George Santayana is credited for saying the original variant of the quote: "Those who do not learn from history are doomed to repeat it." In some ways the story of Calomel ( a mercury-based drug) and gadolinium-based contrast agents (gadolinium-based ofcourse), share some properties. I do not intend to represent those shared qualities, as all of the truth; but they are some, starting with that they are both heavy metal-based drugs that were (Calomel) and are (GBCAs) highly touted in their day/present day. It is also worth adding Salvarsan in, as it is a heavy-metal based drug developed around 1910 (arsenic-based) to treat syphillis. Maybe though the relationship between these heavy-metal

I am posting for all individuals to see what my current recommendations for treatment are at the present time (Sept 2018) , and what areas are still in evolution. This also reveals my concerns about various issues. A number of early stage GDD patients get severe Flare from the Ca-/Zn- protocol. My opinion is this protocol pulls out Gd through the blood system in too much quantity and too quickly in them. Hence for these individuals, a gentler chelation of only Zn-DTPA and with the 5ml ampule injected into a 1 litre bag of normal saline and a slow 2 hr drip infusion. Just the one session and repeated weekly x 5. The Ca-/Zn- protocol will have a high unacceptance rate in these patients, just b

A number of health care practitioners and GDD subjects have asked me about the comparative binding strengths of DTPA compared to other chelating agents for Gd and other heavy metals. This is from John Prybylski, PhD, derived from the stability constant data base NIST 46. Missing data is not present in that data base. Stability Constants for Currently Available Chelators Table: Note that the stability constants favor the use of DTPA over the other chelating agents for all the exogenous heavy metals. We will attempt to find the missing data points from other sources.

The best method to evaluate the success of chelation is to measure 24 hr urine Gd. I think the minimum is a 24 hr urine for Gd within 1 week prior to chelation (maybe the easiest and most accurate is the day before, bringing the urine in the day of chelation). The most dramatic urine Gd content should be the day after the first chelation, which is after Ca-DTPA (if using the standard Ca-/Zn-DTPA protocol) or after the sole injection of Zn-DTPA (if using the Zn-DTPA only infusion), so collection starting immediately after chelation finished. I think the next day collection, after Zn (if using the Ca-/Zn-DTPA protocol) is good as well, but not as essential. I would do the same at the 5th chel

The following blog revisits the subject of the gentle chelation protocol because of the incredible interest on this subject. Individuals who have recent onset GDD (3-6 months, possibility up to 1 year) and/or having received macrocyclic GBCA tend to experience greater Flare reactions to the standard Ca-/Zn-DTPA protocol. It would seem prudent to employ a 'gentle chelation' protocol. We describe this as injecting the 5ml ampule of Zn-DTPA in a 1 Litre bag of normal saline, with a slow drip infusion over 2 hours. Regardless of chelation or not, drinking lots of fluids is important. A fair amount of this fluid should be alkaline water. Additional supplements will be visited in a future blog.

Dry eyes and blurred vision is a common complaint of many sufferers of GDD. There are many locations that eye problems can occur: from internal eye issues, optic nerves, orbital muscles, and optic nerve tracks in the brain through to the brain locations of vision in the occipital lobes. Gd can affect all locations in the vision pathway, and there may be variability in the structures involved between patients. My current opinion is that the most prominent cause for this set of findings is local involvement at the level of the eye-balls themselves. Sodium chloride (NaCl) is the major constituent of tears. As it occurs with Ca in many locations throughout the body, that Gd substitutes in for Ca

In a few of my blogs, and in discussion with many sufferers, it is clear that a sizable percentage of GDD sufferers had developed symptoms of GDD from the first or earlier GBCA-enhanced MRIs and yet tragically continued to undergo further GBCA injections, with each time the disease getting progressively worse. Maybe something like 50% of sufferers fall into this situation. So the question that everyone probably has is: what are the warning signs that I may have developed GDD from GBCA-enhancement, so I do not continue to undergo GBCA-injections. In a very recent blog I described also the categories of disease severity (from 1-5), and this prior blog should be reviewed. The severity of diseas