If Gd gets into cells? Then what. It can't come out with chelation, or can it? The great majority of GDD sufferers still get better. Here's why.
I wrote in a recent blog, that Gd indeed has been detected in neurons. This was reported as early as 2017 in the article I cited from MacDonald. On one hand it does make me wonder, since physicians from Mayo have detected Gd in neurons, then how is it possible that none of the physicians in the Mayo system seem to think that it can give people persistent sickness? That is really material for another blog. In a related subject, some physicians who see reports for Doctors Data tell patients, this is junk science, and yet, the few examples I have seen where Doctors Data and Mayo were performed (at my suggestion to the patient) came up with the same numbers for the quantity of Gd. So is Mayo labs also generating junk science? Yes I have considered comparing results from the exact same sample between Doctors Data, Genova, and Mayo. I think a lot of people would like me to do it. My response I have more central core work to do on GDD, to focus on people understanding clearly that it exists, and clearly how to understand how optimal therapy is to be performed. And people who think I should write the lab comparison paper, or other papers, don't really understand how much time and work is involved in writing a paper and getting it published. It is enormous. I do not have unlimited time and unlimited resources to do that. Yes though, I would like to see it done. Yes the mountain of disinformation out there is enormous, so I cannot deal with all of it. But I will deal with what I write below:
At this time, my opinion is that less than 1 % of Gd retained is retained intracellularly, and much of that in cytoplasmic lysosomes, which are like small thick-walled balloons, that also have inserted into them toxins intended to kill the entity.We know that a heavy metal cannot be killed and so Gd is like kryptonite for superman. An unknown amount may be in freely exchanging form across celll membranes.
But if this intracellular Gd is very toxic, why then are the majority of people who get GBCA injections not sick from it? That is why very early on I described that GDD is something like a 50/50 mixture of immunogenicity and toxicity. The immunogenicity (reactogenicity is used when it is harmful to the person) allows the toxicity to occur. I have said repeatedly, to understand what is going right in GSC subjects (Gd in them yet not sick, like me) and what is going wrong in GDD subjects, would provide enormous insight into many diseases, maybe all metabolic diseases (which are the majority of diseases) including cancer and infection. If I had a billion dollars to spend this is what I would spend it on, and not build rockets, to start ruining deep space. Well maybe before solving the disease understanding that GSC vs GDD represents, but clean up the garbage and waste we have created in the land, water, and air.
We also don't know what relation intracellular Gd has with overall homeostasis. If Gd follows Ca in many of its sabotages, then maybe it also follows Ca in membrane channels, and can also exit the cell, and also be part of le Chatelier's form of Gd elimination. Is all the Gd trapped in cells and cannot escape? I don't know, this is an interesting question my opinion is that some amount may freely cross the cell membrane.
Do cell humoral products such as cytokines block these channels in GSC individuals, preventing Gd entry into cells, and we have little or no Gd in the critical functioning somatic cells (neurons in brain, renal cells in kidneys, pancreatic cells and islet cells in pancreas, etc) or do we all have them and they are in a combination of lysosomes and freely exchanging electrolytes.
I return to the concept of how development of knowledge occurs with drugs, that essentially all drugs that work, the original phase of use is the observation that it works, and then subsequently understanding the mechanics. Finally after some 70 years of use, scientists believe they understand how acetaminophen works within the last couple of years, we have over recent years understood how some antidepressants work, we still don't know how electroconvulsive therapy works, we still don't know how most general anesthetics works. Even when we believe we understand the mechanisms of drug action, these are generally theories and not facts.
The bottom line: if people are sick from Gd. They get an effective cation exchange chelator which exchanges Ca or Zn for Gd, Gd comes out in the urine in measurable amounts. And most people get better if they receive enough chelation. That is far better documentation than virtually any other drug possesses. It also carries with it the prospect of )near) cure, whereas most drugs are designed to simply manage diseases. In the real world we live in, it really doesn't get much better than DTPA treating GDD (or lead toxicity).
So individuals who state that chelation does not work are frankly wrong. This is both stupid, and even worse, is dangerous, because this causes confusion in GDD sufferers about whether the only treatment that is shown to work, works.
If some individuals feel that they have shown chelation does not work in rodents, they also clearly do not know that rodents are different than humans. Also, more likely their rodent work is wrong. At some point I intend to write a blog describing that most of the famous fraudulent science that has been done over the years, has been done on rodents. I do frequently cite the Bayer paper on DTPA removing omniscan from the brains of rodents. But in the same report they also say this did not happen with Gadavist. It should be noted Bayer makes Gadavist. But is this the case in humans in the clinical setting of GDD? The clinical setting is vastly different than the experimental setting. Experiments often are done with 2 or so weeks of retention, not months or years as seen in clinical practice. In clinical practice Gadavist generally is removed in very large amount 20 to 100 fold greater than native elimination. Well Bayer makes Gadavist. Clinical setting is different from the lab, and rodents have metabolic differences from humans. Bayer could easily do/pay for this study in humans. Measure 24 hour urines in all people receiving Gadavist, even as few as 10 would do. Measure 24 hour urine at 1 day, 3 days, 1 week, 2 weeks, 1 month, 3 months. The chelate the individual with 5 ml of DTPA. In this population you would find that the native elimination of Gd at 3 months is 0.5 mcg/ 24 hr, and the mean Gd removal post chelation would be in the range of 20 mcg/ 24 hrs. Now this study I am extremely interested in. Much more than the above mentioned study comparing results from Doctors Data, Genova, and Mayo. This would be an extremely easy study to perform for all GBCAs in university centers, and would give the authors an easy publication. So why is it not done? Oh, I know, fear of writing something that will upset the companies. If I was still in a university, I would do this study in a heart beat.
A thoughtful physician scientist like myself does then wonder: what about the 1% of patients with GDD who do not seem to respond to chelation, what is happening in them?
I do have one patient (who I am not treating directly, so this always poses some uncertainty of what is going on), who despite receiving DTPA treatment as I would do it, is not responding to chelation as the vast majority do. The intense neurological symptoms of hearing and visual intolerances seem not to abate. Why? In that person's history they describe having experienced a viral infection that caused intense headaches, and this was still ongoing and the reason for the MR of the brain with GBCA. My current theory is that the virus has acted to open up or create cell membrane channels in visual brain cortical neurons and auditory brain cortical neurons, such that he does not have 1% of the retained Gd being present in non-exchanging intracellular locations as the majority of GDD sufferers have, instead 50% or more of the Gd in the body is in these intracellular locations, which do not experience le Chatelier's exchange and remain fixed? This is an interesting, yet frightening prospect. This is why I have requested this person to enter the trial of Functional Genomics Analysis that I recently wrote a blog on. I hope that they can discover some epigenetic/ inflammasome cause for this near unique lack of response to iv DTPA chelation. Although DTPA chelation alone works for the majority of individuals, in a small subset it is clear they need additional ancillary treatment, and hopefully we can find out what that is.
In closing, anyone who says DTPA chelation does not work does not know what they are talking about, this is Opinion Unconfounded by Knowledge. It is both incorrect and dangerous, especially so if they believe in GDD, because then they serve as pure Agents of Discord. I consider these Agents of Discord even worse than physicians and health care workers who think that GDD does not exist. This latter group are easier to understand. The latter group I hope to progressively lead, as a shepherd would, into knowledge. I believe this is already happening in significant numbers. The Agents of Discord may simply always remain as Agents of Discord., and this is dangerous
DTPA chelation works as well as any drug for any purpose. But no drug is 100% perfect. Drugs that really work well often are described to work in 80% of patients. DTPA works much better than that, if it is done well and in the right amount (Goldilocks principle). DTPA may in expert hands not apparently work in 1-5%, but it is not that Gd is not being pulled out, but that something in addition needs to be done. It may be in that 1-5% their retained locked intracellular location of Gd is 50% of the total and not 1%. So I am looking into that now, working with experts in metabolism. What a responsible scientist does is be clear eyed to realize there are issues, and to try to understand where there are failings and then tries to further correct/ refine things. This of course seems to be one of the problems with vaccines. It appears many of the vaccine enthusiasts believe, here are the vaccines, they work, so shut up. What they should be doing is thinking this vaccine does not work in x % of patients, and in y% it actually makes them worse. How can we change the vaccine? Or how can we identify who will react badly and not give those individuals the vaccine. This what they should be doing. They should follow what I am doing with GBCAs and with treatments for Gd toxicity/ GDD. This is wise and ethical practice of medicine.
Richard Semelka, MD