It can be challenging enough on gluten-free diet, but what if you eat a vegetarian or vegan diet?
It’s well established that there are health benefits to reducing the amount of meat in the diets of most Americans, and the lifestyle has appeal for some people based on ethical and/or environmental reasons. Fortunately, with extra planning, a well-rounded and delicious gluten-free vegetarian diet is possible.
The good news is that many vegetarian staples, like beans, lentils, tofu, dairy, nuts, seeds and eggs are already naturally gluten-free. And some of the best sources of vegetarian and vegan protein are gluten-free pseudo-grains, such as quinoa, buckwheat and amaranth. Also, grains, such as millet, teff and sorghum are very nutritious. In addition to protein and fiber, they all have other vital nutrients, like
Endoscopic Image of Crohn’s Disease Showing Deep Ulceration in the Sigmoid Colon.
What Is Crohn’s Disease?
Crohn’s disease is an inflammatory bowel disease characterized by patchy inflamed areas involving the full thickness of the intestinal wall that can occur anywhere in the intestinal tract, in addition to, mucosal disease.
In Crohn’s disease there is ongoing immune activation which produces inflammation and ulceration but the cause is not known and the severity varies among patients. At diagnosis of Crohn’s disease, factors predictive of subsequent 5-year aggressive disease are an age below 40 years, the presence of perianal disease, and the initial requirement for steroids.1
Dysbiosis is a factor that develops in and worsens Crohn’s disease and stress is a factor in both of these conditions. Psychological stress activates multiple physiological processes aimed at maintaining balance within the body. These physiological processes also have the capacity to influence the composition of microbial communities in the digestive tract, and research now indicates that exposure to stressful stimuli leads to gut microbiota dysbiosis.2
While the relative abundance of many different bacterial types can be altered during stressor exposure, findings in nonhuman primates and laboratory rodents, as well as humans, indicate that bacteria in the genus Lactobacillus are consistently reduced in the gut during stress.2
Q: Is there a cure for Crohn’s disease?
A: Presently, Crohn’s disease cannot be cured. This condition has a course of remissions, when symptoms subside, and flares, when symtpoms get worse. Treatment is aimed to reduce flares and promote remission.
What Is Crohn’s Disease In Celiac Disease and/or Gluten Sensitivity?
Sources:
Beaugerie L, Seksik P, Nion-Larmurier I, Gendre JP, Cosnes J. Predictors of Crohn’s disease. Gastroenterology. 2006;130:650–656. [↩]
Galley JD, Bailey MT. Impact of stressor exposure on the interplay between commensal microbiota and host inflammation. Gut Microbes. 2014 May 1;5(3):390-396. Epub 2014 Apr 1. [↩] [↩]
Underarm showing skin darkening, which is a feature of Addison’s Disease
What Is Primary Addison’s Disease?
Addison’s disease is an autoimmune destruction of the adrenal glands by autoantibodies that target the adrenal cortex, or outer part of these glands, and is characterized by a slow progressive failure of the adrenal glands to adequately produce its steroid hormones.
Symptoms of adrenal fatigue or failure may not develop until the majority of adrenal tissue is destroyed. When untreated, progression leads to coma, called Addisonian crisis, which is a medical emergency.
There are two adrenal glands each located on top of a kidney and enclosed in a connective tissue capsule. Each is a small, triangular shape that is made of two parts: the outer region and the inner region.
The inner region, called the adrenal medulla, produces epinephrine and norepinephrine chemicals that are needed to deal with stress.
The outer region, called the adrenal cortex, produces adrenocortical (steroid) hormones and releases them into the bloodstream in response to pituitary stimulating hormone from the brain.
Q: What is the function of steroid hormones produced by the adrenal glands?
A: Functions of the three steroid hormones produced by the adrenal glands are:
Glucocorticoids restrain inflammation and metabolism of carbohydrates, fats and proteins to maintain a normal glucose blood level. The major glucocorticoid is hydrocortisone.
Mineralocorticoids regulate the retention and excretion of fluids and electrolytes by the kidneys. The most important mineralocorticoid is aldosterone.
Androgen (testosterone) is a male sex hormone.
Secondary adrenal insufficiency may develop from other causes that are not immune related such as chronic infections, tumor, and medications.
What Is Addison’s Disease In Celiac Disease and/or Gluten Sensitivity?
Calcium is the most abundant mineral in the body, with 99% residing in teeth and bones where it constitutes 40% of skeletal bone weight along with 45% phosphorus.
As a component of hard tissues, calcium fulfills a structural role to maintain body size and acts as attachments for musculoskeletal tissues.
Q: What does the non-skeleton calcium do in the body?
A: The remaining 1% of calcium is present in blood and soft tissues. Calcium levels in the blood are maintained within very strict limits by dietary intake, hormonal regulation and a rapidly exchangeable pool in bone tissue. The many important functions are described below.
What Is Calcium Deficiency In Celiac Disease and/or Gluten Sensitivity?
Obesity is an inflammatory metabolic disorder that is characterized by body mass index greater than 30% resulting from excessive body fat stored in adipose tissue.
Q: What is body fat?
A: Body fat is part of the body that functions as a reserve of stored energy. It is composed of fat cells, called adipocytes, having thin membranes between these cells. Adipocytes expand to store fat and shrink as fat is released as needed into the bloodstream for other body cells to use for metabolizing energy.
Each adipocyte contains a drop of triglyceride which is a type of lipid (fat). Triglycerides are a normal component in the bloodstream and, as such, are transported wherever needed as a form of energy. Excess triglycerides are the form of fat that is stored.
Initially, fat that is eaten in the diet is changed by digestive enzymes into the triglyceride form which is a molecule composed of three fatty acids and glycerol. Triglycerides are then absorbed through the small intestinal wall to be delivered to the liver. Of note, the liver can make triglycerides from excess protein and carbohydrates eaten in a meal, especially sugar and alcohol. The liver on the other hand makes cholesterol from triglycerides.
Triglyceride levels in the blood generally increase as weight increases. It is thought that an elevated blood triglyceride level hampers the body’s ability to feel full or satisfied with food that is eaten. Elevated triglyceride levels also increase the risk of clot formation because they cause the blood to become thicker. A normal triglyceride blood level is 150 mg/dL.
The causes of obesity are complex and varied. Those related to gluten sensitivity are discussed below.
What Is Obesity In Celiac Disease and/or Gluten Sensitivity?
What Is Irritable Bowel Syndrome? I rritable bowel syndrome (IBS) is a motility disorder without anatomic cause involving the entire gastrointestinal tract that is characterized by these four features: 1) Abdominal pain usually relieved by…
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 [↩]
Microscopic View of Gastric Biopsy Showing a Collagen Band Stained Pink Under the Surface Mucosal Cells. Courtesy Gastrolab.com
What Is Collagenous Gastritis?
C ollagenous gastritis is a rarely reported stomach disorder characterized by the deposition of a subepithelial collagen band and accompanying inflammatory infiltrate in the stomach wall.
A subepithelial collagen band means that collagen, a tough fibrous protein, has abnormally accumulated under the surface layer of epithelial cells which form the mucosa lining the stomach.
The surface mucosa may remain intact and not show lymphocytosis and/or gastritis on endoscopic examination or it may become stripped off and bleed from entrapped capillaries. Biopsy is necessary to diagnose collagenous gastritis.1
Q: Why does collagen become deposited under the surface lining of the stomach?
A: It is thought that collagen deposition is preceded by inflammation and tissue damage. However, the natural history and pathogenesis of collagenous gastritis remain unclear.2
What Is Collagenous Gastritis In Celiac Disease and/or Gluten Sensitivity?
Sources:
Jain R, Chetty R. Collagenous gastritis. Int J Surg Pathol. 2010 Dec;18(6):534-6. doi: 10.1177/1066896908329588. Epub 2008 Dec 22. [↩]
Leung ST, Chandan VS, Murray JA, Wu TT. Collagenous gastritis: histopathologic features and association with other gastrointestinal diseases. Am J Surg Pathol. 2009 May;33(5):788-98. doi: 10.1097/PAS.0b013e318196a67f. [↩]
Gluten sensitive enteropathy is active celiac disease characterized by inflammation of the small intestinal mucosa that results from an inherited immunologic intolerance to ingested gluten.
Q: What does the inflammation do to the mucosa in the small intestine?
A: Inflammation is a cell level immune response to gluten that has these effects on the mucosa:
Damages the barely visible villi (multitudinous finger-like structures) by causing atrophy or loss.
Likely affects the structural support and microcirculation of the villus, leading to collapse of the villus.
Elongates the crypts between villi. The thickening of the crypt is not so much a response to loss of surface enterocytes but represents inflammation of the mucosa.1
Increases round cells in the lamina propria and surface epithelial cells leaving few, irregular microvilli (brush border) on the surface of villi.
Damage is most intense in the duodenum and decreases toward the large intestine.
The extent of the damage to the intestine determines the malabsorptive consequences of the disease. Both gastric and small intestinal permeability are disrupted in patients with celiac disease.2
Relationship between active celiac disease and intestinal permeability: There is a clear association between degree of mucosal damage and the intestinal-permeability ratio, and a normal ratio generally implies near-normal small intestinal structure. A raised intestinal permeability of the mucosal lining (leaky gut) could predispose to a high absorption of gluten and exacerbate an existing lesion and hence convert a latent to an overt enteropathy.3
Relationship between active celiac disease and tight junction proteins: A study of intestinal permeability showed that the expression of all junction proteins of the small intestinal lining (occludin, claudin 3, zonula occludens 1, and E-cadherin) was already decreased in early stage celiac disease when compared with non-celiac controls, showing leaky gut and confirming the above earlier study by Johnston et al. Junction protein expression correlated positively with mucosal villus structure and negatively with the number of intraepithelial lymphocytes (IELs), the intensity of small-intestinal autoantibody deposits, and serum autoantibodies. The expression of claudin 3 showed a negative correlation with diarrheal score.4
Relationship between active celiac disease and inflammation. In celiac disease there is an over production of inflammatory interleukin-15 (IL-15) which inhibits the correct removal of damaged intraepithelial lymphocytes caused by the reaction to gluten. Serum levels of IL-15 are directly correlated with the seriousness of tissue damage.5
Relationship between active celiac disease and gut microbiota. Results of a study investigating intestinal microbiota (normal bacterial residents) in patients with celiac disease suggest that with lower levels of the genus bifidobacteria, celiac patients have an imbalance in the intestinal microbiota even while on a gluten-free diet. This fact could favor the pathological process of the disorder. The concentration of bifidobacteria per gram of feces was significantly higher in healthy subjects (2.5 ± 1.5 x107 CFU/g) when compared to celiac patients (1.5 ± 0.63 x108 CFU/g).6
Relationship between active celiac disease and endoscopy technique. The most severe degree of villous atrophy was detected when distal duodenal biopsy specimens were taken in addition to a duodenal bulb biopsy specimen from either the 9- or 12-o’clock position (96.4% sensitivity; 95% CI, 79.7%-100%). The difference between the 12-o’clock position biopsy and the 3-o’clock position biopsy in detecting the most severe villous atrophy was 92% (24/26 patients) versus 65% (17/26 patients).7
Relationship between active celiac disease and diet adherence. Patients with consistent gluten free diet adherence experience symptomatic responses to dietary gluten (SRDG) faster and more severe in comparison to their prior gluten exposure possibly demonstrating an adept immunological response. Anxiety and depression also enhance the speed of symptom onset and co-existing visceral hypersensitivity is a risk factor for severe reactions to dietary gluten.8
Relationship between active celiac disease and atrial fibrillation: Patients with celiac disease, verified by intestinal biopsy, are at increased risk of atrial fibrillation. This observation is consistent with previous findings that elevation of inflammatory markers predicts atrial fibrillation.9
How Prevalent Is Gluten Sensitive Enteropathy?
Sources:
Murray JA, the widening spectrum of celiac disease. American Journal of Clinical Nutrition. Mar 1999; 69(3):354-365. [↩]
Murray JA, the widening spectrum of celiac disease. American Journal of Clinical Nutrition. Mar 1999; 69(3):354-365. [↩]
Johnston SD, Smye M, Watson RGP. Intestinal permeability and morphometric recovery in coeliac disease. Lancet. Jul 28, 2001;358(9278):259, 2p. [↩]
Rauhavirta T, Lindfors K, Koskinen O, Laurila K, Kurppa K, Saavalainen P, Mäki M, Collin P, Kaukinen K. Impaired epithelial integrity in the duodenal mucosa in early stages of celiac disease. Transl Res. 2014 Sep;164(3):223-31. doi: 10.1016/j.trsl.2014.02.006 [↩]
Stazi AV, Trinti B. Selenium status and over-expression of interleukin-15 in celiac disease and autoimmune thyroid diseases. Ann Ist Super Sanita. 2010;46(4):389-99.DOI: 10.4415/ANN_10_04_06. [↩]
Golfetto L, de Senna FD, Hermes J, Beserra BT, França Fda S, Martinello F. Lower bifidobacteria counts in adult patients with celiac disease on a gluten-free diet. Arq Gastroenterol. 2014 Apr-Jun;51(2):139-43. [↩]
Kurien M, Evans KE, Hopper AD, Hale MF, Cross SS, Sanders DS. Duodenal bulb biopsies for diagnosing adult celiac disease: is there an optimal biopsy site? Gastrointest Endosc. 2012 Jun;75(6):1190-6. doi: 10.1016/j.gie.2012.02.025. [↩]
Barratt SM, Leeds JS, Sanders DS. Factors influencing the type, timing and severity of symptomatic responses to dietary gluten in patients with biopsy-proven coeliac disease. J Gastrointestin Liver Dis. 2013 Dec;22(4):391-6. [↩]
Emilsson L, Smith JG, West J, Melander O, Ludvigsson JF. Increased risk of atrial fibrillation in patients with coeliac disease: a nationwide cohort study. Eur Heart J. 2011 Oct;32(19):2430-7. doi: 10.1093/eurheartj/ehr167. [↩]
Reproduction of a lithograph plate showing inside of the stomach from Gray’s Anatomy. Courtesy Wikipedia Commons.
What Is Delayed Gastric Emptying?
D elayed gastric emptying is a stomach motility or movement disorder characterized by abnormally slow movement of gastric contents from the stomach through the pyloric sphincter into the duodenum, causing dyspepsia.
Q: What determines how fast the stomach empties?
A: How fast the stomach empties depends on the pressure of strong coordinated muscle contractions in the top region of the stomach propelling chyme against resistance at the pylorus (base region of the stomach).
Chyme is food that has been dissolved and thoroughly mixed with stomach secretions.
In the digestion of carbohydrate, protein and fat, protein leaves the stomach first (1 hour), then carbohydrates (1 1/2 to 2 hours), and fat takes longest to digest (2-4 hours). Plain water is able to pass through the pylorus within 5 minutes.
What Is Delayed Gastric Emptying In Celiac Disease and/or Gluten Sensitivity?
