Bread is a Major Source of Maltose. Courtesy Johnson Mathey Catalyst
What Is Maltose Intolerance?
M altose intolerance is an enzymopathy (enzyme failure) characterized by inability of the gut to properly break down maltose sugar molecules in food due to low maltase enzyme activity of the small intestinal lining.
Q: What is maltose and maltase?
A: Maltose is a double sugar made up of two molecules of glucose and is derived from starch. Maltase is the enzyme required to digest or release glucose from maltose. Maltase is produced in the microscopic brush border (microvilli) at the base of villi.
Here’s what happens when maltose is not digested:
Undigested maltose cannot be absorbed into the body but remains inside the small intestine where it acts osmotically to draw an unnatural amount of water from the body into the intestine which produces diarrhea.
Additionally, normal gut bacteria ferment the abnormal abundance of unabsorbed maltose, thereby generating an abundance of short-chain fatty acids and hydrogen gas which result in bloating and pain.1
Positive response to a breath hydrogen test (BHT), involving 1 – 3 hours of time post ingestion of maltose test dose, signifies malabsorption in the small intestine and fermentation in the colon. If BHT is positive before 60 minutes, the result implies bacteria is abnormally present in the small intestine, causing fermentation there.
What Is Maltose Intolerance In Celiac Disease and/or Gluten Sensitivity?
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:
National Digestive Diseases Information Clearinghouse [↩]
Lost patch of hair at base of scalp due to alopecia areata. Courtesy Wikimedia,
What Is Alopecia Areata?
A lopecia areata is an autoimmune attack on hair follicles characterized by sudden hair loss involving scalp or beard, although any hairy area may be affected.
Areas of hair loss have a patchy pattern with sharply defined edges.
Q: Can all hair be affected?
A: All body hair may be lost, which is called alopecia universalis although this is uncommon.
In alopecia areata, white blood cells of the immune system attack the rapidly growing cells in the hair follicles. The affected hair follicles become small and drastically slow down hair production. Fortunately, the stem cells that continuously supply the follicle with new cells do not seem to be targeted. So the follicle always has the potential to regrow hair but regrowth is unpredictable.1
What Is Alopecia Areata In Celiac Disease and/or Gluten Sensitivity?
Pitting edema. Right photo shows that indent remains from pressing. Courtesy wikimedia.
What Is Edema?
E dema is an abnormal swollen condition of the skin characterized by excess extracellular fluid volume, meaning there is an increase of the fluid that normally surrounds cells. Edema may be hardly noticeable or it can become extensive.
Edema can have various appearances and can develop from various causes.
Q: What are the appearances and causes of edema?
A: Here are the appearances of edema:
Pitting edema. It is called pitting edema if when the skin is pressed with a finger, the indent remains. This edema results from fluid leaking out of the bloodstream into the surrounding tissues. Pitting edema can be a feature of many disorders including heart disease, kidney disease, vascular disease, cancer, and malnutrition.
Myxedema is a firm swelling or thickening of subcutaneous skin that does not pit, as seen in thyroid disease.
Here are causes of edema:
Local edema as a response to trauma or infection.
Lower extremity edema from poor circulation and malnutrition.
Edema in the lungs from right sided heart disease.
Abdominal edema from liver disease, intestinal disease.
Body wide edema from heart disease, kidney disease, thyroid disease.
What Is Edema In Celiac Disease and/or Gluten Sensitivity?
S ucrose intolerance is the inability to digest sucrose, a widely available sugar, while sucrosemia is the abnormal presence of sucrose in the bloodstream.
Q: Why cannot the body digest sucrose?
A: Sucrose, such as cane or beet sugar, is a double molecule sugar which must first be digested before being absorbed from the gut into the bloodstream. That is, sucrose must be split into its component single molecules of fructose and glucose, which are then properly absorbed.
The inability to properly digest sucrose results directly from low production and activity of sucrase in the small intestine. Sucrase is the specific enzyme that splits or digests sucrose.
Undigested sucrose does not remain idle. Its presence acts osmotically to draw water from the body into the intestine, causing watery diarrhea.
Meanwhile, microbiota (normal bacteria) in the colon eagerly ferment the abnormally present sucrose that arrives from the small intestine. Fermentation generates short-chain fatty acids and hydrogen gas, which results in bloating pain.1
In sucrosemia, sucrose molecules abnormaly pass through an unhealthy small intestinal lining and enter the bloodstream where there presence is abnormal. Sucrose in the blood is filtered out by the kidneys and excreted in urine.
Positive response to a breath hydrogen test (BHT), involving 1 – 3 hours of time post ingestion of sucrose test dose, signifies malabsorption in the small intestine and fermentation in the colon. If BHT is positive before 60 minutes, the result implies bacteria is abnormally present in the small intestine, causing fermentation there. Endoscopy is used to measure sucrase activity in tissue samples.
What Is Sucrose Intolerance And Sucrosemia In Celiac Disease and/or Gluten Sensitivity?
Arrows Show Abnormal Movement of Gastric Acid in Gastroesophageal Reflux Disease.
What Is Gastroesophageal Reflux Disease (GERD)?
G ERD is an upper digestive disorder that is characterized by a decrease in lower esophageal sphincter pressure (LES,) which allows the abnormal reflux or backflow of stomach contents into the esophagus. It is also called erosive esophagitis or reflux esophagitis and is the most common disorder of the esophagus.
The esophagus is a muscular tube that transports swallowed substances to the stomach. It begins at the cricoid cartilage (Adam’s apple) as a continuation of the pharynx and ends at the lower esophageal sphincter (LES).
The lower esophageal sphincter is located at the junction of the esophagus and the stomach. It functions like a circular band to tighten after food is ingested in order to prevent its going back up the esophagus.
Q: How does reflux damage the esophagus?
A: Damage to the lining of the esophagus is induced by the caustic, chemical action of acid and pepsin in gastric juice and, in severe cases, also bile salts, that back upwards from the stomach through an impaired LES. Gastric acid combined with pepsin or bile salts seems to be more harmful to the esophageal epithelial layers than gastric acid alone.1
Pepsin is normally produced by the stomach to dissolve protein in swallowed food. Unfortunately, when the esophagus is inflamed, pepsin will act on it to break down the protein in its sore wall. These sores are called erosions.
Importantly, refluxate to the esophagus in patients with acid suppression therapy is different from those in patients without. Higher levels of secondary bile acids are detected in patients with acid suppression therapy. Even if acid suppression is successful, weakly acidic reflux with bile acids can damage the esophagus.1
Damage starts at the luminal surface (inside where food passes through) of the squamous epithelium (tough surface cells) and progresses through the underlying layers into the submucosa.
One of the primary functions of the esophageal epithelium is to protect the underlying tissue from mechanical and chemical damage by acting as a barrier. The epithelial layers of the distal esophagus need to withstand reflux from the stomach and its contents. When the epithelium fails to protect the underlying tissue from this damage, it leads to erosions, esophagitis, and may lead to Barrett’s esophagus.1
Barrett’s esophagus and esophageal small cell cancer are severe complications of GERD that can be fatal.
GERD can result from too much, or more commonly, too little stomach acid.
What Is Gastroesophageal Reflux Disease (GERD) In Celiac Disease and/or Gluten Sensitivity?
Sources:
Chen X, Oshima T, Tomita T, Fukui H, Watari J, Matsumoto T, Miwa H. Acidic bile salts modulate the squamous epithelial barrier function by modulating tight junction proteins. Am J Physiol Gastrointest Liver Physiol. 2011 Aug;301(2):G203-9. doi: 10.1152/ajpgi.00096.2011. Epub 2011 May 26. [↩] [↩] [↩]
O bnoxious gas, or flatus, is gas that is not only offensive when passed but also lingers in the air longer than ordinary gas does.
Gas is a natural digestive product within the colon that is composed mainly of hydrogen and carbon dioxide gases. These gases are given off in the necessary bacterial breakdown of undigested fermentable food entering the colon from the small intestine.
Q: What makes gas obnoxious?
A: The production of obnoxious gas depends on the type and quantity of undigested food residue that is passed into the colon from the small intestine, dysfunctional motility instead of normal peristalsis, and dysbiosis. Dysbiosis is the condition of having unhealthy or insufficient populations of microbes responsible for digesting (fermenting) foodstuffs in the lower gut or colon.
Gases produced by intestinal microbes may modulate intestinal motor function (muscle movement) in individuals with functional bowel disease. Methane, produced by enteric bacteria in the human gut, is associated with slowed intestinal transit and constipation.1
What Is Obnoxious Gas In Celiac Disease and/or Gluten Sensitivity?
Sources:
Jahng J, Jung IS, Choi EJ, Conklin JL, Park H. The effects of methane and hydrogen gases produced by enteric bacteria on ileal motility and colonic transit time. Neurogastroenterol Motil. 2012 Feb;24(2):185-90, e92. doi: 10.1111/j.1365-2982.2011.01819.x. Epub 2011 Nov 20.
Methane is produced in the colon by intestinal methanogens (microbes) that metabolize hydrogen, one of the end products of normal anaerobic (meaning without oxygen) bacterial fermentation. Fermentation of the undigested starchy part of carbohydrates produces hydrogen in the intestine, which is the food for methane production by intestinal methanogens.
Hydrogen and methane are excreted in the flatus and in breath giving the opportunity to indirectly measure their production using breath testing. ((Triantafyllou K, Chang C, Pimentel M. Methanogens, Methane and Gastrointestinal Motility. J Neurogastroenterol Motil. 2014 Jan;20(1):31-40. Epub 2013 Dec 30. [↩]
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?
Unexpected weight loss is unintentional loss of body mass composition or inability to gain weight marked by decreased serum proteins and increased stool fat.1
What Is Unexpected Weight Loss In Celiac Disease and/or Gluten Sensitivity?
Chronic diarrhea is an intestinal motility disorder characterized by 1) alteration in stool formation causing loose to fluid movements and quantity of movements with or without abdominal pain and 2) interference with normal carbohydrate salvage by the intestinal microbe population.
The severity of diarrhea is determined by the frequency and quantity of fluid lost.
Q: What is carbohydrate salvage by microbes in the colon?
A: Carbohydrate salvage in the colon is the necessary process whereby billions of microbes normally present in the colon work to breakdown undigestible carbohydrate foodstuffs such as fiber that continually arrive from the small intestine.
The microbial action releases energy to the body that would otherwise be lost with defecation, generates short-chain fatty acids, and stimulates sodium and fluid absorption. In this important process, butyrate and proprionate are produced which nourish the colonocytes (cells that line the colon), and acetate is produced for the liver.
While diarrhea may be a common symptom of small bowel mucosal disease, the consequent malabsorption can lead to substantial malnutrition and nutrient deficiencies. The small intestine, unlike the colon, has been relatively inaccessible, and systematic evaluation is often necessary to identify and treat small intestinal mucosal diseases that lead to diarrhea. All patients with severe diarrhea or diarrhea associated with features suggestive of malabsorption may have a disease of the small intestinal mucosa that requires careful evaluation and targeted management.1
What Is Chronic Diarrhea In Celiac Disease and/or Gluten Sensitivity?
Sources:
Murray JA1, Rubio-Tapia A. Diarrhoea due to small bowel diseases. Best Pract Res Clin Gastroenterol. 2012 Oct;26(5):581-600. doi: 10.1016/j.bpg.2012.11.013. [↩]
