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Showing results for tags 'hashimoto’s'.
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Celiac.com 08/10/2022 - Celiac disease is a common inflammatory disease of the small intestine. Hashimoto's thyroiditis and Graves' disease make up most cases of autoimmune thyroid disease, and are marked by lymphocytic infiltration of the thyroid parenchyma. Both Hashimoto's thyroiditis and Graves' disease are often seen together with celiac disease. Meanwhile, patients with monoglandular and polyglandular autoimmunity have a higher rates of celiac disease. Rising rates of celiac disease among autoimmune thyroid disease patients has prompted researchers to investigate the link between the two. A team of researchers recently set out to review the medical literature to more clearly illuminate the connections between celiac disease and thyroid autoimmunity. The team's goal was to study the shared genetic background, the incidence of celiac disease in autoimmune thyroid disease, the effect of a gluten-free diet on autoimmune thyroid disease, and the need for routine screening of celiac disease in autoimmune thyroid disease patients. The research team included Tejaswini Ashok, Nassar Patni, Mahejabeen Fatima, Aselah Lamis, and Shiza W. Siddiqui. They are variously affiliated with the Research at Dubai Medical College in Dubai, ARE; Research, Dubai Medical College for Girls in Dubai, ARE; and Internal Medicine, Deccan College of Medical Sciences in Hyderabad, India. Researchers think that shared genetic background is likely the main reason for the connection, as there seems to be a substantial overlap in genetic variables between celiac disease and autoimmune thyroid disease. Because of the subclinical aspects of the celiac disease, doctors often miss the diagnosis or make it coincidentally during screening. The rising rates of celiac disease in autoimmune thyroid disease patients is well documented. Moreover, most studies on the effects of a gluten-free diet in autoimmune thyroid disease patients with celiac disease have shown beneficial effects for the management of both diseases. To create a clinical therapy regimen to manage these two concurrent disorders, the team calls for more study on autoimmune thyroid disease patients for genes related to celiac disease, and to subclinical and clinical celiac disease rates. They note that the multi-system nature of celiac disease warrants a multidisciplinary research and treatment approach that meshes with the diagnostic algorithm of autoimmune thyroid diseases to give patients with both autoimmune thyroid disease and celiac disease the best possible treatment. Read more at Cureus.com
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Celiac.com 09/14/2018 - If it is really true that nobody really wants to see a grown man cry, then certainly nobody would have wanted to hang around me near the onset of a long illness whose mystery would take 14 years to solve. It began subtly and mildly in 1989, my 43rd year. I had just finished a long and exhausting malpractice suit on behalf of my daughter, an attractive, genetically-normal child who had contracted quadriplegic cerebral palsy in a completely avoidable incident of post-natal asphyxia which had radically changed the nature of life for my spouse and I. By the time 1989 rolled around, I was thoroughly exhausted and carrying a toxic load of anger directed at an incompetent member of the medical profession who had never learned the importance of state-of-the-art skills in a profession that literally has the power of life, death, and disability. From late 1989 on through 1990, I experienced strange episodes of profound sadness, usually of one to two hours duration, that became increasingly disruptive to my ability to handle a job and child-care duties. Initially, these episodes seemed to come from nowhere. Later on, I found that playing certain pieces of music of which I was fond, would send me into such intense sobbing that I would be forced to pull over if this occurred while driving. By the time 1991 rolled around, something was to be added to these periodic bouts of intense sadness. Early in that year, my daughter became very ill, keeping both my spouse and I awake at night for weeks on end. By the time the problem was diagnosed to be a dental infection and dental surgery was done, I had begun to have a sensation of “hollowness”, as though I really weren’t part of this world, most of the time. In late summer of that year, a series of events in which my subconscious had informed me that a friend had a serious illness, sent me into a final “dive”: I simply stopped sleeping more than about two hours per night. When I first stopped sleeping, I soon noticed that even low-level use of alcoholic beverages would further interrupt sleep and throw me into a state in which I couldn’t think of anything but how terrible I felt. This state of pronounced alcohol intolerance would continue for 14 years. The final blow came in November 1991, when I went into a completely disabling panic/anxiety attack that sent me to bed, cowering. I had no alternative but to seek treatment from the psychiatric profession. Unfortunately, the first two psychiatrists prescribed drugs which either had no effects, or had effects that seemed worse than the problem they were supposed to solve. The third psychiatrist, whom I stuck with for about six months, came up with a treatment plan that was partially effective (but certainly not restorative). I stayed with this psychiatrist until it became clear that his treatment was equivalent to Jefferson Airplane singing “one pill makes you larger, and one pill makes you small”. I was being jacked up every morning by a toxic, activating SSRI anti-depressant so I could semi-function, and then dropped by benzodiazepenes every night into a non-restorative twilight sleep state. In retrospect, the most amazing thing about these first three psychiatrists was that not one of them ordered any tests of my endocrine function. Treatment consisted solely of a series of benzodiazepenes, anti-depressants, mood stabilizers, and anti-psychotics, administered in a trial-and-error fashion that yanked my psyche and body chemistry around like a manic pit bull on a two-foot leash. Throughout the latter part of 1992, I transitioned to care with my primary-care physician, mostly because I trusted him more than any of the psychiatrists I had seen up to that time. He was able to stabilize me with one of the old tri-cyclic anti-depressants, doxepin, along with low doses of valium. Although doxepin packs a big morning hangover for many who use it, and has very strong anti-cholinergic effects, its ability to put me out at night helped me function satisfactorily for much of the 1990s, even at doses as low as 10mg, once daily in the evening. In 1993 I consulted a highly-recommended psychiatrist, who was the first psychiatrist who actually looked at my thyroid function. When my TSH was measured at 3.5, without also checking my FT3 and FT4, that doctor concluded that thyroid was not my problem. Of course, standards of thyroid diagnosis and treatment have changed radically in the 12 years since. Under the new AACE guidelines, a TSH of 3.5 would now be suspect, because studies of patients with TSH over 3.0 have shown that most progress to hypothyroidism (i.e., TSH greater than 5.5). The new AACE guidelines would mean that further testing and evaluation should be done. Until the fall of 1997, I continued treatment with doxepin and intermittent valium, adding the practice of meditation to help calm myself. At that time, I came back to my primary-care physician with the symptom of profound exhaustion on top of the symptoms of insomnia, anxiety, and depression I had suffered for years. Fortunately, my GP was suspicious of thyroid function, and found that my TSH was floating above 8. Since this was well above the old/traditional limit of 5.5, he was ready to start treatment, with (as would be expected of most GPs) T4-only replacement. I began taking thyroxine (T4) shortly thereafter with high hopes. Initially, the treatment was successful: getting the added thyroxine into my system caused an immediate improvement in quality of sleep. However, the use of T4 did not turn out to be an unqualified success. After use of T4 for about a month, it was apparent that use of thyroxine alone did not produce a full recovery—I still suffered from anxiety, which the medication seemed to be increasing. In the meantime, hair loss became an issue. Several years earlier, I had noticed that running my fingers through my hair would produce an unpleasant sensation, almost as though the hair roots were tender. By the time of my 50th birthday, in 1996, I had noticed that my pillow was virtually coated with hair by the time I would remove it for washing. Unfortunately, nobody, including my GP, reminded me that hair loss is a prime symptom of hypothyroidism; and, like most males, I was ready to assume it was plain old male pattern baldness. By the time I was treated correctly and the hair loss stopped, I had pronounced thinning on the crown which was too advanced to be reversed in response to the treatment of the thyroid problem. In about 1998, I began experimentation with amino acids which was to last for almost seven years. I found that use of tryptopan, 5-HTP, and GABA could reduce (but not correct) the worst of my symptoms. In retrospect, though, use of amino acids is a poor substitute for a well-functioning thyroid, as well as being expensive and inconvenient. By the summer of 1999, I had reached a paradoxical situation. Experimentation had shown that my body needed on the order of 100 micrograms of thyroxine (T4) to keep my TSH down to a reasonable level; yet taking that much T4 was causing intense anxiety, requiring me to use strong sleeping medications. By late summer 1999, I had noticed another distressing symptom—my acute sense of hearing was being increasingly impacted by tinnitus. Evidently, the root cause that drove me into hypothyroidism, could also impact hearing. It was soon after a household move in the spring of 2000, that I had a partially-disabling attack of severe epicondylitis (more commonly known as tennis elbow). It was obvious that my body was no longer able to handle the short-term stresses of the hard physical work required by a move. This obvious physical symptom, accompanied by increasing periodontal issues and continuing mental issues, prompted me to seek other treatment. In September 2000, I began seeing a prominent “metabolic” doctor (M.D.) who is well known for his treatment of the metabolic disorders of diabetics. This doctor has written a number of books related to dietary changes and supplements needed to stave off metabolic degeneration as one ages. I was switched to Armour thyroid, and began treatment with other hormones (primarily hydrocortisone in low doses to supplement adrenal function, and pregnenolone). I took an enormous range of nutritional supplements recommended by this doctor, and also made radical changes in diet, which I maintained for nearly two years. Unfortunately, nothing seemed to really work—I did not obtain substantial relief of my symptoms. A thyroid test in Sep 2001 still showed unsatisfactory results—my TSH was 4.7, and my FT3 was below the bottom of the normal range. By the spring of 2002, I had decided I would have to take my care elsewhere if there were to be progress. After doing a brief telephone consult with a naturopath outside my home state, I began seeing a naturopath in my home town for whom I had obtained very positive recommendations via a web search. By March 2002, the naturopath had informed me that testing showed my hypothyroidism was due to anti-thyroid antibodies, i.e., my body was attacking its own thyroid gland. This condition is officially known as Hashimoto’s Autoimmune Thyroiditis (HAIT—as I now know, HAIT is the leading cause of hypothyroidism). I found this discovery quite amazing; how come the three endocrinologists I had seen between 1998 and 2002, had not given me this information? I was started on Thyrolar (synthetic combination T3/T4) by the naturopath, because she said that my body’s ability to make T3 may have been compromised by HAIT. Soon after beginning to see the naturopath, I learned that Dr. Stephen Langer of Berkeley, CA might have additional information on the problem I had been having with thyroid hormone causing anxiety in a hypothyroid patient. I had searched for information about this syndrome in a number of places but found nothing; for instance, the well-known book “Thyroid Solution”, by Ridha Arem M.D., contains no information on the condition. So, I consulted with Dr. Langer and learned that a small percentage of people with Hashimoto’s are exquisitely sensitive to even low doses of Thyrolar. In fact, the condition is rare enough that virtually no GPs, and only a few endocrinologists, know of its existence. Apparently, it does not have an official name attached to it. I decided to refer to it as “HAIT anxiety syndrome”, although there are a few doctors who prefer to refer to any neurological symptoms accompanying HAIT as “Hashimoto’s Encephalopathy”. I began to feel a little better between March 2002 and June 2003. I’m not sure why the message about gluten grains had not penetrated before, but by June 2003, the naturopath reminded me again that she had seen a positive result to a test for antibodies to gliadin (one of the two major proteins in gluten grains) in 2002, and that I really should consider removing gluten grains from my diet. This recommendation was based on three factors: I had antibodies to the protein gliadin found in wheat and other gluten grains such as rye and barley; I had anti-thyroid antibodies which were over the threshold that defines HAIT; Medicine really is an experimental science, and this experiment, in spite of its inconvenience, appeared to be worth a try. In a numbers sense, the response of my anti-thyroid antibodies to the removal of gluten grains from my diet was slow, but gratifying. My thyroperox test started off at 25, dropped to 19 within 6 months, 7 within 10 months, and became zero in less than 2 years. I eventually concluded that the removal of gluten grains from my diet was not all that difficult, partly because I wasn’t a celiac who had to worry about that last 1%. I also concluded that removal of gluten would have a positive health effect in terms of the reduced glycemic index of the foods I consumed. My symptomatic improvement thereafter was not immediate. It soon became obvious that T3/T4 treatment is not an exact science, and the proportion of T3 to T4 needs to be closer to the human body’s need, not the pig’s need (Both Armour and Thyrolar have the T3/T4 ratio of one part T3 for every four parts T4, typical of the pig’s biochemistry). For instance, in late 2003, my TSH had dropped very low, i.e. I had become clinically hyperthyroid due to excess T3 as revealed by a free T3 test. I have since gone through a couple more of these “yo-yo” episodes while being treated, which is a not uncommon event—thyroid treatment is as much art as science. Cost of treatment also became a problem. By June 2004, I began seeing a highly-recommended Physician’s Assistant (P.A.), who was known locally to be very good at thyroid treatment, and whose clinic would accept my health insurance. I continued to see the naturopath, although at less frequent intervals, since my insurance (like most) would pay nothing for naturopathy. The P.A. and the naturopath did not completely agree on treatment methods, particularly the use of adrenal supplements (hydrocortisone and DHEA in low/biologic doses) along with thyroid supplements; but they were both in agreement that I should continue to pursue combination T3/T4 therapy. So, I blended recommendations from the two for awhile, transitioning to T3 and T4 in separate tablets of Cytomel and Synthroid, so the percentage of T3 could be altered. I gradually transitioned off adrenal supplements during 2005, and very gradually increased my T3/T4 supplementation over the course of the year. Finally, by September 2005, I began to realize that I truly had recovered my health—I had episodes of feeling really good again! Still, my sleep was not perfect—I had discovered what Ridha Arem M.D. has documented in the book Thyroid Solution: a return to the euthyroid state may not immediately eliminate all symptoms. After going to a small dose of the atypical anti-depressant mirtazapine, I finally could feel, every day, like I had in my 30s. Unfortunately, it had taken an agonizing 14 years to get there. Today, I religiously take my 10 micrograms T3, and 75 micrograms T4, split into two doses each day. I also religiously avoid all traces of gluten grains in my diet because I now understand that the gluey, hard-to-digest proteins in them are a substance which can cause major metabolic disruption. Like the co-author of the book “Dangerous Grains”, Ron Hoggan, with whom I have corresponded, I have come to realize that our society’s over-use of a potentially toxic substance isn’t just dangerous to the 1 in 133 people who have full-blown celiac disease—it can cause a very poor quality of life for the approximately 1 in 5 who have gluten intolerance. I have also come to the realization that, to those few who are unlucky enough to encounter the HAIT Anxiety Syndrome, you may require combination T3/T4 therapy to feel better; and, you may never feel as well as you did when you were young, unless you find a way to stop your immune system from waging war on your thyroid. Most of all, 14 years after it started, I feel as though a significant part of my life has been taken from me. I was unable get joy or pleasure from life, I was unable to work effectively, and I was unable to be the kind of parent I could have been between my 45th and 59th years of life. I never imagine that I would be looking forward to the relatively advanced age of 60. However, given that I now feel better than I did at anytime between the ages of 43 and 59, 60 looks like a good place to be. Summary: In retrospect, the most important things I ended up learning from 14 years of very unpleasant experience are: If you have psychiatric symptoms, e.g., depression, anxiety, panic disorder, etc., make sure your endocrine system is evaluated, with thyroid testing as the cornerstone. Beware of doctors who offer an antidepressant first thing, without endocrine evaluation. The emotional/psychiatric effects of hypothyroidism are just as important, and just as damaging, as the physical ones. Unfortunately, many MD’s focus on the physical. If you want to get well, you have to apply all your skills and intelligence to investigating your problem, which most MD’s may not understand. You may also have to turn to “alternative” practitioners. If your TSH is above 3.0, or maybe even 2.5, and your doctor will not do more comprehensive testing (e.g. FT3/FT4), and/or try a test run of thyroid supplementation, find another doctor. If your doctor diagnoses you as hypothyroid, demand that a test for anti-thyroid antibodies be done. If you have any antibodies, even if they are under the threshold where HAIT is considered to start, get testing for allergy to foods, and testing for allergy to common environmental toxins if food testing reveals nothing. You may find, as did I, that you won’t feel as well as possible until you free your body from antibodies.
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Celiac.com 04/25/2020 - Do you know or suspect that you may have a sensitivity to wheat (or gluten)? According to the European Journal of Endocrinology, 43% of people with gluten sensitivity will manifest a form of thyroid dysfunction. (1) The American Journal of Endocrinology reports 30.3% of people with celiac disease will have thyroid dysfunction. (2) If you have a gluten sensitivity, a common manifestation is that it impacts your thyroid. In fact, thyroid dysfunction is four times higher in people with celiac disease than in the general population. (3) Your thyroid is a butterfly shaped gland located in your neck. The two main hormones produced are triiodothyronine (T3) and thyroxine (T4). The most common types of thyroid dysfunction are related to the levels of hormones. For instance, hyperthyroidism is an overproduction, as seen in conditions such as Graves disease. Hypothyroidism is when you are not producing enough or your thyroid is underactive, as seen in conditions such as Hashimoto’s. Hormones get into the cell through receptor sites specific to that particular hormone. Estrogen goes into an estrogen receptor site. Testosterone goes into the testosterone receptor site. Thyroid hormone will only go into a thyroid receptor site. There is a thyroid receptor site on every single cell of your body. It is an incredibly important hormone. Have you ever turned the thermostat down in your home on a winter night when everyone goes to sleep to save fuel? And in the early morning, turn it up to warm your home before everyone wakes up? Your thyroid is the thermostat that controls the temperature inside every cell of your body, otherwise known as your metabolism. And your metabolism is how fast or slow every function in your body occurs. Because the thyroid regulates the level of function of every cell in your body, any symptom in your body can be the result of thyroid dysfunction. The most commonly recognized symptoms of thyroid dysfunction are: Cold hands and feet Lack of vital energy Brain lacks clarity of thought Difficulty losing weight Depression Hitting snooze multiple times in the am Physical symptoms that may suggest a thyroid condition: Distal third of the eyebrows are thinned out Dry, cracked skin, such as the bottoms of your feet Brittle hair Fatigue Increased sensitivity to cold Constipation Dry skin Weight gain Puffy face Hoarseness Muscle weakness Elevated blood cholesterol level Muscle aches, tenderness and stiffness Pain, stiffness or swelling in your joints Heavier than normal or irregular menstrual periods Thinning hair Slowed heart rate Depression Impaired memory Enlarged thyroid gland (goiter) Medication Warnings for People with Thyroid Dysfunction Of course, if it is determined that you need medication, always follow your doctor’s advice. But at the same time, investigate. ‘WHY’ does my body need medication right now? The FDA warns that some thyroid medications may cause serious consequences, including liver disease, liver dysfunction and death. (4) Although uncommon, if you are taking medications and are not seeing improvement, discuss concerns with your doctor before stopping any medications. Try eliminating gluten from your diet to see if you notice any improvement with your thyroid-related symptoms. People with a sensitivity to gluten who still eat wheat require 49% more thyroid hormone to ‘get the job done’ compared to when they stop eating gluten. (5) That means that IF gluten is a problem for you, when you stop being exposed to gluten, your thyroid begins working better, requires less ‘outside help’ - thus less medication, and less risk of side effects from the medication. If you improve on a thyroid healing protocol, some people find antidepressants are no longer necessary. But before going off any medications, you should first check with your doctor on how to safely do this and confirm it is advisable. Thyroid function is critical to your sense of well being. Whatever it takes to improve its function so you can feel good, keep digging away to discover what may help you. You may be among the many people who have a sensitivity to gluten, and it is triggering an autoantibody response. If so, eliminate gluten from your diet. If gluten is not your trigger, you will need to identify what the trigger(s) are. There is often more than one thing. For example, once BPA, a chemical used to mold plastic found in our food and drinks gets into our bloodstream, it is notorious for binding to thyroid and causing chaos. (6) Removing substances (foods and chemicals) offensive to the thyroid,allows this very important gland to function more normally. Testing is advisable to drill down and uncover the source of the problem. What can impact the thyroid negatively? Chlorine is a common one that binds to the receptor sites. (7) An easy ‘base hit’ is to add a chlorine shower filter to your shower head. It may also improve your skin and hair. Bromine - Overexposure to bromine can cause hypothyroidism. (8) Bromine can be found in baked goods, carbonated soft drinks, hot tubs, and even your car upholstery. Your thyroid relies on iodine for hormone production. Bromine tricks those receptor sites into thinking it is binding with iodine. Ultimately, this results in an iodine deficiency and likely thyroid dysfunction. Fluoride - Some people benefit from choosing fluoride-free toothpaste or fluoride-free water. Fluoride effects appear to be more severe in people with iodine deficiencies and is more closely associated with hypothyroidism. (9) Goitrogenic foods - Goitrogenic means they may inhibit thyroid function. The following are very good foods for you but it is worth seeing if any of them may be inhibiting thyroid function. This would include cruciferous vegetables like broccoli, cabbage, or cauliflower. If you have thyroid problems, screening these foods, keenly observing how you feel and function may be of value. Gluten Sensitivity with or without celiac disease - A recent 2019 study of 34 women with thyroid disease was performed to examine the impact of a gluten-free diet. After six months, the results showed that the group on a gluten-free diet had significantly less antibodies affecting thyroid globulin (TG) and thyroid peroxidase (TPO). (10) Rapid weight loss - When you lose a lot of weight or starve yourself, your thyroid slows down its metabolic activity. Ancestrally, this is your body’s way of protecting you for those times when food is scarce, to prevent death from starvation. When your gas gauge says empty and the nearest station is a few miles away, you slow down to burn less fuel and hopefully you’ll make it to the station for a fillup (your next meal). Responsible weight loss is slow and steady. Estrogen - Yes, estrogen is needed for both men and women, but you can have too much of a good thing. Many studies have been done on the association between estrogen and your thyroid levels. Estrogen dominance produces thyroxine binding globulin (TBG) which binds to that thyroid receptor site, reducing your available thyroid hormone availability. A Case of Mistaken Identity The primary offensive gluten molecule is 33 amino acids long. It’s a long molecule. If your immune system is searching (antibodies) for the food you are sensitive to it may attack other molecules that look like the food. The surface of your thyroid is made up of proteins and fats. The proteins are made up of many amino acids, which can include a section that looks like the gluten molecule. Now the immune system may go after the thyroid damaging your thyroid cell. The ‘geek’ term for this is Molecular Mimicry. Once the immune system goes after the thyroid damaging your thyroid cell because of Molecular Mimicry (in this example), now your body needs to make thyroid antibodies to get rid of that damaged cell. If you have a sensitivity to gluten, every time you eat gluten, your body creates antibodies to gluten. These may also go after the thyroid where it looks like it (if that is your genetic weak link). Eventually, over time, your body develops the mechanism where it starts making antibodies to the thyroid ongoing. Some celiac patients or people with gluten sensitivity find that when they go on a gluten-free diet, the thyroid antibodies also go down. Sometimes dramatically, full remission. Thus, sometimes you can reduce the antibodies to your thyroid just by removing the irritating foods. Foods That Contain Gluten Many foods contain gluten, but the concerning ones (to everyone) stem from wheat, rye, and barley. These are toxic forms of gluten that nobody is able to digest, and it is one of the most common foods people eat. In general, when referring to a gluten-free diet, this means avoidance of foods containing wheat, rye, and barley. Now there is gluten in many other grains, corn, rice, quinoa,... But it’s the toxic family of glutens in wheat, rye and barley we’re talking about here. You may be sensitive to corn. Or rice, or quinoa, or any other food. If you are, stop the food. But it would not be included in the family of gluten sensitivity. That term is allocated to wheat, rye and barley. And remember these grains are used as fillers in many different foods as well as hidden sources, such as sauces, cosmetics and shampoos (which can be inhaled). You want to eliminate all forms of gluten to reap the benefits. A recent study on women with Hashimoto’s showed that a gluten-free diet may offer clinical benefits. (11) And it isn’t just hypothyroidism that seems to show improvement. People with Graves are also reporting improvement. (12) Why? Gluten is a common trigger for a lot of people. You may be one of them and not even realize it. If you are struggling to manage your thyroid symptoms, try a gluten-free diet for a few months. You should notice symptom improvement relatively quickly if gluten is the only trigger making your condition worse. Scientific References Valentino, Rossella & Savastano, Silvia & Maglio, Maria & Paparo, Francesco & Ferrara, Francesco & Dorato, Maurizio & Lombardi, Gaetano & Troncone, Riccardo. (2002). Markers of potential coeliac disease in patients with Hashimoto's thyroiditis. European journal of endocrinology / European Federation of Endocrine Societies. 146. 479-83. 10.1530/eje.0.1460479. Sategna-Guidetti, C & Volta, U & Ciacci, Carolina & Usai, Paolo & Carlino, A & Franceschi, L & Camera, A & Pelli, A & Brossa, C. (2001). Prevalence of thyroid disorders in untreated adult celiac disease patients and effect of gluten withdrawal: An Italian multicenter study. The American journal of gastroenterology. 96. 751-7. 10.1111/j.1572-0241.2001.03617.x. Baharvand P, Hormozi M, Aaliehpour A. Comparison of thyroid disease prevalence in patients with celiac disease and controls. Gastroenterol Hepatol Bed Bench. 2020;13(1):44–49. fda.gov Virili, Camilla & Bassotti, Giulia & Santaguida, Maria & Iuorio, Raffaella & Duca, Susanna & Mercuri, Valeria & Picarelli, Antonio & Gargiulo, Patrizia & Gargano, Lucilla & Centanni, Marco. (2012). Atypical Celiac Disease as Cause of Increased Need for Thyroxine: A Systematic Study. The Journal of clinical endocrinology and metabolism. 97. E419-22. 10.1210/jc.2011-1851. Gore AC, Chappell VA, Fenton SE, et al. EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals. Endocr Rev. 2015;36(6):E1–E150. doi:10.1210/er.2015-1010 Bercz JP, Jones LL, Harrington RM, Bawa R, Condie L. Mechanistic aspects of ingested chlorine dioxide on thyroid function: impact of oxidants on iodide metabolism. Environ Health Perspect. 1986;69:249–254. doi:10.1289/ehp.8669249 Allain P, Berre S, Krari N, et al. Bromine and thyroid hormone activity. J Clin Pathol. 1993;46(5):456–458. doi:10.1136/jcp.46.5.456 Malin, Ashley & Riddell, Julia & Mccague, Hugh & Till, Christine. (2018). Fluoride exposure and thyroid function among adults living in Canada: Effect modification by iodine status. Environment International. 121. 667-674. 10.1016/j.envint.2018.09.026. Krysiak, Robert & Szkróbka, Witold & Okopien, Boguslaw. (2018). The Effect of Gluten-Free Diet on Thyroid Autoimmunity in Drug-Naïve Women with Hashimoto’s Thyroiditis: A Pilot Study. Experimental and Clinical Endocrinology & Diabetes. 127. 10.1055/a-0653-7108. Gier, Dominika. (2019). EVALUATION OF THE PREVALENCE IgG-DEPENDENT FOOD INTOLERANCE IN WOMEN PATIENTS WITH THYROID DISORDERS. Joshi AS, Varthakavi PK, Bhagwat NM, Thiruvengadam NR. Graves' disease and coeliac disease: screening and treatment dilemmas. BMJ Case Rep. 2014;2014:bcr2013201386. Published 2014 Oct 23. doi:10.1136/bcr-2013-201386
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Celiac.com 06/20/2019 (originally published 07/12/2010) - Autoimmune diseases taken together are the third leading cause of death in the US. The list of autoimmune diseases is long and varied—M.S., type 1 diabetes, lupus, Hashimoto’s thyroiditis, rheumatoid arthritis, Sjogren’s, and fibromyalgia to name just a few. But the autoimmune disease celiac, unlike all the others, has a unique feature—it’s the only autoimmune disease where the exact trigger is known. Gluten is the trigger for celiac disease and when that trigger is removed the body stops destroying its own small intestine. Why is this profound? Two reasons: There is no other autoimmune disease where the exact trigger is known. Gluten and the damage it causes to the small intestine may very well be the root cause of other autoimmune diseases! We have appreciated the interesting phenomenon where people “develop” gluten intolerance at different ages. It used to be perplexing because it was assumed that if the problem was genetically driven, as soon as the body received its first gluten “insult” damage should begin to occur. When patients stated that they felt perfectly fine until a certain age, it was thought that the damage had probably begun far earlier but the patient had just not noticed. What we have come to realize is that a genetic propensity plus the presence of gluten in the diet are only two of the three necessary constituents of the puzzle—the third is damage to the small intestine. A completely healthy, intact small intestine seems to be quite able to defend itself against gluten. But once damage has occurred, the gut becomes “leaky” and not only can digestive complaints result but symptoms arise in other body systems. There has been proof for many years that the intestine is not the only tissue targeted by the immune reaction to gluten. The prime example of this is a disease called dermatitis herpetiformis where the gluten sensitivity manifests primarily in skin, with only mild or no intestinal involvement. Now, more recent research reveals that perhaps a vast number of autoimmune diseases may also involve an immune response to dietary gluten as well as its consequent autoimmune reaction to tissue transglutaminase. This may be the main immunologic cause. [Note: Although we typically think of tissue transglutaminase as an enzyme in the gut, it is, in fact, an enzyme found throughout the body. This is perhaps another reason why gluten has such far-reaching effects in other systems of the body.] The substance that dictates the permeability between the barrier cells that line the small intestine is called zonulin. Increased zonulin causes the intestine to become leaky, thereby allowing substances to leave the intestine that normally shouldn’t. Research has shown that in patients with celiac disease, gliadin activates zonulin signaling, leading to increased intestinal permeability. But how does this extend to other autoimmune diseases? Dr. Alessio Fasano performed a brilliant study on rats that were genetically predisposed to develop type 1 diabetes. The premise was that if the gut was not affected negatively by zonulin and remained intact and healthy, then perhaps the auto-antibodies made against specific cells of the pancreas that create diabetes would be prevented from leaving the gut and thereby stopped from causing damage to the pancreas. Sure enough 2/3 of these rats who were highly predisposed to develop diabetes did not! This study was the first time that an autoimmune disease was prevented by blocking intestinal permeability. It further puts a new face on the entire concept of how and why autoimmune disease develops. We’ve always thought that the genetic predisposition was an overriding characteristic of autoimmune diseases that overshadowed any effort to sublimate it. This study opens a new field of investigation into the relationship between the health of the intestine and the basis of many diseases. Imagine if the “unknown trigger” of autoimmune disease turns out to be gluten and its effect of creating a leaky gut! It is for this reason that I am so passionate about early diagnosis of gluten intolerance. Whether it be celiac disease or gluten sensitivity, the effect that gluten imposes on the integrity of the small intestine has far-reaching implications. I see it clinically in my patients on a daily basis, but the above research puts a point on it that we must consider seriously. A study from Italy showed that the longer gluten sensitive people eat gluten, the more likely they are to develop autoimmune diseases. They found that in childhood celiacs, the prevalence of autoimmune disease rose from a baseline of 5% at age 2 to almost 35% by age 20. Imagine if screening of all children for gluten intolerance resulted in reductions of future autoimmune diseases! I am currently working on a program with my patients who are gluten intolerant to restore their small intestines to the healthiest possible condition. This is important from the obvious viewpoint that optimal digestion and absorption is critical to good health. But it is also vital from the perspective of understanding and managing zonulin and its long-term effects on health. I would recommend that you take the following steps to ensure that you are doing everything you can to restore your small intestine to optimal functioning. Have a comprehensive stool analysis performed to ensure that no pathogenic organisms (bacteria, amoeba, parasites, etc) are present. Such a test should also measure the effect of your body’s enzymes to see how effectively your food is being broken down and absorbed. It should also assess the health of your intestinal bacteria or probiotics. Eliminate dairy foods from your diet. There is considerable evidence to suggest that consuming milk from other mammals is not conducive to good health, especially in our digestive tracts. The inflammation that dairy can cause could well be contributing to a leaky gut, despite the elimination of gluten. Once you have taken the above steps, see how you’re feeling. Some patients require supplements such as glutamine, quercitin, reduced glutathione, N-acetylcysteine, omega 3 fatty acids, and vitamins A, E, B and zinc to help the intestinal lining heal fully. Once the above have been done, have a lab test performed for leaky gut. It’s called a lactulose/mannitol test and will show whether large molecules are crossing the intestinal barrier. This is a non-invasive, non-drug test. Just to reiterate: encourage parents you know to have their children evaluated for gluten intolerance. The more we can affect an early diagnosis, the healthier our future generations will be. Last but not least, show your doctor this data. There is still too much ignorance in our profession about gluten and its broad reaching negative effects. I hope you find this information helpful. Many of the steps mentioned above are best administered with the help of a clinician so let me know if I can assist you to find someone in your area who can help. References: Scandinavian Journal of Gastroenterology. 2006 Apr;41(4):408-19. Annals N Y Academy Science. 2009 May;1165:195-205. “Tight junctions, intestinal permeability, and autoimmunity: celiac disease and type 1 diabetes paradigms.” Clinical Gastroenterology & Hepatology. 2005 Apr;3(4):335-41. “Permeability, zonulin production, and enteropathy in dermatitis herpetiformis.” Gut. 2003 Feb;52(2):218-23. “Early effects of gliadin on enterocyte intracellular signalling involved in intestinal barrier function.”
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