Chronic Inflammation Causes and Treatment

Constant inflammation of body parts Chronic inflammation, according to new research, is a process that is essentially controlled by the electric potential (abundance or deficiency of free electrons) of the organism. What has been taught and known for decades is an artificial scenario that models the situation based on our modern abnormal lifestyle.

In our current understanding, inflammation is a response of the immune system to injury. As a part of this response, the immune system sends white blood cells to the site of injury. These white cells include neutrophils that produce an oxidative burst in the injured area. The neutrophils release reactive oxygen- and reactive nitrogen species (also known as free radicals) in order to efficiently destroy pathogens (bacteria) that usually penetrate across the skin into the human body. These free radicals also break apart damaged cells so as to rebuild healthy tissue and ensure healing. This process of destruction is based on chemical aggressiveness of free radicals based on their ability to "steal" electrons from other molecules.

Now we come to the main problem that causes chronic nflammation. Together with destruction of damaged cells, free radicals also leak into surrounding areas and destroy healthy cells causing the classic quintet of hallmarks of inflammation: PRISH or Pain, Redness, Immobility (loss of function), Swelling and Heat. However, this (abnormal) scenario takes place in modern humans (and during animal studies) only in conditions of electrical insulation from Earth and results from electron deficiency.

Body electricity and constant inflammation

Humans, just several generations ago, used to be electrically grounded to Earth (due to barefoot life and absence of artificial fabrics) for nearly 24/7 just several generations ago, and this provided the human body with a slightly negative electrical charge that corresponds to Earth's negative potential. However, nearly all modern research is performed on insulated humans and animals who have a positive charge or electron deficiency. What are the effects? Let us consider the key problem associated with chronic inflammation.

Grounding the human body results in deactivation of free radicals in healthy tissues since Earth can provide an abundant supply of electrons to neutralize free radicals, prevent damage of healthy cells, and "quench" chronic inflammation. As a result, grounding, within 10-30 minutes, reduces chronic inflammation and pain. Here is a link to one of the studies that provides references and thermal images related to effects of grounding on chronic inflammation.

Therefore, the first and easy step in order to reduce chronic inflammation is to provide free electrons for the body or ensure those natural conditions that existed during human and animal evolution.

However, this is not the end of the story. Chronic inflammation also requires low blood supply and reduced O2 levels in tissues (cell hypoxia).

Another cause of constant inflammation

Breathing rates in healthy, normal people vs diseases

Sick people with constant inflammation We see that sick people are affected by chronic overbreathing that leads to tissue hypoxia (regardless of the ventilation-perfusion mismatch and CO2 levels in the arterial blood). Among other factors associated with chronic inflammation, according to recent research studies, are pro-inflammatory transcription factors, such as nuclear factor kappa B (NF-kappaB), activator protein (AP)-1 (Safronova & Morita, 2010; Ryan et al, 2009), and hypoxia-inducible factor 1 (Imtiyaz & Simon, 2010; Sumbayev & Nicholas, 2010).

Therefore, hyperventilation (or breathing more than the medical norms) is an additional effect and cause of chronic inflammation in modern people.

Constant Inflammation Treatment

In order to reduce chronic inflammation we need to breathe slower and less 24/7. Why is this so? We need more oxygen in tissues to normalize key physiological processes and eliminate symptoms of chronic diseases and chronic inflammation. Just Earthing is not enough.

Hence, fast and effective treatment of chronic inflammation is based on:
- grounding yourself by standing on Earth barefoot or using methods for grounding during sleep and work (here are more details for practical steps: Earthing)
- restoration of normal breathing parameters in order to increase body oxygenation and normalize chief physiological parameters.

Furthermore, prevention and avoidance of allergic reactions leading to chronic inflammation is necessary for clinical remission of chronic inflammation. Upon achievement of about 35-40 s for the body-oxygen test (this corresponds to the medical norm for breathing), different types of chronic inflammation disappear within 2-3 weeks or even faster. This is true for asthma, bronchitis, gastritis, sinusitis, pancreatitis, duodenitis, hepatitis, arthritis, problems with liver, and many others conditions. Furthermore, Russian Buteyko breathing doctors had a successful clinical trial on patients with liver cirrhosis and hepatitis B, while thousands of their patients solved problems with chronic inflammation using breathing retraining.


Lancet. 1999 Oct 9;354(9186):1283-6.
Carbon dioxide and the critically ill--too little of a good thing?
Laffey JG, Kavanagh BP.
Department of Anaesthesia and Medical-Surgical Intensive Care Unit, Toronto General Hospital, University Health Network, University of Toronto, Ontario, Canada.
Permissive hypercapnia (acceptance of raised concentrations of carbon dioxide in mechanically ventilated patients) may be associated with increased survival as a result of less ventilator-associated lung injury. Conversely, hypocapnia is associated with many acute illnesses (eg, asthma, systemic inflammatory response syndrome, pulmonary oedema), and is thought to reflect underlying hyperventilation. Accumulating clinical and basic scientific evidence points to an active role for carbon dioxide in organ injury, in which raised concentrations of carbon dioxide are protective, and low concentrations are injurious. We hypothesise that therapeutic hypercapnia might be tested in severely ill patients to see whether supplemental carbon dioxide could reduce the adverse effects of hypocapnia and promote the beneficial effects of hypercapnia. Such an approach could also expand our understanding of the pathogenesis of disorders in which hypocapnia is a constitutive element.

Curr Opin Organ Transplant. 2010 Aug;15(4):411-5.
Inflammation and the balance of Treg and Th17 cells in transplant rejection and tolerance.
Hanidziar D, Koulmanda M.
Transplant Institute, Department of Surgery, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Ave., Boston, MA 02215, USA.
PURPOSE OF REVIEW: Inflammation of the allograft, occurring as a consequence of hypoxia and ischemia/reperfusion injury, adversely influences short-term and long-term transplant outcomes. Thus far, imbalance of tissue-protective Treg and tissue-destructive Th17 cells has been confirmed in a number of tissue-inflammatory states, including autoimmune disease. Hence, benefits of tilting Treg-Th17 equilibrium toward dominance of Tregs may promote transplant tolerance.
RECENT FINDINGS: Adverse graft inflammation creates extreme resistance to the induction of donor-specific tolerance. Proinflammatory cytokines, when abundantly expressed within the graft and draining lymph nodes, prevent commitment of donor-activated T cells into graft-protective, T-regulatory phenotype, while fostering generation of donor-reactive Th1, Th2 or Th17 effector subsets. In addition, the inflammatory milieu may destabilize the program of both natural and induced Tregs, converting them into inflammatory, effector-like phenotypes. Therefore permanent, Treg-dependent acceptance of an allograft may not be achieved without limiting adverse tissue inflammation.
SUMMARY: Balance of graft-protective regulatory and graft-destructive effector T cells largely depends on the balance of proinflammatory and anti-inflammatory cytokines in the milieu, in which donor-directed T-cell response occurs. In the absence of proinflammatory cytokines, the constitutive expression of TGF-beta may guide recipient T cells into a tissue-protective, pro-tolerant mode. Therefore, targeting adverse tissue inflammation may represent a powerful means to tilt antidonor immunity towards tolerance.

Curr Top Microbiol Immunol. 2010;345:105-20.
Hypoxia-inducible factors as essential regulators of inflammation.
Imtiyaz HZ, Simon MC.
Abramson Family Cancer Research Institute, University of Pennsylvania, 438 BRB II/III, 421 Curie Boulevard, Philadelphia, PA 19104-6160, USA.
Myeloid cells provide important functions in low oxygen (O(2)) environments created by pathophysiological conditions, including sites of infection, inflammation, tissue injury, and solid tumors. Hypoxia-inducible factors (HIFs) are principle regulators of hypoxic adaptation, regulating gene expression involved in glycolysis, erythropoiesis, angiogenesis, proliferation, and stem cell function under low O(2). Interestingly, increasing evidence accumulated over recent years suggests an additional important regulatory role for HIFs in inflammation. In macrophages, HIFs not only regulate glycolytic energy generation, but also optimize innate immunity, control pro-inflammatory gene expression, mediate bacterial killing and influence cell migration. In neutrophils, HIF-1a promotes survival under O(2)-deprived conditions and mediates blood vessel extravasation by modulating ▀ (2) integrin expression. Additionally, HIFs contribute to inflammatory functions in various other components of innate immunity, such as dendritic cells, mast cells, and epithelial cells. This review will dissect the role of each HIF isoform in myeloid cell function and discuss their impact on acute and chronic inflammatory disorders. Currently, intensive studies are being conducted to illustrate the connection between inflammation and tumorigenesis. Detailed investigation revealing interaction between microenvironmental factors such as hypoxia and immune cells is needed. We will also discuss how hypoxia and HIFs control properties of tumor-associated macrophages and their relationship to tumor formation and progression.

Arch Immunol Ther Exp (Warsz). 2010 Aug;58(4):287-94. Epub 2010 May 26.
Hypoxia-inducible factor 1 as one of the "signaling drivers" of Toll-like receptor-dependent and allergic inflammation.
Sumbayev VV, Nicholas SA.
Medway School of Pharmacy, University of Kent, Anson Building, Central Avenue,
Chatham Maritime, Kent ME44TB, UK.
Hypoxia-inducible factor 1 (HIF-1) is a heterodimeric transcription complex which plays a crucial role in cellular adaptation to low oxygen availability. In the last years there has been increasing evidence about the role of this factor in inflammatory/innate immune reactions. It has also been found to contribute to different types of allergic inflammation.

Mediators Inflamm. 2010;2010:585989. Epub 2010 Apr 20.
Systemic inflammation in chronic obstructive pulmonary disease: may adipose tissue play a role? Review of the literature and future perspectives.
Tkacova R.
Department of Respiratory Medicine and Tuberculosis, Faculty of Medicine, P J Safarik University, L. Pasteur Teaching Hospital, Kosice, Slovakia.
Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide. Low-grade systemic inflammation is considered a hallmark of COPD that potentially links COPD to increased rate of systemic manifestations of the disease. Obesity with/without the metabolic syndrome and cachexia represent two poles of metabolic abnormalities that may relate to systemic inflammation. On one hand systemic inflammatory syndrome likely reflects inflammation in the lungs, i.e. results from lung-to plasma spillover of inflammatory mediators. On the other hand, obesity-related hypoxia results in local inflammatory response within adipose tissue per se, and may contribute to elevations in circulatory mediators by spillover from the adipose tissue to the systemic compartment. The extent to which systemic hypoxia contributes to the adipose tissue inflammation remains unknown. We assume that in patients with COPD and concurrent obesity at least three factors play a role in the systemic inflammatory syndrome: the severity of pulmonary impairment, the degree of obesity-related adipose tissue hypoxia, and the severity of systemic hypoxia due to reduced pulmonary functions. The present review summarizes the epidemiological and clinical evidence linking COPD to obesity, the role of adipose tissue as an endocrine organ, and the role of hypoxia in adipose tissue inflammation.

J Dent Res. 2010 May;89(5):430-44. Epub 2010 Mar 26.
Transcriptome remodeling in hypoxic inflammation.
Safronova O, Morita I.
Department of Cellular Physiological Chemistry, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8549, Japan.
Hypoxia is an integral component of the inflamed tissue microenvironment. Today, the influence of hypoxia on the natural evolution of inflammatory responses is widely accepted; however, many molecular and cellular mechanisms mediating this relationship remain to be clarified. Hypoxic stress affects several independent transcriptional regulators related to inflammation in which HIF-1 and NF-kappaB play central roles. Transcription factors interact with both HATs and HDACs, which are components of large multiprotein co-regulatory complexes. This review summarizes the current knowledge on hypoxia-responsive transcriptional pathways in inflammation and their importance in the etiology of chronic inflammatory diseases, with the primary focus on transcriptional co-regulators and histone modifications in defining gene-specific transcriptional responses in hypoxia, and on the recent progress in the understanding of hypoxia-mediated epigenetic reprogramming. Furthermore, this review discusses the molecular cross-talk between glucocorticoid anti-inflammatory pathways and hypoxia.

Adv Exp Med Biol. 2010;662:27-32.
Alveolar hypoxia-induced systemic inflammation: what low PO(2) does and does not do.
Gonzalez NC, Wood JG.
Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Reduction of alveolar PO(2) (alveolar hypoxia, AH) may occur in pulmonary diseases such as chronic obstructive pulmonary disease (COPD), or in healthy individuals ascending to altitude. Altitude illnesses may develop in non-acclimatized persons who ascend rapidly. The mechanisms underlying these illnesses are not well understood, and systemic inflammation has been suggested as a possible contributor. Similarly, there is evidence of systemic inflammation in the systemic alterations present in COPD patients, although its role as a causative factor is not clear. We have observed that AH, induced by breathing 10% O(2) produces a rapid (minutes) and widespread micro vascular inflammation in rats and mice. This inflammation has been observed directly in the mesenteric, skeletal muscle, and pial microcirculations. The inflammation is characterized by mast cell degranulation, generation of reactive O(2) species, reduced nitric oxide levels, increased leukocyte-endothelial adherence in post-capillary venules, and extravasation of albumin. Activated mast cells stimulate the renin-angiotensin system (RAS) which leads to the inflammatory response via activation of NADPH oxidase. If the animals remain in hypoxia for several days, the inflammation resolves and exposure to lower PO(2) does not elicit further inflammation, suggesting that the vascular endothelium has "acclimatized" to hypoxia. Recent experiments in cremaster microcirculation suggest that the initial trigger of the inflammation is not the reduced tissue PO(2), but rather an intermediary released by alveolar macrophages into the circulation. The putative intermediary activates mast cells, which, in turn, stimulate the local renin-angiotensin system and induce inflammation.

Expert Opin Ther Targets. 2009 Nov;13(11):1267-77.
Targeting the A2B adenosine receptor during gastrointestinal ischemia and inflammation.
Eltzschig HK, Rivera-Nieves J, Colgan SP.
University of Colorado, Mucosal Inflammation Program, Department of Medicine, Denver, 12700 E 19th Avenue, Mailstop B112, Research Complex 2, Room 7124, Aurora, CO 80045, USA.
... In addition, we discuss the role of this pathway in dampening hypoxia-elicited inflammation, specifically in the setting of intestinal ischemia and inflammation.

Thorax. 2009 Jul;64(7):631-6.
Systemic inflammation: a key factor in the pathogenesis of cardiovascular complications in obstructive sleep apnoea syndrome?
Ryan S, Taylor CT, McNicholas WT.
Sleep Research Laboratory, St Vincent's University Hospital, Dublin, Ireland.
... Intermittent hypoxia, the hallmark of OSAS, results in activation of pro-inflammatory transcription factors such as nuclear factor kappa B (NF-kappaB) and activator protein (AP)-1. These promote activation of various inflammatory cells, particularly lymphocytes and monocytes, with the downstream consequence of expression of pro-inflammatory mediators that may lead to endothelial dysfunction. This review provides a critical analysis of the current evidence for an association between OSAS, inflammation and cardiovascular disease, discusses basic mechanisms that may be responsible for this association and proposes future research possibilities.

Respir Res. 2009 Jun 22;10:54.
Alveolar hypoxia, alveolar macrophages, and systemic inflammation.
Chao J, Wood JG, Gonzalez NC.
Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160, USA.
... Evidence obtained in intact animals and in primary cell cultures indicate that alveolar macrophages activated by hypoxia release a mediators into the circulation. This mediator activates perivascular mast cells and initiates a widespread systemic inflammation. The inflammatory cascade includes activation of the local renin-angiotensin system and results in increased leukocyte-endothelial interactions in post-capillary venules, increased microvascular levels of reactive O2 species; and extravasation of albumin.

Eur Respir J. 2009 May;33(5):1195-205.
Cardiovascular disease in obstructive sleep apnoea syndrome: the role of intermittent hypoxia and inflammation.
Garvey JF, Taylor CT, McNicholas WT.
Respiratory Sleep Disorders Unit, St. Vincent's University Hospital, Dublin,
There is increasing evidence that intermittent hypoxia plays a role in the development of cardiovascular risk in obstructive sleep apnoea syndrome (OSAS) through the activation of inflammatory pathways....

Semin Immunopathol. 2009 Jun;31(1):113-25. Epub 2009 Apr 29.
Obstructive sleep apnea, immuno-inflammation, and atherosclerosis.
Arnaud C, Dematteis M, Pepin JL, Baguet JP, LÚvy P.
INSERM ERI17, Grenoble, 38043, France.
Obstructive sleep apnea (OSA) is a highly prevalent sleep disorder leading to cardiovascular and metabolic complications. OSA is also a multicomponent disorder, with intermittent hypoxia (IH) as the main trigger for the associated cardiovascular and metabolic alterations. Indeed, recurrent pharyngeal collapses during sleep lead to repetitive sequences of hypoxia-reoxygenation. This IH (intermittent hypoxia) induces several consequences such as hemodynamic, hormonometabolic, oxidative, and immuno-inflammatory alterations that may interact and aggravate each other, resulting in artery changes, from adaptive to degenerative atherosclerotic remodeling.... Oxidative stress, inflammation, and vascular remodeling can be directly triggered by IH, further aggravated by the OSA-associated hormonometabolic alterations, such as insulin resistance, dyslipidemia, and adipokine imbalance.

Arthritis Res Ther. 2009;11(1):215. Epub 2009 Feb 23.
Hypoxia. Regulation of NFkappaB signalling during inflammation: the role of hydroxylases.
Oliver KM, Taylor CT, Cummins EP.
School of Medicine and Medical Science, Conway Institute, University College Dublin, Belfield, Dublin 4, Ireland.
... Microenvironmental hypoxia has long been identified as being coincident with chronic inflammation...

Acta Med Port. 2008 Sep-Oct;21(5):489-96. Epub 2009 Jan 16.
[The role of adipose tissue and macrophages in chronic inflammation associated with obesity: clinical implications].
[Article in Portuguese]
Ramalho R, GuimarŃes C.
Servišo e Laboratˇrio de Imunologia, Faculdade de Medicina da Universidade do Porto, Porto.
... so, hypoxia can be a critical factor in inflammatory obese state manifestation...

J Physiol. 2008 Sep 1;586(Pt 17):4055-9. Epub 2008 Jul 3.
Interdependent roles for hypoxia inducible factor and nuclear factor-kappaB in hypoxic inflammation.
Taylor CT.
UCD Conway Institute, University College Dublin, Belfield, Dublin 4, Ireland.
Decreased oxygen availability (hypoxia) is a hallmark feature of the microenvironment in a number of chronic inflammatory conditions including arthritis and inflammatory bowel disease (IBD). Recent advances in our understanding of oxygen-dependent cell signaling have uncovered several mechanisms by which hypoxia impacts upon the development of inflammation through the coordinated expression of adaptive, inflammatory and apoptotic genes...

Methods Enzymol. 2007;435:405-19.
Regulation of hypoxia-inducible factors during inflammation.
Frede S, Berchner-Pfannschmidt U, Fandrey J.
Institut fŘr Physiologie, Universitńt Duisburg-Essen, Essen, Germany.
The microenvironment of inflamed and injured tissue is characterized by low levels of oxygen and glucose and high levels of inflammatory cytokines, reactive oxygen, and nitrogen species and metabolites....

Proc Am Thorac Soc. 2005;2(1):26-33.
Local and systemic inflammation in chronic obstructive pulmonary disease.
Wouters EF.
Department of Pulmonary Diseases, University Hospital Maastricht, P.O. Box 5800,
6202 As Maastricht, The Netherlands
There is growing evidence for systemic inflammation in chronic obstructive pulmonary disease (COPD)... The main causes of systemic inflammation in COPD remain to be elucidated, although systemic hypoxia is a candidate factor.

Ophthalmologe. 2003 May;100(5):363-70.
[Diabetic retinopathy. Pathophysiology and therapy of hypoxia-induced inflammation].
[Article in German]
Joussen AM, Fauser S, Krohne TU, Lemmen KD, Lang GE, Kirchhof B.

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