BIOLOGICAL MECHANISMS OF VACCINE INJURY
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WHEN DR. CHRIS EXELEY and his research team discovered aluminum co-localized with amyloid plaques in the brains of patients who died from Alzheimer’s, it made big news, even though a study in 1985 discussed the aluminum silicate portion of amyloid. That’s right. We’ve known since 1985 at least that amyloid plaque in the brain is partly aluminum silicate. Now, Exeley’s findings completely destroy any hope that aluminum somehow stayed out of the brain,
Aluminum, it turns out, plays a critical role in our understanding of the biological mechanisms of vaccine injury. In this article, I will review the scientific evidence of four major ways that vaccines can cause harm. These are (1) Vaccine-Induced Mitopathy; (2) Vaccine-Induced Persistent Gliosis; (3) Vaccine-Induced Endoplasmic Reticulum Damage, and (4) Vaccine-Induced Autoimmunity (to appear as a separate article). My intent and purpose is not and has never been to discourage anyone from accepting vaccines, nor to provide medical advice of any kind; rather, my intent is to make a clear path toward safer routes to artificial immunization and communicate the state of scientific knowledge about mechanisms of the pathophysiology of disease caused by vaccines, and how such human pain and suffering can be mitigated.
mitopathy(1) Vaccine-Induced Mitopathy
Individuals born with mitochondrial disorders have partially disable cellular energetics. Mutations that alter proteins in the various specific mitochondrial pathways lead to a variety of congenital conditions, including encephalomyopathy and seizures. We need mitochondria to work in all of our tissues. However, our brains consume so much energy, any weakening of mitochondrial ATP flux will almost certainly lead to neurological disorders.
Environmental damage to mitochondria is known to occur from exposure to lead and includes depletion of mitochondrial membrane potential (ΔΨ) and intracellular glutathione (GSH), elevation of caspase-3 activity, intracellular reactive oxygen species, and malondialdehyde levels, and inhibition of GSH peroxidase (GSH-Px) activity (Liu et al., 2014).
Why discuss lead-induced mitochondrial toxicity in an article on vaccine injury? In part because many individuals familiar with brain injuries and conditions that lead to brain injuries will recognize the critical role of GSH, the importance of shutting down ROS, and the potential use of malondialdehyde as a screen for brain injury following vaccination. Another reason is that 25% of the homes in Pittsburgh have higher lead levels in the water coming into the homes than the levels found in the water in Flint, MI, and individuals with mitochondrial damage due to lead are likely to be a higher risk of the toxic effects from vaccines.
The science of the specific actions and mechanisms of mitochondrial injury from vaccines include some of these events, including recognition of aluminum as an intracellular ROS generator (Han et al., 2013). Aluminum is present in vaccines as an adjuvant in a variety of forms, most commonly aluminum hydroxide (a well-known neurotoxin). Vaccine risk denialists spend a lot of time denying the massive literature on the neurotoxicity of aluminum. Nevertheless, studies show that aluminum also disrupts cytoskeletal dynamics (Lemire et al., 2009).
Thimerosal also has damaging influences on mitochondria, including direct damage to the mitochondrial genome. Sharpe et al. (2012) found that thimerosal induced a five-fold increase in the levels of oxidant damaged mitochondrial DNA bases and increases in the levels of mtDNA nicks and blunt-ended breaks.