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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/ [↩]

Anemia, Iron Deficiency

Red Blood Cell Comparison. Courtesy medindia.com
Red Blood Cell Comparison. Courtesy medindia.com

What Is Iron Deficiency Anemia?

Iron deficiency anemia is a blood cell disorder that is characterized by formation of small, pale red blood cells, causing tissue hypoxia. Hypoxia is the inability to meet the demands of the body for oxygen.

Q: Why do small, pale red blood cells cause tissue hypoxia?

A: Small, pale red blood cells (erythrocytes) cause tissue hypoxia because they are not able, as do normal erythrocytes, to pick up adequate oxygen from the lungs and carry it to cells that use oxygen.

Red blood cell production and function are dependent on a sufficient level of iron in the body and also the ability to use available iron to make hemoglobin in red blood cells.

Hemoglobin is a protein that binds oxygen in red blood cells to be carried by the bloodstream to cells throughout the body. In iron deficiency anemia,  hemoglobin in females is below 12.5g/dl (normal range is 12.5 to 16g/dl) and in males it is below 13.5g/dl (normal range is 13.5 to 17.5g/dl).

Iron must be obtained from the diet, since the body cannot make it, but there are various factors that can interfere with absorption and use in the body, causing anemia. Iron absorption from the gut first requires ionization, or gaining a positive electrical charge, in the strongly acidic environment of stomach juice. Ionized iron, only, can be absorbed in the duodenum, which receives the acidic contents of the stomach before it is neutralized further along.

Dietary iron can be heme or non-heme depending on the food source. Heme iron obtained only from animal food sources is absorbed into the bloodstream by active transport across the brush border (microvilli) which cover the multitudinous villi of the small intestinal lining.

Non-heme iron obtained from plants must bind with apoprotein after entering the enterocyte (surface cell of small intestinal lining) to be ferried to the underlying basolateral membrane and exited by active transport into the bloodstream.

Frequently, chronic anemia due to iron deficiency is accompanied by increased platelets, and this thrombocytosis resolves with iron repletion (normal iron level). Conversely, in severe iron deficiency anemia, patients may have thrombocytopenia (low platelets), which also resolves with iron therapy.1

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

Sources:
  1. Koury M and Rhodes M. How to approach chronic anemia. Hematology Am Soc Hematol Educ Program. 2012;2012:183-90. doi: 10.1182/asheducation-2012.1.183. [↩]

Osteoporosis

Woman with long standing osteoporosis. Courtesy of Wikimedia.
Woman with long standing osteoporosis. Courtesy of Wikimedia.

What Is Osteoporosis?

Osteoporosis is a metabolic bone disorder characterized by diminished bone mass (density) with normal cell appearance but fragile bone strength that prediposes to broken bones, and with high bone turnover.

This condition usually goes undetected until late when loss of height or a bone fracture occurs. In fact, each year  1.5 million fractures mainly of the hip, spine and wrist are attributed to osteoporosis. Compression fractures of vertebrae bones are the most common, accounting for 700,000 cases.

Bone is composed of specialized connective tissue called osseous tissue. Osseous tissue is made up of living bone cells (osteocytes) that are embedded in a hard matrix (framework) of calcified substance.

Bone matrix contains collagen fibers and the minerals calcium phosphate and calcium carbonate, which provide strength to bone. The copper enzyme, lysyl oxidase, is involved in the cross-linking of collagen in forming the framework for depositing calcium and other minerals to build and repair bone.

Q: How do osteocytes function in bone?

A: Osteocytes maintain the health of bone by their metabolic activity in regulating normal bone turnover. Bone turnover is the breaking down and removal of old or damaged bone and rebuilding or remodeling of healthy bone that is ongoing throughout life. The bone formation process takes about 3 months to complete.

Osteoporosis develops from failure of the body to maintain health and to provide bone tissue with adequate nutrition for proper function. Risk factors that can be modified include: low calcium intake, sedentary lifestyle, smoking, drinking alcohol excessively, eating a diet with excessive caffeine, protein, and phosphate, and taking certain medications over a long time such as steroids, thyroid preparations, the anti-convulsive drug phenytoin, aspirin, antacids, anticoagulants, some diuretics, and some chemotherapeutic drugs. See below for a fuller description.

In addition to celiac disease, osteoporosis is associated with advancing age, family history, nulliparity (no pregnancies) and post-menopause in females, certain disorders such as hyperthyroidism, hypogonadism, inflammatory bowel disease like Crohn’s disease, multiple myeloma, anorexia nervosa, and Cushing’s disease.

Bone strength is easily measured by testing bone mineral density (BMD). BMD is evaluated by DEXA scan (dual-energy X-ray absorptiometry).  DEXA at the femoral neck and lumbar spine is considered the gold standard to confirm the diagnosis of osteoporosis.  Results are expressed as T and Z scores. T scores compare the result with a 20 to 40 year old helathy person while  Z scores compare the result with persons in the same age group. Both are measured in standard deviations (SD).

According to WHO criteria (World Health Organization), a T-score of -1 SD or greater denotes normal bone, a T-score between −1 to −2.5 SD denotes osteopenia, and a T-score of −2.5 or more denotes osteoporosis.1

Treatment is aimed to preserve and increase bone density, minimize symptoms for better quality of life and reduce risk of bone fractures.

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

The cumulative effects of gluten-induced inflammation, treatment delay, and malabsorption result in lower bone density and bone fragility.2

Sources:
  1. Pantaleoni S, Luchino M, Adriani A, Pellicano R, Stradella D, Ribaldone DG, Sapone N, Isaia GC, Di Stefano M, Astegiano M. Bone mineral density at diagnosis of celiac disease and after 1 year of gluten-free diet. ScientificWorldJournal. 2014;2014:173082. doi: 10.1155/2014/173082. [↩]
  2. Grace-Farfaglia P. Bones of Contention: Bone Mineral Density Recovery in Celiac Disease-A Systematic Review. Nutrients. 2015 May 7;7(5):3347-3369. [↩]

Copper Deficiency

mmm...copper is in chocolate!
mmm…copper is in chocolate and nuts!

What Is Copper Deficiency?

Copper is an essential trace element that is required for a number of enzymes which are necessary for normal metabolic function.

In the body almost all the copper is present as a component of copper proteins which are produced and controlled by the liver.

Q: How does the liver control copper?

A: The liver maintains proper copper balance by binding free copper to proteins and by excreting excess copper as part of bile that is then emptied into the intestinal tract and excreted in stool.

Metabolic balance studies have demonstrated that daily copper losses are approximately 1.3 mg/day.1

Among its specific functions listed below, copper is essential for energy production, blood and nerve functions, blood components, immunity, and collagen tissue. The copper enzyme, lysyl oxidase, is involved in the cross-linking of collagen in forming the framework for depositing calcium and other minerals to build and repair bone.

Animal studies suggest that adequate copper levels during pregnancy are critical to development of higher brain function in the offspring.2

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

Sources:
  1. Williams DM. Copper deficiency in humans. Semin Hematol. 1983 Apr; 20(2):118-28. [↩]
  2. Fisgin T, Yarali N, Duru F, Usta B, Kara A. Hematologic manifestation of childhood celiac disease. Acta Haematol. 2004;111(4):211-4. [↩]

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?

Bone Fractures 

Proptosis and lid retraction are features of Grave's disease, or hyperthyroidism. Courtesy of Wikimedia.
Proptosis and Lid Retraction are Features of Grave’s Disease, or Hyperthyroidism.

What Is Grave’s Disease (Hyperthyroidism)?

G rave’s disease, or hyperthyroidism, is an autoimmune thyroid disease characterized by diffuse nontender goiter, elevated thyroxine hormone levels (T4, T3), suppressed thyroid stimulating hormone (TSH), and presence of thyroid receptor antibodies in the blood.

The autoantibodies involved are anti-thyroid peroxidase and anti-thyroglobulin antibodies. They bind to the thyroid stimulating hormone receptors, causing thyroid stimulation. These antibodies are detected by blood tests.

Q: What happens to the thyroid gland in Grave’s disease?

A: The thyroid gland is located in the front of the neck. This butterfly shaped gland consists of a large number of closed vesicles that contain a homogenous substance called colloid, which contains the thyroglobulin. Thyroglobulin is an iodine-containing protein secreted by the thyroid gland and stored within its colloid, from which the thyroid hormones thyroxine (T4) and triiodothyroinine (T3) are derived.1

Thyroxine molecule, chemical structure. Thyroid gland hormone that plays a role in energy metabolism regulation. It is a iodine containing derivative of thyrosine. Atoms are represented as spheres with conventional color coding: hydrogen (white), carbon (grey), oxygen (red), nitrogen (blue), iodine (purple).
Thyroxine molecule. Atoms are represented as spheres with conventional color coding: hydrogen (white), carbon (grey), oxygen (red), nitrogen (blue), iodine (purple).

T3 is the active hormone and is made from T4. Thyroid hormones are released into the bloodstream as needed to control metabolism, brain development, breathing, heart and nervous system functions, body temperature, muscle strength, skin dryness, menstrual cycles, weight, and cholesterol levels.

Thyroid hormone production is regulated by thyroid-stimulating hormone (TSH), which is made by the pituitary gland in the brain. Normally, when thyroid hormone levels in the blood are low, the pituitary releases more TSH in response to stimulation by the nearby hypothalamus which is continually monitoring levels of thyroxin. When thyroid hormone levels are high, the pituitary decreases TSH production. So in Grave’s disease, release of TSH by the pituitary gland is suppressed by the hypothalamus because thyroid hormone is elevated. Goiter develops from growth stimulation by thyroid stimulating autoantibodies.

What Is Grave’s Disease In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Taber’s Cyclopedic Medical Dictionary. 19th ed. F.A. Davis Company. Philadelphia, PA. [↩]

Antiphospholipid Syndrome

Testing Thigh Strength. Courtesy Charlie Goldberg, M.D., UCSD School of Medicine
Testing Thigh Strength. Courtesy Charlie Goldberg, M.D., UCSD School of Medicine

What Is Hypophosphatemia?

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

Q: How important is phosphorus in metabolism?

A: Phosphorus is crucial to  life, being present in every cell of the body and constitutes 45% of skeletal bone weight along with 40% calcium needed to support the body as a framework.

A low blood phosphate level is characterized by alterations in blood acid-alkaline balance and serious neuromuscular, hematologic, renal, skeletal, and dental abnormalities.

Symptoms result primarily from decreased production of adenosine triphosphate (ATP), the main energy source in cells, and phosphocreatine, a secondary energy source for muscle contraction.

  • Acute phosphorus deficiency may precipitate rhabdomyolysis which is destruction of muscle.
  • Nervous system dysfunction is observed in severe hypophosphatemia.
  • Chronic phosphorus deficiency causes proximal myopathy (upper arms and thighs).1
  • Severe phosphorus deficiency has widespread and ultimately fatal consequences.

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

Sources:
  1. Takeda E, Ikeda S, Nakahashi O. Lack of phosphorus intake and nutrition. Clin Calcium. 2012 Oct;22(10):1487-91. [↩]

Osteopenia In Childhood 

sclerodermaWhat Is Scleroderma?

S cleroderma is a chronic skin manifestation of progressive systemic sclerosis characterized by generalized thickened, edematous skin firmly bound to subcutaneous tissue which causes limited movement.

Systemic sclerosis a connective tissue disease that involves destructive changes in the skin, blood vessels, muscles, and internal organs. The course can be mild or it can be fatal. Cardiopulmonary complications from fibrosis are the most common cause of death.

Gastrointestinal problems mainly due to fibrosis affect 50 to 90% of patients.1

Q: Is there a cure for scleroderma?

A: There is no cure for scleroderma. Treatment is aimed at improving symptoms.

  • Heartburn (acid reflux) can be treated with antacid drugs.
  • Scleroderma kidney disease can be treated with blood pressure medications called “angiotensin converting enzyme inhibitors” (ACE inhibitors). These can often effectively control kidney damage if started early and use of these drugs has been a major advance for treating scleroderma.
  • Muscle pain and weakness can be treated with anti-inflammatory drugs such as prednisone, intravenous immunoglobin (IVIg), and/or immunosuppressive medications. Physical therapy may be useful to maintain joint and skin flexibility.2

 

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

Sources:
  1. Forbes A, Marie I. Gastrointestinal complications: the most frequent internal complications of systemic sclerosis. Rheumatology (Oxford). 2009 Jun;48 Suppl 3:iii36-9. doi: 10.1093/rheumatology/ ken485. [↩]
  2. http://www.rheumatology.org [↩]

Cutis Laxa, Acquired

Image on left shows how atherosclerosis impedes blood flow through coronary arteries while blood clots block blood flow. Courtesy Google.
Figure on right shows how atherosclerosis impedes blood flow through coronary arteries while blood clots block blood flow. Courtesy Google.

What Is Coronary Artery Disease (CAD)?

C oronary artery disease (CAD), also called ischemic heart disease, is a gradual narrowing of medium and large arteries of the heart by fatty buildups, called atherosclerotic plaques.

It is characterized by slowly developing interference with blood flow to heart tissue itself, resulting in oppressive chest pain called angina and, ultimately, thrombosis (clot) causing heart attack.  

The heart is a muscular organ that is working all the time, so it needs a constant supply of oxygen. Oxygen is brought to the working heart tissue by the coronary arteries with each beat of the heart. When heart muscle has to work harder, it needs more oxygen delivered to itself. Lack of oxygen causes pain.

In fact, failure of diseased coronary arteries to deliver adequate oxygen to heart tissue is the most common cause of angina pectoris – substernal pain (under breastbone) or pressure brought on by exertion and relieved by rest. 

Thrombosis, or clot formation, occurs when blood cells within a narrowed artery can no longer get through. Trapped, blood cells pile up and block the artery thus triggering a cascade of events called heart attack. Coronary arteries that are narrowed by atherosclerotic plaques can rupture causing injury to the coronary blood vessel resulting in blood clotting which blocks the flow of blood to the heart muscle. Blood clots may form, partially dissolve, and later form again and angina can occur each time a clot blocks blood flow in an artery.1

Q: How does coronary artery disease develop?

A: Coronary artery disease slowly develops from this combination of events:

  • Dysfunction of epithelial cells that line the inside of arteries cause the vessels to stiffen, and subsequently

  • Accumulation of lipid (fat) in smooth muscle cells beneath the inside lining of arteries and in foam cells cause buildup of fatty deposits on the inside walls progressing to fibrous plaque formation.

Oxidized low-density lipoprotein (oxLDL), so-called bad cholesterol, and oxysterols play important roles in the development of  atherosclerosis. OxLDL triggers the immune system to produce autoantibodies against oxLDL that are detectable in serum. These antibodies are called anti-oxLDL. Anti-oxLDL antibody and oxysterol concentrations are associated with coronary artery stenosis. Oxidative stress may be greatly increased in unstable angina.2 and Chronic inflammation in the general population is a major risk factor for ischemic heart disease.

The pathophysiology of atherosclerosis is, clearly, different in women when compared to the men. The women have a higher risk of blood coagulability making them at high risk for the blood clot formation. In a large number of women endothelial dysfunction, small vessel size and diffuse atherosclerosis have been identified as causes of ischemia without evidence of blockade in the coronary arteries.3

Also, atherosclerotic plaque in women is less fibrotic and contains more lipid filled foam cells, implying greater potential for reversibility but also potentially greater vulnerability for plaque rupture and thrombosis.4

Who is Affected in the General Population?

  • Coronary artery disease remains the leading cause of death in developed countries despite significant progress in primary prevention and treatment strategies.

  • It is the leading cause of death in women, as well as an important cause of disability.

  • Older patients are at particularly high risk of poor outcomes following acute coronary syndrome.5

What Is Coronary Artery Disease In Celiac Disease and/or Gluten Sensitivity?

Ischemic heart disease is the leading cause of death in the United States, making cardiovascular risk assessments and potential interventions or treatments imperative for patients with celiac disease.6

Sources:
  1. http://www.heart.org/HEARTORG/Conditions/HeartAttack/SymptomsDiagnosisofHeartAttack/Unstable-Angina_UCM_437513_Article.jsp# [↩]
  2. Yasunobu Y, Hayashi K, Shingu T, Yamagata T, Kajiyama G, Kambe M. Coronary atherosclerosis and oxidative stress as reflected by autoantibodies against oxidized low-density lipoprotein and oxysterosis. Atherosclerosis. Apr 2001;155(2):445-53. [↩]
  3. Kunadian V, Ford GA, Bawamia B, Qiu W, Manson JE. Vitamin D deficiency and coronary artery disease: A review of the evidence. Am Heart J. 2014 Mar;167(3):283-291. doi: 10.1016/j.ahj.2013.11.012. Epub 2013 Dec 19. [↩]
  4. Kunadian V, Ford GA, Bawamia B, Qiu W, Manson JE. Vitamin D deficiency and coronary artery disease: A review of the evidence. Am Heart J. 2014 Mar;167(3):283-291. doi: 10.1016/j.ahj.2013.11.012. Epub 2013 Dec 19. [↩]
  5. Kunadian V, Ford GA, Bawamia B, Qiu W, Manson JE. Vitamin D deficiency and coronary artery disease: A review of the evidence. Am Heart J. 2014 Mar;167(3):283-291. doi: 10.1016/j.ahj.2013.11.012. [↩]
  6. Robinson BL, Davis SC, Vess J, Lebel, J. Primary care management of celiac disease. Nurse Practitioner. February 2015: Vol 40 – Issue 2; 28–34. [↩]

Edema

Cachexia with Wasted Muscles, Weakness, and That Developed over 3 Years Time.
Cachexia with Wasted Muscles, Weakness, Weight Loss, Anemia, Skin Hemorrhages, Anorexia. GFW

What Is Cachexia?

C achexia is a state of ill health involving deteriorating body composition that is characterized by general malnutrition and loss of lean tissue such as muscle.

Q: What are typical findings in cachexia?

A: Arm muscle triceps (the muscles at the back of the upper arm), skin folds, subscapular skin folds, fat area index, and bone mineral content are significantly lower than normal.

Cachexia may develop in protein-losing enteropathy such as celiac disease, chronic or severe infection such as pneumonia, tuberculosis, malaria, or many chronic diseases such as heart failure and cancer.

Cachexia can develop in persons of any age.

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