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Vitamin C Deficiency

vitamin c gluten celiac disease symptomWhat Is Vitamin C?

[dropcap]V[/dropcap]itamin C, also called ascorbic acid or ascorbate, is an essential water soluble vitamin.

Fresh supplies of vitamin C are required every day to perform vital roles throughout the body among which are the production of connective tissue such as skin, blood vessels and bone, anti-inflammatory responses and anti-oxidant performance. See below for all roles.

Vitamin C fights for us! It has an anti-cancer effect stemming from its role as a potent anti-oxidant in blood plasma and within cells. It also protects nucleic acids (DNA) from oxidative damage and inhibits the formation of nitrosamines (carcinogenic compounds formed in the digestive tract).

Importantly, vitamin C can regenerate vitamin E from an oxidized state after vitamin E performs its own anti-oxidant role against free radicals and vitamin C works together with other anti-oxidants, such as beta-carotene and glutathione, to increase their overall anti-oxidant effect.

A study investigating the specific anti-inflammatory and anti-oxidant micronutrients that reduce oxidative stress found that in adolescents with metabolic syndrome (MetS) the lower the vitamin C level in blood the worse the MetS status and blood uric acid level.  MetS prevalence was estimated at 7% among boys and 3% among girls.1

Vitamin C reverses osteoporosis by reducing or preventing oxidative stress that destroys living bone tissue. Osteoporosis is a disorder of bone inflammation that results in thin, weak bones that may easily fracture. In normal bone structure, vitamin C is required to form collagen, which is living bone tissue.

In humans, vitamin C reduces the duration of common cold symptoms, even if its effect is not clear.2

Vitamin C must be obtained from food daily because our bodies, unlike monkeys and other animals, cannot produce it.

Urinary excretion of vitamin C 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.3

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

Sources:
  1. TGBeydoun MA, Canas JA, Beydoun HA, Chen X, Shroff MR, Zonderman AB. Serum antioxidant concentrations and metabolic syndrome are associated among U.S. adolescents in recent national surveys. J Nutr. 2012 Sep;142(9):1693-704. doi: 10.3945/jn.112.160416. [↩]
  2. Shaik-Dasthagirisaheb YB, Varvara G, Murmura G, Saggini A, Caraffa A, Antinolfi P, Tete’ S, Tripodi D, Conti F, Cianchetti E, Toniato E, Rosati M, Speranza L,Pantalone A, Saggini R, Tei M, Speziali A, Conti P, Theoharides TC, Pandolfi F. Role of vitamins D, E and C in immunity and inflammation. J Biol Regul Homeost Agents. 2013 Apr-Jun;27(2):291-5. [↩]
  3. 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. [↩]

Inflammation

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inflammation-post-4What Is Inflammation?

[dropcap]I[/dropcap]nflammation is our body’s necessary self-defense response and repair mechanism for these assaults:

1) injuries such as cuts, scrapes, sprains, broken bones, burns, insect bites, toxins; 2) invading organisms such as bacteria; and 3) allergens and food sensitivities such as gluten.

Inflammation can be immediate (acute) or persistent (chronic).

Acute inflammation is marked by increased blood flow, migration of white blood cells, and release of defensive proteins and chemicals to the site of injured tissue. Among these chemicals are free radicals in the immune response to injury that are beneficial yet require the activity of anti-oxidants such as vitamin E and vitamin C to control.

Free radicals are chemical particles containing one or more unpaired electrons, which may be part of the molecule. They cause the molecule to become highly reactive.1

The majority of this response takes place in the first 12 to 24 hours after the assault. The inflammatory process continues until all the damaged tissue or invading germs are removed (usually about 5 days).2

Chronic inflammation is marked by persistence weeks to months or longer after tissue damage. Note: high concentrations of free radicals generated in chronic inflammation may be important causes of damage to cell structures. The defensive activity of anti-oxidants such as vitamin E and vitamin C are required to remove free radicals.

Chronic inflammation increases the risk for systemic diseases such as type II diabetes, obesity, heart disease, high blood pressure, arthritis, osteoporosis, chronic fatigue, migraine, autoimmune disease, and vasculitis which may cause stroke, heart attack or deep vein thrombosis (DVT).

Importantly, chronic inflammation is a risk factor for the onset of cancer.3

Q: Are there blood tests available for detecting inflammation?

A: Yes. Your medical health practitioner can order either or both of the following blood tests that measure the amount of inflammation present although not the source of inflammation. Abnormal is an elevation in blood levels.

  1. C-reactive protein (CRP). This test measure C-reactive proteins that are released into the bloodstream within a few hours of tissue injury or infection. CRPs are cytokines called ‘acute phase reactants,’ meaning first on the scene. The CRP test is also useful to monitor treatment response and flare-ups of chronic inflammatory disease such as vasculitis, systemic lupus, and inflammatory bowel disease.
  2. Erythrocyte sedimentation rate (ESR or sed rate). This test measures the rate of fall of blood cells in a sample tube of blood. An increase in the rate of fall shows inflammation due to an increase of C-reactive proteins in the blood specimen. Alone or with the CRP test, the ESR is especially useful for monitoring inflammation of veins and arteries.

In regards to celiac disease, disappearance of blood antibody levels of tissue transglutaminase IgA (tTG-IgA) indicate that inflammation has also subsided. These antibodies should be checked at 3 months, 6 months if indicated, and one year after diagnosis to monitor healing. On the other hand, raised antibodies indicate that there is definitely ongoing inflammation in the small intestine.

In regards to non-celiac gluten sensitivity, disappearance of blood antibody levels of anti-gliadin IgA and IgG at 3 months, 6 months if indicated, and one year after diagnosis indicate that inflammation has also subsided. On the other hand, raised antibodies indicate that there is definitely ongoing inflammation caused by gluten within the body.

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

Sources:
  1. Ruttkay-Nedecky B, Nejdl L , Gumulec J. The Role of Metallothionein in Oxidative Stress. Int. J. Mol. Sci. 2013, 14(3), 6044-6066; doi:10.3390/ijms14036044. [↩]
  2. Taber’s Cyclopedic Medical Dictionary. 19th ed. F A Davis Company. Philadelphia, PA. [↩]
  3. Brighenti E, Giannone FA, Fornari F, Onofrillo C, Govoni M, Montanaro L, Treré D, Derenzini M. Therapeutic dosages of aspirin counteract the IL-6 induced pro-tumorigenic effects by slowing-down the ribosome biogenesis rate. Oncotarget. 2016 Aug 20. doi: 10.18632/oncotarget.11441. [↩]

Helicobacter Pylori Infection (H. Pylori)

What Is Helicobacter Pylori (H. Pylori) Infection? [dropcap]H[/dropcap]elicobacter pylori infection is a potentially deadly stomach disease characterized by chronic superficial inflammation and ulcerations in 100% of infected patients. This infection disrupts normal defense and repair… 

Gastric (Stomach) Ulcer

Photo by gastroscopy showing ulcer in the antrum area of the stomach.
Photo by gastroscopy showing ulcer in the antrum area of the stomach (lower area).

What Is A Gastric Ulcer?

[dropcap]G[/dropcap]astric ulcer is a painful stomach disorder characterized by an open sore involving the mucosa lining and deeper muscle layer of the stomach.

Gastric ulcer is associated with lymphocytic gastritis which is inflammation of the mucosal lining of the stomach. The thick mucosal lining normally protects the stomach from the erosive action of stomach acid.

Q: How do ulcers develop?

A: Ulcers develop if  hydrochloric acid secreted by the gastric glands of the stomach for the purpose of digesting food damages the normally resistant mucosal walls of the stomach. In the reverse, ulcers may be accompanied by achlorhydria (insufficient acid production).

Damage occurs when there is a predisposing factor that alters the health of the mucosal lining. The most common cause is infection with a bacteria called h. pylori bacter, stress and chronic use of the pain relievers aspirin and non-steroidal drugs like ibuprofen.

Smoking tocacco and consuming alcohol aggravate an ulcer but do not cause it to develop.

The most common location for ulcer formation is along the stomach antrum which is the area of the stomach before the pylorus, the lower region that empties liquid stomach contents into the small intestine.

What Is A Gastric Ulcer In Celiac Disease and/or Gluten Sensitivity?

Vitamin D Deficiency

Sunshine Delivers Free Vitamin D To Everyone.
Sunshine Delivers Free Vitamin D To Everyone.

What Is Vitamin D?

[dropcap]V[/dropcap]itamin D is the principle regulator of calcium homeostasis (balance) in the body.  This “vitamin” is really a prohormone, meaning it acts like a hormone but is not. Vitamin D does, however, contain cholesterol in its molecular structure like steroid hormones.

The physiological importance of vitamin D encompasses much more than the regulation of bone metabolism although this is a mighty function.

Q: How does vitamin D regulate bone metabolism?

A: In regulation of bone metabolism, vitamin D works in three ways: 1) enables active absorption of calcium from the small intestine, 2) enhances reabsortion of calcium by the kidneys that would otherwise be excreted in urine, and 3) plays an active role in skeletal development and bone mineralization. Mineralization gives strength to living bone tissue.

Vitamin D interacts with receptors within cells to effect transcriptional changes in many cell types including those in gut, bone, breast, prostate, brain, skeletal muscle, and the immune system.1

In regards to the essential role of vitamin D in muscle tissue, it has been recently shown that vitamin D regulates both muscle function and structure of primary myofibers.2

Vitamin D is converted in the body to a molecule that is biologically active. The active form is 1,25-dihydroxyvitamin D, usually referred to as vitamin D3. About 80% comes from sun exposure and the remaining from food.

Vitamin D3 is synthesized in the skin from 7-dehydrocholesterol via photochemical reactions requiring UV light (sunlight). That is, light that contains energy from the sun is incorporated into molecules of  7-dehydrocholesterol in the underlying dermis of skin to make this vitamin. This is why inadequate exposure to sunlight contributes to vitamin D deficiency.

Blood concentration of 25(OH)D is the best indicator of vitamin D status. It reflects vitamin D produced in the skin and that obtained from food and supplements and has a fairly long circulating half-life of 15 days.3

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

Sources:

  1. McCarty DE, Chesson AL Jr, Jain SK, Marino AA. The link between vitamin D metabolism and sleep medicine. Sleep Med Rev. 2014 Aug;18(4):311-9. doi: 10.1016/j.smrv.2013.07.001. [↩]
  2. Girgis CM, Mokbel N, Cha KM, Houweling PJ, Abboud M, Fraser DR, Mason RS, Clifton-Bligh RJ, Gunton JE. The vitamin D receptor (VDR) is expressed in skeletal muscle of male mice and modulates 25-hydroxyvitamin D (25OHD) uptake in myofibers. Endocrinology. 2014 Sep;155(9):3227-37 [↩]
  3. http://ods.od.nih.gov/factsheets/VitaminD-HealthProfessional/ [↩]

Cancer Predisposition In Children 

In this impressive photo, the large round cell is a lymphocyte. Macrophages with projectile-looking surfaces are interacting with it. Photo is Courtesy of Dr. Timothy Triche. National Cancer Institute.
In this impressive photo, the large round cell is a lymphocyte. Macrophages with projectile-looking surfaces are interacting with it. Courtesy of Dr. Timothy Triche. National Cancer Institute.

What Is Cancer Predisposition In Children?

[dropcap]C[/dropcap]ancer predisposition in children signifies a higher than normal risk of developing cancer. Cancer is the uncontrolled division of abnormal cells in the body.

Among the 12 major types of childhood cancers, leukemias (blood cell cancers) and cancers of the brain and central nervous system account for more than half of the new cases. About one-third of childhood cancers are leukemias.

The most common type of leukemia in children is acute lymphoblastic leukemia. The most common solid tumors are brain tumors (e.g., gliomas and medulloblastomas), with other solid tumors (e.g., neuroblastomas, Wilms tumors, and sarcomas such as rhabdomyosarcoma and osteosarcoma) being less common according to the National Cancer Institute.

On average, 1 to 2 children develop the disease each year for every 10,000 children in the United States.

What Is Cancer Predisposition In Children In Celiac Disease and/or Gluten Sensitivity?

Adenocarcinoma Of Small Intestine (Cancer)

Section of small bowel surgically removed for adenocarcinoma that grew through the wall. By: CDC/ Dr. Edwin P. Ewing, Jr.
Section of small bowel surgically removed for adenocarcinoma that grew through the wall. By: CDC/ Dr. Edwin P. Ewing, Jr.

What Is Adenocarcinoma Of Small Intestine?

[dropcap]A[/dropcap]denocarcinomas are malignant tumors, or cancer, of the small bowel arising out of glandular tissue. They fall in the category of rare neoplasm, comprising only 3% of all gastrointestinal malignancies.

Primary adenocarcinoma is the most common histological (cell) subtype constituting 35–50% of cases.1 

Q: What does adenocarcinoma look like?

A: Adenocarcinoma may manifest as strictures, nodules, excavating masses, or annular lesions.2

What Is Adenocarcinoma Of Small Intestine In Celiac Disease and/or Gluten Sensitivity?

Sources:

  1. Benhammane H, El M’rabet FZ, Serhouchni KI, El yousfi M, Charif I, Toughray I, et al. Small Bowel Adenocarcinoma Complicating Coeliac Disease: A Report of Three Cases and the Literature Review. Case Rep Oncol Med. 2012; 2012: 935183. Published online 2012 December 1. doi: 10.1155/2012/935183 [↩]
  2. Ramachandran I, Sinha R, Rajesh A, Verma R. Multidetector row CT of small bowel tumors.  Clinical Radiology. 2007; 62:607-614. [↩]

Primary Sclerosing Cholangitis 

A 3D Image From Magnetic Resonace Cholangiography. NIHMS
A 3D Image From Magnetic Resonace Cholangiography showing biliary tree. NIHMS

What Is Primary Sclerosing Cholangitis?

[dropcap]P[/dropcap]rimary sclerosing cholangitis (PSC) is an uncommon, slowly progressive bile duct disease that results in stagnation or build-up of bile in the liver, called cholestasis.

Primary sclerosing cholangitis is characterized by sclerosis, or scarring inflammation in bile ducts both within the liver (intra-hepatic ducts), and outside the liver (extra-hepatic ducts), causing progressive narrowing and, eventually, obliteration of the bile ducts.

Primary sclerosing cholangitis comes under the umbrella term autoimune liver disease in which the end result is immune-mediated hepatocellular (liver cell) or hepatobiliary (bile duct) injury.1

Q: What happens when scarred bile ducts can no longer transport bile out of the liver?

A: Bile that cannot be removed from the liver by the biliary duct system backs up and damages the liver, causing cirrhosis.

Bile is continually made by the liver from phospholipids salt, cholesterol, and aging blood cells that it removes from circulation to be carried out of the liver. Bile also carries away waste products produced by normal metabolism and toxic substances that are removed by the liver for eventual elimination in stool. As such, bile must continually flow out of the liver to prevent build-up in the liver.

Bile is a greenish brown liquid made by the liver. Bile ducts carry it out of the liver to the gall bladder for storage until needed to aid in the digestion and absorption of fat from the small intestine. Bile emulsifies fat eaten in the diet so that the pancreatic enzyme called lypase can break it down into its fatty acid and glycerol components.

The liver is the largest organ within the body. It lies mostly in the upper part of the abdomen on the right side just under the diaphragm. About 70% of liver tissue is made up of cube shaped cells called hepatocytes that do the main work of the liver. Other cells (epithelial) form structure and are arranged in single layers around blood vessels, sinusoids, and bile ducts. 

Build-up of bile in the liver is the end result of the inflammatory process in primary sclerosing cholangitis, that by swelling and scarring of bile ducts impedes and eventually prevents bile flow out of the liver, leading to liver failure. There is no curative treatment available for primary sclerosing cholangitis, besides liver transplantation.2

The appearance of the intrahepatic and extrahepatic biliary ducts can be assessed by use of cholangiography, and magnetic resonance (MR) imaging is the best way to identify patients.  See image above.3

MR cholangiography offers a noninvasive method of obtaining images of the biliary system without the use of a contrast agent. There is no radiation exposure. Pulse sequences can be chosen to obtain bright bile or black bile cholangiograms. Image processing algorithms can be selected to obtain a three-dimensional representation of biliary anatomy and pathology, and those images can be rotated in any plane so that ductal anatomy and pathology can be seen to best advantage.4

There is no cure for primary sclerosing cholangitis but there are symptom treatments one of which is supplementation for low levels of vitamins A,D,E, and K. Liver transplant is the only effective option.

What Is Primary Sclerosing Cholangitis In Celiac Disease and/or Gluten Sensitivity?

Sources:

  1. Trivedi PJ, Adams DH. Mucosal immunity in liver autoimmunity: a comprehensive review. J Autoimmun. 2013 Oct;46:97-111. doi: 10.1016/j.jaut.2013.06.013. [↩]
  2. Kummen M, Schrumpf E, Boberg KM. Liver abnormalities in bowel diseases. Best Pract Res Clin Gastroenterol. 2013 Aug;27(4):531-42. doi: 10.1016/j.bpg.2013.06.013. [↩]
  3. Eaton JE, Talwalkar JA, Lazaridis KN, Gores GJ, Lindor KD. Pathogenesis of primary sclerosing cholangitis and advances in diagnosis and management. Gastroenterology. 2013 Sep;145(3):521-36. doi: 10.1053/j.gastro.2013.06.052. Epub 2013 Jul 1. [↩]
  4. Meakem TJ 3rd, Schnall MD. Magnetic resonance cholangiography. Gastroenterol Clin North Am. 1995 Jun;24(2):221-38. [↩]

Melanoma: definition

A cutaneous malignancy (cancer) with rapid invasion and metastasis (spread) characterized by growth from melanocytes (pigment containing skin cells) appearing as a new mole or enlarging from an exisiting mole, changing shape, size or color.…