I expanded my post on low dose naltrexone and SED came up — I thought that it is time to look at SED and the microbiome — is there a relationship?
According to Dave Berg, Hemex (hypercoagulation theory):
“The ESR (erythrocyte sedimentation rate – red blood cell sed rate) is called SED RATE for short. We are close to having enough data to publish that the normal range for SED RATES should start above 3 or 4. Values below this are correlated with high SFM values. As the Soluble Fibrin Monomer (SFM) goes up in the plasma, these molecules form dimers (2 stuck together). This physically blocks the RBCs from settling out of the plasma, thus a low sed rate.” [Townhall]
That is, if your SED rate is 0,1,2 you have a high probability of having excessive soluble fibrin monomer. This results in one (of several types) of hypercoagulation (thick blood). It can be treated. SED rates are common taken (with MDs focused on high SED rates instead of low — just like they are focused on high temperature and not low temperatures)
So, to PubMed, as usual.
- “Clumping reaction, using standard suspension of Staphylococcal aureus Newman D-2-C strain and various substrates, was quantitatively tested. It has been shown that clumping occurs in fibrin lysate containing soluble fibrin monomer complexes unclottable by thrombin.” 
- ” One hundred eleven strains of S. haemolyticus, 10 strains of viridans group Streptococcus, … were clumped by human plasma.” 
- ” Purified fibronectin was capable of clumping Staphylococcus aureus strains in concentrations identical with concentrations of fibronectin in human plasma” 
It is interesting that Staphylococcus aureus which I covered in an earlier post showed up so often (there could be others bacteria also). A vaccine against this resulted in significant remission of CFS.
“Staphylococcus aureus is notorious for its ability to become resistant to antibiotics. Infections caused by antibiotic-resistant strains often occur in epidemic waves initiated by one or a few successful clones.” 
“Staphylococcus aureus can exemplify better than any other human pathogen the adaptive evolution of bacteria in the antibiotic era, as it has demonstrated a unique ability to quickly respond to each new antibiotic with the development of a resistance mechanism, starting with penicillin and methicillin, until the most recent, linezolid and daptomycin. Resistance mechanisms include enzymatic inactivation of the antibiotic (penicillinase and aminoglycoside-modification enzymes), alteration of the target with decreased affinity for the antibiotic (notable examples being penicillin-binding protein 2a of methicillin-resistant S. aureus and D-Ala-D-Lac of peptidoglycan precursors of vancomycin-resistant strains), trapping of the antibiotic (for vancomycin and possibly daptomycin) and efflux pumps (fluoroquinolones and tetracycline). Complex genetic arrays (staphylococcal chromosomal cassette mec elements or thevanA operon) have been acquired by S. aureus through horizontal gene transfer, while resistance to other antibiotics, including some of the most recent ones (e.g., fluoroquinolones, linezolid and daptomycin) have developed through spontaneous mutations and positive selection. Detection of the resistance mechanisms and their genetic basis is an important support to antibiotic susceptibility surveillance in S. aureus.”