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Melanoma

Enamel_celiac[1]What Are Dental Enamel Defects?

D ental enamel defects (DED) comprise a variety of abnormalities in the dental enamel of the second or permanent teeth and of primary or baby teeth.

Teeth may appear with pits, thin or missing enamel, non-white enamel (yellow, orange, or gray colored teeth), and demarcated opacities (very white spots) even if teeth are white.

Q: What is enamel?

A: Dental enamel is the shiny, hard, white, dense, inorganic substance covering the crowns of the teeth. The crown is the tooth portion above the gum. Under the enamel is hard dentin which surround the living pulp. In teeth with missing enamel, the areas with exposed dentin appear dull and tan colored.

What Are Dental Enamel Defects In Celiac Disease and/or Gluten Sensitivity?

Migraine (Headache)

Baby with Allergic Reaction to Peanuts. GFW
Baby with Allergic Reaction to Peanuts. GFW photo.

What Is Food Allergy?

F ood allergy is an abnormal immune response to food proteins that may damage the small intestinal  lining and produce malabsorption of food. The reaction is usually delayed which makes it difficult to identify the offending food that is causing symptoms.

Q: How does food allergy develop?

A: The gastrointestinal tract serves not only to digest and absorb foodstuffs but also to protect the body from unwanted substances. When allergic food substances are eaten, the immune response that is triggered in the gut produces inflammation with symptoms such as pain, vomiting and loose bowels.

Inflammation causes swelling of the gut lining that can interfere with the passage of nutrients through it to the body which results in malabsorption. Malabsorption deprives the body of nutrients needed for normal function.

Symptoms other than digestive may involve skin rashes, hives, and respiratory difficulties that can be distressing and life-threatening.

What Is Food Allergy In Celiac Disease and/or Gluten Sensitivity?

Cancer, Parathyroid

hypocupremia low copper and celiac disease gluten symptom
Paleness and Tendon Problem: Symptoms of Hypocupremia.

What Is Hypocupremia?

H ypocupremia, or low plasma copper, means the level of copper is too low to meet metabolic needs of the body for copper and is characterized by these many features:

  1. Impaired energy production causing weakness.
  2. Impaired ability as part of an enzyme to oxidize vitamin C which is required to breakdown histamine.
  3. Faulty blood cell formation and instability of blood cell membranes causing anemia, shortened life span of neutrophils causing susceptibility to infection, faulty platelet formation causing impaired blood clotting.
  4. Faulty elastin formation causing weak blood vessels.
  5. Poor collagen and connective tissue strength causing joint and tendon problems and weak bones causing deformities, faulty bone mineralization causing fragile bones.
  6. Loss of proprioception causing ataxia.
  7. Loss of pigmentation of hair and skin.
  8. Impaired thyroid function.
  9. Impaired adrenalin production.

Untreated, copper deficiency can advance to brain degeneration. Failure to make normal blood cells can result in death.

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

Pityriasis Rubra Pilaris

Vitamin C Deficiency: Clean Teeth with Swollen Gums.
Vitamin C Deficiency: Swollen Gums.

What Are Bleeding / Swollen Gums?

B leeding and/or swollen gums is  an inflammatory disorder characterized by changes in gum integrity that may result in tooth loss.

Sponginess of the gum (swelling) indicates inflammation, called gingivitis. 

Q: What causes gingivitis?

A: Gingivitis that is caused by inadequate dental hygiene shows as pockets of swollen gum between or along the base of teeth where sticky plaque was allowed to build up. Plaque holds bacteria that inflames the gums where it occurs.

Gingivitis that is caused by vitamin C deficiency, pregnancy, certain drugs such as the anti-epileptic drug phenytoin, and leukemia affects the whole gum irrespective of mouth care.

What Are Bleeding / Swollen Gums In Celiac Disease and/or Gluten Sensitivity?

Occipital Lobe Epilepsy With Cerebral Calcifications

Close-up Slice of a Small Intestinal Villus Showing How Enterocytes Appear Tightly Lining the Entire Outside Surface Of A Villus. Courtesy Cleo Libonati

What Is Increased Intestinal Permeability?

I ncreased intestinal permeability is characterized by dysfunctional intestinal permeability (leakiness) allowing for the penetration of harmful entities from the gut into the bloodstream such as undigested proteins and microbes. The popular name is “leaky gut.”

Q: Why does intestinal permeability increase?

A: Intestinal permeability is an essential function of the small intestinal mucosal lining by which wanted substances such as properly digested foodstuffs are allowed to permeate through the lining to enter the body via the bloodstream and lymphatics. At the same time unwanted substances are kept out.

The mucosal lining is one cell thick and makes up the surface between the digested foodstuffs inside the hollow of the intestine and the underlying tissues.

The mucosal lining is covered by millions of microscopic finger-like structures called villi that project toward the inside of the intestine giving the appearance of a shag rug.

Each one, called a villus, contains a capillary bringing blood to absorb nutrients, a vein to take away nutrients, and a lacteal to absorb and take away digested fat. Its wall is made up of a single layer of tightly connecting cells, called enterocytes.

This single layer of cells separates the contents of our small intestine from the lamina propria (underlying tissues of the small intestine) and the rest of our body. Breaching of this single layer of cells by leakiness can expose lymphocytes (immune cells) located in the lamina propria to a myriad of microorganisms and food antigens, leading to immune reactions.1

To protect the body from unwanted substances, a gatekeeping barrier system operates to regulate the passage of nutrients, or permeation, through the surface mucosal lining. This system acts to seal the inside body from the gut.

The integrity of intestinal permeability is determined by interactions among several barrier components including the unstirred water layer, mucosal surface hydrophobicity, the surface mucous coat, and cell factors (especially tight junctions).

Tight junctions hold cells tightly together side-by-side to prevent unwanted substances from passing through the lining. Tight junctions are complex structures comprising over 50 proteins, such as the claudin proteins which are considered to be the structural backbone of tight junctions.

Tight junctions include a series of special proteins forming fibrils (springy like proteins) that cross the plasma membrane and interact with proteins in the adjoining cells. Tight junctions are regulated by the protein zonulin.2

If zonulin deregulates from the action of substances such as gliadin (gluten in wheat) and bacteria, the tight junction barrier fails which results in increased intestinal permeability. Dysfunction of the barrier system allows unwanted substances to enter the body where they are damaging to many tissues.

Tight junction dysfunction has been shown to be a part of certain autoimmune diseases such as celiac disease, type I diabetes mellitus, multiple sclerosis, and rheumatoid arthritis. Other diseases associated are cancer, allergies, and infections.3

Important gastrointestinal infections that cause leaky gut include rotavirus, parasites, pathogenic bacteria (escherichia coli, clostridium difficile), and mycotoxins produced by fungi found in stored grain and dried fruit.4

Fortunately, the presence of some commensal (friendly intestinal bacteria) and probiotic strains leads to an increase in tight junctions  proteins at the cell boundaries and in some cases prevents or reverses the adverse effects of pathogens, food and stress. Various dietary components are also known to regulate epithelial permeability by modifying expression and localization of  tight junctions proteins.2

What Is Increased Intestinal Permeability In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Fahardi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease. Journal of Gastroenterology and Hepatology. 2003; 18: 479-497. []
  2. Ulluwishewa D, Anderson RC, McNabb WC, Moughan PJ, Wells JM, Roy NC. Regulation of tight junction permeability by intestinal bacteria and dietary components. J Nutr. 2011 May;141(5):769-76. doi: 10.3945/jn.110.135657. [] []
  3. Fasano A. Zonulin and Its Regulation of Intestinal Barrier Function: The Biological Door to Inflammation, Autoimmunity, and Cancer. Physiological Reviews. January 2011Vol. 91no. 151-175DOI: 10.1152/physrev.00003.2008 []
  4. Farhadi A, Banan A, Fields J, Keshavarzian A. Intestinal barrier: an interface between health and disease. Journal of Gastroenterology and Hepatology. 2003;18:479-91. []

Allergic Rhinitis

hypomagnesemiaWhat Is Hypomagnesemia?

H ypomagnesemia means the level of magnesium in the bloodstream is too low to meet metabolic needs of the body for this mineral.

Q: What are the metabolic needs of the body for magnesium?

A: The metabolic needs of the body for magnesium are numerous which gives rise to very many distressing symptoms when this mineral is deficient.

A major function of magnesium is to stabilize the structure of an enzyme called adenosine triphosphate (ATP) within cells for the production of energy. In the brain, magnesium plays important roles in all the major metabolisms such as oxidation-reduction and regulation of ions (charged minerals).1

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

Sources:
  1. 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. []

Itchy (Pruritic) Skin  

tongue in B12 deficiencyWhat Is Beefy Red, Smooth, Burning Tongue?

B eefy, red, smooth, burning tongue is an inflammatory alteration in tongue tissue characteristic of vitamin B12 deficiency.

Inflammation makes the tongue red and sore which, when untreated, progresses to atrophied papillae (shrunken taste buds) that makes the tongue smooth.

Q: Why does vitamin B12 alter the tongue?

A: Vitamin B12 is essential for the metabolism of all cells, especially for those of the digestive tract of which the tongue is an organ.1

These easily seen changes to tongue tissue are an important diagnostic feature of deficient vitamin B12, which causes other devastating unseen damage, because the discomfort generally causes the individual to seek medical care.

What Is Beefy Red, Smooth, Burning Tongue 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. []

Autoimmune Disorders In Dermatitis Herpetiformis

bloodvialWhat Is Prolonged Prothrombin Time?

P rolonged prothrombin time (PT) is a laboratory blood test result showing that blood clots too slowly which makes the patient subject to abnormal bleeding.

Q: What does the prothrombin time (PT) test measure?

A: The prothrombin test measures the clotting ability of blood protein factors I, II (prothrombin), V, VII, and X. If any of these factors are too low, it takes longer than normal for the blood to clot. Prothrombin is a vitamin K dependent factor meaning a deficiency of vitamin K will cause low prothrombin.

Blood is drawn into a blood collection tube with a light blue stopper which has a buffering additive. Tubes must be completely filled.

What Is Prolonged Prothrombin Time In Celiac Disease and/or Gluten Sensitivity?

Lymphoma, B-Cell Non-Hodgkin’s

e3343bf0a689b5f974a852fa2e84a718What Is Laryngospasm?

L aryngospasm is an acute disorder of the larynx that is characterized by life-threatening spasms of the muscles of the larynx located in the throat.

Laryngospasm is a rare feature of hypocalcemia (low blood calcium level) characterized by severe alteration in nerve conduction and muscle contraction.

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

Common Variable Immunodeficiency 

Folic acid deficiency anemia gluten celiac disease symptom
Red Blood Cells.

What Is Folic Acid Or Folate Deficiency Anemia?

F olic acid deficiency anemia, also called folate deficiency anemia, is a macrocytic anemia characterized by defective DNA synthesis of red blood cells that results from a lack of folate in the body.

Q: How does folate deficiency cause anemia?

A: Folates are a family of B vitamins and folic acid is an active form.

Folate is required for the formation of both red and white blood cells in the bone marrow and for their maturation.

Also, folate serves as a carrier in the formation of heme, which contains iron, and is the non-protein part of the hemoglobin molecule.1

Red blood cells provide oxygen to body tissues. When there are not enough red blood cells or when they cannot properly carry oxygen, the condition is called anemia. In folic acid deficiency anemia, the red blood cells are abnormally large. Such cells are called macrocytes (macro size cells). They are also called megaloblasts (mega size cells) as seen in the bone marrow where they are produced. This is why this macrocytic anemia is also called megaloblastic anemia.2

Tests that may be done to determine folate adequacy are complete blood count (CBC), red blood cell folate level, methylmalonic acid level, and homocysteine level. Folic acid deficiency anemia shows a decrease in red blood cell folate and/or serum folate levels and normal plasma methylmalonic acid level with elevated homocysteine blood level. These levels distinguish folic acid deficiency anemia from vitamin B12 deficiency anemia.3

What Is Folate Deficiency Anemia 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. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001578/ []
  3. Mark Beers and Robert Berkow. The Merck Manual, 17th Edition. Whitehouse Station, N.J. USA: Merck Research Laboratories, 1999. []