Photo by gastroscopy showing ulcer in the antrum area of the stomach (lower area).
What Is A Gastric Ulcer?
Gastric ulcer is a painful stomach disorder characterized by an open sore involving the mucosa lining and deeper muscle layer of the stomach.
Gastric ulcer is associated with lymphocytic gastritis which is inflammation of the mucosal lining of the stomach. The thick mucosal lining normally protects the stomach from the erosive action of stomach acid.
Q: How do ulcers develop?
A: Ulcers develop if hydrochloric acid secreted by the gastric glands of the stomach for the purpose of digesting food damages the normally resistant mucosal walls of the stomach. In the reverse, ulcers may be accompanied by achlorhydria (insufficient acid production).
Damage occurs when there is a predisposing factor that alters the health of the mucosal lining. The most common cause is infection with a bacteria called h. pylori bacter, stress and chronic use of the pain relievers aspirin and non-steroidal drugs like ibuprofen.
Smoking tocacco and consuming alcohol aggravate an ulcer but do not cause it to develop.
The most common location for ulcer formation is along the stomach antrum which is the area of the stomach before the pylorus, the lower region that empties liquid stomach contents into the small intestine.
What Is A Gastric Ulcer In Celiac Disease and/or Gluten Sensitivity?
Vitamin E is not a single vitamin but naturally occurs as a fat-soluble vitamin family that consists of at least 8 distinct molecules.
These molecules include 4 tocopherols (alpha, beta, gamma, and delta) and 4 tocotrienols (alpha, beta, gamma, and delta).
Generally, tocotrienols are more active against chronic disease while tocopherols are more protective of the nervous system.
Vitamin E (for short) is a powerful antioxidant that protects cell membranes and other fat-soluble compounds from oxidative damage by free radicals (molecules that damage cells).
Q: How does vitamin E protect cells from oxidative damage by free radicals?
A: As an example, the oxidative damage to low density cholesterol (LDL – bad type) appears to lead to the deposition of cholesterol in the arterial wall (plaque formation) leading to atherosclerotic disease, commonly called hardening of the arteries.
Regarding inflammation, mast cells are activated by oxidized LDL which results in increased expression of inflammatory cytokines. This finding suggests that vitamin E antioxidant activity in reducing oxidation of LDL lipoprotein may also reduce mast cell activation. Mast cells reside near small blood vessels and, when activated, release potent mediators involved in allergy and inflammation.1
In neutralizing free radicals, vitamin E itself is oxidized (changed) to a free radical. Importantly, conversion of vitamin E back to the original form occurs by reaction with vitamin C. These two vital anti-oxidants go hand in hand.
Vitamin E is essential for normal cerebellar brain function (lower brain), peripheral nerve health and healthy skin.
What Is Vitamin E Deficiency In Celiac Disease and/or Gluten Sensitivity?
Sources:
Shaik-Dasthagirisaheb YB, Varvara G, Murmura G, Saggini A, Caraffa A, Antinolfi P, Tete’ S, Tripodi D, Conti F, Cianchetti E, Toniato E, Rosati M, Speranza L,Pantalone A, Saggini R, Tei M, Speziali A, Conti P, Theoharides TC, Pandolfi F. Role of vitamins D, E and C in immunity and inflammation. J Biol Regul Homeost Agents. 2013 Apr-Jun;27(2):291-5. [↩]
Iron deficiency anemia is a blood cell disorder that is characterized by formation of small, pale red blood cells, causing tissue hypoxia. Hypoxia is the inability to meet the demands of the body for oxygen.
Q: Why do small, pale red blood cells cause tissue hypoxia?
A: Small, pale red blood cells (erythrocytes) cause tissue hypoxia because they are not able, as do normal erythrocytes, to pick up adequate oxygen from the lungs and carry it to cells that use oxygen.
Red blood cell production and function are dependent on a sufficient level of iron in the body and also the ability to use available iron to make hemoglobin in red blood cells.
Hemoglobin is a protein that binds oxygen in red blood cells to be carried by the bloodstream to cells throughout the body. In iron deficiency anemia, hemoglobin in females is below 12.5g/dl (normal range is 12.5 to 16g/dl) and in males it is below 13.5g/dl (normal range is 13.5 to 17.5g/dl).
Iron must be obtained from the diet, since the body cannot make it, but there are various factors that can interfere with absorption and use in the body, causing anemia. Iron absorption from the gut first requires ionization, or gaining a positive electrical charge, in the strongly acidic environment of stomach juice. Ionized iron, only, can be absorbed in the duodenum, which receives the acidic contents of the stomach before it is neutralized further along.
Dietary iron can be heme or non-heme depending on the food source. Heme iron obtained only from animal food sources is absorbed into the bloodstream by active transport across the brush border (microvilli) which cover the multitudinous villi of the small intestinal lining.
Non-heme iron obtained from plants must bind with apoprotein after entering the enterocyte (surface cell of small intestinal lining) to be ferried to the underlying basolateral membrane and exited by active transport into the bloodstream.
Frequently, chronic anemia due to iron deficiency is accompanied by increased platelets, and this thrombocytosis resolves with iron repletion (normal iron level). Conversely, in severe iron deficiency anemia, patients may have thrombocytopenia (low platelets), which also resolves with iron therapy.1
What Is Iron Deficiency Anemia In Celiac Disease and/or Gluten Sensitivity?
Sources:
Koury M and Rhodes M. How to approach chronic anemia. Hematology Am Soc Hematol Educ Program. 2012;2012:183-90. doi: 10.1182/asheducation-2012.1.183. [↩]
Woman with long standing osteoporosis. Courtesy of Wikimedia.
What Is Osteoporosis?
Osteoporosis is a metabolic bone disorder characterized by diminished bone mass (density) with normal cell appearance but fragile bone strength that prediposes to broken bones, and with high bone turnover.
This condition usually goes undetected until late when loss of height or a bone fracture occurs. In fact, each year 1.5 million fractures mainly of the hip, spine and wrist are attributed to osteoporosis. Compression fractures of vertebrae bones are the most common, accounting for 700,000 cases.
Bone is composed of specialized connective tissue called osseous tissue. Osseous tissue is made up of living bone cells (osteocytes) that are embedded in a hard matrix (framework) of calcified substance.
Bone matrix contains collagen fibers and the minerals calcium phosphate and calcium carbonate, which provide strength to bone. The copper enzyme, lysyl oxidase, is involved in the cross-linking of collagen in forming the framework for depositing calcium and other minerals to build and repair bone.
Q: How do osteocytes function in bone?
A: Osteocytes maintain the health of bone by their metabolic activity in regulating normal bone turnover. Bone turnover is the breaking down and removal of old or damaged bone and rebuilding or remodeling of healthy bone that is ongoing throughout life. The bone formation process takes about 3 months to complete.
Osteoporosis develops from failure of the body to maintain health and to provide bone tissue with adequate nutrition for proper function. Risk factors that can be modified include: low calcium intake, sedentary lifestyle, smoking, drinking alcohol excessively, eating a diet with excessive caffeine, protein, and phosphate, and taking certain medications over a long time such as steroids, thyroid preparations, the anti-convulsive drug phenytoin, aspirin, antacids, anticoagulants, some diuretics, and some chemotherapeutic drugs. See below for a fuller description.
In addition to celiac disease, osteoporosis is associated with advancing age, family history, nulliparity (no pregnancies) and post-menopause in females, certain disorders such as hyperthyroidism, hypogonadism, inflammatory bowel disease like Crohn’s disease, multiple myeloma, anorexia nervosa, and Cushing’s disease.
Bone strength is easily measured by testing bone mineral density (BMD). BMD is evaluated by DEXA scan (dual-energy X-ray absorptiometry). DEXA at the femoral neck and lumbar spine is considered the gold standard to confirm the diagnosis of osteoporosis. Results are expressed as T and Z scores. T scores compare the result with a 20 to 40 year old helathy person while Z scores compare the result with persons in the same age group. Both are measured in standard deviations (SD).
According to WHO criteria (World Health Organization), a T-score of -1 SD or greater denotes normal bone, a T-score between −1 to −2.5 SD denotes osteopenia, and a T-score of −2.5 or more denotes osteoporosis.1
Treatment is aimed to preserve and increase bone density, minimize symptoms for better quality of life and reduce risk of bone fractures.
What Is Osteoporosis In Celiac Disease and/or Gluten Sensitivity?
The cumulative effects of gluten-induced inflammation, treatment delay, and malabsorption result in lower bone density and bone fragility.2
Sources:
Pantaleoni S, Luchino M, Adriani A, Pellicano R, Stradella D, Ribaldone DG, Sapone N, Isaia GC, Di Stefano M, Astegiano M. Bone mineral density at diagnosis of celiac disease and after 1 year of gluten-free diet. ScientificWorldJournal. 2014;2014:173082. doi: 10.1155/2014/173082. [↩]
Grace-Farfaglia P. Bones of Contention: Bone Mineral Density Recovery in Celiac Disease-A Systematic Review. Nutrients. 2015 May 7;7(5):3347-3369. [↩]
A nti-endomysium antibodies (EmA) are connective tissue autoantibodies produced in persons who have inherited the genes for celiac disease, an autoimmune disease, and are reacting to gluten in their diet.
Autoantibodies are abnormal in that they attack the body’s own tissue.
Q: What is endomysium?
A: Endomysium is the delicate connective tissue that surrounds individual muscle fibers. The autoantigen, or target, that stimulates the autoimmune response is the naturally occuring enzyme in endomysium called tissue transglutaminase (tTG), or more specifically tranglutaminase-2 (TG2). Anti-tissue transglutaminase antibodies recognize the same antigen as EmA, from which they differ in terms of detection method.
Anti-endomysium antibodies (EmA) are tested by the indirect immunofluorescence method and directed against “reticulin-like” fibres in connective tissue around smooth muscle fibres in the esophagus, liver, stomach, and bladder of monkeys, in the sections of the jejunum and kidneys of rats and in sections of the human umbilical cord. In comparison, for the determination of anti-tissue transglutaminase IgA and IgG antibodies, ELISA with human extractive or recombinant transglutaminase is recommended.1
EmA‐binding patterns in serum samples from patients with celiac disease have proved to be exclusively TG2‐targeted and the correlation between EmA and TG2 antibodies is therefore good. Evidence shows that celiac autoantibodies are produced in the small‐bowel mucosa.2
What Are Anti-Endomysium Antibodies In Celiac Disease and/or Gluten Sensitivity?
Sources:
Trigoni E, Tsirogianni A, Pipi E, Mantzaris G, Papasteriades C. Celiac disease in adult patients: specific autoantibodies in the diagnosis, monitoring, and screening. Autoimmune Dis. 2014;2014:623514. doi: 10.1155/2014/623514. [↩]
Salmi TT, Collin P, Korponay-Szabó IR, Laurila K, Partanen J, Huhtala H, Király R, Lorand L, Reunala T, Mäki M, Kaukinen K. Endomysial antibody‐negative coeliac disease: clinical characteristics and intestinal autoantibody deposits.Gut. 2006 Dec;55(12):1746-53. [↩]
Thiamin, also called vitamin B1, is an essential vitamin that is required to convert foodstuffs into energy and for the health and proper functioning of the nervous, muscular and cardiovascular systems.
In the bloodstream, 90% of active thiamin (TPP) is carried by red blood cells while 10% is transported in the bloodstream as free thiamin and thiamin monophosphate bound mostly to the protein albumin.
In the diet, animal food sources provide active thiamin while plant food sources provide free thiamin.1
Urinary excretion of thiamin cannot be detected when vitamin intake is below the required levels. On the other hand, when intake exceeds saturation in the body, thiamin and/or its metabolites are actively excreted into urine to prevent excessive toxicity of the vitamins.2
In patients who have thiamin deficiency, the most common conditions that bring them to a clinician include neuropathies, depression, myalgia, cardiomyopathies or takes diuretics and/or eat a high carbohydrate diet.3
What Is Thiamin Deficiency In Celiac Disease and/or Gluten Sensitivity?
Shibata K, Hirose J, Fukuwatari T. Relationship Between Urinary Concentrations of Nine Water-soluble Vitamins and their Vitamin Intakes in Japanese Adult Males. Nutr Metab Insights. 2014 Aug 5;7:61-75. doi: 10.4137/NMI.S17245. [↩]
Vitamin D is the principle regulator of calcium homeostasis (balance) in the body. This “vitamin” is really a prohormone, meaning it acts like a hormone but is not. Vitamin D does, however, contain cholesterol in its molecular structure like steroid hormones.
The physiological importance of vitamin D encompasses much more than the regulation of bone metabolism although this is a mighty function.
Q: How does vitamin D regulate bone metabolism?
A: In regulation of bone metabolism, vitamin D works in three ways: 1) enables active absorption of calcium from the small intestine, 2) enhances reabsortion of calcium by the kidneys that would otherwise be excreted in urine, and 3) plays an active role in skeletal development and bone mineralization. Mineralization gives strength to living bone tissue.
Vitamin D interacts with receptors within cells to effect transcriptional changes in many cell types including those in gut, bone, breast, prostate, brain, skeletal muscle, and the immune system.1
In regards to the essential role of vitamin D in muscle tissue, it has been recently shown that vitamin D regulates both muscle function and structure of primary myofibers.2
Vitamin D is converted in the body to a molecule that is biologically active. The active form is 1,25-dihydroxyvitamin D, usually referred to as vitamin D3. About 80% comes from sun exposure and the remaining from food.
Vitamin D3 is synthesized in the skin from 7-dehydrocholesterol via photochemical reactions requiring UV light (sunlight). That is, light that contains energy from the sun is incorporated into molecules of 7-dehydrocholesterol in the underlying dermis of skin to make this vitamin. This is why inadequate exposure to sunlight contributes to vitamin D deficiency.
Blood concentration of 25(OH)D is the best indicator of vitamin D status. It reflects vitamin D produced in the skin and that obtained from food and supplements and has a fairly long circulating half-life of 15 days.3
What Is Vitamin D Deficiency In Celiac Disease and/or Gluten Sensitivity?
Sources:
McCarty DE, Chesson AL Jr, Jain SK, Marino AA. The link between vitamin D metabolism and sleep medicine. Sleep Med Rev. 2014 Aug;18(4):311-9. doi: 10.1016/j.smrv.2013.07.001. [↩]
Girgis CM, Mokbel N, Cha KM, Houweling PJ, Abboud M, Fraser DR, Mason RS, Clifton-Bligh RJ, Gunton JE. The vitamin D receptor (VDR) is expressed in skeletal muscle of male mice and modulates 25-hydroxyvitamin D (25OHD) uptake in myofibers. Endocrinology. 2014 Sep;155(9):3227-37 [↩]
U rticaria is an immune based skin disorder characterized by multiple eruptions of well-demarcated edematous, intensely pruritic (itchy) plaques that may be small or reach the diameter of many centimeters with surrounding erythema (redness) each lasting less than 24 hours.1
Q: What is the immune reaction in hives?
A: Hives form when, in response to histamine, blood plasma leaks out of small blood vessels in the skin. Histamine is a chemical released from specialized cells along the skin’s blood vessels. Allergic reactions, chemicals in certain foods, insect stings, sunlight exposure, or medications can all cause histamine release.2
In many patients, in spite of extensive investigations, the cause remains elusive. The term idiopathic is often used to denote this category. Now it is known that autoimmunity is the cause of chronic urticaria in 50% of cases.
Treatment is generally started with nonsedating antihistamine in the daytime and sedating antihistamine in the night.3
What Is Chronic Urti caria In Celiac Disease and/or Gluten Sensitivity?
Sources:
Scala E, Giani M, Pirrotta L, Guerra EC, DePita O, Puddu P. Urticaria and adult celiac disease. Allergy. 1999;54:1008-9. [↩]
Niacin is an essential water-soluble B vitamin that is required by all cells of the body.
During digestion of food containing it, niacin (the form in food) is changed in the small intestines to the active form niacinamide (niacin plus an amide group), which is then absorbed into the bloodstream.
Niacinamide is converted by the body into co-enzymes which are present in all cells. These are niacinimide adenine dinucleotide (NAD) and NADP. NADP is formed when the body adds a phosphate to NAD.
Q: How do these enzymes work?
A: These enzymes function in oxidation-reduction reactions essential for release of energy from carbohydrates, fats, and proteins and are needed as components for more than 200 enzymes involved in metabolism.
In addition to producing energy, niacinamide is essential for healthy skin and the mucosal lining of the digestive tract, normal functioning of the brain and nervous system, and production of steroid hormones in adrenal glands and hormones in sex glands. Functions are more fully described below.
Urinary excretion of niacin cannot be detected when vitamin intake is below the required levels. On the other hand, when intake exceeds saturation in the body, the vitamin and/or its metabolites are actively excreted into urine to prevent excessive toxicity of the vitamins.1
What Is Niacin Deficiency In Celiac Disease and/or Gluten Sensitivity?
Sources:
Shibata K, Hirose J, Fukuwatari T. Relationship Between Urinary Concentrations of Nine Water-soluble Vitamins and their Vitamin Intakes in Japanese Adult Males. Nutr Metab Insights. 2014 Aug 5;7:61-75. doi: 10.4137/NMI.S17245. eCollection 2014. [↩]
Reversible hypertension is a pressure disorder of arteries associated with increased systemic (body wide) blood vessel resistance to blood flow due to endothelial (cell) dysfunction of arterial blood vessels that can improve with nutritional treatment.
Hypertension itself is defined as a systolic blood pressure (SBP) of 140 mm Hg (mercury) or greater and/or diastolic blood pressure (DBP) of 90 mm Hg or greater.
Q: What is blood vessel (vascular) resistance to blood flow?
A: Vascular resistance to blood flow means the arteries carrying blood away from the heart cannot relax or dilate when needed to lower blood pressure but stay constricted, which in turn, keeps the pressure high.
Here’s an analogy: if you replace your garden hose having a one inch inside diameter with one that has a smaller half inch diameter and open the water valve as usual, the result would be water shooting out with more force.
What Is Reversible Hypertension In Celiac Disease and/or Gluten Sensitivity?
![Grade_1_hypertension[1]](https://glutenfreeworks.com/health/wp-content/uploads/sites/10/Grade_1_hypertension1.jpg)