Chronic Inflammation Causes and Its Natural Treatment

- Updated on August 1, 2019

Chronic Inflammation Causes and Its Natural Treatment 1By Dr. Artour Rakhimov, Alternative Health Educator and Author

Constant inflammation of body parts Do you suffer from constant inflammation on the face or in the sinuses, throat, lower back, muscles, stomach, or other 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 effectively 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 the 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 inflammation. Together with the 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 chronic 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 provide 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).

Main cause of chronic or 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: Natural 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 are necessary for the 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. Numerous students completely eliminated their inflammation on the face, in the throat, sinuses, stomach, lower back, muscles and other body parts. 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.

Medical references

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Chao J, Wood JG, Gonzalez NC, Alveolar hypoxia, alveolar macrophages, and systemic inflammation., Respir Res. 2009 Jun 22;10:54.

Eltzschig HK, Rivera-Nieves J, Colgan SP, Targeting the A2B adenosine receptor during gastrointestinal ischemia and inflammation., Expert Opin Ther Targets. 2009 Nov;13(11):1267-77.

Frede S, Berchner-Pfannschmidt U, Fandrey J, Regulation of hypoxia-inducible factors during inflammation., Methods Enzymol. 2007;435:405-19.

Garvey JF, Taylor CT, McNicholas WT, Cardiovascular disease in obstructive sleep apnoea syndrome: the role of intermittent hypoxia and inflammation., Eur Respir J. 2009 May;33(5):1195-205.

Hanidziar D, Koulmanda M, Inflammation and the balance of Treg and Th17 cells in transplant rejection and tolerance., Curr Opin Organ Transplant. 2010 Aug;15(4):411-5.

Imtiyaz HZ, Simon MC, Hypoxia-inducible factors as essential regulators of inflammation, Curr Top Microbiol Immunol. 2010;345:105-20.

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

Laffey JG, Kavanagh BP, Carbon dioxide and the critically ill–too little of a good thing?, Lancet. 1999 Oct 9;354(9186):1283-6.

Oliver KM, Taylor CT, Cummins EP, Hypoxia. Regulation of NFkappaB signalling during inflammation: the role of hydroxylases., Arthritis Res Ther. 2009;11(1):215. Epub 2009 Feb 23.

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Ryan S, Taylor CT, McNicholas WT, Systemic inflammation: a key factor in the pathogenesis of cardiovascular complications in obstructive sleep apnoea syndrome?, Thorax. 2009 Jul;64(7):631-6.

Safronova O, Morita I, Transcriptome remodeling in hypoxic inflammation., J Dent Res. 2010 May;89(5):430-44. Epub 2010 Mar 26.

Sumbayev VV, Nicholas SA, Hypoxia-inducible factor 1 as one of the “signaling drivers” of Toll-like receptor-dependent and allergic inflammation., Arch Immunol Ther Exp (Warsz). 2010 Aug;58(4):287-94. Epub 2010 May 26.

Taylor CT, Interdependent roles for hypoxia inducible factor and nuclear factor-kappaB in hypoxic inflammation., J Physiol. 2008 Sep 1;586(Pt 17):4055-9. Epub 2008 Jul 3.

Tkacova R, Systemic inflammation in chronic obstructive pulmonary disease: may adipose tissue play a role? Review of the literature and future perspectives., Mediators Inflamm. 2010;2010:585989. Epub 2010 Apr 20.

Wouters EF, Local and systemic inflammation in chronic obstructive pulmonary disease., Proc Am Thorac Soc. 2005;2(1):26-33.

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