Lately, it seems like more and more celebrities and professional athletes are openly talking about going gluten free. Whether it’s due to a diagnosis of celiac disease or a gluten sensitivity, or simply because they want to get healthy, many of them have noted a weight loss as part of the benefits they’ve been seeing. Then why is it, that so many doctors and specialists will dismiss a diagnosis of celiac disease in a patient simply because the patient is not underweight?
In a recent article by Sonia Kupfer, MD, the belief that people with un-diagnosed celiac disease are all underweight is revealed to
Close-up shows inflammation and infected patches on roof and back of the mouth caused by candidiasis. Uvula is swollen, hanging near the tongue. Courtesy: Wikimedia.
What Is Candida Albicans Infection?
Candida albicans infection, called candidosis or candidiasis, is an opportunistic invasion of mucous membrane or skin by candida albicans, an endogenous yeast found in 40 to 80% of normal human beings. A former name for this small, budding fungus is monilia albicans.
Opportunistic means that yeast living on mucosal and skin surfaces does not invade (infect) unless these tissues become unhealthy and therefore cannot protect themselves.
Q: How does candida albicans cause infection?
A: Candida albicans lives on the mucosal surfaces and skin in most people without causing infection (colonizes) because of our normal defenses against invasion. In fact, candida albicans is a very effective colonizer of humans. For example, Russell and Lay found that 47% of 1-month-old infants were orally colonized with candida albicans, and 49% were colonized with other fungi.
During growth within the intestinal tract, the organism senses pH (acidity), oxygen, carbon sources, and the presence of surfaces allowing it to optimize gene expression for a particular environment. With these mechanisms for sensing, candida albicans is able to efficiently colonize humans in infancy.1
Candida Infection Of The Esophagus (White Area) On X-ray. Courtesy Radiology Assistant.nl
Lowered host defenses allow yeast already present on mucosal and skin surfaces to take advantage and can grow rapidly, becoming pathogenic (disease producing) so that infection results.
Infection is characterized by superficial, irregular white patches on mucosal surfaces and possible invasion of the bloodstream by a filamentous form (thread-like structures) that can rapidly develop.
Candida albicans is unique among oral pathogens in its ability to invade cornified layers of stratified squamous epithelium of the tongue, mouth surfaces, hard and soft palate, esophagus, and gut. Stratified squamous epithelium is the tough surface cells that ordinarily protect underlying tissues from damage or invasion by microbes.
Candida albicans is also capable of invading the lungs and causing pneumonia and septicemia, which is the spread of infection into the bloodstream.
Here is a time honored simple do-it-youself test for infection of the mouth or throat: First thing in the morning before brushing your teeth or eating, fill a small see through glass with water then gently spit onto the surface. If after an hour the spit remains on the water surface, it is unlikely you have candida in the mouth. If it grows legs downward, it indicates that yeast is growing. If the spit sinks to the bottom, you have this problem. Yeast in the mouth can quickly travel down the esophagus and into the gut.
Medical diagnosis. Difinitive diagnosis for the oral cavity is made by your clinician by swabbing the areas of your mouth and/or throat and viewing under a microscope for evidence of candida.
Infections of the esophagus and gut require inspection by gastroscopy or endoscopy procedure and the taking of samples to be examined under microscope. This examination also give the opportunity to rule out other problems. Barium swallow can show the extent of infection and any disfiguration of the esophagus that results.
What Is Candida Albicans Infection In Celiac Disease and/or Gluten Sensitivity?
Sources:
Rosenbach A, Dignard D, Pierce JV, Whiteway M, Kumamoto CA. Adaptations of Candida albicans for growth in the mammalian intestinal tract. Eukaryot Cell. 2010 Jul;9(7):1075-86. doi: 10.1128/EC.00034-10. Epub 2010 Apr 30. [↩]
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?
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. [↩]
“I should look like Brad Pitt.” Back before I went gluten free, I remember looking in the mirror and saying these exact words to myself. I was working out 5 to 6 days a week,…
A Gluten Free Works Notification for Health Guide Subscribers Is this email not displaying correctly? View it in your browser. Subscriber Newsletter Dear << Test First Name >>: Welcome to the Gluten Free Works Health…
Hypoglycemia means the level of glucose within cells is too low to meet metabolic needs of the body for this essential sugar.
Q: What are the metabolic needs for glucose?
A: Glucose is the most important simple sugar in human metabolism mainly because it is the primary source of energy for most cells of the body.
Energy contained in the glucose molecule is obtained by the body from its reaction with oxygen (oxidation). This oxidation reaction occurs in power producing mitochondria structures that are located within cells.1
Hypoglycemia is characterized by alterations in neurologic, metabolic and muscular functions:
Neurologic function because brain tissue is particularly dependent on glucose for energy,
Metabolic function of glucose-dependent tissues which include red blood cells, white blood cells, bone marrow, eye, inner heart of the kidney, and peripheral nerves because these tissues cannot metabolize fatty acids as an alternate source of energy, and
Muscle function because muscle cells continually require glucose for energy production.
Glucose is made available to cells through the regulating action of insulin, a hormone produced by specialized cells located on the surface of the pancreas.
What Is Hypoglycemia In Celiac Disease and/or Gluten Sensitivity?
I was looking back at old drafts of posts that I’ve written over the years but never published, and I found this rant on the 1200 calorie weight loss myth. Since it’s the last day of National Eating Disorders Awareness Week and the first day of National Nutrition Month, I figured it would be a good time to share it. (Editor’s note: Originally published March 1, 2014)
Not a week goes by that I don’t see a client who truly believes she/he needs to be following a 1200 calories diet to lose weight or be healthy. It seems to be the #1 nutrition myth.
Despite what the intertubes may say, a 1200 cal diet is not considered standard professional weight loss advice. Honest.There is, of course, plenty of bad advice and/or controversy out there, because that sells. There’s also a whole lot of standard nutrition advice that I heartily disagree with, but that’s another post. Take a look at
T etany is a painful feature of low blood calcium or low blood magnesium causing hyperexcitability of all nerves which in turn stimulates involuntary sudden, intermittent and repetitious tonic spasms of muscles. Tonic spasms are steady rather than jerky.
Causes include low function of the parathyroid glands which regulate calcium blood levels, vitamin D deficiency which inhibits calcium absorption from the gut that leads to calcium deficiency, and alkalosis.
In alkalosis, the chemical pH (acid/alkaline measure) of blood is too high, or alkaline, which inhibits adequate free calcium ions from being available for cell use.
Q: Why do low blood levels of calcium or magnesium cause muscles to spasm?
A: Calcium controls the readiness of muscle to respond to nerve stimulation. In muscle action, calcium and magnesium are minerals that oppose each other. Calcium allows a muscle to contract while magnesium allows it to relax. Inadequate levels of these opposing minerals affect the ability of muscles to properly function.
A simple test for tetany is called Trouseau’s named after the doctor who developed it. A blood pressure cuff is placed on an upper arm as usual and pumped up to a pressure sufficient to stop blood flow. The pressure must be held for 3 minutes. A positive result is shown in the above photo of carpopedal spasm: the wrist and hand flexes inward while the fingers extend (opposite of wrist and hand) and the thumb goes against the palm.
What Is Tetany In Celiac Disease and/or Gluten Sensitivity?
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Lately, it seems like more and more celebrities and professional athletes are openly talking about going gluten free. Whether it’s due to a diagnosis of celiac disease or a gluten sensitivity, or simply because they want to get healthy, many of them have noted a weight loss as part of the benefits they’ve been seeing. Then why is it, that so many doctors and specialists will dismiss a diagnosis of celiac disease in a patient simply because the patient is not underweight?
Not a week goes by that I don’t see a client who truly believes she/he needs to be following a 1200 calories diet to lose weight or be healthy. It seems to be the #1 nutrition myth.