Vaccine Injury
*This article is not medical advice. Before starting on any health related regimen, seek the advice of your Primary Care Physician or an M.D.
Are Vaccine Injury, Long Covid, ME / CFS, and Mold Illness Similar ?
Yes and No, As Usual, Its Complicated
After seeing multiple vaccine injury cases, patterns develop. In symptoms, in the functioning of certain bodily systems, in physiology, in bio-chemistry, and in treatments being recommended by some.
The insult in various chronic illnesses, varies, but how the system gets stuck, and stays in some dysfunctional loop - unable to resolve it on its own, is not different from what I see. And it varies across different people. Just like in ME / CFS or Long Covid, there is heterogeneity in these populations when you look deeply into their physiology - and yes there are some common things too.
You may find this article interesting if you:
Want to understand the some of the physiological markers that can dysregulated in vaccine injury cases.
Want to understand the potential mechanisms involved in any ‘insult’ to the system - and what it means for downstream systems in the body.
Want to understand why symptoms may not be your way out.
Want to understand why the treatments being offered may not provide you what you are hoping for in terms of resolution
What Happens When We Have An Immune Insult
Yes, there are recruitment of neutrophils, monocytes, macrophages, and dendritic cells. Yes, this results in various cytokines - IL-1B, IL-6, TNFA, Interferons, and Chemokines like CCL2, CXCL8. Yes, T-Cell activation happens.
Tissue injury from these processes can keep the innate immune system inflammatory reaction sustained, as the body responds.
Neutrophils and monocytes are the early responders.
They activate a series of genes NADPH Oxidases (NOX1, NOX2, NOX4, NOX5, etc) - which produce significant amounts of oxidative radicals such as Super Oxide, Hydrogen Peroxide.
They kick of MPO and hypochlous acid forms - casutic on our endeothelium.
They form NET’s (Neutrophil activated traps) - which is implicated in thrombosis, endothelial injury, and microvascular dysfunction.
Monocytes and macrophages can engulf the antigen, present antigen to the T cells, and also produce cytokines - resulting in additional oxidative stress load. These cytokines include IL-1B, IL-6, TNFA, and kick on our dear friend NOS2
Dendritic cells migrate to lymph nodes and activate: CD4 T cells, CD 8 T Cells, and B cells. B Cells mature into plasma, and produce anti bodies, which is the desired phase, but this is where things go amiss.
And perhaps more importantly, NOS2 Immediately Kicks Into Gear - Producing Large Amounts of Nitric Oxide
NOS2 is calcium dependent, is induced by cytokines, and triggers like IFN Gamma, TNFA, IL-1B, and LPS / TLR signalling from gut based issues are often in play.
This is one of the cornerstones of our immune system - it needs NADPH, B2/Flavins, Zinc, Cysteine, Heme Iron, BH4 (tetrahydrobiopterin), and Arginine to function. When chronically activated without resolution of an immune response, it will drain NADPH, one of the most common cofactors our bodies need - and you will be beyond “tired”. Systems shut down.
Excess Nitric Oxide - has various effects beyond killing pathogens. It can S-Nitrosylate cysteine residues on various genes - disabling them. Yep. This is our friend “NAC”. ADH5 is the primary gene that steps in to protect cysteine residues on genes to keep them functioning. Wanna guess one of the pheno types i see ? ADH5 genetic weakness, and NOS2 over expression. Across all these chronic illnesses. It is a specific pheno type with specific weaknesses.
NOS2 over expression will suppress NOS3.
NOS3 is the primary enzyme responsible for vasodilation in our endothelial structure , especially in the heart and longs. When NOS3 is disabled, endothelial health is compromised, as is circulation, blood flow. Disablement of NOS3 results in NOS Uncoupling where significant amounts of peroxynitrite (OHNOO-) is formed - from the combination of excess nitric oxide and excess super oxide.
Needed cofactors for NOS3 - yep - NADPH , Zinc, FAD/FMN Flavins, Arginine, Copper indirectly for SOD3, Cysteine, Arginine, BH4, Calcium and Calmodulin.
If excess super oxide is present in the endothelium - SOD3 (copper and zinc dependent) is the enzyme that is supposed to step in and handle the super oxide - unless there is no copper - and then we have a major issue. SOD3 is located in the extracellular matrix, vascular wall, endothelial glycocayx, and lungs.
SOD1 (dependent on Zinc and Copper) is similar and its role is to buffer intracellular superoxide. Its located in the cytosol, mitochondria intermembrane space (think endoplasmic reticulum where GPX8 operates), and the nucleus. SOD1 is important for mitochondrial electron leakage, NOX-derived intracellular super oxide, protecting Aconitase (ACO2) in the krebs cycle, protecting the Electron Transport Chain Complexes.
About copper - the most mysterious of our metal cofactors. It depends on a variety of genes to reduce it from Cu2+ to Cu, and also deliver it intracellularly, and also specifically where its needed in certain compartments. Some of the key genes in this proces are : SLC31A1 (intracellular transport), ATOX1 (loads copper onto ATP7B), CCS (copper chaperone), ATP7B, ATP7A, MT1a, MT2a, SP1.
When copper transport goes amiss - we wont deliver it to SOD1, and SOD3 and we will have significant oxidative stress that is not resolved, and also endothelial compromised. Additionally this copper usually is directed to places like the liver in some instances, but can create a significant toxic and oxidative burden. When this copper load is ‘moved out’, it can be significant, often 5-10x above normal high limits on urine, serum, and hair tests. Usually, after this happens, there is a nervous system correction that takes places (calms down).
All of the above reactions can occur in various chronic illnesses - and they can occur all over the body in different systems. So symptomatic presentation can look different depending on ‘where’ it is more prominantly occuring. If there is dysfunction occuring along the NOS2/NOS3 Axis - it will drive significantly oxidative stress, and endothelial dysfunction, effecting symptoms related to circulation, orthostatic tolerance, oxygen delivery, breathing, / respiration, and mitochondrial function.
Mitochondrial Function / Dysfunction: We have all heard the term, ‘mitochondrial dysfunction’, but that isn’t specific, doesn’t indicate what and where the specific issue is, nor how to resolve the dysfunction.
Side Tangent / Analogy / Joke: Saying you have mitochondrial dysfunction, would be similar to this story. Lets say you have a bunch of hiking friends and you are dividing up into groups, each group doing a long through hike - Appalachian Trail (AT), Continental Divide Trail (CDT), John Muir Trail (JMT), or Pacific Crest Trail (PCT). You are all on a group chat / text. And your friend John texts the group chat - “There is a bear on the trail!”. Um, well, which trail are we talking about. “The Pacific Crest Trail” John says, well most of the group can relax. The Pacific Trail Group members, text back, “Where on the PCT did you see the bear ?”. John responds, “in the Sierra’s”. Well, the rest of the friends on the JMT, are in the Sierra’s, but that is still hundreds of miles of trail. “Where in the Sierra’s?” the PCT hikers text back. John texts back, “near mile marker 875”. Now, that is getting to be helpful, but still the other hikers want to know where near mile marker 875 the bear is located. “What part of the trail near mile marker 875?” they text back. “On top of the boulder stack at the top of the hill after you cross a creek that has 3 logs across it near the trail”. Now we have a pretty good idea where the bear was seen, and to be on the look out for it and can prepare appropriately.
Inside the mitochondria there are hundreds of enzymes / genes, and each has its own role, has its own cofactors it needs to have in sufficiency to function, and also each have specific contaminants (certain oxidative radicals, certain metabolites, certain toxins - mycotoxins / heavy metals) that can disable them based on the structure of that enzyme. When you understand the structure of the enzyme you can see how it can be compromised - not having its cofactor(s), a disabled transcription factor, or having genetic compromise. Most of the time it is a combination of converging factors across genetics, across cofactors, across contaminants that results in ‘mitochondrial dysfunction’.
MitoSwab / Mitome - gaining popularity - helpful but not sufficient
These tests have been gaining popularity, but without a deep understanding of the different mitochondrial complexes, what the cofactors are of the genes in them (yes there are many many genes in some of these complexes), what contaminants disable them, and what systems protect them…….patients and MD’s routinely don’t know what to do when they have “Complex I” inhibition, or “Complex II and Complex III combined” inhibition. Its like yelling, “There is a bear on the Pacific Crest Trail”. Yes, its helpful, but certainly not sufficient to understand what to do, how to do it, and in what order.
In all of the chronic illness cases i have seen, it is relatively uncommon that there is a specific genetic compromise on specific genes in Complex I, II, III, IV, V that is driving the mitochondrial dysfunction. It occurs in about 5-10% of cases in Complex I, about 5-10% of the time in Complex II, and in about 5-10% of cases on Aconitase2. About 85% of the time, its a combination of things that stack up that are resulting in the dysfunction.
I have seen parents and patients spend years staring at mito swab tests, throw up their arms, and just say, I/my child has mito dysfunction there is nothing we can do. Yet these same folks have declined to actual get the testing that pinpoints where the dysfunction is, what is causing it, and what can be done to resolve it. I have seen this in leaders of FaceBook groups, MD’s and their children, and self annointed experts with significant social media followings.
It reminds me of an old friend when we were hiking in Yosemite in the 1990’s. We pulled out our map and we were trying to figure out where to go. I pulled out my compass, and my friend said, “The compass isn’t helpful because it doesnt tell you to right or left!”. I chuckled, and stared in dis belief. The Eagle Scout in me, said, “you actually have to know how to use the tools we have, and interpret what they are telling us.” He looked at me dumbfounded, “thats not helpful if it doesnt say left or right.”. You have to have the right tools (genetics, labs), and you have be able to interpret the information they are providing. This is physiology and bio-chemistry at its core.
You have to know how our body creates heme, and the cofactors required and the contanimants that inhibit certain points in the heme biosynthesis pathway. You have to know how to interpret the differences in blood based and urine based heme biosynthesis functional tests (porphyrins testing).
You have to understand how our body makes iron sulfur clusters and what can go wrong in their production, delivery, and their protection.
You have to understand how our body makes Coq10, and various other facilitating agents.
You have to understand how our body uses and converts various forms of NAD: NAD+, NADP, NADPH, NADH, and what happens when this system becomes dysfunctional.
You have to understand how zinc plays a critical yet little understood role in enabling transcription factors that each govern dozens to hundreds of genes
You have to understand how things like nitric oxide, that we cannot measure with labs directly because it is a transient local gas that dissipates in milliseconds.
You have to be able to assess system like copper metabolism - when individual labs alone will not provide clarity.
You have to understand how to interpret krebs cycle metabolites through various lenses to understand where blockages may be, if you are in an M1 or M2 metabolic state, or if the mitochondria have self proectively down regulated.
You have to understand how your nutrient transporters are functioning to see what forms of various nutrients can open up blocked pathways.
You have to understand how various gut metabolites can degrade and inhibit the absorption of things like Thiamine. Ah. Now you begin to see why random treatments like “high dose thiamine” therapy can be helpful for some and not others when there are not genetic factors in play.
You have to understand how certain gut metabolites can inhibit certain mitochondrial complexes.
You have to understand the role of our bodies anti oxidant, quinone, Nad systems play in regulating all of this - and what nutrients and cofactors they need to work well.
And you have to understand the important role of transporters - and if they are compromised - how to work around the transporter defect.
What if i told you excess nitric oxide degrades de activates B12 ? This in-active B12 stays in our blood, and often measures as ‘high serum b12’. Yet their is a functional deficiency intracellularly. Ever wonder why there are loads of people in chronic illness social media groups who claim they have “high b12” but don’t supplement with b12 ? This is an example of one of hundreds of nuances.
To create solutions and treatments to move people forward - one needs to be able to see what the problems are, where they are, what is driving them, and specifically how to intervene and in what order - this is not a simple “vaccine injury protocol”. Its highly specific to the individual.