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Circumstances for pain development and other symptoms (eg: brain fog) in GDD

There are 6 principal circumstances that generate pain and other symptoms (such as brain fog) in GDD sufferers.

1. entry of Gd into tissue site.

2. Gd residing in tissue

3. removal of Gd from tissue site.

4. creation of autoimmune condition.

5. micromovement of Gd in tissues.

6. Stress/ anxiety.

The immune cells involved probably are centered on T-cells, but almost certainly incorporate many other immune cell types.

Overall there is likely a T-cell imbalance involving imbalance of T regulatory cells (part of the family of T suppressor cells, cell types in these categories likely quite large), T effector cells (family T Helper cells), PRIME cells may be involved, and at the tissue level the work horse cells likely are tissue resident memory T cells, trained immunity in macrophages, and detrimental epigenetic scars.

Many of these immunological understandings are very current, and hence not so well understood. The take home message: the immunology is remarkably complex and incompletely understood by even Immunologist experts (which I am not one).

Looking at the 5 above circumstances:


1.Entry.

The major event is the GBCA administered that elicited GDD, or multiple GBCAs which compounded and worsened GDD. But this also occurs with redistribution (problem: choice of poor chelator) and re-equilibration (control by keeping treatment session intervals around 3 weeks (range 1-4 weeks)).

2. Residence.

Residence creates the situation of ongoing disease. This can decrease with time, be stable over time, or worsen over time. The principal source is ongoing release of cytokines and other cell products in response to the recognition that the foreign substance is still present and not destroyed.

3. Removal.

Chelation removal (and other forms of removal like sweating) results in cytokine and other cell products release from immune cells sensing movement of Gd, and re-entry of Gd in the vascular system. For essentially everyone this needs to be controlled with an immune dampening strategy. This immune dampening serves to both decrease the acute symptoms of removal, but also to diminish immunological memory and thereby increase immune tolerance for Gd. This also likely results in de-training of macrophages.


4. Autoimmune condition.

Although GDD is under the rubric of self- destructive disease states: immune, auto-immune, and auto-inflammatory conditions, as generally Gd is present, the cause is both known and present. Excessive chelation without concurrent immune dampening can generate essentially a true auto-immune condition, that is Gd no longer needs to be present in any amount, but self-destruction conditions persist. This is because each chelation causes a Flare (a re-ignition of immunological memory) and also continued training of the innate immune system (macrophages principally), so eventually it develops a life of its own, with no need for Gd to be present. This is why concurrent immune dampening treatment is generally essential.


5. Micromovement.

Many GDD sufferers also find they can no longer tolerate even a noncontrast MRI or various forms of electromagnetic (EM) energy (such as cell phone use). The inciting event is micromovement of Gd in tissues by the effects of EM energy. So the Gd may not actually leave tissue but experience shifting (such as flipping of the polar orientation of protons from low to high energy state, and vice versa) in the exposed EM energy environment. Note that the above mentioned shifting of orientation of protons, refers to the cloud of protons (principally in water and fat) surrounding the GBCA. This reflects one of the mysteries of MRI and GBCAs- in MRI the GBCA is not imaged directly, what is imaged is the magnetic effect of Gd on surrounding protons (principally in water and fat).

The micromovement effect is controlled by avoiding circumstances that this phenomenon is experienced, until the number of chelation sessions has removed sufficient Gd to diminish or remove this effect.

6. Stress/ Anxiety

Once the pathway for symptoms have been established for GDD, other events that can initiate cytokine release can also follow those pathways. Perhaps the most common scenario is excess anxiety on the part of the sufferer. The answer is simple, but for some may be difficult to achieve: Stay calm.

Notes:

No doubt other effects are also in play that are not yet known.

To use a real-life example: if a subject claims to experience brain fog following 1 chelation session, that she did not have before. If the correct chelator has been used (hence re-distribution noncontributory) this may reflect symptoms of Gd removal (removal is always a good thing if done correctly) if originates early, and reflect re-equilibration if originates late. If substantial Gd has been removed from the site (in this example the brain) early origination with continued presence, may reflect persistence of symptoms from the removal, on its own, or blended into later symptomatology from re-equilibration. The added factor that could be responsible for all of this is anxiety, either compounding the above or existing on its own.

Why is it with Flares (removal) symptoms may develop that did not seem to be present before? First of all, it is important to understand that Gd will always be present in the brain following GBCA injection, and certainly in the setting of GDD. So its new symptoms reflects either: i) other symptoms were more dominant at the time of disease initiation (Gd entry) hence this not so noticed, and ii) in the interval following entry and removal, tissue resident memory T cells have taken up residence in that location, and may be particularly larger in number than other sites, so removal generates symptoms not before experienced.

There are a multiple of different symptoms and different cell and subcell defects that have arisen following Gd, mentioning a few topical ones: mitochondrial injury, leaky gut, electrophysiological cardiac abnormalities, sympathetic dystrophy, vision abnormalities, hearing abnormalities, imbalance. There are a bewildering array of treatments for these conditions, most if not all, not scientifically proven.

My recommendation: at least 5, and those who received multiple GBCA injections, at least 10, properly performed DTPA chelations with immune dampening, before entertaining management of any other individual symptom. Almost certainly these symptoms are due to Gd, and the treatment is: controlled Gd removal. Aggressive attempted treatment of these symptoms without an adequate trial of controlled Gd removal, more likely than not will cause more harm, which may be disastrously more harm.

Richard Semelka, MD


 
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