Find out what your nails are telling you about your health in this important video tutorial. These nail problems reveal underlying causes that need to be corrected – and are usually simple to fix –…
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My mother, Cleo Libonati, RN, BSN was giving a presentation to medical school students at a major medical school in Philadelphia. The topic was “Identifying and Correcting Nutrient Deficiencies in Celiac Disease.”
A student approached her after the presentation. She was a tall, athletic looking woman with short blond hair. She introduced herself as Amanda and told Cleo she was afraid she might have to drop out of medical school. She said she was a West Point graduate, but no one could diagnose her.
She said she had constant gastrointestinal problems and fatigue. She couldn’t concentrate. Something was terribly wrong. She could feel it.
Fall is here and that means pumpkins are starting to appear on your neighbor’s door step and in grocery stores, which is the universal signal to start carving and cooking pumpkin. Why is it most of us tend to cook with pumpkin only around Halloween and Thanksgiving? Pumpkin is loaded with vitamin A, fiber and it is low in calories, so we should find ways to work it into our diet throughout the year.
Pumpkin is very versatile to cook with, so it can be used in both sweet and savory recipes. This Examiner did a little research for gluten-free pumpkin recipes and was amazed at all of the drool-worthy recipes we found. Listed below are just a fraction of the gluten-free pumpkin recipes available online.
What is your favorite way to cook with pumpkin?
Pumpkin – General Recipes
What Is Eczema?E czema, or atopic dermatitis, is a chronic recurring inflammatory skin disorder characterized by itching, eczematous plaques and a defective epidermal barrier (surface layer of skin cells) that fails to hold moisture, with affected areas becoming dry then inflamed.
Q: Why does eczema develop?
A: Patients with atopic dermatitis have genetically determined risk factors that affect the barrier function of the skin and immune responses that interact with environmental factors.1
Atopic eczema is associated both with an abnormal skin matrix and impaired systemic immune response. Therefore, isolated topical treatment may have suboptimal effect.2
Atopic eczema is a common presentation of immune response towards food proteins in infancy.3
Global evidences reflect a marked increase in prevalence, which has tripled since 1960. In the United States, the current prevalence rates range from 10% to 20% in children and 1 to 3% in adults.4
A cquired ichthyosis is an uncommon, nonhereditary cutaneous disorder characterized by dry, rough skin with prominent symmetrical scaling that involves significant portions of the body.
Most microscopic studies of acquired ichthyosis exhibit hyperkeratosis (thickened skin) with a reduced or absent granular layer.1
Q: What is the granular layer of skin?
A: The granular layer is the third cell layer (of five) composing the epidermis, or outer surface of skin.
Acquired icthyosis has been associated with internal disease including malignancies, autoimmune/inflammatory, metabolic, endocrine, and infectious diseases, and medication use.
Candida albicans infection, called candidosis or candidiasis, is an opportunistic invasion of mucous membrane or skin by candida albicans, an endogenous yeast found in 40 to 80% of normal human beings. A former name for this small, budding fungus is monilia albicans.
Opportunistic means that yeast living on mucosal and skin surfaces does not invade (infect) unless these tissues become unhealthy and therefore cannot protect themselves.
Q: How does candida albicans cause infection?
A: Candida albicans lives on the mucosal surfaces and skin in most people without causing infection (colonizes) because of our normal defenses against invasion. In fact, candida albicans is a very effective colonizer of humans. For example, Russell and Lay found that 47% of 1-month-old infants were orally colonized with candida albicans, and 49% were colonized with other fungi.
During growth within the intestinal tract, the organism senses pH (acidity), oxygen, carbon sources, and the presence of surfaces allowing it to optimize gene expression for a particular environment. With these mechanisms for sensing, candida albicans is able to efficiently colonize humans in infancy.1
Lowered host defenses allow yeast already present on mucosal and skin surfaces to take advantage and can grow rapidly, becoming pathogenic (disease producing) so that infection results.
Infection is characterized by superficial, irregular white patches on mucosal surfaces and possible invasion of the bloodstream by a filamentous form (thread-like structures) that can rapidly develop.
Candida albicans is unique among oral pathogens in its ability to invade cornified layers of stratified squamous epithelium of the tongue, mouth surfaces, hard and soft palate, esophagus, and gut. Stratified squamous epithelium is the tough surface cells that ordinarily protect underlying tissues from damage or invasion by microbes.
Candida albicans is also capable of invading the lungs and causing pneumonia and septicemia, which is the spread of infection into the bloodstream.
Here is a time honored simple do-it-youself test for infection of the mouth or throat: First thing in the morning before brushing your teeth or eating, fill a small see through glass with water then gently spit onto the surface. If after an hour the spit remains on the water surface, it is unlikely you have candida in the mouth. If it grows legs downward, it indicates that yeast is growing. If the spit sinks to the bottom, you have this problem. Yeast in the mouth can quickly travel down the esophagus and into the gut.
Medical diagnosis. Difinitive diagnosis for the oral cavity is made by your clinician by swabbing the areas of your mouth and/or throat and viewing under a microscope for evidence of candida.
Infections of the esophagus and gut require inspection by gastroscopy or endoscopy procedure and the taking of samples to be examined under microscope. This examination also give the opportunity to rule out other problems. Barium swallow can show the extent of infection and any disfiguration of the esophagus that results.
What Is Atherosclerosis?A therosclerosis is a disease of arteries involving the buildup of fatty material called plaque along the walls of medium and large arteries characterized by patchy subintimal thickening, hardening, and loss of elasticity of blood vessels.
The intima is the innermost layer of an artery, having contact with blood. The subintima is beneath it.
Q: What happens when arteries become narrowed and less flexible?
A: Narrowing of the inside diameter of blood vessels and hardening of their walls reduce or obstruct blood flow through them which impairs their ability to supply tissues of the body with oxygen and nourishment.
When tissues are deprived of oxygen, pain and dysfunction results such as angina pectoris involving heart muscle because the heart continually needs oxygen never being able to rest.
It is thought that atherosclerosis develops from 1) epithelial cell dysfunction of the intima, and 2) lipid (fat) accumulation in smooth muscle cells and in foam cells, causing buildup of fatty deposits on the inside walls progressing to fibrous plaque formation. That is, intimal smooth muscle cells are surrounded by connective tissue and intracellular and extracellular lipids (fat build-up inside and outside of these cells).
Collagenous colitis is a disease of the large intestine (colon) that is characterized by microscopic inflammation of the surface mucosal lining and an abnormally thickened collagen band of tissue that develops wthin the lining of the colon.
The thicker than normal layer of collagen of at least 10 µm (reference value: 2–7 µm) can vary in different locations. Inflammation occurs with increased numbers of lymphocytes (white blood cells) and plasma cells and epithelial (surface cell) damage. These changes can only be seen under microscopic examination of multiple biopsied tissue samples taken during a colonoscopy procedure.
Q: What is collagen?
A: Collagen is a strong, fibrous protein found in connective tissue of the colon and many other tissues such as tendons. The normal basement membrane in the bowel consists mainly of collagen type IV, laminin, and fibronectin. The increased collagen band observed in collagenous colitis consists basically of collagen type I and III, which are the subtypes produced by repair functions, indicating a reactive origin to some irritant or drug.1
The biopsies should preferably be taken from the ascending colon, since the pathological hallmarks may be absent in the descending colon, and in the normally occurring thicker collagen layer in the rectosigmoid region.1 Inflammation of the ileum (last segment of the small intestine next to colon) is common.2
Endoscopy and radiological (x-ray) examinations are usually normal.3
Autoimmune disorders are frequently seen in adult patients with collagenous colitis.4 In the study below by Koskela et al. concomittent autoimmune diseases were present in 53% of patients with collagenous colitis.5
Importantly, the finding of collagenous colitis in patients with autoimmune diseases may reflect the treatment with NSAIDs (non-steroidal anti-inflammatory drugs), such as Ibuprofin and aspirin, PPIs (proton pump inhibitors), and other drugs. However, if secondary forms of collagenous colitis are not taken into consideration, underlying, treatable diseases may be overlooked, while only the gastrointestinal symptoms are treated symptomatically or with budesonide (a steroid).6
Treatment with budesonide steroid is efficacious irrespective of bile acid malabsorption.7
Budesonide at a mean dose of 4.5 mg/day maintained clinical remission for at least 1 year in the majority of patients with collagenous colitis and preserved health-related quality of life without safety concerns. Treatment extension with low-dose budesonide beyond 1 year may be beneficial given the high relapse rate after budesonide discontinuation.8
See below for nutritional deficiency problems caused by steroid usage and steps to be taken for correction.
Lymphocytic colitis is a microscopic inflammation of the large intestinal mucosa with infiltration of lymphocytes (IELs) that is characterized by non-bloody secretory diarrhea.
Secretory diarrhea describes bowel movements that consist of a large volume of liquid stool.
Q: What are IELs?
A: IELs is an abbreviation for intraepithelial lymphocytes, which are white blood cells that infiltrate within epithelial cells or between them. Epithelial cells form the surface mucosa of the large intestine also called the colon.
The histopathological criteria (biopsy) for lymphocytic colitis are a density of at least 20 IELs per 100 surface epithelial cells; chronic inflammatory infiltrate of mononuclear cells in the lamina propria; epithelial damage; and a subepithelial collagen layer of less than 10 µm. The increased collagen band consists basically of collagen type I and III, which are the subtypes produced by repair functions, indicating a reactive origin.1That is, the mucosa is reacting to some irritative substance.
Up to 10% of adults undergoing colonoscopy for investigation of chronic diarrhea and having visibily normal appearing mucosa may have lymphocytic colitis.2
Bile acid malabsorption has been shown to coexist in 60% of patients with lymphocytic colitis.1
Lymphocytic colitis (LC) is categorized as primary or secondary. Primary LC is a clinical and histopathological disease of unknown cause. Secondary LC may develop as the result of iritating factors acting on the colon such as smoking or many medications. In one study, the most common drug treatments as a percentage of the study group were corticosteroids (32.1%), proton pump inhibitors (26.0%), antidepressant drugs, specifically selective serotonin reuptake inhibitors (21.4%), angiotensin-converting enzyme inhibitors or angiotensin II receptor antagonists (18.3%), statins (17.6%), thyroid hormones (17.6%), and beta-blockers (16.0%).3
Secondary lymphocytic colitis is associated with several concomitant diseases including celiac disease. This is why lymphocytic changes must be interpreted with caution before considering them as a separate entity of autoimmune origin, instead of secondary reactions to ischemia and toxic stimulants. Efforts must be made to better classify and diagnose patients with real, primary lymphocytic colitis to avoid over-prescription of corticosteroids for treatment.3
Ulcerative colitis is an inflammatory disorder of the colon characterized by continuous inflammation of the mucosa and submucosa usually with small ulcers, extending from the rectum and typically involving the distal colon, rectum, and anus and producing bloody diarrhea.
While the severity of ulcerative colitis varies among patients, iron deficiency anemia often develops due to blood loss especially when there are many bloody bowel movements in a day.
The onset of ulcerative colitis is most commonly in young adulhood.
Q: Is this disease painful?
A: Yes with the passage of stool.
Psychological stress and subsequent dysbiosis exacerbate ulcerative colitis.
Psychological stress activates multiple physiological processes aimed at maintaining balance within the body. These physiological processes also have the capacity to influence the composition of microbial communities in the digestive tract, and research now indicates that exposure to stressful stimuli leads to gut microbiota dysbiosis.1
While the relative abundance of many different bacterial types can be altered during stressor exposure, findings in nonhuman primates and laboratory rodents, as well as humans, indicate that bacteria in the genus Lactobacillus are consistently reduced in the gut during stress.2
Presently, ulcerative colitis cannot be cured. This condition has a course of remissions, when symptoms subside, and flares, when symtpoms get worse. Treatment is aimed to reduce flares and promote remission. In all cases, correction of dysbiosis improves the condition.
Ulcerative colitis is associated with increased incidence of cancer of the colon.3