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Celiac.com 11/22/2023 - A recent study focused on investigating intestinal gluconeogenesis in children with untreated celiac disease. Gluconeogenesis is a process in the small intestine that converts glutamine into glucose, and it plays a crucial role in metabolic control. Animal studies have suggested that impaired intestinal gluconeogenesis may have long-term effects on metabolic health and be associated with the development of type 2 diabetes and non-alcoholic fatty liver disease (NAFLD). The Research Team The research team included Olof Karlson, Henrik Arnell, Audur H. Gudjonsdottir, Daniel Agardh & Åsa Torinsson Naluai. They are variously affiliate with the Department of Laboratory Medicine, Institute of Biomedicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden; the Department of Paediatric Gastroenterology, Hepatology and Nutrition, Queen Silvia Children’s Hospital, Sahlgrenska University Hospital, Gothenburg, Sweden; the Department of Clinical Sciences, Unit of Celiac Disease and Diabetes, Lund University, Malmö, Sweden; and the Department of Laboratory Medicine, Institute of Biomedicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden. Quantitative Polymerase Chain Reaction to Measure the Expression of 11 Target Genes The researchers aimed to examined intestinal gluconeogenesis at the gene expression level in children with untreated celiac disease. They used quantitative polymerase chain reaction (qPCR) to measure the expression of 11 target genes related to intestinal gluconeogenesis in duodenal biopsies collected from 84 children with untreated celiac disease and 58 disease controls. The expression levels were compared to assess any differences. Impaired Intestinal Gluconeogenesis Process Discovered in Children with Untreated Celiac Disease The findings revealed that children with untreated celiac disease exhibited significantly lower expression of nine target genes involved in intestinal gluconeogenesis compared to the control group. These genes included FBP1, G6PC, GLS, GPT1, PCK1, PPARGC1A, SLC2A2, SLC5A1, and SLC6A19. However, there was no significant difference in the expression of G6PC3 or GOT1. The decreased expression of these important genes suggests an impaired intestinal gluconeogenesis process in children with untreated celiac disease. It remains unclear whether this decrease is a consequence of intestinal inflammation, or a shared metabolic pathway associated with other chronic metabolic diseases. However, this impaired intestinal gluconeogenesis may contribute to the increased risk of non-alcoholic fatty liver disease observed in celiac disease patients. Further research is needed to fully understand the mechanisms underlying these findings and to explore potential interventions or treatments that could alleviate the metabolic consequences of impaired intestinal gluconeogenesis in individuals with celiac disease. Read more in BMC Medicine volume 20, Article number: 440 (2022)

Celiac.com 11/08/2021 - Researchers know that non-alcoholic fatty liver disease is strongly associated with metabolic syndrome. But, are rates for non-alcoholic fatty liver disease higher in patients with celiac disease on a gluten-free diet? What about rates of celiac disease in patients with non-alcoholic fatty liver disease? A team of researchers recently set out to determine risk of non-alcoholic fatty liver disease for people with celiac disease on a gluten-free diet. The research team included M Aggarwal, P Kumar, R Garg, CC Lindenmeyer, J Wakim-Fleming, and A Rubio-Tapia. For their systemic review and meta-analysis, they included 12 studies involving nearly 5,000 subjects. Five of those studies, totaling 1,268 participants, determined rates of non-alcoholic fatty liver disease in patients with celiac disease, while seven studies on just over 3,700 subjects assessed rates of celiac disease in patients with non-alcoholic fatty liver disease. Their analysis included only studies with fifty or more cases of celiac disease with most participants over 15 years of age. They assessed new diagnoses of serology- and histology-positive celiac disease. Researchers reported pooled rates of non-alcoholic fatty liver disease of 12.3% in celiac patients before initiating a gluten-free diet, and 21.4% in celiac patients after initiating a gluten-free diet. They saw a significant increase in the odds of celiac patients developing non-alcoholic fatty liver disease after starting a gluten-free diet. They saw a pooled rate of 5.3% (95% CI, 3.5-8.0; I2 = 76%) and 3.1% (95% CI, 1.7-5.6; I2 = 79%) in patients with non-alcoholic fatty liver disease with serology-positive and histology-positive celiac disease, respectively. Based on their data, the team concludes that the odds of people with celiac disease developing non-alcoholic fatty liver disease nearly double after they begin a gluten-free diet. The team recommends close monitoring of celiac patients for non-alcoholic fatty liver disease over time. Given the long-term metabolic consequences of non-alcoholic fatty liver disease, the team suggests that doctors consider non-alcoholic fatty liver disease screening in celiac patients. The information was presented at the Annual Meeting of the American College of Gastroenterology, from October 22 to 27, 2021. Read more in Gastroenterology Advisor

Celiac.com 08/11/2021 - It takes a well-trained CIA operative to decipher some of this stuff. If the consumption of fat is thought to contribute to fatty liver (which it doesn’t), then why is it found in the context of starvation? Why is alcoholism the leading cause of fatty liver disease in people? And why does gastric bypass surgery, which involves a dramatic reduction in calories, trigger fatty liver disease? This same surgery is also associated with the precipitous development of iron deficiency anemia, bone density issues (osteoporosis) and immune failure in many cases. The morbidity rate following this harmful surgical invention is staggeringly high, and totally explainable. They’re making acute surgical celiacs out of these people. The symptoms they show could be the direct result of malabsorption of vital nutrients that would normally be picked up by the duodenum (calcium, iron, iodine, B complex, vitamin C, and trace minerals). This kind of physiological stress could trigger just about anything, including a subclinical viral infection (or viral adaptation) of the liver. But why do I get so upset over seemingly insignificant news items claiming that fatty liver disease is the result of eating fat? Because the low fat diet is one of man’s worst dietary inventions! Fat is crucial to a healthy diet, serving as a vehicle for certain vitamins to enter our body (the fat soluble A,D,E,K) the source of essential fatty acids (omegas), and the provider of protection against things trying to affect and invade our body, including these pesky lectins I keep writing so much about. Yes, dietary fat (animal fat not man-made trans fats) helps to block the attachment of certain dietary glycoproteins (e.g. the harmful ones from gluten, dairy, soy, etc.) to the villi of our intestinal tract. Other things that help in this regard are good carbs and glycoproteins from fruits and veggies such as pectin from apples. Pectins actually bind lectins. Fats more or less coat the GI tract and prevent the attachment of lectins. That is why whole milk is less harmful than skim milk, as I have discussed before. About five years ago I started seeing more and more chicken allergies in dogs. I wondered if it was because dogs were eating more chicken and that it was a secondary food allergen due to the damage being done by the “big 4” (gluten, casein, soy, and corn) like so many other food allergies, or whether there was something in the chicken that was inducing the problems.   I decided to check out what they were feeding poultry on the hunch that they were loading them up with gluten grains and corn. Five minutes into an Internet search yielded my answer. As of about 10 years ago now, they have been pouring the wheat to chickens and turkeys. If they fed them too much wheat, do you know what happened? They died of fatty liver syndrome. Until now, fatty liver syndrome has been considered “idiopathic: in veterinary medicine. Cats die from fatty liver syndrome. Fatty liver disease is the leading cause of liver disease and failure in the cat.   And what is the leading cause of fatty liver disease in people? Alcohol—grain alcohol. Most alcohols are made from grains, including beer. Could it really be the lectins in the grains that are inducing the fatty liver disease more than the alcohol itself? That makes sense when you think about the number of people who drink (excessively) versus the number who develop fatty liver disease. There has to be something special about those people. Either they have gluten sensitivity or a resident virus or both.   We are making great strides in expanding our understanding of lectins (e.g. those in the “big four”, legumes, grains, corn and dairy), environmental pollutants, trans fats, and the damage done by some drugs. Celiac awareness has opened a number of doors and will lead to improved understanding of dairy, soy and corn intolerance as well. I can’t wait for cow milk to finally be publicly convicted for what it has done to human and veterinary health. That time is coming soon.   We have had this wrong for years and the evidence has pointed us in a better direction for a number of years as well. Fat is not the enemy. You don’t get fat from eating fat. Dr. Atkin’s helped prove this. Similarly, your cholesterol does not go up primarily from eating dietary cholesterol. Further, an unusually low cholesterol diet is not healthful. Cholesterol, for example, is the building block for all of our hormones, including sex hormones and cortisones. It is an essential component in immune responses and in the protection of individual cells from invasion by harmful substances and organisms. The anti-cholesterol and anti-fat campaigns are ill-conceived, misguided, and harmful to our health, thus my passion on this topic.

Celiac.com 06/22/2021 - People with celiac disease have a higher risk for developing non-alcoholic fatty liver disease (NAFLD) and other related metabolic disorders, especially if they are not on a gluten-free diet. A team of researchers recently set out to explore the prevalence of NAFLD and metabolic-associated fatty liver disease in celiac patients at the time of celiac diagnosis and after 2 years of GFD; and to assess the role of PNPLA3 rs738409 in the development of NAFLD and metabolic-associated fatty liver disease in the celiac population. Recently, a new category of metabolic-associated fatty liver disease (MAFLD) has been proposed to move beyond the constraints of the NAFLD definition. The research team included Antonio Rispo; Nicola Imperatore; Maria Guarino; Raffaella Tortora; Anna Alisi; Valentina Cossiga; Anna Testa; Simona Ricciolino; Andrea Fiorentino; and Filomena Morisco. They are variously affiliated with the Gastroenterology, Department of Clinical Medicine and Surgery, School of Medicine Federico II of Naples, Naples, Italy; the Gastroenterology and Endoscopy Unit, AORN Antonio Cardarelli, Naples, Italy; the Hepatology Unit, AORN A. Cardarelli, Naples, Italy; and the Research Unit of Molecular Genetics and Complex Phenotypes, Bambino Gesù Children's Hospital, IRCCS, Rome, Italy. For the study, the team retrospectively enrolled all newly diagnosed celiac patients who underwent clinical, laboratory and ultrasonography investigations, both at diagnosis and at a two year follow-up. They also conducted a PNPLA3 rs738409 genotyping assay. They found that 65 of 221 newly diagnosed celiac patients, nearly 30%, presented NAFLD upon celiac diagnosis, while 32 of 221 met the criteria for metabolic-associated fatty liver disease. There were no major differences between NAFLD and metabolic-associated fatty liver disease, though 3 out of 4 metabolic-associated fatty liver disease patients had higher rates of insulin resistance (IR) compared with 2 out of 5 for NAFLD patients. The study shows that the newly established metabolic-associated fatty liver disease definition better describes the metabolic changes common when celiacs adopt a gluten-free diet. The new classification may help to spot patients at risk of worse metabolic outcomes, who will likely benefit from a close multidisciplinary approach for their multi-systemic disease. Keep an eye on celiac.com for more stories on celiac disease and metabolic-associated fatty liver. Read more in Liver International. 2021;41(4):788-798.

Celiac.com 10/24/2018 - Although some research has shown a connection between a gluten-free diet, altered macronutrient intake and metabolic syndrome, not much good data exists on the risk of nonalcoholic fatty liver disease in patients with celiac disease who follow a gluten-free diet. A team of researchers recently set out to assess the prevalence and relative risk of nonalcoholic fatty liver disease in celiac patients treated with a gluten-free diet. The research team included F. Tovoli; G. Negrini; R. Farì; E. Guidetti; C. Faggiano; L. Napoli; L. Bolondi; and A. Granito of the Department of Medical and Surgical Sciences, University of Bologna, Bologna, Italy. For many patients with metabolic syndrome, nonalcoholic fatty liver disease is common. To try to get some better information, the researchers devised a case-control study, with prospective enrollment of celiac disease outpatients following a gluten-free diet and control subjects. For the study, the team matched patients by age, gender and metabolic risk factors, such as overweight, diabetes mellitus, total cholesterol, and triglycerides, using a 1:1 ratio. The team diagnosed nonalcoholic fatty liver disease according to the criteria set by the European Association for the Study of the Liver. In all, they compared 202 celiac disease patients and 202 control subjects. The raw rate of nonalcoholic fatty liver disease was 34.7% and 21.8% in the celiac disease and control group, respectively. Using binary logistic regression, the team demonstrated that those with celiac disease faced an increased risk for nonalcoholic fatty liver disease. Meanwhile, the relative risk for nonalcoholic fatty liver disease was substantially higher in non-overweight celiac disease patients. Nearly 35% of celiac disease patients on a gluten-free diet also had nonalcoholic fatty liver disease, that’s a risk three times greater than the general population. The team recommends that doctors tailor their celiac treatment approaches to better help celiac disease patients with nonalcoholic fatty liver disease to get proper nutritional intake, which will help to reduce the risk of long-term liver-related events. Source: Aliment Pharmacol Ther. 2018;48(5):538-546.