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Found 5 results

  1. Sandi Star, HHP, CNC, CCMH

    The MTHFR Mutation

    Celiac.com 02/08/2018 - Have you ever considered being tested for a genetic defect called MTHFR? If you have a family history of heart disease or stroke, migraines, trouble getting pregnant or have a child with Autism you might want to consider reading on to learn more. These are just a few of the list of conditions linked to MTHFR mutation. Surprisingly, 60% of our population has this mutation and most do not even know what MTHFR is. I recently came up positive myself for MTHFR A1298C. We will talk more about the two common markers in a bit. This changes everything when it comes to choices and is important to have the knowledge when choosing foods and supplementation. It's also important to monitor your folate levels. More to come. Interestingly, Untreated celiac disease may be associated with hyperhomocysteinemia caused by a combination of vitamin deficiencies and variants in the MTHFR gene. If you are not healing with a gluten free diet this might be a test to consider. [1] So, what is MTHFR? The MTHFR gene (methylenetetrahydrofolate reductase) is an enzyme that plays an important role in processing amino acids, the building blocks of proteins. Now you know why it's an acronym! Methylenetetrahydrofolate reductase is important for a chemical reaction involving forms of the vitamin folate (also called vitamin B9). This enzyme converts a molecule called 5,10-methylenetetrahydrofolate to a molecule called 5-methyltetrahydrofolate. This reaction is required for the multistep process that converts the amino acid homocysteine to another amino acid, methionine. The body uses methionine to make proteins and other important compounds. [2] Although, there are over fifty known MTHFR variants, two are commonly tested C677T and A1298. Some of the key things methylation process is responsible for are: Cellular Repair – DNA repair is a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its genome (genetic material of an organism). Detoxification and Neurotransmitter Production – The interconversion of amino acids. Healthy Immune System Function – Formation and maturation of red blood cells, white blood cells and platelet production. What's the Difference Between the Two Most Common Types? The 677T Variant is associated with heart disease and stroke whereas the 1298C is associated with a variety of chronic illness. Either one however can cause general health problems. Homozygous vs Heterozygous An organism can be homozygous dominant, if it carries two copies of the same dominant allele (allele - one of two or more alternative forms of a gene that arise by mutation and are found at the same place on a chromosome.), or homozygous recessive, if it carries two copies of the same recessive allele. Heterozygous means that an organism has two different alleles of a gene. If you are homozygous (2 abnormal copies) your enzyme efficiency drops to 10% - 20% of normal which can be problematic. A more serious combination is 677T/1298C which has both genetic anomalies. If you are having symptoms and can't quite put your finger on it I would suggest getting tested for the MTHFR. That will help your practitioner determine what supplementation best suits your needs. Diet will also be a factor as with MTHFR the body cannot process synthetic folate which is in fortified foods such as cereal, nutritional yeast (can get unfortified), breads, rice, pastas, flour, etc., This explains why I always got a headache after I ate fortified nutritional yeast. I switched to unfortified and I don't have the headaches. As mentioned above, there are many chronic conditions linked to MTHFR. Here are a few: Alzheimer's Autism Autoimmune Disorders Breast cancer Chronic Fatigue Down's Syndrome Fibromyalgia Heart Disease IBS (irritable bowel syndrome) Infertility in both men and women Mental disorders such as bipolar and schizophrenia Migraines Multiple Sclerosis (MS) Sensitivity to chemicals Stroke The Great Detoxifier Glutathione is the body's main antioxidant and detoxifier. What happens with MTHFR mutation is it can make you susceptible to disease by lowering your body's ability to make glutathione. Most people with MTHFR have low glutathione levels. With low glutathione levels, you are more sensitive to toxins and chemicals including heavy metals. The good news is you can supplement glutathione in the correct methyl form and change up your diet. More to come on this. With oxidative stress, we are more likely to have premature aging as well. Another reason to be aware of MTHFR and maintain a healthy high folate diet along with supporting supplementation. Testing If you have any of the symptoms above or have a family history with MTHFR mutations I highly recommend testing for both C677T and A1298. Testing can be done through a practitioner. You can go to 23andme and order the test or work with your health practitioner. It's inexpensive and well worth it. Also, testing your levels of glutathione and folate would be beneficial so your practitioner knows where your levels are before recommending supplementation. Supplementation for MTHFR If you are taking a B vitamin, make sure it's methyl-B12, methyl-folate. Taking synthetic forms (folic acid) can be more harmful than good because the body cannot do the conversion. It's essential to make sure that your method delivers the antioxidant efficiently to your cells. One of the B vitamins I recommend from Pure Genomics is their B Complex available on our marketplace. Glutathione is also important but hard to absorb so a liposome form is recommended or get one with a precursor called NAC (N-acetyl-cysteine). Glutathione is important for detoxification as mentioned. Here are a few to consider – Liposomal Glutathione by Pure Encapsulations as a liposome form With any supplement, you can have adverse effects so make sure you work with a knowledgeable practitioner. Diet and Lifestyle Folic Acid vs. Folate While folic acid and folate may be marketed interchangeably, as mentioned earlier, their metabolic effects can be quite different, especially for those with the MTHFR mutation. Folate is the bioavailable, natural form of vitamin B9 found in a variety of plant and animal foods. Folic acid, on the other hand while readily utilized by the body is synthetic. Folate is found in supplements and fortified foods such as cereals and might I add nutritional yeast. The body is more adept at using folate and regulates healthy levels by discarding excess folate in urine. With MTHFR folic acid can be problematic so make sure you purge the folic acid rich foods and supplements. For those who love the flavor of nutritional yeast and use it in vegan recipes there are a few companies who make unfortified versions you can get off amazon. Daily lifestyle activities such as dry brushing (lymphatic circulation) Epsom salt baths, exercise, sauna's (infrared sauna is amazing) and of course a healthy diet rich in natural forms of folate such as: Beans and lentils Leafy green vegetables including raw spinach Asparagus Romaine Lettuce Broccoli Avocado Bright-colored fruits, such as papaya and orange Here are just a few examples of some folate rich foods. As you can see spinach packs a powerful punch of folate as well as papaya and lentils coming in the highest. [2] Source Spinach Asparagus Papaya Orange Lentils Pinto Beans Sunflower Seeds Serving Size 1 Cup 1 Cup 1 papaya 1 orange 1 Cup 1 Cup ¼ Cup Folate 263 mcg 262 mcg 115 mcg 40 mcg 358 mcg 294 mcg 82 mcg DV % 65% 64% 29% 10% 90% 74% 21% Did you know your liver needs glutathione to produce bile in addition to the detoxification process? Look at addressing health issues such as leaky gut, IBS and Inflammation as these can affect absorption and neurotransmitter levels as well as hormones with MTHFR A1298C mutations. MTHFR mutations are tied to higher mental disorders such as anxiety, depression, bipolar and schizophrenia as well as chronic fatigue and fibromyalgia. It's important to find ways to manage the stressors in addition to healing the gut as symptoms can be heightened with MTHFR. Protect the heart with an anti-inflammatory diet rich in omegas, fiber and plants. Omega 3 and COQ10 supplementation is helpful. A good multi is beneficial as long as you get one with B12 (methyl cobalamin) and Folate (methyl tetrahydrofolate) forms. Drug Interactions to consider You should not use any supplements without first talking to your health care provider. For example, folate should not be taken at the same time as the antibiotic tetracycline because it interferes with the absorption and effectiveness of this medication. Folate is necessary if taking medications for birth control, cholesterol or seizures for example as they may lower folic acid levels in the body. Dosage and timing is important to know. Here are some medications to keep in mind: Antacids, H2 blockers, proton pump inhibitors Bile acid sequestrants Carbamazepine Nonsteroidal anti-inflammatory drugs (NSAIDs) Sulfasalazine Triamterene When taken for long periods of time, these medications, as well as other anti-inflammatory and anti-seizure medicines, can increase the body's need for folic acid. Also consider drugs used for cancer, rheumatoid arthritis and psoriasis as those also reduce the folic acid in the body. Supplementing folic acid can help reduce symptoms of these disorders however with cancer, folic acid may interfere with methotrexates effects on treatment. Talk with your practitioner if you are taking any medications. [3] Knowing your DNA make up is important as is knowing your numbers (blood pressure, cholesterol, etc.) so you can keep a handle on your health and do your best to control stress. Getting tested for the MTHFR mutation is worth knowing whether it comes up or not. It can make all the difference in aging and detoxing and give you a peace of mind. Sources: https://draxe.com/mthfr-mutation/ http://doccarnahan.blogspot.com/2013/05/mthfr-gene-mutation-whats-big-deal.html https://www.jillcarnahan.com/2014/02/23/health-tips-for-anyone-with-a-mthfr-gene-mutation/
  2. Celiac.com 01/15/2018 - Cerebellar ataxia with sensory ganglionopathy is a disabling combination of neurological dysfunction that usually occurs as part of certain hereditary ataxias. However, some patients present this combination with no apparent genetic cause. A team of researchers recently set out to if autoimmunity might have a role to play in SG. The research team included Panagiotis Zis, Ptolemaios Georgios Sarrigiannis, Dasappaiah Ganesh Rao, Nigel Hoggard, David Surendran Sanders, and Marios Hadjivassiliou. They are variously affiliated with the Academic Department of Neurosciences, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK; the University of Sheffield, Sheffield, UK; the Department of Neuroradiology, Sheffield Teaching Hospitals NHS Foundaiton Trust, Sheffield, UK; the University of Sheffield, Sheffield, UK; and the Academic Unit of Gastroenterology, Sheffield Teaching Hospitals NHS Foundation Trust, Sheffield, UK. The team reviewed records of all patients that have been referred to the Sheffield Ataxia Centre who had neurophysiological and imaging data suggestive of SG and cerebellar ataxia respectively. We excluded patients with Friedreich's ataxia, a common cause of this combination. All patients were screened for genetic causes and underwent extensive investigations. They found 40 patients with combined cerebellar ataxia and sensory ganglionopathy. The majority of patients were initially diagnosed with cerebellar dysfunction, and about one-third were initially diagnosed with sensory ganglionopathy. For that one-third, the two diagnoses were made together. The average time between the two diagnoses was 6.5 ± 8.9 years, ranging from 0 up to 44 years. The most common initial symptom was unsteadiness, in 77.5% of patients, followed by patchy sensory loss in 17.5%, and peripheral neuropathic pain in 5%. Nineteen patients had gluten sensitivity, of whom 3 patients had biopsy proven celiac disease. Other abnormal immunological tests were present in another 15 patients. Six patients had malignancy, which was diagnosed within 5 years of the neurological symptoms. Only 3 patients were classified as having a truly idiopathic combination of cerebellar ataxia with sensory ganglionopathy. This study shows that immune pathogenesis plays a significant role in patients with the unusual combination of cerebellar ataxia and sensory ganglionopathy. Source: Cerebellum & Ataxias 20174:20
  3. Celiac.com 10/26/2017 - Making an accurate count of intraepithelial lymphocytes (IEL) is important to making an accurate diagnosis of celiac disease, but so far, researchers have not been able to establish a definitive 'normal' IEL range. In a recent multi-center study, a team of researchers set out to do just that. The research team included Kamran Rostami, Michael N Marsh, Matt W Johnson, Hamid Mohaghegh, Calvin Heal, Geoffrey Holmes, Arzu Ensari, David Aldulaimi, Brigitte Bancel, Gabrio Bassotti, Adrian Bateman, Gabriel Becheanu, Anna Bozzola, Antonio Carroccio, Carlo Catassi, Carolina Ciacci, Alexandra Ciobanu, Mihai Danciu, Mohammad H Derakhshan, Luca Elli, Stefano Ferrero, Michelangelo Fiorentino, Marilena Fiorino, Azita Ganji, Kamran Ghaffarzadehgan, James J Going, Sauid Ishaq, Alessandra Mandolesi, Sherly Mathews, Roxana Maxim, Chris J Mulde, Andra Neefjes-Borst, Marie Robert, Ilaria Russo, Mohammad Rostami-Nejad, Angelo Sidoni, Masoud Sotoudeh, Vincenzo Villanacci, Umberto Volta, Mohammad R Zali, Amitabh Srivastava. They are variously affiliated with the twenty-eight institutions listed below. The study was designed at the International Meeting on Digestive Pathology, Bucharest 2015. Investigators from 19 centers in eight countries on three continents, recruited 198 patients with Marsh III histology, and another 203 control subjects. They used a single agreed upon protocol to count IEL/100 enterocytes in well-oriented duodenal biopsies. They also collected demographic and serological data. The research team used receiver operating characteristic (ROC) curve analysis to determine the optimal cut-off between normal and celiac disease (Marsh III lesion) duodenal mucosa, based on IEL counts on >400 mucosal biopsy specimens. The average ages of celiac and control groups were 45.5 and 38.3 years, respectively. They found that mean IEL count was 54±18/100 enterocytes in celiac disease and 13±8 in normal controls (p=0.0001). ROC analysis indicated an optimal cut-off point of 25 IEL/100 enterocytes, with 99% sensitivity, 92% specificity and 99.5% area under the curve. Other cut-offs between 20 and 40 IEL were less discriminatory. Additionally, there was a sufficiently high number of biopsies to explore IEL counts across the sub-classification of the Marsh III lesion. Their ROC curve analyses show that a cut-off of 25 IEL/100 enterocytes for Marsh III lesions provides the best way to distinguish between normal control and celiac disease biopsies. They saw no differences in IEL counts between Marsh III a, b and c lesions. There was an indication of a continuously graded dose–response by IEL to environmental gluten antigenic influence. Source: GUT Affiliations: The team members for this study are affiliated with the Department of Gastroenterology and Pathology, Milton Keynes University Hospital, Milton Keynes, UK; the Department of Gastroenterology, Luton and Dunstable University Hospital, Luton, UK; the Wolfson College, University of Oxford, Oxford, UK; the Gastroenterology and Liver Diseases Research Centre, Research Institute for Gastroenterology and Liver Diseases, Shahid Beheshti University of Medical Sciences, Tehran, The Islamic Republic of Iran; the Centre for Biostatistics, Faculty of Biology, Academic Health Science Centre, University of Manchester, Manchester, UK; the Department of Gastroenterology, Royal Derby Hospital, Derby, UK; the Department of Pathology, Ankara University Medical School, Ankara, Turkey; the Department of Gastroenterology, Warwick Hospital, Warwick, UK; the Service de Pathologie, Centre de Biologie et Pathologie Groupe Hospitalier du Nord, Hospices Civils de Lyon, Lyon, France; University of Perugia Medical School, Perugia, Italy; the Department of Cellular Pathology, University Hospital Southampton NHS Foundation Trust, Southampton, UK; Department of Pathology, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania; Institute of Pathology Spedali Civili, Brescia, Italy; Internal Medicine and Pathology Unit, University of Palermo, Giovanni Paolo II Hospital, Sciacca, Italy; Department of Pediatrics and Surgical Pathology, Università Politecnica delle Marche, Ancona, Italy; Department of Medicine and Surgery, Scuola Medica Salernitana, University of Salerno, Salerno, Italy; Departments of Gastroenterology and Pathology, Grigore T. Popa University of Medicine and Pharmacy, Iasi, Romania; College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, UK; Digestive Disease Research Center, Tehran University Medical Science, Tehran, Iran; Center for Prevention and Diagnosis of Coeliac Disease and Pathology Unit, Fondazione IRCCS Ca' granda Ospedale Maggiore Policlinico, Milano, Italy; Department of Medical and Surgical Sciences, University of Bologna and Diagnostic and Experimental, University of Bologna, Bologna, Italy; Gastroenterology and Hepatology, Faculty of Medicine, Mashhad University 0f Medical Sciences, Mashhad, Iran; Pathology department, Razavi hospital, Mashhad, Iran; Department of Pathology, Southern General Hospital, Lanarkshire, UK; Department of Hepatogastroenterology and Pathology, Free University Medical Centre, Amsterdam, The Netherlands; Department of Pathology and Medicine, Yale University School of Medicine, New Haven, USA; Digestive Disease Research Center, Tehran University Medical Science, Tehran, Iran; Department of Pathology, Brigham & Women's Hospital, Boston, USA.
  4. Celiac.com 06/21/2017 - Circulating gluten-specific FOXP3+CD39+ regulatory T cells have impaired suppressive function in patients with celiac disease. What does that mean? Although researchers understand the effector T-cell response in patients with celiac disease pretty well, they really don't know very much about the role played by regulatory T cells (Treg cells) in the loss of tolerance to gluten. To get a better picture, a team of researchers recently set out to define whether patients with celiac disease have a dysfunction or lack of gluten-specific forkhead box protein 3 (FOXP3)+ Treg cells. The research team included L Cook, CML Munier, N3 Seddiki, D van Bockel, N Ontiveros, MY Hardy, JK Gillies, MK Levings, HH Reid, J Petersen, J Rossjohn, RP Anderson, JJ Zaunders, JA Tye-Din, AD Kelleher. For the study, gluten-free patients with celiac disease underwent oral wheat challenge to stimulate recirculation of gluten-specific T cells. The research team collected peripheral blood before and after challenge. To effectively measure the gluten-specific CD4+ T-cell response, they combined traditional IFN-γ ELISpot with a test for antigen-specific CD4+ T cells that does not rely on tetramers, antigen-stimulated cytokine production, or proliferation, but relies instead on antigen-induced co-expression of CD25 and OX40 (CD134). During the gluten challenge, levels of circulating gluten-specific Treg cells and effector T cells both rose sharply, peaking on the sixth day. The team recounts surprise on discovering that about 80% of the ex vivo circulating gluten-specific CD4+ T cells were FOXP3+CD39+Treg cells, which reside within the pool of memory CD4+CD25+CD127lowCD45RO+ Treg cells. Even though they saw normal suppressive function in peripheral polyclonal Treg cells from celiac patients, after a short in vitro expansion, the gluten-specific FOXP3+CD39+ Treg cells showed sharply reduced suppressive function compared with polyclonal Treg cells. The team's study offers the first estimates of FOXP3+CD39+ Treg cell frequency within circulating gluten-specific CD4+ T cells after oral gluten challenge of celiac patients. FOXP3+CD39+ Treg cells made up the majority of all circulating gluten-specific CD4+ T cells, but they showed reduced suppressive function, indicating that Treg cell dysfunction might be a key factor in celiac disease development. This type of research is crucial to help document the genetic physiology of celiac disease, which will help researchers to better understand and treat the disease itself. Source: J Allergy Clin Immunol. 2017 Mar 8. pii: S0091-6749(17)30343-3. doi: 10.1016/j.jaci.2017.02.015. The researchers are variously affiliated with the Immunovirology and Pathogenesis Program, The Kirby Institute, UNSW Sydney, Sydney, Australia, St Vincent's Centre for Applied Medical Research, St Vincent's Hospital, Sydney, Australia; the Infection and Immunity Program, The Department of Biochemistry and Molecular Biology, Biomedicine Discovery Institute, Monash University, Clayton, Australia; Australian Research Council Centre of Excellence in Advanced Molecular Imaging, Monash University, Clayton, Australia; the Immunovirology and Pathogenesis Program, The Kirby Institute, UNSW Sydney, Sydney, Australia; St Vincent's Centre for Applied Medical Research, St Vincent's Hospital, Sydney, Australia, Immunology Division, Walter and Eliza Hall Institute, Parkville, Australia; Department of Medical Biology, University of Melbourne, Parkville, Australia; Department of Surgery, University of British Columbia, Vancouver, British Columbia, Canada; the Institute of Infection and Immunity, Cardiff University School of Medicine, Heath Park, Cardiff, United Kingdom; the Immunology Division, Walter and Eliza Hall Institute, Parkville, Australia; Department of Medical Biology, University of Melbourne, Parkville, Australia; ImmusanT, Cambridge, Massachusetts; and the Department of Gastroenterology, Royal Melbourne Hospital, Parkville, Australia.
  5. Celiac.com 02/20/2017 - Nickel is the most common cause of contact allergy, and nickel exposure can result in systemic nickel allergy syndrome, which mimics irritable bowel syndrome (IBS). Nickel is also found in wheat, which invites questions about possible nickel exposure from wheat in some cases of contact dermatitis. However, nickel hasn't really been studied in relation to glutenâ€related diseases. A research team recently set out to evaluate the frequency of contact dermatitis due to nickel allergy in NCWS patients diagnosed by a doubleâ€blind placeboâ€controlled(DBPC) challenge, and to identify the characteristics of NCWS patients with nickel allergy. The research team included Alberto D'Alcamo, Pasquale Mansueto, Maurizio Soresi, Rosario Iacobucci, Francesco La Blasca, Girolamo Geraci, Francesca Cavataio, Francesca Fayer, Andrea Arini, Laura Di Stefano, Giuseppe Iacono, Liana Bosco, and Antonio Carroccio. The are variously affiliated with the Dipartimento di Biologia e Medicina Interna e Specialistica (DiBiMIS), Internal Medicine Unit, University Hospital, Palermo, Italy; the Surgery Department, University Hospital, Palermo, Italy; Pediatric Unit, "Giovanni Paolo II" Hospital, Sciacca (ASP Agrigento), Italy; DiBiMIS, Gastroenterology Unit, University Hospital, Palermo, Italy; Pediatric Gastroenterology Unit, "ARNAS Di Cristina" Hospital, Palermo, Italy; Dipartimento di Scienze e Tecnologie Biologiche Chimiche e Farmaceutiche (Ste.Bi.CeF), University of Palermo, Palermo, Italy. Their team conducted a prospective study of 54 women and 6 men, with an average age of 34.1 year, and diagnosed with NCWS from December 2014 to November 2016. They also included a control group of 80 age†and sexâ€matched subjects with functional gastrointestinal symptoms. Patients reporting contact dermatitis related to nickelâ€containing objects were given a nickel patch sensitivity test. The tests showed that six out of sixty patients (10%) with NCWS suffered from contact dermatitis and nickel allergy, and this frequency was statistically higher than observed in the 5 percent seen in the control group. Compared to NCWS patients who did not suffer from nickel allergy, NCWS patients with nickel allergy commonly showed a higher rates of skin symptoms after wheat consumption. Contact dermatitis and nickel allergy are more frequent in NCWS patients than in subjects with functional gastrointestinal disorders. Moreover, large numbers of these patients showed cutaneous manifestations after wheat ingestion. Nickel allergy should be evaluated in NCWS patients who have cutaneous manifestations after wheat ingestion. More study is needed to determine the relationship between nickel sensitivity and NCWS. Source: Nutrients 2017, 9(2), 103; doi:10.3390/nu9020103
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