Chronic fatigue syndrome (CFS)/myalgic encephalomyelitis (ME) has long been associated with the presence of infectious agents, but no single pathogen has been reliably identified in all patients with the disease.

Recent studies using metagenomic techniques have demonstrated the presence of thousands of microbes in the human body that were previously undetected and unknown to science. More importantly, such species interact together by sharing genes and genetic function within communities.

It follows that searching for a singular pathogen may greatly underestimate the microbial complexity potentially driving a complex disease like CFS/ME. Intracellular microbes alter the expression of human genes in order to facilitate their survival.

We have put forth a model describing how multiple species-bacterial, viral, and fungal- can cumulatively dysregulate expression by the VDR nuclear receptor in order to survive and thus drive a disease process.

Based on this model, we have developed an immunostimulatory therapy that is showing promise inducing both subjective and objective improvement in patients suffering from CFS/ME.

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Paradoxically,  immunosuppressive  therapies  often result  in  short-term  symptom  improvement  or resolution  by  decreasing  the  cytokine,  antibody  and endotoxin  release  associated  with  an  inflammatory response  towards  acquired  pathogens. This  temporary symptom  improvement  should  not  be  mistaken  for actual  reversal  of the  disease  process. The  monoclonal antibody  rituximab,  which  has  recently  been  used  to deplete  the  B  cells  of  patients with CFS/ME[4],  may  be an  example  of  a  therapy  that  elicits  “improvement”  in this  fashion.  It’s  instructive  to  note  that  the  apparent
progress  noted  among  CFS/ME  patients  taking  the medication  is  almost  always  followed  by  profound relapse.  Furthermore,  the  use  of  rituximab  has  been linked  to the  resurgence  of  latent  infections  including hepatitis  B  reactivation,  multifocal leukoencephalopathy, and Pneumocystis  pneumonia [93].

Subsequently,  over  the  last  decade,  our  group  has developed  a  novel  therapy  that  seeks  to  stimulate rather  than  suppress  the  innate  immune  system [94]. Instead  of  slowing  the  immune  response,  we  aim  to directly  target  microbes  by  stimulating  immune defenses.  Central  to  the  treatment  is  the  use  of olmesartan  medoxomil. While  this  drug  was  approved as  an angiotensin  II  receptor  agonist  (ARB), we  showed that  it  also  has  a  high  affinity  for  the  VDR  nuclear receptor,for which it is most likely a partial agonist [95].

In  a  VDR- compromised  individual,  olmesar tan medoxomil  stimulates  the  expression  of  the  many endogenous  antimicrobials  under  VDR  control,  and helps  to  gradually  restore  the  activity of  other  nuclear receptors,  which  may  have  been  impacted  by  VDR dysregulation.

Immunostimulation in the treatment for chronic fatigue syndrome/myalgic encephalomyelitis by AD Proal et al in Immunologic Research, 11 April 2013


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