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    Scott Adams
    ¾ teaspoon of xanthan gum per cup of flour & one teaspoon of methylcellulose per cup of flour. Clear Gel in place of methylcellulose has the advantage of being much cheaper and more readily available than methylcellulose.
    If flour is the only ingredient that contains gluten, then you can convert it to a gluten-free recipe. Just replace the flour with Bette Hagmans gluten-free flour mix:
    2 parts white rice flour
    2/3 part potato starch flour
    1/3 part tapioca flour and a teaspoon of xanthan gum
    Beware of spices which contain wheat flour! Many manufacturers use wheat flour to keep spices from clumping.

    Scott Adams
    Knox un-flavored gelatin is readily available in regular grocery stores in the baking supplies area. It adds moisture and helps bind ingredients. It is a welcome addition to bread recipes with gluten-free flours. Besides commercially prepared Egg Replacer, Flaxseed can be used as an egg substitution. Mixing one tablespoon ground flaxseed with two tablespoons warm water for each egg. Let it sit after adding. If you are soy tolerant, add one half teaspoon lecithin to this mixture plus one teaspoon baking powder to help the leavening process. When substituting this mixture for a regular egg, add one extra. Duck eggs are often tolerated by those who have problems with chicken eggs. They can be hard to find. Look for them in Chinese markets. Coconut milk is a good substitute for cow and soy milk.

    Scott Adams
    This recipe comes to us from Lori Nies.
    (Dose: 1-2 tablespoons per day for adults)
    1 pound prunes
    1 pound raisins or pitted dates
    1 pound figs
    4 ounces Senna tea leaves (found at health food stores)
    1 cup gluten-free brown sugar
    1 cup lemon juice
    Boil 4 cups of water, add to the tea leaves and steep for five minutes. Strain the tea and pour two cups of the tea liquid into a large pot, discard the rest. Add the fruit (except lemon) to this pot and boil for five minutes.
    Remove from heat; add the sugar and lemon juice and mix. Allow the mixture to cool.
    Use mixer, blender or food processor to turn the fruit mixture into a smooth paste. Spoon it into jars or freezer containers and store in the freezer.
    Note: This fruit paste does not freeze solid, but keeps well indefinitely in the freezer. It can be spread on toast or used as topping - or if all else fails, just take it like medicine.

    Carol Fenster, Ph.D.
    This article originally appeared in the Summer 2004 edition of Celiac.com's Journal of Gluten-Sensitivity.
    Celiac.com 10/13/2014 - Sugar—the very word brought the lively conversation at my dinner party to a screeching halt.  As my guests savored their cake, I could feel ten pairs of ears eavesdropping as I discussed this emotionally laden word with the woman seated next to me.
    “My friend made a chocolate cake,” she was saying, “and wanted to cut back on sugar in her diet, so she made a few adjustments to the recipe.  Instead of semisweet chocolate, she used unsweetened chocolate.  In place of the sugar, she used a few tablespoons of Splenda.”  But, my guest continued with a look of puzzlement on her face, “the cake didn’t taste like cake at all and it was hard and chewy and kind of rough-looking.  My friend had to throw it away.”
    In these days of low-sugar diets, many of us—like my guest’s friend—are tempted to skip the sugar in baking, or at least reduce it somewhat.  Much maligned and often relegated to the back of the pantry, most of us regard sugar as a source of calories and are unaware of its other roles.
    Now, before I go any further let’s set the record straight.  I think we eat far too much sugar.  I look for ways to reduce it in my diet whenever I can.  I avoid sugary soft drinks, only eat desserts on special occasions, and watch for hidden sugar in commercial foods.
    Nonetheless, after over 10 years of developing gluten-free recipes, I have a healthy respect for the role of sugar in baking.  It is particularly important for us gluten-free bakers, because we already have to alter the flavor of our foods by removing wheat flour.  If you thinking about omitting sugar in your baking, here’s what you should know:
    First, the obvious.  Sugar makes things taste sweet.  You can replace sugar with a substitute sweetener but the cake may taste different because we associate “sweetness” with the distinct flavor of sugar (even though you may think of sugar as “neutral” because it’s white). Sugar accentuates the flavor of food.  A chocolate cake tastes downright strange without sugar, but delicious with the right amount.  Try this experiment: Drink unsweetened tea and then add a little sugar to it and notice how much stronger the flavor is. Sugar tenderizes the crumb and makes it finer and moister.  In contrast, substitutes like Splenda tend to produce a crumb that is larger, tougher, and somewhat drier. Sugar encourages the browning process on the crust of baked goods.  It’s this browning that we often use as an indicator that a cake is “done,” and, it’s that tendency to brown that relates to its next benefit. Sugar produces a slightly crispy, shiny exterior on baked goods that makes them more attractive.  It’s the sucrose in sugar that does this and, since sucrose is missing in Splenda, it can’t promote the same level of browning.   Next time you’re tempted to reduce or omit the sugar in baked goods, follow these tips:
    Instead of using all Splenda, use half sugar and half Splenda.  You will lower the calorie content, but your cake will be more tender, brown more attractively, and have a finer crumb than if you use all Splenda.  A cake may bake a little faster, so check it about five minutes before the recommended cooking time.  It may also have a little less volume and not rise as high. Add a couple tablespoons of honey to the batter.  Honey is a natural humectant and encourages the cake to retain moisture so it won’t dry out as quickly.  Of course, honey has its own flavor which you may detect if you use a lot of it. Increase the amount of fat in the recipe by 25%, but be sure to use healthier fats.  Canola oil and (light) olive oil are good in baking and are good for you.  Of course, this will increase the fat content and calorie content (a tablespoon of these oils is roughly 100 calories), but your baked goods will taste better and look better because fat is a flavor carrier and also tenderizes the crumb. Use a topping to conceal the rough crust found in low-sugar baked goods.  For example, a streusel topping on muffins will partially conceal their rough tops. Rather than drastically reducing the amount of sugar at the beginning of your sugar-reduced diet, gradually cut back on the sugar a little more each time you bake.  Your palate will adjust and eventually you won’t want “ultra-sweet” foods as much. Try an alternative sweetener such as agave nectar.  Even though it has calories, it has a low glycemic level (the rate at which it raises your blood sugar levels). Finally, (and this is the tough one) just try eating less of those sugary baked foods to reduce your sugar intake.  Maybe half a muffin, or a smaller slice of cake, or only one small cookie instead of a large one.  Our portion sizes have crept up over the past couple of decades to the point where our muffins are anywhere from 3-5 times larger than a standard USDA serving. Oh, you’re probably wondering about that dessert my guests were eating.  It was a flourless chocolate cake from my book Gluten-Free 101 made with one-third sugar, one-third Splenda, and one-third agave nectar.  It was topped with whipped cream (sweetened with agave nectar) lightly dusted with Dutch cocoa, and garnished with a bright red strawberry and a few chocolate-covered espresso beans.  The slices were reasonably-sized—not the massive servings we often find in restaurants.  My guests were relieved to learn that this dessert was a sweet, yet sensible ending to the meal…and, they ate every last crumb!

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/18/2018 - Celiac disease has been mainly associated with Caucasian populations in Northern Europe, and their descendants in other countries, but new scientific evidence is beginning to challenge that view. Still, the exact global prevalence of celiac disease remains unknown.  To get better data on that issue, a team of researchers recently conducted a comprehensive review and meta-analysis to get a reasonably accurate estimate the global prevalence of celiac disease. 
    The research team included P Singh, A Arora, TA Strand, DA Leffler, C Catassi, PH Green, CP Kelly, V Ahuja, and GK Makharia. They are variously affiliated with the Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Lady Hardinge Medical College, New Delhi, India; Innlandet Hospital Trust, Lillehammer, Norway; Centre for International Health, University of Bergen, Bergen, Norway; Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Gastroenterology Research and Development, Takeda Pharmaceuticals Inc, Cambridge, MA; Department of Pediatrics, Università Politecnica delle Marche, Ancona, Italy; Department of Medicine, Columbia University Medical Center, New York, New York; USA Celiac Disease Center, Columbia University Medical Center, New York, New York; and the Department of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, India.
    For their review, the team searched Medline, PubMed, and EMBASE for the keywords ‘celiac disease,’ ‘celiac,’ ‘tissue transglutaminase antibody,’ ‘anti-endomysium antibody,’ ‘endomysial antibody,’ and ‘prevalence’ for studies published from January 1991 through March 2016. 
    The team cross-referenced each article with the words ‘Asia,’ ‘Europe,’ ‘Africa,’ ‘South America,’ ‘North America,’ and ‘Australia.’ They defined celiac diagnosis based on European Society of Pediatric Gastroenterology, Hepatology, and Nutrition guidelines. The team used 96 articles of 3,843 articles in their final analysis.
    Overall global prevalence of celiac disease was 1.4% in 275,818 individuals, based on positive blood tests for anti-tissue transglutaminase and/or anti-endomysial antibodies. The pooled global prevalence of biopsy-confirmed celiac disease was 0.7% in 138,792 individuals. That means that numerous people with celiac disease potentially remain undiagnosed.
    Rates of celiac disease were 0.4% in South America, 0.5% in Africa and North America, 0.6% in Asia, and 0.8% in Europe and Oceania; the prevalence was 0.6% in female vs 0.4% males. Celiac disease was significantly more common in children than adults.
    This systematic review and meta-analysis showed celiac disease to be reported worldwide. Blood test data shows celiac disease rate of 1.4%, while biopsy data shows 0.7%. The prevalence of celiac disease varies with sex, age, and location. 
    This review demonstrates a need for more comprehensive population-based studies of celiac disease in numerous countries.  The 1.4% rate indicates that there are 91.2 million people worldwide with celiac disease, and 3.9 million are in the U.S.A.
    Source:
    Clin Gastroenterol Hepatol. 2018 Jun;16(6):823-836.e2. doi: 10.1016/j.cgh.2017.06.037.

    Jefferson Adams
    Celiac.com 06/16/2018 - Summer is the time for chips and salsa. This fresh salsa recipe relies on cabbage, yes, cabbage, as a secret ingredient. The cabbage brings a delicious flavor and helps the salsa hold together nicely for scooping with your favorite chips. The result is a fresh, tasty salsa that goes great with guacamole.
    Ingredients:
    3 cups ripe fresh tomatoes, diced 1 cup shredded green cabbage ½ cup diced yellow onion ¼ cup chopped fresh cilantro 1 jalapeno, seeded 1 Serrano pepper, seeded 2 tablespoons lemon juice 2 tablespoons red wine vinegar 2 garlic cloves, minced salt to taste black pepper, to taste Directions:
    Purée all ingredients together in a blender.
    Cover and refrigerate for at least 1 hour. 
    Adjust seasoning with salt and pepper, as desired. 
    Serve is a bowl with tortilla chips and guacamole.

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia.
    So how, you may ask, is all this related to gluten? As a starting point, one report from the medical literature identifies a patient who developed aphasia after admission for severe diarrhea. By the time celiac disease was diagnosed, he had completely lost his faculty of speech. However, his speech and normal bowel function gradually returned after beginning a gluten free diet (8). This finding was so controversial at the time of publication (1988) that the authors chose to remain anonymous. Nonetheless, it is a valuable clue that suggests gluten as a factor in compromised speech production. At about the same time (late 1980’s) reports of connections between untreated celiac disease and seizures/epilepsy were emerging in the medical literature (9).
    With the advent of the Internet a whole new field of anecdotal information was emerging, connecting a variety of neurological symptoms to celiac disease. While many medical practitioners and researchers were casting aspersions on these assertions, a select few chose to explore such claims using scientific research designs and methods. While connections between stuttering and gluten consumption seem to have been overlooked by the medical research community, there is a rich literature on the Internet that cries out for more structured investigation of this connection. Conversely, perhaps a publication bias of the peer review process excludes work that explores this connection.
    Whatever the reason that stuttering has not been reported in the medical literature in association with gluten ingestion, a number of personal disclosures and comments suggesting a connection between gluten and stuttering can be found on the Internet. Abid Hussain, in an article about food allergy and stuttering said: “The most common food allergy prevalent in stutterers is that of gluten which has been found to aggravate the stutter” (10). Similarly, Craig Forsythe posted an article that includes five cases of self-reporting individuals who believe that their stuttering is or was connected to gluten, one of whom also experiences stuttering from foods containing yeast (11). The same site contains one report of a stutterer who has had no relief despite following a gluten free diet for 20 years (11). Another stutterer, Jay88, reports the complete disappearance of her/his stammer on a gluten free diet (12). Doubtless there are many more such anecdotes to be found on the Internet* but we have to question them, exercising more skepticism than we might when reading similar claims in a peer reviewed scientific or medical journal.
    There are many reports in such journals connecting brain and neurological ailments with gluten, so it is not much of a stretch, on that basis alone, to suspect that stuttering may be a symptom of the gluten syndrome. Rodney Ford has even characterized celiac disease as an ailment that may begin through gluten-induced neurological damage (13) and Marios Hadjivassiliou and his group of neurologists and neurological investigators have devoted considerable time and effort to research that reveals gluten as an important factor in a majority of neurological diseases of unknown origin (14) which, as I have pointed out previously, includes most neurological ailments.
    My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
    Sources:
    1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
    2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
    3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
    5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
    6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
    7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
    9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
    14. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.

    Jefferson Adams
    Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs). 
    However, researchers really don’t have much data regarding the frequency and significance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. Such data could provide useful comparison information for patients with RCDII, among other things.
    To that end, a research team recently set out to try to get some information about the frequency and importance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. The research team included Shafinaz Hussein, Tatyana Gindin, Stephen M Lagana, Carolina Arguelles-Grande, Suneeta Krishnareddy, Bachir Alobeid, Suzanne K Lewis, Mahesh M Mansukhani, Peter H R Green, and Govind Bhagat.
    They are variously affiliated with the Department of Pathology and Cell Biology, and the Department of Medicine at the Celiac Disease Center, New York Presbyterian Hospital/Columbia University Medical Center, New York, USA. Their team analyzed results of TCR-GR analyses performed on SB biopsies at our institution over a 3-year period, which were obtained from eight active celiac disease, 172 celiac disease on gluten-free diet, 33 RCDI, and three RCDII patients and 14 patients without celiac disease. 
    Clonal TCR-GRs are not infrequent in cases lacking features of RCDII, while PCPs are frequent in all disease phases. TCR-GR results should be assessed in conjunction with immunophenotypic, histological and clinical findings for appropriate diagnosis and classification of RCD.
    The team divided the TCR-GR patterns into clonal, polyclonal and prominent clonal peaks (PCPs), and correlated these patterns with clinical and pathological features. In all, they detected clonal TCR-GR products in biopsies from 67% of patients with RCDII, 17% of patients with RCDI and 6% of patients with gluten-free diet. They found PCPs in all disease phases, but saw no significant difference in the TCR-GR patterns between the non-RCDII disease categories (p=0.39). 
    They also noted a higher frequency of surface CD3(−) IELs in cases with clonal TCR-GR, but the PCP pattern showed no associations with any clinical or pathological feature. 
    Repeat biopsy showed that the clonal or PCP pattern persisted for up to 2 years with no evidence of RCDII. The study indicates that better understanding of clonal T cell receptor gene rearrangements may help researchers improve refractory celiac diagnosis. 
    Source:
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023

    Jefferson Adams
    Celiac.com 06/13/2018 - There have been numerous reports that olmesartan, aka Benicar, seems to trigger sprue‐like enteropathy in many patients, but so far, studies have produced mixed results, and there really hasn’t been a rigorous study of the issue. A team of researchers recently set out to assess whether olmesartan is associated with a higher rate of enteropathy compared with other angiotensin II receptor blockers (ARBs).
    The research team included Y.‐H. Dong; Y. Jin; TN Tsacogianis; M He; PH Hsieh; and JJ Gagne. They are variously affiliated with the Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School in Boston, MA, USA; the Faculty of Pharmacy, School of Pharmaceutical Science at National Yang‐Ming University in Taipei, Taiwan; and the Department of Hepato‐Gastroenterology, Chi Mei Medical Center in Tainan, Taiwan.
    To get solid data on the issue, the team conducted a cohort study among ARB initiators in 5 US claims databases covering numerous health insurers. They used Cox regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for enteropathy‐related outcomes, including celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy. In all, they found nearly two million eligible patients. 
    They then assessed those patients and compared the results for olmesartan initiators to initiators of other ARBs after propensity score (PS) matching. They found unadjusted incidence rates of 0.82, 1.41, 1.66 and 29.20 per 1,000 person‐years for celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy respectively. 
    After PS matching comparing olmesartan to other ARBs, hazard ratios were 1.21 (95% CI, 1.05‐1.40), 1.00 (95% CI, 0.88‐1.13), 1.22 (95% CI, 1.10‐1.36) and 1.04 (95% CI, 1.01‐1.07) for each outcome. Patients aged 65 years and older showed greater hazard ratios for celiac disease, as did patients receiving treatment for more than 1 year, and patients receiving higher cumulative olmesartan doses.
    This is the first comprehensive multi‐database study to document a higher rate of enteropathy in olmesartan initiators as compared to initiators of other ARBs, though absolute rates were low for both groups.
    Source:
    Alimentary Pharmacology & Therapeutics