Friday 11 May 2012

definition intestinal permeability leaky gut syndrome

definition intestinal permeability leaky gut syndrome

In the past few years, the interest in changes to gut permeability has risen as the association among intestinal inflammation, increased permeability, and autoimmune disease has become well established. The penetration of the intestinal mucosal barrier appears to correlate with clinical disease manifested as infection, food allergy, Crohn’s disease, coeliac disease, dermatologic conditions, colitis, or autoimmune diseases (such as rheumatoid arthritis, ankylosing spondylitis, Reiter’s syndrome, eczema, and other allergy disorders). Decreased permeability appears as a fundamental cause of malnutrition, malabsorption, and failure to thrive.

The small intestine has the paradoxical, dual function of being a digestive and absorptive organ as well as a barrier to the penetration of toxic compounds and macromolecules. The mucosal membranes accomplish this barrier function through a combination of intestinal immune function and mechanical exclusion. Elaborate immunologic and mechanical processes for excluding harmful dietary antigens, bacterial products, and viable microbial organisms are present at the mucosal level.

The distal intestine contains numerous dietary and bacterial products with toxic properties, including actual bacterial cell wall polymers, chemotactic peptides, bacterial antigens capable of inducing antibodies that cross react with host antigens, and bacterial and dietary antigens that can form systemic immune complexes.

Abnormalities of the immune system or mechanical barriers lead to enhanced uptake of inflammatory mediators and pathogenic bacteria. With clinical intestinal injury, mucosal absorption of substances that are normally excluded increases dramatically. Intestinal inflammation enhances the uptake and systemic distribution of potentially injurious macromolecules.

Peters and Bjarnason, in an excellent review of uses of permeability testing noted, “Measurement of intestinal permeability will play an increasing role in clinical investigation and monitoring of intestinal disease.”

The measurement of passive permeability using the dual sugar technique (lactulose and mannitol) may be the most useful and precise noninvasive method for assessing mucosal integrity in the small bowel. Mannitol (a monosaccharide) and lactulose (a disaccharide) are water-soluble molecules that are not metabolized by the body. Mannitol (molecular weight 182) is readily absorbed, and lactulose (molecular weight 360) is only slightly absorbed. An oral dose containing 5 g lactulose and 3 g mannitol in 10 g of glycerol is given and a timed urine sample is analyzed for the ratio of the percentage recovery of lactulose and mannitol.

Clinical Significance Studies on a wide range of illnesses have demonstrated alterations in the uptake of monosaccharides, disaccharides, or both and have correlated these changes with clinical and pathologic conditions. These illnesses, which disrupt the structural barrier of the GI tract, often result in pathologic changes in distant organs and tissues.

The clinical conditions associated with altered intestinal permeability include IBD, irritable bowel disease, malnutrition and malabsorption, accelerated aging, Crohn’s disease, intestinal infections, ulcerative colitis, endotoxemia, autism, nonsteroidal antiinflammatory drug (NSAID) enteropathy, celiac disease, chemotherapy, inflammatory joint disease, giardiasis, food allergy, trauma, alcoholism, and human immunodeficiency virus (HIV) positive status.

Some of the symptoms associated with increased intestinal permeability include abdominal pain, arthralgias, cognitive and memory deficits, diarrhea, fatigue and malaise, fevers of unknown origin, food intolerances, myalgias, poor exercise tolerance, shortness of breath, skin rashes, and toxic feelings.

The permeation of water-soluble molecules through the intestinal mucosa can occur either through cells (transcellular uptake) or between cells (paracellular uptake).

Small molecules (mannitol) readily penetrate cells and passively diffuse through them. Larger molecules such as disaccharides (lactulose) normally are excluded by cells. The rate-limiting barrier in this case is the tight junction between cells, which help maintain epithelial integrity.

The intestinal permeability test directly measures the ability of two nonmetabolized
sugar molecules, mannitol and lactulose, to permeate the intestinal mucosa. Lactulose is only slightly absorbed and serves as a marker for mucosal integrity. Mannitol is readily absorbed and serves as a marker for transcellular uptake. Low levels of mannitol and lactulose indicate malabsorption.

Elevated levels of mannitol and lactulose are indicative of general increased permeability and leaky gut. Permeability to mannitol may decrease, which is indicative of malabsorption of small molecules.

The lactulose/mannitol ratio is a useful parameter. An elevated ratio indicates that the effective pore size of the gut mucosa has increased, allowing access (to the body) of larger, possibly antigenic, molecules. One should consider the possibility of mild IBD or gluten enteropathy in these cases.

Clinical Therapeutics Treatment of altered intestinal permeability is very important for several reasons. Increased permeability can contribute to, or cause, a wide range of systemic reactions. Decreased permeability can cause malabsorption and
malnutrition, leading to a wide range of systemic effects. Correcting the altered permeability can have an immediate effect on relief of symptoms and a gradual improvement on the underlying condition. Eliminating the cause can often stop the pathologic process, allowing the body to heal and return to homeostasis.

One of the first considerations is to identify and eliminate the cause of altered permeability. Some of the most common causes of increased permeability are NSAID use, intestinal infection, dysbiosis, parasites, maldigestion, deficient immunoglobulins, allergenic foods, alcoholism, toxic chemicals, trauma, and endotoxemia. Decreased permeability may be caused by chemotherapy, gastroenteritis, IBS, food allergy, and ulcerative colitis. Identifying the cause is an important first step in reversing altered permeability.

There are a number of therapeutic substances, such as L-glutamine; zinc; vitamins A, E, and C; pantothenic acid; folic acid; glycyrrhiza; gamma oryzanol; slippery elm; aloe vera; cat’s claw; selenium; carotenoids; N-acetyl cysteine; bioflavonoids; and EFAs, which can be used for mucosal support to lower intestinal permeability. In determining which substance to use, it is helpful to understand the proposed mechanism of action. Administration of therapeutic substances must be carried out under the supervision of a medical practitioner. Application of this test to children between the ages of 2 to 12 must be conducted under the supervision of a medical practitioner, as well.

list of supplements to help ibs vitamins herbs and minerals

here is a list of popular supplements to help ibs vitamins herbs and minerals, though never take too many as you will only make your ibs worse by overloading your system.

first are some of the ones i have found to help with ibs in moderation: calcium, probiotic plain yoghurt, l-glutamine, msm powder.

the list below:

Digestive herbs/Nutrients

Hydrastis canadensis (goldenseal root)
Gentiana lutea (gentian root)
Betaine hydrochloride
Bromelain
Papain


Antiinflammatory herbs/Nutrients


Curcuma longa (tumeric)
Zingiber officinale (ginger)
Uncaria tomentosa (cat’s claw)
Tanacetum parthenium (feverfew)
Boswellia serrata (boswellia)
Quercetin
Zinc and copper

Antiparasitic and Antimicrobial Herbs

Juglans nigra (black walnut)
Artemisia annua (wormwood)
Berberis vulgaris (bearberry)
Allium sativum (garlic)
Pau d’arco

Therapeutic Oils

Eicosapentaenoic acid (EPA) (n-3)—salmon, mackerel, sardine
Docosahexaenoic acid (DHA) (n-3)
Gamma-linoleic acid (GLA) (n-6)—evening primrose oil, borage oil
Alpha-linolenic acid (ALA) (n-3)—linseed oil, pumpkin see oil,

Prebiotics and Probiotics

Fructo-oligosaccharieds
Lactobacillus acidophilus
Bifidobacterium bifidum

Fiber (35-40 g/day)

Psllium husks
Slippery elm
Wheat, oat, and rice bran

Water

Drink 1.5 L of filtered water daily

Mucosal Support

L-glutamine
Zinc

other potential help

Vitamin A
Vitamin E
Vitamin C
Pantothenic acid
Folic acid
Glycyrrhiza
Gamma oryzanol
Slippery elm
Aloe vera
Cat’s claw
Selenium
Carotenoids
N-acetyl cysteine
Bioflavonoids
Essential Fatty Acids (EFAs)

a cdsa stool test for ibs

a cdsa stool test can be used to check for ibs

The CDSA profile is recommended for an initial, thorough evaluation of GI tract function. The information provided includes the following:

● Macroscopic (color, form, consistency, mucus, blood, pus, fibers, food remnants)

● Microscopic (starch, meat fibers, vegetable cells and fibers, red blood cells,
white blood cells, fat globules)

● Biochemical (pH, occult blood, chymotrypsin, cholesterol, triglycerides,
total fecal fat, long-chain fatty acids, SCFAs)

● Parasitology (all pathogenic and nonpathogenic parasites)

● Bacteriology (normal flora, imbalanced flora, potential pathogens)

● Mycology (yeasts and molds, specifically Candida albicans)

A CDSA comprises the stool parasitology and culture and the microscopy and biochemistry panels. The stool parasitology and culture provides an analysis of parasitology, bacteriology, and mycology. A 3-day follow-up analysis is performed when a parasitic infection is detected in the CDSA.

The stool microbiology follow-up provides an analysis of bacteriology and mycology.

Patients should be instructed on the importance of proper specimen collection (refer to collection instructions). Only those specimens collected in appropriate kits (provided by the laboratory) should be analyzed. To obtain the most accurate laboratory results, specimens must arrive at the laboratory within 72 hours of collection. Delay in samples reaching the laboratory can cause bacterial overgrowth or death and biochemical changes that may produce inaccurate results and diagnoses.

bacterial overgrowth fermentation and yeasts in the stomach and small intestine

bacterial overgrowth fermentation and yeasts in the stomach and small intestine

Fermentation (Bacterial Overgrowth). Fermentation is a condition of overgrowth of endogenous bacteria and yeasts in the stomach and small intestine. It is exacerbated by gastric hypochlorhydria (stomach hydrochloric acid deficiency), abnormal motility, immune deficiency, and poor nutrition.

Bacterial overgrowth can also occur without any specific symptoms. Fermentation increases the risk of systemic infection and gastric cancer in individuals with hypochlorhydria and can increase intestinal permeability in susceptible individuals. Bacterial overgrowth (fermentation dysbiosis) may cause mucosal damage (degradation of intestinal brush border enzymes by bacterial proteases), pancreatic insufficiency, altered fat absorption, reduced vitamin B12 availability (bacterial consumption of cobalamine), bacterial conversion of nitrates to nitrites and nitrosamines, and elevated levels of SCFAs.

Deficiency. Reduced concentration of normal fecal flora such as Bifidobacterium sp., Lactobacillus sp., and Escherichia coli create an imbalance that leads to deficiency dysbiosis. An unfavorable alteration in the balance of normal flora can be caused by antibiotic therapy or a diet depleted in soluble fiber. In rare situations, chronic exposure to ingested xenobiotics can have the same effect. Individuals suffering from symptoms of irritable bowelsyndrome (IBS) and food intolerance may have imbalance of fecal flora (decreased ratio of anaerobes to aerobes) and decreased fecal SCFAs.
Deficiency dysbiosis and putrefactive dysbiosis are conditions generally treated using similar protocols.

Sensitization. Inappropriate immunologic responses to organisms inhabiting the gut lumen and adhering to the intestinal mucosal surface can be triggered by products of dysbiosis and components of normal intestinal flora. Such responses lead to inflammatory conditions, which are associated with IBS and inflammatory bowel disease (IBD), and increased intestinal permeability, which permits the absorption of enterotoxins, bacterial and food antigens, and bacterial debris. Increased intestinal permeability is involved in the cause of inflammatory joint diseases (arthropathies) and allergy (asthma, eczema).

Infection. Susceptibility to infection by viruses, bacteria, fungi, and parasites is higher in dysbiosis. The prevalence of these infectious agents has increased dramatically in recent years, because of factors such as international travel, contaminated processed foods, and increased antibiotic use.

Changes in global climatic conditions may also have an effect on the normal balance and the abundance of infectious agents. Intoxication. Chemical poisoning of vital biochemical and microbiologic processes by xenobiotics and therapeutic agents (e.g., antibiotics) can cause physiologic imbalances and contribute to dysbiosis. Adetailed assessment of a patient’s history should identify whether intoxication is implicated.

Putrefaction dysbiosis and the GI tract digestion and absorption of food

Putrefaction dysbiosis and the GI tract digestion and absorption of food

The GI tract, for the purposes of understanding the process of digestion and absorption, can be divided into four main areas: the mouth, stomach, small intestine, and large intestine. The mouth is responsible for mastication and the physical break up of food. Saliva and enzymes mix with food to facilitate transit, digestion, and protection of the pharyngeal and esophageal mucosa.

The stomach mixes and digests food by gastric juices (emulsifiers, enzymes, acids) and orders delivery to the small intestine. In turn, the small intestine is the major site for digestion and absorption, mediated by pancreatic enzymes and bile acids. Residency time of nutrients is crucial to efficiency of absorption. The large intestine is responsible for the absorption of water and microbial fermentation of soluble fiber, resistant starch, and undigested carbohydrates, as well as the production of short-chain fatty acids (SCFA) and pH control of feces.

The GI tract provides an ideal environment for a vast and diverse array of normal flora. These bacteria exert positive effects and are vital for well-being and health. As a consequence of their metabolic activities and when dysbiosis occurs, they may also exert negative effects.

Few of the bacteria ingested with food or drink or which originate in the nose, mouth, or oropharynx survive the very acidic conditions in the stomach. Hence, colonization of the stomach is an infrequent event (<10 viable organisms/mL of stomach contents is the norm), although it may occur when Helicobacter pylori invade the stomach mucosa.

Putrefactive dysbiosis is more likely when diets high in animal protein and fat and low in fiber are consumed. Significant imbalances in stool bacteria populations occur (i.e., increased Bacteroides sp. and decreased Bifidobacterium sp.) with consequent major disturbances to enzyme activity and metabolism, causing the following: decarboxylation of amino acids (production of vasoactive and neurotoxic amines like histamine, octopamine, tyramine), catalysis of tryptophan by bacterial enzyme tryptophanase (production of indoles, skatoles, phenols, etc.), hydrolysis of urea to
ammonia by increased bacterial urease (Bacteroides sp., Proteus sp., Klebsiella sp. activity) that results in raised stool pH and yeast/fungal overgrowth, hydrolysis of conjugated bile acids and hormones by bacterial enzymes (increased stool levels of bile acids and increased plasma levels of estrogens), bacterial reduction of primary bile acids (production of secondary bile acids such as deoxycholate), reduced production of SCFAs (impaired energy synthesis in colonic epithelial cells), and compromised liver detoxification enzyme systems.

Putrefactive dysbiosis is strongly implicated in the pathogenesis of colon and breast cancer.

ibs and the complete digestive stool analysis cdsa

ibs and the complete digestive stool analysis cdsa

Optimal health is every individual’s desired state, in which well-being is achieved by a balance between nutrition and lifestyle. Lifestyle essentially includes physical condition, psychologic disposition, and the physical environment.

The many nutrients, which are absorbed by the GI tract, act to maintain the body’s homeostasis in optimal balance.

The synergy of balanced nutrition and lifestyle are fundamental to the control of predisposing factors involved in the onset and progress of disease.

Normal human bacterial microflora in the small and large intestine maintain a delicate balance. Their metabolic and enzymatic activity is critical in the metabolism, biotransformation, and absorption of nutrients. These nutrients include all compounds taken orally and all substances entering the intestine via the biliary tract or by direct secretion into the lumen.

When the microflora balance is disturbed (dysbiosis), these metabolic and enzymatic
activities can be severely compromised. Dysbiosis is a state in which imbalances in intestinal flora cause changes to normal GI processes, manifesting in clinical and preclinical conditions, which can lead to varying degrees of unwellness. The symptoms of dysbiosis can vary significantly between individuals; however, the causes can be placed into four major categories, namely, putrefaction, fermentation, deficiency, and sensitization.

Infection by viruses, bacteria, fungi, and parasites and chemical attack (intoxication) by xenobiotics and therapeutic agents (drugs, etc.) can also be implicated. Dysbiosis can lead to the breakdown of mucosal integrity (leaky gut), contributing to increased absorption and compromised liver function.

The complete digestive stool analysis (CDSA) offers a practical and economical noninvasive assessment of the functional health of the entire GI tract.

The CDSA may provide an important opportunity in the assessment of chronic disorders and imbalances in the GI tract by investigating biochemical and microbiologic parameters resulting from altered digestion, absorption, motility, microflora imbalance, metabolic activity, immune function, and disease processes such as infection and inflammation.

The GI tract is arguably the body’s most strategic organ for metabolism, biotransformation, and absorption of nutrients. Microbiologic and biochemical enterohepatic functions are important factors in human health and may be etiologic agents in the onset of disease. Therefore assessment of chronic health issues should include a thorough evaluation of GI tract and enterohepatic status.

The CDSA provides baseline diagnostic information on which current and future GI well-being can be gauged. The CDSA is not indicated as a procedure for the diagnosis of underlying disease.

leaky gut gastrointestinal (GI) tract and the liver

leaky gut gastrointestinal (GI) tract and the liver explained

You are what you eat is a common saying that is referred to in the context of general health. However, it is an oversimplification of an individual’s potential to achieve optimal health. It assumes that he or she consumes a balanced nutritional diet, lives and works in a clean environment, is stress and infection free, and has inherited defective-free genes. A balanced diet alone should act as the foundation for excellent health and well-being—if only it were that simple. For example, it is well-established that some foods are grown in nutrient deficient soils!

The manifestation of chronic ill health is determined, in most instances, by the low-level impact of prevailing factors causing a cascade of interrelated stresses on physiologic processes and organ functions, which results in critical disturbances to homeostasis and health. The major organs governing the initiation and progression of these processes are the gastrointestinal (GI) tract and the liver, respectively.

The GI tract must digest and process food, selectively absorb essential nutrients and biochemicals and eliminate toxic, allergenic, and inflammatory compounds. The microflora in the small and large intestine must be in balance to ensure the health and function of the intestinal mucosa.

Imbalances in microflora can alter the immunologic and mechanical integrity of the mucosa (“leaky gut”), thus permitting absorption of inflammatory, allergenic, and toxic molecules.

The liver must detoxify the body by removing endogenous waste products (i.e., end products of metabolism), xenobiotics (i.e., ingested, inhaled, and dermally absorbed toxic chemicals), and absorbed endotoxins (i.e., GI products absorbed through a leaky gut).

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