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Categories of GDD and their Effect on Treatment Success

On the surface it is absurd to think there could be only two forms of Gd toxicities: acute hypersensitivity reaction (AHR) and NSF. There are atleast 4 types of anaphylaxis, 4 types of anaphylactoid and 2 types of overlap anaphylaxis-anaphytoid reactions, and only 2 forms of Gd toxicity? 7 types of Ehlers Danlos, and only 2 types of Gd toxicity? You get the idea.

Knowing that GDD exists, it begs the question: is there only one type of GDD?

Ofcourse not, there are atleast several known variants ... which means there is atleast 10, recognizing there must be 10, means that there are likely 100+ variants.

Being lost in the maze of variants should not distract from recognizing the shared principals of treatment: the most effective treatment is chelation with the most stable (and include adequately bio-available) chelators (as measured by stability constant) with concurrent management of the host response. In some variants modifications of this principle will be necessary, for atleast portions of the treatment period.

GDD itself (and probably all autoimmune and T-cell dysregulation conditions) arise almost like the pulling of the arm of a slot machine in Los Vegas or Macau, most of the time the pull on a slot machine arm, does not result in success, once in a rare while you hit jackpot. In a similar fashion, with the 1000 moving parts of the immune system, most of the time a great number of antigens which have entered the body are ignored (immune tolerance) but on occasion the cylinders click in the correct pattern in order that you hit jackpot, or in this case bad jackpot or anti-jackpot. This can also be like swimming in the ocean where there is a lot of powerful sharks around, the great majority of the time they recognize that humans are not their natural prey, but sometimes their instincts fail them > anti-jackpot. As with both the slot machine and the shark, certain conditions exist that make hitting the anti-jackpot more likely. With the shark analogy, the anti-jackpot more likely if you are swimming with a number of great whites, compared to swimming with a school of hammer head sharks. A roulette table could also be used as an analogy, except a slot machine more closely reflects the immune system, as often a number of cell lines have to act together (for example the dendritic cell has to present to the T-cell the antigen), so often a few mis-steps have to occur in order to hit the anti-jackpot.

So let us look then at the major categories of anti-jackpot GDD categories to GBCA:


Powerful immune system variant (PISV). Almost certainly its own unique genetics. A large number of sufferers describe that they have generally never been sick in their lives before GDD, no colds, no flus. I anticipate their base-line likelihood of cancer also extremely low. Either the first dose of GBCA, or a subsequent one, each time a pull of the slot machine arm, then they hit anti-jackpot. Once they have hit anti-jackpot the immune system will remember it, and each injection of GBCA the anti-jackpot pays off a larger amount of anti-payout. I have previously described this as superman and kryptonite. It would be interesting to see if in this variant if their powerful immune system actually also splits the bonds in macrocyclic agents. In this variant concurrent immune dampening with chelation is essential, for atleast large stretches of treatment, to manage Flare and to decrease immunological memory for Gd. In principle these are the easiest to treat and most likely to experience 'complete cure'.

T-cell dysregulation variant (TCDV). There may be overlap with the powerful immune system variant, or separate, it is a somewhat contorted powerful immune system either from birth or developed, I think likely can be either. These individuals already have a pre-existent T-cell dysregulation. Common causes presently are preexistent chronic parasitic (eg Lyme) or viral (eg: Epstein Barr) or immune disruptive states (autoimmune disease). Chronic neuropathies can also result in increased susceptibility (fibromyalgia, CRPS, sympathetic dystrophy) They already have one T-cell disruptive state, so are susceptible to other T-cell disruptive states (they are swimming with great whites and not hammer head sharks).

More difficult to treat. The more disrupted the immune system, the more difficult to treat to a cure (impossible?) with the chelation/immune dampening treatment strategy. More ancillary treatments will likely be necessary. Shifting to an ultra-safe chelation strategy may need to be resorted to (see below). An ongoing process of discovery.

Recent decrease of immune system variant (RDISV). Most common situation is high potency antibiotic therapy immediately prior to or in close relation to GBCA administration. This is analogous to the one-two punch that can occur in NSF: an iodinated contrast enhanced CT, that has decreased renal function, followed in short order by the knock-out blow of a linear GBCA. This variant likely can occur on its own, or overlie PISV or TDISV. In addition to chelation/immune dampening for Gd, they will need restoration of the native immune system. For example probiotics (+ other) to correct for destruction of the host healthy bowel tract bacteria secondary to high potency oral antibiotic intake.

Transient physiology imbalance variant. (TPIV). The concept the same as RDISV, but the underlying imbalance in general much easier to correct. This variant seen in subjects dehydrated before receiving the GBCA (hence always, always, always a patient should not be thirsty before getting a GBCA injection - same true for iodine injection). The other common setting is an individual undergoing intense physical activity immediately before or after receiving GBCA. The answer: also don't do this.

Multiple Chemical Sensitivity Syndrome (MCSS). Co-existent MCSS can be a major problem both for the subject (for the subject because it encompasses everything in their life) but also for the therapy plan. I recommend starting with the optimal chelation strategy: Ca-/Zn-DTPA with immune dampening, but patients may not be able to tolerate the Flare, tolerate the steroid, tolerate imbalance of native electrolytes (Mg, Mn, Cu, etc), tolerate even an iv or the stress of everything. This is now a new treatment concept I am revealing here: which others have recommended to me in the past (thanks Gail Montani) but I resisted. These subjects may need 1/2 volume (2.5 ml) Zn-DTPA alone as the entire chelation session, ultrasafe chelation, with no additional drugs, or with just very little immune dampening. This is then like mini-extent precision microsurgery for Gd removal. Less chelator- therefore less Gd removal and resultant less impetus for Flare; use of the most effective chelating ligand (DTPA) so no/negligible redistribution; the Zn- form of DTPA, so no/negligible native metals removed, and only pure Gd and other heavy metal removal. This is like playing competitive pick-up-sticks, or competitive 'Operation' (the old board game) where the space around the femur bone is decreased by 1 mm. Some immune dampening likely will be required at times, but possibly also in mini-amounts. The obvious question the reader may have - why then Dr S not use this for everyone? The simple answer: travel, time, money and veins for the patient. In simple terms: Ca-DTPA is approximately 2/3 more effective than Zn-DTPA to remove Gd - so a typical Ca-/Zn- DTPA session results in 1 and 1/3 or 1.33` chelation units. 1/2 volume of Zn-DTPA results in 0.167 chelation units. (1/8th as much Gd removal) This means if a standard patient who had received complicated multiple GBCA injections and likely requires 20 Ca/Zn chelation sessions. The equivalence with 1/2 dose Zn-DTPA is 160 chelations. In some patients however this may be necessary, and I recommend stepping down from standard chelation to get to 1/2 dose Zn-DTPA. The answer never is weaker chelators because of redistribution. Since the great majority of our patients come from distance, we want to maximize the amount of Gd coming out of their body in each visit (hence standard treatment). The calculation when to switch to more ultrasafe chelation, therefore is done more hesitantly. If patients are local, it may not be unreasonable to do this in reverse: start ultrasafe and work up.

Concurrent GDD and Mast Cell Activation Syndrome (MCAS). This may be a common co-existent state with GDD, as GDD is a T-cell dysregulation state and MCAS is a Mast cell overactivity/dysregulation- which is essentially an extended Acute Hypersensitivity Reaction (AHR) to GDD. Overlap of Gd toxicites is not rare, and this by far the most common. This rarely results in extremely serious outcome (anaphylaxis) none-the-less a complicating factor for GDD. The simplest approach is to manage MCAS concurrently with GDD, which is done already in treating GDD by chelation and FRAME drugs.

Female Variants of GDD. Women tend to have profound vision changes, and other cranial findings, for example, compared to men. But this is only a relative difference.

Male Variants of GDD. Men will experience a GDD variant which primarily effects extremities (primarily legs) and involves pain, fasciculations, and skin changes. This variant generally does not have cranial findings. Noteworthy is that brain fog is generally absent.

Minimal severity GDD. In reality, minimal severity GDD is likely by far the most common situation. A patient receives a GBCA, has symptoms of GDD for less than 1 week (up to 3 months), then either decides for themselves to never get another GBCA again, or simply never has another MRI with GBCA ordered on them again. They never come to attention, even their own, as having GDD. GDD itself possesses a full range of severity of disease, as with any other similar, auto-immune disease, Crohn's, Rheumatoid Arthritis, etc.


Each of the above variants may well have their own distinct gene-basis. They may be unique individual locus gene variants, or may be altogether part of a gene cluster, that may include various combinations of the GDD genes, that may also include other genes, such as MTHFR (and others), in the cluster. Gene detection is the next major enterprise.


Richard Semelka, MD