Below is a simple picture of the model that I use in understanding CFS. This model also leads me into certain direction for items to investigate.
CFS starts by health gut bacteria incorporating foreign RNA when they reproduce. The RNA will often come from an acute virus. Stress increases the “willingness” of bacteria to incorporated RNA (trying to find something that addresses the stress), this may be stress-induced mutagenesis or adaptive mutation. The result is an alteration of microflora populations families. Bacteria have a friend-foe identification, so some species may flip to the dark side because of the new RNA. Normally, the bacteria will eliminate these mutations over time and return to their prior state, however in some cases this will fail to happen (or take a very long time). In general, about 95% will return to normal in 6 months or less. The remaining 5% will likely be diagnosed as CFS.
Once the bacteria population shifts, there may be dramatic changes of what the body gets, two examples:
- Decrease of E.Coli results in reduced NADH
- Decrease or L. Reuteri results in reduced B12
These changes allow past bacterial or viral infection to be come active in a similar manner to Chickenpox / Shingles — both are caused by the same virus. Chickenpox happens on initial exposure. Shingles is the reactivation. Most bacterial infections have resisters, sleeping cells of bacteria (antibiotics usually act by interfering with the reproduction – if some cells sleep through this, they can become active later given the right situation).
These reactivated pathogens contribute to the gut bacteria dysfunction. They also can increase coagulation (which interact with the inherited coagulation defects very often found in CFS patients) causing “fibrin-walled cities of pathogens” that cannot be reached by antibiotics or antivirals. Any bacterial reactivation can result in biofilms forming, creating additional protected cities of viruses and bacteria.
This is the model — there are many factors that may need to be addressed for effective treatment:
- Gut Bacteria dysfunction
- Fibrin Deposits / Coagulation
- Reactivated virus
- Reactivated bacteria