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GDD in children


I have been asked a few times recently about GDD in children. Here is my current thinking.

GDD is very rare in children primarily because the incitement of GDD in a person often requires that the immune system is mature enough to mount an aggressive response to a foreign antigen (Gd). That is why the disease usually presents beyond 20 years of age.

Can children get GDD though? Probably yes.

In Medicine we often divide children in atleast the following categories by age(and probably more is appropriate).

Neonates (up to 1 year of age) often for medications they are clustered up to 2 years of age, but likely there is difference between 0-1 years, and 1-2years. 0-1 years the immune reaction often is highly reflective of the maternal immune system that the neonate is still experiencing (also with breast milk). 1-2 years it is likely a more pure child's immune reaction, but a highly immature form.

2-13 years (prepubescent childhood), probably significant differences 2-8 years and 8-13 years.

14-18 (pubescent), probably early pubescent and late pubescent are different.

As GDD is not widely recognized (for various reasons, as I have mentioned before) any treatment for anyone is considered 'experimental' or 'unproven', and applying this to children is a whole other level of risk. There are 2 risks: 1) the risks of treating children in an ethical medical sense (are we doing the right thing for the child?), and 2) the medicolegal risks of trying something novel in children. My suspicion is the pt 2 often is the prevailing concern. It also is important for me.

In the perfect non-litigious world this is how treatment should go:

In reverse order (since treatment most obvious in older children)

14-18 years. Certainly from 16-18 years, treat as one would do an adult: Ca-/Zn-DTPA with FRAME followed and accompanied by Amase drugs. Children over 100 pounds, standard doses, less than 100 pounds half doses. Simple at home remedies always smart to do first: Diet, alkaline water, gentle exercise, sweating, sun-shine. Children 14-16, probably Zn-DTPA alone. Zn-DTPA removes much less if any, intrinsic metals in the body, unlike Ca-DTPA, so this is advisable in all younger children, if they will receive chelation.

2-13 years. Start with at home remedies, and hopefully stop there. The immune system should be so immature that true GDD is not occurring. As we observe in nature programs, the mother is the most fearsome member of a species (polar bears, wolves, etc), so the first thought, are the parents over-interpreting findings? Since there are no weight based formulas for DTPA, reliance on experts for an appropriate dose- probably using a similar strategy that is used with GBCAs to begin with. So as thumbnail estimates: 2 year olds probably should get no more than 0.5 ml of Zn-DTPA, 8 year olds probably no more than 2.0 ml of Zn-DTPA.

0-2 years old. A primary consideration in this group: how did the neonate get the GBCA? If it was from mother's milk the amount the neonate would have received is infinitesimally small, so GDD extremely, extremely unlikely. If Gd was received as a fetus because the mom received GBCA then the risk is just extremely unlikely, but probably real enough, as the fetal circulation is closely aligned with the maternal with only a placental buffer. If received directly as a neonate, then the most direct Gd delivery has occurred. So direct neonatal injection atleast 1000 times more Gd than through maternal milk and probably 50 times greater than fetal exposure. The other critical aspect is in children 0-6 months of age, much of their immunity may still be maternal, hence they may manifest GDD symptoms without actually having GDD but just residual maternal activity. That is why watchful waiting early on is critical. To ease parental concern, urine Gd could be obtained as spot Gd urine. If there is no Gd, especially if the issue is: does my child have GDD from breast milk? then in this case: no native urine Gd - no GDD. This would be true if urine testing is done within 3-6 months of the breast feeding.

My assumption in the 0-2 year old group that maternal anxiety may play an enormous factor. Simple at homes remedies should be used for a long time (read my blogs on this). This would include pectin fruit containing baby food (SOME not ONLY), cilantro and possibly chlorella sprinkled on baby food (JUST A LITTLE). Maybe there are other diseases responsible- even just colic, or allergies. If GDD seems almost certain, treatment as for 2 year olds, above, but thumb-nail at most 0.3 ml of Zn-DTPA.

Issues: Urine testing for Gd could be done as spot testing. A very large problem with diagnosis is that the patient description of symptoms is critical. This may not be reliable/possible with children < 8 years of age. Similarly one may not want to do a challenge DTPA provocation to observe Flare symptoms.

Much of my current thinking on urine Gd is still proprietary, but I will say that generally the importance of urine Gd pre-chelation, urine Gd post-provocation/ chelation (I only use Ca-DTPA for provocation) is over-rated for determining the presence of GDD (but not for GSC). Brain signal on MRI not of value, and tissue content of Gd not important. These just tell you if the patient has received Gd (tissue presence, and this is known from history, the number of GBCA injections, when, and the brand of GBCAs, will be the best determiners of how much Gd is present in the body), and if the GBCA was linear (brain MRI signal, this is known from history of GBCA agents used and how many injections). You will have to wait for future blogs and publications to learn what actually is important. In brief though, the current state of knowledge is, GDD is determined by the following: 1. administration of a GBCA agent, 2. the type of symptoms developed (as I have written in a blog), 3. symptom timeline (within 1 month of GBCA injection, often arising within minutes), 4. occurrence of Flare reaction to the injection of Ca-DTPA. This is a reflection that Ca-DTPA is the best chelator currently available for Gd, not because there is a problem with Ca-DTPA. Quite the opposite actually, weak chelators may not mobilize enough Gd to result in a Flare. Lab tests are currently under investigation.

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