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Found 10 results

  1. Celiac.com 04/24/2019 - We now live in a society where much of our population, including our children, are overfed but undernourished. Dietary supplements can play an important role in closing the nutritional gap. For a child’s body to develop normally, essential nutrients need to be consumed each and every day. Children need vitamins and minerals for their normal growth and for the nourishment of their organs and bones. This can be quite a task, especially since many young children are picky about the foods they eat. A good way to be sure children get the nutrients required to produce a healthy body and brain is to give them a daily multivitamin and mineral. Multivitamin supplements in the form of liquids or drops, are often the best option for children who are sometimes unable to swallow a tablet. And there are other advantages: Liquid supplements allow a multivitamin/mineral to be mixed with food or a child’s favorite beverage and make it easier to take, regardless of the child’s age Often liquids contain higher doses of active ingredients and lower levels of sugar Liquid formulas allow for greater bioavailability and absorption of the nutrients Unfortunately, most multi liquid formulas include only the vitamins, not the minerals, needed for healthy development at a young age. But you can count on ChildLife Liquid Multi Vitamin and Mineral to supply all the primary minerals as well. In addition, ChildlLife Multivitamin & Mineral contains Calcium, Iodine, Magnesium, Selenium, Manganese, Potassium, Chromium & Potassium as well as Choline and Inositol for healthy brain neurotransmitter support. And like all our products, ChildLife Multivitamin & Mineral is gluten free, casein free, alcohol free with no artificial colorings, flavorings or sweeteners. It is a complete multi formula you can be comfortable and confident giving your child. For more info visit: Visit Our Site.
  2. Celiac.com 11/23/2015 - A new study looks at the impacts of introducing gluten to infants and the development of celiac disease. A research team recently set out to assess the evidence regarding the effect of time of gluten introduction and breastfeeding on the risk of developing celiac disease. The research team included MI Pinto-Sánchez, EF Verdu, E Liu, P Bercik, PH Green, JA Murray, S Guandalini, and P Moayyedi. Their team conducted a comprehensive review of studies from the following electronic databases: Cochrane Central Register of Controlled Trials (CENTRAL); MEDLINE (Ovid); EMBASE (Ovid); and System for Information on Grey Literature in Europe (SIGLE). Two independent authors collected the data. Their analysis included randomized controlled trials and observational studies that assessed proper timing for introducing gluten to the infant diet, appropriate quantity of gluten consumption at weaning, and the effect of breastfeeding on celiac disease risk. Out of a total of 1982 studies they identified, 15 matched their criteria for data extraction. The team performed a meta-analysis on 2 randomized controlled trials, 10 cohort studies, and 1 case-control study. That analysis showed a 25% increase in celiac disease risk with gluten-introduction after 6 months, compared to the recommended 4 to 6 months (risk ratio [RR], 1.25; 95% CI, 1.08-1.45). There was no difference between breastfeeding vs no breastfeeding on celiac disease risk (OR, 0.55; 95% CI, 0.28-1.10), with substantial heterogeneity (I2 = 92%) among studies. There is currently no evidence to support that early introduction of gluten to the infant diet increases the risk of celiac disease. However, introduction of gluten after six months of age might promote an increased risk of celiac disease. More studies are needed that control for potential confounders and that evaluate environmental factors in low-risk families. Source: J Pediatr. 2015 Oct 20. pii: S0022-3476(15)01045-8. doi: 10.1016/j.jpeds.2015.09.032.
  3. Celiac.com 08/03/2017 - Some evidence indicates that feeding in the first months of life might have an impact on the risk of later celiac disease. Numerous patients with celiac disease or type 1 diabetes show high levels of antibodies against cow milk proteins. For infants with genetic susceptibility for type 1 diabetes, avoiding of cow’s milk-based formula can lower the levels of diabetes-associated autoantibodies. Could the same be true for celiac disease? To find out if weaning to an extensively hydrolyzed formula lowered the risk of celiac disease of celiac disease autoimmunity, a research team performed a randomized controlled trial. The research team included Mila Hyytinen, Erkki Savilahti, Suvi M. Virtanen, Taina Härkönen, Jorma Ilonen, Kristiina Luopajärvi, Raivo Uibo, Outi Vaarala, Hans K. Åkerblom, and Mikael Knip for the Finnish TRIGR Pilot Study Group. For their double-blind controlled trial, they enrolled 230 infants with HLA-defined predisposition to type 1 diabetes and at least 1 family member with type 1 diabetes. The infants were randomly assigned to groups, with 113 fed a casein hydrolysate formula, and 117 receiving a conventional formula whenever breastmilk was not available during the first 6–8 months of life. The team collected serum samples over an average of 10 years, and screened for antibodies to tissue transglutaminase (anti-TG2A) using a radiobinding assay, to endomysium using an immunofluorescence assay, and antibodies to a deamidated gliadine peptide using an immunofluorometry assay. In patients with anti-TG2A levels over 20 relative units, the team conducted duodenal biopsy. They measured cow’s milk antibodies during the first 2 years of life. Their results showed that about 13% of the 189 participants they analyzed for antiTG2A 25 tested positive. Just ten of the 230 study participants were diagnosed with celiac disease. The team found no significant differences in total cases of anti-TG2A positivity (hazard ratio, 1.14; 95 % CI, 0.51–2.54) or celiac disease (hazard ratio, 4.13; 95% CI, 0.81–21.02) between the casein hydrolysate and cow's milk group. Interestingly, children who developed celiac disease did show higher levels of cow's milk antibodies before the appearance of anti-TG2A or celiac disease. This study of infants with genetic risk factors for celiac disease showed evidence that weaning to a diet of extensively hydrolyzed formula compared with cow’s milk-based formula would lower the risk for celiac disease later in life. Elevated levels of cow's milk antibody before anti-TG2A and celiac disease indicates that many people may experience increased intestinal permeability before they develop celiac disease. Source: GASTROENTEROLOGY
  4. Celiac.com 12/14/2015 - Recently, several studies have set out to determine how intake of gluten during infancy influences later risk of celiac disease. One such study, conducted in Sweden, investigated whether gluten intake before 2 years of age increases the risk for celiac disease in genetically susceptible children. The research team included Carin Andrén Aronsson, Hye-Seung Lee, Sibylle Koletzko, Ulla Uusitalo, Jimin Yang, Suvi M. Virtanen, Edwin Liu, Åke Lernmark, Jill M. Norris, and Daniel Agardh. They are variously affiliated with the Digestive Health Institute, Children's Hospital Colorado, University of Colorado Denver, Aurora, Colorado, the Department of Epidemiology, Colorado School of Public Campus, University of Colorado Denver in Aurora, Colorado, the Department of Clinical Sciences at Lund University and Skåne University Hospital in Malmö, Sweden, with Dr. von Hauner Children's Hospital, Ludwig Maximilians University in Munich, Germany, the National Institute for Health and Welfare, Nutrition Unit in Helsinki, Finland, the School of Health Sciences, University of Tampere, Finland, the Research Center for Child Health, Tampere University and University Hospital, Science Center of Pirkanmaa Hospital District, University of Tampere, Finland, and with the Health Informatics Institute, Morsani College of Medicine, University of South Florida, Tampa, Florida. The research team conducted a case-control study of 436 pairs of children, generated from a Swedish database of 2525 children with genetic susceptibility to celiac disease, matched for sex, birth year, and HLA genotype from September 2004 to February 2010. The children were screened each year for celiac disease using an assay for tissue transglutaminase autoantibodies (tTGAs). To confirm celiac disease, the team conducted intestinal biopsy on children who tested positive for tTGA. The team also calculated gluten intake from 3-day food records collected when the children were 9, 12, 18, and 24 months old. The results showed that the duration of breastfeeding, lasting 32 weeks, on average, and average age at first introduction to gluten of 22 weeks was basically the same for the target group and the tTGA-negative control group. At the visit prior to tTGA seroconversion, the target group reported a larger intake of gluten, 4.9 grams a day, compared to 3.9 grams a day for controls (odds ratio [OR], 1.28; 95% confidence interval [CI], 1.13–1.46; P = .0002). More of the target group consumed amounts of gluten in the upper third tertile (ie, >5.0 g/d) before they tested positive for tTGA seroconversion compared to control subehects (OR, 2.65; 95% CI, 1.70–4.13; P < .0001). Interestingly, this increased risk was similar for children homozygous for DR3-DQ2 (OR, 3.19; 95% CI, 1.61–6.30; P = .001), heterozygous for DR3-DQ2 (OR, 2.24; 95% CI, 1.08≥4.62; P = .030), and for children not carrying DR3-DQ2 (OR, 2.43; 95% CI, 0.90–6.54; P = .079). Intake of gluten before 2 years of age at least doubles the risk of celiac disease in genetically susceptible children. This association was uniform among HLA-DR3-DQ2 haplotypes. These findings may be taken into account for future infant feeding recommendations. So, basically, if kids have a genetic susceptibility to celiac disease, regardless of their genetic haplotypes, then parents should wait until after 2 yearss of age to introduce gluten into the child's diet. This study, taken together with another recent study that shows that introduction of gluten after six months of age might promote an increased risk of celiac disease, might help provide some guidance for parents looking to introduce gluten to their children's diets. The earlier study, the children did not have a genetic predisposition to celiac disease. That means that, according to research, the best window for optimal gluten introduction is after two years, especially for children with genetic predisposition, and before six months, regardless of genetic status. SOURCE: Clinical Gastroenterology and Hepatology, October 07, 2015. DOI: http://dx.doi.org/10.1016/j.cgh.2015.09.030
  5. Celiac.com 06/24/2010 - I have previously suggested vitamin D deficiency and the makeup of gut bacteria during pregnancy and infancy, while breast-feeding and prior to and during the introduction of gluten, may be factors leading to the onset of celiac disease. The question of how much vitamin D should be given to infants remains open. The current recommendation, by the American Academy of Pediatrics, is that children of all ages should receive 400 IU of vitamin D each day. A recent limited study of 74 diabetic children, however, suggests that this recommended dose may still be insufficient for most children. The children were given daily vitamin D doses ranging from 400 IU to 2000 IU over a 12-month period and their vitamin D status was monitored. Most of the children remained vitamin D insufficient or deficient at the end of the study. The study concluded that all children younger than 5 years should probably receive at least 1000 IU of vitamin D daily. Further study is needed, especially with specific emphasis on the onset and prevention of celiac disease during infancy. Source: Medscape Medical News - June 22, 2010: More Evidence That Current Pediatric Vitamin D Recommendation is Often Inadequate http://www.medscape.com/viewarticle/723993
  6. Celiac.com 11/03/2014 - Some data have suggested that introducing gluten to infants at 4 to 6 months of age can help to lower the risk of celiac disease. To get a clearer picture of any potential benefits of introducing gluten within this time period, a team of researchers performed a multi-center, randomized, double-blind, placebo-controlled dietary-intervention study. The research team included Sabine L. Vriezinga, M.D., Renata Auricchio, M.D., Enzo Bravi, M.S., Gemma Castillejo, M.D., Anna Chmielewska, M.D., Ph.D., Paula Crespo Escobar, B.Sc., Sanja KolaÄek, M.D., Ph.D., Sibylle Koletzko, M.D., Ph.D., Ilma R. Korponay-Szabo, M.D., Ph.D., Eckart Mummert, Ph.D., Isabel Polanco, M.D., Ph.D., Hein Putter, Ph.D., Carmen Ribes-Koninckx, M.D., Ph.D., Raanan Shamir, M.D., Ph.D., Hania Szajewska, M.D., Ph.D., Katharina Werkstetter, M.Sc., M.P.H., Luigi Greco, M.D., Ph.D., Judit Gyimesi, M.D., Corina Hartman, M.D., Caroline Hogen Esch, M.D., Ph.D., Erica Hopman, R.D., Ph.D., Anneli Ivarsson, M.D., Ph.D., Tunde Koltai, Ir., Frits Koning, Ph.D., Eva Martinez-Ojinaga, M.D., Chantal te Marvelde, B.Sc., Ana Pavic, M.D., Jihane Romanos, Ph.D., Els Stoopman, Vincenzo Villanacci, M.D., Ph.D., Cisca Wijmenga, Ph.D., Ricardo Troncone, M.D., Ph.D., and M. Luisa Mearin, M.D., Ph.D. For their study, the team recruited 944 children who were positive for HLA-DQ2 or HLA-DQ8, with at least one first-degree relative with celiac disease. From 16 to 24 weeks of age, 475 participants received 100 mg of immunologically active gluten daily, and 469 received placebo. The team then made periodic measurements of anti–transglutaminase type 2 and antigliadin antibodies. The overall goal was to determine the frequency of biopsy-confirmed celiac disease at 3 years of age. The team confirmed celiac disease through biopsy in 77 children, while three more received a celiac diagnosis of based on the 2012 European Society for Pediatric Gastroenterology, Hepatology, and Nutrition diagnostic criteria for a total of 80 celiac children. The cumulative incidence of celiac disease among patients 3 years of age was 5.2% (95% confidence interval [CI], 3.6 to 6.8), with similar rates in the gluten group and the placebo group (5.9% [95% CI, 3.7 to 8.1] and 4.5% [95% CI, 2.5 to 6.5], respectively; hazard ratio in the gluten group, 1.23; 95% CI, 0.79 to 1.91). Both groups also showed similar rates of elevated levels of anti–transglutaminase type 2 and antigliadin antibodies (7.0% [95% CI, 4.7 to 9.4] in the gluten group and 5.7% [95% CI, 3.5 to 7.9] in the placebo group; hazard ratio, 1.14; 95% CI, 0.76 to 1.73). The team also noted that breast-feeding, regardless of whether it was exclusive or whether it was ongoing during gluten introduction, had no substantial impact on the later development of celiac disease. Compared to the placebo, introducing small quantities of gluten to high-risk children at 16 to 24 weeks of age had no impact on rates of celiac disease at 3 years of age. So, basically, the data show that there is no need for parents to fret or worry about when their child first begins to consume gluten. There is no magic window or timeframe for introducing gluten to their child’s diet that will change the risk for developing celiac disease later on. Source: N Engl J Med 2014; 371:1304-1315October 2, 2014. DOI: 10.1056/NEJMoa1404172
  7. Celiac.com 06/10/2013 - Researchers have known for some time that immunoglobulin G antibodies against deamidated gliadin peptides are about as accurate as tissue transglutaminase and endomysium autoantibodies in diagnosing celiac disease in adults. However, not much is known about their predictive value in infants with a suspected gluten enteropathy. A team of researchers recently set out to determine if antibodies to deamidated gliadin peptides could be an accurate predictor of celiac disease in infants. The research team included S. Amarri, P. Alvisi, R. De Giorgio, M.C. Gelli, R. Cicola, F. Tovoli, R. Sassatelli, G. Caio, and U. Volta. They are affiliated with the Pediatric Unit, IRCCS - Arcispedale Santa Maria Nuova, Reggio Emilia, Italy. To test whether deamidated gliadin immunoglobulin G antibodies are more reliable than traditional tests for screening celiac disease in infants, the researchers tested 65 children under 2 years of age for deamidated gliadin immunoglobulin G, tissue transglutaminase and endomysium immunoglobulin A, and gliadin immunoglobulins A and G. The group included 42 infants with malabsorption, along with 23 infants as control subjects. Thirty-seven of the 42 children with malabsorption had deamidated gliadin antibodies, associated with tissue transglutaminase and endomysial antibodies in 33, and with gliadin immunoglobulins A and G in 21 and 29, respectively. The team conducted intestinal biopsy in 34 of the 37 children who tested positive for deamidated gliadin antibodies. Thirty-two of the 34 showed villous atrophy consistent with celiac disease, while one of the remaining two had a Marsh 1 and the other showed normal mucosa. The control group showed only gliadin immunoglobulins A (4.3 %) and G (39.1 %). The results showed that deamidated gliadin, tissue transglutaminase and endomysial antibodies were significantly more sensitive for celiac disease than gliadin immunoglobulins G and A. High levels of deamidated gliadin antibodies correlated with severe intestinal damage. For infants, deamidated gliadin antibodies showed a higher diagnostic accuracy for celiac disease than gliadin antibodies. High levels of deamidated gliadin antibodies are good predictors of severe gluten-dependent duodenal damage. Source: J Clin Immunol. 2013 Apr 5.
  8. Celiac.com 05/30/2012 - From what we understand about celiac disease, both genetic and environmental factors play a part in its development: eople with certain genetic dispositions are more likely to develop it, but studies of twins at high risk of developing celiac disease have shown that in 25% of cases, only one of the twins will develop the disease. This indicates an environmental effect, and with more research it might be possible to discover what these environmental factors are so that parents with celiac disease can take steps to prevent their children from developing the disease themselves. Breast-feeding has already demonstrated some protective effect on infants at risk of developing celiac disease, but it is still unclear how the modulation of intestinal bacteria affects the formation of the disease. Understanding the role various strains of intestinal bacteria play in the intestine could be the key to understanding why breast-feeding helps prevent celiac disease, and perhaps why celiac disease develops at all. In the present study, 75 newborns with at least one first degree relative with celiac disease were broken into breast-feeding, formula-feeding groups, high (7-28%) and low (less than 1%) genetic risk groups, then tested at 7 days, 1 month and 4 months for prevalence and diversity of intestinal bacteria. Infants at high risk of developing celiac disease had more Bacteroides vulgatus, regardless of feeding methods while infants at low risk of developing celiac disease had more Bacteroides ovatus, Bacteroides plebeius and Bacteroides uniformis. Formula-fed infants had more Bacteroides intestinalis, Bacteroides caccae and Bacteroides plebeius, though prevalence depended on the testing stage. The most striking finding of the experiment seems to indicate that both low genetic risk of celiac disease development and breast-feeding are positively correlated with the prevalence of Bacteroides uniformis in the intestines. This might explain why breast-feeding can help protect against development of the disease, by introducing more Bacteroides uniformis into the infant's intestinal bacteria community. The implications of this research are still unclear, but a follow-up study on these infants is intended. Further research may explain how the prevalence of these bacteria in the intestine actually affects the development of celiac disease in infants. Source: http://www.ncbi.nlm.nih.gov/pubmed/21642397
  9. JAMA. 2005;293:2343-2351, 2410-2412 Celiac.com 05/31/2005 – Researchers in the United States have found that introducing gluten too early or too late in an infants diet may play a key role in whether or not they eventually develop celiac disease autoimmunity. From 1994 to 2004 the researchers followed 1,560 high-risk children (those with either HLA-DR3 or DR4 alleles, or with a first-degree relative with type 1 diabetes) who were periodically screened for celiac disease autoimmunity. Positive results were defined by two positive tissue transglutaminase (tTG) blood serum tests, or one positive tTG and a positive small bowel biopsy. The researchers conducted a prospective observational study in which the parents of the children in the study responded to a questionnaire regarding the timing of gluten introduction into their childrens diets. To avoid a bias on the answers the researchers purposely did not include children who already had celiac disease. During the mean duration period of the study (4.8 years), 51 children developed celiac disease autoimmunity. Their findings indicate that children who were first introduced to gluten when they were less than 3 months of age had a five-fold increased risk of developing celiac disease autoimmunity when compared to children who were first introduced to gluten at 4-6 months old. Additionally, those who were first introduced at 7 months or older had a marginally increased risk of getting celiac disease autoimmunity when compared with the same group. Based on these findings the researchers recommend that parents should introduce cereals into their childrens diets at 4-6 months of age—even though this conflicts with recent recommendations by the American Academy of Pediatrics, who recommend breast-feeding only until 6 months of age. The researchers stress that much larger international prospective studies need be done in this area to answer the many questions that this study raises.
  10. AU- Fallstrom SP; Kristiansson B; Ryd W JN- Acta Pathol Microbiol Scand [A]; 89 (6) p431-8 PY- Nov 1981 AB- Eighty-one children aged 4-18 months with unsatisfactory weight gain were investigated for organic diseases; the investigation included small-intestinal biopsy. Sixteen had total villous atrophy, in most cases due to gluten intolerance. Transient disease, e.g. cows milk protein intolerance, was probable in 7 children with subtotal atrophy. In 18 children the only abnormal finding was an increased number of inflammatory cells in the mucosa, a finding which was probably of no clinical significance. Planimetric measurement showed good agreement between the mucosal surface/volume ratio and an ordinary histological grouping of the mucosa. A significant correlation was found between the rate of weight gain during the period preceding investigation and mucosal surface/volume ratio.
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