Heavy Metals in the body. Transient Presence, Retention, and Durability of Retention (Deposition)
Heavy metals in the body turns out to be an entire field of science/medicine, and we are just now scratching the surface. I came to recognize this importance in treating GDD and looking at 24 hour urine reports in reports that list 20+ metals... Everyone has atleast 5 heavy metals (read 20) retained in their body, 100% have lead (Pb). These metals on their own have the prospect for Deposition Disease, and almost certainly they interact with each other in the patient's symptom complex.
The level of durability of presence of a heavy metal depends to a large extent on what it binds to in the body. In general binding to bone (as Gd and Pb do) results in durable deposition - that may mean durable for the life of the individual, and if in females deposition that can be transferred to the fetus (a sort of nasty reincarnation).
Before panicking too much, it is remarkable how the human body can manage corralling a fair amount of these potentially toxic substances and still be ok- the Storage Condition circumstance.
Being corralled into bone probably is the result of two processes (at least): 1. that the metal can substitute for Ca, passive deposition and 2. bone marrow infiltrate cells (cd 34+ circulating fibrocytes being one member, likely of 10 cell types [read 100]) corral them into bone, active deposition. My theory is that this active deposition is the last defense mechanism of the integrated host immune system: if the immune system can't kill, or eliminate (by kidneys, bile, bowel, lung, sweat, salivary secretions) the offending particles, then its last option is to corral it in a situation where it can cause the least harm - this is generally the skin and the bones.
One of the most common transient presence (I believe transient) is Bismuth, which patients acquire from products like Peptobismol that have been taken for GI upset. Again transience reflects that there is no natural effective binder in the body, and it gets (near) fully eliminated.
Other toxins may be neutralized by binding primarily in fat (this may include in neural tissue). Empirically fat-binding should be less permanent than bone, and can with some time be eliminated, over a course of 1 year or so.
Many toxins there is no molecule that can bind and remove it (yet). That is one of the (few) positives of having GDD - there is a binding agent that can remove it well (DTPA, in the future HOPO)... Almost all other drug toxicities do not have binding agents that can remove it. They get removed (hopefully) with the tincture of time, and other, not yet fully understood, strategies of the immune system (ignoring the toxin works for many- also ofcourse for Gd).
The first step in treatment is always to eliminate the intake of the toxin. With GDD, this means never receive another additional, introduction of Gd into the system, so never another GBCA injection again. Based on durability of the reservoir (bone) this may not be sufficient to eliminate the disease in most cases. This would also be true for true Lead Deposition Disease(LDD) (that is not Lead Storage Condition, which the vast majority of people have, LDD also extremely rare- but based on numbers, everyone has lead in them, common enough).
It is not clear with Thallium Deposition Disease (TDD) if simply stopping the continued intake, this means stopping eating kale, maybe cabbages, and green plant extract powder, is sufficient to treat successfully the disease. Or if the addition of oral Prussian Blue capsules (maybe combined with iv DTPA) is essential. But as with simple GDD, the first step is stop the intake,. With GDD it is also important presently to wait 3 months after disease initiation, and see if the subject is largely better., before starting chelation. For Thallium Deposition Disease, immediate treatment though with Prussian Blue does not seem to be as deleterious as immediate treatment with DTPA after GDD onset (this Flare reflects a heightened immunological memory effect). This may reflect the following differences: sudden onset of disease development (GDD) versus long term progressive onset (TDD)- so there is not the sudden development of intense immunologic memory (iv administration), but more of a progressive slower development with oral consumption; between oral vs iv intake of treating agent; and the nuanced type of host immune response. But there may be no difference- I do not know this.
With radioactive metals there is probably not enough dose to achieve a Deposition Disease state (so no Plutonium Deposition Disease), they die with much lower doses than result in direct tissue destruction. With radioactive heavy metals the key is to get them out as quickly as possible, and try to manage the metabolic imbalance of chelation subsequently. So with Plutonium the best treatment available is Ca-DTPA iv. Probably administered daily. With additions of Zn-DTPA to restore Zn, and supplements of Mg, Mn, and other native metals, as depleted. A Goldilocks approach; because supplements of native metals will compete with Plutonium for removal using Ca-DTPA.
Sources of acquisition of heavy metals, reservoirs of localization of the metals, native host binding agents, pattern and type of toxicity, method of intake, durability of deposition, all factor in how heavy metal toxicity, Heavy Metal Deposition Disease, must be treated.
We are just at the beginning of understanding these processes and the interplay between host, heavy metal, other heavy metal, other toxins.
The starting point: where is the heavy metal coming from? Stop the continued intake. See if the subject gets better with just stopping intake.
In using a chelator, use one with broad high stability for multiple heavy metals (since everyone has multiple heavy metals). Presently DTPA is the best choice. Perhaps Zn-DTPA alone for most situations. Occasionally Ca-DTPA or our standard Ca-/Zn-DTPA for very serious Deposition Disease or for mild toxicity from radioactive heavy metals. Daily Ca-DTPA for radioactive heavy metal poisoning. In the future this may be HOPO and hopefully more agents. It is all about stability: stability of the chelator with the spectrum of heavy metals, paired with relatively low stability for host native metals and cations.
Richard Semelka, MD