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  • Connie Sarros
    All About Eggplant
    Image Caption: Image: CC--Jeff Peterson
    Celiac.com 09/15/2018 - People have a love/hate relationship with the purple fruit called ‘eggplant’. Eggplants, first cultivated in southern India and Sri Lanka, are also known as aubergine, Guinea squash, melazana, and ‘poor-man’s caviar’. Like potatoes they are members of the nightshade family, and despite the fact that we all consider eggplant to be a vegetable, biologically it is defined as a berry, and therefore it is a fruit.
    When selecting the fruit, select ones that are firm to the touch, have a smooth and shiny skin and are heavy. Avoid those with brown or soft spots and have a dull color. Gently push with your thumb or forefinger. If the flesh gives slightly but then bounces back, it is ripe. If the indentation remains, it is overripe and the insides will be mushy. If there is no give at all, the eggplant was picked too early. Once you bring it home, avoid placing it near tomatoes and apples, as they give off a gas that quickens the ripening process. Try to use the eggplant within two days of purchase.
    There are several cooking hints that will make your ‘eggplant experience’ more tasteful. Do not cook this fruit in an aluminum pan as it may cause discoloration (both of the pan and the fruit!). The skin is edible on small, younger plants, but should be removed on coarser, older ones. Once you cut the eggplant and cook it right away because the flesh will brown (similar to cut bananas). This fruit absorbs oil very easily, so it is recommended that you coat the slices with cornmeal before frying or baking. To help reduce the bitter flavor in older plants, ‘de-gorge’ the eggplant—Slice the eggplant into ½-inch pieces, salt well, then weigh down each slice in a colander to allow the liquid to drain out of the eggplant for 30 minutes—then rinse with cold water and pat dry.
    Equivalents and Nutritional Value—one pound of eggplant equals 3½ cups of diced eggplant and 1¾ cups cooked eggplant. One medium eggplant weights about 1 pound. It contains vitamin C and potassium, has anti-bacterial and diuretic effects, as well as flavanoids (cancer fighting antioxidants). One cup cooked eggplant contains 25 calories.
    The different ways to prepare eggplant are limited only by your imagination. Cut it into matchsticks to add to a stir-fry. Cube it for vegetable stews (Ratatouille). Shred it to make fritters, or puree it for a hummus-style dip. You can also slice it lengthwise and grill it.
    This fruit is probably most famous for the Italian rendition of Eggplant Parmigiana. But the Greeks have taken this dish one step further, ‘Moussaka’. If you have never eaten this, it is a delight to savor. Lean ground beef may be substituted for the ground lamb. Three zucchini may be used in place of the eggplant (if you prefer). Even if you hate eggplant, you will love Moussaka.
    The beauty of Moussaka is that this casserole may be made in advance, then covered and refrigerated overnight, or covered with foil and frozen—before you bake it (thaw in the refrigerator completely before baking). Time is precious for us all, and this concoction does take some time to assemble, but every moment is worth it. This makes an impressive side dish for company, it is perfect for a buffet table, or it can be used as a main dish for a family dinner.
    The following recipe is from my “Wheat-free Gluten-free Reduced Calorie Cookbook”. Traditional Moussaka is ‘loaded’ with calories and fat and cholesterol. This version is lower in calories and fat without sacrificing any of the delicious taste.
    Moussaka (Greek Casserole Dinner)
    Ingredients:
    1 large eggplant, peeled 2 teaspoons olive oil 1 large onion, chopped ½ pound lean ground lamb 5 teaspoons tomato paste ¼ cup white wine ¼ cup chopped fresh parsley 1/8 teaspoon cinnamon 18 teaspoon salt 1/8 teaspoon pepper 1 tablespoon margarine 1 ½ tablespoon cornstarch 1 cup scalded 1% milk 1 egg beaten until frothy 1/8 teaspoon nutmeg ½ cup gluten-free lowfat cottage cheese 1/3 cup gluten-free corn muffin crumbs, dried 1/3 cup Parmesan cheese, shredded Directions:
    Preheat broiler. Cut the peeled eggplant lengthwise into ½-inch thick slices. Spray both sides of the slices with gluten-free nonstick spray; set on a broiler pan and broil until browned, turning once. Preheat oven to 350F. Heat olive oil in a skillet; add onion and sauté until lightly browned. Add the lamb and cook, breaking meat up with a fork, for 10 minutes or until the meat is browned. In a small bowl, stir together the tomato paste, wine, parsley, cinnamon, salt and pepper; add to the meat and simmer, stirring frequently, until all liquid has been absorbed. Remove from heat. Melt the margarine in a medium-size saucepan; blend in the cornstarch with a whisk. Slowly stir the hot milk into the cornstarch; cook over medium heat, stirring constantly, until thickened. Cool slightly, and then stir in the beaten egg, nutmeg, and cottage cheese. Spray a 9-inch square pan with gluten-free nonstick spray. Sprinkle the bottom lightly with 2 tablespoons of the corn muffin crumbs. Arrange alternate layers of eggplant slices and meat mixture in the pan. Sprinkle each meat layer with the Parmesan cheese and remaining corn muffin crumbs. Pour the cottage cheese mixture over the top. Bake 45 minutes or until the top is golden. Cool slightly before cutting. Makes 6 (4 ½ X3-inch) serving.

    Jefferson Adams
    Nima Labs Claps Back at Gluten Free Watchdog Over Gluten Sensor Data
    Image Caption: Image: Nima Labs
    Celiac.com 09/14/2018 - Celiac.com was all set to do a story on the latest peer-reviewed data on the Nima gluten testing device, when along comes Gluten-Free Watchdog with another of their famous non-recommendations. Gluten-Free Watchdog says they cannot recommend the Nima gluten test kit because of alleged flaws.
    But what does the science say? The latest Nima article and Gluten-Free Watchdog’s complaint both focus on the science, so let’s start there.
    Nima makes two different food sensors: one detects gluten, the other detects peanuts. Each sensor comprises a small, handheld electronic device and a cartridge. To test food, consumers place a pea sized amount into the cartridge, place the cartridge inside the sensor, and run the device.  They then receive a smiley face or wheat symbol with "gluten found," depending on whether or not the Nima device detected the allergen.
    Nima reported their original data in a peer-reviewed scientific journal. Among the conclusions: “Compared with reference R5, Nima antibodies (13F6 and 14G11) had 35- and 6.6-fold higher gliadin affinities, respectively. Nima demonstrated device performance using a comprehensive list of foods, assessing detection sensitivity, reproducibility, and cross-reactivity. Nima presented a 99.0% true positive rate, with a 95% confidence interval of 97.8%–100%.”
    Gluten Free Watchdog says that:
    “Based on third party testing data, the Nima Sensor fails to detect gluten at the 20 ppm level over 20 percent of the time. It isn’t until a sample contains a level of gluten at the 40 ppm level, that a gluten found result is received close to 100% of the time.” Gluten Free Watchdog suggests that this is a problem, because:
    “At a level of gluten in a sample from less than 2 ppm up to a level of gluten between 30 ppm and 40 ppm, the result displayed on the Nima Sensor may be either smiley face or gluten found. If a sample is tested with a Nima Sensor and the result is a smiley face, there is no practical way for a consumer to know if the level of gluten in the sample is less than or more than 20 ppm. If a sample is tested with a Nima Sensor and the result is gluten found, there is no practical way for a consumer to know if the level of gluten in the sample is less than or more than 20 ppm. As a result, the data point received from the Nima Sensor for gluten presents major interpretation problems.” Gluten Free Watchdog charges that Nima uses “NOT the scientifically validated Ridascreen Gliadin R5 ELISA Mendez Method from R-Biopharm used by Gluten Free Watchdog.” The fact is that R5 Elisa remains the industry standard for most testing applications. 
    Gluten Free Watchdog closes its warning with a word from their independent expert: According to Adrian Rogers, Senior Research Scientist at Romer Labs, “It could be argued that the device is not fit for purpose as the company states that there is a clear differentiation between safe and unsafe products based on a 20 ppm level which the validation data does not corroborate.”
    It’s worth noting that for all his accomplishments, Rogers is neither a doctor, nor a PhD. Rogers' LinkdIn page lists his education as: Bsc (Hons), Microbiology, University of Wales, Aberystwyth. A Bachelor of Science degree may not necessarily make an expert in this subject, yet he is presented as one.
    Rogers also seems to have a potential conflict of interest that was omitted in Thompson’s press release. Directly from Rogers’ LinkdIn site:
    “Romer Labs®, Inc. developed an immunochromatographic lateral flow assay for the qualitative detection of gluten in raw ingredients, processed foods, finished food products, and environmental surfaces, using the G12 antibody developed by Belén Morón. The G12 antibody targets a 33-mer peptide which is resistant to enzymatic digestion and heat denaturation, as well as being the fragment of the gliadin protein to which celiac disease sufferers react, making it a reliable analytical marker.” The company Rogers works for, Romer Labs, makes its own gluten testing kits. It seems a bit disingenuous for Gluten Free Watchdog to use a spokesperson from a potentially competing company to try to counteract a peer-reviewed scientific publication for a device which is made by a potential competitor.
    Nima’s Scientific Advisory Board includes some of the most highly respected celiac disease researchers and scientists in the world. They include: Peter HR Green, MD Phyllis and Ivan Seidenberg Professor of Medicine. Director, Celiac Disease Center at Columbia University; Jody Puglisi, PhD Stanford University Professor of Structural Biology; Lucille Beseler, MS, RDN, LDN, CDE, FAND Family Nutrition Center of South Florida; Benjamin Lebwohl, MD, MS Director of Clinical Research Celiac Disease Center at Columbia University; John Garber, MD Gastroenterology, Mass General; and Thanai Pongdee, MD Consultant, Division of Allergic Diseases, Mayo Clinic.
    Nima says that Gluten Free Watchdog’s view of their recently published validation is incomplete and misleading. Nima wrote:
    “All the studies show Nima is highly sensitive across a range of both low and high levels of gluten." "The Nima third party data accurately reported gluten found at 20 ppm and above between 93.3% for food as prepared (a food item that is spiked with an intended quantity of gluten) and 97.2% for food as quantified by an ELISA lab kit (used to determine the exact ppm of gluten in the food)." "The Nima peer reviewed study published in the Food Chemistry Journal reported gluten found at 20 ppm and above at 96.9% accuracy." The statement that:
    “'Nima will fail to detect gluten at 20 ppm 20% of the time' is almost entirely driven by 1 specific food out of 13 tested. That sample, when quantified, was actually below 20 ppm." "In real life, people get glutened at many different ppm levels, not just 20 ppm. Nima has been shown to detect gluten at levels below, at and above 20 ppm across a variety of foods in a number of studies.” Reading the peer reviewed data provided by Nima, and reading Gluten Free Watchdog’s complaints, it becomes clear that Gluten Free Watchdog’s complaints sound serious and authoritative, but ring a bit hollow. 
    Consider the Following Analogy
    Imagine a gluten-sniffing dog that performed as well as Nima in scientific trials; same performance, same exact data. 
    You can give this dog a sniff, or a small bite of food, and he can signal you if the food’s got gluten in it with 97% accuracy at 20ppm or below. Nearly 100% accuracy at 40ppm or above (as stated by Gluten Free Watchdog).
    People would think that the dog was not only cute and fluffy, but wonderfully helpful and everyone would love it, and everyone with celiac disease would want one. And it would be a great big gushing warm and fuzzy feel-good story. Pretty much no one would be arguing that the dog was potentially dangerous, or somehow unfit for people with celiac disease. Such dogs would also be far more expensive to own and maintain than the Nima device. Apparently such dogs can cost upwards of $16,000, not including the cost of food, vet bills, etc.
    So, what’s the accuracy rate of a gluten-sniffing dog, anyway? From Mercola.com: Willow, a German shorthaired pointer, is another gluten-sniffing dog, in this case living in Michigan. Her owner, Dawn Scheu, says she can detect gluten with 95 percent to 98 percent accuracy. She worked with a trainer (the same one who trained Zeus) to teach her own dog to detect gluten, with excellent results.
    Gluten-sniffing dogs may detect gluten in amounts as small as .0025 parts per million with 95 percent to 98 percent accuracy. So, will Gluten Free Watchdog be warning against gluten-sniffing dogs anytime soon?
    Somehow, because Nima is a mechanical device made by a company, it's not so warm and fuzzy, not so feel-good. Maybe Nima needs to shape their device like a cute little doggy, or a Pez candy dispenser?
    But the data remains, as does the fact, whatever its drawbacks, anything that detects gluten like Nima does, as well as it does, is potentially very helpful for celiac disease in numerous situations. And it is extremely unlikely to do them any harm.
    Nima seems very much committed to transparency, scientific excellence, and continual product improvement. These are noble goals and generally a win for people with celiac disease. Think of it, just ten years ago, a portable gluten-sensor with the kind of accuracy Nima is reliably achieving would have been the stuff of fantasy. Yet here it is. More accurate than any gluten-sniffing dog, and for a couple hundred bucks. People with celiac disease are living in a very different world than just a few years ago.
    Nima did not have to publish its data, but it chose to do so, and in a reputable, peer-reviewed scientific journal. Nima conducted its research using solid scientific standards, and reported those results publicly. They explained their methodology and results, they acknowledged product limitations and expressed a commitment to improvement. How is this remotely controversial?
    The celiac disease community is fortunate to have companies committed to investing time and money into products and devices that help to improve the lives of people with celiac disease. We feel strongly that the perfect should not be the enemy of the good. Devices like the Nima gluten sensor can be helpful for numerous people with celiac disease.  
    Disclosure: Nima is a paid advertiser on Celiac.com. Celiac.com's advertisers do not influence our editorial content. 
    Read Nima’s full report on test data at: Food Chemistry.com Read Gluten Free Watchdog’s Statement on the Nima device at: Glutenfreewatchdog.org Read Nima’s Reply to Gluten Free Watchdog at: Nimasensor.com

    Edward R. Arnold
    To HAIT and Back: The Musings of a Thyroid Patient on the Vagaries of Medical Diagnosis and Treatment in America
    Image Caption: Image: CC--katieg93
    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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    Jefferson Adams
    Lawsuit Claims Bob’s Red Mill Ignores RoundUp Pesticide in its Oat Products
    Image Caption: Image: CC--Mike Mozart
    Celiac.com 09/13/2018 - Bob’s Red Mill finds itself under fire by two women who claim the company knowingly hides the presence of an allegedly cancer-causing weed killer in its steel cut oat and rolled oat products, and falsely advertises those products as healthy. 
    Tamara Frankel and Natasha Paracha filed a federal class action in San Francisco, alleging that parent company Bob’s Red Mill Natural Foods knows that its oat products contain or likely contain glyphosate, but fails to disclose it on the label. The women cite a recent report by the Environmental Working Group, an environmental research and advocacy group, which claimed to find traces of controversial herbicide glyphosate in Cheerios, Quaker Oats and other oat-based breakfast foods. The women contend that Bob’s uses labels such as “gluten free,” “wheat free” and “purity tested,” which lead consumers to falsely believe them to be healthy.
    Both U.S. and European regulators have concluded that glyphosate is safe, while that World Health Organization’s International Agency for Research on Cancer classifies it as a probable human carcinogen.
    Bayer subsidiary Monsanto, maker of the glyphosate-based herbicide Roundup has faced numerous lawsuits over its product.  A San Francisco jury recently found that exposure to Roundup caused the cancer of a school groundskeeper, and awarded him $289 million in damages. Shortly after that verdict, the Environmental Working Group released a report claiming that 31 of 45 oat-based food samples tested positive for glyphosate, and that levels exceeded safety limits of 160 parts per billion.
    EWG applies a more stringent standard than the 2 mg/kg/day of glyphosate standard used by the U.S. Environmental Protection Agency, and the 1.1 mg per day standard used by the State of California.
    Frankel and Paracha are represented by Patricia Syverson of the San Diego law firm Bonnett, Fairbourn, Friedman & Balint.
    Stay tuned for more developments on this and related stories.

    Jefferson Adams
    Gluten-Free Diet Likely Improves Neuropathic Pain in Patients with Gluten Neuropathy
    Image Caption: Image: CC--Thanh Liêm
    Celiac.com 09/12/2018 - Many people with celiac disease develop peripheral neuropathy, also known as gluten neuropathy. A team of researchers recently set out to determine rates of neuropathic pain in patients with seemingly idiopathic peripheral neuropathy and gluten sensitivity, and to make note of any contributing factors. They included patients with positive antigliadin, endomysial, and/or transglutaminase antibodies, with or without enteropathy.
    The research team included P Zis, PG Sarrigiannis, DG Rao, and M Hadjivassiliou. They are affiliated with the Academic Department of Neurosciences, Sheffield Teaching Hospitals NHS Foundation Trust, Royal Hallamshire Hospital, Glossop Rd, Sheffield, South Yorkshire, UK.
    They invited all consecutive patients with gluten neuropathy attending a specialist gluten/neurology clinic to participate in the study. They used the DN4 questionnaire and the visual analog scale to assess pain levels. They used the Overall Neuropathy Limitations Scale to assess the severity of neuropathy, along with the Mental Health Index (MHI-5) to assess patients' general mental health status.
    A total of 33 out of 60 patients with gluten neuropathy showed neuropathic pain. The team found no significant differences between the painful, and the non-painful groups in terms of age, gender, neuropathy severity and neuropathy type. 
    Over half of patients with painless gluten neuropathy followed a strict gluten-free diet, compared with just 21.2% of those with painful neuropathy. Patients with painful gluten neuropathy also showed significantly worse MHI-5 scores. 
    After adjusting for age, gender and MHI-5 scores, multivariate analysis showed that, strict gluten-free diet lowered the odds of peripheral neuropathic pain by nearly 90%.
    Most patients with gluten neuropathy commonly have neuropathic pain, which is associated with poorer mental health status. 
    A strict gluten-free diet might substantially reduce rates of peripheral neuropathic pain in patients with gluten neuropathy.
    Read more at: J Neurol. 2018 Jul 21. doi: 10.1007/s00415-018-8978-5.PMID: 30032386

    Jefferson Adams
    Pentraxin 3 Tied to Major Gastrointestinal Damage in Celiac Disease Patients
    Image Caption: Image: CC--altemark
    Celiac.com 09/11/2018 - Gluten sensitivity is the most common sign of celiac disease. Clinical celiac diagnosis usually involves a positive blood test followed by biopsy confirmation of a typical enteropathy.
    The body’s immune response to celiac disease involves both adaptive and innate immunity, and is marked by anti-gliadin (AGA) and anti-transglutaminase 2 antibodies (tTGA), lymphocytic infiltration in the intestinal epithelial membrane, and expression of multiple cytokines. Researchers know that long pentraxin 3 (PTX3), an acute-phase inflammatory molecule, plays an important role in innate immunity.
    A pair of researchers recently set out to assess the relationship between Pentraxin 3 and biopsy status in celiac patients. Roberto Assandri and Alessandro Montanelli of the Department of Clinical Pathology, Clinical Chemistry Laboratory ASST Ospedale Maggiore di Crema, Italy, and the Clinical Chemistry Laboratory, Spedali Civili di Brescia, Italy, set out to explore a possible relationship between PTX3 and celiac disease.
    They used Marsh Histological grade following Marsh criteria classification to dividing 108 celiac disease patients into three groups: Group 1: Marsh 0, patients with a known history of celiac disease under gluten free diet, complete remission; Group 2: Marsh 1 and Marsh 2; Group 3: Marsh 3.
    As a control group, they used 30 healthy age-matched individuals with no known history of celiac disease or gastrointestinal symptoms. They used sandwich ELISA on an automated platform to measure PTX3 serum levels.
    They found that PTX3 serum levels were substantially higher in group 3 and group 2 compared with the healthy control group. They found no statistically significant differences between group 1 and the healthy control group. They noted a strong linear correlation between PTX3 serum levels and AGA levels in group 2, and group 3, but no such correlations between PTX3 serum levels and tTGA levels. 
    Blood tests showed that PTX3 correlated with major gastrointestinal damage in celiac patients. PTX3 is a part of the innate immune system’s humoral branch. Data from this study show that PTX3 serum levels are high in active disease patients with pathological levels of AGA. They also show that patients with normal AGA IgA levels had PTX3 serum levels compared to healthy control subjects. 
    The team proposes that PTX3 can modulate the innate response to gliadin in celiac disease, and may also regulate the adaptive immune response. 
    Read more at: Gastroenterology and Hepatology

    Jefferson Adams
    How Much Gluten Exposure Do Celiacs Get on a Gluten-Free Diet?
    Image Caption: Image: CC--Stig Nygaard
    Celiac.com 09/10/2018 - Anyone diagnosed with celiac disease needs to eat a gluten-free diet if they hope to see their condition improve, and not lead to worse outcomes. So, how much gluten exposure do celiacs get on a gluten-free diet?
    William F. Balistreri, MD, Director Emeritus, Pediatric Liver Care Center; Medical Director Emeritus, Liver Transplantation at Cincinnati Children's Hospital in Cincinnati, Ohio presented data at this year's Digestive Disease Week that focused on the challenges celiac patients face in trying to follow a gluten-free diet. 
    Gluten-free standards and labels help improve awareness, but even so, eating gluten-free can be a challenge. Anyone with celiac disease can tell you that the chances of accidental gluten contamination are many, and that consent vigilance is required.
    Even ”gluten-free foods" are not always free from variable amounts of gluten, whether by imprecise food production, processing, packaging, or preparation.  Accidental gluten exposure can also come via non-foods, such as lipstick, shampoo, toothpaste and the like. Regular, low-level gluten exposure can cause many celiac patients to have mucosal inflammation despite maintaining a gluten-free diet.
    Product by product, gluten levels are generally well-known, but not much is known about how much gluten exposure levels in people with celiac disease who are following a gluten-free diet. Such information could be quite helpful in designing disease management and patient follow-up strategies.
    Gluten immunogenic peptide (GIP) analysis provides direct and quantitative measurement of gluten exposure, has proven useful in diagnosis and clinical management of non-responsive or refractory celiac patients. To figure out the amounts of gluten ingested by highly motivated, educated celiac patients following a gluten-free diet, the research team measured levels of GIPs in food, urine, and stool. They noted the connections between gluten exposure and persistent villous atrophy or related conditions. 
    The study also analyzed food samples from restaurant “doggie bags" saved by the study subjects. The team detected gluten in at least one food sample from nearly 90% of patients consuming a gluten-free diet. That indicates that nearly nine out of ten people with celiac disease, who are trying hard to follow a gluten-free diet, as being exposed to gluten when they eat out.
    Overall, approximately 33% of food samples tested positive for GIPs above 20 ppm, and the estimated GIPs ingested ranged from 0.23 mg to > 40 mg per exposure.
    This new information confirms what many people with celiac disease have long suspected. Namely, that avoiding gluten is really hard to do, even for who are highly aware of gluten-related celiac disease issues, and who work hard to avoid gluten.
    Read more at: Medscape.com

    Carol Fenster, Ph.D.
    Aw Nuts! There’s More Than Meets the Eye in Nut-Crusted Entrees
    Image Caption: Image: CC--Brock Roseberry
    Celiac.com 09/08/2018 - On a recent trip to Hawaii I was often attracted to a particular entrée on the menu of several restaurants. It went by many different names, but basically the dish was fish dredged in a mixture of spices and pulverized nuts to produce a chunky crust. Since Hawaii is the home of macadamia nuts, this popular nut was often used.
    I love fish and I’m very fond of macadamia nuts, so I was particularly enticed by this entrée but I was wary because I know that many chefs like to use panko (Japanese bread crumbs) and add flour to such mixtures even though it isn’t absolutely necessary and is often not mentioned in the entrée’s description on the menu. So, I found myself engaged in a very typical conversation with the waiter. It went something like this:
    Me: I’m wondering about the nut mixture used to coat the fish. Is there wheat flour or bread crumbs in it? Waiter: I don’t know, but I’ll check with the chef and let you know. Me to husband: I better choose another entrée just in case he/she comes back with bad news. Waiter: The chef says there is (flour or bread crumbs or both) mixed in with the nuts and spices. Sorry. Me: That’s fine. Thanks for checking on that for me. Instead, I’ll have the… After I returned from this otherwise fabulous trip, I vowed to create my version of this entrée so I could have it at home whenever I wanted. I will share it here with you, but first a little background on macadamia nuts.
    Macadamia Nuts
    Though expensive, macadamia nuts are a treat and Hawaii is well known for this delicious nut. If macadamia nuts are too expensive or not available in your area, you can use slivered almonds instead. Despite their sometimes “bad” reputation, nuts offer important nutrients and good, healthy fat. But the real reason I was attracted to this dish was the crunchy texture that is so important to me in my gluten-free diet.
    The best way to crush the macadamia nuts is to put them in a small coffee grinder or food processor and grind just until they reach a coarsely chopped stage. Don’t grind them any further or you might end up with “mush” instead of pulverized nuts. To prevent the nuts from sticking together, I grind them with a small amount of cornstarch.
    Some of you may never have traveled to Hawaii. Others, like me, may not get a chance to return to Hawaii for a long time but at least we can bring a little bit of the islands to our dinner table with this tempting dish.
    Macadamia-Crusted Snapper with Pineapple Salsa
    Ingredients:
    4 fish fillets (red snapper, mahi mahi, or firm-flesh fillets--about 6 ounces each) 4 tablespoons olive oil, divided 1 teaspoon ground ginger 1 teaspoon ground coriander 1 teaspoon paprika, plus some for dusting 1 teaspoon salt ½ teaspoon freshly ground pepper 1 cup coarsely ground macadamia nuts or almonds (ground with ¼ cup cornstarch) Additional salt and pepper to taste Salsa Ingredients:
    1 can (8 ounces) pineapple tidbits, drained ½ cup finely diced red bell pepper ½ cup chopped fresh cilantro ¼ cup finely diced red onion 1 tablespoon fresh lime juice 1 tablespoon rice vinegar 1 teaspoon olive oil 1 serrano chile pepper, seeded and finely diced ¼ teaspoon salt ¼ teaspoon sugar Directions:
    At least an hour before dinner, combine all of the salsa ingredients in a small serving bowl, cover, and let sit at room temperature. Preheat the oven to 400°F. Lightly grease a baking dish or sheet large enough to hold the fish fillets side by side and at least 2 inches apart. Use 1 tablespoon of the olive oil or you may line the pan with aluminum oil and lightly coat with cooking spray. Grind the nuts and cornstarch together. Evenly spread the nut mixture on a large dinner plate.
    Combine remaining 3 tablespoons of the oil, ginger, coriander, and paprika. Brush each filet with this mixture; sprinkle both sides with salt and pepper. Dredge each fillet in the nuts, pressing mixture on fish with your fingers to cover it evenly on both sides. Gently transfer fish to prepared baking dish. Sprinkle with a dusting of paprika. Bake fish fillets until they are cooked through and the nut crust is golden brown, anywhere from 10 to 15 minutes or more depending on the thickness of the fish. Season with additional salt and pepper to taste. Serve immediately with 1/3 cup of Pineapple Salsa per serving. Serves 4.
    You don’t have to save this nut crust for fish. It works great on chicken fillets, too. Plan ahead by grinding more nuts than you need then freezing the remainder. That way, it’s just a simple step to mix in the necessary spices or whatever else the recipe calls for.

    Jefferson Adams
    Celiac.com’s Twenty Most Popular Gluten-Free Dinner Recipes
    Image Caption: Image: CC--Quinn Dombrowski
    Celiac.com 09/07/2018 - For the first time in one place, here are Celiac.com’s most popular recipes for gluten-free dinner entrees. These recipes have been enjoyed by hundreds of thousands of readers and have anchored more than a few gluten-free dinner tables. They are sure to please even the most hungry gluten-free eaters. 
    Celiac.com’s Twenty Most Popular Gluten-Free Dinner Recipes are:
    Really Good Gluten-free Beef Stew Recipe Really Good Gluten-Free Chinese-style Fried Rice Recipe Easy Gluten-free Meatloaf Recipe Gluten-free Lobster Mac and Cheese with Truffle Oil Recipe Basic Gluten-Free Cheese Risotto Recipe Easy Gluten-Free Slow Cook Pot Roast Recipe Really Good Gluten-free Shepherd's Pie Recipe Really Good Gluten-Free Chicken Marsala Recipe Really Good Gluten-free Lasagna Recipe Gluten-free Italian-style Meatballs Recipe Gluten-Free Potato Salad Recipe Easy Gluten-Free Ground Beef Tacos Recipe Classic Gluten-Free Mexican-Style Rice Recipe Gluten-Free Chinese-style Lemon Chicken Recipe Celiac.com's Best Ever Gluten-free Thanksgiving Recipe Gluten-Free Corned Beef Recipe Gluten-Free Irish Soda Bread Recipe Easy Gluten-Free Bacon and Cheese Cornbread Recipe Gluten-Free Chicken Vegetable Curry Recipe Easy Gluten-Free Oven-baked Salmon Recipe

    Jefferson Adams
    These Nine Common Foods Cause Most Allergic Reactions
    Image Caption: Image: CC--NIAID
    Celiac.com 09/06/2018 - What are the most common foods that can trigger allergic reactions in people? 
    First, and it's important to be clear about this, a food allergy is not to be confused with a food sensitivity. Food sensitivities are common and usually harmless, if sometimes uncomfortable. Food sensitivity can cause symptoms like gas, bloating, stomach upset, indigestion, and the like when some people eat certain foods. 
    A food allergy, on the other hand, is an immune reaction that happens when the body mistakes harmless food, a peanut for example, for something that could make you sick. When you eat a food you're allergic to, your immune system thinks you’re body is being harmed, and reacts to protect you from that harm. This reaction can be as mild as a light skin rash or red, itchy eyes, or it could be serious enough to cause difficulty breathing, swelling, pain, shock and even death. An allergic reaction can happen very soon after eating an allergenic food, or it can happen many hours later. Either way, food allergies are potentially serious, and should be treated as such.
    According to WebMD, these nine foods account for about 90% of all food allergies:
    Peanuts Tree nuts, such as walnuts, almonds, pine nuts, brazil nuts, and pecans Soy Milk Eggs Wheat, barley, and rye—Celiac disease Oats Fish Shellfish Mild symptoms of a food allergy reaction include:
    Red, swollen, dry, or itchy skin and rash (hives or eczema) Runny or stuffy nose, sneezing, or a slight, dry cough Itchy, watery, red eyes Itchy mouth or inside your ear Funny taste in your mouth Upset stomach, cramps, vomiting, or diarrhea Though any of these foods can cause an allergic reaction, peanuts, nuts, fish, and shellfish are well known for causing severe allergic reactions. 
    Symptoms of a sever allergic reaction to food include:
    Trouble breathing or swallowing Swollen lips, tongue, or throat Feeling weak, confused, or light-headed, or passing out Chest pain or a weak, uneven heartbeat If you suspect that you or someone you know is having an allergic reaction to food, especially a severe reaction, definitely seek medical attention immediately.

    Jefferson Adams
    Researchers Find Key Gene Locus Behind Progression from Celiac to Refractory Celiac Disease
    Image Caption: Image: CC--Elentir
    Celiac.com 09/05/2018 - About one out of every twenty celiac patients fails to respond to a gluten-free diet, and goes on to develop refractory celiac disease (RCD). RCD is a serious condition marked by appearance of intraepithelial T lymphocytes. Depending on the phenotype of the lymphocytes, people develop either RCD I or RCD II. Patients with RCD type II (RCDII) show clonal expansions of intraepithelial T lymphocytes, and face an especially poor prognosis. Just over half of these patients will die within five years of onset due to aggressive enteropathy-associated T-cell lymphoma. 
    At this time, researchers don’t know whether genetic variations might play a role in the severe progression from celiac disease to RCDII. A team of researchers recently set out to try to get some answers.  The team began by conducting the first genome-wide association study to identify the causal genes for RCDII, along with the molecular pathways at play in cases of RCDII. 
    For their genome-wide association study, the team used 38 Dutch patients with RCDII, and replicated the 15 independent top-associated single nucleotide polymorphism (SNP) variants (P<5×10) in 56 independent French and Dutch patients with RCDII.
    The team found that, after replication, SNP rs2041570 on chromosome 7 was significantly associated with progression to RCDII (P=2.37×10, odds ratio=2.36), but not to celiac disease susceptibility. They also found that SNP rs2041570 risk allele A was associated with lower levels of FAM188B expression in blood and small intestinal biopsies. Stratifying RCDII biopsies by rs2041570 genotype revealed differential expression of innate immune and antibacterial genes that are expressed in Paneth cells.
    The team’s efforts resulted in the identification of a new SNP associated with the severe progression of celiac disease to RCDII.  Their data suggest that genetic susceptibility to celiac disease might be unrelated to celiac progression to RCDII, and suggests that Paneth cells might play a role in RCDII progression.
    Source:
    Eur J Gastroenterol Hepatol. 2018 Aug;30(8):828-837.  
    The research team included B Hrdlickova, CJ Mulder, G Malamut, B Meresse, M Platteel, Y Kamatani, I Ricaño-Ponce, RLJ van Wanrooij, MM Zorro, M Jan Bonder, J Gutierrez-Achury, C Cellier, A Zhernakova, P Nijeboer, P Galan, S Withoff, M Lathrop, G Bouma, RJ Xavier, B Jabri, NC Bensussan, C Wijmenga, and V Kumar. They are variously affiliated with the Department of Genetics, University Medical Center Groningen, University of Groningen, Groningen, the Department of Gastroenterology, VUMC, Amsterdam, The Netherlands, INSERM U1163, Imagine Institute and Paris Descartes University, the Department of Gastroeneterology, Georges Pompidou European Hospital, the Paris 13 University Sorbonne Paris Cité, UREN, Inserm (U557), Inra (U1125), Cnam, Bobigny, France, the scientific director of McGill University and Génome Québec Innovation Centre, Montréal, Québec, Canada, the Gastrointestinal Unit and Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital and Harvard Medical School, Boston, The Broad Institute of MIT and Harvard, Cambridge, Massachusetts, the Department of Medicine, University of Chicago, Chicago, Illinois, USA., and the K.G. Jebsen Coeliac Disease Research Centre, Department of Immunology, University of Oslo, Norway.

    Jefferson Adams
    Gluten-Free Salted Cod and Potatoes
    Image Caption: Image: CC--Eugene Kim
    Celiac.com 09/04/2018 - Want a tasty, simple, reasonably quick gluten-free dinner that is sure to satisfy? This recipe for salted cod and smashed potatoes is just the ticket. Add some arugula with a delightful vinaigrette, and you're home free.
    This recipe pairs smashed potatoes with slated cod, milk, garlic, and herbs for a big, gluten-free suppertime hit.
    Ingredients:
    4 cod fillets, 4-6 ounces each 1½ cups whole milk 2 shallots, sliced 1½ teaspoons salt 1 teaspoon dried thyme 2 bay leaves 3 cloves garlic, crushed 1 pound red baby potatoes 2 tablespoons salted butter ¼ cup chives 1 ounce arugula pinch of salt pinch of cracked black pepper 2 teaspoons extra virgin olive oil Tomato and thyme vinaigrette:
    5 ounces plum tomatoes ½ teaspoon thyme 1½ cups tomato juice 1 tablespoon sherry vinegar 2 pinches of salt 1 pinch of cracked black pepper Directions:
    For the vinaigrette, add all the ingredients in a blender and puree until smooth. 
    Strain, and season to taste, and put aside.
    Rub the cod fillets with salt and set aside for 25 minutes. 
    Place the potatoes in a pot, bring to a simmer and cook until tender. 
    When potatoes are done, drain away the water, and place potatoes in a bowl. 
    While still warm, crush the potatoes in the bowl, add the melted butter, salt, and the chopped chives.
    Run cod under cold water to rinse all the salt off. 
    Place cod in a large saucepan with the cold milk, thyme, crushed garlic, sliced shallots and bay leaves.
    Bring to a simmer, cook for four minutes, remove and place on plate for serving.
    Place the potato just off the middle of the plate, place the cod on top and spoon over the dressing. 
    Dress the rocket with the olive oil, salt and pepper, and add place beside the cod. 

    Jefferson Adams
    Why a Faster, Easier Celiac Test is Only Part of the Diagnostic Challenge
    Image Caption: Image: CC--Alden Chadwick
    Celiac.com 09/03/2018 - Can an office-based point of care test (POCT) improve celiac disease detection and diagnosis? A team of researchers recently set out to measure the diagnostic performance of an IgA/IgG-deamidated gliadin peptide (DGP)-based POCT for celiac disease detection, patient acceptability, and inter-observer variability of the POCT results.
    The research team included Michelle S. Lau MBChB, Peter D. Mooney MD, William L. White MBChB, Michael A. Rees BMedSci, Simon H. Wong MBChB, Marios Hadjivassiliou FRCP, Peter H. R. Green MD, Benjamin Lebwohl MD & David S. Sanders FRCP.  They are variously affiliated with the Academic Department of Gastroenterology, the Academic Department of Neurosciences and University of Sheffield, Royal Hallamshire Hospital, Sheffield Teaching Hospitals, Sheffield, UK, and with the Celiac Disease Centre at Columbia University Medical Centre in New York, NY, USA.
    Beginning in 2013, and running through 2017, the team recruited patients who had been referred for secondary care with gastrointestinal symptoms, anemia and/or weight loss (group 1), along with a group of patients with self-reported gluten sensitivity, but unknown celiac disease status (group 2).  Every patient in the study received a POCT, tests for IgA-tissue transglutaminase (IgA-TTG), IgA-endomysial antibodies (IgA-EMA), total IgA levels, and a duodenal biopsy. 
    A total of 500 patients completed acceptability questionnaires, and the team compared inter-observer variability of the POCT results among five clinical staff for 400 cases.
    Group 1 included 1,000 patients. The team saw forty-one patients (4.1%) diagnosed with celiac disease. The sensitivities of the POCT, IgA-TTG, and IgA-EMA were 82.9, 78.1, and 70.7%; the specificities were 85.4, 96.3, and 99.8%. Group 2 included 61 patients. The POCT showed 100% sensitivity, but negative predictive value in detecting celiac disease in group 2. 
    A majority of patients preferred the POCT to a blood draw (90.4% to 2.8%). A Fleiss Kappa coefficient of 0.895 reflected good inter-observer agreement on the POCT results. The POCT had comparable sensitivity to a blood test, and accurately spotted all celiac disease cases in a gluten sensitive group. But, because its low specificity may could cause further unnecessary tests, it’s not good enough to take the place of blood testing.
    It turns out that spotting celiac disease is only part of the battle. Making sure to rule out people who don’t have celiac disease is equally important. That’s why it’s important that any diagnostic test be both sensitive, to spot celiac disease, and specific, to rule out celiac disease in those who don’t have it. 
    Until we get a PCOT with high enough sensitivity and specificity to make accurate celiac diagnosis and accurate elimination of those without celiac disease, the current blood testing regime will continue.
    Read more at: The American Journal of Gastroenterology; volume 113, pages1238–1246 (2018)

    Jonas F. Ludvigsson, M.D.
    Being Pregnant with Celiac Disease: What does it Mean to the Fetus?
    Image Caption: Image: CC--Mysudbury.ca Ouisudbury
    Celiac.com 09/01/2018 - Celiac disease is a common disease triggered by gliadin exposure in genetically sensitive individuals.  It has long been known that untreated celiac disease is associated with intestinal malabsorption, but it is also associated with ongoing inflammation.  This inflammation may have adverse effects on the uptake of important nutrients.  This is probably the underlying reason for the increased risk of osteoporosis demonstrated in patients with celiac disease.  Malabsorption and ongoing inflammation in untreated celiac disease could also potentially have a negative effect on fetal development.
    Several reports have indicated an adverse effect of untreated celiac disease on pregnancy outcome.  We set out to use the national registers of Sweden to:
    Evaluate the association of untreated celiac disease and birth weight, pregnancy duration and intrauterine growth. Evaluate the same association in treated celiac disease. Compare the risk of the above two groups with a reference group of 2.8 million births to mothers who never had a diagnosis of celiac disease. A fourth objective was to evaluate placental weight to see if lower placental weight was more frequent in women with celiac disease. We found that untreated celiac disease (women diagnosed after pregnancy, but most likely having untreated celiac disease at time of pregnancy) was associated with a two-fold risk of low birth weight, pre-term birth, intrauterine growth retardation and cesarean section.
    The low birth weight and intrauterine growth retardation may have been mediated through malabsorption, since placental weight was lowest in women with untreated celiac disease.
    This study was published in Gastroenterology Aug 2005. A link to this paper can be found here: gastrojournal.org
    After that we set out to evaluate the association between adverse pregnancy outcome in males with untreated and treated celiac disease.  In a previous paper, we had found an increased risk of adverse pregnancy outcome when the father had celiac disease (Ludvigsson et al, Gut, 2001).  Now, taking advantage of the large Swedish national registers (all births since 1973 and onwards are recorded), we found no increased risk of low birth weight, pre-term birth or cesarean section in infants to fathers with untreated or treated celiac disease.  This study was published in the Scandinavian Journal of Gastroenterology in Feb 2006.

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