Skip to content

DHA (Docosahexaenoic Acid) Deficiency

Smoked Salmon...Brain Food that's Good for the Eyes!
Salmon…Brain Food That’s Good for Your Eyes, Heart, Blood Vessels, Blood Sugar, Liver, Muscles, and Fights Inflammation!

What Is DHA?

[dropcap]D[/dropcap]ocosahexaenoic acid (DHA) is an essential omega-3 fatty acid that is abundant in the brain, being crucial in brain structure. As such DHA is a key component of neuronal membranes together with arachidonic acid (a major opposing omega-6 fatty acid), making up 15-20% of the brain’s dry mass.

This polyunsaturated fatty acid is obtained from fish sources of food.

In healthy human volunteers, positron emission tomography (PET) has shown that the normal human brain consumes 4.6 mg/day of DHA.1

DHA is particularly concentrated in highly active membranes such as nerve synapses (junctions) and photoreceptors in the eye (retina).

Q: How much DHA is in the retina?

A: DHA makes up more than 30% of the retina.2

In other roles, DHA is an  important building material for the eicosanoids, a large group of highly bioactive hormone-like substances including prostaglandins, leukotrienes, and thromboxanes that are involved in blood clotting, inflammation, and vasoconstriction.

DHA has been shown to increase insulin sensitivity as opposed to the opposite problem of insulin resistance, to improve muscle mass, and protect against non-alcoholic fatty liver disease.3

Egert et al. in a study of people aged 19 to 43 years with normal cholesterol showed that DHA intake significantly increased serum HDL (good) cholesterol. Also, DHA significantly decreased fasting serum triglycerides.4

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

Sources:
  1. Rapoport SI. Brain arachidonic and docosahexaenoic acid cascades are selectively altered by drugs, diet and disease. Prostaglandins Leukot Essent Fatty Acids. 2008 Sep-Nov;79(3-5):153-6. Epub 2008 Oct 29. [↩]
  2. Richardson AJ. The importance of omega-3 fatty acids for behavior, cognition, and mood. Scandinavian Journal of Nutrition. 2003;47(2):92-8 [↩]
  3. Espinosa A, Valenzuela R, González-Mañán D, D’Espessailles A, Guillermo Gormaz J, Barrera C, Tapia G. Prevention of liver steatosis through fish oil supplementation: correlation of oxidative stress with insulin resistance and liver fatty acid content. Arch Latinoam Nutr. 2013 Mar;63(1):29-36. [↩]
  4. Egert S, Kannenberg F, Somoza V, et al. Dietary alpha-linolenic acid, EPA, and DHA have differential effects on LDL fatty acid composition but similar effects on serum lipid profiles in normolipidemic humans. J Nutr. 2009;139:861–868. doi: 10.3945/jn.108.103861 [↩]

Vitamin B1 (Thiamin) Deficiency

thiamin deficiency What Is Thiamin?

[dropcap]T[/dropcap]hiamin, also called vitamin B1, is an essential vitamin that is required to convert foodstuffs into energy and for the health and proper functioning of the nervous, muscular and cardiovascular systems.

In the bloodstream, 90% of active thiamin (TPP) is carried by red blood cells while 10% is transported in the bloodstream as free thiamin and thiamin monophosphate bound mostly to the protein albumin.

In the diet, animal food sources provide active thiamin while plant food sources provide free thiamin.1

Urinary excretion of thiamin cannot be detected when vitamin intake is below the required levels. On the other hand, when intake exceeds saturation in the body, thiamin and/or its metabolites are actively excreted into urine to prevent excessive toxicity of the vitamins.2

In patients who have thiamin deficiency, the most common conditions that bring them to a clinician include neuropathies, depression, myalgia, cardiomyopathies or takes diuretics and/or eat a high carbohydrate diet.3

What Is Thiamin Deficiency 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. 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. [↩]
  3. Spectracell Labs, Inc. [↩]

Dry Eyes, Chronic

Dry Eye Due to Riboflavin Deficiency. GFW
Dry Eye Due to Riboflavin Deficiency. GFW

What Is Chronic Dry Eye Syndrome?

[dropcap]C[/dropcap]hronic dry eye syndrome is an inflammatory condition of the conjunctiva with inadequate tear production or distribution over the eye surface. It is characterized by surface damage to the conjunctiva, giving the appearance of redness.

This complex condition involves the lacrimal glands, eyelids, and tear film, as well as a variety of eye surface tissues, including epithelial, inflammatory, immune, and goblet cells.1

Q: What is the conjunctiva?

A: The conjunctiva is the mucous membrane that lines the inside of the eyelids and covers the eyeball surface, also called the white of eye. The conjunctiva has a rich blood supply that can quickly bring microbe fighting cells to prevent invasion and overcome infection.

While infection and inflammation go hand-in-hand, they are not the cause of, but may result from, chronic dry eyes.

Dry eye syndrome develops from poor health of the conjunctiva that is associated with inadequate nutrition and poor quality of the tears that steadily lubricate the eye surface. These tears are called the tear film and are not the same as tears produced when crying or that result from irritating substances such as onions. Blinking spreads the tears that protect the surface from drying and flushes away unwanted matter.

The tear film is made up of three layers: mucous layer produced by goblet cells in the conjunctiva, aqueous (water) layer produced by the lacrimal glands, and lipid (fat) layer produced by the meibomian glands in the eyelids. Dysfunction of any of these layers impairs the the tear film. Without an adequate tear film the conjunctiva becomes dry and inflamed.

When the meibomian glands fail to produce sufficient lipid that is clear and fluid but rather cloudy and thick, the condition is called meibomian gland dysfunction (MGD). The main cause of MGD is hyperkeratinization (thickening of the glands) and its related pathogenesis (for example, ductal dilatation and acinar atrophy). Other disorders such as atopy, pemphigoid acne, rosacea, and seborrhea are related to MGD and may result in a chronic inflammation of the eye surface.2

MGD is “the most underrecognized, underappreciated and undertreated disease in ophthalmic care. It is so common as to be taken as ‘normal’ in many clinical practices,” according to Joseph Tauber, MD, an anterior segment subspecialist and refractive surgeon in Kansas City, Mo.3

Untreated dry eye progresses to xerophthalmia, a condition of extreme drying and thickening of the conjunctiva characterized by hazy, dry cornea. Other causes of dry eye, beside celiac disease, include certain systemic conditions such as Sjogren’s syndrome, an autoimmune disease.

What Is Chronic Dry Eye Syndrome In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Liu A, Ji J. Omega-3 essential fatty acids therapy for dry eye syndrome: a meta-analysis of randomized controlled studies. Med Sci Monit. 2014 Sep 6;20:1583-9. doi: 10.12659/MSM.891364. [↩]
  2. Oleñik A, Jiménez-Alfaro I, Alejandre-Alba N, Mahillo-Fernández I. A randomized, double-masked study to evaluate the effect of omega-3 fatty acids supplementation in meibomian gland dysfunction. Clin Interv Aging. 2013;8:1133-8. doi: 10.2147/CIA.S48955. Epub 2013 Aug 30. [↩]
  3. Rethinking Meibomian Gland Dysfunction: How to Spot It, Stage It and Treat It. Linda Roach, PhD. OPHTHALMIC PEARLS. [↩]

Vitamin B12 Deficiency

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

What Is Vitamin B12?

[dropcap]V[/dropcap]itamin 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. [↩]

Cataracts

Slit lamp view of cataract in human eye. Courttesy Wikimedia
Slit lamp view of cataract in human eye. Courtesy Wikimedia

What Are Cataracts?

[dropcap]C[/dropcap]ataract is a clouding of the normally clear lens in an affected eye characterized by blurred vision and progressive blindness due to loss of the len’s ability to focus light rays on the retina. Cataracts can occur in either or both eyes.

Q: How does a cataract form?

A: The lens is a transparent, colorless, oval-like structure of the eye made of mostly water and protein. The protein is arranged in a precise way that keeps the lens clear and lets light coming through the pupil to pass through it to reach the retina where it is recorded. Once an image reaches the retina, it is changed into nerve signals that are sent to the brain.1

In each eye, the lens is enclosed in a capsule that is held in place directly behind the pupil by the ciliary body and the suspensory ligaments. The lens consists primarily of lens fibers that at the periphery are soft, forming the cortis lentis, and in the center are of a harder consistency, forming the nucleus lentis. Beneath the capsule on the front surface is a layer of cells, the lens epithelium. The shape of the lens is changed by the ciliary muscle to focus light rays onto the retina.2

A cataract begins to form when some of the protein clumps together and starts to cloud a small area of the lens. Over time, the cataract may grow larger and cloud more of the lens, making it harder to see.3

A cataract is diagnosed by an ophthalmologist, who is a medical doctor specializing in the treatment of eye conditions. The eye examination involves viewing the anterior (front) of the eye by means of a slit lamp microscope. This instrument allows detailed observation of the lens and its supporting structures.

What Are Cataracts In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Tabers Cyclopedic Medical Dictionary. 19th ed. FA Davis Company, Philadelphia, PA. [↩]
  2. Tabers Cyclopedic Medical Dictionary.C 19th ed. FA Davis Company, Philadelphia, PA. [↩]
  3. http://www.nei.nih.gov/health/cataract/cataract_facts [↩]

Bitot’s Spots 

Classic Bitot's spot in a 29-year-old man that shrunk dramatically with vitamin A therapy. (Sommer A: Nutritional Blindness: Xerophthalmia and Keratomalacia. New York, Oxford University Press, 1982)
Classic Bitot’s spot in a 29-year-old man that shrunk dramatically with vitamin A therapy.*

What Are Bitot’s Spots?

[dropcap]B[/dropcap]itot’s spots are superficial foamy patches that develop on the exposed bulbar conjunctiva (white of the eye) as a manifestation of advanced vitamin A deficiency.

This painless eye disorder is reversible only with vitamin A therapy. It is named after Charles Bitot, who first described it.

Q: What makes up these foamy alterations of the conjunctiva?

A: Bitot’s spots are composed of epithelial debris (dead surface cells) and secretions.1

Bitot’s spots may develop in malnutrition, reduced intake including alcoholism, medication adverse effect, old age, low stomach acid, and disease causing vitamin A deficiency such as celiac disease, Crohn’s disease, pancreatic insufficiency, and short bowel syndrome.  Other conditions associated with vitamin A deficiency may include disordered transport (Abetalipoprotenemia, a genetic disorder) and reduced liver storage caused by liver disease.

What Are Bitot’s Spots In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Sadowski B, Rohrback JM, Steuhl KP, Weidle EG, Castrillon-Obendorfer WL. Corneal manifestations in Vitamin A deficiency. Klinische Monatsblatter fur Augenheilkunde. Aug 1994;205(2)76-85. [↩]

Uveitis, Non-Infectious  

Drawing of eyeball to illustrate uveitis. Courtesy National Eye Institute
Drawing of Eye to Illustrate Uvea Tract. Courtesy
National Eye Institute

What Is Non-Infectious Uveitis?

[dropcap]N[/dropcap]on-infectious uveitis, as opposed to that which is caused by an infection, is an inflammatory eye disorder characterized mainly by swelling of the uveal tract structures in the anterior (front) of the eye.  

Inflammation can also affect the lens, retina, optic nerve, and vitreous, producing reduced vision or blindness if left untreated. 

Q: What are structures of the uveal tract?

A: Structures of the uveal tract are composed of the iris, the ciliary body, and the choroid: 

  • The iris is the colored circle at the front of the eye. It defines eye color, secretes nutrients to keep the lens healthy, and controls the amount of light that enters the eye by adjusting the size of the pupil (opening).
  • The ciliary body is located between the iris and the choroid. It helps the eye focus by controlling the shape of the lens and it provides nutrients to keep the lens healthy.
  • The choroid is a thin, spongy network of blood vessels, which primarily provides nutrients to the retina in the back of the eye.1

Uveitis may be caused by problems or diseases occurring in the eye itself or it can be part of an inflammatory disease affecting other parts of the body. The uveal tract has a rich supply of blood vessels that contain immune cells to fight microbial invasion. These immune cells are lymphocytes, phagocytes, and plasma cells.

The uvea can be attacked by autoimmune antibodies produced in autoimmune diseases that affect similar tissues in other parts of the body such as psoriasis, Behcet’s syndrome, multiple sclerosis, sarcoidosis, Vogt Koyanagi Harada’s disease, and celiac disease.

Uveitis can last for a short (acute) or a long (chronic) time. The severest forms of uveitis reoccur many times.

What Is Non-Infectious Uveitis In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. http://www.nei.nih.gov/health/uveitis/uveitis.asp [↩]

Xerophthalmia

Marked conjunctival and corneal xerosis. The entire bulbar conjunctiva is dry and thickened and almost skinlike. (Sommer A, Sugana T, Djunaedi E, Green R: Vitamin A-responsive panocular xerophthalmia in a healthy adult. Arch Ophthalmol 96:1630, 1978)
Marked conjunctival and corneal xerosis. The entire bulbar conjunctiva is dry and thickened and almost skinlike. (Sommer A, Sugana T, Djunaedi E, Green R: Vitamin A-responsive panocular xerophthalmia in a healthy adult. Arch Ophthalmol 96:1630, 1978)

What Is Xerophthalmia?

[dropcap]X[/dropcap]erophthalmia is a serious condition of extreme drying and thickening of the conjunctiva following chronic inflammation and failure to make tears, characterized by hazy, dry cornea.

Vitamin A is obtained from the diet and is required in the cornea for maintaining epithelial (surface cell) health.1

Xerophthalmia is most often associated with malnutrition involving chronic, severe vitamin A deficiency and may develop from chronic liver disease, intestinal disorders such as celiac disease, pancreatitis, and extensive bowel surgery that cause malabsorption.

It may also develop in autoimmune diseases such as Sjogrens syndrome.

Q: What is the prognosis for xerophthalmia?

A: Xerophthalmia has the potential to rapidly advance to corneal necrosis (keratomalacia) and blindness.

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

Sources:
  1. Alwitry A. Vitamin A deficiency in coeliac disease. Br J Ophthalmol. 2000 September; 84(9): 1075. doi:  10.1136/bjo.84.9.1075e [↩]

Smell, Loss of  

Courtesy encyclopedia.lubopitko-bg.com
Courtesy encyclopedia.lubopitko-bg.com

What Is Loss of Smell?

[dropcap]L[/dropcap]oss of smell is a disorder that is characterized by impaired olfactory sense, or olfaction.

Partial or complete loss of smell can result from malnutrition, chronic rhinitis, polyps, chronic sinusitis, medications, old age, head trauma, Alzheimer’s disease and Parkinson’s disease.

Q: How do we smell things?

A: The sense of smell is complex. It involves specialized olfactory cells that are chemoreceptors, that is, they detect odor molecules in the air we breathe in through our nose and transmit the information to the olfactory area of our brain, called the olfactory cortex, by way of the olfactory tract.   Olfactory cells are located in the top of the nasal cavity.

The ability to smell strongly contributes to the ability to taste, so that individuals with loss of smell have great difficulty in perceiving the taste of food. The result is loss of the appetite for and pleasure from food.

What Is Loss of Smell In Celiac Disease and/or Gluten Sensitivity?

Tuberculosis – Non-Response to Treatment 

Chest x-ray showing tuberculosis. Courtesy wikipedia.
Chest x-ray showing tuberculosis with consolidation of left lung (white area). Courtesy wikipedia.

What Is Non-Response to Tuberculosis Treatment?

[dropcap]N[/dropcap]on-response to treatment for tuberculosis means that proper medical treatment failed to control active disease. Tuberculosis is an infection that may be dormant or active.

Q: What happens in active tuberculosis?

A: Tuberculosis is an infectious disease caused by a bacteria called mycobacterium tuberculosis. It is characterized by chronic bacterial infection most commonly affecting lungs that develops in stages.

Active tuberculosis  produces inflammation and formation of tubercles, necrosis, abcess, fibrosis, and calcification. Calcification is the body’s action to encapsulate the bacterial invasion. Active tuberculosis is life-threatening and may result in death.

About one third of the world’s population is infected with tuberculosis bacteria. In 2012 the number reached a staggering 8.6 million people. Of these, 1.3 million people died from tuberulosis.  About 95% of tuberulosis deaths occur in low- and middle-income countries and it is among the top three causes of death among women aged 15 to 44.1

People with weakened immune systems have a much greater risk of falling ill from tuberculosis. For example, a person living with HIV is about 20 to 30 times more likely to develop active tuberculosis.2

What Is Non-Response To Tuberculosis Treatment In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. http://www.who.int/features/factfiles/tb_facts/en/index.html [↩]
  2. http://www.who.int/features/factfiles/tuberculosis/en/ [↩]