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Gadolinium Deposition Disease Brain Fog

One of the most vexing issues with Gadolinium Deposition Disease from a scientific perspective, is what is the explanation for brain fog? From a historical perspective, for centuries cognitive impairment has been recognized with other heavy metals, notably mercury and lead, so the concept of brain fog with heavy metals is a well recognized disorder for a very long time. It would seem reasonable to assume that the cause for brain fog may be a feature common with heavy metal toxicities. So studying literature on lead toxicity and brain function impairment should provide supportive information on Gd toxicity.

Gadolinium is a positively charged atom, like calcium, and also has an ionic radius not too dissimilar to Calcium, so Gd can substitute for calcium in a number of metabolic processes. This appears to be the issue with brain fog as well as for other neuropathic disorders.

A number of articles have been written that have described the effects on Gd on isolated neuron and neuronal units. The basis of the brain fog may be on direct cellular interference by Gd on the pre- and post-synaptic receptors. Gd appears to be able to regulate the transport and release of synaptic transmitters and block some membrane receptors. Articles specifically describing the effects of gadolinium in neuronal function have focused on the effects of membrane based glutamate receptor channels specifically GABA and AMPA types, with differing types of channels on pre- and post- synaptic receptor surfaces. Defects or deficiencies or hyperactivity of these channels have been shown to result in mood changes and memory loss in animal models.

As with most things, there are some limitation issues that must be paid attention to in articles, especially with animal models. The type of Gd molecule administered is critical, the most convincing data is when actual commercial GBCA agents are used, and least convincing when less stable Gd formulations are used, such as Gd-Cl or Gd-citrate. Also the route of administration is critical. A number of animal studies on the brain have used direct intracisternal injection (that is injection directly into the brain and into brain spaces [ventricles, subarachnoid space]). So effects both on the type of Gd molecule and the location of administration are of critical importance. In humans Gd is administered as a GBCA (and in fairness all GBCAs must be studied individually) and by intravenous route in the great majority of cases. So seizures or motor defects observed in animal models where injection has been directly into the brain, is entirely different than if GBCA is administered intravenously. That being said, these type of worst case scenario injections do provide some indication of what GBCAs are capable of doing.

A major point that I struggle with all articles that focus on the metabolic effects of Gd, which correctly describe that Gd can substitute in for calcium in all metabolic pathways, with maybe 100 known, and hence 1,000 actually present, why does this not occur then in everyone? If 10 million people have appreciable Gadolinium Storage Condition, why do the great majority have no problems with the agents and do not develop brain fog? This is why I have focused on the immune system, which is the most variable system in humans, that the immune system plays an active role as a gate keeper for metabolic processes. So somehow the immune system blocks the capacity to cause these metabolic effects in the vast majority of patients, but in a few it seems to neglect that role and may even be a participant or potentiater of these metabolic dysfunctions - but at any rate negligent in its role to protect the host from foreign invaders, in this case Gd. In fact, in a number of the disease effects (burning skin/skin substrate pain, bone/joint boring pain) I am convinced that the major perpetrator of illness is the immune system itself with an exuberant and excessive immune response to a small inanimate intruder, the Gd atom. Finally, none of these host systems operate in unique isolation, there is always a complex interrelationship with all the organ systems, which makes understanding complex diseases like GDD so challenging. Effects have to be considered in their totality, as a web of interplay between multiple systems.

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