Skip to content

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?

Headache (Emicrania)

Infant with Acute Diarrhea and Swollen Belly - Hallmarks of Celiac Disease.
Malnourished Infant With Acute Diarrhea and Swollen Belly.

What Is Acute Diarrhea?

A cute diarrhea is a small intestinal motility disorder characterized by excessively rapid movement of intestinal contents through the small intestine with excessive loss of fluid and electrolytes that leads rapidly to a life threatening hypokalemia (low potassium blood level) and acidosis.

Q: What is hypokalemia?

A: Hypokalemia is characterized by dehydration that may result in vascular collapse, muscular malfunction that may result in paralytic ileus (bowels do not move), paralysis (cannot stand), and respiratory hypoventilation (shallow breathing) or failure, metabolic acidosis resulting from diarrhea, and impaired nerve conduction.1

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.2

What Is Acute Diarrhea In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Kathleen Mahan and Sylvia Escott-Stump, ed. Krause’s Food, Nutrition & Diet Therapy, 10th Edition. Philadelphia, PA. USA: W.B. Saunders Company, 2000. [↩]
  2. 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. [↩]

Chronic Fatigue / Lassitude / Tiredness

What Are Erosions In The Second Part Of The Duodenum?

E rosions in the second part of the duodenum typically are superficial excoriations (sores) in the mucosal lining that do not penetrate into the muscle layer as does an ulcer.

Of note, most erosions develop in the first part of the duodenum rather than the second part.

Q: Are duodenal erosions serious?

A: Yes duodenal erosions are serious and can be life-threatening for the following reasons:

  • Duodenal erosions may occur together with gastric erosions, therefore they can jointly induce massive bleeding.
  • Duodenal erosions may be associated with duodenal ulcer but hemorrhage originates from the erosion and the ulcer itself does not bleed.
  • Duodenal erosion in itself might induce bleeding. The intensity of bleeding, if there is no hemorrhage from other places, is not so severe, as the one originating from gastric erosions.1

What Are Erosions In The Second Part Of The Duodenum In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Preisich P, Farkas I, Konyár EJ. The role of duodenal erosions in the occurrence of upper gastrointestinal haemorrhage. Scand J Gastroenterol Suppl. 1989;167:36-8. [↩]

Chronic Fatigue Syndrome 

Intestinal Edema in an 11 Month Old Baby. Courtesy: Nature.com
Intestinal Edema of Duodenum in an 11 Month Old Baby. Courtesy: Nature.com

What Is Small Intestinal Edema?

S mall intestinal edema is characterized by fluid accumulation within the intestinal mucosa so that the intestinal wall appears thick and swollen.

Intestinal edema hampers peristalsis that can result in pain and gas build-up. Peristalsis is the normal rhythmic muscular wave-like action that moves residue along the gastrointestinal tract.

Q: What part of the small intestinal lining is swollen?

A: Any part of the small intestine may be affected. Some causes of edema include allergic reactions, enteropathies such as celiac disease, cow milk enteropthy, yeast infection, parasite infection, inflammatory bowel disease such as Crohn’s disease, and certain medications.

For example, the anti-hypertensive drugs known as Angiotension Converting Enzyme (ACE) inhibitors can cause intestinal angioedema and therefore the patient may present with gastrointestinal complaints.1

What Is Small Intestinal Edema In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. LoCascio E J,  Mahler  S A, and  Arnold TC. Intestinal Angioedema Misdiagnosed as Recurrent Episodes of Gastroenteritis. West J Emerg Med. Sep 2010; 11(4): 391–394. [↩]

Stroke in Childhood 

Lymph System. National Cancer Institute.What Are Extraintestinal Lymphomas?

E xtraintestinal lymphomas (non-Hodgkin’s) are malignancies that arise in peripheral lymphatic tissue outside the intestinal tract from B-cell and T-cell lymphocytes.

Q: What is peripheral lymphatic tissue?

A: Peripheral lymphatic tissue includes lymph vessels, lymph, lymph nodes, and lymphocytes.

Lymph vessels branch into all the tissues of the body, carrying lymph, a clear fluid that contains white blood cells, especially B-cell and T-cell lymphocytes.

Lymph vessels are connected to lymph nodes which are small, round masses of tissue that store white blood cells. They also trap and remove bacteria or other harmful substances that may be in the lymph. Groups of lymph nodes are found in the neck, underarms, chest, abdomen, and groin.

Ninety percent (90%) of extraintestinal lymphomas are B-cell type and ten percent (10%) are T-cell type. In this malignancy, lymph nodes are replaced by cancer cells. Some are more aggressive than others.

In 2010, there were an estimated 509,065 people living with non-Hodgkin lymphoma in the United States according to the National Cancer Institute.

What Are Extraintestinal Lymphomas In Celiac Disease and/or Gluten Sensitivity?

Iron Deficiency

ferritinWhat Is Iron?

Iron is an essential mineral that is required for normal body function.

Almost two-thirds of iron in the body is found in hemoglobin, the protein in red blood cells that carries oxygen to tissues. Smaller amounts of iron are found in myoglobin, a protein that helps supply oxygen to muscle, and in enzymes that assist biochemical reactions.

Iron is also found in proteins that store iron for future needs and that transport iron in blood.

Q: How are iron stores regulated?

A:Iron stores are regulated by intestinal iron absorption.1That is, whenever iron is needed, more iron is absorbed than when iron is sufficient. This mechanism prevents excess iron in the body which is harmful.

In the brain, iron is necessary to ensure oxygenation and to produce energy in the cerebral parenchyma (via cytochrome oxid. ase), and for the synthesis of neurotransmitters and myelin.

Iron concentrations in the umbilical artery are critical during the development of the fetus, and in relation with the IQ in the child.2

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

Sources:
  1. http://ods.od.nih.gov/factsheets/Iron-HealthProfessional accessed 12/11/12 [↩]
  2. Bourre JM. Effects of nutrients (in food) on the structure and function of the nervous system: update on dietary requirements for brain. Part 1: micronutrients. J Nutr Health Aging. 2006 Sep-Oct; 10(5):377-85. [↩]

Vitamin B3 (Niacin) Deficiency

SumptuousTuna For Niacin.
Sumptuous Tuna For Niacin.

What Is Vitamin B3 (Niacin)?

Niacin is an essential water-soluble B vitamin that is required by all cells of the body.

During digestion of food containing it, niacin (the form in food) is changed in the small intestines to the active form niacinamide (niacin plus an amide group), which is then absorbed into the bloodstream. 

Niacinamide is converted by the body into co-enzymes which are present in all cells. These are niacinimide adenine dinucleotide (NAD) and NADP. NADP is formed when the body adds a phosphate to NAD.

Q: How do these enzymes work?

A: These enzymes function in oxidation-reduction reactions essential for release of energy from carbohydrates, fats, and proteins and are needed as components for more than 200 enzymes involved in metabolism.

In addition to producing energy, niacinamide is essential for healthy skin and the mucosal lining of the digestive tract, normal functioning of the brain and nervous system, and production of steroid hormones in adrenal glands and hormones in sex glands.  Functions are more fully described below.

Urinary excretion of niacin cannot be detected when vitamin intake is below the required levels. On the other hand, when intake exceeds saturation in the body, the vitamin and/or its metabolites are actively excreted into urine to prevent excessive toxicity of the vitamins.1

What Is Niacin 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. eCollection 2014. [↩]

Autism and Learning Disabilities

Malignant lymphoma high grade B-cell. Courtesy Wikimedia
Malignant lymphoma high grade B-cell. Courtesy Wikimedia

What Is B-Cell Non-Hodgkin’s Lymphoma?

B cell non-Hodgkin’s lymphoma is a malignant, monoclonal (arising from a single cell) proliferation of lymphocytes that is preceded by lymphadenopathy and characterized by varying, less predictable spread than Hodgkin’s disease.

Lymphadenopathy is enlargement of lymph nodes greater than 1.5 cm caused by activation and increased production of lymphocytes and phagocytes (type of white blood cell that engulfs pathogens during infection) or invasion by a tumor.

Q: How does this type of lymphoma develop?

A: 80% to 85% of non-Hodgkin’s lymphoma arise from B-lymphocytes (B-cells).

What Is B Cell Non-Hodgkin’s Lymphoma In Celiac Disease and/or Gluten Sensitivity?

Multiple Sclerosis

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. [↩]