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Obesity

KONICA MINOLTA DIGITAL CAMERAWhat Is Obesity?

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?

Amino Acid Deficiency (Essential)

phWhat Are Essential Amino Acids?

Amino acids are small molecules, or subunits, that link together in various combinations to make up big, complicated proteins. As such, amino acids are commonly referred to as “the building blocks” of proteins.

Q: How many amino acids are used in our body?

A: There are 20 amino acids that are used within our body to synthesize or produce our unique human proteins.  Of these amino acids,  9 are termed essential, meaning our bodies require them to live but cannot make them. Therefore, the essential amino acids must come from the food we eat, whether from plant or animal sources.

The essential amino acids include histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine.

What Is Deficiency Of Essential Amino Acids In Celiac Disease and/or Gluten Sensitivity?

Non-Alcoholic Fatty Liver Disease

Smooth muscle. Courtesy pathguy.com
Smooth Muscle. Courtesy pathguy.com

What Are Anti-Endomysium Antibodies?

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:
  1. 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. []
  2. 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. []

Gluten Sensitive Enteropathy (Active Celiac Disease)

canstockphoto17997339What Is Gluten Sensitive Enteropathy?

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:
  1. Murray JA, the widening spectrum of celiac disease. American Journal of Clinical Nutrition. Mar 1999; 69(3):354-365. []
  2. Murray JA, the widening spectrum of celiac disease. American Journal of Clinical Nutrition. Mar 1999; 69(3):354-365. []
  3. Johnston SD, Smye M, Watson RGP. Intestinal permeability and morphometric recovery in coeliac disease. Lancet. Jul 28, 2001;358(9278):259, 2p. []
  4. 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 []
  5. 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. []
  6. 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. []
  7. 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. []
  8. 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. []
  9. 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. []

Low Plasma Proteins

Image of a protein molecule.
Image of a protein molecule.

What Are Low Plasma Proteins?

Low plasma proteins found in blood indicates an abnormal blood level.

Plasma proteins are any of the proteins that constitute about 6% to 7% of the blood plasma in the body. They include albumin, fibrinogen, prothrombin, and the gamma globulins. All plasma proteins except the gamma globulins are produced in the liver.1

Q: Which protein is most abundant in blood?

A: Of the dozens of plasma proteins, albumin makes up more than half. Albumin level is the most frequently tested in the presence of weight loss and other signs of poor nutrition. Albumin helps maintain water balance that affects osmotic pressure, increase blood viscosity, and helps maintain blood pressure.1

Other commonly tested blood proteins are globulins which make up about a third of plasma proteins. Lab reports show the ratio between albumin and globulin, as well as, their individual values. Fibrinogen, essential for clot formation, makes 7% of plasma proteins while regulatory proteins, which include enzymes and hormones, make up 1%.

What Are Low Plasma Proteins In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Mosby’s Medical Dictionary, 8th edition. © 2009, Elsevier. [] []

Muscle Weakness 

Microscopic View of Gastric  Biopsy Showing a Collagen Band Under the Surface Mucosal Cells. Courtesy Gastrolab.com
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:
  1. Jain R, Chetty R. Collagenous gastritis. Int J Surg Pathol. 2010 Dec;18(6):534-6. doi: 10.1177/1066896908329588. Epub 2008 Dec 22. []
  2. 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. []

Cataracts

Glucose Meter Reading Showing Hypoglycemia. Courtesy Abbott.
Glucose Meter Reading.Courtesy Abbott.

What Is Diabetic Instability?

D iabetic instability, also called brittle diabetes, is poor control of blood sugar characterized by frequent rise (hyperglycemia) and fall (hypoglycemia). These fluctuations can be life-threatening and cause unnecessary complications.

Q: What are complications in diabetes?

A: Complications of diabetes include any/all of the following:

  • Peripheral neuropathy that causes burning, numbness, or tingling in the extremities.
  • Skin infections and ulcers that do not heal and can lead to amputation of toes, feet or legs.
  • Damage to retina that can progress to blindness.
  • Cataracts and glaucoma that impair vision and can cause blindness.
  • Increased susceptibility to serious infections of the genitourinary tract, lung and upper respiratory tract that can become systemic and life-threatening.
  • Kidney disease that can lead to kidney failure.
  • Heart disease that can lead to heart failure.
  • Vascular disease that can lead to stroke.
  • Impaired motility in digestive tract that can lead to dyspepsia and constipation.
  • Pregnancy complications.
  • Shortened life expectancy.

The main causes of brittleness include malabsorption, certain drugs (alcohol, antipsychotics), defective insulin absorption or degradation, defect of hyperglycemic hormones especially glucocorticoid and glucagon, and above all delayed gastric emptying as a result of autonomic neuropathy.1

What Is Diabetic Instability In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Vantyghem MC, Press M. Management strategies for brittle diabetes. Ann Endocrinol (Paris). 2006 Sep;67(4):287-96. []

Nails, White Spots And White Bands

Cardiomegaly-Heart-frontWhat Is Cardiomegaly?

C ardiomegaly is a non-inflammatory disorder of the myocardium (heart muscle) causing the heart to enlarge.

Q: What happens when the heart enlarges?

A:The heart enlarges because excessive growth of muscle tissue (hypertrophy) thickens the heart walls which in turn reduces the size of the lower chambers (ventricles) and impairs the filling of the heart chambers with blood. In consequence, the heartbeat quickens.

Also, the enlarging heart encroaches on lung space which impairs their ability to expand with inspiration of air.

Cardiomegaly can result in heart failure because of inability to pump sufficient blood for the needs of the body and ventricular arrhythmias (irregular or missed beats) that can stop the heart. An echocardiogram, which is a test that uses sound waves to produce a picture of the heart, is used to detect and diagnose cardiomegaly.

What Is Cardiomegaly In Celiac Disease and/or Gluten Sensitivity?

Bitot’s Spots 

 

Jaundice, or yellowing of the skin and sclera of eyes.
Jaundice, or yellowing of the skin and sclera of eyes, is a symptom of autoimmune hepatitis.

What Is Autoimmune Hepatitis?

A utoimmune hepatitis is an autoimmune attack against liver cells that is characterized by inflammation and results in chronic liver disease which includes low blood albumin and cirrhosis.

Autoimmune hepatitis is diagnosed by detection of autoantibodies in blood and liver biopsy.

Q: What is cirrhosis?

A: Cirrhosis is a degenerative process of the liver that can be fatal. Normal lobular liver structure is distorted and replaced with nodules of regenerating liver cells separated by bands of fibrous tissue that cannot properly carry out liver function and block the necessary flow of blood through the liver, ending in liver failure.

The liver is the largest organ within the body and lies mostly in the upper part of the abdomen on the right side just under the diaphragm. About 70% of liver tissue is made up of cube shaped cells called hepatocytes that do the main work of the liver. Other cells form structure and are arranged in single layers around blood vessels, sinusoids, and bile ducts.

Bile ducts carry bile, a greenish brown liquid made by the liver, to the gall bladder for storage until needed to aid in the digestion and absorption of fat from the small intestine. Bile emulsifies fat eaten in the diet so that the pancreatic enzyme called lipase can break it down into its fatty acid and glycerol components.

The liver is a very busy organ, carrying out over 500 metabolic processes! Nutritionally, it is the first to receive all the blood carrying nutrients freshly absorbed from the digestive tract. Hepatocytes then convert the nutrients to provide the body with energy, a host of amino acids as building blocks for numerous cell activities, and proteins such as albumin and fibrinogen. In fact, hepatocytes build the structural proteins for the liver itself. Imagine the array of nutrients the liver uses and keeps at its disposal for its metabolic functions. Included in liver storage are vital vitamins and minerals such as vitamin A and vitamin B12.

As a detoxifier, Kupffer cells located in the sinusoids act like amoebas to engulf and digest unwanted matter. As a blood cleanser, the liver removes waste products produced by normal metabolism and toxic substances and rids it by preparing these substances for elimination in urine, such as ammonia converted to urea, and/or excreting them in bile for eventual elimination in stool. Bile is continually made by the liver from phospholipids salt, cholesterol, aging blood cells it removes from circulation.

Autoimmune hepatitis is classified into several types. Type 1 autoimmune hepatitis is the most common form in North America. Type 1 can occur at any age; however, it most often starts in adolescence or young adulthood. People with type 1 autoimmune hepatitis commonly have other autoimmune disorders (see listed below).

Type 2 autoimmune hepatitis is less common and occurs more often in children than adults. People with type 2 can also have any of the autoimmune disorders (see listed below).

Both types of autoimmune hepatitis are treated with prednisone, a corticosteroid hormone to control inflammation and reduce the body’s immune activity against the liver.1

What Is Autoimmune Hepatitis In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. National Digestive Diseases Information Clearinghouse []