(Dave Berg’s theory that ME/CFS patients were in a state of hypercoagulation or thickened blood which reduced oxygen and nutrient flow to their tissues appeared around 2000. The theory, like so many other theories, (eg. Chia’s enterovirus findings), received little attention from the research community. One small study (n=17) did not find evidence of hypercoagulation and that was it for the theory. Ken Lassesen, however, benefited greatly from hypercoagulation therapy and his research lead him to suspect an intriguing blood-gut-infection combination was present in ME/CFS)
“Overall, our findings suggest that clot formation can be a physiological weapon that helps to fight off pathogenic microbes. Indeed, activation of the blood coagulation process is probably an important and widespread antimicrobial defence mechanism.” Englemann
You know B and T-cells go ballistic when confronted with an infection. You may know that natural killer cells poke holes in infected cells or that monocytes into killing machines called macrophages when they ‘hear’ a pathogen is around, but you probably don’t know that immune cells called neutrophils actually thicken our blood to fight pathogens as well.
It turns out that upon encountering a microbe the innate immune system initiates an ‘unspecific inflammatory response’ which includes producing small blood clots that trap pathogens in the small blood vessels. (What an interesting finding that is given Dr. DeMeirleirs assertion that the small blood vessels are already clamped down.. )
The Dave Berg/Hemex model for CFS and GWI involves an infection causing excessive coagulation due to a genetic or an acquired (often from organphosphates) coagulation defect. A coagulation defect occurs when a glitch in the complex coagulation process that allows coagulation products to remain and build up over time.
To give an analogy, coagulation is more complex then burning fossil fuels. When we burn such fuels, carbon monoxide, carbon dioxide, water, sulphur dioxide (“bad eggs smell”), even arsenic are released into the air and local environment. Nature re-absorbs most of these chemicals — but if the right circumstances happen, one or more may start to accumulate and may cause a local health issue — it may be just smog or can even be toxic ground water.
The same is true for coagulation disorders, even more so.
A coagulation defect means that one or more of the above arrows are missing or not working. For myself, it’s the links between Prothrombin(F II) –> Thrombin (F IIa) –> Fibrinogen –> Fibrin monomer. Correcting this particular defect required nothing more than adding turmeric and piracetam. Another ME/CFS sufferer had problems with the Protein S link. This style of defect is rarely clinically significant(i.e. not worth exploring by MDs) unless there was something causing coagulation to keep the process going and going at a higher level than normal. If a stroke occurs, then MDs will take action.
That something could be an infection or a toxin.
Dave Berg discovered this CFS connection because his lab specialized in testing for coagulation issues associated with infertility. (Accumulated coagulation products can interfer with the flow of oxygen to the fetus can cause an abortion.) The treatment for this type of infertility is low doses of the body’s natural anticoagulant compound – heparin.
Similar to what happened with Rituximab 10 years later, the MD’s of these infertility patients noticed that many of their ME/CFS patients got better when on heparin. Many of these patients had thick enough blood to receive a diagnosis of anti-phospholipid syndrome (APS) or Hughes Syndrome. Berg’s investigations lead to several publications before he retired.
- Berg D, Berg LH, Couvaras J, Harrison H. Chronic fatigue syndrome and/or fibromyalgia as a variation of antiphospholipid antibody syndrome: an explanatory model and approach to laboratory diagnosis. Blood Coagul Fibrinolysis. 1999 Oct;10(7):435-8.
- Harrison H, et al. Procoagulant genetic factor in a pooled cohort of 582 chronic fatigue syndrome, fibromyalgia and related chronic illnesses, AACFS, Oct 2004
- Hannan KL, Berg E, et al. Activation of the coagulation system in Gulf War Illness: a potential pathophysiologic link with chronic fatigue syndrome: a laboratory approach to diagnosis. Blood Coag Fibrinolysis 2000, 11:7
For more on anti-phospholipid syndrome, ME/CFS and David Berg, check out “Conversations with David Berg” here.
So that’s the back story for this post…
Microbiome or Infection or Both?
Last time around, I was working off an infection causing model. In my readings, I found that the infections associated with a condition called Hughes Syndrome a.k.a. antiphospholipid antibody syndrome appear to be the same ones that are over-represented in the CFS population. My primary sources for APS infections was From “Hughes Syndrome Antiphospholipid Syndrome” Springer, 2000 (2nd printing 2002), editor M.A. Khamashta. Chapter 14, “Infections and Antiphospholipid Syndrome”(by A.E. Gharavi and S.S. Pierangeli), p. 135.
|Chronic Fatigue Syndrome Associated Infections||APS Infections|
|EBV (20% – 72%) — 11 articles on pubmed||Epstein-Bar Virus (EBV or HHV4)|
|VZV – 2 articles on pub med||Varicella zoster virus (VZV or HHV3 -chicken pox)|
|**||Human Immunodeficiency virus (HIV)|
|HHV6 (25% – 58%) – 12 articles on pub med||Human Herpes Virus 6 (HHV6)|
|CMV (29%) – 4 articles on pub med||Cytomegalovirus (CMV) (HHV5)|
|Coxiella Burnetii (Rickettsia)(90% – 50%) – 6 articles on pub med||Coxiella Burnetii (Enteroviruses)|
|Lyme – 2 articles on pub med||Lyme Disease (Rickettsia)|
|Mediterranean spotted fever (Rickettsia)|
|Mycoplasma (41% – 69%) – 13 articles on pub med||Mycoplasma|
|Anecdotal – see below||Leprosy|
|Parvovirus B Three articles on pub med||Parvovirus B|
|Chlamydia-Pneumonia (8%) – 4 articles on pub med||Chlamydia-Pneumonia – 3 articles on pub med|
|Human Enteroviruses (32% – 82%) 2 articles on pub med|
The bottom line is simple: infections known to cause APS tend to be over represented in ME/CFS patients. Most of the infections associated with ME/CFS are known to cause APS (with one exception)
The anecdotal case of leprosy is interesting because I met someone at a Seattle ME/CFS Support group meeting who had and was successfully treated for Leprosy but came down with ME/CFS afterwards. Retesting her for leprosy indicated she was all clear. My assumption at that time was that a co-infection was responsible…. In 2012, however, a mathematical modelling article changed my opinion totally….
This article, which ironically, dealt with the same type of machine learning I was doing at Amazon before my relapse, proposed that an analysis of a person’s gut microbiome could provide greater than 90% accuracy in determining what infection/illness. It suggested that each of the above infections alters the gut microbiome for its own benefit and that the symptoms caused by the infection could, in some cases, be due to the altered microbiome – not the infection, per se. This article suggested that sometime in the future, your family MD may ask you to bring in a stool sample in order to figure out what’s wrong the matter with you!
Then another mathematical modelling study, found that the longer that a person has an infection, the more likely that the microbiome will stay in its altered state. That is, the microbiome associated with the infection will persist (and thus accounts for the ease of re-infection for some diseases). This altered / unhealthy microbiome will keep pumping out signal chemicals causing coagulation and other symptoms without the infection being present.
You may test negative for every one of the infections above and still have the symptoms!
This ‘hit and run’ theory in which a pathogen hits, does its damage by altering the homeostasis of an organism, and then disappears, is a prevalent one in ME/CFS given how difficult the Dubbo studies indicated it was to find active virus/bacterial infections in people with infectious onset. That suggested to me that the search of an infection causing CFS may be an ideological quest doom to failure. It might be far better to look for evidence of chronic system dysregulation, and, for me, that system was the gut.
Ten years later, doctors are not ordering stool samples in order to find out what infection you have but based on my experience and my readings, I believe that an altered microbiome alone could account for many symptoms of chronic fatigue syndrome. I am not saying that checking for the above infections should not be done — definitely they should (and if found treated), but that may be only part of the CFS engine. The other parts need to be addressed also.
In the next posts I will look at what what we know about the microbiome (not that much) and how to alter it (even less)…
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