That's not quite autoimmunity...

It seems we are having even more issues with overextrapolation.

I admire the work that Bret Weinstein and Heather Heying put out, including on their Darkhorse Podcast. It’s always interesting to see how their mind works and how they perceive the world. Heather tends to be a clear example illustrating how one goes out and views the world, including such examples as when she mentions one of her PhD mentors who would take her and other students out in the wilderness and make remarks such as, “look at all of the questions!” I can’t recall which mentor she refers to in particular, but it serves as a reminder that we tend to assume that things are just out there without understanding how those things operate, or why they may operate in the manner that they do.

Although I find both of their works to be enjoyable and generally food for thought, there are some moments where I have found issues in their interpretations of data.

Part of this is due to my own conceptualization of information. I’m more mechanisms-driven relative to other people and I’ve become more aware of that the more I write. I don’t like the basic explanation of “X treats Y”, but am more curious of how X can treat Y. What exactly is going on that seems to explain the relationship between the two aside from the fact that using X makes Y go down…somehow. This is just a minor aside and is just one noticeable difference in my thinking vs Bret and Heather’s way of thinking for some concepts.

When it comes to COVID one thing I have drawn criticism of is Bret’s model of heart damage, in which he refers to the targeting of the heart by the vaccines as an autoimmune event. More specifically, he uses the argument that the heart via transfection of the mRNA vaccines will lead the production of spike within the heart, which would then be targeted by the immune system and be removed, in which case the immune system’s attack on the heart can be considered an autoimmune-related response. He also suggests that this event isn’t related to the heart in particular but any cells that are made to express spike protein.

For context, he made such comments in a recent Darkhorse Podcast episode (timestamped below):

There’s a lot to consider in regards to why and how myocarditis presents post-vaccination, but for all intents and purposes this justification of autoimmunity doesn’t quite work because, well, it’s not quite autoimmunity.

Autoimmunity refers to a phenomenon in which the immune system directs attacks against the body’s own antigens, whether through targeting self receptors or other proteins within the body normally produced by our own cells.

For instance, Type 1 diabetes mellitus is argued to be related to autoimmune responses in some individuals (termed autoimmune diabetes mellitus or Type 1a diabetes)¹, in which case the immune system inappropriately targets the insulin-producing cells of the pancreas called beta cells.

Note that the critical factor in autoimmunity is the auto part, or “self”. It’s the inappropriate recognition of self antigens by the immune system that causes these diseases to manifest.

It’s also worth noting that there appears to be evidence of autoimmune responses following a severe COVID infection, as well as post-vaccination:

But again, in these cases of autoimmunity the immune system somehow incorrectly targets self antigens, possibly by way of cross-reactive antibodies that target both the virus/spike antigen as well as our own proteins.

All this to say that targeting of the spike in transfected cells doesn’t quite fit the definition of autoimmunity because our own cells don’t normally produce spike protein. It’s also the fact that this doesn’t mean that the immune system may be incorrectly trained to target the heart if it was made to express spike protein.

It’s one of Bret’s models that I had a bit of trouble rationalizing, and to be honest I didn’t give it much thought until Jessica Rose’s recent piece that also emphasized that this wouldn’t fit a model of autoimmunity:

Spike-mediated (CTL)-mediated immunity is NOT autoimmunity

This article is really important and draws attention to the distinction between autoimmunity and acquired T and B-cell-mediated immunity. We can define the difference using only two words: self and foreign.

I wrote these words before here:

“The thing that people are talking about with regard to injection-related spike embedded cell destruction, is not autoimmunity. It is the immune system working properly to clear cells with destroy-me flags on their surfaces.”

Bear in mind that the immune-mediated clearance of spike-producing cells isn’t far off from what the immune system normally does to an infected cell anyways. A virus enters into a host cell, begins producing genetic material and proteins, some of which may be collected by the infected cell and presented on the surface. Immune cells tasked with surveying cells to make sure that they aren’t produce wrong peptides would then target these cells for destruction.

That’s not what that means…

Far be it from me to argue that terms are being used inappropriately. I’m learning things as I write, and because of that I have misused terms in the past and more than likely will misuse terms in the future.

That being said, what’s becoming a bit apparent is that the misuse of words has become rather common, and when it comes to dissemination of information misuse of words may lead to improper interpretations.

Although I much admire Bret and Heather, I will also argue that Bret’s model is a bit simplistic, and it doesn’t quite fit what we would consider to be an autoimmune phenomenon. It would be a bit improper to reinterpret autoimmunity in such a manner, especially if cells of the heart are being made to produce spike. You don’t need to rely on a justification of autoimmunity to explain that the death of heart cells is not a good thing.

Bear in mind I’m viewing this perspective from the idea that the heart is being transfected. This argument seems to be highly controversial, and a study from Barmada, et al.² that Bret and Heather have cited once has even argued that autoimmunity does not seem to be the reason for myocarditis, but may be related to cytotoxic immune responses that may lead to heart damage, although I’ve raised some issues with the study’s design and authors’ denouncements of other hypotheses.

Even with these issues, the Barmada, et al. study would at least contradict an autoimmune model proposed by Bret.

It’d be interesting to see if Bret reworks his model and provides better context for his model, but this is again an issue in which terms may be used that are distant from their original meaning.

Not to sound like a broken record, but we’ve seen this when it comes to original antigenic sin in which everyone and their mother seemed to have a different, rather superficial definition of what OAS is, and yet everyone’s definition seemed to appear correct. It doesn’t help that many studies that looked at immune imprinting or OAS fail to have proper study designs that actually model OAS.

We’re seeing this now with “VAIDS”, which simultaneously draws parallels to AIDS but also doesn’t fit the model of what AIDS is.

Untreated AIDS should, hypothetically, lead to continuous depletion of CD4 cells and waning immunity. People within the early stages of AIDS may not recognize that they have AIDS because their body can sufficiently deal with infections. However, as the disease progresses and the immune system weakens then the ability to deal with infections gets worse, and otherwise mild infections may lead to worse illnesses in these AIDS patients. It’s argued that many AIDS patients die from secondary infections due to their inability to deal with infections.

VAIDS, if invoked, should fit a model similar to this. We should expect people to not only get sick more frequently but to also be even worse off without intervention, and eventually many people are likely to succumb to secondary infections.

The problem I have with VAIDS is that the former (more frequent infections) are used as an argument that the latter (worse illness and death) is occurring. It’s true that many people, and children in particular, are getting ill more frequently. However, it doesn’t appear that these illnesses are leading to far greater degrees of hospitalizations and death, and we probably shouldn’t expect people to be able to manage their frequent illnesses at home if their immune systems are shot.

And yet VAIDS continues to widely circulate. I even see saw someone mention that Megyn Kelly’s recent remarks about testing positive for some sort of autoimmunity is an example of VAIDS. Great, that just means that there is even less consistency in a made-up word and anyone can define VAIDS whichever way they see fit.

This is one of the growing issues in which terms that are used as a term of art with a clear definition may become bastardized when used colloquially, so now the term has a different meaning in the public eye, and is made worse when the colloquial definition is used to refer back to scientific ideas or concepts.

I find it strange that there tends to be this high degree of inconsistency. There’s a cultural argument over the colloquial use of “gender” and “sex” compared to the scientific use of these words, and yet these same people may use scientific words colloquially to infer whatever they want.

And because of this inconsistency there isn’t a proper method of organizing ideas. Words can mean whatever they want so long as it harkens back to your group or invokes some idea of hysteria.

Words have meaning. Words used within a specific context cannot be overgeneralized to refer to ideas or concepts. And more importantly, words allow us to disseminate information in a consistent manner. We can’t do with words whatever we see fit.

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1. Type 1 diabetes requires a distinction between autoimmune-mediated insulin deficiency or insulin deficiency related to other variables. Autoimmune-mediated type 1 diabetes can be confirmed through autoantibody screening measures.

2. Barmada, A., Klein, J., Ramaswamy, A., Brodsky, N. N., Jaycox, J. R., Sheikha, H., Jones, K. M., Habet, V., Campbell, M., Sumida, T. S., Kontorovich, A., Bogunovic, D., Oliveira, C. R., Steele, J., Hall, E. K., Pena-Hernandez, M., Monteiro, V., Lucas, C., Ring, A. M., Omer, S. B., … Lucas, C. L. (2023). Cytokinopathy with aberrant cytotoxic lymphocytes and profibrotic myeloid response in SARS-CoV-2 mRNA vaccine-associated myocarditis. Science immunology, 8(83), eadh3455. https://doi.org/10.1126/sciimmunol.adh3455