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Risk Factors and Complicating Factors- definitions for GDD (also true for other heavy metals) and variations true for most other diseases

  • Writer: Richard Semelka
    Richard Semelka
  • Aug 12
  • 4 min read
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Up till the present I have lumped risk factors and complicating factors togther. Although there is considerable overlap they are different entities.

To begin with, risk factors are factors which predispose to developing GDD. This is a predisposition but not necessarily mean inevitable.

In distinction, my use of the term complicating factors, are factors which make treatment for GDD, more complicated than the simple approach: patients with GDD recover with a standard approach of for every 1 GBCA, 5 iv DTPA chelations with steroids and antihistamines. will effectively cure them.

Historically, for NSF the term cofactor was used, with the implication that cofactors were essential cofactors, which they were not, yet many of the the cofactors considered were contributory, such as metabolic acidosis..

A number of risk factors and essentially all complicating factors relate to the larger process of broad-based immune system dysregulation.


Risk Factors

So to start with , I have used the estimate that 1 in 10,000 of all comers would develop GDD who undergo MRI with GBCA. . But, depending on the number and severity of risk factors, the risk escalates. To start with among the highest risk categories, stepping through the risks:

white- perhaps increases risk by 25%

female- perhaps increases another 25%

pre-existent severe Multiple Chemical Sensitivity Syndrome- 50%

severe infection within 1 week of obtaining MRI with GBCA - 50%

These percentages reflect percentages not of the total of 10,000, but of each decreasing number of possible sufferers. So the final risk considering this above list, is 1 in 1,406, which is now real risk to be considered.


The question I get from many individuals: "I am getting an MRI with GBCA in a week's time" what can I do to mitigate risk. The most obvious risks are avoiding activities that will result in transient immune system perturbation from 1 week before to 1 week after GBCA, and to increase elimination.

So:

  1. Drink 20% more water before and after GBCA, for about 2 days before and after. Note: not too much water, as this will have the opposite effect (see earlier blog).

  2. Do not engage in intense activity for 1 week before to 1 week after GBCA injection.

  3. If possible undergo MRI 1 week after a moderately severe infection. This may be most feasible with a viral infection, such as an enteric virus, influenza, or COVID. Renal infection may pose a greater risk than many other infections.


    The basic key is to avoid getting MRI if your immune system is out of balance... if possible.


    Complicating factors.


Complicating factors make treatment more difficult. The first to mention is particularly intense sensitivity to the presence of Gd (think of peanut allergy as a comparison). Not uncommonly this may only be elucidated following the start of a chelation regimen. But pre-treatment status usually provides important insight).

Severe chemical sensitivity syndrome is an important risk factor, as it effects what drugs can be used in patients and also the individual's overall sensitivity to Gd,

Recent literature has described the importance of goo in creating the environment for dementia and many other diseases, both intra- and extracellular. I have for a long time focused on the importance of protein as a symptomatic form of Gd, Gd bound to protein. Essentially protein goo. Recent research from SUNY Buffalo has described the presence of tangled mRNA in the cytoplasm as a cause for forms of dementia and other neurological diseases, and the use of antisense RNA to disentangle and break up these RNA goos. Maybe an approach like this can be accomplished for GDD and similar toxicities. In the meantime, although Gd- protein may be the most symptomatic Gd, it may also be the form that Gd is most easily removed by an effective chelator from the binding protein molecule, and then eliminated in urine.

So states where there is increased protein goo in the body prior to MR with GBCA, or immediately after. What I have observed as a very important complicating factor is prior recent surgery, especially major surgery, which is known to result in significant granulation tissue (immature fibrosis), which is fibrin-type, essentially protein goo. Back surgery and prior back injury also results in significant granulation tissue (immature AKA early fibrosis) and fibrosis, essentially protein goo. The central spine especially problematic since in adults this is the last center present for creation of various blood cell tissues (these include Tcells, (which I consider the principal cell lines for GDD) .

Both collagen (the scaffolding of tissues and organs, creating normal structure) and fibrin (involved in repairs of injuries and thrombosis of vessels, which can both be good and bad) are protein which have adherence, essentially stickiness (what I am calling goo).


.Superimposed infection of tissues then magnifies the amount and gooey-ness of fibrin and likely collagen. As ofcourse do other pre-existent Immune Mediated Inflammatory Diseases.


This blog emphasizes protein goos (think spiderman webs) which serve to trap Gd, increasing the risk of GDD and also complicating treatment with the only effective treatment : chelation with a powerful and effective chelator.



Risk factors and complicating factors are overlapping sets that relate to the development of GDD and(risk) and the prolongation/perseverance post DTPA-chelation. All of these contribute to the state of a broad-based Immune System Dysregulation.


Richard Semelka, MD






 
 
 

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