I have written a lot on the mechanism, symptoms, treatments for GDD. I have opined on that GDD is primary an immunological disease. Also I have reflected on the plethora of reports on animals that describe an enormous range of awful consequences of Gd in the rodent model - everything from Gd inserting into Ca channels in metabolic pathways (which is essentially all of them), nerve tissue effects, and mitochondrial disruption.. So it is amazing to think that even with the majo

Gd toxicity and treatment with chelation are relatively uncommon disease-treatment combinations in medicine in that it is possible to measure directly with numerical results, the status of predictors of disease and of the response to treatment. In this way similar to type 1 diabetes and insulin treatment. In contrast, GDD as the example, iv glutathione for treatment, there is no numerical way to see benefit, and lack of Flare, although patients may see as a good thing, proba

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 seve

In a recent blog I described that Acute Hypersensitivity Reaction (AHR) (Mast cell reaction) can exist as an overlap condition with GDD (T-cell dysregulation). Earlier studies on AHR that described failure of steroid treatment ,or recurrent AHR (also described for iodine contrast, used in CT), some of these failures may be actually early reporting of GDD. But, what is recurrent AHR: Mast Cell Activation Syndrome. MCAS has not been specifically tied to GBCA use, and in my opi

I watched the movie Dark Waters recently. It turns out we all have PFOA in our bodies. At least as scientifically fascinating that GDD can be so devastating in humans, recognizing the range of injuries Gd has been observed in animal models, is that most humans do not experience these adverse injuries. There clearly is protective measures, such as toll-like receptors, that block Gd from inserting into Ca- driven metabolic pathways. It is likely that the immune system blocks i