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COVID-19 and GDD: Interesting similarities and differences

What I have emphasized very early on in my research on GDD is this essential feature: that disease depends on both the presence of the invading entity and the host response. 99.9% of recipients of a GBCA injection seem not to experience long-lasting consequences to receiving the antigen, while 0.01% experience lasting consequences (GDD) with 0.001% of the total of recipients experiencing extremely severe disease. Notice these numbers are similar to the mortality rate of the common Flu and also in the range of COVID-19 (0.5%)

It has been interesting to learn that probably 50% of individuals who have the COVID-19 virus are asymptomatic. Yet despite being asymptomatic can still infect other individuals, and these other individuals may actually then die from the disease. I am not certain what level of asymptomatic individuals occur with other viruses, like the Flu, it may be about the same percentage, and likely varies considerably for different infective organisms. A number of individuals who have transmitted disease are asymptomatic carriers (famously Typhoid Mary) and most often because their immune system ignores the invading enemy (which is good for them, and potentially very bad for everyone else).

So a remarkable similarity between GDD and COVID-19, many people can be perfectly asymptomatic from the foreign antigen, while others can be desperately sick.

What I deduced for GDD is that it had to be primarily the immune system that was the difference: the host response. If the immune system ignores Gd then the individual is fine after GBCA (the 99.99%) The variable severity of the disease reflects the extent of the immune system response, and likely the variety of cells conscripted into the response.

Other critical aspects of foreign antigens (including infections [Covid-19], cancer, and heavy metals [Gd]) are how readily it can be spread from one individual to another (transmissibility, which takes into account the infectious dose[below] and the route of transmission [blood; air borne, mist, particulate; urine; sexual; skin contact; etc) and the related concept of how many particles (for infections: microbes) is necessary to ensure infection, termed ID50, and also called the infectious dose. Generally the fewer particles needed to cause disease the more aggressive and often the more lethal the infection. The infectious dose smaller and transmissibility greater than most Flu strains. What has been clear though with COVID-19, which ofcourse makes perfect scientific sense is the longer the human-to-human contact, and the more confined the space, the more likely for spread (transmissibility to occur) a perfect example is a meat packing plant. Add in more susceptible individuals (nursing homes) then one arrives at a perfect storm for infection spread. So, greater viral load exposure the more likely spread will occur and the more likely the recipient will get severe disease. This ofcourse is also the case with Gd exposure and humans. What was recognized initially with Nephrogenic Systemic Fibrosis: the greater the total body load of Gd, the more likely to get disease and the more likely the disease is severe. This is also true with GDD. The novel observation with GDD, in many respects very similar to a comparison with a virus, is that although the larger the dose (often meaning multiple repeat GBCA injections) generally the more severe disease (and the more difficult to treat as there is more Gd to be removed by chelation), it can also arise from very small dose, if that dose is administered into a small contained space. This is analoguous to a vaccine for a virus. Often the vaccine is injected in a contained space (muscle, subcutaneous fat, intradermal) such that the antigens provide a sufficient local concentration that immune cells congregating around the pocket of vaccine have enough particles to develop a cellular and antibody reaction/response to it. In essentially the exact same immune system process, GBCA injected in a contained space (accidentally, such as an interstitial injection; or deliberately, such as MR arthrography) it is possible to develop GDD from a small dose> often subcutaneous injections may represent 5 ml of GBCA and MR arthrography may be only 1 ml of GBCA. Yet in this setting, a small volume of GBCA can cause GDD. This is not well known, and in not recognizing it, it is even easier for a doctor to dismiss that the patient could not possibly have developed disease to such a tiny amount of GBCA. This type of event defies the strict Bradford Hill criteria (read my blog on GDD and Bradford Hill criteria), but ofcourse fits a more informed Bradford Hill criteria.

With COVID-19, it seems not so clear in humans if the immune system ignoring the virus explains the asymptomatic nature of the disease, or if it is effective killing/neutralizing of the virus. It may be 1 or the other, or both. I did listen recently to an interesting interview on CNN of one of the expert virus hunters. It seems most of the zoonotic viruses that have afflicted humans in the last century (maybe for many centuries) are derived from bats. Poor bats getting such a bad wrap. Zoonotic means transmission from animals to humans. He explained that many bats contain a multitude of viruses in their gastrointestinal tract: Ebola, many species of Corona. Somehow they are perfectly fine from that, they do not make the bats sick. His explanation was that since bats fly, and this causes a great strain on the system, they do not have the reserve to deal with other strains, so their immune system has evolved and adapted such that it ignores the presence of these viruses that are so lethal in humans. This would suggest that often times ignoring the presence of viruses may render them innocuous. The obvious question is: in humans how often is this the case that the immune system ignoring viruses renders them safe. By further extension, to what extent is it the host reaction that makes viruses proliferative? Some cytokine, antibody or other cell product that stimulates or facilitates the virus to replicate or enter cells and replicate? The other scary thought about viruses, is that a number of viruses live in us for the entirety of our lives, starting from the time we first acquired them. Herpes viruses, Epstein Barr virus (mumps), Varicella virus (chicken pox/shingles) all are living in us> they're ok, we're ok. One has to wonder how many others. Many also reside on nerve roots by the spinal chord > also frightening to think of (Herpes, Varicella). Yet, by and large these do not cause enormous problems for most humans, we live with them fine enough, essentially because our immune system has learned to ignore them, except in moments of stress. Perhaps it is the moments of stress with release of immune cell products that these viruses replicate. Will COVID-19 then simply live in us for all of our lives?

A very interesting aspect of COVID-19 is the loss of the sense of taste and smell. To me, this also harkens to the variety of unusual neurological issues we see with GDD. I have discussed this in greater length in prior emails. With COVID-19 does this relate to the common feature of viruses that live with us that they also have a predilection for developing a relationship with the nervous system. Is it some relation with the nervous system, seen also with some other viruses that is causing this? It may also be a local effect from the propensity of COVID-19 to infect nasopharyngeal membrane tissue, because of the presence of cell surface membrane receptors. In some respect the nerve issue with GDD is easier to understand: Gd substitutes for Ca, and maybe only 1 atom in 1 million is sufficient to disrupt/ cause havoc with the nervous system: severe pins and needles, hearing issues, some of the visual disturbances, gait and balance issues. I have opined that the dysregulation of the immune system may allow access to these Ca channels, which otherwise in normal circumstances are blocked: a toll-like function. Does the immune system possess a toll-like function in controlling these calcium channels even in other cells?

What about stroke in young healthy adults with COVID-19? This is a result of the dysregulation caused in the immune system- that cell products released are also stimulating the clotting system, recently experts (see below) have described complement-mediated microvascular angiopathy with COVID-19. As I have mentioned in many previous blogs, there is probably 1,000 + moving parts in the complex immune system and from that interactions with the complement system, clotting system, nervous system... and essentially everything else. Vascular calcification and smooth muscle vessel wall affliction are not a rare longterm consequences in GDD, this is likely a similar concept of clotting/vascular wall issue that COVID-19 causes with general blood cell dysregulation.

My opinion is that when diseases predilect young to middle aged individuals the primary cause of the disease is the host response: the individual's own immune system. This is the case with GDD, in the vast majority of individuals disease originates in young to middle age adults. Cytokine storm is the strong response that the healthy immune system creates in the presence of an antigen, that the immune system is going all out to attack. My opinion, as I have written previously, is that cytokine storm is responsible for severe GDD. There are variations of severity of cytokine storm, and cytokine storm can readily kill the host - and may be the principle cause of death in young to middle aged sufferers with COVID-19, and other infections (Swine Flu of 1918). Cytokine storm is also the most probably cause of death in patients with severe anaphylactoid reactions to drugs (including GBCA). Interestingly, the cytokine storm of GDD almost never results in death, just severe disease - hence there must be different types and different severities of cytokine storm - like there are variations of weather storms.

Diseases that target the immature immune system (young children) and the senescent immune system (the elderly), the principle effect is of the invading antigen and not the host response. Most flus for example. But even then, there are differences in the targeting between the immature system and the senescent system, which I won't discuss. It is interesting that very recently a variant disease from COVID-19 has been described in children, ultimately with more experience the similar concept of a variant, will be seen with GDD.

Perhaps the over-riding similarity between COVID-19 and GDD is that they are both multisystem disorders, and as is common with multisystem disorders, various tissues/organs may predominate. The lung though plays the dominant role in severe COZVID-19 infection, but other organs can be seriously affected as well. The principle cause of the multisystem disorder for severe COVID (I have just learned by listening to a video by Cynthia Magro, MD, chief of Dermatopathology at Cornell University) is complement-mediated microvascular angiopathy, which results in endothelial damage and thrombosis (there is a lot more detail to this). The lung, brain, heart, skin, and kidneys are dominantly effected with COVID-19, but all organs fundamentally can be effected, as the disease is vessel-based. The intestines can also be effected, either by vascularity or direct COVID-19 infiltration. The multisystem pathology of GDD likely reflects a combination of direct Gd deposition with local immune cell reaction (skin, bones), nerve cell involvement, including a sympathetic neuropathy, which may be due to substitution of Gd- for Ca in Ca channels, and diffuse muscle, including smooth muscle (vessel walls, bowel wall) dysfunction both from Gd-Ca substitution, reaction to Gd deposition, and blood cell dysregulation. A number of organs of frequent involvement overlap between COVID-19 and GDD (skin and brain for example) and differ (lung with COVID-19 and bone with GDD). There is also COVID toe which likely represents microangiopathy, and appears to be quite permanent, and GDD foot where a vast array of different colors may arise, and remarkably also be transient, reflecting a combination of the above features of GDD, but possibly primarily a sympathetic dystrophy.

The key for treatment of a foreign antigen disease that is from a non-replicating antigen and where host response is the principle cause of disease, is twofold: 1. remove (much of) the foreign antigen, and 2. control the immune response. This is the case with GDD.