Free Course | Celiac disease and gluten sensitivity
Proliferation of humankind and spread all over the globe was primarily fueled by wheat energy. Who would have imagined that wheat would be demonized as a killer grain in twentieth century? How did it come to pass that every self-respecting grocery store would stock shelf after shelf with gluten-free foods?
The answer: In the United States, we own and pride in our diseases.
We fiercely fight to protect our right to own our diseases – more than the gun lobby fights to protect the right to own guns. We must always have a disease of the decade or two. And these are the decades of gluten diseases. No self-respecting American can tolerate opposition to celiac disease and gluten sensitivity.
Until fifty years ago, the terms celiac disease and gluten sensitivity were known only to doctors. In 1960, in my third year at King Edward Medical College, Lahore, Pakistan, I considered these entities to be learned and remembered until I passed the examination in my pediatric course. I desired to be a surgeon and I did not think surgeons then were interested in such gut problems. In 1968, I arrived in the United States and saw little reason to ever open my textbooks to look for celiac disease and gluten sensitivity.
Celiac disease (sprue by another name) is an immune-inflammatory entity. It is believed to be caused by a family of gluten proteins in wheat, oat, barley, rye, and in smaller amounts in other grains. True celiac disease accounts for a relatively small number of individuals clinically diagnosed to have gluten sensitivity. It occurs in genetically predisposed people of all ages from middle infancy onward. Symptoms include pain and discomfort in the digestive tract, chronic constipation and diarrhea, failure to thrive (in children), anemia and fatigue, but these may be absent, and symptoms in other organ systems have been described. Vitamin deficiencies are often noted in people with celiac disease owing to the reduced ability of the small intestine to properly absorb nutrients from food.
How Did Celiac Disease Become a Darling of Disease-lovers?
Before I answer this question, let us consider the findings of a landmark study conducted by Italian researchers and published in the journal BMC Gastroenterology on November 18, 2014. The three graphs reproduced below from that study tell the story of how celiac disease has changed.
Disease onset was symptomatic in 610 patients (79%), while 160 celiacs showed a subclinical phenotype. In the symptomatic group the non-classical prevailed over the classical phenotype (66% vs 34%). Diarrhea was found in 27%, while other gastrointestinal manifestations were bloating (20%), aphthous stomatitis (18%), alternating bowel habit (15%), constipation (13%) and gastroesophageal reflux disease (12%). Extraintestinal manifestations included osteopenia/osteoporosis (52%), anemia (34%), cryptogenic hypertransaminasemia (29%) and recurrent miscarriages (12%). Positivity for IgA tissue transglutaminase antibodies was detected in 97%. Villous atrophy was found in 87%, while 13% had minor lesions consistent with potential celiac disease. A large proportion of patients showed autoimmune disorders, i.e. autoimmune thyroiditis (26.3%), dermatitis herpetiformis (4%) and diabetes mellitus type 1 (3%). Complicated celiac disease was very rare.
Our early primordial ancestors were fermenters. Throughout human evolution, some of those fermenting cells thrived in oxygen-poor nitches in the human body, serving many purposes, including food digestion. These were “good fermenters.” Our later human ancestors learned—experientially or intuitively, it seems—learned ferment foods to enhance their value. We can call it “good fermentation.”
Every chronic disease begins with fermentation. This need not raise any eyebrows. Diseases involve inflammation with buildup of acids and alcohols. Fermentation, of course, is conversion of sugars into alcohols and acids. We can call it “bad fermentation.”
Then came the age of fermenting human cells—most notably during the last century—ushered in by the era of antibiotics, sugar abuse, and industrial pollutants. The modern epidemics of inflammatory, immune, and degenerative disorders are rooted in cellular fermentation. In a broader evolutionary context, I recognize these epidemics as evolution-in-reverse. This is “ugly inflammation.”
This article is a part of my series (begun in the early 1980s) on good fermentation.
Gluten Sensitiivity or Gut Fermentation With Leaky Gut State Majid Ali MD
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on PROBLEMS OF FERMENTATION IN THE GUT
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Gluten-free Diet for Gluten Sensitivity
Glutens are two grain proteins – glutenin and gliadin enmeshed in starches – that cause a wide spectrum of clinical disorders in some individuals. One simple form is wheat intolerance. At the other end of the spectrum is the severe form of gluten-sensitive enteropathy (GSE) called celiac disease. In Part Three of this series, I include a very long list of celiac disease-associated conditions to define the scope of clinical problems associated with gluten proteins. I begin this three part series about gluten sensitivity by first summarizing my experience with gluten-related clinical problems:
1. The frequency of problems caused by wheat, rye, oats, and barley is increasing among people with chronic health issues.
2. Nearly all my patients with gluten-related symptoms ate bread and other gluten foods freely and without symptoms before they developed gluten sensitivity.
3. Gluten intolerance developed when the bowel became inflamed and “leaky,” leading to entry into the blood of undigested gluten proteins.
4. Gluten-free diet only partially improved health.
5. Gluten-sensitive individuals regained their health only after bowel-liver detox was achieved and other oxygen-related issues—mold allergy, mold toxins, thyroid-adrenal weakness, hormonal imbalance, anger, and deep disappointments that caused the leaky gut state—were addressed.
6. The recovery in some cases with severe stress, mold toxicity, and instability of the autonomic nervous system, and continuing stress was sometimes delayed or incomplete or both.
7. Complete elimination of gluten grains was usually helpful in the short-term but was necessary in the long run only for a small number patients.
Dr. Ali’s Leaky Gut Protocol
From the above summary, many readers with puzzling chronic health disorders might ask: should I try a gluten-free diet trial? My answer: absolutely yes. I suggest that such readers consider a six-week trial of Dr. Ali’s Leaky Bowel (DALB) Protocol, which includes gluten-free diet trial (described below) as well as elimination of dairy (except yogurt), and sugar. I also prescribe castor oil rubs and Nystatin to reduce the population of fermenting microbes. Nystatin, of course, requires a physician’s prescription. Fortunately, more and more doctors are willing to support this request from patients. The less effective alternatives to Nystatin are echinacea, astragalus, burdock root, goldenseal, pau d’arco, and oregano.
A Valuable Suggestion
I recommend that readers first consider all elements of Dr. Ali’s Leaky Gut Trial described in Part Two. Once clinical improvement is achieved with all elements combined, then one can eliminate some aspects to narrow down the negative effects of gluten proteins. If that is not possible, I suggest readers first conduct a four-week gluten-sugar-dairy-free trial. Trials limited to gluten-free diet sometimes are not as revealing.
The Oxygen (Dysox) Model of Gluten Sensitivity
Readers will note that my oxygen view of gluten sensitivity—and celiac disease, by extension—is radically different from other prevailing theories of the disorders. In past publications I marshaled evidence for the central—and fundamental—roles of oxygen-related factors in the cause of the leaky gut state. My colleagues at the Institute of Integrative Medicine and I have also published a series of clinical outcome studies in which we documented the role of bowel derangements caused by dysox (dysfunctional oxygen homeostasis) and healing with oxystatic therapies. This, in essence, is the Oxygen Model of Gluten Sensitivity.
Oxygen is the organizing principle of human biology and governs the aging process. I began my book Oxygen and Aging (2000) with these words and then I began a series of articles in which I marshaled evidence for the unifying oxygen model of disease. Specifically I presented oxygen models of inflammation, pain, liver injury, asthma, allergy, colitis, heart disease, stroke, kidney failure, cancer, and other disorders. This article outlining the Oxygen Model of Gluten Sensitivity is an extension of that work.
Gluten-sensitive persons need to avoid completely the following grains, in any form, for a period of at least six weeks to assess the effects of such elimination on their health:
Other grains such as amaranth, buckwheat, quinoa, milo, teff, rice and corn contain small amounts of “bound gluten” that, in general, do not cause food incompatibility reactions in gluten-sensitive persons.
Spelt and Kumat are two types of ancient wheats that appear to be genetically different from the common variety of wheat. Many gluten-sensitive individuals can tolerate these grains well, especially when consumed sparingly. Both varieties are usually grown without pesticides. Spelt has a strong hull that protects its kernel. Teff, an Ethiopian staple, is a highly nutritious grain that contains more than ten times as much calcium as wheat and barley.
Suggestions for Snacks
Sunflower seeds, sesame seeds, pumpkin seeds, melon seeds, watermelon seeds, soy nuts (actually a grain), cashew nuts, macadamia nuts, pine nuts, Brazil nuts, chestnuts, pecans, and litchi nuts. Peanuts and walnuts are common causes of allergic reactions and should be eaten infrequently. For additional information, please read chapter 8 of The Butterfly and Life Span Nutrition (1992).
Evidence for the Oxygen Model of Gluten Sensitivity
In Part Three of this series, I present evidence of the Oxygen Model of Gluten Sensitivity under the following headings: (1) microscopic features of bowel biopsies:
(2) coexistence of mold allergy and mold toxins;
(3) association of antibodies against gluten proteins with gluten-sensitivity;
(4) the gluten-sensitivity-associated conditions; and
(5) incomplete healing with gluten-free diets alone.
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