Celiac.com 05/12/2018 - Dear researchers/scientists at NIDDK: RE: Misinformation on your website?

I am encouraged that you have information about celiac disease on your website (Provider Points: Testing for Celiac Disease). My wife has had celiac disease (CD) for more than 35 years and we always welcome more public/professional exposure for this perplexing condition. I'm a gluten-sensitive-patient advocate and concerned that your information does not appear to be supportable by laboratory science. (Yes, I saw the references and the reviewers—very prestigious literature and referees for your document.) Let's review the information from an accountant's perspective.  

Before we get into the details of your site, I must mention that I was a medical laboratory technologist in California for 15 years and am quite familiar with the issues that you discuss related to laboratory testing. I was actually working in the lab years ago when the PSA (prostate-specific antigen) was proclaimed the ultimate test for prostate cancer. Now the U.S. Preventive Services Task Force (USPSTF) recommends against PSA screening. Because of this reversal of support for the PSA and other similar tests that were first introduced with blazing reviews throughout the years, I take a skeptic's view whenever I see amazing claims about lab tests. I have read much of the CD research literature and have not changed my cynical ways after reviewing the astounding claims for the blood tests and the biopsy in preparation for writing my book, Celiac Disease & Gluten Sensitivity: A Troubled Past but a Promising Future.

Before we put the accountant to work, I want to point out that you have taken the safe road when stating that, "For accurate diagnostic test results, patients must be on a gluten-containing diet." One reason you made that statement is because the news sources certainly give us the impression that an expanding portion of the population is attempting the gluten-free diet (GFD) first, before any testing. Many patients would therefore need to return to a gluten-containing diet. Most major celiac organizations designate a certain number of weeks or months for a person to be on this diet in order to get the accurate results to which you refer. I assume you are aware that no one really knows exactly how long patients must consume gluten to ensure high rates of accuracy for the blood tests. You will find a variety of time spans on the various university and public advocacy websites. 

Since yours is a Provider Points site, it would seem prudent for you to explain to the providers that the exact length of time is unknown—therefore the doctor would need to take his/her best guess because each person is unique. It's worth noting that currently most doctors know little or nothing about CD and its myriad ramifications. This is my first point. Before we stick that needle in the patient's arm, we may already be in error by specifying a certain time span for the gluten-containing diet and therefore introducing inaccurate results for those patients who did not perform within the limitations. And neither you nor the providers know how large, or small, that number may be. 

Now the accountant can clock in. You seem to favor the tTG test as the best. You say that it has a sensitivity of more than 90% (very few false negatives) and a specificity of more than 95% (very few false positives). As you know, those are remarkably good numbers for any lab test (not to mention the EMA, which Dr. Green says is approaching 100% accuracy). Let's break those figures down. You assert that 2–3% of celiac patients have selective IgA deficiency. Are those people included in the 90/95? I assume they are, since we can't know who these patients are until they're tested. If they are included, then those 90/95 numbers are even more amazing, because we now have a small (but significant) percentage of cases who will immediately show up as false negatives. 

Let's move to the other group that you've stated might not be accurate because the "tTG and EMA tests may yield false negative results"—young tykes. Again, every individual is unique, and to assume that your 18-month cutoff age will work for every child is pushing the limits. I noticed you also did not include the elderly here, although the two clusters have similar problems—immune systems that are immature (kids) or faulty (seniors). So both ends of the age continuum may show false negative results for the tTG. 

In fact, it wouldn't be a scientific stretch to expand this idea further, because we know there are millions worldwide within these age specifications that are immunocompromised due to undernutrition. When you add the age factor plus the nutrition factor together in one patient, he/she is even more unlikely to be able to produce a robust autoantibody response, and therefore would show up as a false negative. I'm not sure the accountant can keep track of these numbers—they keep adding up and making those 90/95 values seem like a dream. 

I've already introduced the undernutrition topic, so let's throw in a few million people who are undernourished, and therefore may be immunocompromised but are not at the extremes of the age spectrum. Let's now go beyond the undernutrition group and identify more of the immunocompromised. That list is quite long, but here are just a few examples of patient conditions/illnesses: HIV/AIDS, alcoholism, diabetes, corticosteroid use, and immunosuppressant use.
There are two recent developments that help answer a question that may be rolling around in the back of your mind, "How many more hours do I need to pay this accountant before she's finished calculating the total number of patients who may show false negative results on the CD blood tests?" The answer is, "You're going to need to her full time." 

First, new research on patients' responses to vaccines (International Journal of Obesity, "Obesity Affects Influenza Vaccine Response", October, 2011) suggests that obesity may impede a person's immune system such that they may not be able to produce sufficient antibodies as would normally be expected: another subset of the population who may show false negatives when tested for CD. This is preliminary research which will be further explored because the finding is critical to the vaccine industry.  If true, can you imagine the number of people added to the accountant's ledger in the U.S. alone?

Second, on page 27 of a monograph titled, 21st Century Medicine: A New Model for Medical Education and Practice, by David Jones, MD, Laurie Hofmann, MPH, and Sheila Quinn, the researchers describe the affect that various influences may have on gene expression. 

"The evidence clearly reveals that each patient is a unique individual—one whose gene expression patterns are constantly in flux and whose complex and ever-changing response to treatment, environment, and lifestyle will challenge physicians to listen differently, see differently, and respond differently than taught by the linear model of acute care."
That statement allows us to question the accepted position of the CD community which clings to the principle that once the celiac genes are turned on, they stay on forever—theoretically at the same level of expression—such that once a patient becomes sensitive to gluten, that patient is forever relegated to a gluten–free diet.  

The authors' statement adds support to the controversial concept of "transient celiac disease," which suggests that a person may have a full blown case of symptomatic CD with all the tests showing positive, and then at some time later in life, the gene expression modulates and the person either becomes less sensitive to gluten or even may return to a totally normal diet without any untoward consequences. The patients' blood tests and biopsies would also potentially resort to normal. If you decide to read my book, you will observe that we already have documented cases of blood tests that reverted back to normal in people who had been officially diagnosed with CD but continued on a normal diet (fluctuating antibody levels).

I think you get the picture. All of the aforementioned patients may show up as false negatives; I suspect the accountant can give you a strong estimate as to how accurate the 90/95 numbers are. Since you have only briefly discussed the biopsy on these web pages, I won't critique it, beyond stating that using that test as the "gold standard" also pushes the limits of credibility. If you would like to read my ebook it's on Amazon.com. It clearly identifies the shortcomings of the testing suggested for CD using accepted research and common laboratory knowledge. 

I am, as you are, a gluten-sensitive-patient advocate, but misinformation can be just as bad as no information. I'd love to have a professional conversation with you about the issues I have raised. 

Thank you for your time,
Gordon Heinrichs, DC

P.S. I am retired from seeing patients and write about gluten-health issues as a hobby and passion.

Celiac.com 05/04/2018 - It has been recognized for several decades that both children and adults with celiac disease have a significantly increased frequency of osteoporosis and increased risk of fractures as compared to the age-matched non-celiac healthy individuals. Based on published data the prevalence of osteoporosis among celiac patients varies from as low as 4% to as high as 70%. The data from our clinic indicate that prevalence of osteoporosis among adults with gluten intolerance and celiac disease is in the vicinity of 30-40%.

Characteristics and causes of osteoporosis 
Osteoporosis is a bone disease characterized by the reduced bone mineral density and impaired bone architecture that leads to an increased risk of fracture. The three main mechanisms by which osteoporosis develop include an inadequate peak bone mass, excessive bone resorption and inadequate formation of new bone during remodeling. 

At a given age, bone mass results from the amount of bone acquired during growth (the peak bone mass) minus the acquired bone loss due to variety of reasons including age-related processes, malabsorption syndromes, chronic steroid use etc.  The rate and magnitude of bone mass gain during the pubertal years may markedly differ from one individual to another. It has been demonstrated that pediatric onset of celiac disease and poor compliance with gluten-free diet during childhood do significantly reduce peak bone mass. 

One of the main causes of osteoporosis is an alteration in bone remodeling due to imbalance between bone formation and resorption, with a predominance of resorption resulting in a reduction in bone mass and increased risk of fractures. Formation of the new bone is facilitated by specialized cells, osteoblasts, which actively synthesize bone matrix. Bone resorption is mediated by other specialized cells, osteoclasts.

One of the main regulators of bone remodeling is the RANK/RANKL/OPG system. During bone remodeling, bone marrow cells and osteoblasts produce RANKL(receptor activator for nuclear factor kB ligand), which bonds with a transmembrane receptor of the osteoclast precursor, RANK(receptor activator of nuclear factor kB), causing their differentiation and activation. Osteoprotegerin (OPG) binds to RANKL before it has an opportunity to bind to RANK, and hence suppresses its ability to increase bone resorption.

Normal bone remodeling is based on the permanent renovation of the skeleton and consists of an initial phase of bone resorption followed by a phase of formation, both of which are regulated by general (endocrine) factors and local (paracrine) factors. The main endocrine factors include parathyroid hormone [PTH] and vitamin D as well as estrogens and, to a lesser extent, testosterone, thyroid hormones, growth hormone and leptin. Local factors include various cytokines (IL-1, IL-6 and TNF-a playing a role) key growth factors that regulate the process.

There are several well-characterized risk factors which contribute to the development of osteoporosis in celiac patients. These include:

1. Malabsorption of vitamin D and secondary hyperparathyroidism
Villous atrophy in celiac patients reduces the active absorption surface and induces steatorrhea (exces fat in feces), which has a chelating effect on calcium and vitamin D, making their absorption difficult. This reduces levels of the vitamin D transporting protein (calbindin and calciumbinding protein) and increases PTH synthesis which, in turn, lead to increased bone resorption causing osteoporosis.

2. Malabsorption of vitamin K
Malabsorption of fat soluble vitamins including vitamin K is a common finding in celiac patients. Three vitamin-K dependent proteins have been isolated in the bone: osteocalcin, matrix Gla protein (MGP), and protein S. 

Osteocalcin is a protein synthesized by osteoblasts. The synthesis of osteocalcin by osteoblasts is regulated by the active form of vitamin D—1,25-dihydroxy-cholecalciferol. The mineral-binding capacity of osteocalcin requires vitamin K-dependent gamma-carboxylation of three glutamic acid residues. 

MGP has been found in bone, cartilage, and soft tissue, including blood vessels. The results of animal studies suggest MGP facilitates normal bone growth and development. 

The vitamin K-dependent anticoagulant protein S is also synthesized by osteoblasts, but its role in bone metabolism is unclear. Children with inherited protein S deficiency suffer complications related to increased blood clotting as well as decreased bone density.

The data on the role of vitamin K in osteoporosis came from the clinical observations indicating that a chronic use of vitamin K antagonists such as warfarin increases risk of vertebral and rib fractures. Accordingly, vitamin K supplementation significantly lowers risk of vertebral and hip fractures. 

3. Magnesium deficiency
Magnesium deficiency may be an additional risk factor for celiac-associated osteoporosis. This may be due to the fact that magnesium deficiency alters calcium metabolism and the hormones that regulate calcium. Several human studies have suggested that magnesium supplementation may improve bone mineral density. Magnesium deficiency is easily detected with laboratory tests (eg, low serum magnesium, low serum calcium, resistance to vitamin D) or clinical symptoms (eg, muscle twitching, muscle cramps, high blood pressure, irregular heartbeat). Screening for magnesium deficiency should be routinely included in the screening of celiac patients with osteoporosis.

4. Chronic diarrhea and metabolic acidosis
Chronic diarrhea in patients with celiac disease results in significant bicarbonate losses and development of metabolic acidosis. Bone is a major site for the extracellular buffering of the retained acid. Therefore, one of the main compensatory mechanisms maintaining a stable serum bicarbonate level in the face of an uncorrected metabolic acidosis is the dissolution of bone buffers and net efflux of calcium from bone. Bicarbonate supplementation in patients with metabolic acidosis decreases urinary calcium, phosphorus and hydroxyproline wasting supporting the concept of negative effects of acidosis on bone health.

5. Hypogonadism
Decline of estrogen production and activity is one of the main events in the development of age-related osteoporosis. It is well known that estrogen deficiency is important in the pathogenesis of osteoporosis not only in women but also in men. Increase in bone mineral density in young men and declines in older men are related to circulating free estrogen, not testosterone. In general, patients with celiac disease are characterized by low levels of circulating estrogens which contributes to the development of premature osteoporosis. 

6. Chronic use of Proton Pump Inhibitors 
Proton pump inhibitors (PPIs) are one of the most widely used classes of drugs. The commonly used PPIs include such drugs as Omeprazole (brand name: Prilosec), Lansoprazole (brand name: Prevacid), Dexlansoprazole (brand names: Kapidex, Dexilant), Esomeprazole (brand name: Nexium), Pantoprazole (brand name: Protonix) and Rabeprazole (brand name: AcipHex). Chronic use of PPIs for gastroesophageal reflux disease and other related conditions has been associated with impaired calcium and magnesium absorption and increased risk of vertebral and nonvertebral fractures. 

7. Chronic use of Selective Serotonin Reuptake Inhibitors 
Selective Serotonin Reuptake Inhibitors (SSRIs) are frequently used in celiac patients for treatment of depressive disorders. The commonly used SSRIs include such drugs as Citalopram (brand name: Celexa), Escitalopram (brand name: Lexapro), fluoxetine (brand name: Prozac), fluvoxamine (brand name: Luvox), Paroxetine (brand name: Paxil) and Sertraline (brand name: Zoloft). It has been demonstrated that SSRIs increase extracellular 5-HT (5-Hydroxytryptophan) levels that have deleterious skeletal effects. The skeletal serotonergic system consists of 5-HT receptors and the 5-HT transporter (5-HTT) in osteoblasts and osteocytes. 5-HTT is a transmembrane protein targeted by SSRIs. 5-HT restrains osteoblastic activity, thus leading to bone loss. 

8. Autoimmune mechanisms
Autoimmune mechanisms have been long suspected as risk factors contributing to development of osteoporosis in celiac patients. Near a decade ago, it was demonstrated that sera from celiac patients with osteoporosis contains significantly high titers of antibodies against bones as compared to non-celiac osteoporotic patients. The immunostaining was localized in areas where an active mineralization process occurred and was similar to the distribution of the native bone tissue transglutaminase. Recently, it has been described that a subset of patients with celiac disease has autoantibodies to osteoprotegerin, which block the inhibitory effect of osteoprotegerin on signaling by the receptor activator of nuclear factor (NF)-kappaB (RANK), and are associated with severe osteoporosis and high bone turnover. 

9. Chronic inflammation
Chronic inflammatory diseases, including celiac disease, are associated with overproduction of proinflammatory cytokines such as TNF-a, interleukin(IL)-1, IL-6, IL-11, IL-15 and IL-17 among others which activate osteoclasts and accelerate bone resorption leading to osteoporosis.

In conclusion, osteoporosis associated with celiac disease is not a coincidental problem. It is a consequence of disease-specific (autoantibodies to osteoprotegerin), disease-nonspecific (malabsorption of vitamin D, K and magnesium, hypogonadism, chronic inflammation, chronic diarrhea and metabolic acidosis) and jatrogenic (overuse of PPIs and SSRIs) events accelerating resorptive processes in the skeleton. Correction of the aforementioned risk factors in celiac patients can reverse the development of osteoporosis and reduce the risk of osteoporosis-associated fractures.

Bibliography:

• Bab I, Yirmiya R. Depression, selective serotonin reuptake inhibitors, and osteoporosis. Curr Osteoporos Rep. 2010 Dec;8(4):185-91.
• Bianchi ML. Inflammatory bowel diseases, celiac disease, and bone. Arch Biochem Biophys. 2010 Nov 1;503(1):54-65.
• Ito T, Jensen RT.  Association of long-term proton pump inhibitor therapy with bone fractures and effects on absorption of calcium, vitamin B12, iron, and magnesium. Curr Gastroenterol Rep. 2010 Dec;12(6):448-57.
• Katz S, Weinerman S.  Osteoporosis and gastrointestinal disease. Gastroenterol Hepatol (N Y). 2010 Aug;6(8):506-17.
• Riches PL, McRorie E, Fraser WD, Determann C, van't Hof R, Ralston SH. Osteoporosis associated with neutralizing autoantibodies against osteoprotegerin. N Engl J Med. 2009 Oct 8;361(15):1459-65.
• Stazi AV, Trecca A, Trinti B.  Osteoporosis in celiac disease and in endocrine and reproductive disorders. World J Gastroenterol. 2008 Jan 28;14(4):498-505.
• Sugai E, Cherñavsky A, Pedreira S, Smecuol E, Vazquez H, Niveloni S, Mazure R, Mauriro E, Rabinovich GA, Bai JC.  Bone-specific antibodies in sera from patients with celiac disease: characterization and implications in osteoporosis. J Clin Immunol. 2002 Nov;22(6):353-62.
• Turner J, Pellerin G, Mager D.  Prevalence of metabolic bone disease in children with celiac disease is independent of symptoms at diagnosis. J Pediatr Gastroenterol Nutr. 2009 Nov;49(5):589-93.
• Vasquez H, Mazure R, Gonzalez D, Flores D, Pedreira S, Niveloni S, Smecuol E, Mauriño E, Bai JC. Risk of fractures in celiac disease patients: a cross-sectional, case-control study. Am J Gastroenterol. 2000 Jan;95(1):183-9.
   

Celiac.com 04/21/2018 - Dear Friends and Readers,

I have been writing articles for Scott Adams since the 2002 Summer Issue of the Scott-Free Press. The Scott-Free Press evolved into the Journal of Gluten Sensitivity. I felt honored when Scott asked me ten years ago to contribute to his quarterly journal and it's been a privilege to write articles for his publication ever since.

Due to personal health reasons and restrictions, I find that I need to retire. My husband and I can no longer travel the country speaking at conferences and to support groups (which we dearly loved to do) nor can I commit to writing more books, articles, or menus. Consequently, I will no longer be contributing articles to the Journal of Gluten Sensitivity. 

My following books will still be available at Amazon.com:

• Gluten-free Cooking for Dummies
• Student's Vegetarian Cookbook for Dummies
• Wheat-free Gluten-free Dessert Cookbook
• Wheat-free Gluten-free Reduced Calorie Cookbook
• Wheat-free Gluten-free Cookbook for Kids and Busy Adults (revised version)

My first book was published in 1996. My journey since then has been incredible. I have met so many in the celiac community and I feel blessed to be able to call you friends. Many of you have told me that I helped to change your life – let me assure you that your kind words, your phone calls, your thoughtful notes, and your feedback throughout the years have had a vital impact on my life, too. Thank you for all of your support through these years.

Celiac.com 04/14/2018 - There is a revolutionary new book about gluten sensitivity and celiac disease, written by Dr. Gordon Heinrichs, D.C. (whose article appears in this issue). His careers as a medical laboratory technologist, then a chiropractor, have uniquely located him to see gluten's impact on health in an entirely new way. His book critiques relevant scientific explorations and discoveries and the ensuing clinical practices. Titled "Celiac Disease & Gluten Sensitivity: A troubled past, but a promising future", this exciting book is a breath of fresh air in the field of gluten sensitivity and celiac disease. Dr. Heinrichs' thoughtful analysis of relevant data combined with the application of practical common sense explodes some of the common medical myths that claim to distinguish gluten sensitivity from celiac disease. He also explores conventional wisdom around dietary experimentation, and offers a rational approach to diagnosing gluten sensitivity. 

The evidence Heinrichs provides raises questions about the view that we should continue to eat gluten until we can visit a gastroenterologist and get a biopsy taken. He also challenges the belief that HLA analysis is beneficial for those who are aware that gluten causes some or all of their health problems. 

After a preview of the final draft, I can confidently predict that anyone who is interested in thoughtful, objective, and health promoting insights into gluten's impact on human health will be intrigued and motivated by the offerings of this inexpensive, powerful new ebook. I recommend it without reservation. It is very well researched and written and is now available on Amazon. I hope it will become the new best seller among books that explore the gluten syndrome.

Celiac.com 03/29/2018 - Fatigue is the most common symptom plaguing a majority of patients. Trouble sleeping, weight issues, PMS, headaches, fertility or libido issues, and achy joints are also very common and can all be affected by hormonal imbalance that continues after gluten has been removed from the diet.  The trouble with trying to resolve such symptoms is that the root cause can vary. If every patient with fatigue had a thyroid problem, it would be easy to correct because we would know exactly where to look. 

If you're gluten intolerant you may have suffered from some of the complaints listed above prior to discovering your celiac disease or gluten sensitivity. But perhaps now, despite your gluten-free diet, some of these same symptoms continue to plague you.  If so, read on.

Let's review the list of symptoms and add a few more:

• Fatigue
• Trouble sleeping
• Weight trouble
• PMS
• Migraines
• Infertility or miscarriage
• Achy joints or muscles
• Allergies
• Light headedness
• Frequent illness
• Asthma

While the list is long, believe it or not, there is a common cause to all of them.  I'm not saying it's the only cause, but what I do wish to discuss is the reason why someone can be found gluten intolerant, successfully institute a gluten-free diet, yet continue to suffer from many of the above symptoms.

There are two glands in your body called the adrenal glands. They sit atop each of your kidneys and they are the masters of multi-tasking! If I asked you if one part of your body was responsible for:

Giving you energy, maintaining your weight, keeping your immune system strong, maintaining stable mood, anti-aging, controlling sleep quality, assisting with hormonal balance, keeping allergies at bay and more…what would you say? 

You might think to yourself that if there was one type of body part responsible for all those things then you had better start treating it well! You'd be very right in your analysis.

As you've probably guessed the aforementioned adrenal glands are responsible for that very long list and, unfortunately, those very same adrenal glands tend to be quite stressed in the gluten intolerant individual.

Why? Because adrenal glands are sensitive to, and get very stressed with, unstable blood sugar. Stable blood sugar comes from eating healthy food that your body finds nourishing. As you well know if you're gluten intolerant, gluten, for you, is a poison. Therefore years of eating gluten created unstable blood sugar and thereby put a tremendous strain on your adrenal glands.

Because of the many, many jobs that the adrenal glands do, simply removing gluten as a stressor is typically insufficient to restore them to normal function. They need to be 're-set' with a nutritional and dietary program, to restore their good health. This explains why many who are gluten intolerant continue to suffer with the symptoms mentioned above.

Therefore, even if your gluten intolerance has been diagnosed and you've instituted a strict gluten-free diet, if you haven't also found a clinician who understands and specializes in restoring health and function to the adrenal glands, you may very well continue to suffer with symptoms associated with adrenal stress.

The good news is that the treatment to normalize adrenal function is not at all difficult. It is a completely natural program, when done correctly, involving no dangerous drugs or surgery. There are lab tests to determine the level of adrenal malfunction occurring but these are functional specialized lab tests rather than traditional ones. I mention this because I want to ensure that there is no confusion created when I mention adrenal function lab testing.

The adrenal glands can become diseased but the disease isn't common. If you ask your traditional doctor to test for adrenal malfunction he or she will test for adrenal disease – once again a rare occurrence – and will likely pronounce your adrenal glands 'fine'. What I am discussing is malfunction vs. disease, two very different conditions. While adrenal gland disease is rare, adrenal gland malfunction is extremely common. It is this latter condition that we are discussing here. 

This is an important distinction because I want to make sure that if you are suffering from adrenal fatigue that you aren't given a 'clean bill of health' incorrectly. Unfortunately this happens often. If it took you a while to receive a diagnosis of gluten intolerance then you will understand this phenomenon. Sadly this area of health is fraught with misunderstanding and it is the patient who suffers, often unnecessarily.

If you need any help finding a clinician to help you, feel free to contact me. Normalizing adrenal function is one of our areas of expertise and patients visit us for treatment, at our destination clinic, from across the country, as well as internationally. If we cannot find a clinician close to you that specializes in this then we are more than happy to see you here. The good news is that the treatment is natural and inexpensive.

I look forward to hearing from you.

Celiac.com 03/23/2018 - I should probably add severe dermatitis herpetiformis to that title. It was numerous doctors' guessing games, a medical misadventure, and years of improper eating that led to my arrival at "severe". I often wonder why 'misadventure' was the legal term they used to describe a doctor giving me a neuroleptic drug for "spots". After all, there was no adventure in what occurred and the only thing that was 'missed' was the correct diagnosis. But my tale is one of a beginner's trials. I described my medical 'misadventure' in a previous issue. Perhaps this article could be called "The Perils of Pauline" if my name was Pauline.

When I was diagnosed with celiac disease and severe dermatitis herpetiformis (DH) I was told that the diet was very difficult to follow and I would have to be vigilant or Dapsone might not stand in the gap as my savior from the itching, I was told that I would suffer abdominal pain, outbreaks of sores, anemia, and, (big swallow) horrible bowel disorders.

About ten years ago I submitted an article about celiac disease and DH to a magazine. I was told that nobody wants to hear about 'bowels'. Thank goodness times have changed and we now have our own magazine. I can use terms like "flattened villi", "flatulence" and "stools", and know that you understand the need to discuss these issues.

Early in this process, I left my dermatologist's office with a prescription for Dapsone to treat the attack of sores on my scalp, my arms, and thighs, and a slip of paper directing me to see the dietitian at our local hospital. I was told to avoid "wheat", which meant avoiding bread and bread products. "Duh!" I went home, had a bowl of Campbell's Mushroom Soup and thought "I can do this. I am a nurse after all. It won't be long before these sores have cleared up, I can gain weight, my nails will grow again, and I will stop this blessed itching" (Why do we say "blessed" when we mean a swear word?)

I was on such high doses of Dapsone and the sores cleared up but what a price my body paid! We continued using the same toaster. (Goodness what is a crumb after all?) The more I traversed this "adventure" the more I found flour, or to be precise GLUTEN in almost everything I ate, liked, or touched.

I visited the dietitian at our hospital after weeks of waiting, and she was curious to see the sores on my scalp, never having seen dermatitis herpetiformis before! Her file on celiac disease was smaller than the one that I had started to develop. I am embarrassed to say, as a nurse and writer, that I did not search the Internet for help during those first months. The dietitian was my only resource. I did not know anyone with celiac disease. And dermatitis herpetiformis was something I did not want to tell anyone about. It sounded contagious to me.

Some of the 'shockers' to me, the person who thought the gluten free diet was going to be a piece of cake were simple things and stupid things. Some of the words I was frequently saying were "I just did not think gluten would be in that!" and "I did not think to read that!" and, "Who would have thought?" Certainly not me!

That first Christmas someone bought us a bottle of Irish Cream Liqueur, a thing we seldom imbibe. Again, not thinking, I used it in coffee for a drink after Christmas dinner and "wondered" why I had diarrhea the next day and why DH spots appeared on my scalp.

Food surprises: Oh my, such a lot of them. McDonald's French fries are not French fries. They are reconstituted flours, lard and "some" incidental potato products. My favorite, Costco fries, were hardly fries at all. They contained a lot of flour, which I suppose gave them the crunchy texture that I loved and paid dearly for afterward. I found out that most sausages contained toasted bread crumbs, as did sausage meat. Processed hamburger patties, big surprise, also contained toasted bread crumbs. I finally found that one can get sausages labeled gluten free, with that wonderful little "Wheat Sign" that I was learning to look for. Milk shakes? Oh, come on! Milk and ice cream... right? Not necessarily because not all ice creams are the same, some actually contain wheat germ or other grains used as fillers. This is similar to the way they use fillers in our medications, not only our pills but our liquid medications, our cough syrups, and pain liquids. Some indicate that they are made on machines that use wheat products and are not carefully cleaned before they begin another batch of medications. It is the same with those lovely sour lemon candies I love. They are coated with this lovely lemony powder. I can eat a bag of them without much thought. That is, thought was suspended until I was awake all night with abdominal pain and suffered the next day with diarrhea, and the next week with DH spots and the itch. Oh boy the itch! It is not a normal itch you know. It is not one that you just scratch for a bit and forget it. You HAVE to scratch it until it draws blood, and then scratch the scab until you have a burning pain like no other. Thankfully we found a Corticosteroid liquid called "Scalpacin". It is an over the counter liquid.

I was forced to get serious about this search for traces of gluten, but why do they make the product analysis writing so small? Picture me pulling things out of the freezer department of the supermarket and trying to read the product analysis. I cannot leave the door open because the hairs in my nose will freeze and I'm afraid that the department manager will become annoyed, so I end up opening the freezer doors again and again, searching for something I can eat.

I discovered, like most serious long-term celiacs, that quick, pre-made dinners are something you might as well ignore when shopping. And those wonderful rotisserie chickens - so nice and warm and "fatty" - have to be taken out of the warmer and the label has to be read because most of them seem to contain MSG and other unknowns. Acronyms - initials that scared me because I could not remember which ones were on my "Danger List". Eventually I printed off and laminated a sheet of "OKAY TO GO" and 'DANGER LIST" and took it with me when we shopped. (These lists are available at www.celiac.com.) Spices contain flour to prevent them from sticking, and who knew that baking powder would contain flour, and icing sugar? I was giving away most of my baking products cupboard to my grown daughters. Of course they did not mind and my husband was slowly learning to eat gluten free. Really, he was better for it. I kept telling him that. I seldom made cakes and pies in the beginning. Then, I had so many gluten free baking disasters because I was so used to baking with a "dash of this, and a dash of that", and you cannot do that with celiac baking or you will have a flop. I dug so many cakes out of the pan and threw them in the garbage. The first loaf of bread I tried to make in our break maker, the loaf actually went down instead of rising, and my husband ended up digging it out of the pan with a screw driver!

We rarely went to restaurants. I was embarrassed at having to give the waiter the third degree about the menu. And so many of the chain restaurants have large tins of pre-made products and the waiters, so time oriented out of necessity, cannot read every label. I now find, to their credit, that a lot of these chain restaurants have a book listing ingredients of each of their menu items. They are great, IF waiters will take the time to read them. A waiter in Hawaii, after grilling him (not the steak) about the "au jus" in the dish, finally came back to our table with my meal. My husband asked him again if he had checked that the meal was gluten free. Although he said it was safe, it became clear that he had not checked. It was that little hesitation that should have "clued us". I would not have spent the next three days of my holiday dastardly sick if I had handled it differently.

My family physician has told me to emphasize that gluten "is poison to me, and I get very ill from it". He went on to say, "That will scare them because they will be thinking you will be rolling on the floor in the restaurant". Eventually we found one restaurant in our area, a small family owned business where everything was made by the chef/owner, that was safe for me to eat. The chef even came out to see if everything was okay. I was so delighted I wrote an article in our local newspaper about the restaurant and sent information to the Vancouver Chapter of the Canadian Celiac Association because they welcome new information about restaurants and new bakeries offering gluten free baked goods, new information regarding retail grocery stores offering new gluten free products, etc.

I have learned to avoid caramel because even though I'm told it is not made with flour, it often has other forms of gluten in it that manufacturers are sneaky and not listing, like malt! A big shocker for me was the John Frieda shampoos. I just loved it when the hair lightener products by John Frieda came out.. They had blonde hair lighteners, burgundy hair colors, caramel, and chocolate brown. Oh my, the colors were endless and lovely. I bought the blonde hair products, the anti-frizz, the shine products and sprays. My cupboard was full of John Frieda blonde hair products for the wonderfully expensive streaks in my hair. Why oh why was my hair itching so badly? And the sores, and the blood! Why it was Wheat Germ Oil! And my scalp was alive once again.

But I had a bigger problem. By this time, my wonderful Dapsone was becoming a danger to me. I had always been told by my dermatologist to assist the DH to dry up by going {5-4-3-2-1 with the Dapsone pills. And if that did not work, doing it again along with yet another prescription pill Prednisone! Out came his trusty prescription pad for Prednisone, {5-4-3-2-1 of Dapsone and Prednisone.

I was not told however, of the potential side effects of Prednisone, like aching joints and mood swings. But Dapsone is one of the drugs that can cause methemaglobinemia, a blood disorder where the oxygen is taken out of the blood and your oxygen saturation can drop dangerously into the low 80's. I learned this after two hospital admissions into the ICU this year. They used Methane Blue (a potentially lethal mixture if not used correctly) to clean my blood. The oxygen is hidden behind a door somewhere and the Methane Blue helps open those trap doors and releases the oxygen into the blood again. That is how the internist described it to my husband who was sitting terrified in the other room. I had an infusion of two units of whole blood and a four day stay to monitor my oxygen saturation levels and was told I could never use Dapsone again.

What??!! Dapsone was my life-line; I could never live without Dapsone! Three days without that "stuff" and the dreaded spots were back. I was referred again to a dermatologist, now fifteen years after my diagnosis, and he prescribed Cimetidine, a medication used for stomach disorders. Who would have known? But it works - three times a day that is. Another dratted pill! We purchased a SAT machine (It measures the oxygen saturation of hemoglobin) online from the U.S.A. for $38.00. It is a very good deal. Twice a week we check my SAT levels and if they are 92-93 I consider it okay to continue my Dapsone.

I have been told if my SAT levels drop below 89 I should go to the Emergency Department because these small machines are not totally accurate. But this little guy has checked out with my physician's SAT machine and the hospital's machine every time; It's a real winner, and a life saver for me! IF you are afflicted with dermatitis herpetiformis and have to take Dapsone regularly you may want to consider purchasing one of these machines. A few shots of Zylocaine for pain, coupled with the Dapsone, and you could be in trouble. Zylocaine, in combination with a few other drugs, can cause Methemaglobinemia.

I have just listed "some" of the things that surprised (shocked) me when I was a new gluten checker. I am sure you can write in and tell us your "shocking" stories.

Celiac.com 03/16/2018 - Celiac awareness has increased exponentially over the last decade among physicians and the general public alike. Increasing numbers of research publications and very active support groups and individuals have contributed to this growing awareness.  Knowledge of the many and varied manifestations is also growing rapidly although some individuals continue to cling to the notion that celiac disease is characterized by malabsorption and that nutrient deficiency is the dominant feature of this ailment. This misses the broader understanding of the many ways in which gluten grains negatively impact on human health. From toes to head, any and all of our human body systems may be harmed by ingesting gluten under some circumstances. Although the wide range of signs and symptoms of celiac disease is impressive, a similar, even broader range of impacts may be attributed to gluten in the context of non-celiac gluten sensitivity. Those with celiac disease only comprise a small portion of the population of people who are afflicted by non celiac gluten sensitivity. Dr. Rodney Ford has offered the all encompassing term of 'gluten syndrome' to identify everyone whose health is compromised by gluten consumption (1). 

From Dr. Fasano's most conservative estimate that 6% of the population is afflicted by non-celiac gluten sensitivity (2), to Dr. Rodney Ford's estimate that 10% is afflicted (3), to Dr. Kenneth Fine's finding that IgG class anti-gliadin antibodies are found in about 11% of the population (4), to this writer's assertion that non-celiac gluten sensitivity includes well more than 20% of the population, the paucity of research in this area offers a wide range of estimates without a solid basis for refuting any of them. Nonetheless, it is clear that those with non-celiac gluten sensitivity outnumber those with celiac disease by a ratio of somewhere between 6 to 1 and more than 20 to 1. The gluten syndrome may therefore include from seven percent to more than twenty percent of the population. 

The importance of these percentages and ratios is that we are seeing growth in the diagnosis of celiac disease, and in the number of people who have celiac disease (4). It has been argued that a similar trend may be seen across the spectrum of the gluten syndrome, attributing that trend to the genetic modifications that have been made to grains, and the increased consumption of these foods (5). 

But this is just the tip of the iceberg. Dr. Fasano bases his estimate of non-celiac gluten sensitivity on those who mount an innate immune reaction to gluten grains. While there is likely some overlap between innate immune reactions and selective antibody reactions, most estimates of non-celiac gluten sensitivity are based on IgG class antibodies against one of the proteins of several protein families found in gluten. It makes eminent sense to me that when our bodies are mounting a measurable immune response against the most common food in our diets, whether the reaction is by the innate immune system or by creating selective antibodies, that food might be harmful to our health. I do not quarrel with the basis on which these sensitivities are identified. I simply argue that they are only identifying a sub-fraction of many more possible cases of non-celiac gluten sensitivity.  

To put this issue into sharper focus, there are several protein families to be found in each of the gluten grains. In wheat, for instance, each family, glutelin, gliadin, and glutenin contains a number of individual proteins. The antibody test for gliadin ignores possible reactions to proteins in either of the other two families.  Further, IgG class antibodies are the most common and widespread class of selective antibody we produce.  But they form only one of five types of selective antibodies (known as immunoglobulins). Further, as is obvious from Dr. Fasano's conservative approach to identifying non-celiac gluten sensitivity, there are other facets of the immune system that do not involve selective antibodies, and can also be enlisted in a reaction against gluten grains.

Thus, when we test for IgG anti-gliadin antibodies, the most common test for non-celiac gluten sensitivity, positive results are identifying reactions against only one of the several protein families found in gluten, and only one of the five possible selective antibody reactions against this single protein family. 

It therefore seems wholly improbable that testing for reactions against a single protein family in only a single class of selective antibody would identify all or even most cases of gluten sensitivity. Admittedly, some researchers test for IgA antibodies but those investigators usually do not test for IgG antibodies. However, even with testing for both classes of selective antibodies, which most published reports on this issue have not done, it is clear that many possible immune reactions to any other protein fractions of gluten might well be overlooked, either in the form of other selective antibodies or as other immune reactions and various innate reactions against gluten grains.

 I'm sure that, by now, the reader will see that there are many possible immune reactions against this most common food, and that most of these reactions will go undetected, both in the context of standard medical testing and in most research conducted in this venue. On a more practical plane, when Dr. Curtis Dohan identified significant improvements among patients with schizophrenia patients eating a gluten-free, dairy-free diet (6), and Singh and Kay replicated their findings (7), many looked for celiac disease among patients with schizophrenia and found only a small increase.

Dohan and Singh's publications were followed by several sloppy studies that ignored the guiding principles expressed in this pioneering work. These weak studies further undermined acceptance of the connection between gluten and schizophrenia. The net result was a growing belief that Dohan had erred and his heroic work was widely dismissed. Yet, more than twenty years after his death, one of Dohan's most vigorous critics is listed among the authors of a paper that reports an immune reaction against gluten that, while different from the reaction seen in celiac disease, is common among people with schizophrenia (8). 

Similarly, I think that we can expect, sometime in the future, to see research that identifies immune reactions and damaging dynamics caused by gluten consumption among people with learning disabilities. There is, for instance, one newspaper report of an informal study conducted at the Nunnykirk School in Northumberland, a school that serves only children with dyslexia, a condition that is reported to afflict about 10% of children in the United Kingdom. After six months of eating a gluten free diet, more than 80% of these children improved their reading at a rate of at least twice that of normal children. Some leaped ahead, in their reading skills, by as much as 2.5 years over this six month period (9). 

Relatedly, I had the privilege of working with Dr. Rodney Ford on a retrospective analysis of indicators of school readiness among children who had celiac disease, non-celiac gluten sensitivity (as measured by selective antibody testing) and children who showed no signs of either reaction to gluten. A large majority of those who reacted to gluten improved dramatically. There was a small but significant sub-group whose school readiness improved following a gluten free diet, and these improvements happened within 6 months of avoiding gluten (unpublished data).

Autism, especially where normal development was curtailed after one or several years, is another condition in which excluding gluten seems to provide substantial improvements even in the absence of celiac disease. Some research in this area suggests that toxins (generated by bacteria resident in the intestines) are allowed access to the bloodstream and the brain (10). Perhaps exclusion of dietary gluten is the factor that limits access to the bloodstream through reducing zonulin production.   

Similarly, although not as well supported, there is some evidence to suggest that gluten contributes to bi-polar disorder. Just how frequent and significant the contribution may be is still open to debate, but I have observed some evidence to support this hypothesis in my own family.  

A range of types of epilepsy have been found in association with celiac disease, many of which are mitigated by the gluten free diet (11). 

The manifestations of undetected non-celiac gluten sensitivity are not limited to brain function. We know that celiac disease is much more frequent in the context of other autoimmune diseases. We also know that antibody tests show even higher rates of non-celiac gluten sensitivity. Since we are only identifying a fraction of those who may be reacting to gluten, it seems reasonable to suggest that everyone with an autoimmune disease, or antibodies suggesting that an autoimmune disease is imminent, should begin a strict gluten free diet and follow it for at least one year. If there is any reduction of auto-antibodies or symptoms of autoimmunity, the diet should be continued. Although difficult in the early stages, it is an entirely benign intervention/treatment. There are no unwanted side effects or hazards. 

There are more than 200 autoimmune and other medical conditions reported in association with gluten and are listed in Appendix D of Dangerous Grains (12). In each case, a lengthy trial of a gluten free diet would be well advised. Again, there are no negative side effects of the gluten free diet. It is an entirely benign intervention.

A significant proportion of those who suffer from IBS, Crohn's or any of the various types of colitis have also been reported to benefit from a gluten free diet on various websites. Similarly, many people with MS and a host of other neurological diseases have been shown to benefit from a gluten free diet (13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23).  

Even many AIDS patients are helped by a gluten free diet. It reduces their diarrhea and improves nutrient absorption (24). This is an important discovery that can be harnessed in conjunction with the improved treatments now available for this very serious illness. 

Overweight, obesity, and weight loss are contentious issues with regard to the gluten free diet. Until quite recently, there were two reports of small studies of changes in body mass index in the USA and one report from Ireland, following institution of a gluten free diet. The two American studies showed weight loss among overweight subjects on a gluten free diet. The study from Ireland showed only weight gain among overweight subjects after following a gluten free diet. In November of 2011, another small study was published. Their conclusion states "The GFD (gluten free diet) has a beneficial effect upon the BMI (body mass index) of overweight children with celiac disease" (25), which is congruent with the earlier two American studies. I have previously suggested that the discrepancy between the findings may be due to the acceptance of wheat starch as part of the gluten free diet in the United Kingdom. However, regardless of the cause, the preponderance of evidence supports the notion that a gluten free diet can be used as an effective weight loss strategy in some cases of celiac disease. Other evidence suggests it may be a more broadly effective weight loss tool.

Thus, my estimate of the prevalence of non-celiac gluten sensitivity includes the 6% who show signs of innate immune reactions to gluten, in addition to those who show IgG  antibodies against gluten, at about 11% of the population (although there may be some overlap between these 6% and 11% groups). My estimate also includes many of those with schizophrenia who number about 1% of the general population, and a portion of those with autism who are quickly approaching 1% of the population. I am also including 80% of the approximately 10% of the population with some degree of dyslexia. Because of overlaps between groups, and because gluten's impact is often only demonstrable through a gluten free diet, I only assert that non-celiac gluten sensitivity is a factor in more than 20% of the general population. However, I remain open to findings that will show a much greater negative impact from eating foods derived from gluten grains.  The portion of the human population that may be negatively impacted by gluten consumption can range as high as the 80% portion that produce haptaglobin 2, for which zonulin is the precursor. 

The take away point here is that the gluten free diet may aid overall health for up to as much as 80% of the general population. In that context, my estimate that 20+% of the population is showing signs that they are variously mounting immune reactions against gluten or are otherwise harmed by gluten appears modest. The overlapping symptoms make it extremely difficult to narrow my estimate further. Nonetheless, gluten is one of the most harmful substances in our diet. Yet it is the most ubiquitous factor in our diets.    

Sources:
1. Dr. Rodney Ford
2. Sapone A, Lammers KM, Casolaro V, Cammarota M, Giuliano MT, De Rosa M, Stefanile R, Mazzarella G, Tolone C, Russo MI, Esposito P, Ferraraccio F, Cartenì M, Riegler G, de Magistris L, Fasano A. Divergence of gut permeability and mucosal immune gene expression in two gluten-associated conditions: celiac disease and gluten sensitivity. BMC Med. 2011 Mar 9;9:23.
3. personal communication
4. personal communication
5. Wheat Belly
6. Dohan FC, Grasberger JC. Relapsed schizophrenics: earlier discharge from the hospital after cereal-free, milk-free diet. Am J Psychiatry. 1973 Jun;130(6):685-8.
7. Singh & Kay
8. Samaroo D, Dickerson F, Kasarda DD, Green PH, Briani C, Yolken RH, Alaedini A. Novel immune response to gluten in individuals with schizophrenia. Schizophr Res. 2010 May;118(1-3):248-55.
9. Blair, Alexandra. Wheat-free diet gives food for thought. http://www.timesonline.co.uk/tol/news/uk/article444290.ece
10. Sandler RH, Finegold SM, Bolte ER, Buchanan CP, Maxwell AP, Väisänen ML, Nelson MN, Wexler HM. Short-term benefit from oral vancomycin treatment of regressive-onset autism. J Child Neurol. 2000 Jul;15(7):429-35.
11. Ribaldone DG, Astegiano M, Fagoonee S, Rizzetto M, Pellicano R. Epilepsy and celiac disease: review of literature. Panminerva Med. 2011 Dec;53(4):213-6.
12. Braly J, Hoggan R, Dangerous Grains. Avery, New York,  2002.
13. Hadjivassiliou M, Sanders DS, Grünewald RA, Woodroofe N, Boscolo S, Aeschlimann D. Gluten sensitivity: from gut to brain. Lancet Neurol. 2010 Mar;9(3):318-30. 
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15. Hadjivassiliou M, Chattopadhyay AK, Grünewald RA, Jarratt JA, Kandler RH, Rao DG, Sanders DS, Wharton SB, Davies-Jones GA. Myopathy associated with gluten sensitivity. Muscle Nerve. 2007 Apr;35(4):443-50.
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18. Hadjivassiliou M, Williamson CA, Woodroofe N. The immunology of gluten sensitivity: beyond the gut. Trends Immunol. 2004 Nov;25(11):578-82. Review. 
19. Hadjivassiliou M, Sanders DS, Grünewald RA, Akil M. Gluten sensitivity masquerading as systemic lupus erythematosus. Ann Rheum Dis. 2004 Nov;63(11):1501-3.
20. Hadjivassiliou M, Grünewald RA, Davies-Jones GA. Gluten sensitivity as a neurological illness. J Neurol Neurosurg Psychiatry. 2002 May;72(5):560-3. 
21. Hadjivassiliou M, Grünewald RA, Lawden M, Davies-Jones GA, Powell T, Smith CM. Headache and CNS white matter abnormalities associated with gluten sensitivity. Neurology. 2001 Feb 13;56(3):385-8.
22. Hadjivassiliou M, Grünewald RA, Davies-Jones GA.  Gluten sensitivity: a many headed hydra. BMJ. 1999 Jun 26;318(7200):1710-1. 
23. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.
24. Quiñones-Galvan A, Lifshitz-Guinzberg A, Ruíz-Arguelles GJ. Gluten-free diet for AIDS-associated enteropathy.  Ann Intern Med. 1990 Nov 15;113(10):806-7.
25. Reilly NR, Aguilar K, Hassid BG, Cheng J, Defelice AR, Kazlow P, Bhagat G, Green PH. Celiac disease in normal-weight and overweight children: clinical features and growth outcomes following a gluten-free diet. J Pediatr Gastroenterol Nutr. 2011 Nov;53(5):528-31.
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