Posted 6/19/2016 1:25 PM (GMT -7)
So here is the information that was shared with me to read by my doctor. The link is below. Obviously, he explained this to me further, but this will at least provide some context. My doctor said I am definitely TH2 dominant now and we needed to move towards a happy medium between the 2.
Pro-inflammatory cytokines Anti-inflammatory cytokines
Interleukin one (IL-1) Interleukin ten (IL-10)
Interleukin two (IL-2). Interleukin four (IL-4)
Interleukin twelve (IL-12)
Gamma interferon (IFN-g)
Tumor necrosis factor (TNF)
-Th1 cells (which stands for “T helper one” cells), which secrete the pro-inflammatory cytokines mentioned above and are very effective at killing invading germs (even those inside of cells), but may cause potentially damaging excessive inflammation
-Th2 cells (which stands for “T helper two” cells), which secrete the anti-inflammatory cytokines mentioned above and also direct the cells that produce antibodies to begin their antibody production
-Treg cells (which stands for “T regulator” cells), which “regulate” the balance between Th1 pro-inflammation and Th2 anti-inflammation
All three CD4 components are critical to the successful control of Lyme disease. At the onset of Lyme infection, the Th1 response is vital to controlling Lyme. But the Th2 response is important to “cool off ” the Th1 and to produce antibodies for help to control Lyme. Finally, the Treg response is absolutely necessary to keep the system balanced. That is to say, the Th1 system tends to suppress the Th2 system and vice versa—a process similar to a see-saw. The Treg system keeps things in balance.
Here are some examples of how problems can occur when the T cell system does not work properly.
Example one: When Lyme invades the body, it wants to avoid the Th1 response, because that is the most deadly immune system attack on it. Therefore, Lyme actually induces the body to make IL-10 (an anti-inflammatory cytokine) for the purpose of suppressing the Th1 response. If the body’s Th1 system is not strong enough to overcome the premature Th2 (IL-10) suppressive action, then Lyme can penetrate deeper into the body tissues. Therefore, a Lyme-weakened Th1 (from excess IL-10) response will allow Lyme to successfully invade the body.
Example two: As previously stated, Lyme causes excess IL-10 production. But there are situations in which the body may already be in a state of overproduction of IL-10. This preexisting excess IL-10 condition is called “Th2 dominance.” Th2 dominance is a setup for a poor outcome from Lyme. Conditions such as chronic fatigue syndrome, chronic viral infections (like Epstein-Barr virus), mercury overload, parasitic infections, and chronic allergies all lead to the Th2 dominant state. In that state, the Th1 is suppressed not only by Lyme but also by the other situations that we just mentioned. Once again, the Th1 is limited in what it can do and Lyme is able to establish itself in the body.
Example three: In either of the above examples, if Lyme has successfully invaded, the Th1 system continues to try to attack The Lyme Disease Solution 1 4 4 Lyme but unsuccessfully. In this circumstance, there are four possible reasons. The first reason for this lack of success could be due to Th1 weakness/exhaustion (for example, if nutritional deficiencies are present). The second is that it could be due to ongoing suppression of Th1 by Th2. The third possibility is that a person has ongoing co-infections such as Babesia or Bartonella. Finally, it could be due to Treg’s lack of regulation of the process. I believe that the unfortunate result is that the weakened and inadequate Th1 system loses its ability to distinguish infected tissue from “self tissue.” This leads to what we call “autoimmunity” and chronic inflammation (which I will discuss in the next chapter). This is very frequently the picture of a typical Lyme patient when coming into a Lyme-aware doctor’s office—a long history of inadequately treated, active, or persistent Lyme with accompanying autoimmune manifestations.