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Celiac.com 04/21/2023 - If you're trying to lose weight, you might want to think about the amount of gluten in your diet. A study from 2015 found that wheat gluten intake can contribute to weight gain and fat accumulation, at least in mice. The study sheds some light on the relationship between gluten and weight gain by investigating the effects of gluten intake on weight gain, fat metabolism, and energy expenditure in mice. The Study For the study, researchers fed mice different diets for eight weeks. The diets included a control-standard diet, a standard diet with added wheat gluten, a high-fat diet, and a high-fat diet with added wheat gluten. Mice that had wheat gluten added to their diets gained more weight, and had more fat deposits, despite having the same energy intake as mice in the control group. The Findings Tests also found gluten in the blood, liver, and visceral adipose tissue, suggesting that it can reach organs beyond the intestinal tract. The study found that gluten intake reduced thermogenesis-related protein expression in subcutaneous and brown adipose tissues and lowered oxygen volume consumption, which points to reduced energy expenditure. Mice on a high-fat diet with added gluten also had lower levels of adiponectin, peroxisome proliferator-activated receptor (PPAR)-α and PPARγ, and hormone-sensitive lipase in cultures of isolated adipocytes. By contrast, in mice on a standard diet, added gluten intake increased interleukin-6 expression, and tended to increase tumor necrosis factor expression. This suggests that gluten may have different effects on fat metabolism and inflammation, depending on the diet. Conclusions: Wheat Gluten Intake Can Lead to Increased Weight Gain and Fat Deposits Overall, the study suggests that wheat gluten intake can lead to increased weight gain and fat deposits, along with reduced thermogenesis and energy expenditure, especially in mice on a high-fat diet. The study also highlights the potential systemic effects of gluten, which can reach organs beyond the intestine. While the study was conducted in mice, the findings suggest that gluten may play a role in human weight gain as well. While more research is needed to better assess any connection between these findings and gluten consumption in humans, the study does offer some interesting food for thought. Stay tune for more on this and related stories. Read more at Int J Obes (Lond)

Celiac.com 05/09/2022 - Data from gene expression, lipidomic and growth impairment indicate that celiac disease begins long before the body starts to have an immune response to gluten. The influence of gluten intake in the first years of life as a potential risk factor for celiac disease is currently debated among researchers. A team of researchers recently set out to estimate the risk of developing celiac disease based on the amount of gluten intake and the serum inflammatory profile in genetically predisposed infants. The research team included Auricchio Renata, Calabrese Ilaria, Galatola Martina, Cielo Donatella, Carbone Fortunata, Mancuso Marianna, Matarese Giuseppe, Troncone Riccardo, Auricchio Salvatore & Greco Luigi They are variously affiliated with the Department of Translational Medical Science, University Federico II, Via S. Pansini 5, 80131, Naples, Italy; the European Laboratory for Food Induced Diseases, University Federico II, Via S. Pansini 5, 80131, Naples, Italy; the Department of Clinical Medicine and Surgery, University Federico II, Naples, Italy; the Laboratory of Immunology, Institute for Experimental Endocrinology and Oncology, National Research Council (IEOS-CNR), Naples, Italy; the Neuroimmunology Unit, IRCCS Fondazione Santa Lucia, Rome, Italy; and the the Department of Molecular Medicine and Medical Biotechnology, University Federico II, Naples, Italy. The team evaluated an Italian cohort of children at risk for celiac disease, and enrolled twenty-seven children who developed celiac disease, along with fifty-six control subjects, matched by sex and age. The team also conducted a dietary interview at 9, 12, 18, 24 and 36 month intervals. They assessed serum levels of cytokines INFγ, IL1β, IL2, IL4, IL6, IL10 IL12p70, IL17, and TNFα, at four and thirty-six months. They found that infants who went on to develop celiac disease by six years of age showed increased serum cytokine levels at four months of age before gluten introduction. Elevated cytokines included INFγ, IL1β, IL2, IL6, IL10, IL12p70 and TNFα. Children who later developed celiac disease consumed substantially more gluten in their second year of life than the controls. For those children, gluten intake in the second year of life was strongly correlated with serum cytokines INFγ, IL2, IL4, IL12p70, IL17 at thirty-six months. The dietary pattern of infants who developed celiac disease was marked by high consumption of biscuits and fruit juices and low intake of milk products, legumes, vegetables and fruits, which may invite questions about pre-celiac gut microbiota health in these subjects. The researchers found that genetically predisposed infants who developed celiac disease showed a unique serum cytokine profile at 4 months before gluten consumption. In these children, gluten intake was strongly correlated with an inflammatory profile in serum cytokines at thirty-six months. This is one of the first studies to demonstrate such a clear relationship between cytokine profiles and infant gluten intake in advance of the development of celiac disease. Further study could help to develop preventative screening that Read more in Scientific Reports volume 12, Article number: 5396 (2022)

Celiac.com 07/02/2019 - Does gluten intake in childhood influence the development of celiac disease later in life? It's a basic question that hasn't had a good answer, until now. That's mainly due to an absence of good data. Looking to change that, a team of researchers recently set out to examine the connection between the amount of gluten intake in childhood and later celiac disease. The research team included Karl Mårild, MD, PhD; Fran Dong, MS; Nicolai A Lund-Blix, PhD; Jennifer Seifert, MPH; Anna E Barón, PhD; Kathleen C Waugh, MS; Iman Taki, BS; Ketil Størdal, MD, PhD; German Tapia, PhD; Lars C Stene, PhD; Randi K Johnson, MPH; Edwin Liu, MD; Marian J Rewers, MD, PhD; and Jill M Norris, MPH, PhD. For their prospective Diabetes Autoimmunity Study in the Young, the team included 1,875 at-risk children with annual estimates of daily gluten intake from age 1 year. From 1993 through January 2017, the team used repeated tissue transglutaminase (tTGA) screening to identify 161 children with celiac disease autoimmunity and persistent tTGA positivity. A total of eighty-five children from this group met the celiac disease criteria of biopsy-verified histopathology or persistently high tTGA levels. The team used Cox regression to model gluten intake in children between ages 1 and 2 years, along with joint modeling of total gluten consumption throughout childhood to estimate hazard ratios adjusted for confounders (aHR). The data showed that children with the highest third of gluten intake between the ages of 1 and 2 years had double the chance of developing celiac disease, and celiac disease autoimmunity, compared with those in the lowest third. The results showed that every daily gram increase in gluten intake in 1-year olds increases the risk of developing celiac disease autoimmunity by 5%. The child's human leukocyte antigen genotype had no influence on the association between gluten intake in 1-year-olds and later celiac disease or celiac disease autoimmunity. Rates of celiac disease rose in direct relation to increased overall gluten intake throughout childhood. This is one of the first studies to show that gluten intake in 1-year-olds can influence the development of celiac disease, and celiac disease autoimmunity, in children at risk for the disease. Obviously, further study is needed, but the main takeaway from this study is that parents of 1-year old children with known risk factors for celiac disease might want to consider reducing the gluten intake in those children. Read more at the American Journal of Gastroenterology The researchers in this study are variously affiliated with the Division of Epidemiology, Norwegian Institute of Public Health, Oslo, Norway; the Department of Pediatrics, Queen Silvia Children's Hospital, Gothenburg, Sweden; the Barbara Davis Center, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA; the Department of Pediatric and Adolescent Medicine, Oslo University Hospital, Oslo, Norway; the Department of Epidemiology, Colorado School of Public Health, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA; the Department of Biostatistics and Informatics, Colorado School of Public Health, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA; and the Department of Pediatrics, Østfold Hospital Trust, Grålum, Norway.

Celiac.com 05/31/2021 - For people without celiac disease, does eating gluten have an impact on brain health, specifically on cognitive function? A recent study of nearly 14,000 non-celiac women at midlife revealed no statistical evidence of any association of long- or short-term gluten intake with cognitive function. More and more people are eating gluten-free for perceived health benefits that may not be real. It's true that cognitive impairment, sometimes called "brain fog," is a common symptom reported by many people before they are diagnosed with celiac disease. In those cases a gluten-free diet generally results in improvement of the symptoms. However, data are lacking in individuals without celiac disease. A recent study set out to "examine whether gluten intake is associated with cognitive function in women without celiac disease." Their study included US women who participated in the longitudinal, population-based Nurses’ Health Study II and had not previously or subsequently been diagnosed with celiac disease. Subjects answered a questionnaire that was used to cumulatively average gluten intake cycles prior to cognitive assessment. They then took a battery of tests on psychomotor speed and attention score, learning and working memory score, and global cognition score. They research team found no connection between long-term gluten intake and cognitive scores in middle-aged women without celiac disease. Their results, "do not support recommendations to restrict dietary gluten to maintain cognitive function in the absence of celiac disease or established gluten sensitivity." But how useful was the study? What did they actually measure? What did they actually show us? The study actually reveals very little, if anything. Celiac.com does not recommend a gluten-free diet for people who do not have celiac disease or gluten sensitivity, but we also do not oppose it. A properly structured gluten-free diet can be every bit as nutritious and health-promoting as a diet that contains gluten. However, we also do not agree with studies with conclusions that seem to be designed to scare people off of a gluten-free diet, or to soft-pedal a diet that contains wheat. The study does not say that there is no cognitive benefit to giving up gluten for people who do not have celiac disease or gluten intolerance, or that those without celiac disease might also benefit from a gluten-free diet. The benefits or harm of a gluten-free diet in people who are not gluten-free remains poorly studied. Even in people with celiac disease, the implications of a long-term gluten-free diet have not been well-studied, and plenty of studies make unproven nutritional assumptions about those implications based on scant data. We believe that each person must choose their diet for themselves, and that many folks without celiac disease may choose to eat gluten-free for reasons that make sense to them. Some may do so because they perceive themselves to think more clearly when they do not eat wheat. The problem, from our perspective is that the study basically says: We looked at a bunch of women who eat wheat and gluten in various quantities. Their brains seem fine. Nothing to see here. People concerned about a potential connection between brain function and wheat consumption deserve more than a study that says, in effect, "hey, plenty of women eat gluten, and whether they eat a lot or a little, their brain test results seem fine." Telling us that eating wheat does not seem to cause brain impairment in non-celiacs is helpful. It is. But it's only part of the picture. As far as we can see, none of these subjects had brain function tests when eating gluten compared with tests when they were gluten-free. Nor did the test compare women who ate wheat to similar women on a gluten-free diet (but really, what was needed here was the former, a comparison of the same group of people, perhaps tested when eating different gluten levels, then re-tested after a prolonged gluten-free diet). For all of the seemingly grand implications of the study, it really doesn't tell us much about brain function in people who eat gluten. It doesn't tell us if there are any benefits brain wise to giving up gluten. Look, it could be that giving up gluten has a negative impact on non-celiacs, but that remains unproven. We really need a more comprehensive and focused study to help tell us what, if any, impact gluten has on the cognitive function of non-celiacs, along with what benefits, if any, they might have when giving up gluten. Read more in JAMA Netw Open. 2021;4(5):e2113020 The research team included Yiqing Wang, PhD; Benjamin Lebwohl, MD, MS; Raaj Mehta, MD; et al Yin Cao, ScD, MPH; Peter H. R. Green, MD; Francine Grodstein, ScD; Manol Jovani, MD; Paul Lochhead, MBChB, PhD; Olivia I. Okereke, MD, MS; Laura Sampson, MS, RD; Walter C. Willett, MD, DrPH; Qi Sun, MD, ScD, MMS; Andrew T. Chan, MD, MPH. They are variously affiliated with the Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Harvard Medical School, Boston; the Division of Gastroenterology, Massachusetts General Hospital, Harvard Medical School, Boston; the Celiac Disease Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York; the Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, New York; the Division of Public Health Sciences, Department of Surgery, Washington University in St Louis, St Louis, Missouri; the Division of Gastroenterology, Department of Medicine, Washington University in St Louis, St Louis, Missouri; the Rush Alzheimer’s Disease Center, Rush University Medical Center, Chicago, Illinois; the Department of Internal Medicine, Rush Medical College, Chicago, Illinois; the Division of Gastroenterology and Hepatology, Johns Hopkins Hospital, Baltimore, Maryland; the Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts; the Department of Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston; the Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts; and the Department of Nutrition, Harvard T. H. Chan School of Public Health, Boston, Massachusetts.

Celiac.com 06/04/2012 - Non-responsive celiac disease is very much what it sounds like: celiac disease where symptoms seem to resist treatment and continue even in the face of a gluten-free diet. A team of researchers recently set out to look for the most likely causes of persistent symptoms in celiac disease patients on a gluten-free diet. The research team included David H. Dewar, Suzanne C. Donnelly, Simon D. McLaughlin, Matthew W. Johnson, H. Julia Ellis, and Paul J. Ciclitira. They are variously affiliated with King's College London, Division of Diabetes and Nutritional Sciences, Department of Gastroenterology, and The Rayne Institute at St. Thomas' Hospital in London. Their goal for the study was to investigate all patients referred to our center with non-responsive celiac disease (NRCD), to establish a cause for their continued symptoms. For their study, the research team assessed all non-responsive celiac disease who were referred to their gastroenterology center over an 18-mo period. They then established the etiology of ongoing symptoms for these patients. For all patients, the team established a thorough case history and conducted a complete examination with routine blood work including tissue transglutaminase antibody measurement. Additionally, each patient was examined by a specialist gastroenterology dietician to try to spot any gaps in their diets, or any hidden sources of gluten consumption. When possible, the team conducted a follow-up small intestinal biopsy, and compared the results against the biopsies from the referring hospital. Patients with persistent symptoms received colonoscopy, lactulose hydrogen breath testing, pancreolauryl testing and a computed tomography scan of the abdomen. The team monitored patient progress over a minimum of two year period. Overall, the team looked at 112 patients with non-responsive celiac disease. They determined that twelve of those did not actually have celiac disease. Of the remaining 100 patients, nearly half, 45%, were not adequately following a strict gluten-free diet. Of these, 24 (53%) were found to be accidentally consuming gluten, while 21 (47%) admitted to not faithfully following a gluten-free diet. Microscopic colitis was found in 12% and small bowel bacterial overgrowth in 9%. Refractory celiac disease was found in 9%. Three of these were diagnosed with intestinal lymphoma. After 2 years, 78 patients remained well, eight had continuing symptoms, and four had died. In most cases of non-responsive celiac disease, the team found a reversible cause can be found in 90%. In the vast number of those cases, continued consumption of gluten was the main cause. The team is proposing the use of an algorithm for further investigation of the matter. Source: World J Gastroenterol. 2012 Mar 28;18(12):1348-56.

Celiac.com 04/18/2019 - Cases of type 1 diabetes have been on the rise in western countries, which suggests an environmental role in the development of the disease. Still, after decades of study, researchers have yet to nail down the factors driving the increase, and so they have no clear way to prevent new cases. A potential association that deserves closer scrutiny is one of environmental causes as a driver of diabetes, including dietary factors, such as gluten. At the moment, there is a great deal of focus on maternal and childhood dietary factors. To remedy the current impasse, researchers Maija E Miettinen and Suvi M Virtanen of the National Institute for Health and Welfare in Helsinki, Finland, cite the need for comprehensive prospective studies with carefully collected data to define and confirm associations. Only with such data can effective solutions be devised and tested. In a linked article, also in the BMJ, Antvorskov and colleagues investigated the association between maternal gluten intake during pregnancy and risk of type 1 diabetes in offspring. The authors analyzed data from the large Danish National Birth Cohort, covering about a third of all pregnancies in Denmark during the recruitment period of 1996-2002, in which more than 70,000 pregnant women reported their diet with a food frequency questionnaire. That analysis revealed that risk of type 1 diabetes in offspring increased proportionally with maternal gluten intake during pregnancy per 10 grams per day increase of gluten. Compared to women with the lowest gluten intake of under 7 grams per day, those with the highest gluten intake, who consumed 20 or more grams a day, had double the risk for type 1 diabetes development in their children. Basically, higher gluten intake during pregnancy meant higher diabetes risk for the children. However, that’s one study with good data. The authors stress the urgency to understand what is driving alarmingly fast-rising diabetes rates. People’s health, well-being, and lives are at stake. For that, further study is needed, and soon. Read more at BMJ 2018; 362

Celiac.com 11/26/2019 - High gluten intake during childhood may confer risk of celiac disease, and celiac autoimmunity. A team of researchers recently set out to determine if the amount of gluten consumed during the first 5 years of life is associated with celiac disease autoimmunity and celiac disease in genetically at-risk children. The research team included Carin Andrén Aronsson, PhD; Hye-Seung Lee, PhD; Elin M. Hård af Segerstad, MSc; Ulla Uusitalo, PhD; Jimin Yang, PhD; Sibylle Koletzko, MD, PhD; Edwin Liu, MD, PhD; Kalle Kurppa, MD, PhD; Polly J. Bingley, MD; Jorma Toppari, MD, PhD; Anette G. Ziegler, MD; Jin-Xiong She, PhD; William A. Hagopian, MD, PhD; Marian Rewers, MD, PhD; Beena Akolkar, PhD; Jeffrey P. Krischer, PhD; Suvi M. Virtanen, MD, PhD; Jill M. Norris, MPH, PhD; Daniel Agardh, MD, PhD; in association with the TEDDY Study Group. The participants in The Environmental Determinants of Diabetes in the Young (TEDDY), a prospective observational birth cohort study designed to identify environmental triggers of type 1 diabetes and celiac disease, were followed up at 6 clinical centers in Finland, Germany, Sweden, and the United States. The team enrolled 8,676 newborns carrying HLA antigen genotypes associated with type 1 diabetes and celiac disease between 2004 and 2010. They conducted annual screening for celiac disease with tissue transglutaminase autoantibodies in 6,757 children from the age of 2 years. Data on gluten intake were available in 6,605 children (98%) by September 30, 2017. Gluten intake was estimated from 3-day food records collected at ages 6, 9, and 12 months and biannually thereafter until the age of 5 years. The data show that higher gluten intake is associated with a statistically significant increase in celiac disease autoimmunity (absolute risk difference, 6.1%) and celiac disease (absolute risk difference, 7.2%) for every gram increase of gluten intake per day. The primary outcome was celiac disease autoimmunity, defined as positive tissue transglutaminase autoantibodies found in 2 consecutive serum samples. The secondary outcome was celiac disease confirmed by intestinal biopsy or persistently high tissue transglutaminase autoantibody levels. Every increase in gluten consumption was associated with higher risk of celiac disease. Absolute risk was 20.7% by age of 3 years if the reference amount of gluten was consumed, compared with an absolute risk of 27.9% when gluten intake was 1-gram per day higher than the reference amount, for an absolute risk difference of 6.1%. High gluten consumption during the first 5 years of life increases the risk of celiac disease autoimmunity and celiac disease in genetically predisposed children. The main takeaway here is that genetically predisposed children consuming just 1 gram per day over baseline can face increased risk levels celiac disease, or celiac disease autoimmunity. That's something to keep an eye on. Stay tuned for more on this and related stories. Read more, including more detailed results in JAMA. 2019;322(6):514-523. doi:10.1001/jama.2019.10329 The researchers are variously affiliated with the Department of Clinical Sciences, Lund University, Malmö, Sweden; the Health Informatics Institute, Department of Pediatrics, Morsani College of Medicine, University of South Florida, Tampa; the Dr von Hauner Children’s Hospital, Ludwig Maximilians University, Munich, Germany; University of Warmia and Mazuri, Olsztyn, Poland; the Digestive Health Institute, University of Colorado Denver, Children’s Hospital Colorado, Denver; the Tampere Centre for Child Health Research, University of Tampere, Tampere University Hospital, Tampere, Finland; the School of Clinical Sciences, University of Bristol, Bristol, England; the Research Centre for Integrative Physiology and Pharmacology, Institute of Biomedicine, University of Turku, Turku, Finland; the Department of Pediatrics, Turku University Hospital, Turku, Finland; the Institute of Diabetes Research, Helmholtz Zentrum München, Klinikum rechts der Isar, Technische Universität München, and Forschergruppe Diabetes eV, Neuherberg, Germany; the Center for Biotechnology and Genomic Medicine, Augusta University, Augusta, Georgia; the Pacific Northwest Diabetes Research Institute, Seattle, Washington; the Barbara Davis Center for Childhood Diabetes, University of Colorado School of Medicine, Aurora; the National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland; the National Institute for Health and Welfare, Department of Public Health Solutions, Helsinki, Finland; the Faculty of Social Sciences/Health Sciences, University of Tampere, Tampere, Finland; Research Center for Child Health, Tampere University, University Hospital, Science Center of Pirkanmaa Hospital District, Tampere, Finland; and the Colorado School of Public Health, Department of Epidemiology, University of Colorado, Aurora.

Celiac.com 09/30/2019 - We know from recent studies that high gluten intake in infancy can raise risk for celiac disease, and we know that the amount of gluten eaten by infants at 18 months heavily influences their risk of developing type 1 diabetes later in life. An earlier study conducted in Denmark suggested that a high maternal gluten consumption during pregnancy increased the risk of type 1 diabetes in the child. Until now, researchers have not looked at levels of gluten intake by both the mother during pregnancy and the child in early life, and how that influences risk of developing type 1 diabetes in childhood. Now, a new study shows that every 10 grams of extra gluten eaten at age 18 months is associated with a 46% increased risk of developing type 1 diabetes. The researchers recently conducted a Norwegian population-based nationwide study of 86,306 people to examine the association between the mother's intake of gluten during pregnancy, child's gluten intake at age 18 months, and the risk of type 1 diabetes in the child. The research team included Dr Nicolai Lund-Blix, and colleagues at Oslo University Hospital, and the Norwegian Institute of Public Health in Oslo, Norway. Their research was presented at the Annual Meeting of the European Association for the Study of Diabetes (EASD) in Barcelona, Spain from September 16-20. The outcome was clinical type 1 diabetes cases in the nationwide childhood diabetes registry. The team calculated increased risk using statistical modeling for maternal gluten intake during pregnancy and child's gluten intake at 18 months. The authors estimated grams per day of gluten intake based on a semi-quantitative food frequency questionnaire at week 22 of pregnancy, and from a questionnaire completed by the guardian when the child was 18 months old. Researchers are not calling upon expectant mothers to reduce gluten content in the infant diet at this point in time. According to the authors, "This study suggests that the child's gluten intake at 18 months of age, and not the maternal intake during pregnancy, could increase the risk of type 1 diabetes in the child." Read more at: Diabetes Times and at Celiac.com: High Childhood Gluten Intake Increases Risk of Celiac Disease and Celiac Autoimmunity

Celiac.com 08/26/2019 - Does the amount of gluten consumed during the first 5 years of life influence the risk of celiac disease autoimmunity and celiac disease in at-risk children? A new study says it does. There's been some previous study data to suggest that high gluten intake during childhood may increase risk of celiac disease. A team of researchers working for The Environmental Determinants of Diabetes in the Young (TEDDY) study group recently set out to investigate if gluten intake levels are associated with celiac disease autoimmunity and celiac disease in genetically at-risk children. The TEDDY group is a prospective observational birth cohort study designed to identify environmental triggers of type 1 diabetes and celiac disease. The research team included Carin Andrén Aronsson, PhD; Hye-Seung Lee, PhD; Elin M. Hård af Segerstad, MSc; et al Ulla Uusitalo, PhD; Jimin Yang, PhD; Sibylle Koletzko, MD, PhD; Edwin Liu, MD, PhD; Kalle Kurppa, MD, PhD; Polly J. Bingley, MD; Jorma Toppari, MD, PhD; Anette G. Ziegler, MD; Jin-Xiong She, PhD; William A. Hagopian, MD, PhD; Marian Rewers, MD, PhD; Beena Akolkar, PhD; Jeffrey P. Krischer, PhD; Suvi M. Virtanen, MD, PhD; Jill M. Norris, MPH, PhD; Daniel Agardh, MD, PhD; for the TEDDY Study Group For their multinational prospective birth study, the team looked at gluten consumption in 6,605 genetically predisposed children in 6 clinical centers in Finland, Germany, Sweden, and the United States. The team defined celiac disease autoimmunity as positive tissue transglutaminase autoantibodies found in 2 consecutive serum samples. The team defined celiac disease as cases confirmed by intestinal biopsy or persistently high tissue transglutaminase autoantibody levels. The team estimated gluten intake from 3-day food records collected at ages 6, 9, and 12 months and biannually thereafter until the age of 5 years. Their results showed that children with higher gluten intake levels had a significantly higher risk of celiac disease autoimmunity, with an absolute risk difference of 6.1%. Children with higher gluten intake levels also had a significantly higher risk of celiac disease, with an absolute risk difference of 7.2%, for every gram increase of gluten intake per day. This study shows that genetically predisposed children with higher gluten intake during the first 5 years of life face an increased risk of celiac disease autoimmunity and celiac disease. Read more at JAMA. 2019;322(6):514-523. doi:10.1001/jama.2019.10329 The researchers are variously affiliated with the Department of Clinical Sciences, Lund University, Malmö, Sweden; the Health Informatics Institute, Department of Pediatrics, Morsani College of Medicine, University of South Florida, Tampa; the Dr von Hauner Children’s Hospital, Ludwig Maximilians University, Munich, Germany; the University of Warmia and Mazuri, Olsztyn, Poland; the Digestive Health Institute, University of Colorado Denver, Children’s Hospital Colorado, Denver; the Tampere Centre for Child Health Research, University of Tampere, Tampere University Hospital, Tampere, Finland; the School of Clinical Sciences, University of Bristol, Bristol, England; Research Centre for Integrative Physiology and Pharmacology, Institute of Biomedicine, University of Turku, Turku, Finland; Department of Pediatrics, Turku University Hospital, Turku, Finland; the Institute of Diabetes Research, Helmholtz Zentrum München, Klinikum rechts der Isar, Technische Universität München, and Forschergruppe Diabetes eV, Neuherberg, Germany; the Center for Biotechnology and Genomic Medicine, Augusta University, Augusta, Georgia; Pacific Northwest Diabetes Research Institute, Seattle, Washington; the Barbara Davis Center for Childhood Diabetes, University of Colorado School of Medicine, Aurora; the National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland; the National Institute for Health and Welfare, Department of Public Health Solutions, Helsinki, Finland; the Faculty of Social Sciences/Health Sciences, University of Tampere, Tampere, Finland; the Research Center for Child Health, Tampere University, University Hospital, Science Center of Pirkanmaa Hospital District, Tampere, Finland; and the Colorado School of Public Health, Department of Epidemiology, University of Colorado, Aurora, Colorado.

Celiac.com 02/14/2017 - In 1999, Loren Cordain, the renowned professor of Exercise Physiology at Colorado State University who has since popularized the Paleodiet, published an extensive exploration of why our cultivation and consumption of cereal grains has been disastrous for the human race, resulting in many autoimmune, nutrient deficiency, and other modern diseases (1). Previously, in 1987, the famous physiologist, Jared Diamond characterized humanity's shift to agriculture as "The Worst Mistake in the History of the Human Race" (2). A year later, medical doctor and professor of Anthropology, S. Boyd Eaton and colleagues suggested a mismatch between the human genome and our current agricultural diet/lifestyle (3). And more than a decade prior to that, gastroenterologist, Walter L. Voegtlin, M.D., self published a book apparently asserting, based on his treatments and observations of patients, that dietary avoidance of cereal grains and sugars, offset by increased consumption of meats and animal fats, is an effective treatment regimen for a variety of intestinal ailments including Crohn's disease, colitis, irritable bowel syndrome, and indigestion (4). Each of these perspectives was informed by a different but solidly scientific approach to human health. The academic field of each of these authors varied from Exercise Physiology to Physiology, to Gastroenterology, to Anthropology. Yet each of these specialist researchers arrived at the very similar conclusion that cereal grains are not healthful foods for humans. Their strident declarations to that effect leave little room for doubt. Dr. Cordain acknowledges that the roots of some of his thinking lie with Dr. Eaton and his colleagues. Nonetheless, there is a convergence here, of ideas and insights drawn from separate bodies of data and investigative approaches. While there is some overlap between these scientific disciplines, they all lead to a clear indictment of cereal grains as little more than a starvation food for humans. These scientists point to myriad signs of illness that arise more commonly when populations make the transition to eating diets dominated by grains, especially when the grains are refined and when they are combined with sugar. One critic of this paradigm is the evolutionary biologist, Dr. Marlene Zuk of the University of California at Riverside. According to Alison George at New Scientist, Zuk asserts that the 10,000 years that humans have been cultivating and consuming cereal grains is an adequate time period for humans to evolve an adaptation to these foods (5). But surely this is a Eurocentric view. Simply because some Europeans have been cultivating and consuming cereal grains for ten or more thousands of years does not mean that the entire world's population, or even all Europeans, would or could have adapted to consuming these foods. Let's look back to see what we currently know about our human roots and how those early humans spread all over the world. A group thought to number about 200 humans left Africa sometime between 85,000 and 70,000 years ago, during a glacial maximum that lowered worldwide sea levels by about 300 feet below current levels. The enormous glaciers of the time so depleted the oceanic barriers we see today, that these bodies of water were made navigable even with very primitive flotation devices. The progeny of this relatively small group of early modern people multiplied and went on to parent almost all of today's non-African people of the world with some 1% to 4% of today's human, non-African genes having been derived from the Neanderthal branch of the hominid tree (6). This predominantly early modern human group's progeny would quickly find its way to Australia, the South Pacific, across Asia, to China, east to the Americas and west across India, finally arriving in Europe, where they would supplant the long-time Neanderthal residents who had survived some of Europe's harsh and inhospitable glaciations but apparently could not survive having our forebears as neighbors. While specific paths and dates for exiting Africa, and worldwide patterns and timing of human distribution remain controversial, most experts now accept that indigenous Australians had arrived there at least 60,000 years ago (6). A similarly recent finding places people in the Americas by at least 55,000 years ago, long prior to the date at which the Bering Land Bridge was thought to be available for human movement from Siberia into the Americas (8). This newer, admittedly controversial date raises the likely possibility that people arrived in the Americas, from Asia, by boats or rafts on which they followed the shoreline east to what is now Alaska, then south of the glaciated wastelands of much of what is now Canada. (Or perhaps they arrived by some other means that we have not yet imagined.) But only a small portion of these early Americans would eat wheat, rye, oats, or barley before the last 200 years or so, especially those living on the Great American Plains, or in the frigid north, the dense jungles or places that were otherwise isolated from the encroaching wave of "immigrants" from Europe and beyond. And none of those aboriginal peoples of the Americas were eating these grains prior to 1492. The epidemics of autoimmunity and obesity that may be seen among indigenous Americans are clear reflections of their recent shift to the gastronomic wonders of foods derived from these European grains. Further, even among Europeans, grain cultivation and consumption had not uniformly spread across most of Europe until, at most, less than half of the 10,000 years that Zuk says would be sufficient for human adaptation. In Britain, for instance, grain farming was only getting under way about 4,000 years ago, and availability of grains varied according to local geographies and economies. Also, in parts of Scandanavia, wheat bread was a rare treat until after World War II. Some Europeans are thought to have been cultivating grains for even longer than the 10,000 years ago suggested by Cordain, but the evidence is contradictory and accompanied by a range of expert opinions. Further, the health consequences of this nutritional path are consistently seen in the skeletal remains of those early farmers, many of which can now be seen reflected among indigenous peoples of the Americas, as they assimilate our grain and sugar dominated diet. Adaptation to eating grains is not a gentle, joyful process. Early farmers may have produced many more children than their hunting and gathering neighbors, but their lives were shorter, their bodies were less robust, with substantial reductions in stature, and they experienced widespread infectious diseases and ailments driven by nutritional deficiencies. By the time grains became a cash crop for many European farmers, cereals were disproportionately consumed by affluent urbanites. Those who were large consumers of cereal grains did not include all Europeans, even where yields were prodigious. In more remote, northerly, or mountainous areas, cereal grains, or foods made from them, were likely a rare treat rather than a daily staple. Jared Diamond points out, that in addition to "..... malnutrition, starvation, and epidemic diseases, farming helped bring another curse upon humanity: deep class divisions." He goes on to argue that only with farming and the storage and accumulation of food can Kings "and other social parasites grow fat on food seized from others". He also presents evidence that farming led to inequality between men and women. Conversely, contemporary hunter-gatherers have repeatedly been shown to be quite egalitarian, both regarding gender and political leadership (9). Roger Lewin is another critic of the health impact of European grain cultivation on humans. He points out that even in the very heart of the Fertile Crescent, where agriculture got its start, there was not a uniform adoption of farming. One agricultural center at Abu Hureyra, experienced two cycles of abandonment, one at 8,100 B.C.E., lasting about 500 years, and another at 5,000 B.C.E. These periods when agriculture at this locale was abandoned are "thought to be related to climatic change that became less and less conducive to agriculture" (10). Lewin also harkens to Mark Nathan Cohen's collation of "physical anthropological data that appear to show increasingly poor nutritional status coincident with the beginnings of agriculture.... " (10) suggesting, again, that grains were a starvation food. Eaton et al also approach grain cultivation from an anthropological perspective, suggesting that increased dietary protein and fats from animal/meat sources likely gave rise to increased stature of earlier humans, along with providing the necessary fatty acids for building larger brains, and allowing smaller gut sizes over the past 2.5 million years. It seems reasonable to assume that if it took our pre-historic ancestors that long to adapt to eating meats and animal fats, the very irregular adaptation period of between less than one hundred years and about 10,000 years that various world populations have been cultivating and consuming wheat, rye, barley and oats would be insufficient to allow full adaptation to eating these immune sensitizing cereal grains. Dr. Zuk's perspective might be tempered a bit if she considers that Europeans and their descendants do not comprise the entirety of the world's populations. There are several Asian populations that are not insignificant when compared with European populations and their progeny, including the residents of China, India, Pakistan, and South-East Asia. Even among those of us who appear quite European, there may be a mixture of genes derived from peoples of any of the other five populated continents. The approximately 10,000 year maximum period since humans began to cultivate cereal grains would have little adaptive impact on populations that have only been exposed to these grains for a period of somewhere between four or five centuries and seven or eight decades, as is the case among the indigenous people of the Americas, Australia, New Zealand, and much of Asia (6). Even if all humans had been cultivating and consuming cereal grains for the 10,000 years since this practice was first begun in the Middle East, the high frequency of intestinal, autoimmune, and other diseases that can be mitigated by a gluten free diet, even among descendants of Europeans, leaves little room to doubt that Dr. Zuk's projected adaptation simply has not occurred. The current prevalence of celiac disease and non-celiac gluten sensitivity identifies, at a bare minimum, between 7% and 12% of the American population that has not adapted to cereal grain consumption. While a few research projects suggest that molecular mimicry and the opioids from cereal grains contribute to autoimmunity, obesity, type 2 diabetes and cardio-vascular disease, current research does not provide any clear sense of how many cases or to what degree these health conditions are driven by gluten consumption. We know that foods derived from cereal grains are often laced with refined sugar, but the insulin stimulating properties of gluten alone are such that their role in these conditions cannot, reasonably, be denied. I feel vindicated by these many experts who decry the folly in humanity's embrace of the European grains. I wonder how long it will take for this information to filter into, and be acknowledged by, those who claim that science has led them to advocate cereal grain consumption for everyone without celiac disease and, more recently, non celiac gluten sensitivity? Sources: Cordain, Loren. Simopoulos AP (ed): Evolutionary Aspects of Nutrition and Health. Diet, Exercise, Genetics and Chronic Disease. World Rev Nutr Diet. Basel, Karger, 1999, vol 84, pp 19–73 http://thepaleodiet.com/wp-content/uploads/2012/08/Cerealgrainhumanitydoublesword.pdf Jared Diamond, "The Worst Mistake in the History of the Human Race," Discover Magazine, May 1987, pp. 64-66. http://www.ditext.com/diamond/mistake.html Eaton SB, Konner M, Shostak M. Stone agers in the fast lane: chronic degenerative diseases in evolutionary perspective. Am J Med. 1988 Apr;84(4):739-49. Voegtlin, Walter L. (1975). The stone age diet: Based on in-depth studies of human ecology and the diet of man. Vantage Press. ISBN 0-533-01314-3 George, A. " The Paleo Diet Is a Paleo Fantasy" New Scientist. April 7, 2013. http://www.slate.com/articles/health_and_science/new_scientist/2013/04/marlene_zuk_s_paleofantasy_book_diets_and_exercise_based_on_ancient_humans.single.html Oppenheimer, Stephen. The Real Eve: Modern Man's Journey Out of Africa. Basic Books, NY, NY. 2004 Fagan, Brian. Cro-Magnon: How the Ice Age Gave Birth to the First Modern Humans. Bloomsbury Press, New York. 2011 http://www.utep.edu/leb/Pleistnm/sites/pendejocave.htm Brody, Hugh. The Other Side of Eden: Hunters, Farmers and the Shaping of the World. Douglas 7 McIntyre Ltd., Vancouver, B.C., Canada. 2000 Lewin, Roger. A Revolution of Ideas in Agricultural Origins. Science. vol 240, May 20, 1988