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NSF is the designation which is incorrect, should be GCSF-RF... GDD is correct.

When the term GDD is challenged, actually it is more scientific to challenge NSF as a designated term; it is more accurately termed what Brent Wagner has done in a 2016 review article Gadolinium Associated Systemic Fibrosis ... although one probably now could call it Gadolinium Caused Systemic Fibrosis (in Renal Failure) GCSF-RF.

Also it is worth noting that essentially all the studies on GASF are observational, Oxford Level of Evidence (LOE) 2 a, at best. None have looked at cytokines as we have done in humans with GDD.. and ofcourse none have looked at challenges to recreate the immune reaction as we have done. This challenge occurs as a distinctive phenomenon of the appropriate treatment, removal/chelation of Gd from the body, which also happens to simulate a GBCA injection by the remobilizing Gd in the vascular system. The general disappearance of GCSF-RF in the world around 2009 was from stopping the use of linear agents in renal failure patients is LOE 2a.

Probably incorrect that GASF is untreatable.. The same approach as we use should be employed in them, and if they are dialysis-dependent then dialysis shortly after chelation would be appropriate. I usually do not give away important insights until I have written the paper... but this is another one I am providing to the world of investigators.

What must be happening is that chronic renal failure, probably over the course of time, induces changes in CD 34+ bone marrow cells that they become more reactive to perceived injures/ antigens, and more readily react with fibrosis to contain antigens. Something along these lines must be the plausible explanation, otherwise why have subjects with normal kidney function who have received 20+ GBCA injections, and therefore will have substantial Gd retention, not also experience this condition? So this has been an important unanswered question. Animal studies with partially nephrectomized kidneys show greater skin changes with the less stable agents than the more stable agents, which sort of fits with GCSF-RF, so it is possible that one of the systemic responses of diminished renal function is an immune system response that puts bone marrow cell immune cells in a more active state to deal with antigens- and what they do is fibrose antigens. The other unanswered question, and again just observational, why do less stable linear agents cause the condition more. The explanation is that they release more 'free' Gd.... but Gd is never free, it rapidly becomes bound to another anionic species.... So what species of Gd is it that results in GCSF-RF?

Finally, why do only 5% of chronic renal failure patients who receive Omniscan (or Optimark, Magnevist, which are a lower percentage) develop GCSF-RF? Since only 5% of renal dialysis patients develop NSF after GBCA injection, there must be a genetic component as well. It may well be the same gene as GDD or a gene in a network of Gadolinium toxicity genes, and probably more broadly heavy metal toxicities.

Find the gene for GDD, will be the key to unlock some of the mysteries of all heavy metal toxicities... all heavy metal deposition diseases.

There are many unanswered questions still with GCSF- RF, and essentially the majority of the assertions are observational and not experimental. GCSF-RF likely arises both due to GBCA instability and bone marrow cell infiltrate immunogenicity, which are both complex and not scientifically explained phenomenon. In contrast, GDD falls more in line with classic medical knowledge: it is an allergy- and more specifically a T-cell dysregulation type of allergy. This is much more straightforward than the underlying causes of GCSF-RF: GDD is essentially like peanut allergy, with the difference that the micropeanuts of Gd have durable retention in your body. In the case of GDD, it is a million micropeanuts hammered into your skeleton and skin,. On top of that, we have opened the door to understanding GDD by cytokine studies, and the unique application of dynamic cytokine analysis following a disease-inciting challenge. Never done with any other entity before. Unfortunately though, the cytokine profile will probably look like the cytokine profile of the various forms of asthma that have been worked out, which is remarkably complex. This asthma cytokine work probably took decades and 10s of millions of dollars.

My primary goal: find the gene(s) for GDD. Open one of the major locks on the door to more fully understand all heavy metal toxicities. Like the opening images of Maxwell Smart in the Get Smart series from the 1960s.


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