I read the new post about hyaluronic acid, give some minor news updates and introduce the next series on kefir and the importance of autophagy in normal cell process.
Commentary:
News note reminder on the next possible series regarding kefir and diabetes and another beneficial substance/extract, possibly a ferment that enhanced the Langerhans islet in the pancreas and β-cells in diabetic rats. Also possibly shows that trans fatty acid profile and insulin resistance are not major factors involved toward developing diabetes but instead that gut health, probiotics and microbiota play a major role in healthy insulin production and response.
Update video that will be added to intro to colostrum in features on home page.
Part B of some of the conditions that I forgot. GC protein deficiency, by chemo type drug, it was a T cell destroying MS drug that affected liver function. The term CFS and the first actual case that led to the terminology was due to a toxic event; (chemical spill) therefore CFS refers to this toxicity syndrome event involving a chemical with the suffix ‘ene’, unless you’ve been exposed to that chemical you do not have CFS. Many toxic events have occurred in history with similar chemicals, benzene, kerosene etc. Toxicity and fatigue can worsen over time (and be severe) but CFS is condition specific to a particular toxic event, I was not exposed. The major presidential initiative, ‘The War On Cancer’ ending in the 1970’s, failed to find cancer causing ‘viruses’, funding dried up and thus began the new fear mongering marketing technique where ‘epidemics’ du jour began to make headlines in order to boost ‘sales’ and raise research dollars, especially for ‘vaccines’. A thought provoking reminder, ‘Polio’ and ‘smallpox’ ‘vaccines’ remain remarkably successful? while all others based on more advanced ‘technology’ require many, many, many ‘boosters’ which should lead anyone to question entire events. Colostrum prevents and treats endotoxemia. The genetic expression regarding mold is HLA-DR, I provide evidence in my book that this ‘genetic’ expression can be switched at will (with fish oil) undermining another concept that ‘genetic’ is a fixed state, just one of many written in stone concepts that I have helped expose over the years as being questionable.
The Nature Of Things – Refuting The Scientific Establishment
Why I think being precise in language and meaning matter. The great divide, see The Breakfast Club – Sticky – Refuting The Scientific Establishment Worldview if you want a greater understanding of ‘circular arguments’ and non-sensical meaning such as ‘asymptomatic carrier’ or ‘passenger virus’, our endless label syndromes, assigning meaningful importance to nonsense, ‘in silico’ etc. If you want to know how we got here, the definition of letting ‘man’ define and assign meaning to ‘the nature of things’ with no correspondence to a universal is nominalism. Example, if I say the grass is yellow, it’s yellow and the concept of green is a label that I determine. A modern viewpoint. I think you get where that has led. There was a time where if two parties did not see green grass in the absence of color blindness one of them would be in a straightjacket. How you get to no science, no health but an end game of money, power or prestige.
Anyway, how we get ahead is by disputing nominalism instead of going along to get along. As Dr. Cowan and others reiterate if we let this slide we will only be subject to more of the same. I propose attacking the term ‘infective’ as opposed to does a thing exist or not exist as being more productive and when we avoid this straw man we will likely be much further ahead. As in; autophagy, how your body utilizes it’s own nutrients (hyaluronic acid) to recycle and repair and prolong the life of cells.
Utilize: To make practical or effective use of, how plants (living things) utilize nutrients to produce seeds.
Very simple, 99% with ‘flu’ don’t die of ‘flu’, they die of bacterial pneumonia, therefore pick up the real ball and tackle the real problem instead of promoting falsehoods via nominalism.
95% of chronic conditions aren’t caused by anything you read about in general media but risk is assigned to three or four (toxicity/drugs) major factors which can be addressed and which were understood quite clearly until the modern era.
1. In 1991 Anthony Fauci proved that the “HIV” phenomena could be inhibited by antioxidants.
(Kalebic T, Kinter A, Poli G, Anderson ME, Meister A, Fauci AS. Suppression of human immunodeficieny virus expression in chronically ‘infected’ monocytic cells by glutathione, glutathione ester, and N-acetylcysteine. Proc. Natl. Acad. Sci. U S A 1991;88:986-990).
2. Hence material from ‘infected’ and non-infected cultures contain the same proteins.
So which ones can make you sick?
Only the gremlins know.
Hyaluronic Acid For Acute Kidney Injury
Hyaluronic acid (HA) is a member of a large family of glycosaminoglycans (GAGs).
Recently, it has been demonstrated that empty hyaluronic acid without bearing any therapeutic agent can be used therapeutically for the treatment of inflammatory diseases via modulating inflammatory responses. However, when combined with other common supplements such as Vitamin C it appears that hyaluronic acid can increase the benefits of those substances. Another recent application combines hyaluronic acid with curcumin advancing effectiveness of curcumin by increasing solubility.
CD44 receptor is implicated in the inflammatory process of diabetes and acute kidney inury. Based on the abnormally increased expression of CD44 receptors on renal tubule epithelial cells during ischemia/reperfusion-induced acute kidney injury, a product was developed a hyaluronic acid-curcumin polymeric prodrug targeting to epithelial cells and then relieving oxidative stress damages. The water solubility of hyaluronic acid-curcumin was significantly enhanced and approximately 27-fold higher than that of curcumin. Cellular uptake test showed hyaluronic acid-curcumin was preferably internalized by H2O2-pretreated tubular epithelial (HK-2) cells compared with free curcumin benefiting from the specific binding between hyaluronic acid and CD44 receptors. Biodistribution results further demonstrated the increased accumulation of hyaluronic acid-curcumin in kidneys with 13.9-fold higher than that of free curcumin. Pharmacodynamic studies indicated hyaluronic acid-curcumin effectively ameliorated acute kidney injury, and the exact mechanism was that hyaluronic acid-curcumin protected renal tubule epithelial cells from oxidative stress damage via inhibiting PtdIns3K-AKT-mTOR signaling pathway. This study provides a new therapeutic strategy for the treatment of acute kidney injury based on the pathogenesis of the disease.
Autophagy, aging and chronic kidney disease
Autophagy is a fundamental cellular process that maintains normal function and structure of the cell. It can be induced during stress and serves as an adaptive response for cell survival. Normal kidneys have high metabolic demands yet are relatively hypoxic. Injury or aging aggravates metabolic perturbation and activates autophagy in many types of renal cells. In the kidney, tubular epithelial cells consume the most energy due to active transport mechanisms and therefore are the most susceptible to injuries from hypoxic or low-energy states.
Autophagy is an evolutionarily conserved mechanism in which lysosomes mediate bulk degradation of cellular components as an adaptive response to starvation. Progress in the research field has led to the discovery that autophagy is active in all cells under basal conditions and can be further activated in response to many types of stress stimuli.
A lysosome is a membrane-bound cell organelle that contains digestive enzymes. Lysosomes are involved with various cell processes. They break down excess or worn-out cell parts. They may be used to destroy invading viruses and bacteria. If the cell is damaged beyond repair, lysosomes can help it to self-destruct in a process called programmed cell death, or apoptosis.
Autophagy functions to recycle nutrients, remove damaged organelles and protein aggregates and eliminate invading pathogens. The key morphologic feature of autophagy is the formation of intracellular autophagic vesicles that include autophagosomes and autolysosomes. The earliest description of autophagic structures was in the kidneys of newborn mice that underwent an initial starvation period following birth. Sam Clark, a researcher who was interested in cellular differentiation of newborn kidneys, first reported the ‘round bodies’ that contained ‘lamellar structures and mitochondria’ under electron microscope in 1957. In 1963, Belgian biologist Christian de Duve coined the term autophagy (‘self-eating’ in Greek) (De Duve 1963) and eventually won the Nobel Prize in Physiology or Medicine in 1974 for his discovery of lysosomes. Once again, in 2016, autophagy received the highest level of recognition when the Nobel Committee honoured Yoshinori Ohsumi for his scientific contributions to the field of autophagy with the Nobel Prize in Physiology or Medicine. This further exemplified the importance of autophagy as a fundamental cellular process that regulates cell homeostasis and provides a mechanism for cell survival during stress and injury. As such, autophagy has been shown to play a critical role in development, physiology, ageing and disease in many organ systems including the kidney.
Autophagy requires initiating signals followed by coordinated activities among proteins encoded by the Atg genes and other regulatory molecules. Activation of these proteins triggers the formation of isolation membranes that elongate to form autophagosomes, which then fuse with lysosomes to form autolysosomes. Autolysosomes contain enclosed cargo that is to be degraded. Starvation is a powerful stimulus for autophagy, and this response is regulated in part by the main nutrient sensor, (mTOR). Under nutrient-rich and growth factor-abundant conditions, mTOR complex 1 (mTORC1) is activated, which phosphorylates and inactivates the autophagy-activating kinase 1 complex. In contrast, nutrient deprivation, especially amino acid deficiency, leads to mTORC1 inactivation thus removing its inhibitory effect on autophagy.
Kidneys receive 20–25% of cardiac output to maintain glomerular filtration and energy-dependent ion transport. Although the renal cortex has a rich blood supply, there is pre-glomerular diffusional shunting of oxygen from arteries to veins and this limits oxygen delivery to tubules rendering epithelial cells susceptible to hypoxic injury.
Aging kidneys are more susceptible to hypoxia. Both hypoxia and incomplete reduction of O2 in the mitochondria result in accumulation of reactive oxygen species (ROS). Mitochondrial damage and ROS have been shown to be one of the mechanisms involved in age-related tissue injury. Caloric restriction, which increases the expression and activity of NAD-dependent deacetylase sirtuin 1 (Sirt1), reduces mitochondrial oxidative damage in the aging kidney by stimulating mito-phagy to remove dysfunctional mitochondria, thus protecting kidneys from aging.
Autophagy serves as an injury response in renal tubules. Severe ischaemic, chemical or obstructive injuries to renal tubules could result in necrosis, apoptosis, necroptosis, ferroptosis or other forms of regulated cell death. Under stress conditions, tubular epithelial cells utilize autophagic machinery as a survival mechanism.
Taken together, the biological function of autophagy in renal tubular epithelial cells could be summarized as the following. Autophagy maintains cell homeostasis of the healthy tubules. Aging kidneys experience more hypoxia and oxidative stress and exhibit physiological and metabolic adaptations including changes in autophagic activity. Although controversies remain as to whether autophagy declines during aging, a recent publication indicates that aging kidneys demonstrate a high level of autophagy and that this is crucial for mitochondrial quality control. Following injury, autophagy is stimulated for energy reutilization to improve the chances of cell survival as well as removing damaged organelles to facilitate tubular repair. Perturbations in renal repair have been shown to increase the risk of developing chronic kidney disease. Interestingly, aging kidneys share these features. It is possible that non-productive renal repair may accelerate renal aging where vascular damage and hypoxia play a key role in the metabolic alterations.
Recent studies indicate that hyaluronic acid-curcumin effectively ameliorated acute kidney injury via inhibiting PtdIns3K-AKT-mTOR signaling pathway, therefore increasing solubility and enhancing benefit of curcumin and perhaps providing treatment strategies for chronic kidney disease as well as acute kidney injury.
More:
The production of hyaluronic acid is related to nutrition and is naturally produced but can decline with age related malnutrition, this article highlights some of the important benefits of this glycosaminoglycan as an overview. 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.
Corrections:
Collagen and GAG Types
Collagen is made up of proteins within a family of GAG’s, some are sulfated, chondroitin sulfate is one example. Hyaluronic acid is not a protein but a muco-polysaccharide. Both are considered GAG’s. The main difference between collagen and hyaluronic acid is that collagen is a polymer of protein while hyaluronic acid is the biopolymer of carbohydrates. Both are often found in the same bodily constituents (synovial fluid for example). Vitamin C, sodium ascorbate plays a critical role for both in bio synthesis and is required for the production of collagen.
Autophagy explained.
This series on hyaluronic acid will be finished next week with a combined benefits piece. Worth a review of ‘dysfunctional’ autophagic syndromes like IBD. This includes macrophage activation ‘proper’ immune response including the return to homeostasis.
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
The Elderly
Mammal milk is required for enhanced phagocytosis as shown by research, especially in the elderly. Whole fat mammal milk can actually restore phagocytosis in senescent cells in the elderly. Phagocytosis, by which immune cells ‘eat’ bacteria or infected cells, is one of the mechanisms that help to resist infections. Lactic acid bacteria strains like acidophilus also increases phagocytosis.