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Tcell dysregulation predisposes to Tcell dysregulations. L Haul/GDD. One bad thing leads to another.

I have touched on this subject in several blogs. One large category of GDD is the individual has a pre-existent Tcell dysregulation condition which predisposes then to acquiring GDD. The types of Tcell dysregulation change in populations with changes in behavior, endemic infections, and pollutants.

To illustrate another disease that has experienced this shifting demographics: hepatocellular cancer. Disease afflicting the liver directly is the primary underlying cause. In North America, 20 years ago, and for decades before this, alcohol overuse was the most common underlying condition, this gradually changed to Hepatitis C, 20 years ago to the present, which became the most common maybe 10 years ago. Now the transition is evolving that unless health practices change, obesity

will be the commonest underlying cause over the next decade.

I envisage a similar demographic shift with GDD. Presently the most common Tcell dysregulations are chronic infections such as Lyme, EBV, and other self-destructive conditions like fibromyalgia. I envisage the transition in GDD will be rapid and is already occurring: COVID long haul, I anticipate, will be by far the most common underlying condition, and post COVID vaccine long haul a distant second.



Why does one Tcell dysregulation lead to another. Very simple: an appropriate immune response involves 1,000 + moving parts that have to act together in a coordinated fashion - there is always a balance ongoing of pro-inflammatory action (often mediated by cytokines) and immune calming action (also mediated by cytokines, but other ones) and probably a third major category of signaling cytokines that tell the entire body system to either calm down or gear up for battle. These all occur simultaneously and in synchronicity.

The basic reason. that 99.9% + of individuals do not react to GBCA and do not develop GDD, is actually their immune system follows the ancient Chinese philosophy of Wu Wei - the active pursuit of doing nothing. My original thinking had been that in GSC subjects (normals) the immune system simply ignored the presence of Gd. Our work on cytokines suggests this passive approach is probably not fully correct, because GSC subjects can also release a lot of cytokines to the presence of Gd. The difference between GSC and GDD then? The type of cytokines released: GSC primarily calming cytokines, GDD primarily pro-inflammatory cytokines. Once this imbalance of cytokines has developed in an individual, because of underlying chronic inflammatory disease and hence chronic underlying T-cell dysregulation, then they are a set up to react in the same imbalanced way to other antigens that their immune system is exposed to.

A major problem with the combination of Tcell dysregulation conditions is that the treatment for each of them, may not only be different, but actually be in conflict. With the approach that I have developed: essentially removing Gd and concurrent management of severe hypersensitivity reaction, success rate for treating pure GDD is extremely high. The only failures for pure GDD, historically (and to the present time at centers not recognizing the critical nature of this combination) is starting chelation too early and getting into uncontrolled Flare, or patients opting to stop chelation too early because of their fear or bad early experience with Flare- this latter is always a mistake, but people will sometimes do what they will do regardless of advice. Presently 80% of individuals who undergo chelation do well to extremely well, the variable often is the number of GBCA injections they had. 15% do not so well, but because they have stopped chelation too early, even after the first one, and this ofcourse is completely avoidable. The third category, 5% who do not so well, is because of a pre-existing Tcell condition, in which either there is no treatment for that condition (most common), or the treatment for that Tcell condition conflicts with the treatment for GDD. In general though it is not a given that if a subject has an underlying Tcell dysregulation that treatment for GDD will fail, most actually do quite well (not as fast as pure GDD) but quite well. It is still uncommon for an underlying Tcell condition with GDD to fare poorly with treatment, but when there are failures it is because of this.

I do not anticipate that there will be an intrinsic high failure rate with combined long haul and GDD, but ofcourse I am not 100% certain, because it is too early to know. There are certain elements of treatment that are actually identical (which is extremely good) and I am hopeful that with 10,000 physicians and scientists working on COVID, new treatments, that will also be effective for GDD, will be developed.

Beware of COVID long haul and GDD, COVID vaccine long haul and GDD. Particularly be aware that individuals with long haul are highly susceptible to GDD, and once they get GDD from one GBCA injection, each additional GBCA injection will make them worse and less treatable- so recognize GDD when it first develops, and they never get another GBCA injection again.

One bad thing leads to another.


Richard Semelka, MD