel much more at peace for making my at-risk youngest go through having an endoscopy and small bowel biopsy earlier this summer. The statistics from this study are definitely eye-opening.

Reference: Liu E, Lee HS, Aronsson CA, et al. TEDDY Study Group. Risk of pediatric celiac disease according to HLA haplotype and country. N Engl J Med. 2014 Jul 3;371(1):42-9.

Also, if you are a research geek like I am, here are some other interesting findings from the TEDDY study thus far (found via a Pubmed.gov search):

  • The HLA-DQ2/2 genotype may predispose to obesity among 2-4-year-old children.
  • Between 15% and 20% of the infants in the study were introduced to solid foods before the age of 4 months.
  • The median age of early-onset diabetes is at 2.3 years. 33% of the subjects with an early diagnosis of diabetes had no symptoms of diabetes.
  • Findings have not supported the presence of viremia (recent viral infection) around the time of seroconversion in young children with rapid-onset type 1 diabetes.
Email This Page
gluten challenge

Hope for a Less Challenging “Gluten Challenge”

The current “gold standard” tests for celiac disease include testing for celiac antibodies in patients’ blood and performing an endoscopy to obtain small bowel biopsies. In order for these tests to be accurate, one has to be eating gluten up until the time of testing.  If a patient is already on the gluten-free diet when these tests are done, the diagnosis of celiac disease can easily be missed.

Since starting this page I’ve encountered many people who have decided that they’d like to be tested for celiac disease after starting on the gluten-free diet.  Per the celiac disease experts, a “gluten challenge” must be performed in these cases to assist in the diagnosis of celiac disease. A gluten challenge requires eating foods containing gluten for a prescribed period of time prior to an endoscopy and/or blood testing for celiac disease. The length of time and amount of gluten that need to be consumed for a gluten challenge vary from source to source. Here are some examples of different recommendations for a gluten challenge (current as of July 5, 2014):

University of Chicago Celiac Disease Center: “For a gluten challenge we recommend eating 1/2 slice of bread or a cracker each day for the duration of the challenge. Prior to blood testing we recommend 12 weeks of eating gluten. Prior to an endoscopic biopsy we recommend 2 weeks of eating gluten. In the case of a severe reaction to gluten, a medical professional may opt to shorten the 12-week challenge and move immediately to an endoscopic biopsy.”

Celiac Disease Center at Columbia University: “In individuals who are willing to further pursue the question of whether they have celiac disease, we will advise a gluten challenge. This consists of ingesting at least 4 slices of bread a day for one to three months followed by an endoscopy and biopsy. There is no evidence that following antibody tests is beneficial in establishing a diagnosis of celiac disease because these tests are not sensitive in this setting.”

Celiac Disease Center at Beth Israel Deaconess Medical Center: “Gluten is reintroduced into the diet and after a period of time (ideally 6 to 8 weeks if the challenge can be tolerated for that long) blood tests and an intestinal biopsy are performed. If the gluten challenge is not tolerable for the full 8-week period blood tests and biopsy can be performed sooner but this can lead to a false negative result.”

In addition, Dr. Leffler and colleagues published a paper in 2013 showing that the majority of patients with celiac disease will test positive after eating >3g gluten/day for 2 weeks. A typical piece of wheat bread contains about 5g of gluten.

Despite all of the confusion, there is hope on the horizon for a shorter gluten challenge in the future.  Researchers at the Walter and Eliza Hall Institute in Australia have been developing a blood test that measures gluten-reactive T cells, immune cells that increase in response to gluten in those with celiac disease, via cytokine release assays.  In a pilot study published earlier this year, patients with celiac disease had a significant jump in blood levels of gluten-responsive T cells, compared to controls, after only 3 days of consuming gluten. Per Dr. Jason Tye-Din, one of the researchers working on this test, “We hope that larger studies can validate these findings and establish its role in the diagnosis of celiac disease.” For the sake of my gluten-light kids, and everyone else who is in a similar situation in regards to diagnosis, I hope he is right.

A press release regarding the study can be found here.

Out of curiosity, have any of you been diagnosed with celiac after doing a gluten challenge? If so, do you remember how much gluten you had to eat and for how long prior to testing?

Full reference:

Ontiveros NTye-Din JAHardy MYAnderson RP. Ex-vivo whole blood secretion of interferon (IFN)-γ and IFN-γ-inducible protein-10 measured by enzyme-linked immunosorbent assay are as sensitive as IFN-γ enzyme-linked immunospot for the detection of gluten-reactive T cells in human leucocyte antigen (HLA)-DQ2·5(+) -associated coeliac disease. Clin Exp Immunol. 2014 Feb;175(2):305-15.

 

Email This Page

Update on the CeliAction Study

The CeliAction Study will be continuing to enroll subjects with celiac disease through this summer. This medication has the potential to help many of us with celiac disease. All questions and comments will be answered by a CeliAction study representative, as this is a sponsored post. Thank you for reading!   -Jess

celiaction

 

National study to help advance celiac disease research

The CeliAction Study is a clinical research study designed to evaluate an investigational drug for celiac disease. The study will explore whether the investigational drug is able to improve the damage in the lining of the intestine caused by ingesting even small traces of gluten. The study will also evaluate whether the investigational drug improves any symptoms of celiac disease.

You may qualify for the CeliAction Study if you:

  • Have been diagnosed with celiac disease by a healthcare professional
  • Are attempting to be on a gluten-free diet
  • Have experienced at least one moderate or severe symptom of celiac disease in the past month

There are other criteria that you must meet to qualify for participation. The study staff will explain the requirements to you and answer any of your questions.

As a volunteer in a clinical trial, you may:

  • Participate in a research process that may lead to new treatment options
  • Learn new information about your health
  • Receive study-related care from qualified physicians

To learn more about this research study, visit CeliActionStudy.com or call 1-855-3333-ACT.

Email This Page
Neurogluten

Gluten-Related Neurologic Symptoms in Children

There is a well-established relationship between celiac disease (and non-celiac gluten sensitivity) and the development of neurologic problems in adults.   According to Dr. Marios Hadjivassiliou, a neurologist in the UK who is one of the world’s experts in this area, up to 50% of adults with newly diagnosed celiac disease have signs or symptoms of neurological problems. I have personally experienced a peripheral neuropathy (nerve damage) as a result of celiac disease and it was my neuropathy that prompted me to start writing about my experiences in 2012 (see link).  If you are interested in learning more about gluten-related neurologic problems in adults, I urge you to read Christine Boyd’s article “Gluten and Your Brain” in the April/May 2014 issue of Living Without Magazine. I was fortunate to be interviewed for Ms. Boyd’s story, and the article contains a wealth of information from experts, including Drs. Fasano and Hadjivassiliou.

Although there is definitely a link between gluten-related disorders and nerve and brain problems in adults, much less in known about the neurologic signs and symptoms in children with gluten sensitivity. This may be in part due to a 2008 paper in the Journal of Pediatrics that concluded that neurologic problems in children with celiac disease are rare. I have personally interacted with many parents of children with both celiac disease and non-celiac gluten sensitivity who have had their children’s neurologic and behavioral symptoms improve on the gluten-free diet.  In addition, in just the last few weeks, there have been several published case reports regarding gluten-induced neurologic problems in kids. If you are interested in learning about the case reports, I have summarized them below:

  1. The 1st case report is of a 15 year old girl with celiac disease who developed a peripheral neuropathy out of the blue that consisted of weakness and a pricking sensation in her legs.  It was discovered that she had been accidentally eating biscuits that contained gluten for about 2 months prior to the neuropathy starting.  Her neuropathic symptoms resolved when she stopped eating the non-GF biscuits (see reference #3).
  2. The 2nd case report is of a 3 year old girl who developed an acute disseminated encephalomyelitis (brain inflammation) and white matter lesions that were visible on her brain MRI. After going on the GF diet her neurological symptoms resolved and the white matter lesions stopped growing in size (see reference #4).
  3. The 3rd case report is of a 2 year old boy with epilepsy who continued to have seizures despite being on multiple seizure medications.  He did not have any digestive symptoms, outside of canker sores in his mouth, but was found to carry one of the 2 main celiac genes (HLA-DQ8).  Within 6 months of being on the GF diet, his seizures improved, his EEG became normal, and he was able to be weaned off of all his seizure medications (see reference #5).

According to Dr. Guandalini, the founder and medical director of The University of Chicago Celiac Disease Center, who wrote a recent review article about celiac disease in children, neurologic signs and symptoms of celiac disease in the pediatric population can include all of the following: cerebellar ataxia, recurring headaches, peripheral neuropathy, seizures, and psychiatric disorders, including anxiety, panic attacks, and depression.

In writing and sharing this post I am not trying to state that all neurologic problems in kids are as a result of gluten, as this is clearly not the case.  I am sharing this information in hopes that both celiac disease and non-celiac gluten sensitivity may be on both parents’ and doctors’ radars when neurologic signs and symptoms appear in kids, as well as to help prevent others from having a long delay in diagnosis like I did.

Thank you for reading and please feel free to share your personal experiences in the comments section.

References:

Hadjivassiliou, M, Sanders, D, Grubewald, R, et al.  Gluten sensitivity: from gut to brain.  The Lancet. March 2010. 9: 318-330.

Ruggieri MIncorpora GPolizzi A, et al. Low prevalence of neurologic and psychiatric manifestations in children with gluten sensitivity. J Pediatr. 2008 Feb; 152(2):244-9.

Boskovic AStankovic I. Axonal and demyelinating polyneuropathy associated with celiac disease. Indian Pediatr. 2014 Apr 8; 51(4):311-2.

Jorge RAguiar CEspinheira C, et al. A pediatric case of gluten sensitivity with severe neurological presentation. Eur J Pediatr. 2014 May 13. [Epub ahead of print]

Bruni ODosi CLuchetti A, et al. An unusual case of drug-resistant epilepsy in a child with non-celiac gluten sensitivity. Seizure. 2014 Apr 18. pii: S1059-1311(14)00106-X. doi: 10.1016/j.seizure.2014.04.005. [Epub ahead of print]

Email This Page

The CeliAction Study

A significant percentage of patients with celiac disease continue to have gastrointestinal symptoms and/or small bowel inflammation while on the gluten-free diet. The Celiaction Study is recruiting subjects with celiac disease to test a medication that will help improve symptoms of celiac patients who are already on the gluten-free diet. Since this is a sponsored post, all questions will be answered by a CeliAction Study representative. Thank you!  -Jess

celiaction

Did you know there isn’t a single drug approved to treat celiac disease? Currently, attempting a gluten-free diet is the only option recommended by doctors, but a clinical research study called the CeliAction Study is researching if an investigational drug improves any symptoms of the disease.

You may qualify for the CeliAction Study if you:

  • Have been diagnosed with celiac disease by a healthcare professional
  • Are attempting to be on a gluten-free diet
  • Have experienced at least one moderate or severe symptom of celiac disease in the past month

If you participate in the CeliAction Study, you:

  • Will be able to maintain your current diet restrictions
  • Will be provided with study-related care at no cost
  • Do not need medical insurance to take part
  • May be compensated for time and travel
  • Will help advance medical research for celiac disease

To learn more about this research study and see if you qualify, visit www.CeliActionStudy.com
or call 1-855-3333-ACT.

Email This Page

“Gluten intolerance” can actually be subclinical celiac disease

glutenintolerant

I think most of us have met people who have symptoms of celiac disease, but when tested, are told that their celiac antibody blood tests and biopsy results are negative (normal). Some of these people are labeled “gluten intolerant” or “gluten sensitive” by their doctors, others are told they may have “early” celiac disease, or “pre” celiac disease, and the rest are told that they have nothing wrong and are often advised to continue to eat gluten.  Many continue to eat gluten and find themselves getting sicker and sicker, with an improvement or disappearance of symptoms when they go gluten-free.  Then, when they go gluten-free, since they are “gluten intolerant” as opposed to having celiac disease, it is unclear how closely they need to be followed for vitamin deficiencies, the development of additional autoimmune disorders, and other problems that are associated with long-standing celiac disease.

Whenever I hear that a person is “gluten intolerant” I wonder whether or not the diagnosis of celiac disease was actually missed.  Celiac blood antibody testing can be unreliable in infants and toddlers, people who have a condition called serum IgA deficiency (occurs in up to 3% of celiacs), and when patients are tested after they have already started on the gluten-free diet. Likewise, endoscopies and biopsies are often done incorrectly (see link) which can lead to celiac-induced intestinal damage being missed.

I recently read, with much interest, an article called, “Intestinal-mucosa anti-transglutaminase antibody assays to test for genetic gluten intolerance,” which was published this month by a group of celiac researchers in Italy. Although it’s a bit technical, I will do my best to summarize it for you.

In this study, the gluten-intolerant subjects consisted of 78 pediatric patients who had symptoms of celiac disease but normal celiac antibodies (anti-TTG, also called TTG IgA) and normal small bowel biopsies.  None of the subjects were IgA deficient. Of the 78 gluten intolerant subjects, 12 were found to have anti-TTG antibodies present in the tissue biopsies from their intestines–to clarify, anti-TTG antibodies were found in their intestines, but not in their blood. 3 of the 12 patients in this “gluten intolerant” group, with TTG antibodies localized to the intestine only, were started on a GFD diet and they all had improvement in symptoms and anemia after 24 months on the gluten-free diet. Of the 9 patients with anti-TTG antibodies in the intestines who were continued on a gluten-containing diet, 2 of the 12 had celiac disease at 24 month follow-up. The remaining 7 “gluten intolerant” subjects who remained on gluten-containing diets appeared to have an improvement in symptoms at the 24 month mark, but it is unclear if this reflected a period of remission v. a true resolution of the intestinal antibody response, as there has been no long term follow-up, and as far as I can tell, biopsies were not repeated.

Although this study has a very small sample size, it demonstrates that there are some “gluten intolerant” patients who actually have subclinical celiac disease. In these cases, the celiac immune response is contained to the intestines only and villous atrophy (the hallmark of celiac disease) has not yet occurred. It appears that these individuals benefit from treatment with the gluten free diet.

I am curious to see if the long-term follow-up of the remaining 7 gluten intolerant subjects will be published in the future, and if some of them will also go on the develop celiac disease. I am also curious to see if celiac antibody testing of intestinal biopsy specimens will eventually become part of the standard of care in the clinical investigation of celiac disease.

Reference:

Quaglia, S, De Leo, L, Ziberna, F, et al. Intestinal-mucosa anti-transglutaminase antibody assays to test for genetic gluten intolerance. Cellular and Molecular Immunology advance online publication, 28 April 2014; doi:10.1038/cmi.2014.32.

Email This Page

An Introduction to the CeliAction Study

This is the first of a series of sponsored posts about the Celiaction Study on my page. Since being diagnosed with celiac disease in 2010 I have been patiently waiting for treatment options to augment the GF diet.  Although I eat strictly GF and am safely able to do so in my home, I am at risk of gluten cross-contamination whenever I travel and/or eat outside of my home.  The enzyme being studied has the potential to reduce intestinal damage from gluten cross-contamination, and is also being evaluated as a treatment for those with nonresponsive celiac disease.  All comments and questions will receive a response from a Celiaction Study representative. -Jess

celiactionblogpost

Managing celiac disease may be more than just a gluten-free diet.

A clinical research study called the CeliAction Study is researching if an investigational drug – which would be taken as a supplement to an attempted gluten-free diet – improves any symptoms of celiac disease.

You may qualify for the CeliAction Study if you:

  • Have been diagnosed with celiac disease by a healthcare professional
  • Are attempting to be on a gluten-free diet
  • Have experienced at least one moderate or severe symptom of celiac disease in the past month

If you participate in the CeliAction Study, you:

  • Will be able to maintain your current diet restrictions
  • Will be provided with study-related care at no cost
  • Do not need medical insurance to take part
  • May be compensated for time and travel
  • Will help advance medical research for celiac disease

To learn more about this research study and see if you qualify, visit CeliActionStudy.com
or call 1-855-3333-ACT.

Email This Page
GFgoodjpg

Dr. Fasano’s Gift of Gluten Freedom

Dr. Alessio Fasano, founder and director of the Center for Celiac Research at Massachusetts General Hospital, is one of the world’s leading experts in celiac disease and non-celiac gluten sensitivity. Without his dedication and research, there’s a good chance that many of us with celiac disease would still be walking around undiagnosed and chronically ill. As I have stated before, he is one of my heroes.

I had the fortune to read Dr. Fasano’s brand new book, Gluten Freedom, as I sat at O’Hare airport earlier this week due to a flight delay.   It made for one of the most fascinating flight delay experiences of my life.

Gluten Freedom explains the history of celiac disease, celiac disease awareness in the medical community, and the amazing leaps in celiac research over the past two decades.  Most significant research findings related to celiac disease are discussed and summarized in an easy to read manner. Dr. Fasano shows how celiac disease can have effects on all areas of the body, not just the digestive system, and discusses new research on the neurological and psychiatric/behavioral effects of gluten.  Non-celiac gluten sensitivity is discussed in depth as well, and Dr. Fasano makes it clear that non-celiac gluten sensitivity is a separate diagnosis from celiac disease that occurs in up to 6% of Americans. In addition, Dr. Fasano paints us a picture of why not all of us are successful on the gluten free diet, and justifies the need for additional medical treatment options for celiac disease.

My favorite part of the book was Part 3, in which the chapters deal with living with celiac disease during specific phases of life, including pregnancy, childhood, college, and the elderly years. A lot of the questions I have had others ask about me about being gluten free during pregnancy are discussed in this book.

One of my favorite quotes was Dr. Fasano’s discussion of what happens at the time of diagnosis. He states, “As a physician, I’m very sympathetic with this complex combination of emotions.  I never minimize the feelings of someone who has just realized that his or her life has been changed forever by this restriction on one of the most enjoyable activities of humankind, that is, eating.” He truly “gets it” like I wish other doctors would.

Although I’d love to be able provide a summary of the entire book for you, like I often do for journal and research articles, I cannot, as my post would end up being about 500 pages long!  If possible, I urge you to read this book on your own.  No matter what age you are, or where you are in your gluten-free journey, you will be helped by the information in it and will gain a better understanding of your medical condition.

Although the hardcover version of Gluten Freedom will not be available until April 29th, the Kindle version is already available on Amazon.com for $11.99. If you can swing it, it is money well spent, I promise.

And Dr. Fasano, if you (or one of your representatives) ever do read my post, thank you for all you’ve done and continue to do for all of us with gluten-related disorders.  We truly appreciate it!

 

Email This Page
ID-100149378

Happy Gluten-Free Spring

I intended for this post to be an overview of a recent review article about celiac disease written by three prominent celiac researchers in the UK, Drs. Mooney, Hadjivassiliou, and Sanders. However, after just doing 7 hours of online continuing medical education modules, my heart and brain are not cooperating, and I am also ready to throw my laptop out the window. So I’m going to shorten my post by quite a bit and save the life of my computer…

Below are the “take home” messages of the article, as well as some interesting comments on the original article that were published by another physician. Please bear in mind that I am “translating” from medical terminology to lay terminology, so if anything seems confusing, just post a comment and I will clarify.

1. The prognosis for celiac disease is good and those with celiac have a normal life expectancy.

2. The gluten free diet is currently the only treatment for celiac disease (this is the only 1 of the 6 that I was told when I was diagnosed).

3. Although the risk of lymphoma is greater than the general population, it is small, and being on the gluten free diet reduces the risk of lymphoma.

4. The average celiac patient has low bone mineral density, therefore, adequate vitamin D and calcium intake must occur.

5. If patients do not get better on the gluten free diet, then they need to seek medical advice as this indicates that there is either ongoing gluten exposure, or another condition that needs to be evaluated.

6. Close family members have a 1 in 10 chance of also having celiac disease; 1st degree relatives (parents, siblings, and children) should be screened.

Dr. Andrew Smith, also from the UK, had some interesting comments about this article in regards to the role of an endoscopy and biopsy in the diagnosis of celiac disease. I’ve cut and paste a few of Dr. Smith’s statements below (originally published online in the British Medical Journal on 3-12-14).

“The article is an interesting and informative overview of coeliac disease. However, the discussion related to the necessity of a duodenal biopsy in adults seems comparatively inadequate; especially considering that it is reported that European guidelines provide an algorithm for avoidance of biopsy in children.”

“The formal diagnosis of coeliac disease seems to be an academic endeavour in certain cases. If an adult patient has resolution of symptoms on a gluten-free diet, especially if combined with high serological markers, can this not be enough to recommend continued trial of dietary gluten avoidance? Even if the patient has Irritable Bowel Syndrome with an element of gluten-sensitivity, the treatment will be the same. The insistence on endoscopy seems unnecessary in these cases; both in relation to patients’ perceptions and experience of such an invasive procedure and to the financial costs associated with it.”

“Another factor is that of an ethical one. It is well known that a fundamental basis of medicine is ‘primum nil nocere’ (‘first, do no harm’). It therefore seems erroneous to encourage patients to continue with gluten-containing diets whilst awaiting an endoscopy appointment, especially when serological tests can be taken within one or two days. Even more conflicting is prescribing individuals a ‘gluten challenge’ with the explicit aim to create the histological features, but also concomitant symptoms, to aid the diagnosis of a disease for which the treatment may have already had benefit.”

I think that Dr. Smith brings up some of the same questions that many of us, as patients, have had through the years, and it is nice to see that this is being debated and discussed.

On a totally unrelated note, sometime this week is my 4 year anniversary of being diagnosed with celiac disease and going gluten free (I’m not sure of the exact date but know it was around St.Patrick’s Day).

As a tribute I would like reflect on the ways that this diagnosis has changed my life for the better:

-I have energy and can run, chase my kids around the yard, ski, do yoga, and stay awake all day (and sometimes all night for work) without feeling like sleeping all of the time. My joint pains are gone and I feel younger than I did 4 years ago.

-I have been forced to eat healthier and provide my entire family with more nutritious food. I no longer take what I eat for granted, and I have mastered the art of label reading. I have also learned to cook and bake from scratch, something that I had never had to confidence to try to do in the past. I also have an excuse not to eat all of the junk food in the break room at work, donuts at conferences, etc.

-When we road trip and travel we have to plan out our food-related stops ahead of time, and no longer rely on eating at fast food places like McDonald’s. This has been a blessing, and just last week we discovered a super great eatery called Egg Harbor Café, with GF options, outside of Chicago while on a road trip. I highly recommend checking them out if you live or travel through the area, there are a bunch of locations.

-I have formed an incredible network of people with celiac disease and non-celiac gluten sensitivity around the world. And although I have met only a few of you in person, it is a joy to be able to communicate, email, and share ideas, stories, articles, laughs, etc. I am so grateful for your love, advice, and support.

-I’ve realized that I can live a full life, even with celiac disease and 2 other autoimmune conditions. Although it’s not always a piece of cake, celiac disease is not a death sentence (see #1 above) or a reason to hate the world. It has been empowering for me to triumph over celiac disease.

The next time I get glutened, I’ll have to remember to look back on this post. Dear Tom, if you are reading this, please remind me to do so!

Have any of you had experienced positive life changes following your diagnosis? If so, please feel free to share. I would love to balance some of the negativity and bitter feelings about celiac disease and living gluten free that seem to be increasingly prevalent these days in the internet world.

I won’t be writing much this spring, but feel free to post questions and comments either here or on my Facebook page, and I’ll respond as soon as I can. Thanks for reading and Happy Spring!

Reference:

Mooney, P., Hadjivassiliou, M., Sanders, D. Coeliac disease. BMJ 2014;348:g1561. Published online 3 March 2014.

Email This Page
top

Notes from the 2014 International Nutrition and Growth Conference in Barcelona

I was fortunate to be able to escape the “polar vortex” 3 weeks ago and travel to sunny Barcelona, Spain for the 2nd International Conference on Nutrition and Growth, a 3-day gathering of doctors, researchers, nutritionists, nurses, and other specialists from around the world. During this conference I learned about the most recent research regarding neonatal and pediatric nutrition, breastfeeding, probiotics, obesity, maternal diet and nutrient supplementation during pregnancy, epigenetics, and the microbiome. I was also given a fair amount of free time to explore one of the most beautiful cities in the world. As an added bonus I was able to eat GF like a queen throughout the city (there will be an upcoming post about this). If it was not for my family, job, and other “real life” things I am not sure that I would ever have left Barcelona!

Although I have pages and pages of notes, abstracts, and presentation slides to sort through, there were some common themes that were repeated over and over again at the conference. Although we’ve heard many of these ideas before, and none of them are “rocket science,” I feel compelled to share, as they are all very important. Here they are, in no particular order:

1. We need for our children to play outside as much as they can. It is good for them to play in and eat dirt, as this strengthens their microbiomes. Having a healthy population of gut bacteria helps to prevent against the later development of allergies and celiac disease. Exposure to sunshine, even on cold winter days, is crucial for the development of healthy bones and teeth.

2. All us need to eat more fish and green leafy vegetables, especially when we are pregnant. The “good” fats in fish, such as salmon, play a huge role in the development of a fetus’ immune system. Green leafy vegetables, such as kale, are full of micronutrients that are important for the development of fetal and infant brains. We need to really pay attention to what we are eating and drinking when we are pregnant, as our diets during pregnancy play a large role in the lifetime health of our unborn babies.

3. We should probably all be taking probiotics, or at least considering doing so. The higher one’s level of Lactobacilli and Bifidobacterium (good bacteria) in the gut, the less likely one is to develop celiac disease and food allergies later on. Researchers are also finding that an overgrowth of “bad” gut bacteria can predispose both to obesity and mental health issues. The best source of probiotics for babies is breast milk.

4. Rapid weight gain during infancy is not a good thing. If a newborn infant gains too much weight during the first few months of life, he or she will have a much higher risk of obesity, type 2 diabetes, and metabolic syndrome as an adult. Infant obesity is being recognized as an emerging problem in first world countries. Healthy term infants should not be fed on a schedule and should not be forced to continue eating when they no longer seem hungry.

5. All infants need to get their own mother’s breast milk, even if the breastfeeding is partial. The evidence is clear that breastfeeding leads to decreased infections during infancy, improved immune system functioning, optimal brain development, and the establishment of a healthy microbiome. Some breast milk is much better than none at all! When a mother cannot provide breast milk, donor breast milk should be considered, especially for premature infants.

6. Solid foods (including those containing eggs, milk, gluten, etc.) should be introduced to an infant between 4 and 6 months of age, while still being breastfed. This is a critical time in the development of the immune system, and there’s enough research out there showing that babies who receive breast milk when solids are introduced during this time frame have a much lower risk of the later development of both food allergies and celiac disease.

I could keep going but am going to stop for the sake of brevity. As I make my way through some more of my notes, I’ll post information that may be of interest to you. Feel free to ask questions too. I love when readers comment, ask questions, and share their experiences and ideas.  I’ll definitely share my Barcelona dining experiences in an upcoming post as well, as it truly is a great destination for those of us with celiac disease (and non-celiacs too!)

Email This Page
ID-100142496

Celiac Disease Can be a Pain in the Joint

Unexplained joint pains (arthralgias) were one of the main symptoms that I dealt with prior to my celiac diagnosis. Throughout my twenties I had pain and stiffness in my fingers, knees and ankles that would come and go with no apparent explanation.  I ran track for part of high school and continued to run for fitness during college, but shortly after graduating had to stop running for a long time due to my joint issues. I was evaluated over and over again for lupus, rheumatoid arthritis, Lyme Disease, etc. but there were never any answers for why I had developed the pains. So I learned to live with them and I stopped running. Fortunately, since going GF in 2010 my arthralgias have almost entirely disappeared, and I was able to resume running again.

Based on previous research, up to 25% of people with celiac disease may experience joint pains. In just the last few months there have been a few interesting studies published about the relationship between celiac disease and joint issues.

A group of researchers published a paper last week showing a significant relationship between joint inflammation and celiac disease in children. They evaluated the knees, hips, and ankles of children with celiac disease (n=74) by ultrasound. They compared ultrasound findings of those with treated v. untreated celiac disease and found that 50% of those who were not on the GF diet had evidence of joint inflammation v. only 11% of those who were GF.

In a recent Tunisian study, researchers tested over 200 women with unexplained arthralgias (joint pains) for celiac disease.  They found much high rates of undiagnosed celiac disease in their sample (2.37%) than in the general population in their country (0.28%).  Interestingly enough, all of the women who were diagnosed did have other symptoms of celiac disease, such as anemia and infertility, when their medical records were reviewed after-the-fact.

In addition, Dr. Guandalini refers to the relationship between celiac disease and arthritis in his review of celiac disease in children that was published earlier this month in JAMA Pediatrics (see my previous post for a summary and for the actual reference).

Although the relationship (or lack of one) between juvenile idiopathic arthritis (JIA) and celiac disease appears to be debatable in the medical literature, this story, which was published last year in the NY Times, does present a compelling case for a link, at least in some cases.

Have any of you experienced celiac-related joint pains? If so, please share, as your stories may lead others to be diagnosed…

References:

  1. Lubrano E, Ciacci C, Ames PR, et al. The arthritis of coeliac disease: prevalence and pattern in 200 adult patients. Br J Rheumatol. 1996;35(12):1314.
  2. Iagnocco ACeccarelli FMennini M, et al. Subclinical synovitis detected by ultrasound in children affected by coeliac disease: a frequent manifestation improved by a gluten-free diet.Clin Exp Rheumatol. 2014 Jan 20. [Epub ahead of print]
  3. Ghozzi MSakly WMankaï A, et al. Screening for celiac disease, by endomysial antibodies, in patients with unexplained articular manifestations. Rheumatol Int. 2013 Dec 1. [Epub ahead of print]
Email This Page
image-17

Celiac Disease in Children (Summary of January 2014 Review Article)

Drs. Guandalini and Assiri have written a summary of pediatric celiac disease that was published in the online edition of the journal JAMA Pediatrics last week. In this post I will share some of the highlights of their review article.

Although the overall prevalence of celiac disease is 1% in the pediatric population, only 10-15% of children with celiac disease have been diagnosed and treated.

The celiac genes (HLA-DQ2 and DQ8) contribute 40% of the risk of developing celiac. Environmental risk factors for celiac disease include infant feeding patterns, early infections, gut microbiota, and the amount and timing of initial gluten exposure.

The two major autoantibodies used in the diagnosis of celiac disease include the anti-TTG IgA and antiendomysial IgA. The antibody against deamidated gliadin peptides IgG (DGP IgG) is a 3rd antibody that has been identified. The DGP IgG may be the best one to use for diagnosing celiac disease in young children (under the age of 2) as it has the highest sensitivity in this age group.

During the past few decades there has been a shift from children presenting with celiac disease having typical symptoms (gastrointestinal) to having extraintestinal (atypical) symptoms.

“Typical” symptoms include abdominal pain (most common), diarrhea, chronic constipation, weight loss, vomiting, abdominal distension, and malnutrition.

“Atypical” (extraintestinal) symptoms in children include all of the following:

  • fatigue
  • iron deficiency anemia
  • dermatitis herpetiformis
  • dental enamel defects
  • aphthous ulcers (canker sores)
  • arthritis and arthralgias (joint pains)
  • low bone mineral density, fractures of bones
  • elevated liver enzymes
  • short stature
  • delayed puberty
  • cerebellar ataxia
  • recurring headaches
  • peripheral neuropathy
  • seizures
  • psychiatric disorders, including anxiety, panic attacks, depression

Celiac disease is associated with other pediatric conditions, including type 1 diabetes mellitus, selective IgA deficiency, Down syndrome, Turner syndrome, and Williams syndrome.

Patients with celiac disease are at an increased risk of all of the following (I was not aware of many of these associations until I read this article):

  • adrenal insufficiency
  • asthma
  • IgA nephropathy
  • lupus
  • pancreatitis
  • hyperparathyroidism
  • endometriosis
  • cataracts
  • ischemic heart disease
  • dilated cardiomyopathy

Dr. Guandalini recommends that celiac diagnosis in children involve celiac antibody testing, endoscopy with small bowel biopsy, and response to the gluten free diet. He does discuss that the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN) has recently issued guidelines for diagnosis in which, in select cases, the small bowel biopsy can be omitted. Dr. Guandalini’s major concern is that if children undergoing evaluation do not have biopsies done, that other GI diagnoses that may need treatment, such as eosinophilic esophagitis, can be missed.

Celiac Disease resources that were discussed toward the end of the article include the Academy of Nutrition and Dietetics website, www.eatright.org, and an e-book created by the University of Chicago Celiac Disease Center called “Jump Start Your Gluten-Free Diet.”

In summary, this is a nicely written paper that is a great summary for pediatricians and other practitioners who need to be on the look out for celiac disease in their pediatric patients. I also thought that some of you non-medical folks might be interested as well!

Reference: Guandalini S, Assiri A. Celiac Disease: A Review. JAMA Pediatr. 2014 Jan 6. doi: 10.1001/jamapediatrics.2013.3858.

Lastly, the super cute children in the photo are my baby brothers and nieces who are now in their late teens and twenties. Since none of them read my blog, as they seem to be in denial that they have a risk of celiac disease, I had no qualms about sharing their adorable photo. Also, I became an aunt for 19th time this past week! Welcome baby Gabriel Dominic and congratulations to my sister and her family on his birth.

Thank you for reading!

 

Email This Page
ID-10073499

Non-celiac gluten sensitivity in children

I was thrilled to come across a paper about non-celiac gluten sensitivity in children in the Journal of Pediatrics, one of the main pediatric journals. Many of my pediatrician colleagues read this journal on a regular basis. In this article, a group of Italian researchers have described the symptoms and lab test results in 15 children with gluten sensitivity (GS) compared to 15 children with active celiac disease and 15 controls (children with IBS-type symptoms that have no correlation with gluten intake). None of the children included in the GS group had an IgE-mediated wheat allergy causing symptoms. Most of the children in the study were between 8 and 10 years old.

Here is a brief overview of the research study:

  • The main symptoms in the gluten sensitive group included abdominal pain, chronic diarrhea, bloating, failure to thrive (poor growth), vomiting, and constipation. These symptoms were similar to those seen in the group of children with active celiac disease. The “control” group of children with functional (IBS-type symptoms) had only abdominal pain and indigestion as symptoms.
  • The gluten sensitive children had “extraintestinal” symptoms of tiredness, headaches, and limb pains. Interestingly, these were not seen in children with active celiac disease. The celiac group of children had anemia and elevated liver function enzymes but the gluten sensitive children did not.
  • Two thirds of the gluten sensitive children had abnormally high antigliadin IgG antibodies (this is an older antibody that was used in the past to assess for celiac disease, but is no longer used because it is non-specific for celiac disease). None of the gluten sensitive children had elevated celiac antibodies (TTG IgA and endomysial IgA). All of the children with active celiac disease had abnormally high TTG IgA and endomysial IgA levels and 13/15 with celiac disease had elevated antigliadin antibodies. The control group kiddos with functional abdominal pain were negative for all antibodies (antigliadin, TTG, and endomysial).
  • Seven of the 15 children with GS had one of the celiac genes (DQ2/8) and 8 did not. The 8 gluten sensitive children who were DQ2/8 negative all had some combination of HLA DQ1, DQ5, and DQ7.
  • Eleven of the 15 GS children had an intestinal biopsy while on a gluten-containing diet. All of those with GS had normal to mildly inflamed intestinal mucosa, corresponding to Marsh stage 0 to 1.

In summary, the authors provide findings that support the existence of gluten sensitivity in children as a distinct problem from celiac disease. Children with gluten sensitivity have celiac-like symptoms that resolve on a gluten free diet and return when gluten is reintroduced. Although gluten sensitive children often have elevated antigliadin IgG levels, they have normal TTG IgA and endomysial IgA levels, at least in this study. Their small bowel biopsies show no evidence of villous blunting and, in the majority of cases, the biopsies are normal. In addition, these children’s symptoms are not as a result of being allergic to wheat. Although this is a small study, it is a step in the right direction toward the recognition of non-celiac gluten sensitivity in the pediatric population, and I am thankful that there is finally a research study to support its existence. I am looking forward to being able to read and share similar articles with you.

Reference:

Francavilla, R., Cristofori, F., Castellaneta, S., et al. Clinical, serologic, and histologic features of gluten sensitivity in children. Journal of Pediatrics. E-pub ahead of print. Nov. 16, 2013.

Email This Page
ID-100125319

Risk Factors for Celiac Disease

I’ve had a very difficult week getting my act together to watch any of the Gluten Summit videos, and was unable to make it to my local celiac support group’s dinner tonight due to traffic difficulties (sorry Mary Lynne!), but I was able to get my hands on Dr. Benjamin Lebwohl’s latest manuscript called “The Unfolding Story of Celiac Disease Risk Factors.” If you have Celiac Disease and haven’t heard of Dr. Lebwohl, he is one of the main researchers at the Celiac Disease Center at Columbia University in New York with Dr. Peter Green. Just this past summer Dr. Lebwohl published a landmark paper (see link) showing an increased risk of lymphoma in untreated celiac disease. If you haven’t read this paper, I recommend reading it and showing it to your family members to convince them that they need to be screened for celiac disease if they’d like to prevent getting cancer.

It is currently known that there are 3 components to developing celiac disease: ingestion of gluten, having one of the celiac genes (HLA DQ2 and/or DQ8 in most cases), and a yet to be determined environmental factor. Researchers are working hard to figure out what the environmental trigger is, as avoiding it may be the key to preventing the development of celiac disease in genetically susceptible individuals. About 40% of the U.S. population carries one of the celiac genes, and as I learned at the International Celiac Disease Symposium in Chicago this fall, Celiac can also develop in people who do not have the 2 main genes (myself included, I am double DQ7 positive).

In his latest paper, Dr. Lebwohl discusses the current theories regarding risk factors for the development of celiac disease that have been well-researched. They include the following:

1. Infant feeding practices. There was an epidemic of celiac disease in Sweden in the 1980s and 1990s which corresponded with a change in feeding practices. Babies during this time period were exposed to large amounts of gluten after they had been weaned from breast milk. The lovely Cristen Pantano wrote a guest post for me about this very topic in October 2013. Thus, the timing of the introduction of gluten during infancy may have an effect on the later development of celiac.

2. Infections, including rotavirus infections in children and campylobacter infections in adults, have been associated with an increased risk of celiac disease.

3. Hygiene hypothesis. Research has shown an increased risk of celiac disease in developed countries (i.e. Finland) than in less developed regions, such as the Russian Karelia region. A decrease in exposure to bacteria and microbes may lead to an increased risk of autoimmune and allergic conditions. Kids are supposed to be dirty to some extent.

4. Infants born via c-section are at higher risk for celiac disease than infants delivered vaginally. This is likely due to a change in the colonization of babies’ intestinal flora. For more on this topic, you can see my post about probiotics from February 2013 (and I’ve also heard through the grapevine that this is being discussed quite a bit during the Gluten Summit).

5. Gastrointestinal tract colonization with H pylori, a bacteria, is associated with a lower risk of celiac disease.

6. Medications associated with a higher risk of celiac include antibiotics (especially multiple doses) and proton pump inhibitors (i.e. Prilosec or Prevacid). I cringe when I think of how many antibiotics and anti-reflux medications I was on during college when I was repeatedly treated for ulcers and acne (in retrospect my symptoms were from untreated celiac disease and I have a feeling that this is the case for many people).

7. Infants whose mothers take iron supplements during pregnancy are at a higher risk of celiac disease than infants whose mothers did not take iron. Excess iron may have an effect on the makeup of the bacterial microbiome and have an influence on the innate immune system. More research into this area is needed before specific recommendations can be made and/or changed in regards to iron supplementation during pregnancy.

Overall, this paper by Dr. Lebwohl is the most comprehensive, up-to-date summary of our current understanding of celiac disease risk factors that I have come across, and every risk factor has research to support its inclusion. I am optimistic that, in the future, as more information becomes available, that we will be able to better identify those at risk for celiac disease and prevent it. Right now the only way to prevent celiac disease from developing is to exclude gluten from a newborn baby’s diet for life. And as we all know, in our gluten-filled world, this is much easier said than done! Perhaps for my great-great grandchildren we’ll have an easier way to prevent it. As my 4 year old daughter reminded me today as I dropped her off at school, “Mommy, you are going to be a grandma soon because you look like you are almost 100 years old!” So, perhaps this will be sooner than later!

Reference:

Lebwohl, B, Ludvigsson, JF, Green, PHR. The unfolding story of celiac disease risk factors. Clinical Gastroenterology and Hepatology (2013), doi: 10.1016/j.cgh.2013.10.031.

Email This Page
ID-100114989

2013 International Celiac Disease Symposium Poster Highlights

Although I did not allot enough time to check out all of the posters of abstracts that were on display at the International Celiac Disease Symposium (ICDS) in person, all of us received a spiral bound book that contained the hundreds of scientific posters that were presented. Abstracts are summaries of new research studies, and in many cases, they have not yet been published in a journal. I have started to review the book of abstracts that I received from the ICDS and there are some abstracts that are truly fascinating. We’ll hopefully hear more about these studies in the future as they get published in journals.

Here is a brief synopsis of five of the most interesting studies that I’ve been reading about:

1. “Nine years of follow-up of potential celiac disease in children.” A group of researchers from Naples, Italy (Aurrichio, et al) followed 156 with potential celiac disease who were not on a GF diet. Potential celiac disease, as I discussed here, is when a patient has abnormally high celiac antibodies on blood screening, and often symptoms, but a normal intestinal biopsy. The management is currently controversial. In this study, over a 5-year period, 46.8% of the children with potential celiac disease developed full-blown celiac disease.

2. “Celiac disease detection in asymptomatic children of 2 and 11 years old in a primary care health center using a transglutaminase antibodies quick test.” A Spanish team (Vallejo, et al) screened groups of 2 and 11 year olds for celiac disease in an outpatient clinic using rapid tests. 2% of the 2 year olds had confirmed celiac disease, and 1.5% of the 11 years had celiac disease. The overall rate of celiac disease in their population was 1.7%, which is higher than previously described.

3. “Absence of HLA-DQ2 and HLA-DQ8 does not exclude celiac disease in Brazilian patients.” HLA DQ2 and DQ8 are the 2 main celiac disease genes and are the ones that are currently tested for by most U.S. laboratories. In this study, a Brazilian team (Kotze, et al) performed gene tests on 101 patients with biopsy confirmed celiac disease. They found that 9 (8.9%) of their patients with celiac disease were DQ2 and DQ8 negative. They suspect that this is related to having such an ethnically diverse population in Brazil.

4. “Neurological dysfunction in patients with newly diagnosed celiac disease: a large prospective study.” Dr. Hadjivassiliou and team from the UK performed neurological evaluations on 73 patients with newly diagnosed celiac disease. 63% complained of neurologic symptoms; the most common were frequent headaches, problems with balance, and sensory symptoms. 32% had abnormal white matter lesions on MRI scanning and 43% had abnormal spectroscopy of the vermis of the cerebellum. The cerebellum is the part of the brain involved in balance and posture.

5. “Potential or definite celiac disease: push enteroscopy changes the diagnosis.” A celiac research team from the UK, lead by Dr. Eross, evaluated 16 patients with “potential” celiac disease. Potential celiac disease, as discussed above, is the term for when a patient has abnormally elevated celiac antibodies but no evidence of celiac disease on small bowel biopsy. They found that when their original duodenal biopsies were re-reviewed and biopsies of the jejunum (2nd part of the small intestine that is not typically biopsied when a patient is evaluated for celiac disease) were performed that 15 of the 16 patients actually did have celiac disease. They recommend that a diagnosis of potential celiac disease can only be made if the jejunum has been evaluated by biopsy.

Please let me know if you are interested in reading more about the abstracts that were presented at the ICDS poster session, as there are literally hundreds more that I can summarize for you. Also, I would love to hear about any interesting research that you have stumbled upon!

Email This Page
InfantRisk Center

Early Feeding and Risk of Celiac Disease in a Prospective Birth Cohort

**This is the first guest post on my page by Cristen Pantano, an incredibly talented scientist and mother of two children. Her youngest child was diagnosed with Celiac disease earlier this year. Many thanks to Cristen for tackling this challenging topic! 

Celiac is known to have a large genetic component and people with Celiac disease carry the HLA-DQ2 or HLA-DQ8 genes. However, only around 4% of people that carry these genes develop Celiac. The big question then is, what else is contributing to the development of Celiac?

Scientists are currently looking at other candidate genes, and so far, seven additional genes that make individuals more susceptible to developing Celiac have been identified. Genes are a great place to start, but as we all know, gluten is the big culprit in Celiac. It is the known environmental “trigger” for Celiac. Why is it that some people that carry the “Celiac genes” develop the disease after gluten exposure while others don’t?

Scientists and doctors are asking this question a lot these day. One area that is being investigated is infant feeding. Studies looking back on the Swedish Celiac epidemic of the 1980-1990s have shown that more than half of the epidemic could be explained by infant feeding practices (see link). During the time of the epidemic, Swedish infants were being introduced to gluten, on average, at around five months of age. Breastfeeding ended around this time and was replaced with formula thickened with wheat flour. When breastfeeding averages extended toward seven months and the popularity of wheat-laden formulas decreased, so did the rates of Celiac.

The Swedish epidemic got researchers thinking about infant feeding and many studies have since been published showing an effect of the age of gluten introduction, the amount of gluten introduced, and breast feeding on Celiac development.

A new study looking at the effect of these factors on the development of Celiac was recently published in the journal Pediatrics. This study, out of Norway, looked at the early feeding practices in 324 children that developed Celiac disease compared to a cohort with 81,843 children that did not develop the disease. The strength of the study is that it was prospective. Unlike most population studies where parents have to look back in time and remember details of early milestones, in a prospective study, parents fill out surveys to provide information in real time.

So what did this most recent study find? The authors found that 3.68/1000 children developed Celiac when introduced to gluten at six months compared to 4.24/1000 when introduced at four months and 4.15/1000 after six months. The increased risk for Celiac disease when gluten is introduced before four months, or after six, has been previously observed.

In this new study, the average length of breastfeeding in children that developed Celiac was 10.4 months compared to 9.9 months in the control population. The researchers found a positive association of prolonged (greater than 12 months) breastfeeding and  the development of Celiac disease. When all their breastfeeding data was adjusted for confounding factors such as maternal Celiac disease, this increased risk was borderline significant. That means that statistically speaking, the data set is on the weaker side and needs to be interpreted with caution. However, it does still demonstrate that in this data set, children that were nursed for twelve months or more had a greater risk for developing Celiac.

These findings have been met with frustration by many mothers of children with Celiac. Are women responsible for the development of their child’s Celiac disease because they chose to hold off solid foods and nurse up to, or past, one year? Of course they aren’t, and the authors of this study are not saying that they are. In their discussion, the authors caution that while their data on age of gluten introduction closely matches data from earlier studies, their data on breastfeeding does not.

Many, if not all, previous studies looking at breastfeeding and Celiac disease have found a protective effect from nursing. A 2006 review of the literature found that breastfeeding at the time of gluten introduction provided a 52% reduction in the development of Celiac disease. In 2005, two Swedish studies found a significant reduction in the onset of Celiac in babies that were nursed at the time of gluten introduction and continued to be nursed after that first introduction.

This latest study found that breastfeeding did not protect against Celiac and that nursing past twelve months increased the risk. Sounds strange right? In their discussion, the authors hypothesize that the greater risk in those breastfed past 12 months may have more to do with gluten than with breast milk. When a child is breastfed longer, the introduction of gluten may be later, after six months of age. Furthermore, since the child is older at gluten introduction, he may be exposed to larger amounts. The authors also mention that some mothers may have nursed longer due to perceived food sensitivities.

In the end, what is the take away from this study, and others, looking at infant feeding and the development of Celiac? It seems that there may be a window for gluten introduction between 5-6 months. Introduction before and after this time seem to increase the risk of Celiac. As far as breastfeeding, most studies point toward a large protective effect.

The development of Celiac Disease seems to be a perfect storm of genetic and environmental factors. Factors that may be out of any one person’s control. Studies should continue to look at early infant feeding and disease development, but all data should also be interpreted knowing that as hard as we try, some times, some things just can’t be prevented.

Email This Page
1331341-1331357-932104-1415516

ICDS 2013: The Celiac Iceberg Revisited

The second to last session on day one of the 2013 International Celiac Disease Symposium (ICDS) was a talk entitled, “Melting the Celiac Iceberg-potential, latent, silent: to treat or not to treat?” I was very confused about these terms when I first came across them in the Celiac medical and research literature a few years ago.

“Silent” Celiac Disease refers to patients who have Celiac Disease (elevated Celiac antibodies on blood testing and abnormal small bowel mucosa on endoscopy and biopsy) but no outward symptoms (or at least, do not appreciate any abnormal symptoms). Many silent Celiacs are picked up when they are screened for Celiac Disease due to having a family member with Celiac Disease and/or being in a high risk category for Celiac Disease, i.e. having Type 1 Diabetes.

“Latent” or “Potential” Celiac Disease is the term for when a patient has abnormally high Celiac antibodies on blood testing but either normal, or almost normal, small bowel mucosa on endoscopy. Many with potential Celiac Disease have abnormal symptoms. Some patients with this problem are told they are gluten sensitive, some have been told that they may have “early” or “pre” Celiac Disease, some are told by their doctors that they can continue to eat gluten, and others are advised by their doctors to go gluten free. My understanding is that, in recent years, the word “potential” is preferred over the word “latent” to describe this group.

Dr. Daniel Leffler, from the Celiac Center at Beth Israel Deaconess in Boston, presented the case for the GF diet in patients with potential and silent Celiac Disease, while Dr. Riccardo Troncone, from Naples, Italy, presented the case against the GF diet in these populations. Here are some interesting points that were brought up during both sides of the debate:

Children with first-degree relatives with Celiac Disease (parents and/or siblings) should be screened for Celiac Disease every 2-3 years in the absence of outward symptoms. Many “silent” Celiacs who think they feel “fine” prior to diagnosis will notice improvement on the GF diet. The presenters reminded us that 60% of newly diagnosed Celiacs have atypical symptoms.

There are many types of tissue transglutaminase (TTG) antibodies. Type 2 TTG antibodies can attack the placentas of pregnant women, type 3 cause the skin problem of dermatitis herpetiformis, and type 6 can attack the brain and nervous system. As an aside (from another talk during the ICDS), the commercially available assays in the U.S. test for Type 2 only!

There is conflicting information of the risks to silent Celiacs who do not go gluten free. One study in 2006 (Metzger, et al.) showed that untreated silent Celiacs have an increased risk of mortality and cancer over a 10 year period. But another study in 2009 (Lohi, et al) did not show an increase in cancer for this group. As with many areas, more research is necessary.

According to Dr. Troncone, it is not known if untreated silent Celiac Disease is associated with the development of other autoimmune diseases. He did state that going GF does not improve blood glucose control in patients who have both silent Celiac Disease and Type 1 diabetes.

Dr. Leffler presented research that shows that up to 50% of potential Celiacs will develop full blown Celiac Disease over a 5 year period and reminded us that TTG antibodies can cause harm even if there are no intestinal changes. He also stated that in order to be diagnosed with “potential” Celiac Disease that one must have an abnormally high TTG antibody level on at least 2 separate occasions (this is to rule out a false positive on the initial test).

I felt that the take home message from this lecture/debate was that those with silent and potential Celiac Disease should be on the GF diet, but that much more research is needed. Per my notes, they recommended that silent Celiacs should be GF, but it was not explicitly stated that potential Celiacs need to be GF. My concern is that many potential Celiacs may actually have full blown Celiac Disease that was not picked up on biopsy (see my previous ICDS post for information on how biopsies can be done incorrectly and that the damage from Celiac Disease can be missed). I will update all of my ICDS posts once I can get my hands on the power point presentations from the lectures, which I hope is soon! We were unable to take photos of the slides and although I tried to write as quickly as I could, I will add in key information that I may have missed.

Also, as a total aside, I am thankful to the anonymous reader who has nominated me for the WEGO Health “Geek Health Activist” of the year award. I have never been so proud to be called a geek in my entire life!

Email This Page
ID-10091069-1

Updates on Celiac Disease Screening and Testing from the 2013 International Celiac Disease Symposium

It’s been a busy three weeks since I attended the 2013 International Celiac Disease Symposium (ICDS) in Chicago and I have dedicated only two posts to the symposium thus far (as I was reminded by my friend last night). So, here is some more information for you. This will be post #3 of about 9 or 10 total.

On the first day of the conference, Dr. Benjamin Lebwohl from Columbia gave a lecture entitled “The Correct Diagnostic Approach.” Some of his bullet points on the diagnosis of Celiac Disease included the following:

  • At the current time, most algorithms for diagnosis use both blood tests (serology) and a small bowel biopsy.
  • The TTG IgA antibody is the blood test that is the most sensitive and specific for Celiac Disease. If a patient has a selective IgA deficiency (occurs in about 3% of the population), the deamidated gliadin peptide IgG (DGP IgG) can be useful for screening. The DGP IgA antibody is also more sensitive than the TTG IgA antibody in children under the age of 2.
  • The Celiac antibody tests are imperfect. In approximately 10% of Celiac patients, at time of diagnosis the antibody tests will be negative (normal) but there is still damage seen on biopsy. If these patients had only blood tests performed, their cases of Celiac Disease would be missed.
  • All patients with Irritable Bowel Syndrome (IBS) should be tested for Celiac Disease.
  • It is not feasible to screen all people for Celiac Disease because the positive predictive value (PPV) of the Celiac tests is too low. PPV refers to the percentage of patients with a positive test result who actually have a disease. He stated that if all people were screened, 2/3 of people with abnormal Celiac antibodies would actually not have Celiac Disease (too many false positives) .
  • Lastly, he reminded us that it is crucial that 4 to 6 biopsies be taken during endoscopy, as the damage from Celiac Disease can be missed if too few biopsies are taken. There are many people walking around who have Celiac Disease but were told that their small bowel biopsies were normal because not enough biopsies were taken. If you are interested in reading more about this, I discussed this in a recent post.

Later in the day, Dr. Enzo Bravi from Europe discussed rapid “point of care” tests for Celiac Disease.  There are several tests on the market that require only a few drops of blood and can give results in 5 to 10 minutes.  Simtomax and Biocard are two examples that are used in Europe and other parts of the world.  All of the rapid tests look for some combination of antibodies (TTG IgA, total IgA, DGP IgA and IgG, etc).  There are hopes that these tests will be especially useful in pediatric populations and in developing countries.  Dr. Bravi is currently researching if these tests can be used to assess compliance with the GF diet in Celiac patients who are already GF.   He emphasized that these tests are not intended to be used for the final diagnosis of Celiac Disease.  For more on the Simtomax tests, please see link.  I had an opportunity to briefly speak with Dr. Bravi during one of the breaks and learned that none of these tests are FDA approved for use in the U.S.  If/when they are approved,  I would love to be able to use them in a clinical research study!

Session 4 of the ICDS focused on the pathology of Celiac Disease.  The speakers were Drs. Marsh, Hart, and Bhagat.  We were reminded that small intestinal (duodenal) tissue biopsies are graded from Marsh Type 0 (normal) to Type 3 (villous atrophy and destruction).  Types 1 and 2, the intermediate lesions, have infiltration of tissues with white blood cells, which is called intraepithelial lymphocytosis (IEL). Type 2 also includes tissue hyperplasia, or thickening.

Type 1 lesions, with IEL only, can be seen in IBS and other causes of malabsorption.  If a patient has a Marsh Type 1 lesion in the duodenum and positive TTG antibodies, the diagnosis is either Celiac Disease or Crohn’s Disease.  If anti-endomysial antibodies are present, it is Celiac Disease, and if they are absent, it is Crohn’s Disease.

There are several other diseases that can cause villous blunting that is similar to that seen in Celiac Disease.  They include the following:

  1. Olmesartan associated enteropathy
  2. Common variable immunodeficiency (CVID)
  3. Crohn’s Disease
  4. Giardia infection
  5. Tropical sprue
  6. Autoimmune enterocolitis

CVID, an immunodeficiency, has a mean age of diagnosis of 35.  Two thirds of patients with CVID have increased IEL +/- villous atrophy on their biopsies.  Celiac antibody tests are often negative.  Patients with CVID have no improvement on the gluten free diet. This is one of the biggest red flags that CVID is a possibility for a patient.  CVID needs to be ruled out in cases of refractory (non-responsive) Celiac Disease.

Olmesartan is a medication used for high blood pressure (hypertension) that is in a category of drugs called ACE inhibitors. It can cause duodenal damage that is almost identical to that seen in Celiac Disease. Colchicine is another drug that can cause similar bowel changes.

The speakers emphasized that in patients with refractory Celiac Disease (that do not respond to the gluten free diet), #1-6 need to be excluded.

More information from ICDS to come, including what to do for those with “potential” Celiac Disease and nutrional aspects of Celiac Disease.  Thank you for both reading and being patient with me!

For additional information from the conference, please check out recent posts from both The Savvy Celiac  and Pretty Little Celiac who were official ICDS bloggers.

Email This Page
ID-10039017

“Celiac Disease Now”

Note: This is part 2 of several posts summarizing information discussed at the International Celiac Disease Symposium (ICDS) 2013 in Chicago 9/23-9/25. 

The introductory lecture of the clinical forum of the International Celiac Disease Symposium (ICDS) 2013 in Chicago last week was entitled “Celiac Disease Today: An Overview” given by Drs. Alessio Fasano and Peter Green.

Although the official slides and presentations from the symposium are not yet available for purchase, based on my notes the following topics were addressed during this opening session:

Celiac Disease involves both an innate and an adaptive immune system response to gluten. 1 in 133 Americans have Celiac Disease. The risk of Celiac Disease in 1st degree relatives of Celiac patients (parents, siblings, and children) is 1 in 22. The risk in 2nd degree relatives (aunts and uncles and grandparents) is 1 in 39.  Research has shown that the true prevalence of Celiac Disease has increased by 15% in the last few decades.  Most people with Celiac Disease (83%) are unaware that they have it…

Although the current “gold standard” for diagnosing Celiac Disease is to perform an endoscopy and small intestinal biopsy, Dr. Fasano did bring up the concept of the “4 out of 5” rule, in which some have proposed that Celiac Disease can be diagnosed if a patient meets at least 4 of the following 5 criteria:

  1. Adverse symptoms when gluten is ingested
  2. Elevated Celiac antibodies on serology (blood tests)
  3. An improvement in symptoms when gluten is removed from the diet
  4. Genetic markers (HLA DQ2 and/or 8, although he did mention that 1-2% of Celiacs are DQ2 and DQ8 negative)
  5. Abnormal small intestinal (duodenal) biopsy

Anti-TTG IgA antibodies are greater than 95% sensitive and 95% specific for Celiac Disease.  The DGP IgA antibodies have a sensitivity and specificity of greater than 90%.

No one is born with Celiac Disease and it can develop at any age. Celiac Disease involves a shift from gluten tolerance to an immune (autoimmune) response to gluten.  The current thinking is that in order to develop Celiac Disease, one must have a genetic predisposition, ingest gluten, and be exposed to a (yet to be defined) environmental factor. In order to figure out exactly what the environmental factor(s) are, researchers will need to follow a large cohort of children from birth and monitor them for the development of Celiac Disease.  We did learn later during the conference that this is actually being done as part of the “Prevent Celiac Disease Study” in Europe, which I will discuss in a later post (www.preventCD.com).

It is now believed that a change in the gut microbiome (bacteria) is involved in the pathogenesis and development of Celiac Disease.  Although our gut microbiomes are inherited from our mothers,  the composition of our gut bacteria is continually changing.  There has been some recent research showing that birth by c-section increases a child’s risk of Celiac Disease by 2-3x. During a normal vaginal delivery newborns’ digestive tracts are colonized by bacteria that they pick up from their mothers’ bodies during labor and delivery.  During a c-section this mother to infant transfer of bacteria does not take place.

There are over 70 clinical trials of Celiac Disease going on right now, many of which are currently enrolling subjects.  You can check out www.clinicaltrials.gov and search for “celiac disease” for more information.

Dr. Green stated that currently recognized gluten related disorders include Celiac Disease, gluten ataxia, dermatitis herpetiformis, wheat allergy, and non celiac gluten sensitivity (NCGS).  NCGS was discussed at the ICDS pre-conference (see my previous post for more details).  Celiac Disease can be differentiated from these disorders by the presence of intestinal inflammation and villous atrophy.  Based on a 2012 publication, only 17% of people with Celiac Disease have actually been diagnosed. Young men in the age range of 20-30 have the lowest rates of diagnosis.

Currently recognized risk factors for Celiac Disease include formula feeding, being introduced to gluten before 4 months of life or after 7 months of life, being born during the winter months, PPI (proton pump inhibitor, a type a reflux medication) use, and frequent respiratory infections during infancy.  Much of this information comes from Sweden, where there was an epidemic of Celiac Disease in children during the 1980s and 1990s which triggered much research and analysis.

We were cautioned of a few pitfalls in the diagnosis of Celiac Disease, many of which I will describe in more detail in future posts.  Some of the researchers have found that TTG (tissue transglutaminase) antibody testing from certain labs can be unreliable.  Likewise, some research has shown that only 35% of the biopsies performed during evaluations for Celiac Disease are done correctly. Most GI docs take only 2 samples of small bowel, despite the current recommendations that 4-6 samples be taken.

Although Celiac Disease is often associated with digestive symptoms, many patients do not have any symptoms at all (i.e. they are picked up because they are screened due to having a family member with Celiac).  Some of the most severe cases of Celiac Disease have been found in patients whose only symptom is anemia (low red blood cell count).  On the flip side, a 2009 study showed that only 51% of patients with symptoms of Celiac Disease were actually screened.

A few sort of depressing stats:

-only 20% of patients with Celiac Disease have adequate follow-up after diagnosis

-the average U.S. medical student learns about Celiac Disease for one hour during medical school (I can personally relate to this one!)

And things that I think everyone should know:

-If a patient has dermatitis herpertiformis (DH), then they have Celiac Disease. Dr. Green stated that if one has DH, there is no need for a small bowel biopsy.

-1st degree family members of Celiac Disease patients should be screened every 5 years.

-The Celiac Center at Beth Israel Deaconess Medical Center in Boston has a great new website called “Celiac Now.” Check it out here.

More ICDS information to come soon…Also, any questions are welcome in the meantime!

 

Email This Page
ICDS 2013 Banner

Recap of Non Celiac Gluten Sensitivity ICDS Pre-Conference 9.22.2013

I was fortunate to be able to attend the International Celiac Disease Symposium (ICDS) in Chicago last week, during which I was able to hear lectures given by world expert doctors, researchers, and nutritionists.  Although I got home 3 days ago, my mind is still spinning from all of the information that I learned and tried to absorb during the 22 hours of lectures.  I was also fortunate to meet some awesome people from the Celiac internet community, including Erica from Celiac and the Beast, Rebecca from Pretty Little Celiac, G-Free Laura, and The Gluten-Free Professor. Although I was not one of the official bloggers from the conference, I did learn some information that I’d like to share with you.

Over the next few weeks I plan to summarize much of the information that I learned about both Celiac Disease and Non Celiac Gluten Sensitivity (NCGS) at the symposium, as well as to try to convince you to attend the next ICDS in Prague in 2015 with me, as my dear husband has already declined.

On Sunday night there was a pre-conference on NCGS with a panel of speakers who are world’s experts on NCGS.  I am very interested in this topic as I have several family members who have NCGS and I am amazed by the lack of awareness of this condition in the medical community. There are many doctors who believe that you cannot get sick from gluten unless you have Celiac Disease (intestinal damage) and as you may already know, this is not true!

The experts who presented information about NCGS included Drs. Fasano, Green, Kelly, Mooney, Volta, Schuppan, and Leffler. Below is a summary of some of the information that was shared with the audience:

Patients with NCGS experience adverse symptoms after ingesting gluten but they do not meet the criteria for getting diagnosed with Celiac Disease (namely, they do not have the findings of Celiac Disease on small bowel biopsy).  NCGS is a “diagnosis of exclusion” meaning that, ideally, Celiac Disease is ruled out before a diagnosis of NCGS is given. Despite this, many with NCGS are self-diagnosed.

Between 0.5 to 6% of U.S. population has NCGS, depending on which study is referenced.  The average age of diagnosis is around 40 years, but the research on NCGS is really still in its infancy. Some patients with NCGS have abnormally high antibodies that are associated with Celiac Disease, such as TTG IgA and/or anti-gliadin antibodies, and others do not. About half of patients with NCGS have one of the two main Celiac genes (HLA-DQ2 and/or DQ8) and half do not.  There are currently no biomarkers for NCGS, which plays a large part in the difficulty of diagnosis.

In a large Italian survey, the most common symptoms associated with NCGS included abdominal pain, bloating, diarrhea, fatigue, headache, anxiety, and a “foggy mind.” This mirrors the symptoms that have been described in previous studies.

Dr. Green introduced the acronym PWAWG which stands for People Who Avoid Wheat and Gluten.  According to Dr. Green, not all PWAWGs have NCGS, and many have other problems such as small intestinal bacterial overgrowth (SIBO) and fructose intolerance.  In one recent study, which has gotten a lot of attention, many NCGS patients’ reactions to gluten totally disappear when FODMAPs are also removed from the diet (see link to paper in references below).  However, the researchers only looked for a resolution of abdominal and digestive symptoms and we do not know if other symptoms of NCGS, such as headaches and anxiety, also improved when FODMAPs were removed.  More research is needed in this area. Although I will discuss FODMAPs more in the upcoming weeks, you can refer to Stanford’s website for more information on the low FODMAP diet if interested.

I learned that both autism and schizophrenia have been associated with anti-gliadin antibodies. There was a publication in 2011 that showed that there is subset of autistic children whose symptoms improve on a gluten free and casein free diet.  There are also ongoing clinical trials to see if the GF diet can help improve symptoms associated with schizophrenia.  The tissue transglutaminase antibody (TTG) type 6 looks to be a marker of neuroinflammation and is a possible biomarker for schizophrenia. TTG type 2 antibodies are what are currently measured in blood tests for Celiac Disease.

The pathogenesis of NCGS appears to involve the innate immune system and it is possible that wheat amylase trypsin inhibitors (ATIs), a totally different portion of wheat than the gluten proteins, may be involved. I wrote about this a bit last winter (see link) and the article referenced can be found in the references below.

During the panel discussion, we were reminded that the only way that a NCGS individual who is already GF can find out if he or she has Celiac Disease is to undergo a “gluten challenge.”

One of the last questions to the panel was, “Who should be avoiding gluten?” The answer given was patients with Celiac Disease, NCGS, and possibly autism and schizophrenia.

I also learned that Dr. Fasano recently published a book called “A Clinical Guide to Gluten-Related Disorders,” which I plan to purchase a copy of ASAP. It is available on Amazon.com (see here).

51AXBclt3KL__BO2,204,203,200_PIsitb-sticker-arrow-click,TopRight,35,-76_AA278_PIkin4,BottomRight,-59,22_AA300_SH20_OU01_

Dr. Fasano reminded us that there is currently more confusion than understanding of NCGS, and that it is similar where we were with understanding Celiac Disease 20 to 30 years ago. The great thing is NCGS is finally being recognized and properly studied!

For a great overview of NCGS, please check out the following abstract from PubMed by Dr. Volta, who was one of the experts on NCGS at the symposium:

Volta U, Caio G, Tovoli F, De Giorgio R.Cell Mol Immunol. Non-celiac gluten sensitivity: questions still to be answered despite increasing awareness.  2013 Sep;10(5):383-92. doi: 10.1038/cmi.2013.28. Epub 2013 Aug 10.

Recently, the increasing number of patients worldwide who are sensitive to dietary gluten without evidence of celiac disease or wheat allergy has contributed to the identification of a new gluten-related syndrome defined as non-celiac gluten sensitivity. Our knowledge regarding this syndrome is still lacking, and many aspects of this syndrome remain unknown. Its pathogenesis is heterogeneous, with a recognized pivotal role for innate immunity; many other factors also contribute, including low-grade intestinal inflammation, increased intestinal barrier function and changes in the intestinal microbiota. Gluten and other wheat proteins, such as amylase trypsin inhibitors, are the primary triggers of this syndrome, but it has also been hypothesized that a diet rich in fermentable monosaccharides and polyols may elicit its functional gastrointestinal symptoms. The epidemiology of this condition is far from established; its prevalence in the general population is highly variable, ranging from 0.63% to 6%. From a clinical point of view, non-celiac gluten sensitivity is characterized by a wide array of gastrointestinal and extraintestinal symptoms that occur shortly after the ingestion of gluten and improve or disappear when gluten is withdrawn from the diet. These symptoms recur when gluten is reintroduced. Because diagnostic biomarkers have not yet been identified, a double-blind placebo-controlled gluten challenge is currently the diagnostic method with the highest accuracy. Future research is needed to generate more knowledge regarding non-celiac gluten sensitivity, a condition that has global acceptance but has only a few certainties and many unresolved issues.

Additional References from ICDS pre-conference:

1. DiGiacomo, et al. Prevalence of gluten-free diet adherence among individuals without celiac disease in the USA: results from the Continuous National Health and Nutrition Examination Survey 2009-2010. Scand Journal Gastroenterol. 2013 Aug;48(8):921-5. doi: 10.3109/00365521.2013.809598. Epub 2013 Jul 8.

2. Biesiekierski JR, Newnham ED, Irving PM, Barrett JS, Haines M, Doecke JD, et al. Gluten causes gastrointestinal symptoms in subjects without celiac disease: a double-blind randomized placebo-controlled trial. Am J Gastroenterol 2011;106:508–14.

3. Biesiekierski JR., et al. No effects of gluten in patients with self-reported non-celiac gluten sensitivity after dietary reduction of fermentable, poorly absorbed, short-chain carbohydrates. Gastroenterology. 2013 Aug;145(2):320-8.e1-3. doi: 10.1053/j.gastro.2013.04.051. Epub 2013 May 4.

4. Junker, et al. Wheat amylase trypsin inhibitors drive intestinal inflammation via activation of toll-like receptor 4. J Exp Med. 2012 Dec 17;209(13):2395-408. doi: 10.1084/jem.20102660. Epub 2012 Dec 3.

 

 

Email This Page
ID-10069040

Celiac Disease “Journal Club” 2013 Part 2

This is going to be a quick post, as I am getting ready to head to Cincinnati for a wedding, and then to Chicago for the International Celiac Disease Symposium 9/22-9/25. I look forward to being able to meet some of you in person at this conference, and to hear the experts, including Dr. Fasano, speak about the most recent research, recommendations, and guidelines regarding the diagnosis and management of both celiac disease and non-celiac gluten sensitivity.

Below are summaries of three recent journal articles that may be of interest. Part 1 of my Celiac “Journal Club” series can be seen here. Under each article summary statement I am including a link to some of my previous posts about relevant topics.

1. “2013 update on celiac disease and eosinophilic esophagitis.” Authors: Pellicano, R, et al. Published in Nutrients in Aug. 2013.

-authors reviewed 30 publications regarding celiac disease and eosinophilic esophagitis (EoE), a chronic inflammatory disorder of the esophagus which is on the rise. They found that the prevalence of EoE in subjects with celiac disease is 10x higher than the general population in the majority of the studies. They recommend that all children who get small intestinal biopsies for celiac disease diagnosis also get evaluated for EoE.

-for more information on the relationship between EoE and Celiac Disease, as well as an overview of the symptoms of EoE, please see my post from Jan. 2013.

2. “The rising incidence of celiac disease in Scotland.”  Authors: White, L, et al. Published in Pediatrics in Sept. 2013.

-researchers looked at the incidence of celiac disease in children in Scotland from 1990 to 2009. Overall incidence increased by 640% over this 20 year period, with the incidence of “atypical” celiac disease increasing by 1140%!

-of note, 51% of the children who were actively screened for celiac disease and found to have celiac disease had no symptoms at all. Active screening takes place if a child is in a “high risk” category for celiac disease, i.e. has a sibling or other first degree relative with celiac disease.

-for more information on the screening of children for celiac disease, and who should be screened, please check out my post from June 2013.

3. “Potential new mechanisms of placental damage in celiac disease: anti-tranglutaminase antibodies impair human endometrial angiogenesis.” Authors: Simone, N., et al. Published in Biol Reprod in Aug. 2013.

-the authors demonstrate that tissue transglutaminase antibodies seen in celiac disease damage the placenta by interfering with the development of crucial placental blood vessels.  This finding helps to explain why women with untreated celiac disease often have problems of infertility, miscarriages, and fetal growth restriction.

-I wrote about the topics of Celiac Disease and Pregnancy in Jan. 2013 (see link) and Celiac Disease and Infertility in Mar. 2013 (see link).

I anticipate returning from Chicago with a lot to write about on this page. I will also be making my conference tweeting debut (@PatientCeliac), so feel free to follow me for real-time updates. Lastly, if you will be attending, please reach out and let me know so that we can meet!

Email This Page
ID-10090197

Celiac Disease “Journal Club” 2013 Part 1

As some of you may have figured out, I love to keep up to date with the latest research regarding celiac disease and non-celiac gluten sensitivity (NCGS). My interest in research stems from the countless Journal Clubs that I participated in during my decade of medical training. Journal Club gives medical students, residents, fellows, and other trainees the opportunity to learn how to read, interpret, and critically review research articles. Although there are many things which I do not miss about medical training (especially the sleep deprivation), I do miss Journal Club.

I have created my own overview for you of some of the most interesting research articles about gluten-related diseases that have been published during the past few months. This is part 1 of 2.

1. “Clinical features and symptom recovery on a gluten-free diet in Canadian adults with celiac disease.” Authors: Pulido, et al. Published in the Canadian Journal of Gastroenterology in August 2013.

-Almost 6000 adults with Celiac Disease were surveyed regarding their symptoms of Celiac Disease and their recovery on the GF diet. Average age at diagnosis was 45 and average delay in diagnosis was 12 years.

-Conclusions: Although many subjects had a complete resolution of symptoms after 5 years on the GF diet, almost half reported continuing problems with migraines, lactose intolerance, constipation, itchy skin, and depression after being GF for 5 years. Women were less likely than men to report full recovery from symptoms, especially in the areas of abdominal pain, bloating, weakness, diarrhea, anemia, muscle cramps, constipation, migraine headaches, and swelling of the hands and feet.

2.  “Mucosal healing and risk for lymphoproliferative malignancy in celiac disease: a population-based cohort study.” Authors: Lebwohl, et al. Published in Annals of Internal Medicine in August 2013.

-Researchers found that 43% of adults with Celiac Disease in their study population had persistent villous atrophy on follow-up biopsies after being GF. These patients were found to have a significantly higher (3.5x) risk of lymphoma than the general population.

-Conclusion: Partially treated Celiac Disease is associated with cancer.

-For more information please check out this summary article from Columbia University.

3. “Antibiotic exposure and the development of celiac disease: a nationwide case-control study.” Authors: Marild, K., et al. Published in BMC Gastroenterology in July 2013.

-Main objective of the study was to examine the association between antibiotic use and the subsequent development of celiac disease by comparing subjects with celiac disease with matched controls (subjects without celiac disease).

-Antibiotic exposure was found to be associated with an increased risk of celiac disease, intestinal inflammation, and “potential” celiac disease (elevated Celiac antibodies on blood testing without any small intestinal changes seen on small bowel biopsy).

-Conclusion: The first study to show an association between antibiotic doses and the subsequent development of celiac disease. The authors postulate that an alteration of gut flora (ie. killing off of “good” bacteria) may play a role in the development of celiac disease.

4. “Markers of celiac disease and gluten sensitivity in children with autism.” Authors: Lau, N, et al. Published in PLOS One in June 2013.

-The researchers examined 37 children with autism and found that they had significantly higher levels of anti-gliadin IgG antibodies than children without autism (controls)

-Of the autistic children with anti-gliadin antibodies, most did not have either of the celiac genes (HLA-DQ2 and DQ8) and did not have other celiac antibodies (TTG IgA and IgG and DGP IgA and IgG). However, the majority of autistic children with anti-gliadin antibodies did have gastrointestinal symptoms.

-Conclusion: The anti-gliadin (gluten) immune response in autism involves a mechanism that is different from celiac disease.

5. “Colonic involvement in celiac disease and possible implications of the sigmoid mucosa involvement in its diagnosis.” Authors: Picarelli, A., et al. Published in the Journal of Clinical Immunology in July 2013.

-Researchers took samples of the colon (large intestine) of patients with Celiac Disease and evaluated the samples for celiac antibodies. They found that 75% of patients with Celiac Disease had anti-endomysial antibodies and 81% had anti-TTG antibodies in colonic tissue.

-Conclusion: The immune tissues of the large intestine are affected by Celiac Disease. In the future, large intestinal biopsies may be used in diagnosis.

Part 2 will be coming soon. Please feel free to comment and share articles related to celiac disease and/or non-celiac gluten sensitivity which you have found interesting as well. I would love to discuss.

Email This Page
ID-10094074

Women with celiac disease, we are not alone…

I have spent a good portion of this summer enjoying my time with my family, traveling, and not obsessing about celiac disease (which has led me to not write about it either!) Overall, I am comfortable with my gluten free household and life and have accepted my diagnosis. But, the other day, in part due to fatigue and in part due to accidentally eating a KIND bar with soy protein (soy is one of my other food intolerances and I feel like total garbage after eating it), I totally lost my calm. I found my 4-year-old, Gabby, eating a bag of Goldfish crackers when I picked her up from day camp. Instead of hugging and kissing her, and asking her about her day, like I should have, I began to obsess about celiac disease. Thoughts like, “Now I have to clean all of the gluten off of her face and I don’t have any napkins or wet wipes,” and, “Why the heck is she getting Goldfish crackers as a ‘healthy’ snack’?” and, “I cannot afford to get ‘glutened’ this week because I have to be able to work and function as a mom!” went through my mind. The encounter of picking up Gabby from camp quickly became “all about me,” which is one thing that I truly despise about this disease.

That very night I came across a timely article entitled “Everyday Life for Women with Celiac Disease” in which 16 Swedish women with celiac disease share their experiences. Amazingly, there has not been much published on this topic over the years, so I read it with much interest.

Here are some of the common themes that came up in the discussions in the study:

1. Celiac Disease affects a person’s entire life.

2. The experience of persistent fatigue, even after years on the gluten free diet.

3. Many women reported new signs and symptoms in other areas of the body, such as headaches, after starting the gluten free diet.

4. Anxiety about always having to plan ahead to have food to be able to safely eat and frustration at the lack of spontaneity associated with eating outside of the home.

5.  Reluctance to attend parties and social events due to fears of gluten contamination.

6. Feelings of sadness, vulnerability, anger, and hopelessness surrounding having to follow the gluten free diet. Many women felt lonely in their struggles.

I have experienced #1-6 more times than I can count, and although it has gotten easier with time, I continue to struggle to explain to others how careful I need to be with eating food that is not prepared in my own kitchen. Many of my friends and family members have had no idea how careful I need to be about cross contamination, and that I have to avoid foods that not only contain gluten, but that are prepared on surfaces and in equipment where cross contamination might occur.

Reading about the experience of these women with celiac disease made me feel much less alone, much less “crazy,” and I realized that my reaction to Gabby’s Goldfish crackers was probably not as severe as I had initially thought.  I have decided to be a little easier on myself and move on as I know that Gabby definitely already has. Also, when I pick her up today I’ll be better prepared with some wet wipes and paper towels to clean up the gluten crumbs!

Reference:

Roos, Suzanne, Hellstrom, Ingrid, Hallert, Claes, and Wilhelmsson, Susan. Everyday Life for Women with Celiac Disease. Gastroenterology Nursing. 2013. 36(4), p. 266-273.

Email This Page
patchwork-quilt-100160_640

The Intestinal Villous Blunting (Flattening) in Celiac Disease is often “Patchy”

Villi are the fingerlike projections of the small intestine where nutrient absorption takes place and are the location of Celiac Disease’s assault on the digestive tract.

Untreated celiac disease leads to blunting (flattening) of the intestinal villi that can be seen when a gastroenterologist performs an endoscopy with biopsy. Despite current controversy over whether or not an endoscopy is necessary for all cases of celiac diagnosis, it is still considered by many experts to be the “gold standard” for officially diagnosing Celiac Disease. I look forward to learning more about this moving target at the International Celiac Disease Symposium being hosted by the University of Chicago in September 2013 (see link).

Although in many cases of Celiac Disease the villous blunting is continuous throughout the small intestine, it has been increasingly recognized that the blunting/flattening can be patchy, and in some cases, localized to one specific portion of the small intestine called the duodenal bulb (see references). Thus, in many cases of Celiac Disease, totally normal areas of intestine alternate with diseased areas. Because of this, experts recommend that gastroenterologists take at least 3 to 4 biopsies, including at least one of the duodenal bulb, when evaluating a patient for Celiac Disease. If not enough biopsies are taken, the diseased portions of the small intestine may be missed (and hence, Celiac Disease not properly recognized). Since starting this blog last fall I have interacted with many people who get terribly ill from eating gluten, have many symptoms of Celiac Disease and have abnormal Celiac antibodies on blood testing, only to be told that they do not have Celiac Disease based on “normal” biopsies. I have also encountered one woman in which no biopsies were taken at all! I strongly suspect that some of these “gluten intolerant” people actually have Celiac Disease.

A group of researchers in Italy (Valitutti, et al.) have recently published the findings of a study in which they mapped the patchiness of villous blunting in 41 pediatric patients with Celiac Disease. 17/41 (41.5%) showed diffuse villous blunting throughout and 24/41 (58.5%) had patchy villous lesions. Of note, one child with Celiac Disease had villous blunting in the jejunum, the second portion of the small intestine, only. In most cases only the duodenum, the first portion of the small intestine, is biopsied, so had this child not had his jejunum biopsied for the study, his celiac changes would have been missed. I find this to be very significant, as he would have likely been labeled as being gluten intolerant, or having “Potential” Celiac Disease as opposed to having actual Celiac Disease….for more on Potential Celiac Disease, please see my previous post from March 2013.

In conclusion, if you are one of the gluten intolerant or gluten sensitive patients out there who had a “normal” biopsy (or are parents of one), I encourage you to obtain your biopsy results and check out how many tissue samples were actually taken from your small intestines. Check also to see if your duodenal bulb was evaluated. You may be surprised by what you find!

Also, if you are going to be attending the Celiac Disease Symposium in Chicago next month I would love to connect with you in person. Shoot me an email at thepatientceliac@gmail.com, or comment below. We are very fortunate to be having it be held in the U.S.A. this year and it will be a great opportunity to learn and network.

References:

1. Valitutti, F., et al. Mapping histologic patchiness of celiac disease by push enteroscopy. Gastrointestinal endoscopy. E-pub, ahead of print. June 2013.

2. Kurien, M., et al. Duodenal bulb biopsies for diagnosing adult celiac disease: is there an optimal biopsy site? Gastrointestinal Endoscopy. 2012. 75 (6): 1190-6.

3. Ravelli, A., et al. How patchy is patchy villous atrophy?: distribution of histological lesions in the duodenum of children with celiac disease. American Journal of Gastroenterology. 2010. 105(9): 2103-10.

ICDS 2013 Banner

Email This Page
ID-10076296

Celiac Disease and Endometriosis

As I was doing my weekly glance through the PubMed database (www.pubmed.gov) I came across an interesting letter to the editor in the Archives of Gynecology and Obstetrics entitled, “Celiac Disease and Endometriosis: What is the Nexus?” Endometriosis is a common gynecologic disorder, which effects approximately 10% of women of childbearing age. It involves the development of endometrium, which is the tissue which lines the uterus, in areas of the body outside of the uterus. Symptoms of endometriosis include heavy menstrual periods, abdominal and pelvic pain, abnormal menstrual cycles, and infertility. Although the exact cause of endometriosis is unknown, theories include retrograde menstruation (endometrial cells from the uterus flow backward into the fallopian tubes instead of out of the body during menstruation), an abnormal placement of embryonic stem cells in the pelvic cavity which produce endometrial tissue, and/or an immune system disorder.

Endometriosis is associated with having the HLA-DQ2 and DQ8 genes (which are also present in approximately 96% of patients with Celiac Disease), as well as the DQ7 gene, which has been associated with Celiac Disease in some southern Italians, Sicilians, and Sardinians.

Two studies published within the last few years have shown associations between Celiac Disease and endometriosis. Researchers in Sweden (Stephansson, et al.) reviewed the medical records of over 11,000 women with Celiac Disease in 2011. Compared with controls, women with Celiac Disease were found to be at a much higher risk of having endometriosis, especially in the first year after diagnosis with celiac disease (overall hazard ratio of 1.39).  The authors postulate that there must be a shared inflammatory process in both disorders. Likewise, researchers in Brazil found that 2.5% of women diagnosed with endometriosis also had Celiac Disease (Aguiar, et al, 2009). Please see the references section for links to these two studies.

The gluten free diet has recently been recommended as a strategy to manage the pain of endometriosis. In a pilot study in Italy, 75% of women with endometriosis had a decrease in pain symptoms after 12 months on the gluten free diet (see link in reference section). This strongly suggests that gluten sensitivity and/or Celiac Disease plays a role in endometriosis.

Although I do not have endometriosis, I have interacted with many women through social networking who do have both gluten intolerance and endometriosis. I can say that my periods have become significantly lighter and less painful since going gluten free after my Celiac diagnosis in 2010. I can also say, without a doubt, that my sensitivity to gluten seems to ebb and flow with my menstrual cycle. I seem to be the most sensitive to gluten cross contamination in the 7-10 day stretch before my period, when my estrogen levels are their highest.

With time, I hope that more research is done examining the link between celiac disease and gynecologic disorders. After reading up on endometriosis I did a PubMed search on “Celiac Disease and Polycystic Ovarian Syndrome (PCOS)” and came up with one article from 2002 that was published in Turkey and did not find an association between the two conditions. I have a feeling that if the study was reproduced in the U.S., on a large scale, that an association between Celiac Disease and PCOS would be shown.

For more information on endometriosis, please check out the Mayo Clinic’s website. Rebecca, from “Pretty Little Celiac,” also wrote about endometriosis on her page in January 2013 (see link.)

References:

1. Mormile, R. and Vittori, G. Celiac disease and endometriosis: what is the nexus? Archives of Gynecology and Obstetrics; June 2013 (e-pub, ahead of print).

2. Stephansson, O., Falconer, H., Ludvigsson, J. Risk of endometriosis in 11,000 women with celiac disease. Human Reproduction. 2011; 26 (10): 2896-2901.

3. Aguiar., F., et al. Serological testing for celiac disease in women with endometriosis. A pilot study. Clin Exp Obstet Gynecol. 2009; 36(1): 23-25.

4. Marziali, M. et al. Gluten-free diet: a new strategy for management of painful endometriosis related symptoms? Minerva Chir. 2012 Dec; 67(6): 499-504.

Email This Page
ID-10044135

Update on Celiac Disease Screening in Infants and Toddlers

There are multiple reasons why a young child may need to be evaluated for Celiac Disease. The most obvious reason is if he or she has symptoms, such as chronic diarrhea, poor growth, and/or anemia. Other reasons include having a first degree relative (parent or sibling) who has Celiac Disease or having another autoimmune disorder, such as Type 1 diabetes.

The main blood tests to screen for Celiac Disease are tissue transglutaminase IgA (TTG IgA) antibodies and endomysial IgA (EMA IgA) antibodies. These tests are highly sensitive, which means that if the tests are negative, Celiac Disease can be ruled out most of the time. The problem with using these tests in infants and toddlers is that the sensitivity of these tests is much lower for children under the age of 2 than it is for older children and adults. Some believe that this is because young children with Celiac Disease have not had enough time to develop TTG and EMA IgA antibodies which can be measured. Needless to say, there are probably many toddlers with Celiac Disease who are walking around undiagnosed because they did not have elevated TTG and/or EMA IgA antibodies when they were tested.

Deamidated gliadin peptides (DGPs) are a new test for antibodies against gliadin and are being used with increased frequency for screening for Celiac Disease in the U.S. and Europe. A group of Italian researchers recently studied the utility of using DGP IgG antibodies to screen for Celiac Disease in children under the age of 2. They found that 100% of children under the age of 2 with biopsy-proven Celiac Disease had abnormally high DGP IgG antibodies on blood testing. They also found that DGP antibodies were abnormally high in 4 toddlers who had malabsorption (diarrhea) but who did not have a biopsy consistent with Celiac Disease. One of the 4 children with an abnormal DGP did have mild villous blunting and eventually developed Celiac Disease. The other 3 children with diarrhea and elevated DGPs all had the genes that predispose to Celiac Disease. They plan to follow these 3 children closely for the development of Celiac Disease. The researchers also found that DGP levels correlate very well with the extent of damage on the duodenal biopsies of the children with Celiac Disease and postulate that in the future, children with markedly elevated DGP antibodies may not need to be biopsied for diagnosis with Celiac Disease.

Out of curiosity, I went to the internet sites of some of the major labs that perform Celiac Disease blood screening tests. Labs which DO include DGP IgG antibodies on their celiac panels include Prometheus, Labcorp, ARUP, and Mayo Medical Labs. Labs which DO NOT include DGP IgG antibodies on their celiac panels include Kimball Genetics and Quest Diagnostics (as of 4/17/2013).

If you suspect that your young child may have Celiac Disease, but he or she did not have positive antibodies, it may be helpful to find out which lab their blood was sent to so that you can learn whether or not DGP IgG antibodies were part of the testing.  I recommend that you discuss any concerns with your child’s physician.

References:

1. Antibodies to deamidated gliadin peptides: an accurate predictor of celiac disease in infancy. Amarri, S., et al. J Clin Immunol. Published online 4/5/2013.

2. ARUP Consult. A Physician’s Guide to Laboratory Test Selection and Test Interpretation. Celiac Disease. www.arupconsult.com/assets/print/CeliacDisease.pdf.

3. Screening for celiac disease in average-risk and high-risk populations. Aggarwal, S., Lebwohl, B, and Green, P. Therap Adv Gastroenterol. Jan 2012; 5 (1): 37-47.

Email This Page
baby bottle

A New Food “Allergy” of Infancy: Food Protein Induced Enterocolitis Syndrome (FPIES)

My oldest daughter, Grace, had horribly bad reactions to cow’s milk protein as an infant, which included vomiting, chronic diarrhea with mucus, irritability, reflux, and poor growth. Her first reaction occurred shortly after getting her initial supplemental bottle of formula. She was predominantly breastfed at first, but I did have to supplement her due to milk supply issues (which, looking back, I believe were a result of my undiagnosed Celiac Disease). She went through a series of formula changes (from regular to soy to Alimentum and Nutramigen), and it was not until she was started on Neocate, an amino acid based formula, at 2 months, that she began to grow and thrive. Looking back, I am pretty sure that she had food protein induced enterocolitis syndrome, which is also called FPIES.

FPIES is a severe food sensitivity/intolerance which causes digestive symptoms in infants. Although it is considered by many to be an “allergy,’” it does not involve the formation of IgE antibodies like other food allergies. The most common triggers for FPIES in babies are cow’s milk and soy proteins, although rice, oats, barley, fruits, and vegetables have also been documented as triggers for older infants who have been started on solid foods. Based on recent studies it is believed that 0.3% of infants have an FPIES reaction to cow’s milk. This is in addition to the 3-5% of infants who have milder non-IgE reactions (allergies) to cow’s milk protein during the first year of life.

Infants with FPIES have symptoms shortly after consuming cow’s milk and/or soy proteins, usually within 1-4 hours. The usual trigger is a cow’s milk based formula, but breast fed infants can react to milk proteins in their mother’s breast milk as well. Symptoms can include projectile vomiting, chronic diarrhea with blood and/or mucus, low blood pressure, lethargy, irritability, and/or an elevated white blood cell count. 50% of infants with FPIES who react to milk will also react to soy.

It has recently been recognized that older infants can develop FPIES after solid foods are introduced during the 2nd six months of life. Rice is the most common trigger, followed by oats, barley, chicken, turkey, egg whites, green peas, peanuts, and potatoes. I recently learned that 80% of infants with one solid food trigger will have reactions to at least one other food, and that it is common for infants to have FPIES reactions to multiple foods.

Diagnosing FPIES is difficult because there are currently no blood tests that can be used in detection. This is because the immune reaction of FPIES does not involve the formation of IgE antibodies against the offending foods. This is much different than the IgE-mediated immune reaction that occurs in older children with food allergies. IgE allergies can be detected by blood and/or skin testing.  If a baby has adverse reactions after multiple exposures to the same food, FPIES can be diagnosed clinically. If the diagnosis is unclear, an oral food challenge (OFC) should be performed. It is recommended that an OFC be performed under close medical supervision (i.e. doctor’s office), as there is a risk for low blood pressure and/or dehydration to develop during a food challenge. In the worst cases an infant can develop shock. In some cases infants may need IV fluids after a reaction. Steroids are sometimes needed in severe cases. Based on what I have read, it seems that reactions to trigger foods may get more severe with time, i.e. it may take less and less of the offending food to trigger a reaction.

Research has shown that FPIES to milk and/or soy protein resolves by 3 years of age. It is recommended that children with FPIES get oral food challenges every 12 to 24 months. My oldest daughter is now 7 years old and she has no problems with dairy products (she eats yogurt, cheese, and ice cream) but she has refused to drink plain cow’s milk and has a tendency to avoid soy as well.

Reading and learning about FPIES led me to have many questions and concerns:

1. Why are so many infants born with this problem and why is it increasing in severity? Is it somehow related to their moms having undiagnosed Celiac Disease, and/or some other process causing “leaky gut” while pregnant?

2.  Is this the same disease process which those of us who have multiple food intolerances are experiencing, only babies are getting sicker and having more severe reactions since their immune and digestive systems are less mature?

3. How under-diagnosed is this problem? I had never heard of it 7 years ago when my daughter had it (and I was in my pediatric residency at the time). What are the real numbers?

4. Do infants with FPIES go on to develop Celiac Disease or gluten sensitivity when they are older? Is FPIES, even though it resolves, some sort of marker for the future development of food issues in a patient?

5. Is this somehow linked to the dramatic increase in autism over the last few years? Do the FPIES episodes have some sort of effect on the developing brain of an infant?

6. Does the microflora of the gut play a role? Would probiotics prevent and/or ameliorate the problem?

7. I was going to speculate a bit about GMOs, but I am not sure that I am ready to write about that yet…

I suspect that we are going to hear a lot more about this problem in the future. I wrote this article to share the little which I know about FPIES with you, in hopes that we can learn about it together.

References:

1. American Academy of Allergy, Asthma, and Immunology website: www.acaai.org/allergist/allergies/Types/food-allergies/Pages/food-protein-induced-enterocolitis-syndrome-fpies.aspx

2. Medscape Pediatrics. “FPIES: The ‘Other” Food Allergy.” Dr. Anna Nowak-Wegrzyn, MD. Published online April 3, 2013.

3. Curr Opin Pediatr. 2012 Dec;24(6):739-45. Clinical diagnosis and management of food protein-induced enterocolitis syndrome. Leonard, S. and Nowak-Wegrzyn, A. www.ncbi.nlm.nih.gov/pubmed/23042254

4. Clin Exp Allergy. 2012 Aug;42(8):1257-65. A multicentre retrospective study of 66 Italian children with food protein-induced enterocolitis syndrome: different management for different phenotypes. Sopo, S., et al. Department of Pediatrics, University of Sacred Heart Agostino Gemelli Rome, Rome, Italy. www.ncbi.nlm.nih.gov/pubmed/22805473

 

Email This Page
ID-10087293

“Potential” Celiac Disease

I celebrated the 3-year anniversary of my Celiac diagnosis by attending a Celiac support group meeting in a nearby city. I was a bit hesitant to attend, as my initial experience at a Celiac support group meeting in 2010 was nothing short of a disaster (probably worthy of a blog post in itself, but in short, involved the woman sitting next to me eating a gluten-rich Subway sandwich and chocolate chip cookies throughout the meeting and getting her crumbs on me when she coughed.)

Despite my reluctance, I am grateful that I gave this other support group a chance. The guest speaker was a Gastroenterologist who is also board-certified in Integrative Medicine, so he seemed to have a true understanding of the effect of nutrition on our bodies’ healing.  He presented top notch information on Celiac Diease, and as he spoke I scribbled notes on a manila folder. Upon reviewing my chicken scratching, the phrase “Potential Celiac Disease” jumped out at me because it is a term that I have heard of but did not know much about.

Potential Celiac Disease (PCD) is diagnosed when a patient has abnormally elevated TTG IgA and Endomysial (EMA) antibodies on blood screening tests (the 2 main celiac antibodies) but normal bowel mucosa on biopsy. There is no evidence of the villous blunting seen in Celiac Diease (CD).  PCD often pops up when people who are at high risk for celiac disease are screened, such as first degree relatives of Celiacs, Type 1 diabetics, and/or patients with other autoimmune diseases. Many patients with PCD have no symptoms and do not feel ill from eating gluten. It is essential for the Celiac screening to be done while a patient is still on a gluten-containing diet. If a person is already gluten free when tested it is difficult to tell if the positive celiac antibodies and normal biopsies are from PCD v. full blown CD which is already being treated.

There is a lot of controversy over what to do if a patient is diagnosed with PCD. Some experts believe that if Celiac antibodies are elevated, that one should go gluten free, even in the absence of symptoms. Others believe that asymptomatic potential Celiacs should continue on a gluten containing diet, with close monitoring and follow-up of with small bowel biopsies at regular intervals. The rational behind this 2nd line of thought is that a lot of patients with PCD may never actually go on to develop full CD.

Unfortunately, Potential Celiac Disease has been so under-researched that we really don’t have good information on what percentage of “Potential” Celiacs become actual Celiacs.

A group of researchers in Italy recently studied 47 patients who were diagnosed with PCD. They found that those with PCD did not differ from those with CD in terms of age of diagnosis, digestive symptoms, anemia, or other associated problems. They broke the 47 PCD patients into 2 groups for analysis:

Group 1: 23 patients who immediately went gluten free after being diagnosed with PCD, most due to digestive and other autoimmune complaints. Follow-up biopsies to screen for CD could not be performed since all of these patients were GF.

Group 2: 24 patients who stayed on a gluten-containing diet after being diagnosed with PCD. 14 had repeat biopsies at 1 year. Of these 14, 5 had villous blunting (full celiac disease) and 9 did not. Of the 9 who had normal biopsies at 1 year follow-up, 4 went GF due to symptom development and 5 remained without symptoms and had normal biopsies 3 years later.  The 10 patients with potential celiac disease who remained on a gluten-containing diet and refused follow-up biopsies are described as being in “good clinical condition,” however 5/10 had anemia, 3/10 had thyroid disease, 3/10 had diarrhea, 1/10 had alopecia, and 1/10 had rheumatoid arthritis on follow-up. While these problems might be perceived as being better than having full blown Celiac Disease, I wonder if so many symptoms would be present in this group of potential Celiacs had they gone GF.

The concept of non celiac gluten sensitivity was largely ignored in this paper. There is also no comment on how many intestinal biopsies were taken. The speaker that I listened to last night reiterated that at least 4-6 biopsies need to be taken from the duodenum in order to confirm a diagnosis of CD. If less than 4-6 biopsies are taken, CD can be missed.

In summary, we are in a gray zone as to how to advise others with “potential” celiac disease in terms of the gluten free diet. If one has PCD and feels lousy after eating gluten, then the decision to go gluten free is an easy one. For those who have PCD but do not have any ill effects from eating gluten (at least outward symptoms), I can see how the decision may be quite a bit more difficult.

After living so long with undiagnosed Celiac Disease, I would be hard pressed to not recommend the gluten free diet for those with Potential Celiac Disease. We currently have no idea how high the real risk of Celiac Disease is for this group. I personally know that it is a risk that I would not want my own family members to take….whether or not they would take my advice is an entirely different question!

Reference:

Prevalence and natural history of potential celiac disease in adult patients. Federico Biagi, Lucia Trotta, Claudia Alfano, Davide Balduzzi, et al. Scandanavian Journal of Gastroenterology. Posted online on March 19, 2013. (doi:10.3109/00365521.2013.777470)

*Also, a quick reminder that this is a blog. I am summarizing medical literature, but also adding in my own thoughts and opinions on what I have read. I am not trying to tell anyone what they should do for their own health, nor am I giving medical advice through this page. Thank you!

Email This Page
grade 1_2_2_2_5_2_2

Delay in Diagnosis of Celiac Disease

This is my first grade photo. This was taken right before I began to show signs and symptoms of Celiac Disease. Although it takes, on average, 10 to 13 years after the initial onset of symptoms for a patient with Celiac Disease to be diagnosed, in my case it took almost 30 years.

Undiagnosed, and hence, untreated, Celiac Disease is associated with anemia, osteoporosis, arthritis, infertility, central nervous system damage, and the development of other autoimmune diseases. Celiacs with longstanding exposure to gluten are also at an increased risk of cancer of the digestive system. Although some of these problems, such as anemia and infertility, are reversible once gluten free, others are not. My autoimmune thyroid disease (Hashimoto’s thyroiditis), which I suspect is due to decades of gluten exposure, will never go away.  Through the internet I have interacted with tons of other people with Celiac Disease with long delays in diagnosis (some not until their 50s or 60s). Anecdotally, it seems like a lot of us have multiple autoimmune issues, such as lupus, multiple sclerosis, fibromyalgia, and/or irritable bowel syndrome, as well as multiple food intolerances. It is unclear whether or not we would have developed these additional autoimmune problems had we removed gluten from our diets decades earlier, when we first started to show signs and symptoms of Celiac Disease. My gut tells me that we would have…

There was an interesting study published in Wales in 2007 in which the medical records of patients with Celiac Disease were reviewed. Celiac patients had a significant increase in number of subspecialist consultations in the years before diagnosis, seeing on average 5 different consultants. People with Celiac Disease also had symptoms of depression, anxiety, anemia, and diarrhea in much higher numbers than patients without Celiac Disease prior to diagnosis; 41% had a history of depression and/or anxiety. Swedish researchers examined the quality of life of 1500+ patients with Celiac Disease, both pre- and post-diagnosis, and found, not surprisingly, an improved quality of life for Celiac patients once diagnosed and treated (see link).

Last of all, a case report of a women diagnosed with Celiac Disease in her mid-forties (named Mrs. J) was published in a large medical journal called JAMA in 2011. Mrs. J’s main symptoms of Celiac Disease were recurrent miscarriages and chronic anemia. While I highly recommend that all of you read the article if you can, I am going to cut and paste a few of Mrs. J’s questions after diagnosis and the experts’ answers to her:

Could my miscarriages have been related to celiac disease? Currently the typical newly diagnosed patient with celiac disease is a woman around the age of 40 years who has had symptoms of celiac disease for over a decade. Given that active celiac disease has nutritional and direct inflammatory consequences on fertility, the reproductive life of many patients is irreversibly affected. In particular, the risk of miscarriage appears higher in women with untreated celiac disease compared to the general population. For these reasons, clinicians should maintain a very low threshold for celiac disease testing in this population.

Has my body sustained any irreversible damage from celiac disease over the years? The small intestinal mucosa has enormous regenerative capacity in both health and disease. Even individuals with longstanding, severe celiac enteropathy can expect to achieve complete or near complete intestinal healing with gluten avoidance and nutritional support, although the length of time to healing varies from less than one year to more than five years and healing is associated with younger age at diagnosis and improved GFD adherence. Outside of the intestine, however, healing is not always assured. A number of extraintestinal manifestations of celiac disease such as dermatitis herpetiformis, anemia, and joint pain, typically improve significantly or resolve within the first year of treatment, as was seen in Ms. J. One of the most common associations with celiac disease is reduced bone mineral density (BMD) which is seen in at more than 50% of patients at diagnosis. Although there is often a significant improvement in BMD over the first year of treatment with a GFD, up to 21% of patients will have persistent osteoporosis. There are multiple neurologic manifestations of celiac disease, some of including peripheral neuropathy and headaches which resolve, while case studies suggest that other manifestations including ataxia, may stabilize but rarely improve. Finally, there is a potential increased risk of secondary autoimmune disorders related to longstanding untreated celiac disease, and once triggered, these will not respond to gluten withdrawal.

My hope is that no child with current symptoms of Celiac Disease will have to wait 20+ years for diagnosis, like so many of us did. We need to prevent Celiac-associated problems, such as infertility, neurologic complications, and other autoimmune diseases, from developing in the first place, so that children with Celiac Disease can have an improved quality of life as adults!

References:

1. A case-control study of presentations in general practice before diagnosis of coeliac disease. Cannings-John R, Butler CC, Prout H, Owen D, Williams D, Hood K, Crimmins R, Swift G. Br J Gen Pract. 2007 Aug; 57(541):636-42.

2. Delay to celiac disease diagnosis and its implications for health-related quality of life. Norström F, Lindholm L, Sandström O, Nordyke K, Ivarsson A. BMC Gastroenterol. 2011 Nov 7;11:118.

3. Celiac disease diagnosis and management: a 46-year-old woman with anemia. Leffler D. Source Department of Gastroenterology, Beth Israel Deaconess Medical Center, and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215, USA. dleffler@caregroup.harvard.edu. JAMA. 2011 Oct 12;306(14):1582-92.

Email This Page
ID-10087749

The Gluten Contamination Elimination Diet

As many of us already know, there are some celiacs who are “refractory” and continue to have ongoing symptoms after going gluten free. In addition, there are a bunch of us who are “super sensitive” in terms of reactions to gluten cross-contamination. I am one of the super sensitives. Not too long ago I had a reaction from eating one bite of a Trader Joe’s “no gluten ingredients” brownie which I had prepared in my own gluten free kitchen for a potluck.

Just last week, Dr. Fasano and colleagues published a research paper on the effects of 3-6 months of a diet of exclusively whole, unprocessed foods on the symptoms of celiac patients who had no improvement while eating strictly gluten free. In this study patients were considered to have non-responsive celiac disease (NRCD) if they failed to respond to the gluten free diet or had a recurrence/relapse of symptoms despite being gluten free. Steroids are currently the standard of care for treating NRCD, which as we know can have serious side effects.

The researchers coined their diet the “Gluten Contamination Elimination Diet.” Here is the breakdown of foods with are allowed and prohibited on this diet:

Allowed: brown and white rice; all fresh fruits and vegetables; fresh meats; fish; eggs; dried beans; unseasoned nuts in the shell; butter; plain yogurt; plain milk, and aged cheeses; oils; vinegar (except flavored or malt); honey; salt. Beverages allowed include 100% juices, water, and Gatorade.

Not allowed: millet, sorghum, buckwheat or any other grains, seeds, or flours; frozen, canned, or dried fruits and vegetables; lunch meats; ham; bacon; seasoned or flavored dairy products; processed cheeses; flavored and malt vinegars.

Basically, all processed foods are eliminated. Of note, dairy is not reintroduced until week 4 of the diet.

17 patients with NRCD, all female, were placed on this diet for an average of 3-6 months. 14 of the 17 (82%) significantly improved on the Gluten Contamination Elimination Diet. Of those who did have biopsies performed after the diet, all but one had resolution of their villous atrophy. This is important information as there have been a lot of recent studies showing that persistent villous atrophy is common in celiac disease. Most of the patients in this study were able to eventually resume a “traditional” gluten free diet.

It has taken me over 3 years, and a lot of trial and error, to figure out the foods which my body loves and hates. Interestingly enough, my body’s food preferences are almost identical to the foods on the “allowed” list in this diet. Had I known about this diet, and adhered to it when I was first diagnosed, it would have saved me a ton of pain and anguish. I am optimistic that this diet (or a similar version) will become the standard of care for those newly diagnosed with Celiac Disease, and I hope that this happens sooner than later. If we work together, we can get the word out!

Reference: “Trace gluten contamination may play a role in mucosal and clinical recovery in a subgroup of diet-adherent non-responsive celiac disease patients.” BMC Gastroenterology. 2013. 13:40 (e-pub).

Email This Page

Celiac Disease and the Innate Immune System

256px-Innate_Immune_cells

I know that this title sounds very boring (so much so that I doubt that many will read any further than this).  But, if you can bear with me, there is some fascinating research involving the role of the innate immune system in reactions to wheat. Trust me!

The role of the immune system is to fight infection.  There are two main types of immunity: innate and adaptive. The adaptive immune system is highly evolved and involves antibody formation. The ability of our bodies to “remember” previous infections and respond to vaccines depends on adaptive immunity.

The innate immune system, on the other hand, is our first line of defense against bacteria and viruses. It is primitive, exists in all plants and animals, and does not involve antibody formation. The innate immune system is made up of different types of white blood cells, including neutrophils, monocytes, basophils, and mast cells (see picture above).  When confronted with an “invader,” these cells release chemicals, called cytokines, which cause widespread inflammation.

The traditional teaching is that autoimmune diseases involve the adaptive immune system, as antibodies are created against one’s own tissues and organs, called “autoantibodies.”  For example, in Celiac Disease antigliadin antibodies and tissue transglutaminase antibodies (TTG) are created. However, recent research has shown that the innate immune system may also be involved in the “gluten reaction” experienced in Celiac Disease.

Alpha-amylase/trypsin inhibitors (ATIs) are “pest-resistant” molecules found in wheat and other cereals and grains, such as corn and soy. A team of researchers from Boston and Germany have recently discovered that wheat ATIs trigger an innate immune response, with a release of pro-inflammatory cytokines from monocytes, macrophages, and dendritic cells, when they come into contact with human intestinal cells.  They were surprised to find that inflammation occurred when wheat ATIs came into contact with cells from all of the subjects (both with and without Celiac Disease). I find this to be both fascinating and scary.

I am curious to see if those of us with Celiac Disease who seem to be “super sensitives” may actually have a stronger innate immune reaction to wheat than other Celiacs. I am also wondering if the innate immune system plays a role in why so many of us with Celiac Disease develop additional food sensitivities with time and/or feel like we get “glutened” from gluten free foods from time to time. The fact that other grains contain ATIs, and hence, can likely trigger an innate reaction, may explain why so many of us feel our best when we are on a Paleo, or at least “grain-light,” diet.  Finally, I hope that this information will stimulate research into the mechanism of non celiac gluten sensitivity, which so many suffer from.

For more information on this subject I suggest the following:

1. Gliadin Triggers Innate Immune Reaction in Celiac and Non-Celiac Individuals.  Celiac.com webpage. 12/31/2012.

2. J Exp Med. 2012 Dec 17;209(13):2395-408. doi: 10.1084/jem.20102660. Epub 2012 Dec. Wheat amylase trypsin inhibitors drive intestinal inflammation via activation of toll-like receptor. Junker Y, Zeissig S, Kim SJ, Barisani D, Wieser H, Leffler DA, Zevallos V, Libermann TA, Dillon S, Freitag TL, Kelly CP, Schuppan D. Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.

3. Researchers believe pest resistance molecules in wheat play role in triggering innate immune responses.  National Foundation for Celiac Awareness website. 12/31/2012.

4. Natural “Pesticides” in Wheat: Is There a Role in Gluten Sensitivity and Celiac Disease? By Peter Olins, PhD. December 19, 2012.

Email This Page

So it appears that Celiacs are not slowly dying after all…

Happy celiac

I recently came across the question, “Are Celiacs really slowly dying?” on one of the Celiac Disease forums. My first thought was, “Aren’t we all slowly dying?” Then, as I read, I realized that the person who posted it was concerned about research showing that many adult Celiacs do not have complete healing of their intestinal mucosa (tissue) despite being on the gluten free diet. This is called “persistent villous atrophy” in the medical world.

One of the major studies of persistent villous atrophy was published in 2009 (see link). Italian researchers studied a large group (n=465) of Celiacs who were on the gluten free diet. The average follow-up biopsy was performed 16 months after biopsy-confirmed diagnosis of Celiac Disease. At the time of follow-up biopsy, 75% of the patients reported that their symptoms had disappeared and 87% of the subjects experienced normalization of their celiac antibody tests on the gluten free diet. Of the 465 Celiacs on the GF diet, they found the following on repeat biopsy: 8% had completely normal duodenal (small intestinal) tissue, 65% were in remission (intestines looked better than at diagnosis, but there were still an increased number of white blood cells in the intestinal tissues), 26% had no change from diagnosis, and 1% were actually worse than prior to going gluten free.

At the end of the paper, the researchers hypothesize that the lack of intestinal healing and increased white blood cells may be due to the continual activation of the innate immune system by small amounts of gluten in “gluten free” foods. I plan to discuss this soon in another post. The Italian researchers’ findings and discussion at the end of their paper have, unfortunately, led many to believe that the gluten free diet is harmful and/or killing all of us with Celiac Disease.

In February 2013 Dr. Green and colleagues at both the Celiac Disease Center at Columbia University and in Sweden will be publishing a paper entitled “Mucosal healing and mortality in celiac disease.” Their teams set out to see if a lack of mucosal healing (persistent villous atrophy) is associated with an increased risk of death for patients with Celiac Disease. Similar to the Italian researchers, > 40% of Celiacs were shown to have persistent villous atrophy on follow-up biopsies. However, the researchers found no association between persistent villous atrophy and an increased risk of death for Celiacs. This is definitely a good thing!

After reading both of these papers, I am left with many questions: Why does it take so long for adult Celiacs’ guts to heal after going gluten free? Should we expect the same for children with Celiac Disease? Is the persistence of white blood cells in the intestines contributing to and/or a “marker” of the “leaky gut” that so many of us seem to be experiencing, or is it a normal part of the slow healing process? How is the innate immune system involved? Are follow-up biopsies for Celiacs going to be necessary in the future now that so many patients are diagnosed on the basis of genetics, symptoms, and abnormal antibody testing alone? Isn’t the fact that symptoms resolve and antibodies normalize much more important than what actually shows up on repeat biopsies?

I’ll definitely be hitting the books and reviewing the innate immune system in upcoming weeks with plans to share what I find with you…

**Also, a quick reminder that this is a blog. I am summarizing medical literature, but also adding in my own thoughts and opinions on what I have read. I am not trying to tell anyone what they should do for their own health, nor am I giving medical advice through this page.

 

Email This Page

The Prevent Celiac Disease Study

prevent_cd_logo

I recently wrote about the best available recommendations for when to introduce gluten to babies who may be at risk of developing Celiac Disease. Although most babies are exposed to small amounts of gluten in breast milk, for my 4th baby (first born after my diagnosis), my breast milk was gluten free. Based on the best available evidence in the medical literature, small amounts of gluten should be given between 4 to 6 months of age, as it seems this is a critical window for the development of the immune system. If gluten is introduced later than this, the consensus is that it is important for breastfeeding to still be taking place during gluten introduction (see references in my previous post for more info).

I understand that this is a controversial area, as many parents feel that they should never introduce gluten to the at-risk child. I believe that, despite our best efforts to shield our children from gluten, they are eventually going to be exposed one way or another.

I did recently discover that the question of the timing of gluten introduction is being explored in Europe right now through the PreventCD study (www.preventCD.com).

This study has been sponsored by the European Union and involves 11 countries. More than 1000 infants were enrolled in the study from 2007 through 2011, and they are now being followed for the development of Celiac Disease from infancy until age 3. Based on the latest newsletter on the study website, the last participant will turn 3 in 2013, and the results will be “unblinded” at this point.

The 1000 infants in the study were all considered to be “at risk” for CD by having a first-degree relative (parent and/sibling) with Celiac Disease and being HLA-DQ2 and/or DQ8 positive. The study “intervention” started at 4 months of age and went for 8 weeks. Half of the babies were given a gluten-containing baby food on a daily basis and half were given a placebo. Breastfeeding was encouraged for both groups during the 8 week period.

The endpoint of the study is to see if there is any difference in frequency of Celiac Disease between the two groups at age 3. As a mom, Celiac, and pediatrician, I am eagerly awaiting these results. I am also intereseted to see if they will have the funding and resources to be able to follow the children into later childhood and adolescence. Either way, the results which they share will be valuable for all of us!

Although the study results will not be published for a while, the researchers have published an interesting review paper on infant feeding and Celiac Disease:

Systematic review: early infant feeding and the prevention of coeliac disease. Szajewska H, Chmielewska A, Pieścik-Lech M, Ivarsson A, Kolacek S, Koletzko S, Mearin ML, Shamir R, Auricchio R, Troncone R; PREVENTCD Study Group.Aliment Pharmacol Ther. 2012 Oct;36(7):607-18.

The full details of their study are described in this paper:

The PreventCD Study design: towards new strategies for the prevention of coeliac disease. Hogen Esch CE, Rosén A, Auricchio R, Romanos J, Chmielewska A, Putter H, Ivarsson A, Szajewska H, Koning F, Wijmenga C, Troncone R, Mearin ML; PreventCD Study Group.Eur J Gastroenterol Hepatol. 2010 Dec;22(12):1424-30.

Email This Page

Carrageenan and Celiac Disease

red seaweed

Carrageenan is a food additive that is extracted from red seaweed.  It is used as a thickener and emulsifier and is found in dairy products, processed meat, soymilk, toothpaste, and ready to feed infant formulas. I first came across it on an ingredient list early in on my gluten free (and food label reading) life. Once I learned that it is gluten free and “natural,” I assumed it was safe for me to eat as a celiac. However, a few months ago I began developing GI upset every time I ingested it, and I cut it totally out of my diet. Based on what I have now learned, I am glad that carrageenan is out of my life and kitchen.

First of all, the definitive answer to the question, “Is carrageenan safe for celiacs?” is never going to be known in our lifetimes.  No one is going to pay for a randomized controlled trial in which one group of celiacs are fed carrageenan and one group are fed a placebo, and outcomes of the two groups are measured. It’s just not going to happen.

Carrageenan has antiviral properties and stimulates the immune system.  On a quick search through the Pubmed.gov database, carrageenan aids in killing viruses and is being researched as an additive in treatments for HIV, enterovirus, and human papilloma virus.

When rats are given carageenan, they develop inflammation and arthritis-type symptoms.  Many studies of anti-inflammatory medications involve giving the test medications to Carrageenan exposed, and hence, inflamed rats and monitoring for improvement and side effects.

Research has shown that animals given carrageenan in high doses develop polyps, ulcers, tumors, and inflammation of the intestine. Most of the published research on the effects of carrageenan on human cells and tissues is by Dr. J. Tobacman from the University of Illinois, Chicago.  In the past year she has shown that carrageenan leads to enzyme changes and an inflammatory response in human intestinal and mammary cells as well. See link for more information.

There are two types of carrageenan. The first is degraded, or low molecular weight, and is the type which has been shown to cause inflammation in animals and human cells. It is not used in food products and products for human consumption.  The second type is undegraded, or high molecular weight, and is the type which is added to foods and beauty products.  There is an widespread belief that undegraded carrageenan is safe, and according to the Stonyfield farms website:

The scientific literature overwhelmingly concludes that undegraded carrageenan is safe to eat.  Based on this independent review of the literature, along with the Board’s recommendation to continue to allow it in organic production, we feel that carrageenan continues to be a safe ingredient to use.

What we don’t have any information about is whether or not our bodies convert some of the undegraded (“safe”) form to degraded (“unsafe”) form after we have eaten it. There are a few small studies from the 1970s which show that this chemical change occurs in the intestinal tract of rats and guinea pigs.

The European Union has banned the use of carrageenan in infant formulas due to concerns about safety in this population.  I just checked the website of the major U.S. formula makers and it is still present in most ready-to-feed formulas commercially available in the U.S.

Dr. Weil, M.D., one of the nation’s leaders in integrative health, spoke out against carrageenan in October 2012 (see link), stating, “I recommend avoiding regular consumption of foods containing carrageenan. This is especially important advice for persons with inflammatory bowel disease.”

As a Celiac I’ve made my decision and there’s no turning back now….

Email This Page

Introducing Gluten to the Baby At-Risk for Celiac Disease

IMG_3038 copy

This is Claire. She is my fourth baby, my “last” baby, and one of the greatest gifts of my life. She is the first baby I’ve had since being diagnosed with Celiac Disease and going gluten free. Because of this, I spent a lot of time during the postpartum period obsessing/fretting/freaking out about if/when I should expose my dear baby to gluten. I felt that I needed to do everything that I could to protect her from developing celiac disease. As usual, my husband was much more laid back and calm about the whole situation!

I researched my question and discovered the following:

1. Based on the best available information, gluten should be introduced to the “at risk” baby between 4 and 6 months of age. This runs counter to the current notion that infants should be exclusively breastfed for 6+ months and not have solids introduced until after 6 months.

2. Babies should be breastfed when gluten is first introduced and should continue to receive breast milk for at least 2-3 months after the first introduction to gluten.

Here is some of the science behind what I discovered:

-Anti-gliadin antibodies (antibodies against the major gluten protein) are present in breast milk of all women. The highest antibody titers are in colostrum, or early breastmilk, and levels decrease with time. It is hypothesized that these antibodies, which are passed from mother to baby, provide immunity to babies when gluten is introduced. Please refer to my post from November 2012 for additional information.

-Norris, et al. followed a large cohort of infants (>1500) in the U.S. who were at risk of developing celiac disease between the years 1994 and 2004. Feeding practices were analyzed and their research showed a much higher risk of celiac disease if gluten was introduced between 1 and 3 months of age or after 6 months of age.

- The rates of celiac disease skyrocketed in Sweden between 1984 and 1996; 3% of children born during this time developed celiac disease. This epidemic coincided with a nationwide change in feeding practice recommendations from starting solids between 4-6 months until after 6 months of age. This led to many infants having gluten introduced after being weaned from breastfeeding. See link for more information.

- The European Society for Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN) recommends avoiding both early (<4 months) and late (>7 months) introduction of gluten and to introduce gluten while the infant is still being breastfed. This mirrors the advice given by the University of Chicago Celiac Center (see website). The American Academy of Pediatrics emphasizes the importance of introducing gluten while breastfeeding in their 2012 “Breastfeeding and the Use of Human Milk” policy statement.

Overall, there seems to be a current consensus for an optimal “window” for introducing gluten to the “at-risk” baby between 4 and 7 months.

Back to sweet, little Claire. We started her on wheat-contaminated baby oatmeal at 4.5 months one time/day for about 4 weeks. She received exclusive breast milk for the next 2.5 months and is now a gluten-free baby. We’ll see what develops with time, but at if she develops Celiac Disease, at least I will know that I tried my best to prevent it!

Happy New Year and thank you for reading!

*Also, a quick reminder that this is a blog. I am summarizing medical literature, but also adding in my own thoughts and opinions on what I have read. I am not trying to tell anyone what they should do for their own health, nor am I giving medical advice through this page. Thank you!

Email This Page

Celiac Disease in the December 20, 2012 New England Journal of Medicine

Nejm_logo2011

I am grateful to one of my partners for leaving the December 20th issue of the New England Journal of Medicine in my mailbox with a yellow sticky note stating, “Jess, Thought this might interest you.” She was right, it did interest me, because it includes a review article written by my favorite celiac researcher, Dr. Fasano, from the Center for Celiac Research in Baltimore, MD (which, if you’re interested, will be moving to Boston, MA in 2013).

I love this article as, from the start, it highlights the fact that celiac disease can present in patients in “atypical” ways.

The article begins by describing a 22 year old female who fractures her wrist while playing volleyball. Outside of having fatigue and oral ulcers, she is otherwise healthy. An X-ray of her wrist shows that she has osteopenia (low bone density). Her blood tests show anemia, low iron, and low Vitamin D levels. She had no gastrointestinal symptoms but celiac disease is suspected.

I absolutely love this case presentation, as when I was in medical school (which wasn’t really that long ago) I learned that celiac disease was to be considered in patients with classic gastrointestinal symptoms, such as chronic abdominal pain, diarrhea, and weight loss. During my pediatrics residency (which was even more recently), I learned to suspect celiac disease in toddlers with signs of malnutrition, chronic diarrhea, and failure to thrive. Definitely not in young adults with a wrist fracture and low Vitamin D levels…..

I am so excited that hundreds and thousands of physicians, nurse practitioners, and physician assistants will read this article and learn and/or be reminded that patients with celiac disease can have symptoms NOT related to the GI tract. As Dr. Fasano eloquently states in the article, “The clinical features of celiac disease are protean and reflect its systemic nature.” How beautiful is that?

Dr. Fasano also reminds us of the consequences of untreated celiac disease, which include osteoporosis, spleen dysfunction, infertility and recurrent miscarriages, intestinal ulcers, and cancer. This is important for all doctors and patients to know.

He mentions that for many celiacs, despite adhering to a strict gluten free diet, minimal intestinal damage persists. I think that it is important for more to know this, as it highlights the need for additional research into celiac disease and the “leaky gut” phenomenon which it seems more and more of us are experiencing.

The last segment of the article is called “Areas of Uncertainty” and includes a discussion regarding the appropriate timing of introducing gluten to infants. He reports a 50% lower risk of celiac disease in infants who are receiving breast milk when gluten is introduced. I hope to write more about this in the upcoming months.

In conclusion, this article reaffirmed my admiration and gratefulness for Dr. Fasano, and I sincerely hope that its publication leads to increased diagnosis and treatment for the 97% of celiac patients in the U.S. who are walking around undiagnosed.

Email This Page

What Now? Wheat Sensitivity?

wheat sensitivity 2

I first came across the term “wheat sensitivity” in an editorial entitled, “Non-Celiac Wheat Sensitivity: Separating the Wheat from the Chat,” in the December 2012 issue of the American Journal of Gastroenterology. Thanks to a night of bad insomnia and a pretty interesting original research article by Carroccio, et al., in the same issue, I kept on reading…

Researchers out of Palermo, Sicily, state that “wheat sensitivity” is a both a new and real diagnosis. They reviewed the medical records of 267 patients diagnosed with both Irritable Bowel Syndrome (IBS) and “wheat sensitivity” during the 10-year period from 2001 thru 2011. All of their patients with wheat issues met the following criteria:

  1. Symptoms of irritable bowel syndrome
  2. Negative celiac antibody testing for TTG (tissue transglutaminase) and EMA (endomysial) antibodies
  3. Normal small intestinal biopsies (no villous blunting like that seen in celiac disease)
  4. Negative IgE (skin prick) testing for a wheat allergy
  5. Improvement in gastrointestinal symptoms on a wheat free diet by a double-blind placebo challenge

For the double-blind placebo wheat challenge the patients ate a regular diet, including 30 grams of wheat, daily for 2 to 4 weeks. 30 grams of wheat equals 1 slice of bread. They then had a 2-week elimination period, in which they stopped eating wheat, dairy, tomatoes, eggs, and chocolate, all of which are considered highly allergenic foods in Italy. After the elimination diet period, they were then given one of two pills everyday for 2 weeks. Pill “A” contained wheat and Pill “B” was a placebo sugar pill. Neither the research subjects, nor the researchers, knew which pill each subject was taking during the test period; this is why it is called a “double-blind” placebo study. There was a one week interim period in which subjects avoided all of the allergenic foods again, and then those who received pill “B” for the 1st two weeks were given “A” for the 2nd two week period and vice versa. The beauty of this type of crossover study is that each subject served as his or her own control.

If you’ve actually read this far, you may be wondering what the researchers found when they re-analyzed the 276 cases of wheat sensitivity….see below!

Compared to patients with Celiac Disease and IBS, those with “wheat sensitivity” have the following characteristics:

  • Increased likelihood of having atopic diseases (i.e. eczema, hay fever, environmental allergies)
  • Increased history of food allergies, especially during infancy
  • Elevated numbers of eosinophils (white blood associated with allergic reactions) in both the small and large intestine
  • Abnormally high anti-gliadin antibodies (a type of antibody against one of the gluten proteins) compared with those with IBS
  • Higher rates of anemia and weight loss than seen in those patients with non-wheat sensitive IBS

The researchers were able to break down the 276 wheat sensitive individuals into 2 groups. Those in Group 1 (n=70) shared many characteristics with Celiac patients, including having the genes that predispose to Celiac Disease (HLA DQ2 and/or DQ8). They believe that these wheat sensitive patients with IBS are at risk for the later development of celiac disease. Those in Group 2 (n=206) were found to have multiple food intolerances, including having antibodies to cow’s milk proteins, despite not having IgE mediated food allergies on skin prick testing. This group was referred to as the multiple food sensitivity group.

I believe that the researchers have done a great job demonstrating that there are many people with IBS who may benefit from being wheat free. I wish that I had known this when I was diagnosed with IBS at age 19. I was advised to increase my consumption of healthy whole grains, which I did; unfortunately, most of my increased grain consumption was in the form of whole wheat!

Perhaps in the future gastroenterologists will be able to use the presence/absence of eosinophils in the small and large intestines to help guide nutritional recommendations for patients with IBS. I am especially interested in seeing what the future holds for learning about links between wheat and cow’s milk protein sensitivities. I work with newborn babies and it seems like the numbers of babies with cow’s milk protein allergies are skyrocketing. I hope to write more about this soon.

Email This Page

The Effects of Gluten on the Brain and Nervous System

brain option 3

Most of the articles about gluten and celiac disease I’ve came across in the media have focused on symptoms related to digestion, such as abdominal pain and bloating after eating gluten, and damage to the small intestine. The bulk of the gluten-related discussions on the celiac forums I’ve perused concern questions and answers regarding the diagnosis of celiac disease and tips for following the gluten free diet. There have been several papers published over the last few years about the neurologic effects of gluten exposure for those with celiac disease and non-celiac gluten sensitivity. I do not believe that they have gotten the attention that they deserve in the media or on the forums. I am especially interested in this area as over the last few months I have developed a peripheral neuropathy (nerve damage) related to having celiac disease.

Dr. Hadjivassiliou is one of the leading researchers on neurologic problems related to gluten exposure. Although I have no idea how to pronounce his name, I can tell you that he is on faculty in the Department of Neurology at Royal Hallamshire Hospital in Sheffield, United Kingdom. My favorite paper of Dr. Hadjivassiliou’s is a review article titled, “Gluten sensitivity: from gut to brain,” which was published in the Lancet, a major medical journal, in 2010. In this paper, gluten sensitivity refers to both celiac disease and non-celiac gluten sensitivity. Some of the key points of this paper include the following:

• Most patients with neurologic symptoms related to gluten do not have gastrointestinal symptoms.

• Ataxia (a problem with balance and coordination) and peripheral neuropathy (nerve damage) are the most common neurologic symptoms related to gluten. Up to 25% of celiac patients on a gluten free diet will develop a peripheral neuropathy at some point.

• Patients with neurologic symptoms often have celiac “autoantibodies” on blood testing, usually anti-gliadin (AGA) antibodies and/or tissue transglutaminase (TTG) antibodies. Many patients with these antibodies have non-celiac gluten sensitivity, meaning that they have high celiac antibody levels and symptoms, but no evidence of villous blunting (seen in celiac disease) on small bowel biopsy.

• The average age of onset of gluten ataxia is 53 years and for the gluten-related peripheral neuropathy is 55 years.

• Brain MRI findings can include cerebellar atrophy (loss of volume) and/or white matter lesions which may mimic those seen in multiple sclerosis.

• Neurologic symptoms often improve on a strict gluten free diet but may never resolve completely.

Gluten sensitivity has also been associated with seizures, dementia, and migraines. Obviously, further research on the effects of gluten on the brain and nervous system is needed. I’ve came across many people on the celiac forums who have psychiatric symptoms related to gluten exposure as well, although this has not been well-studied.

It seems especially frightening that many people who develop neurologic problems, like me, do so when they are already on the gluten free diet. This is a reminder that even small traces of gluten can cause serious damage to those of us who are gluten sensitive. If you have any family members or friends who develop ataxia or a peripheral neuropathy of an unknown cause, I urge you to recommend an evaluation for celiac disease and non-celiac gluten sensitivity.

For further reading on the this topic I would suggest the following links:

1. “Brain Abnormalities Common in Celiac Disease Patients,” by P. Harrison, published in Medscape Neurology News on September 10, 2012.

2. Dr. Hadjivassiliou’s Lancet Neurology article, “Gluten Sensitivity: From Gut to Brain,” published in March 2010.

3. Living Without Magazine article, “Gluten Attack: Ataxia,” found in the Feb/Mar 2011 issue.

Email This Page

The Latest and Greatest on Non-Celiac Gluten Sensitivity

Yes, this is a real diagnosis, and it effects between 6 to 8% of our population, or approximately 18 million people. Many doctors and patients are unaware that it exists. Most of the papers on this topic have only been published in the last 2-3 years. The British Medical Journal published a case study and review of gluten sensitivity in their November 30, 2012 edition. It is the first case study I have come across in a major medical journal in which a patient self-diagnoses based on information which he found on the internet. The review article gives a good overview of our current understanding of this disorder.

Gluten sensitivity is a catchall term for a bodily reaction to eating gluten. It is not a food allergy, and the autoimmune process differs from celiac disease in that there is not destruction of the villi of the small intestine. People with gluten sensitivity may experience any of the following symptoms after eating gluten:

1. Gastrointestinal symptoms like diarrhea, abdominal pain, constipation, and/or “irritable bowel syndrome.”

2. Fatigue, depression, or difficulty concentrating. Feeling like one has a “foggy brain.”

3. Joint pains, stiffness, and/or leg numbness and tingling.

Anemia and osteoporosis have also been associated with gluten sensitivity. Some recent work has also shown neurologic problems, such as ataxia and peripheral neuropathy, in gluten-sensitive individuals.

Many of these symptoms overlap with celiac disease, but patients with gluten sensitivity do not meet the diagnostic criteria for celiac disease. Some may not have either of the two major celiac genes (HLA-DQ2 or DQ8), some may not have abnormal celiac antibodies, and most have normal, or almost normal, small bowel biopsies.

There are no tests for gluten sensitivity. Once celiac disease has been ruled out, if your symptoms go away when you stop eating gluten, and they return when you start eating gluten again, then you know that you are “sensitive” to it. You can diagnosis yourself.

We do not yet have information on the long-term effects of continuing to eat gluten if you have a gluten sensitivity. In this recent article, Dr. Fasano, one of the leaders in celiac disease research, states that he doesn’t believe that there are long term effects on health if you choose to do this.

I am a bit uncomfortable with this, as just a few decades ago it was believed that patients could “outgrow” celiac disease. The bottom line is that if a food makes you feel terrible, don’t eat it! You can definitely survive and live a full life without gluten-containing cupcakes, pizza, pancakes, etc. My fellow Celiacs and I are proof of this and we can help you on this journey.

For additional reading on this subject I would suggest Melinda Beck’s article, “Clues to Gluten Sensitivity,” published in the March 15, 2011, Wall Street Journal Health Journal.  There is also some helpful information about gluten sensitivity on the website www.celiaccenter.org.

Email This Page

Why are 97% of American Celiacs Undiagnosed?

Based on prevalence studies, it is estimated that 3 million Americans have Celiac Disease. Of these 3 million people, 2.9+ million have no idea that they have a serious autoimmune disease. This is a huge problem….

A few explanations for the atrocious rates of diagnosis:

-Only 1/3 of Celiacs have “classic” symptoms, such as abdominal pain and chronic diarrhea. Many of the symptoms of celiac disease, such as reflux, fatigue, anemia, oral ulcers, joint pains, hair loss, osteoporosis, seizures, migraines, infertility, etc. can be seen in other conditions and lead to errors and delays in diagnosis. There are probably many people with diagnoses such as chronic fatigue syndrome or fibromyalgia who actually have celiac disease as their underlying problem.

-Doctors used to teach that children with celiac disease would “outgrow” the condition, so there are many adult celiacs who believe that they outgrew their problems with wheat.

-The screening blood tests for celiac disease can be inaccurate.

  • Although there is evidence that patients need to have tests for several celiac antibodies, many labs are not performing all of these.
  • The labs that must be performed are 1. IgA endomysial antibodies, 2. IgA and IgG tissue transglutaminase antibodies, 3. total IgA antibodies, and 4. deamidated gliadin peptides.
  • 3% of celiacs have selective IgA deficiency, so if total IgA antibodies are not tested, the rest of the test results will be meaningless (meaning that celiac antibody tests will be negative even if celiac disease is present).


-Genetic testing is not perfect either. Most labs will test for two genes, HLA-DQ2 and HLA-DQ8, which are found in 95% of people with celiac diease. If a patient doesn’t have these genes, even if they get horribly sick from eating gluten, they are often told that they do not have Celiac Disease and may not be offered further testing. However, in 3-5% of cases, patients with Celiac Disease on biopsy are negative for DQ2 or DQ8. So it is possible to be a Celiac, even if you don’t have the 2 most common genes.

-Many biopsies are done incorrectly. According to most experts, the “gold standard” of diagnosis is an endoscopy with biopsy. Celiac disease destruction of the small intestine can be very patchy, and if the wrong areas are biopsied, and/or not enough tissue samples are taken, it can be missed. It is essential that at least 4 samples are taken. It is essential that the duodenal bulb be biopsied in all cases. Despite the guidelines, only 35% of biopsies are done correctly. Many patients have classic symptoms of celiac disease, positive antibodies and/or gene tests, but have negative biopsies due to the wrong area being biopsied. They are labeled as being gluten intolerant and some are sadly told and advised to continue to eat gluten!

-Right now there is no cure. Celiac disease is treated with the gluten free diet, but there is not a pharmaceutical “magic bullet.” I think that when there is finally a pill to treat this disease, and the associated marketing campaign, that people will finally get diagnosed in large numbers.

The bottom line is that if you or a loved one has any symptoms of celiac, it is worth researching the idea of celiac disease and discussing with your doctor. A lot of people who I have met have been diagnosed after asking their doctors to test them. Also, the book “Celiac Disease: A Hidden Epidemic” by Peter Green, is definitely worth checking out if you have any suspicions or conerns that gluten is causing you harm.

Email This Page

Help, My Gut is Leaking! Celiac Disease and the “Leaky Gut”

Intestine_-_sized

I have heard and read tidbits about the concept of the “leaky gut” for a while, especially in regards to autism, so it was with great interest that I read Dr. Alessio Fasano’s article, “The Leaky Gut and Autoimmune Diseases,” which was published in 2012. Dr. Fasano is one of the leading U.S. researchers of Celiac Disease and is the head of the Center for Celiac Disease Research at the University of Maryland. He was the first to report that 1 in 133 Americans are Celiacs (the majority of which have no idea). He will likely be one of the first to find a cure for us. And, as I recently learned by watching a recent televised interview, he is also very easy on the eyes…

Our digestive tracts are one of the largest immune organs in our body. The tissues of our small and large intestines act as a barrier to keep out proteins and other molecules which may be perceived by our bodies as being “foreign.” According to Dr. Fasano, increased intestinal permeability (or loss of the barrier function of our intestines) may play a role in the development of autoimmune diseases. In autoimmune diseases, our immune systems produce antibodies against our own tissues, called “autoantibodies.” For example, in Hashimoto’s Disease, the first autoimmune disease which I was diagnosed with, autoantibodies have attacked and destroyed my thyroid gland. In Celiac Disease, when our bodies are confronted with “foreign” proteins in gluten, such as gliadin, autoantibodies are formed which lead to an attack that may cause injury to many organs, including the intestines.

We all have “tight junctions” between the cells in the lining of our intestines. These tight junctions prevent the movement of “foreign” proteins to the layer of the intestines where the immune response occurs. Dr. Fasano has found that individuals with autoimmune diseases have increased levels of a molecule called zonulin in their intestines. Zonulin plays a role in making the intestinal tight junctions looser, and thus, “leakier.” Leaks between the tight junctions allow “foreign” proteins, i.e. gliadin, to sneak into the deeper layers of the intestine and for autoantibodies to be created. Dr. Fasano provides evidence that zonulin levels are increased in Celiac Disease as well as other autoimmune diseases, such as Type I Diabetes, Asthma, Multiple Sclerosis, and Inflammatory Bowel Disease.

Trials of a zonulin blocker, called Larazotide acetate, are currently underway. Thus far, patients with Celiac Disease who take this medication have much “tighter” junctions when ingesting gluten. While this would not be a cure for celiac disease, it would be a great way to prevent people on the GF diet from getting accidentally “glutened.” And if you are a Celiac or have a loved one who is a Celiac, you can understand how truly horrendous it is to get “glutened.” I am curious to see if research will show that increased zonulin levels lead to other food intolerances and sensitivities in those of us with Celiac disease. Since going gluten free I have also developed autoimmune/inflammatory symptoms after consuming foods with soy proteins as well as sulfites. I guess that time will tell. Until then I am patiently waiting….

Email This Page

Save the Date (September 22-25, 2013, Chicago, IL)

I am thrilled to learn that the 15th International Celiac Disease Symposium will be taking place in Chicago from September 22-25, 2013. The last symposium was held in Oslo, Norway in 2011. This meeting will bring together celiac researchers, physicians, nurses, dietitians, patients, etc. from around the world. The latest research on celiac disease and non-celiac gluten sensitivity will be presented. There will be 2 separate forums, one for physicians and scientists, and a clinical forum for patients, clinicians, dieticians, etc.

I plan on attending for sure, as I live within driving distance to Chicago, it’s a lovely time of year to visit the city, and I am eager to learn from this conference. I will likely sign up for the “clinical” track, although there is a part of me which would love to participate in the scientific forum as well (each person can only register for the scientific or the clinical forum).  Luckily, I have plenty of time to make a decision.

Please check out the Symposium’s website for full details and registration. I hope to see you/meet you there and/or share information with you after I attend.

 

Email This Page