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    Jefferson Adams
    Celiac.com 11/05/2009 - It's well known that people with celiac disease often show reduced bone mineral density, and that metabolic bone disease is a significant and common complication of celiac disease. A new article in the journal Nutrition Reviews reinforces the benefits of a gluten-free diet in reducing bone problems in children with celiac disease.
    This is important information, because, even though celiac disease can be diagnosed at any age, it most often discovered in children between 9 and 24 months of age.
    By better understanding the benefits of a gluten-free diet in preventing bone disease, parents can make smarter choices that will help build healthy bones in their celiac kids.
    Ideally, this will help the kids to avoid the reduced bone mineral density that can lead to the inability to develop optimal bone mass as children and to the loss of bone as adults, both of which increase the risk of osteoporosis, and contribute to an additional risk of fracture.
    The good news is that the evidence suggests that a gluten-free diet in celiac children paves the way for a rapid increase in bone mineral density, followed by a complete recovery of bone mineralization. Children may attain normal peak bone mass if the diagnosis is made and treatment is given before puberty, thereby preventing osteoporosis in later life.
    Also, regular calcium and vitamin D supplements seem to increase the bone mineral density of children and adolescents with celiac disease.
    In adults, the picture is less rosy. In adults, a gluten-free diet improves, although rarely normalizes, bone mineral density.
    "Our findings reinforce the importance of a strict gluten-free diet, which remains the only scientific proven treatment for celiac disease to date," the authors conclude. "Early diagnosis and therapy are critical in preventing celiac disease complications, like reduced bone mineral density."
    Source:
    Nutrition Reviews


    Jefferson Adams
    Celiac.com 04/09/2012 - Many people with celiac disease suffer from fatigue and may limit theirsocial activities, both of which can lead to a decrease in physicalactivity, and potentially lower bone mass.
    A team of medical researchers recently set out to study the effects of exercise and gluten-free diet on bone-mass in women with celiac disease.
    The research team included Valentina Passanantia, Antonella Santonicolaa, Cristina Buccia, Paolo Andreozzia, Antonella Ranaudoa, Daniel V. Di Giacomoc, and Carolina Ciacci. They are affiliated with the Department of Clinical and Experimental Medicine at the University Federico II of Naples, Italy, the Gastrointestinal Unit of Salerno University Medical School in Salerno, Italy, and the Celiac Disease Center of the Department of Medicine at Columbia University in New York.
    For their study, the team recruited two groups of women. In both groups, they examined physical activity, fatigue and bone mineral density in women with celiac disease, both at diagnosis and while following a gluten-free diet.
    In the first group of 48 women, the team measured bone mineral density at diagnosis and after 2 years of a gluten-free diet. In the second group, this one with 47 women, researchers measured bone mineral density at diagnosis, and after 5 years of a gluten-free diet.
    The researchers questioned and assessed both groups regarding physical activity and ranked them on a visual analogue scale regarding their perception of fatigue at diagnosis and follow-up. The team also gathered data on smoking habits, alcohol use, gastrointestinal symptoms, drug therapy and body mass index.
    Across the board, for all factors, the two groups showed similar results. At follow-up, the mean body mass index and physical activity questionnaire scores were similar to baseline. Both groups showed increased bone density and unchanged scores for physical activity and visual analogue scale.
    For both groups, bone density improved significantly after two years on a gluten-free diet. In both groups, physical activity was often low and played only a small role in changes to bone mineral density.
    So, exercise does not seem to help increase bone mineral density in any significant way, and following a gluten-free diet is sufficient to re-establish bone mineral density to healthy levels.
    Source:

    2011 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd.  doi:10.1016/j.dld.2011.12.012

    Jefferson Adams
    Celiac.com 09/02/2013 - Most people with celiac disease are now diagnosed as adults, and many suffer from impaired bone mineralization.
    Researchers A.J Lucendo and A. García-Manzanares recently conducted a review of bone mineral density in patients with adult celiac disease.
    Their goal was to provide an updated discussion on the relationship between low bone mineral density (BMD), osteopenia and osteoporosis, and celiac disease.
    They conducted a search of relevant articles published in PubMed over the last 15 years. They also reviewed all sources cited in the article results to identify potential sources of information.
    They found that up to 75% of celiac patients can suffer from low BMD, which can occur at any age, independently of positive serological markers and presence of digestive symptoms.
    Patients with osteoporotic issues have significantly higher rates of celiac disease.
    The team proffers two theories which may explain the origins of low BMD in celiac patients. The first says that low BMD may result from malabsorption of micronutrients (including calcium and vitamin D) determined by villous atrophy, which has has been related to secondary hyperparathyroidism and incapacity to achieve the potential bone mass peak;
    The second theory says that low BMD may result from chronic inflammation, which was also related with RANKL secretion, osteoclasts activation and increased bone resorption.
    Whatever the cause of the low BMD, people with celiac disease have more than 40% higher rates of bone fractures compared to matched non-celiac individuals.
    Treatment of low BMD in celiac disease includes gluten-free diet, supplementation of calcium and vitamin D, and the use of biphosphonates, the effects of which on celiac disease have not been specifically studied.
    Up to 75% of people with celiac disease, and 40% of those diagnosed in adulthood show low BMD, along with increased risk of bone fractures.
    This information shows the potential importance of bone density scans for adults with celiac disease.
    Source:
     Rev Esp Enferm Dig. 2013 May;105(3):154-162.

    Jefferson Adams
    Celiac.com 12/15/2014 - Non-celiac gluten sensitivity (NCGS), aka `wheat sensitivity’ (NCWS), is currently included in the spectrum of gluten-related disorders. 
    Many people with celiac disease suffer from low bone mass density, but there has been no good data on low bone mass density in people with NCWS.
    A team of researchers recently set out to determine rates of low bone mass density in NCWS patients and to search for correlations with other clinical characteristics. The researchers included Antonio Carroccio, Maurizio Soresi, Alberto D'Alcamo, Carmelo Sciumè, Giuseppe Iacono, Girolamo Geraci, Ignazio Brusca, Aurelio Seidita, Floriana Adragna, Miriam Carta and Pasquale Mansueto.
    For their prospective observation study, the team assessed 75 NCWS patients (63 women; median age 36 years) with irritable bowel syndrome (IBS)-like symptoms, along with control groups of 65 patients with IBS and 50 with celiac disease. The team recruited patients from two Internal Medicine Departments. The diagnoses of NCWS were established using an elimination diet and double-blind placebo controlled wheat challenge.
    The team determined bone mass density in all subjects using Dual Energy X-Ray Absorptiometry (DXA), in addition to assessing all subjects for duodenal histology, HLA DQ typing, body mass index, and daily calcium intake. The double-blind placebo controlled wheat challenge revealed that 30 of the 75 NCWS patients suffered sensitivity to multiple foods. Osteopenia and osteoporosis frequency increased from IBS to NCWS and to celiac disease (P <0.0001).
    Thirty-five of the patients with NCWS (46.6%) showed osteopenia or osteoporosis. Low bone mass density was related to low body mass index and multiple food sensitivity. Levels of daily dietary calcium intake were significantly lower in NCWS patients than in control subjects with IBS.
    The study showed that patients with NCWS suffered from higher rates of bone mass loss; which correlated with low body mass index, and was more frequent in NCWS patients who showed sensitivity to multiple foods.
    The team also found that patients with NCWS generally had a low daily intake of dietary calcium.
    Source: 
    BMC Medicine 2014, 12:230. doi:10.1186/s12916-014-0230-2

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/19/2018 - Could baking soda help reduce the inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease? Scientists at the Medical College of Georgia at Augusta University say that a daily dose of baking soda may in fact help reduce inflammation and damage caused by autoimmune diseases like rheumatoid arthritis, and celiac disease.
    Those scientists recently gathered some of the first evidence to show that cheap, over-the-counter antacids can prompt the spleen to promote an anti-inflammatory environment that could be helpful in combating inflammatory disease.
    A type of cell called mesothelial cells line our body cavities, like the digestive tract. They have little fingers, called microvilli, that sense the environment, and warn the organs they cover that there is an invader and an immune response is needed.
    The team’s data shows that when rats or healthy people drink a solution of baking soda, the stomach makes more acid, which causes mesothelial cells on the outside of the spleen to tell the spleen to go easy on the immune response.  "It's most likely a hamburger not a bacterial infection," is basically the message, says Dr. Paul O'Connor, renal physiologist in the MCG Department of Physiology at Augusta University and the study's corresponding author.
    That message, which is transmitted with help from a chemical messenger called acetylcholine, seems to encourage the gut to shift against inflammation, say the scientists.
    In patients who drank water with baking soda for two weeks, immune cells called macrophages, shifted from primarily those that promote inflammation, called M1, to those that reduce it, called M2. "The shift from inflammatory to an anti-inflammatory profile is happening everywhere," O'Connor says. "We saw it in the kidneys, we saw it in the spleen, now we see it in the peripheral blood."
    O'Connor hopes drinking baking soda can one day produce similar results for people with autoimmune disease. "You are not really turning anything off or on, you are just pushing it toward one side by giving an anti-inflammatory stimulus," he says, in this case, away from harmful inflammation. "It's potentially a really safe way to treat inflammatory disease."
    The research was funded by the National Institutes of Health.
    Read more at: Sciencedaily.com

    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