Lead Toxicity is Lead Deposition Disease. Optimal treatment is identical to GDD: iv DTPA with steroids/AH. Effective oral chelator (?HOPO) would be the most ideal, based on how lead entered the body.

Lead toxicity is Lead Deposition Disease (LDD or PbDD). Everyone in North America, and by extension almost everywhere in the world has lead retained in their body. When I say everyone, I mean EVERYONE. I know this because everyone who we have done urine studies on for GBCA, also has lead in them. The repository sites for lead are essentially identical to Gd, and the symptom complex of those with LDD are also extremely similar to GDD.

The critical thing that is not understood as yet, is optimal treatment for LDD is actually identical as for GDD: multiple sessions of iv DTPA with oral steroids/antihistmines.

The great majority of individuals treated for the presence of lead actually do not have LDD, but instead Lead Storage Condition (LSC), which is the identical situation as with Gd. Of 10,000 people with Lead in their body only 1 will have LDD. I have used with Lead the same numbers that I have direct knowledge of with Gd, but translate it to lead since it appears to be the same reaction to another very similar behaving metal in the body. I have heard some individuals say, well why do you have to do so many chelations with GDD, when with lead we need to do only one. This is a fundamental misunderstanding of.... everything.... when it comes to heavy metals and chelation. Multiple chelation sessions are also needed for LDD, and if they truly have LDD they will Flare with chelation. LSC (like GSC) will not show Flare, because they do not have an immune reaction to lead. The presence of absence of Flare is a critical observation for disease detection. Here are the main points:

1. LDD is virtually identical to GDD.

2. Stability constant is crucial for chelation of all heavy metals. DTPA has the highest stability constant for Lead of the available agents, as is the case with Gd (although not as marked a difference : the advantage of DTPA over the next most stable agent EDTA is 300,000 times for Gd, and about 600 times for lead).

3. If a person has LDD/ Lead toxicity then they will Flare with effective chelation, as with Gd.

4. If the individual has toxicity then they will need steroids/antihistamines to manage the Flare reaction.

5. Effective chelation requires multiple sessions.

6. Understand the concept of total body heavy metal content. I have written prior blogs on this subject with Gd, so read those).

7. 24 hour urine is the best tool to evaluate removal of Lead. Read the blogs I have written on Gd to understand that.

8. One important difference from Gd, is Lead has been internalized primarily through GI ingestion, hence the primary pathway of lead tire tracks of deposition are in the GI tract, through liver, and without as strong a perivascular interstitial space deposition as Gd has. One has to understand the route of entry when developing a chelation regimen.

9. Lead deposition is always ongoing, so it also cannot be controlled as GDD can be controlled. GDD is controlled by not getting any GBCA injections in the future. You cannot stop continued lead intake. You can however minimize it, by carefully paying attention to diet and environment you are in.

In the past, a few members of the nonprofit group GadTTRAC has reached out to treating doctors for children with lead toxicity in Flynt Michigan...unfortunately I do not have the time or energy to do that. Here is what they, and everyone else who treats lead toxicity everywhere, has to do to treat lead toxicity:

Optimal treatment for lead toxicity (LDD) is iv DTPA chelation with steroids/antihistamines at the present time, done exactly as we treat GDD. Stability constant of chelator for metal is the crucial determination. Multiple chelations with the same principles as we do with GDD. One critical difference is that in the not too distant future HOPO should be FDA approved. As I have written with GDD, the chelation should follow the route of how the metal entered into the body (IV GBCA hence iv chelation, at least to start with Gd) and for lead: oral acquisition of the metal (some respiratory intake) so optimal chelation should follow the same path:

if the heavy metal entered by oral consumption. then oral administration of an optimal chelator (based on stability constant and accessibility of the binding site of the chelator) follows the path of the tire tracks of deposition of that heavy metal. Oral entry of the heavy metal: oral chelation; iv entry of the heavy metal (Gd): iv chelation (and at a comparable rate of administration - so fast administration of chelator for Gd); respiratory intake of heavy metal: inhalational chelation; cutaneous intake: cutaneous (and probably supplemented by iv) chelation.

If I was very concerned about lead toxicity I would want to be treated in a center that actually understands the science of chelation. Exactly as I have written above.

The same logical pathway of thinking about all heavy metal toxicities should be understood.

Richard Semelka, MD.