Therapy Tip

It isn't necessary to

postpone initiation of Inflammation Therapy until 25-D is less than 30 ng/mL. This may take many months for some and would unnecessarily delay treatment. While 25-D is still elevated antibiotics should be increased cautiously, keeping in mind that herxing may increase as 25-D falls.

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Genes don't do anything without an environment says geneticist Richard Lewontin.  You can bet your immune system genes get quite a workout juggling the environment we ingest, breathe, and inject.  A strong immune system requires good nutrition and avoidance of chronic inflammation and immune suppression.  If microbes enter without our strong defenses, they are able to do multitudes of damage from inducing antibody mimicry of our own tissues to living inside our immune cells causing persistent  inflammation, further suppressing our immune system in a vicious cycle.   Ironically many meds and vaccines used to protect us cause immune suppression.  Good science means review and revision of old science with the new, but politics are a fact of life.  Global rates of chronic illness have skyrocketed the last 50 years and all signs point to what we ingest, breathe, and inject.  Genes are attractive to blame, distracting us from a very toxic but lucrative environment.  Otherwise innocuous microbes are terrorizing us because we inadvertently let them in.      

At CIR, our mission is twofold: education promotes prevention and treatment restores immune function and a better you, head to toe.  

-CIR staff 

Clinical Effect of Olmesartan and Antibiotics

In the clinic setting, a Jarisch-Herxheimer reaction (JHR) is usually seen following administration of olmesartan. JHR is a cascade of reactions including inflammation, cytokine release, and endotoxin release as part of the immune response to the disintegration of infected cells. [1,2] These inflammatory symptoms (and inflammatory lab markers) that wax and wane in response to olmesartan administration provide evidence of occult infection. This immunopathology suggests a robust immune response and transcription of AMPs by an activated VDR; and provides additional evidence that olmesartan is a VDR agonist. [3-5] The adaptive immune system may also respond to the presence of fragments of DNA generated by pathogenic and cellular debris, stimulating antibody production in the process. Theoretically, olmesartan restores VDR competence and, thus, phagocytosis leads to bacterial death; consequently, inflammation is increased by cytokine reaction to microbial endotoxins and cellular debris from dead host cells and bacteria. [6, 7] To help eradicate the intracellular pathogens, select antibiotics are administered which, revealingly, cause an exacerbation of inflammatory symptoms (JHR) with each dose. [8] Sub-inhibitory oral antibiotics, are gradually introduced in a pulsed fashion; [9-11] for their ability to weaken bacterial ribosomes, penetrate cell walls and blood brain barrier, accumulate in phagocytes, or interfere with folate synthesis. [12-18] A correlating treatment strategy is the avoidance of excessive sunlight exposure, foods high in vitamin D and vitamin D supplements to maintain serum 25(OH)D at a level (20-30ng/ml) that isn't likely to suppress the immune system and inhibit bacterial elimination.

1. Herxheimer K, Martin H. So-called Herxheimer reaction. Arch Derm Syphilol. Jan 1926;13(1):115-117.
2. Heyman A, Sheldon WH, Evans LD. Pathogenesis of the Jarisch-Herxheimer Reaction: A REVIEW OF CLINICAL AND EXPERIMENTAL OBSERVATIONS. Br J Vener Dis. Jun 1952(28(2)):50-60.
3. Sonawane A, Santos JC, Mishra BB, et al. Cathelicidin is involved in the intracellular killing of mycobacteria in macrophages. Cell Microbiol. Oct 2011;13(10):1601-17.
4. Nickel D, Busch M, Mayer D, Hagemann B, Knoll V, Stenger S. Hypoxia triggers the expression of human beta defensin 2 and antimicrobial activity against Mycobacterium tuberculosis in human macrophages. J Immunol. 2012;188(8):4001-7.
5. Platten M, Youssef S, Hur EM, et al. Blocking angiotensin-converting enzyme induces potent regulatory T cells and modulates TH1- and TH17-mediated autoimmunity. Proc Natl Acad Sci U S A. Sep 2009;106(35):14948-53.
6. Hurley JC. Antibiotic-induced release of endotoxin. A therapeutic paradox. Drug Saf. Mar 1995;12(3):183-95.
7. Mangin M, Sinha R, Fincher K. Inflammation and vitamin D: the infection connection. Inflamm Res. 2014 Jul 22. [Epub ahead of print]
8. Hof H. Antibiotic Treatment of Infections with Intracellular Bacteria. In: Paradise LJ, Friedman H, Bendinelli M, eds. Opportunistic Intracellular Bacteria and Immunity. New York, NY: Kluwer Academic Press; 2002.
9. Davies J, Spiegelman GB, Yim G. The world of subinhibitory antibiotic concentrations. Curr Opin Microbiol. Oct 2006;9(5):445-53.
10. Lo Bue AM, Rossetti B, Cali G, Nicoletti G, Condorelli F. Antimicrobial interference of a subinhibitory concentration of azithromycin on fimbrial production of Porphyromonas gingivalis. J Antimicrob Chemother. Nov 1997;40(5):653-7.
11. Elliot GR, Peterson PK, Verbrugh HA, Freiberg MR, Hoidal JR, Quie PG. Influence of subinhibitory concentrations of penicillin, cephalothin, and clindamycin on Staphylococcus aureus growth in human phagocytic cells. Antimicrob Agents Chemother. Nov 1982(22(5)):781-4.
12. Pechère JC. Phagocytes, antibiotics and intracellular parasites: are the experimental data clinically relevant? Eur J Clin Microbiol Infect Dis. Feb 1991;10(2):97-9.
13. Darouiche RO, Hamill RJ. Antibiotic penetration of and bactericidal activity within endothelial cells. Antimicrob Agents Chemother. May 1994;38(5):1059-64.
14. Nau R, Sörgel F, Eiffert H. Penetration of drugs through the blood-cerebrospinal fluid/blood-brain barrier for treatment of central nervous system infections. Clin Microbiol Rev. Oct 2010(23(4)):858-83.
15. Hand WL, King-Thompson NL. Membrane transport of clindamycin in alveolar macrophages. Antimicrob Agents Chemother. Feb 1982;21(2):241-7.
16. Patel RB, Welling PG. Clinical Pharmacokinetics of Co-trimoxazole (trimethoprim-sulphamethoxazole). Clin Pharmacokinet ;5(5):405-423.
17. Hughes DT. Inhibition of Folate Metabolism in Chemotherapy. Handbook of Experimental Pharmacology. Vol 64; 1983.
18. Jacobs RF, Wilson CB. Activity of antibiotics in chronic granulomatous disease leukocytes. Pediatr Res. Nov 1983(17(11)):916-9.

Has your doctor asked where s/he can read a published scientific explanation of Inflammation Therapy? Now you can refer to our peer-reviewed article recently published by Springer in the print journal Inflammation Research.  

The full text is available online at this link.   

"My results were significant and immediate. Many symptoms, which had persisted for years, began disappearing. Some problems may never resolve. But the quality of my life is measurably improved."  

You can read Jim's case report at this link.    

"In general I feel much better than I have for a couple of years. My back doesn't hurt. I haven't been to the chiropractor for 3 months. My knees are better, but I hope they heal all the way to be stronger when I rise or sit. Headaches are less. I'm grateful to have learned about IT and CIR." Ann