Metal Deposition Disease and Storage Condition States.
I have been asked on a number of occasions why do I use the terms Gadolinium Deposition Disease and not Gadolinium Toxicity or Gadolinium Poisoning. I usually respond: GDD is one of atleast 3 Gadolinium toxicities, the other 2 Acute Hypersensitivity Reaction and NSF, so although toxicity is correct, toxicity is a larger umbrella. Poisoning carries with it a more hostile implication, that may suggest deliberate injury ... which I do not want to convey, also because no health care provider wants to think that they are poisoning someone.
With experience now with measuring heavy metals in urine, is that everyone has atleast 5 different metals in them, and everyone has lead... Yes everyone.
It appears that organic kale has a fair amount of thallium and cesium in it - yet I suspect individuals who for health reasons consume a lot of kale, only a small percentage probably show signs of toxicity. My estimate: 1 in 10,000 have mild disease, . 1 in 100,000 have severe disease.
So lead toxicity should be called Lead Deposition Disease to distinguish sufferers from the rest of us (those with Lead Storage Condition). Thallium toxicity, probably 1 in 10,000 have mild disease, and .. you guessed it, 1 in 100,000 have severe disease. So Thallium Deposition Disease..... and so on with other heavy metals - such as arsenic and mercury.
I am convinced that GDD is genetic... I am similarly certain that these others are also genetic. The question is: is GDD the same gene as Lead Deposition Disease and Thallium Deposition Disease?
In many subjects disease may be a threshold phenomenon (the amount entering the body has to be at a certain volume or concentration before it can overwhelm the immune system , others it seems to be a simple immune reaction to the presence of Gd independent of the volume - although local contained Gd (MR arthrography, subcutaneous injection (as examples)) lends itself to GDD, and may therefore simulate vaccination, but also then not too different from a threshold effect as the local concentration would be high. So are these different genes: threshold and high sensitivity immunogenicity?
The Deposition Disease states may be about the same, and optimal treatment is also probably about the same: chelation with a high stability chelator for that metal while managing the host response. As described in another blog - chelation following the route of acquisition of the metal is probably wise (this is oral quite often), maybe in combination with iv chelation. DTPA has high stability with many of the heavy metals. We are currently looking into whether other chelators may have higher stability for other specific metals.
Richard Semelka, MD