The question comes up often in emails from patients. How does one know if the symptoms I am experiencing is from GDD or from another disease? The reality is, that most patients who get an MRI have some process ongoing which has brought them to getting an MRI. Hence there is a high likelihood of an pre-existent disease process. A number of these diseases, such as Multiple Sclerosis (MS), can have very similar symptoms. Then what to do? The first thing to realize is that you can have two (or more) diseases going on at the same time: GDD and MS, or GDD and Lyme disease (one may predispose to the other actually), GDD and rheumatoid arthritis. Sometimes, maybe often you can tell them apart as GDD

X-ray fluorescence is a technique that had been developed and used to detect the presence of lead in bones. More recently this technique has been described for Gadolinium, another heavy metal that also goes to bone. All research on GDD is to be commended. There are a couple of critical considerations though regarding this technique: 1. Heteogeneity of deposition between cortical and trabecullar bone has been desxcribed with lead, and there is also variability between bones, and various physiologic states can have an impact. All this would be true with Gd. 2. With lead, the question that x-ray fluorescence answers, is lead present? This is of value where uncertainty of lead intake occurs. Thi

I have not seen any data of any kind to suggest that the injected ligand can be the cause of Flare symptoms. In essentially all the animal and in vitro studies I have seen on the subject for GBCA evaluation, the ligand has always been reported as the safe component. That is why extra ligand is present in many of the linear agents, to increase safety. One of the main reasons to do a Zn-DTPA only protocol is that the only cations and metals that should cause DTPA to release the Zn in a transmetalation process are exogenous heavy metals (all of them). All the native cations/metals bind much more weakly to DTPA than Zn does, so they should not release the Zn, and depletion of native cations/meta

I have now had the opportunity to communicate with 100s of patients with GDD. One of the things that I have realized is that because of the newness of recognizing the disease, that there are no magic bullets (yet), and that conventional physicians don't seem to know about it, there is an enormous range of discussions and postings on the disease. Many of these are not founded upon any science. Although some may be founded upon anecdotal experience or experience of that individual, that may have actually worked, but this may not be generally applicable. Below are my recommendations on avoiding mistakes: 1. if you think you have GDD (based on reading my blogs) do not ever get another GBCA admin

Much has been written, including by myself with co-authors of Gd being deposited in the brain following GBCA administrations. This deposition has come to radiologist attention because it is visible on MR images. This has largely been observed with linear agents, and is visually apparent after about 5 doses. Although it has been greatly emphasized, as I have stated in earlier blogs, the amount of Gd deposited in the brain is far less than that in the bones or the skin. Ken Maravila and his team have shown the concentration of Gd in bones to be something like 20 times that in the brain. When you then factor in the difference in overall mass between these organ systems, the actual difference in