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Wickedly Decadent Gluten-Free Brownies for Chocoholics
Carol Fenster, Ph.D. posted an article in Winter 2003 Issue
Celiac.com 04/01/2023 - I confess. I’m a chocoholic! My favorite dessert is anything chocolate, but when I need a good, quick chocolate “fi x”, I often turn to this recipe. I’ve been making it for about 20 years now and, although it’s gone through many evolutions, it never fails to please. My fondness for chocolate dates back to my childhood when almost all of our desserts were chocolate. We enjoyed chocolate cakes, chocolate pies, chocolate puddings, and chocolate cookies––but one of my favorites was chocolate brownies. I’ve recreated that recipe for you here—with a few wickedly decadent embellishments. Luckily, my husband is fond of chocolate too and will look for any excuse to eat it. Upon learning that chocolate comes from the cocoa bean––which is actually a legume–– he announced that he would increase his vegetable consumption by eating more chocolate! Whatever your excuse, Americans apparently LOVE chocolate––on average, we consume about 10-12 pounds of it each year. But before you head to the kitchen, here are a few tips to assure success: Use the best quality cocoa possible. I’m particularly fond of Ghirardelli unsweetened natural cocoa. Look for it at your local health food store. I also like Scharffen Berger natural cocoa, which can be found at kitchen or gourmet food stores. If you can’t fi nd these brands, I recommend Hershey’s natural cocoa which is available at grocery stores. Be sure to use natural cocoa, not Dutch-processed or European-style cocoa. I get many questions on this topic so here’s the explanation: Natural cocoa is always acidic. Dutch processed cocoa is treated to make it alkaline instead of acidic. The baking powder in this particular recipe is designed to balance the acid in the natural cocoa. If you use Dutch processed cocoa, the PH level is “unbalanced” and the recipe won’t work. Carol Fenster’s Gluten-Free Chocolate Brownies Preheat oven to 350˚. Grease 8-inch square nonstick pan. Stir dry ingredients together (fl our to xanthan gum). Set aside. In large mixing bowl, beat butter, sugars, vanilla, and egg with electric mixer on medium speed until well combined. With mixer on low speed, add dry ingredients and hot water. Mix until just blended. Mixture will be somewhat thick. Stir in nuts and additional ingredients, if using (see options below). Spread batter in prepared pan with wet spatula. Bake 20 minutes. Cool brownies completely before cutting. Serves 12. Double Chocolate Brownies: Add 1⁄2 cup gluten-free, dairy-free chocolate chips or finely chopped dark chocolate to batter. Bake as directed. Chocolate Mint Brownies: Prepare batter as directed. Place half of the batter in greased 8 x 8-inch pan. Add a layer of your favorite gluten-free mints such as Junior Mint patties, taking care not to cut the patties. Top with the remaining layer of batter. Bake as directed. Rocky Road Brownies: Prepare batter as directed. Stir in 1⁄2 cup gluten-free, dairy-free chocolate chips, 1⁄4 cup chopped walnuts, 1⁄2 cup dried cranberries, and 1⁄2 cup Jet-Puff® miniature marshmallows. Because of the additional ingredients, you will need to increase pan size to 11 x 7 or 13 x 9-inch pan. Bake as directed, extending baking time by 5 to 10 minutes, or until thoroughly baked. Cool completely before cutting. Ingredients: 1 cup Flour Blend* 1⁄2 cup unsweetened cocoa (not Dutch) 1⁄2 teaspoon baking powder 1⁄2 teaspoon salt 1⁄2 teaspoon xanthan gum 1⁄4 cup melted butter or margarine 1⁄2 cup brown sugar, packed 1⁄2 cup granulated sugar 2 teaspoons vanilla extract 1 large egg 1⁄4 cup hot water (110º) 1⁄4 cup chopped walnuts (optional *Flour Blend: 1 1⁄2 cups sorghum flour 1⁄2 cup corn flour 1 1⁄2 cups potato starch 1 cup tapioca. Makes 4.5 cups. (To make corn flour, grind cornmeal in small coffee grinder until consistency of flour.) -
Why Medical Researchers Prefer Double Blind Testing
Dr. Ron Hoggan, Ed.D. posted an article in Winter 2014 Issue
Celiac.com 12/21/2016 - I have previously criticized the use of a single blind test protocol for a gluten-free diet. In past issues of The Journal of Gluten Sensitivity I have also been critical of some double blind research protocols for investigating dietary variables for a variety of reasons not relevant to the current topic. However, there are good reasons that the double blind protocol continues to be favored, especially among medical researchers. Single blind testing is where the research subjects are not aware of the intervention being used whereas, in a double blind test, both the subjects and the researchers are kept in the dark about the intervention until the end of the trial. Sometimes that requires the use of placebos. In other protocols, it involves masking the intervention. The primary merit of double blind, over single blind tests is that the former eliminates something called "confirmation bias". Single blind testing was first developed because patients' and other experimental subjects' expectations were thought to skew results. Under some circumstances, this problem is called a placebo effect. We can see the placebo effect in action when research subjects are split into two groups. One group is given the medical treatment or drug being investigated, while the other group is given a placebo. This placebo may be a sugar pill or some other substance or treatment that should have no significant or measurable medical impact on the subject. The placebo is given to subjects/patients as if it could provide medicinal properties. Because the patient expects to feel better with this placebo intervention, some subjects do start feeling better. That's the placebo effect. Single blind testing does reduce this problem. Especially for drug treatments, blinding subjects does make sense. However, another confounding variable was soon recognized as arising from single blind tests. It turns out that, in addition to patients' reporting health benefits from sugar pills and other placebos, the physicians and other scientists were skewing the results in another fashion. This is where confirmation bias comes in. The term identifies a situation where researchers miss signs of a problem with gluten. (A fascinating book titled The Structure of Scientific Revolutions (1962), by Thomas Kuhn provides detailed explanations of this phenomenon in his descriptions of several experiments that clearly show this tendency.) To some extent we all have a tendency to confirm our expectations in what we see. This confirmation bias can have an impact on research results in two ways. First, it can lead researchers who are interacting with the test subjects to communicate, either through body language, or verbal "slips" to indicate that they expect a given patient to improve following the intervention or drug being investigated, leading to more of the placebo effect. It can also lead researchers to interpret their results in ways that confirm what they expected to see, rather than in a more objective light. Placebo effect and confirmation bias can be nullified in a double blind study when researchers subtract the portion of the placebo group who are feeling better on the placebo from the number who report feeling better in the experimental group. (The experimental group is the group that was given the actual drug or medical treatment under investigation.) This simple arithmetic eliminates the number of people in the experimental group who were likely to report feeling better even though they were only given the placebo. The remaining number of experimental subjects who report feeling better after the medical intervention are thought to reflect the number of people who actually experience a benefit induced by the treatment. My concern with physicians running single blind tests on patients who believe that they feel healthier on a gluten-free diet is that the physician is likely to see what she/he expects to see (confirmation bias). So skeptical physicians who would request that their patients do a gluten challenge in the form of a single blind test are most likely to see what they expect to see. This may be why more than 95% of people with celiac disease remain undiagnosed in the USA. Confirmation bias seems to afflict many physicians practicing in the USA. Judging from my years of exchanging correspondence with gluten sensitive people from all over the world, similar dynamics seem to be at work, to varying degrees, in many other countries as well. A protocol that requires the patient to undergo a gluten challenge in a single blind test format is offensive in its implications. It denies the limitations of the very physicians who would be charged with conducting these tests, making observations, and treating patients accordingly. I sincerely believe that physicians are intelligent, hard-working individuals who have pursued a career that is dedicated to helping people. I also believe that they are equally fallible in their judgments and pre-conceived notions about others, especially when it comes to dietary interventions. If physicians cannot accept the observations of their patients, why should their patients be willing to accept their physicians' observations and conclusions? Who has more at stake in this relationship? And who is in a better position to observe even very subtle responses to gluten ingestion? As a culture, we seem to have lost track of why we consult physicians. Although we are all subject to confirmation bias, most of us are not seeking insulting instructions that disparage our honesty, integrity and reliability. When I visit my family physician, I want her to act as my guide to the science she is familiar with, and render the best guidance she can offer based on her expertise and paying careful attention to what I report. If my problem is beyond her knowledge or experience, I expect to be referred to a specialist in my area of concern. I usually consult her, on a collaborative level, when she has some relevant expertise that will compliment my own expertise. I can not foresee a set of circumstances in which I would allow her to conduct a single blind trial on me. I do not accept the premise that she is less susceptible to her confirmation bias than I am to the placebo effect. Thus, my expectation of my physician is that we work together to solve any health problems that arise. I must say that both my current physician, whom I have been seeing for the last five years, and my previous physician who worked with me for the previous eleven years, have consistently exceeded my expectations. In both cases, they seem very happy that I am trying to take responsibility for my own health care and that I consider their advice to be a resource rather than the final word in the matter. I'm very grateful for these relationships, as they, and the gluten-free, dairy-free, diet, along with reduced soy and refined sugar consumption, have helped me achieve a much better state of health than I previously considered possible. -
Celiac.com 06/01/2015 - Earlier research on celiac disease and neuropathy has been hampered by the use of inpatient data, low study power, and lack of information on neuropathic characteristics. A team of researchers recently set out to accurately assess both relative and absolute risk of developing neuropathy in a nationwide population-based sample of patients with biopsy-verified celiac disease. The research team included Sujata P. Thawani, MD, MPH; Thomas H. Brannagan III, MD; Benjamin Lebwohl, MD, MS; Peter H. R. Green, MD; and Jonas F. Ludvigsson, MD, PhD. They are variously affiliated with the Peripheral Neuropathy Center at the Neurological Institute of Columbia University College of Physicians and Surgeons, the Celiac Disease Center in the Department of Medicine at Columbia University College of Physicians and Surgeons in New York, New York, with the Department of Medical Epidemiology and Biostatistics at the Karolinska Institutet in Stockholm, Sweden, and with the Department of Pediatrics, Örebro University Hospital, Örebro University, Örebro, Sweden. For their study, the team collected data on small-intestinal biopsies conducted at Sweden’s 28 pathology departments from 1969 to 2008. They compared the risk of neuropathy in a total of 28 ,232 celiac disease patients, all with villous atrophy, Marsh 3, against results from 139, 473 age- and sex-matched non-celiac control subjects. They used Cox proportional hazards regression to estimate hazard ratios (HRs), and 95% confidence intervals (CIs), for neuropathy as defined by relevant International Classification of Diseases codes in the Swedish National Patient Register; including both inpatient and outpatient data. They found that patients with biopsy-verified celiac disease faced a 2.5 times higher risk of developing neuropathy (95% CI, 2.1-3.0; P < .001). Celiac patients also had an increased risk of developing chronic inflammatory demyelinating neuropathy (2.8; 1.6-5.1; P = .001), autonomic neuropathy (4.2; 1.4-12.3; P = .009), and mononeuritis multiplex (7.6; 1.8-32.4; P = .006). However, the team found no association between celiac disease and acute inflammatory demyelinating polyneuropathy (0.8; 0.3-2.1; P = .68). The team found a significantly increased risk of neuropathy in patients with celiac disease, and they are recommending that doctors screen patients with neuropathy for celiac disease. Source: JAMA Neurol. Published online May 11, 2015. doi:10.1001/jamaneurol.2015.0475
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Celiac.com 11/17/2014 - There is a large body of data that show that celiac disease is associated with metabolic bone disorders, such as low bone mineral density. However, it is unclear whether this translates into an association between celiac disease and such hard clinical outcomes as bone fractures. A research team set out to systematically review and pool the data to better understand the nature of the relationship between celiac disease and the prevalence and incidence of bone fractures. The research team included Katriina Heikkilä, Jo Pearce, Markku Mäki, and Katri Kaukinen. They are variously affiliated with the Departments of Internal Medicine at Seinäjoki Central Hospital and Tampere University Hospital, Finland, the School of Medicine at the University of Tampere, Finland, the Tampere Centre for Child Health Research at University of Tampere and Tampere University Hospital, Finland, and with the Division of Nutritional Sciences, School of Biosciences at the University of Nottingham in the United Kingdom. For their study, they conducted a systematic search of Pubmed, Scopus, Web of Science and Cochrane Library in January 2014 for studies of celiac disease and bone fractures. They included observational studies of any design which compared bone fracture outcomes in individuals with and without celiac disease. Two investigators then independently gathered results from eligible studies. A meta-analyses of case-control and cross-sectional studies showed that bone fractures were almost twice as common in individuals with a clinically diagnosed celiac disease as in those without celiac disease. A meta-analyses of prospective studies showed that celiac disease at baseline was associated with a 30% increase (95% CI: 1.14, 1.50) in the risk of any fracture and a 69% increase in the risk of hip fracture (95% CI: 1.10, 2.59). Two studies of patients with high concentrations of celiac disease-specific autoantibodies, but no celiac disease diagnosis, produced contradictory findings. The results of this study suggest that people with clinically diagnosed celiac disease face a greatly increased risk of hip fractures, and of fractures in general. Further research is needed to determine whether unrecognized celiac disease carries a similar risk of bone fractures. Source: The Journal of Clinical Endocrinology & Metabolism. DOI: http://dx.doi.org/10.1210/jc.2014-1858
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Celiac.com 01/14/2009 - For decades now, doctors have known that people with celiac disease face a significantly greater risk of developing non-Hodgkin's lymphoma (NHL), though that risk has steadily declined over the last 40 years. Recently though, a team of doctors at the National Cancer Institute in Bethesda, Md., led by Ying Gao, M.D., has discovered that siblings of celiac patients also face an increased risk of developing NHL. Results of the study appeared in the January issue of Gastroenterology. The research team conducted a study using 37,869 patients with NHL, 8,323 with Hodgkin's lymphoma, and 13,842 with chronic lymphocytic leukemia who were diagnosed between 1965 and 2004. The study included 236,408 matched controls and 613,961 first-degree relatives. The results indicated that people with celiac disease developed NHL at rates that were 5.35 times higher than non-celiacs, but that they faced no increased risk for developing Hodgkin’s lymphoma or chronic lymphocytic leukemia. In some good news, the doctors found that the NHL risk level for people whose celiac disease was diagnosed between 1995 and 2004 dropped to just 3.86 times greater than for non-celiacs. This is a significant improvement over the 13.2 times greater risk of NHL faced by people diagnosed with celiac disease between 1975 and 1984. However, the study also showed that siblings of celiac disease patients developed NHL at rates that were more than double those of the general population (2.03). Clearly, as diagnosis and treatment of celiac disease has improved, the risk levels for NHL have decreased. The study underscores the need for greater vigilance on the part of both doctors and patients regarding NHL, and for greater understanding of the mechanisms that influence the development of NHL in both celiacs and non-celiacs. As diagnosis and treatment and monitoring of celiac disease improves, and as understanding of NHL increases, it is likely that NHL risk levels for celiac patients will drop even further. Until then, celiac patients are encouraged to stay informed, stay vigilant, and to consult with a physician to keep on top of any developments that may influence risk levels for NHL. Journal of Gastroenterology, January 2009; pp 91-98.
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Celiac.com 03/22/2010 - The main cause for gluten intolerance continues to puzzle scientists, but pathogenesis theories include both genetic susceptibility and environmental triggers, like a virus or infection. For the first time, scientists working with the Academy of Finland’s Research Program on Nutrition, Food, and Health have found genes in the body that are associated both with the immune system and with the body's ability to properly digest gluten in the intestinal tract. Gluten intolerance arises from an autoimmune reaction in the small intestine to the gluten protein found in wheat, barley and rye. Academy Research Fellow Paivi Saavalainen, a veteran researcher in hereditary risk factors for gluten intolerance, says that "some of the genes we have identified are linked with human immune defense against viruses. This may indicate that virus infections may be connected in some way with the onset of gluten intolerance.” Data shows that rates of celiac disease in America have increased more than 400% since World War II. Meanwhile, a Finnish scientist internationally known for his gluten research says that the number of people in Finland who suffer from gluten intolerance has doubled over the last two decades. Since the early 1980s, the percentage of Finns with gluten intolerance has risen from about 1 percent of adults to about 2 percent, according to Professor Markku Mäki, head of a research project in the Academy of Finland's Research Program on Nutrition, Food and Health. "We've already seen a similar trend emerge earlier on where allergies and certain autoimmune disorders are concerned. Screening has shown that gluten intolerance occurs in 1.5 per cent of Finnish children and 2.7 per cent of the elderly. The higher figure for older people is explained by the fact that the condition becomes more frequent with age," says Mäki. For the immune study, when researchers scanned the genetic maps of more than 9400 celiac patients, they found areas of immune system disturbance. Their evidence also indicated that genes connected with the inability to digest gluten were also connected with other autoimmune diseases such as type 1 diabetes and rheumatoid arthritis. Saavalainen and his team have succeeded in localizing risk genes in both individual patients and entire families, which adds weight to the notion that gluten intolerance is inherited. The researchers are hoping to use the genetic information to craft better screening tests for gluten intolerance, as up to 75% of people with gluten intolerance remain undiagnosed due to mild or atypical symptoms, and many with condition may unwittingly suffer damage to their intestinal villi. Professor Maki points out that many present first with iron deficient, or folic acid deficient, anemia. Source: Academy of Finland
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Gut. 2004 May;53(5):649-654 A multi-center Swedish study involving eight separate pediatric clinics looked at 116 children with newly diagnosed celiac disease. The group was randomized into two groups, and one group was given a standard gluten-free diet, while the other was given a standard gluten-free diet that also included oats. The study period was one year, small bowel biopsies were performed at the beginning and end of the study, and serum IgA antigliadin, antiendomysium, and antitissue transglutaminase antibodies were monitored at 0, 3, 6, and 12 months. The median intake of oats for the oat-eating group was 15g per day. By the end of the study all patients were in clinical remission for celiac disease. Neither group differed significantly from one another with regard to serology markers or small bowel mucosal architecture (including numbers of intraepithelial lymphocytes). Out of the original 116 children 93 finished the study, and significantly more younger patients withdrew from it than older patients. The researchers conclude: "This is the first randomized double blind study showing that the addition of moderate amounts of oats to a gluten-free diet does not prevent clinical or small bowel mucosal healing, or humoral immunological downregulation in coeliac children. This is in accordance with the findings of studies in adult coeliacs and indicates that oats, added to the otherwise gluten-free diet, can be accepted and tolerated by the majority of children with celiac disease."
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