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Dementia

DementiaWhat Is Dementia?

Dementia is the term used to describe a group of symptoms that show significant deterioration of an individual’s intellectual and social abilities.

The deterioration in intellectual function is progressive and is characterized by memory and cognitive impairment involving deficits in reasoning, judgment, abstract thought, comprehension, learning, use of language, and task execution.

Some types of dementia can be reversed,  while most types of dementia are degenerative or nonreversible.

Q: What causes dementia?

A: There are  many differing causes of dementia.  Here are some causes according to nonreversible and reversible:

  • Nonreversible dementia may not be turned back due to these conditions:
  • Alzheimer’s disease is the most common type of degenerative dementia caused by abnormal protein structures in certain areas of the brain. 
  • Lewy body disease is a leading cause of dementia in elderly adults.
  • Vascular dementia due to many small strokes.
  • Medical conditions: Huntington’s disease, multiple sclerosis, infections that can affect the brain, such as HIV/AIDS and Lyme disease, Parkinson’s disease, Pick’s disease, and progressive supranuclear palsy.
  • Reversible dementia may be stopped or reversed if these conditions are found soon enough:
  • Brain injury.
  • Brain tumors.
  • Chronic alcohol abuse.
  • Changes in blood sugar, sodium, and calcium levels.
  • Changes that can occur with celiac disease, diabetes, thyroid disease, and other metabolic disorders.
  • Nutritional deficiencies.
  • Use of certain medications, including cimetadine and some cholesterol-lowering medications.1

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

Sources:
  1. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001748/ [↩]

Depression

What Is Postbulbar Duodenal Ulceration/Stenosis?

P ostbulbar duodenal ulceration is a chronic inflammatory disorder characterized by thickening of the intestinal lining with excoriation penetrating the muscularis mucosae (muscle layer of the intestine) associated with villous atrophy.

The ulcer is well-defined. Stenosis due to thickening of the area narrows the hollow inside of the duodenum which impairs passage of foodstuffs and may lead to obstruction.

Q: Is postbulbar duodenal ulceration painful?

A: Postbulbar duodenal ulceration may not cause symptoms but usually causes gnawing pain that is relieved by eating food. After eating there develops nausea and bloating.

Complications include obstruction, bleeding, and perforation of the duodenal lining. Ulcers do not usually become malignant.

What Is Postbulbar Duodenal Ulceration/Stenosis In Celiac Disease and/or Gluten Sensitivity?

Hypertension, Reversible

Grade_1_hypertension[1]What Is Reversible Hypertension?

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?

Homocysteine, Elevated Blood Level (Hyperhomocysteinemia)

A 3-D model of homocysteine.
A 3-D model of homocysteine.

What Is Elevated Homocysteine?

Elevated homocysteine in blood, called hyperhomocysteinemia, indicates an abnormal blood level of this transient amino acid.

Q: How does the level of homocysteine become abnormal?

A: In metabolism, homocysteine is briefly formed in the breakdown of the amino acid methionine. It is normally converted to cystathione and then to the amino acid cysteine by means of an enzyme that requires vitamin B6.

In the reverse, conversion of homocysteine to methionine requires an enzyme dependent on adequate folic acid and vitamin B12 levels.

Insufficient methionine levels and/or inefficiency in this process results in elevated homocysteine plasma levels that are toxic to blood vessels.

Folic acid, vitamin B12 and vitamin B6 are involved in the metabolic removal of homocysteine, but folic acid deficit occurs the most often.1

What Is Elevated Homocysteine In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Lim PO, Tzemos N, Farquharson CA, et al. Reversible hypertension following coeliac disease treatment: the role of moderate hyperhomocysteinaemia and vascular endothelial dysfunction. Journal of Human Hypertension. Jun 2002;16(6):411-5. [↩]

Vitamin B12 Deficiency

Clams Are Chock Full of Vitamin B12.
Lovely Clams For Vitamin B12.

What Is Vitamin B12?

Vitamin B12, also called cobalamin, is a highly complex vitamin that functions in two coenzyme forms: adenosylcobalamin and methylcobalamin.

These forms of the vitamin play important roles in the physical and chemical processes by which amino acids become proprionate, proprionate that becomes acetate,  and single carbons.

Q: Why are these steps important?

A: These steps are essential for normal function in the workings of all cells, especially for those of the digestive tract, bone marrow and nervous tissue.

Vitamin B12 is mainly excreted through bile into the duodenum (first part of the small intestine) for excretion in stool.1 However, if vitamin B12 is needed, it is reabsorbed in the ileum (end of the small intestine) while excess is excreted in stool and very little in urine.2

The blood level of vitamin B12 in healthy people ranges between 140 and 750 pg/ml.

What Is Vitamin B12 Deficiency In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. 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. [↩]
  2. Shinton N K. Vitamin B 12 and folate metabolism. Br Med J. Feb 26, 1972; 1(5799): 556–559. [↩]

Peripheral Neuropathy 

Microscopic Slide of Lymphocytic Colitis. Courtesy Quizlet.com
Microscopic  Slide of Biopsy Sample Showing Lymphocytic Colitis. Courtesy Quizlet.com

What Is Lymphocytic Colitis?

L ymphocytic colitis is a microscopic inflammation of the large intestinal mucosa with infiltration of lymphocytes (IELs)  that is characterized by non-bloody secretory diarrhea.

Secretory diarrhea describes bowel movements that consist of a large volume of liquid stool.

Q: What are IELs?

A: IELs is an abbreviation for intraepithelial lymphocytes, which are white blood cells that infiltrate within epithelial cells or between them. Epithelial cells form the surface mucosa of the large intestine also called the colon.

The histopathological criteria (biopsy) for lymphocytic colitis are a density of at least 20 IELs per 100 surface epithelial cells; chronic inflammatory infiltrate of mononuclear cells in the lamina propria; epithelial damage; and a subepithelial collagen layer of less than 10 µm. The increased collagen band consists basically of collagen type I and III, which are the subtypes produced by repair functions, indicating a reactive origin.1That is, the mucosa is reacting to some irritative substance.

Up to 10% of adults undergoing colonoscopy for investigation of chronic diarrhea and having visibily normal appearing mucosa may have lymphocytic colitis.2

Bile acid malabsorption has been shown to coexist in 60% of patients with lymphocytic colitis.1

Lymphocytic colitis (LC) is categorized as primary or secondary.  Primary LC is a clinical and histopathological disease of unknown cause. Secondary LC may develop as the result of iritating factors acting on the colon such as smoking or many medications.  In one study, the most common drug treatments as a percentage of the study group were corticosteroids (32.1%), proton pump inhibitors (26.0%), antidepressant drugs, specifically selective serotonin reuptake inhibitors (21.4%), angiotensin-converting enzyme inhibitors or angiotensin II receptor antagonists (18.3%), statins (17.6%), thyroid hormones (17.6%), and beta-blockers (16.0%).3

Secondary lymphocytic colitis is associated with several concomitant diseases including celiac disease. This is why lymphocytic changes must be interpreted with caution before considering them as a separate entity of autoimmune origin, instead of secondary reactions to ischemia and toxic stimulants. Efforts must be made to better classify and diagnose patients with real, primary lymphocytic colitis to avoid over-prescription of corticosteroids for treatment.3

What Is Lymphocytic Colitis In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Ohlsson B. New insights and challenges in microscopic colitis. Therap Adv Gastroenterol. 2015 Jan;8(1):37-47. doi: 10.1177/1756283X14550134. [↩] [↩]
  2. Abdo AA, Urbanski SJ, Beck PL. Lymphotcytic and collagenous colitis: the emerging entity of microscopic colitis. An update on pathophysiology, diagnosis and management. Canadian Journal of Gastroenterology. Jul 2003;17(7):425-32. [↩]
  3. Roth B, Manjer J, Ohlsson B. Drug Target Insights. 2013 Aug 11;7:19-25. doi: 10.4137/DTI.S12109. [↩] [↩]

Apathy

Cows Milk enteropathyWhat Is Milk Intolerance (Bovine Beta Casein Enteropathy)?

B ovine beta casein enteropathy is characterized by raised serum IgA antibodies to bovine beta casein found by blood testing and damage to mucosa of the jejunum found by biopsy.

The jejunum is the second section of the small intestine, between the duodenum and the ileum.

Mucosa damage is similar to damage caused by gluten.

Q: What is bovine beta casein?

A: Bovine beta casein is a protein found in cow’s milk.

An immune reaction to protein in milk is totally different from lactose intolerance. Lactose intolerance develops from deficiency of an intestinal enzyme called lactase which is required to digest lactose, the sugar in milk.

What Is Milk Intolerance In Celiac Disease and/or Gluten Sensitivity?

Insomnia

Sweet Bon Bons: Courtesy Freepik.
Sugary Bon Bons: Courtesy Freepik.

What Is Sucrose Intolerance And Sucrosemia?

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?

Sources:
  1. Krause’s Food, Nutrition, & Diet Therapy. 10th Edition. Kathleen Mahan, Sylvia Escott-Stump. 2000. W.B. Saunders Company. [↩]

Muscle Pain and Tenderness, Chronic 

Reproduction of a lithograph plate showing inside of the stomach from Gray's Anatomy. Courtesy Wikipedia Commons.
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?

Weight Loss, Unexpected/ Inability To Gain Weight

unexpected weight loss celiac disease symptomWhat Is Unexpected Weight Loss?

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?

Sources:
  1. Krause’s Food, Nutrition, & Diet Therapy. 10th Edition. Kathleen Mahan, Sylvia Escott-Stump. 2000. W.B. Saunders Company. [↩]