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Think of your GUT as a very long tube that starts in your mouth and ends at your butt? Dependent on what you push through this long and windy tube you can develop 2 main problems.
1.) The tube can clog up with deposits of toxins that cause inflammation and damage to the gut lining. Especially heavy metals, pesticides, fungicides and herbicides cause a serious risk to your gut wall and the protective membrane that keep bacteria out of your blood stream.
2.) The deposits in the tube becomes the breeding ground of all sorts of wurmin, parasites and bacteria. Think of a dirty sure-line where the walls are covered with fungi, mold and bacteria. This slimy cover prevents the supply of Oxygen to your healthy cells which leads to anaerobic conditions and cell mutations. (Cancer) . The waste these pathogens produce is just as toxic and causes inflammation and damage to the cell wall.
The inflammation caused by either deposits and toxins or the waste of pathogens, always leads to inflammation, cell mutation, destruction of tight junctions (glue between the membrane cells) and damage of the gut lining. It's like a garden hose with many of little holes where undigested foods, proteins and bacteria sprinkle into the blood stream and cause a systemic reaction.
This condition is commonly known as LEAKY GUT.
The gastrointestinal epithelium (aka the gut lining) forms the barrier between all internal body systems and external environment. This barrier stops the invasion of pathogens, toxins, and pathogens but allows the absorption of water and nutrients.
This selective permeable barrier is regulated via inter-cellular tight junction structures.
Damage to the intestinal tight junction barrier followed by the invasion of harmful substances leads to inflammation and acts as a trigger for the development of intestinal and systemic diseases as well as overall inflammation.
As leaky gut progresses it destroys the tiny finger like projections known as microvilli affecting absorption of vital nutrients and impairs digestion of foods.
As the damage progresses to the tight junctions, the gaps become wider and wider allowing unwanted particles into the bloodstream.
The damage of the intestinal wall (epithelial barrier) and later the dysfunction and inflammation are major factors leading to severe intestinal diseases commonly known as:
So what do all of these conditions and diseases have in common? They all indicate a leaky gut and lead to systemic inflammation which links them directly to cancer, osteoarthritis, food sensitivities, depression and many other chronic degenerative diseases.
Once pathogens and other harmful substances pass through the tight junctions of the gut they enter your bloodstream. Once in your bloodstream they can travel throughout the body creating more inflammation and infection!
These repeated invasions lead your body into a vortex of degeneration, weakness, infections and stress eventfully leading to fatigue, food intolerances, and many other symptoms completely unrelated to the gut.
Very rarely are connections drawn between these diseases and the GUT. They are treated separately and are in conventional medicine completely unrelated.
Ironically the gut is responsible for producing a neurotransmitter needed to combat or avoid depression.
Depression is caused by a lack of the neurotransmitter serotonin. This neurotransmitter aids in the regulation of mood, appetite and metabolism and is produced and secreted by cells in the gut.
So when someone is suffering from depression it doesn’t necessarily mean that there is external stress and unfortunate life scircumstance. Perhaps it’s what this person eats and how far the leaky gut has already destroyed the gut lining.
· Food allergies and food sensitivities
· Poor diet
· Celiac disease
· Pharmaceutical drugs
· Exposure to heavy metals
• Celiac disease
• Multiple sclerosis
• Chronic fatigue syndrome
• Irritable bowel syndrome
• Ulcerative colitis
• Chronic hepatitis
• Cystic fibrosis
• Multiple chemical sensitivities
• Accelerated aging
• Colon cancer
• Crohn's disease
• Food allergies
• Pancreatic dysfunction
• Anyklosing spondylitis
• Inflammatory bowel disease
• Liver dysfunction
Abdominal pain (chronic)
Shortness of breath
Fevers of unknown origin
Gluten intolerance (celiac disease)
Multiple chemical sensitives
Poor exercise tolerance
Recurrent bladder infections
Recurrent vaginal infections
Swollen lymph glands
Constant hunger pains
There are some remedies known to help in repairing leaky gut. One of the more famous therapies for leaky gut is the Gaps Diet with bone broth for 4 weeks to 3 months. Restore for Life also claims good results while no evidence and control studies have been presented and patient observations show very inconsistent results.
The general consensus is that Leaky Gut is very hard to reverse and that it takes a very long time to restore the epithelium and associated lymphatic tissue. Most patients work for years to reverse the damage that has already been created and many of the so called "cures" work very slow.
Here is a mindmap of known remedies to expedite the healing process.
Considering we have evidence of over 40 years and countless studies showing exceptional results with Ozone therapy in the reversal of Leaky Gut it's a wonder how this treatment could have been suppressed for so long. Doctors are scared of using Ozone due to legal implications and private people are scared with unfounded claims that it's toxic.
Everything that is used unwisely becomes toxic. Even drinking excess water can lead to a kidney collapse and death. Oxygen can be harmful if not regulated properly, yet without, we would die instantaneously. The same rule applies to OZONE. We need it to survive but if inhaled in large quantities it causes harm. To propagate that this treatment is harmful and dangerous is a crime to mankind. Especiall as this treatment has a 0.00007% accident rate (related to needles and not ozone). It is the safest and most effective treatment in the world.
68 patients with chronic gastritis was treated with ozone and a clinical effect was observed in 89% of cases, including a decrease in inflammatory activity and normalization of microcirculation in gastric mucosa.
Don't take my word for it. Rather look at some of these
Intestinal Permeability Regulation by Tight Junction: Implication on Inflammatory Bowel Diseases
Sung Hee Lee
Institute of Pharmaceutical Research and Development, Wonkwang University College of Pharmacy; BK21plus program & Department of Smart Life-Care Convergence, Wonkwang University Graduate School, Iksan, Korea
Epithelial tight junctions (TJs) are the key structures regulating paracellular trafficking of macromolecules. The TJ is multi- protein complex that forms a selective permeable seal between adjacent epithelial cells and demarcates the boundary between apical and basolateral membrane domains. Disruption of the intestinal TJ barrier, followed by permeation of luminal noxious molecules, induces a perturbation of the mucosal immune system and inflammation, which can act as a trigger for the de- velopment of intestinal and systemic diseases. Inflammatory bowel disease (IBD) patients demonstrate increased intestinal paracellular permeability. Although it remains unclear whether barrier dysfunction precedes disease or results from active in- flammation, increased intestinal TJ disruption is observed in IBD patients suggest that dysregulation of TJ barrier integrity may predispose or enhance IBD progression. Therefore, therapeutic target to restore the TJ barrier integrity may provide effective therapeutic and preventive approaches against IBD. This review discusses the molecular structure and regulation of intestinal TJs and the involvement of intestinal TJs in IBD pathogenesis.
Changes in intestinal tight junction permeability associated with industrial food additives explain the rising incidence of autoimmune disease
Aaron Lerner & Torsten Matthias
The incidence of autoimmune diseases is increasing alongwith the expansion of industrial food processing and food additive consumption. The intestinal epithelial barrier,with its intercellular tight junction, controls the equilibriumbetween tolerance and immunity to non-self-antigens. As a result, particular attention is being placed on the role of tight junction dysfunc- tion in the pathogenesis of AD. Tight junction leakage is enhanced by many luminal components, commonly used industrial food additives being some of them. Glucose, salt, emulsifiers, organic solvents, gluten,microbial transglutaminase, andnanoparticles are extensively and increasingly used by the food industry, claimthemanufacturers, to improve the qualities of food.However, all of the aforementioned additives increase intestinal permeability by breaching the integrity of tight junction paracellular transfer. In fact, tight junction dysfunction is common inmultiple autoimmune diseases and the central part played by the tight junction in autoimmune diseases pathogenesis is extensively described. It is hypothesized that com- monly used industrial food additives abrogate human epithelial barrier function, thus, increasing intestinal perme- ability through the opened tight junction, resulting in entry of foreign immunogenic antigens and activation of the autoimmune cascade. Future research on food additives exposure-intestinal permeability–autoimmunity interplay will enhance our knowledge of the common mechanisms associated with autoimmune progression.
Valacchi, G, Fortino, V & Bocci, V 2005, ‘The dual action of ozone on the skin’, pp. 1096–1100.
The dual action of ozone on the skin
G. Valacchi, V. Fortino and V. Bocci
The aim of this brief review is to summarize the recent literature on the effect of ozone (O3) on cutaneous tissues. Recently it has been reported that a chronic contact with O3 can be deleterious for the skin. Our group and others have shown a progressive depletion of antioxidant content in the stratum corneum and this can then lead to a cascade of effects resulting in an active cellular response in the deeper layers of the skin. Using an in vivo model we have shown an increase of proliferative, adaptive and proinflammatory cutaneous tissue responses. On the other hand the well known activity of O3 as a potent disinfect- ant and oxygen (O2) donor has been also studied for therapeutic use. Two approaches have been described. The first consists of a quasi-total body exposure in a thermostatically controlled cabin. This treatment has proved to be useful in patients with chronic limb ischaemia. The second approach is based on the top- ical application of ozonated olive oil in several kinds of skin infection (from soreness to diabetic ulcers, burns, traumatic and surgical wounds, abscesses and skin reactions after radiotherapy). We and other authors have observed a striking cleansing effect with improved oxygenation and enhanced healing of these con- ditions. It is now clear that, on the skin, O3, like other drugs, poisons and radi- ation, can display either a damaging effect from a long exposure or a beneficial effect after a brief exposure to O2 and O3 or to the application of ozonated oil to chronic wounds.
Epithelial Tight Junctions in Intestinal Inflammation
Joerg D. Schulzke, Svenja Ploeger, Maren Amasheh, Anja Fromm, Sebastian Zeissig, Hanno Troeger, Jan Richter, Christian Bojarski, Michael Schumann, and Michael Fromm
Department of General Medicine & Pathophysiology of Enteral Nutrition & Department of Gastroenterology, Infectious Diseases and Rheumatology Institute of Clinical Physiology, Charit´e, Campus Benjamin Franklin, Berlin, Germany
The epithelium in inflamed intestinal segments of patients with Crohn’s disease is characterized by a reduction of tight junction strands, strand breaks, and alterations of tight junction protein content and composition. In ulcerative colitis, epithelial leaks appear early due to micro-erosions resulting from upregulated epithelial apoptosis and in addition to a prominent increase of claudin-2. Th1-cytokine effects by interferon- γ in combination with TNFα are important for epithelial damage in Crohn’s disease, while interleukin-13 (IL-13) is the key effector cytokine in ulcerative colitis stimulating apoptosis and upregulation of claudin-2 expression. Focal lesions caused by apoptotic epithelial cells contribute to barrier disturbance in IBD by their ownconductivity and by confluence toward apoptotic foci or erosions. Another type of intestinal barrier defect can arise from α-hemolysin harboring E. coli strains among the physiological flora, which can gain pathologic relevance in combination with proinflammatory cytokines under inflammatory conditions. On the other hand, intestinal barrier impairment can also result from transcellular antigen translocation via an initial endocytotic uptake into early endosomes, and this is intensified by proinflammatory cytokines as interferon-γ and may thus play a relevant role in the onset of IBD. Taken together, barrier defects contribute to diarrhea by a leak flux mechanism (e.g., in IBD) and can cause mucosal inflammation by luminal antigen uptake. Immune regulation of epithelial functions by cytokines may cause barrier dysfunction not only by tight junction impairments but also by apoptotic leaks, transcytoticmechanisms, andmucosal gross lesions.
Regulation of intestinal epithelial permeability by tight junctions
The gastrointestinal epithelium forms the boundary between the body and external environment. It effectively provides a selective permeable barrier that limits the permeation of luminal noxious molecules, such as pathogens, toxins, and antigens, while allowing the appropriate absorption of nutrients and water. This selec- tive permeable barrier is achieved by intercellular tight junction (TJ) structures, which regulate paracellular per- meability. Disruption of the intestinal TJ barrier, followed by permeation of luminal noxious molecules, induces a perturbation of the mucosal immune system and inflam- mation, and can act as a trigger for the development of intestinal and systemic diseases. In this context, much effort has been taken to understand the roles of extracel- lular factors, including cytokines, pathogens, and food factors, for the regulation of the intestinal TJ barrier. Here, I discuss the regulation of the intestinal TJ barrier together with its implications for the pathogenesis of diseases.
Effect of Ozone on Intestinal Epithelial Homeostasis in a Rat Model
Igor Sukhotnik, M.D.1,2*, Alona Starikov, M.D.1 , Arnold G. Coran, M.D.3 , Yulia Pollak, M.Sc.1 , Rima Sohotnik, M.D.1 , and Ron Shaoul, M.D.4
Background: The positive effects of ozone therapy have been described in many gastrointestinal disorders. The mechanisms of this positive effect of ozone therapy are poorly understood. The purpose of the present study was to investigate whether the use of ozone may potentiate the gut intestinal mucosal homeostasis in a rat model.
Methods: Adult rats weighing 250–280 g were randomly assigned to one of three experimental groups of 8 rats each: 1) Control rats were given 2 mL of water by gavage and intraperitoneally (IP) for 5 days; 2) O3- PO rats were treated with 2 mL of ozone/oxygen mixture by gavage and 2 mL of water IP for 5 days; 3) O3- IP rats were treated with 2 mL of water by gavage and 2 mL of ozone/oxygen mixture IP for 5 days. Rats were sacrificed on day 6. Bowel and mucosal weight, mucosal DNA and protein, villus height and crypt depth, and cell proliferation and apoptosis were evaluated following sacrifice.
Results: The group of O3-IP rats demonstrated a greater jejunal and ileal villus height and crypt depth, a greater enterocyte proliferation index in jejunum, and lower enterocyte apoptosis in ileum compared to control animals. Oral administration of the ozone/oxygen mixture resulted in a less significant effect on cell turnover.
The role of IgG hypersensitivity in the pathogenesis and therapy of depressive disorders
Hanna Karakuła-Juchnowicz1, Patrycja Szachta2, Aneta Opolska3,Justyna Morylowska-Topolska1, Mirosława Gałęcka2, Dariusz Juchnowicz3,Paweł Krukow1, Lasik Zofia2
Depressive episodes are associated not only with changes in neurotransmission in the central nervous system, but also may lead to structural changes in the brain through neuroendocrine, inflammatory, and immunological mechanisms. The aim of this article is to present a new hypothesis connecting the inflammatory theory of depression with IgG food hypersensitivity and leaky gut syndrome. This new potential pathway that may mediate the pathogenesis of depression implies the existence of subsequent developmental stages. Overproduction of zonulin triggered, for example, by gliadin through activation of the epidermal growth factor receptor and protease-activated receptor causes loosening of the tight junction barrier and an increase in permeability of the gut wall (‘leaky gut’). This results in a process allowing larger molecules that would normally stay in the gut to cross into the bloodstream and in the induction of IgG-dependent food sensitivity. This condition causes an increased immune response and consequently induces the release of proinflammatory cytokines, which in turn may lead to the development of depressive symptoms. It seems advisable to assess the intestinal permeability using as a marker, for example, zonulin and specific IgG concentrations against selected nutritional components in patients with depression. In the case of increased IgG concentrations, the implementation of an elimination–rotation diet may prove to be an effective method of reducing inflammation. This new paradigm in the pathogenesis of depressive disorders linking leaky gut, IgG-dependent food sensitivity, inflammation, and depression is promising, but still needs further studies to confirm this theory.
Regulation of Tight Junction Permeability by Intestinal Bacteria and Dietary Components
Dulantha Ulluwishewa,3,5 Rachel C. Anderson,3Warren C.McNabb,4,5 Paul J. Moughan,5 JerryM.Wells,6 and Nicole C. Roy3
The human intestinal epitheliumis formed by a single layer of epithelial cells that separates the intestinal lumen from the underlying lamina propria. The space between these cells is sealed by tight junctions (TJ), which regulate the permeability of the intestinal barrier. TJ are complex protein structures comprised of transmembrane proteins, which interact with the actin cytoskeleton via plaque proteins. Signaling pathways involved in the assembly, disassembly, and maintenance of TJ are controlled by a number of signaling molecules, such as protein kinase C, mitogen-activated protein kinases, myosin light chain kinase, and Rho GTPases. The intestinal barrier is a complex environment exposed to many dietary components and many commensal bacteria. Studies have shown that the intestinal bacteria target various intracellular pathways, change the expression and distribution of TJ proteins, and thereby regulate intestinal barrier function. The presence of some commensal and probiotic strains leads to an increase in TJ proteins at the cell boundaries and in some cases prevents or reverses the adverse effects of pathogens. Various dietary components are also known to regulate epithelial permeability by modifying expression and localization of TJ proteins. J. Nutr. 141: 769–776, 2011.
Intramammary Application of Ozone Therapy to Acute Clinical Mastitis in Dairy Cows
Atsuya OGATA and Hajime NAGAHATA
The infusion of ozone into the inflamed quarter of cows with clinical mastitis was performed and the efficacy of ozone therapy was evaluated. Ozone was infused into the inflamed quarter via a teat canal using ozone gas generating equipment. Nineteen Holstein cows with acute clinical mastitis were divided into two groups: 15 cows treated with ozone therapy, and 4 cows treated with antibiotic therapy. Systemic and local clinical signs, California Mastitis Test scores, the mastitis causing pathogens, electronic conductivity of milk, and somatic cell counts in milk from ozone- and antibiotic-treated quarters, were compared between the groups. Sixty percent (9/15) of cows with acute clinical mastitis treated with ozone therapy, did not require any antibiotics for recovery. This newly developed ozone therapy method was proven to be effective, safe, and cost effective, and carries no risk of drug residues in milk.
Bocci, VA 2006, ‘Scientific and Medical Aspects of Ozone Therapy . State of the Art’, vol. 37, pp. 93–104.
Scientific and Medical Aspects of Ozone Therapy. State of the Art
Velio Alvaro Bocci
The aim of this review is to dispel misconceptions and skepticism regarding ozone
Medical ozone therapy reduces oxidative stress and intestinal damage in an experimental model of necrotizing enterocolitis in neonatal rats
Ahmet Guvena,⁎, Gokhan Gundogdua, Sabahattin Vurucub, Bulent Uysalc, Emin Oztasd, Haluk Ozturka, Ahmet Korkmaz
Purpose: Necrotizing enterocolitis (NEC) remains a major cause of morbidity and death in neonates. Evidence suggests that an imbalance between activated proinflammatory response with inadequate antiinflammatory protection results in NEC. Ozone has been proposed as an antioxidant enzyme activator, immunomodulator, and cellular metabolic activator. Therefore, this study was designed to investigate whether medical ozone therapy is effective on neonatal rat model of NEC.
Materials and Methods: Thirty-eight newborn Sprague-Dawley pups were randomly divided into 3 groups of NEC, NEC + ozone, and control (left to breast feed). Necrotizing enterocolitis was induced by enteral formula feeding and exposure to 100% carbon dioxide inhalation for 10 minutes after +4°C cold exposures for 5 minutes and 97% oxygen for 5 minutes 2 times daily. The NEC + ozone group received 0.7 mg/kg per day ozone/oxygen mixture intraperitoneally for a total of 3 days after first day of NEC procedure. The pups were killed at fourth day, and their intestinal tissues were harvested for biochemical and histopathologic analysis. Blood sample from pups were also obtained.
Results: The mortality rate and the weight loss were significantly higher in NEC group than control and treatment groups. Oxidative stress markers (malondialdehyde and protein carbonyl content) significantly increased and antioxidant enzyme activities (superoxide dismutase and glutathione peroxidase) were significantly decreased in NEC group. All these biochemical changes were ameliorated in NEC + ozone group. Nitrate plus nitrite levels and serum tumor necrosis factor α were elevated in NEC group and reduced in treatment group. In addition, histopathologic injury score of NEC group was significantly higher than NEC + ozone group.
Conclusion: Ozone treatment significantly reduced the severity of NEC by modulating antioxidative defense and antiinflammatory protection in our experimental animal model.
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