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Why Flare can be more severe than initial GDD reaction.

If Flare arises from removal of Gd from the body, why can it be more severe than getting Gadolinium Deposition Disease in the first place?

This question arises not infrequently from a number of subjects, and I do not think I have taken this issue head-on in a blog previously.

There are many components to the development of GDD, but the principal one in my opinion is the development of an immunity- mediated inflammatory disease IMIDD) with the generation of Tissue resident Memory T cells (tr- MTcells).

What has happened with the development of GDD, is that dendritic cells ( a presentation immune cell) pick up particles of GBCA injected into the circulation, and show them to Tcells (located primarily in lymph nodes). In the majority of individuals (the Gadolinium Storage Condition group) the Tcells look at the GBCA particles, send off cytokines, but the cytokines are primarily inflammation suppressing and communicating cytokines, and this cytokine release is transient. As a side note this benign Tcell cytokine reaction probably occurs with the injection of any molecule, vitamin C, glutathione, etc.. it just has never been looked at yet). There may be a transient reaction, like flushing, and things settle down, but miniscule amounts of Gd get deposited throughout the body, primarily in bone and skin, and that's it. In a very few individuals, some mainly by pure genetic function, and others confounded by co-factors (metabolic acidosis, certain infections, high potency antibiotics, other IMIDs), when the dendritic cells show T cells the GBCA particles, the Tcells identify the GBCAs as a dangerous foreign invaders. They send off cytokines that are primarily pro-inflammatory. Amongst other things, a principal effect is this causes increased production of tr-MTcells. These cells then migrate to everywhere that Gd is being retained..... which is everywhere, but primarily in bone and skin (and lower down the list brain, liver, kidneys, etc). At the time of the initial contact with GBCA and the initial reaction, there is (an estimate) perhaps 100,000 T cells that react to GBCA. Once the full immune reaction is established (using COVID vaccine data) after about 14 days, full immunity has been created, and that means now approximately 10 million (relative estimate) memory T cells have been developed lined up everywhere Gd is deposited, and associated inflammatory immune cells. These are now all fully on high alert for Gd, and prepared to act at full immune capacity. In many sufferers with time this immune high alert status starts wearing down, so the extent of pro-inflammatory cytokine release and total number of tr-MTcells progressively diminishes. In many GDD sufferers this begins in earnest at about 2 months, so by 3 months one has a reasonable idea which way the immune reaction is heading.

But to get back to the original question about why Flare can appear worse than the initial GDD is simply that there are now many more cells that are reacting to GBCA, and specifically adapted to react to GBCA and now already on high alert, and are now located everywhere Gd is, whereas at the outset only in some of the locations Gd has been retained in.

In general, the largest group of individuals at highest risk for severe Flare are those between 2 weeks and 3 months after disease onset. This propensity for intense Flare progressively decays over time, by 6 months, 1 year, such that by 2 years post development of GDD the likelihood of very severe Flare is low.

Highest risk for severe Flare: 1) initiation of chelation within 3 months of GDD onset, 2) at time of presentation of the sufferer to the health care center, they still have severe symptoms of GDD (meaning the immune system is still reacting strongly to the persistent presence of Gd for months or years beyond disease initiation), and 3) numerous GBCA injections (reflecting that chelation will re-mobilize a lot of Gd because there is a lot of Gd that is retained, and this massive remobilization will result in increased impetus for many Tcells reacting).

This is not to say that removal (chelation) should not be attempted in any of these 3 groups, and in fact groups 2 and 3 likely chelation is absolutely essential. There are always counter risks that one has to consider. In my opinion beginning at 3 months persistent damages from GDD begin to accrue, but also in many these persistent damages are not necessarily irreversible or too debilitating. Many features of GDD are largely reversible certainly by 1 year, perhaps also by 2 years. Clear physical damage tends to begin in earnest at year 1, and in many sufferers these progress. Changes that are likely not significantly reversible is clear tissue destruction and fibrosis (subcutaneous tissue loss/ and or stiffness of subcutaneous tissue), and debilitating handicaps such as decreased ability to walk. This is not to say that chelation cannot improve things, but just that the likelihood of getting back to near-normal becomes progressively more remote.

Because there is a high propensity to have severe Flare is not the same as chelation should not be performed, often chelation is essential in this circumstance. But extreme care and caution is necessary: start with lesser amount of chelator and higher amount of immune dampening, and gradually increase amount of chelator and decrease amount of immune dampening, using the sufferer's perception of Flare severity as the guide. Also it is imperative for the suffer to recognize, especially if they are in the group of GDD onset within 6 months, a severe Flare represents, even if paying attention to low dose chelation with substantial immune dampening, both the most important confirmatory evidence that the individual has GDD, and that it reflects a lot of Gd is being remobilized from the tissues and transported to the kidneys for elimination. Last important point about Flare: usually it is short lived from time of chelation (onset sometimes at day2-3) for 7 days, especially time limited if taking a Frame type steroid regimen.

As with essentially all diseases, early detection and early treatment is crucial to achieve the best outcomes. Because of the nuance of early heightened immune system reactivity to Gd, and at the same time this immune sensitivity can decrease on its own dramatically in many individuals, early treatment usually means starting treatment no sooner than 3 months following onset of disease. Theoretically there may be one exception, I will discuss this in an upcoming blog.

Richard Semelka, MD

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