Hyaluronic Acid For IBD

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What is Hyluronic Acid?

Hyaluronic acid (HA) is a long, unbranched polysaccharide, GAG (glycosaminoglycan).

Glycosaminoglycans’ primary role is to maintain and support collagen, elastin and bounce in the cellular spaces and keep protein fibers in balance and proportion. GAG’s also promote the ability of the collagen and elastin fibers to retain moisture, therefore remaining soluble. Known as the water reserve of the viable epidermis and dermis, these carbohydrates are dependent on fluid intake. Hyaluronic acid molecules can hold nearly 10,000 times their own weight in water due its neutral ph and molecular structure. Glycosaminoglycans are also linked to the lymphatic system. Glycosaminoglycan’s natural uses in the body include heparin as an anticoagulant, hyaluronate as a component in the synovial fluid lubricant in body joints, and chondroitins which can be found in connective tissues, cartilage and tendons. There are no adverse reactions associated with glycosaminoglycans, in part because they are naturally created in the body but as we age production decreases. Bone broth is a natural source of hyaluronic acid due to the nutrient being released from the joints during the slow cooking process.

The molecule is present in many strains of bacteria and is ubiquitous in all Vertebrates, where it is particularly abundant in the embryonic tissues and in the extracellular matrix (ECM) of adult soft connective tissues. However, it reaches its greater concentrations in the vitreous body of the eye and in the umbilical cord.

The first clinical use of hylauronic acid occurred in the 1950s in the field of ophthalmic surgery but nowadays the most widespread use is in arthritis, where it replaces the pathological synovial fluids. Hyaluronic acid is usually sought for treatment of arthritis and joint pain and for skin care.

The view of the role of hyaluronic acid has changed dramatically, unlike other glycosaminoglycans that are synthesized within the cell, HA is synthesized by three transmembrane enzymes at the inner side of the plasma membrane and then extruded directly into the extracellular space.

Hyaluronic acid is decomposed into two- to six-membered polysaccharides by enteric bacteria, and these polysaccharides are then partially absorbed in the body by the small intestine, and can move into the joints and other tissues. Accounting for these degradation mechanisms, it is estimated that the half-life of hyaluronic acid in the skin is 1–2 days, the half-life in the bloodstream about 24 h, in the eye, it is 24–36 h, 1–3 weeks in the cartilage and about 70 days in vitreous humor. The balance between the synthesis and degradation processes of HA plays an essential regulatory role in the human body, as it determines not only the amount of hyluronic acid, but also its molecular weight. It is the molecular weight and circumstances of synthesis or degradation that determine the biological actions. Hyaluronic acid distributes to lymphatic system and connective tissues.

The wide potential of HA in therapy for inflammatory diseases including its benefits in pathologies of the joints, intestines, lungs, heart, vascular system and nerves. Hyaluronic acid has also been shown to exhibit anti-inflammatory, antioxidant and antihyperuricemic effects in vivo for the treatment of gout.

Arthritis

Osteoarthritis is a pathology that is very widespread among the population of middle and senile age. Hyaluronic acid and is a significant advance in the therapy of osteoarthritis helping to regenerate cartilage. Hyaluronic acid is also useful for the treatment of Rheumatoid arthritis (RA).

There are now many other applications for hyaluronic acid as hyaluronic acid has been demonstrated to play a crucial role by influencing inflammatory, proliferative, or re-modeling phases of the healing process. Hyaluronic acid appears to provide cartilage protection by the down regulation of cytokines, free radicals, and proteolytic enzymes in synovial fluid.

Vascular Tissue

Hyaluronic acid is an important component of vascular tissue. HA has proved active in promoting the migration and subsequent activation of tissue macrophages and neutrophils which once activated, are able to secrete angiogenic and mitogenic factors essential to growth and repair. An in vivo and in vitro study investigating the role of HA in embryonic stem cell differentiation toward a smooth muscle cell lineage has proven that remodeling the HA microenvironment is a critical step in directing stem cell differentiation toward a vascular lineage, suggesting a potential role of HA for treatment of vascular diseases. Hyaluronic acid enhances the proliferation of endothelial cells accelerating healing.

Commentary:

Aside from quietness, I re-awakened to the benefits of extracting myself from tv, newspapers, magazines, news, radio etc. and when presented with the next shiny ball in the media; I concluded it was time once again to seek higher benefit as drawn from the well of the aesthetic life. Aside from creativity, history and philosophy has been about the only respite from the mental porn of the last two years; when I realized I was just drifting along and being too distracted by distractions (the plot of the enemy) in so called alt media it seemed necessary to just stop the drift and turn most of it off and seek higher ground as I did over a decade ago …..

The book mentioned is My Daily Bread A Summary of The Spiritual Life by Anthony J. Paone, S.J. – Chapter 73 The Dangers Of Knowledge

Nerve Tissue

Hyaluronic acid has found widespread use in peripheral nerve tissue engineering, supporting nerve outgrowth, differentiation, and proliferation. Hyaluronic acid demonstrated the ability to enhance the survival rates and proliferation of neural precursors, showing great potential for peripheral nerve regeneration and therapeutic potentials for the central nervous system.

A key ingredient in the therapy of inflammation.

Hyaluronic acid turnover is finely regulated by enzymatic synthesis and degradation and when compared to other extracellular components, this turnover is relatively fast. Of the estimated 15 g in humans, about a third is reversed every day. Why this metabolism is so active in the body is unknown, the intrinsic capacity of hyaluronic acid to act as an eliminator of ROS is possibly an advantage in its rapid turnover. During the inflammatory process, this turnover is disturbed, leading to the accumulation of the fragments associated with the spread of the inflammatory response in the extracellular spaces.

Hyaluronic acid in combination with chondroitin sulfate reduced lipid peroxidation, restored GSH (reduced glutathione) and SOD, decreased TNF-α, and reduced infiltration of activated neutrophils.

The fact that hyaluronic acid (HA) is produced by practically all types of cells means that it has multiple fundamental biological functions. HA can be involved in several cellular interactions (differentiation, proliferation, development and recognition) and biological functions (lubrication, hydration, matrix structure and steric interactions). The viscous gel formed by the HA matrices lubricates the joints and acts as a buffer for the surrounding tissues, as well as participating in tissue regeneration and remodeling processes. This molecule has mechanical and dilation properties that can adjust cellular functions, such as adhesion and expansion, and form structures, such as microvilli, which can play an important role in signal transmission. In addition to these properties, hyaluronic acid can alter the local properties of the cell membranes, acting as an external cytoskeleton and modifying and controlling the shape of the cell. During tissue injury hyaluronic acid is actively produced regulating tissue repair and disease processes.

Furthermore, hyaluronic acid can interact with specific cytokines, and thus modulate immune cell function. One example is interleukin-8 (IL-8), released by fibroblasts, monocytes/macrophages, endothelial and epithelial cells in the presence of inflammation. Hyaluronic acid is advantageous in the inhibition of unwanted immune response.

N-butyrylated (BHA hyaluronic acid) was used to assess in vitro and in vivo wound healing. BHA has been shown to significantly promote healing. It appears that the production of pro-inflammatory cytokines (TNF-α, IL-1β and IL-6), associated with M1 macrophages, is reduced in the presence of BHA. This reduction indicates that M1 macrophages are transformed into M2 macrophages, which is a fundamental part of the healing process. This transformation leads to the increased expression of growth factors (e.g., transforming growth factor-β (TGF-β) and VEGF). Improved wound healing was observed after local treatment with BHA compared to the control group, verifying that the healing process is efficient with BHA. Thus the results show that BHA demonstrates anti-inflammatory activities by modulating cytokine expression, indicating BHA’s ability to prevent the wound from becoming trapped in a chronic inflammatory state.

The anti-inflammatory, immunomodulatory, anti-proliferative, anti-diabetic, anti-aging, safe analgesic, wound healing and tissue regeneration, skin repair, and cosmetic properties that this molecule presents make it attractive for biomedical applications.

More:

The production of hyaluronic acid is related to nutrition as naturally produced but can decline with age related malnutrition, this article highlights some of the important benefits of this glycosaminoglycan as an overview. Since most GAG’s aren’t covered in depth in my book aside from chondroitin ‘sulfate’ as they are naturally produced with optimal nutrition I thought I would address the benefits of some as features. As it is a short synthesis of current reviews more articles about hyaluronic acid and perhaps other GAG’s will be coming soon. No specific brands are recommended at this time but it is best to keep hyaluronic acid as a singular supplement rather than in combination supplements if you care to supplement. Vitamin C (sodium ascorbate form is best) is a necessary co-factor for production of collagen and carbohydrate digestion. Lactose can also increase benefit through enzymatic degradation. Hyaluronic acid can also help to activate macrophages in addition to changing polarity. In medicine, like other GAG’s it is also used as a transport molecule.

Mechanisms-based anti-osteoarthritis effects of hyaluronic acid (some important studies).

Antioxidative, antinitrosative, anti-inflammatory, chondro protective, and anti-OA
Antioxidative, anti-chondroptosis, protection of mitochondrial function, and anti-OA
Free radicals scavenging, Antioxidative, and anti-arthritic
Anti-inflammatory and anti-OA
Analgesic and protected cartilage degeneration
Chondroprotective, cartilage repair, and anti-OA
Protection of chondrocytes and cartilage degeneration
Maintains normal structure and function of bone and cartilage
Anti-apoptotic, and anti-cartilage matrix degradation in OA
Cell adhesion, migration, and proliferation in maintaining cartilage homeostasis
Cartilage repair effect
Improves bone metabolism
Disease modifying effect in OA

Inflammatory Bowel Diseases

Inflammatory bowel disease (IBD) is a chronic disease of the gastrointestinal tract (GIT), caused by dysfunctional autophagic immune responses. Ulcerative colitis (UC) is a condition in which the inflammatory response is confined to the colon. Inflammation is mainly limited to the mucosa, with ulceration, edema and hemorrhage along the colon. Unlike UC, Crohn’s disease (CD) can involve any part of the gastrointestinal tract, from the oropharynx to the perianal area. Here, inflammation can be transmural, often extending to the serous, resulting in sinus pathways or fistula formation. It is also characterized by a defect in the integrity of the epithelial barrier, resulting in the translocation of microbial and other antigens, acting as external agents. Endothelial cells are known to express high levels of CD44 in inflamed IBD sites. Therefore hyaluronic acid could be ideal for treatment of the inflamed mucosa.

Study summaries using with HA for the treatment of inflammatory bowel disease.

Promotion of healing of the intestinal mucosa; reduction in intestinal inflammation
Inflammation reduction
Inflammation relief; mucosal healing; combination with hydrogel exhibits increased ability to prevent mucosal damage
Improvement in tissue regeneration
Relief of UC symptoms; increased expression of COX-2 and PGE2
Colon epithelium barrier restored

Did you know?

Slippery Elm

Slippery elm is also a safe and effective supplement for soothing inflammatory bowel conditions, providing a thick mucilage to prevent inflammation and help heal wounds. Upon contact with water, the inner bark, collected in spring, yields a thick mucilage or demulcent that was used as an ointment or salve by American Indians and early settlers. It is also commonly used to treat sore throat.

Historical Use Source:

The slippery elm tree is native to eastern Canada and eastern and central US, where it is found most commonly in the Appalachian mountains. The trunk is reddish brown with gray-white bark on the branches. In the spring, dark brown floral buds appear and open into small, clustered flowers at the branch tips. White elm (U. americana) is a related species used in a similar manner. Slippery elm also is known as red elm, Indian elm, moose elm, and sweet elm.

Demulcent/Protectant
Slippery elm prepared as a poultice coats and protects irritated tissues such as skin or intestinal membranes. The powdered bark has been used in this manner for local application to treat gout, rheumatism, cold sores, wounds, abscesses, ulcers, and toothaches. The tannins present are known to possess astringent actions. It also has been known to “draw out” toxins, boils, splinters, or other irritants.

Powdered bark is incorporated into lozenges to provide demulcent action (soothing to mucous membranes) in the treatment of throat irritation. It also is used for its emollient and antitussive actions, to treat bronchitis and other lung afflictions, and to relieve thirst.

GI/Urogenital effects
When slippery elm preparations are taken internally, they cause reflex stimulation of nerve endings in the GI tract, leading to mucus secretion. This may be the reason they are effective for protection against stomach ulcers, colitis, diverticulitis, gut inflammation, and acidity. Slippery elm also is useful for diarrhea, constipation, hemorrhoids, irritable bowel syndrome, and to expel tapeworms. It also has been used to treat cystitis and urinary inflammations.

Other uses:
The plant also is used as a lubricant to ease labor, as a source of nutrition for convalescence or baby food preparations, and for its activity against herpes and syphilis.

Toxicology:
The FDA has declared slippery elm to be a safe and effective oral demulcent.

Slippery Elm. Any brand will suffice as far as quality. In my own case, Prior to natural oral immune therapy and reversing root issues (SAM), Slippery Elm and Marshmallow Root were the only supplements that provided any relief from constant intestinal inflammation that continued for almost thirty years. They may provide similar benefit to you.

Did you know?

Marshmallow Root

A. officinalis has been traditionally used for cough, inflammation of the mouth and stomach, and peptic ulcers. It appears to have antimicrobial and anti-inflammatory properties and may be used topically to increase epithelialization of wounds. However, there are no recent clinical trials to support these uses.

Historical Use Source:

Marshmallow is a perennial plant that grows up to 1.5 m in height in salt marshes and moist regions throughout Europe, western and northern Asia, and the eastern United States. Its flowers are pink and the 3-lobed leaves are velvety due to a dense covering of hair. The plant blooms from July to September and resembles hollyhock (Althaea rosea). Marshmallow root is collected in the fall from a plant that is at least 2 years old, and is then peeled of its brown corky layer, dried, and used in commerce.

The Malvaceae family is known as the mallow family, and confusion may surround the common nomenclature and identification of plants in this group. A. officinalis should not be confused with confectionary marshmallows, which were once made from A. officinalis but currently consist mostly of sugar.

Marshmallow root has traditionally been recognized as a source of mucilage, which has been used for more than 2 millennia to treat topical wounds and as a remedy for sore throats, cough, and stomach ailments. The first recorded therapeutic use of marshmallow was in the ninth century BC. The mucilage is incorporated into ointments to soothe chapped skin and is added to foods in small quantities (approximately 20 ppm) to provide bulk and texture.

Marshmallow root and leaves contain mucilage polysaccharides (6.2% to 11.6% and 6% to 9%, respectively). The mucilage content varies considerably with the season and is highest in the winter. A purified mucilage is composed of L-rhamnose:D-galactose:D-galacturonic acid:D-glucuronic acid in a molar ratio of 3:2:3:3.3 Asparagine (2%), sugars, pectin, and a tannin have also been identified in the root. Fatty oil of althea has been addressed. Flavonoid compounds of the leaves, flowers, and roots have also been described, including glucosidoesters and monoglucosides. According to one study, flavonoid content of the white flowers of A. officinalis is higher than that of the pink and reddish-pink flowers. However, the reddish-pink flowers possess higher antioxidant activity than the white or pink flowers.

Clinical data:

A clinical trial evaluated the effects of a topical product containing A. officinalis, A. rosea (hollyhock), and other herbals for the treatment of leishmania lesions. Among patients receiving the topical herbal extract (n=86), a complete cure occurred in 74.4%, a partial cure occurred in 11.6%, and treatment failure occurred in 14%. Among those receiving the standard treatment of meglumine antimoniate injection, 24.1% experienced complete cure, 14.1% experienced partial cure, and 58.8% experienced treatment failure.

Antiulcerogenic effects

Marshmallow is possibly beneficial in providing gastroprotection from ulcers due to its mucilaginous properties and flavonoid content, which offers coverage and protection of the GI tract.

Animal and in vitro data

In a murine model, rats with ethanol-induced ulcers showed greater gastric protection with administration of A. officinalis 250 mg/kg than with control (cimetidine) (P<0.05).20 In another murine model, marshmallow did not impact the quantity of ulcers or the ulcer index following administration of indomethacin; however, it did increase histamine release.

Clinical data:

Research reveals no clinical data regarding the use of marshmallow for the treatment of ulcers.

Antitussive effects

The polysaccharides in A. officinalis are believed to exert antitussive effects via formation of a protective film on the oropharyngeal mucosa. A model of lozenges containing marshmallow has been evaluated.

Animal and in vitro data

In a study of cats, an A. officinalis polysaccharide dose of 50 mg/kg exerted cough-suppressing effects. An extract of marshmallow was less effective than the polysaccharide. In a model of airway inflammation in guinea pigs, the polysaccharide : from A. officinalis exerted cough-suppressing effects in a dose-dependent fashion. In another study of guinea pigs, it was theorized that rhamnogalacturonan’s antitussive effects might be attributed to its association with 5-hydroxytryptamine 2 (5-HT2)receptors. In vitro, althea reduced the transport velocity of isolated ciliated epithelium cells of the frog esophagus. Additionally, marshmallow may be useful in the management of cough and cold because of its ability to protect mucosal layers in the hypopharynx, and because of its spasmolytic, antisecretory, and bactericidal activity.

Clinical data:

In a clinical study, 60 patients with angiotensin-converting enzyme inhibitor–induced cough were randomized to receive A. officinalis 40 mg (given as 20 drops) or placebo every 8 hours for 4 weeks. At the end of the study, patients receiving A. officinalis had significantly lower cough scores compared with baseline (P<0.05). No significant changes were noted in the placebo group. Eight patients in the A. officinalis arm experienced almost complete resolution of cough.

Diabetes

Animal and in vitro data

In a murine model, a polysaccharide from A. officinalis reduced blood glucose levels. This may be attributed to the high pectin content in althea.

Clinical data:

Research reveals no clinical data regarding the use of marshmallow in diabetes.

Antimicrobial effects

Animal and in vitro data

In a murine model of wound excision creation, A. officinalis extract demonstrated antibacterial activity against the gram-positive organism Staphylococcus aureus, but did not demonstrate activity against gram-negative organisms.16 In an in vitro study, A. officinalis exerted antimicrobial activity against numerous periodontopathic bacterial strains. In general, the methanolic extract exerted better antibacterial activity than the decoctions, suggesting a potential role in the management of patients with periodontitis.28 In another in vitro study, A. officinalis demonstrated antibacterial effects against methicillin-resistant S. aureus.

Clinical data

Research reveals no clinical data regarding the use of marshmallow for its antimicrobial effects.

Neuroprotective effects

Animal and in vitro data

In a study of rats with induced hemi-Parkinsonism, an A. officinalis 10 mg/kg extract exerted neuroprotective effects.

Clinical data

Research reveals no clinical data regarding the use of marshmallow for its neuroprotective effects.

Other uses:

Effects of varying doses of A. officinalis on lipid parameters, platelet aggregation, inflammation, and gastric ulcers were assessed in rats. Following 1 month of administration, A. officinalis did not reduce total cholesterol, low-density lipoprotein cholesterol, or triacylglycerol concentrations; however, high-density lipoprotein cholesterol levels were improved with the 50 mg/kg dose. Time-dependent inhibition of platelet aggregation was demonstrated with A. officinalis. Improvements in inflammation were noted in both the acute and chronic inflammation models, with an apparent optimal dose of 250 mg/kg to exert these anti-inflammatory effects.

Interactions:

Oral medications

When taken with other oral medications, marshmallow may delay the absorption of the other medications.

Oral hypoglycemic agents/Insulin

Due to potential additive hypoglycemic effects, marshmallow should be used cautiously in patients receiving oral hypoglycemic agents and insulin.

Topical corticosteroids

Marshmallow may enhance the effects of topical corticosteroids. Use caution.

Use caution or avoid use of marshmallow in individuals receiving aminoglycosides such as gentamicin. A. officinalis extract at varying doses did not exert renal protective effects against gentamicin-induced nephrotoxicity; higher doses of the extract actually worsened renal dysfunction.

Adverse Reactions

Anecdotal evidence suggests potential allergic reactions and hypoglycemia.

Toxicology

The acute LD50 of A. officinalis in mice was greater than 5,000 mg/kg.21

Avoid if pregnant.

Marshmallow Root. Any brand will suffice as far as quality. Although there are reports of long term use, addressing cause is best while producing no adverse effects. I personally avoid most supplements unless ‘food based’ such as such salmon oil, cod liver oil. GSE (grapefruit seed extract), sodium ascorbate, taurine, zinc as needed among very few others. Reduced Glutathione is a recent purchase that I decided upon after learning of this new form. I still keep Slippery Elm and Marshmallow Root on hand occasionally for sore throat but there was a time when they were daily staples so I thought I would share as the only two that actually relieved pain. Hyaluronic acid may provide even more benefit as a natural nutrition based supplement with greater properties than either Slippery Elm or Marshmallow Root.

Alternavita: All you need to know (critical info in a nutshell)..... by focusing exclusively on these foundational health and immune development issues up to 90% of chronic conditions can be eliminated.

WHO STATEMENTS: 2017 Millennium Goal

Breastfeeding,
food (security)
and water security (sanitation)

are major protective factors against malnutrition and critical factors in the maturation of healthy gut microbiota, characterized by a transient bifidobacterial bloom before a global rise in anaerobes. Early depletion in gut Bifidobacterium longum, a typical maternal probiotic, known to inhibit pathogens, represents the first step in gut microbiota alteration associated with severe acute malnutrition (SAM). Later, the absence of the Healthy Mature Anaerobic Gut Microbiota (HMAGM) leads to deficient energy harvest, vitamin biosynthesis and immune protection, and is associated with diarrhea, malabsorption and systemic invasion by microbial pathogens. A therapeutic diet and infection treatment may be unable to restore bifidobacteria and HMAGM.

Researchers found that malnourished children’s microbiota failed to follow the healthy pattern they identified in healthy children. The microbiota of malnourished children is immature, lagging in development behind that of their healthy peers. Supplementing these children’s meals with widely used therapeutic foods that increase calories and nutrient density reduces deaths from malnutrition, but it does not fix their persistent microbiota immaturity.

“Perhaps more insidious than slowing growth is malnutrition’s effect on less visible aspects of health, including impaired brain development and dysfunctional immunity, which follow these children throughout their lives”.

The Father of The Microbiome

Dr. Jeffrey Gordon

SIBO

SIBO can cause severe malabsorption, serious malnutrition and immune deficiency syndromes in children (non breastfed) and adults.

Prognosis is usually serious, determined mostly by the underlying disease that led to SIBO.

Immunizations

The WHO recommends that immunization or treatment be orally administered due to economic, logistical and security reasons. Furthermore, this route offers important advantages over systemic administration, such as reducing side effects, as the molecules are administered locally and have the ability to stimulate the GALT immune responses (Levine and Dougan, 1998; Neutra and Kozlowski, 2006; Bermúdez-Humarán et al., 2011).

Infections

For ANY infectious or parasitic disease to start, it is ALWAYS a requisite that the host suffer IMMUNODEFICIENCY. At the same time, infectious and parasitic diseases themselves cause additional IMMUNE SUPPRESSION and more MALNUTRITION. This immune suppression is SECONDARY to the accumulation of free radicals, especially oxidizing species, that occurs during and after infectious and parasitic diseases.

Clinical Aspects of Immunology and Biochem J.

Current IBD Research 2016

Currently available treatments for IBD, which target the systemic immune system, induce immunosuppression, thereby exposing the patient to the risk of infections and malignancy. The interplay between the gut and the systemic immune system determines the final effect on target organs, including the bowel mucosa. Inflammatory bowel diseases (IBD) are associated with an altered systemic immune response leading to inflammation-mediated damage to the gut and other organs.

Clinical & Translational Immunology (2016)
Gastroenterology and Liver Units, Department of Medicine, Hebrew University-Hadassah Medical Center, Jerusalem, Israel

Most importantly, the immune modulatory agents used today for IBD do not achieve remission in many patients.

Not all IBD patients benefit from currently available drugs. Young people with IBD do not want to be on long-term drug therapy. Oral immune therapy, while not yet studied in large cohorts of patients, may provide an answer to this unmet need.

Clinical & Translational Immunology (2016)
Gastroenterology and Liver Units, Department of Medicine, Hebrew University-Hadassah Medical Center, Jerusalem, Israel

Tolerance

Tolerance is the ability of the immune system to ‘see’ and respond appropriately. Without galactose (a necessary sugar) the immune system can not 'see'. Your immune system would not be able to function without galactose Your body wouldn’t know which cells are “good” and what cells are “bad.” Your body wouldn’t know who the invaders were and which ones should be attacked by antibodies. As you will learn the importance of these ‘sugars’ in gut microbiota health is a rapidly expanding field of research, only recently discovered, including HMO's (human milk oligosaccharides).

Why galactose? Milk sugar aka lactose has been shown to be very beneficial for the human body though unlike sucrose, lactose is made up of glucose and galactose. There is no fructose in lactose. It is a healthy disaccharide sugar. Galactose is known as the “brain sugar” and supports brain development of babies and children. Galactose helps triggers long-term memory formation. Galactose has been shown to inhibit tumor growth and stop its spread, particularly to the liver. This beneficial sugar can also enhance wound healing, decrease inflammation, enhances cellular communication, and increases calcium absorption.
What does immune ‘tolerance’ mean in simple language?
Immune tolerance, or immunological tolerance, or immunotolerance, is a state of unresponsiveness of the immune system to substances or tissue that have the capacity to elicit an immune response in a given organism. The Th1 cytokine profile is vital for clearance of certain organisms and ancillary immune activity, and a limiting effect on this cytokine profile may result in reduced chances for overcoming infections especially intra-cellular organisms residing within macrophages. Effective clearance will depend on appropriate macrophage activation (which occurs through IFN≥ release by Th1 and NK cells) and production of nitric oxide. If this pathway is disrupted IFN≥ secretion is blocked, impairing macrophage activation. Persistent blockade of these inhibitory receptors has lead to the breakdown in immune self tolerance, thereby increasing susceptibility to autoimmune or auto-inflammatory side effects, including rash, colitis, hepatitis and endocrinopathies. Many drugs may cause checkpoint blockade toxicity including pharmaceutical drugs termed ‘immuno therapy’ by pharmaceutical companies, these include Mab drugs and cancer treatments. Checkpoint Inhibitor–Induced Colitis: A New Type of Inflammatory Bowel Disease? Madeline Bertha, MD MS, corresponding author1 Emanuelle Bellaguara, MD, Timothy Kuzel, MD, and Stephen Hanauer, MD ACG Case Rep J. 2017; 4: e112. Published online 2017 Oct 11. doi: 10.14309/crj.2017.112 PMCID: PMC5636906 PMID: 29043290

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