The SARS-CoV-2 mRNA Vaccines: Will They Increase Autism Rates?
The US Centers for Disease Control are now recommending that the SARS-CoV-2 mRNA vaccine be administered to children as young as six months of age, and also to pregnant women [259]. We believe there is reason to be concerned that this policy may lead to increases in the prevalence of autism both in vaccinated infants and in the offspring of vaccinated pregnant women. It has become very clear that the SARS-CoV-2 spike protein is extremely toxic, and it may be the primary cause of observed severe vaccine side effects following mRNA vaccination. The spike protein itself is likely a major cause of myocarditis following vaccination, as circulating spike protein, both free and antibody-bound, was found in subjects who developed myocarditis after the vaccine, but not in the control subjects [260]. A study on 28 cases of fatal myocarditis immediately following mRNA vaccination for SARS-CoV-2 established that all 28 deaths were most likely linked to the vaccine [261]. The spike protein is predicted to cause neuroinflammation and neurodegenerative disease, in part through its prion-like properties [262,263].
The lipid nanoparticles in the vaccine are designed so as to protect the mRNA from degradation, and, furthermore, the mRNA itself has been engineered to resist enzymatic breakdown through the substitution of methylpseudouridine for all of the uridine residues [264]. The synthetic cationic lipids assure that the mRNA will be released from the endosome, escaping lysosomal degradation, and then be persistently translated into spike protein. While mRNA normally degrades within a few hours, vaccine spike antigen and mRNA can persist for up to eight weeks in lymph node germinal centers [265].
The nanoparticles can breach the blood brain barrier, and the mRNA nanoparticles can be phagocytized by microglia in the brain and then translated into spike protein, stimulating a massive immune response. This causes upregulation of TNF-α, IL-1β, and IL-6, stimulating ROS production and neuroinflammation. Neuroinflammation in turn provokes astrocytes to release excessive glutamate into the synapse, overstimulating the NMDARs and causing neuroexcitotoxicity [266]. This leads to a reduction in BDNF signaling and impaired neuroplasticity, as is seen in schizophrenia and autism [267]. As we have seen, extracellular glutamate interferes with cystine uptake in neurons, leading to glutathione deficiency. A recent review paper has proposed that glutathione deficiency may be at the core of COVID-19 pathophysiology [268]. Glyphosate’s ability to deplete glutathione would therefore likely lead to more severe outcomes from COVID-19 and/or more severe adverse reactions to the mRNA vaccines.
A seminal study by Erdogan et al. on rat pups found strong evidence that the mRNA vaccines cause autism-like symptoms in rats. Pregnant rat dams were exposed to a full adult dose of the BNT162b2 vaccine, and the offspring were carefully evaluated for behavioral issues and motor performance, as well as monitoring for any changes in brain chemistry. Exposed male rat pups, but not female pups, exhibited pronounced autism-like behaviors, including repetitive behaviors, impaired social interaction, as well as impaired coordination and agility. Notably, the exposed male offspring were found to have statistically significant decreased expression of BDNF and WNT (p < 0.01) and significantly increased expression of mTOR (p < 0.01) [269].
BDNF is an important player in WNT signaling, and its expression has been shown to be essential for synapse maturation in the hippocampus mediated by neuroligin [270]. Downregulation of BDNF leads to decreased levels of Bcl2 through impaired Akt signaling, with a resulting increase in apoptosis in neurons, a mechanism that has been proposed as potentially being responsible for the pathogenesis of autism [271]. We have already seen that WNT signaling is decreased following exposure to glyphosate, making these injections synergistically toxic with glyphosate [118]. Overexpression of mTOR has been linked to increased spine density in excitatory synapses in autism [272]. As we have already stated, an overactive mTOR pathway impairs microglial autophagy, resulting in decreased clearance of unproductive synapses [116].
In the Erdogan et al. study, post-mortem analyses showed that exposed male pups also had significantly fewer neurons in specialized regions of the hippocampus compared to male pups of the unvaccinated mothers, as well as lower counts of Purkinje cells in the cerebellum [269].
While the rat dams in this experiment was exposed to a much higher dose of the vaccine than would be appropriate given their weight, it is also the case that the rat ACE2 receptor has a much reduced capacity to facilitate uptake of the spike protein compared to the human ACE2 receptor, making rats far less susceptible to SARS-CoV-2 [273].
We have shown that children with autism have impairments in melatonin synthesis, and that glyphosate exposure reduces melatonin levels in rats [39]. It has been proposed that melatonin supplementation can be therapeutic in treating long COVID, through its anti-inflammatory, antioxidant and immune enhancing properties [274]. A study on mice humanized to express the human ACE2 protein and exposed to SARS-CoV-2 found that melatonin therapy inhibited SARS-CoV-2 brain entry and protected brain endothelial cells from damage. They showed that melatonin inhibits virus-induced damage of cerebral small vessels, diminishes brain inflammation, and decreases viral load in the brain. This result suggests that melatonin deficiency, such as is seen in autism and induced by glyphosate, would lead to increased risk to severe COVID as well as vaccine adverse reactions.
At the beginning of this paper, we noted the standard categorization of autism onset as “early,” typically onset prior to age 2; and “regressive,” with onset after age 2. We cited studies that have shown that over 50% of regressive cases of autism displayed subtle-yet-perceivable sensory and/or behavioral abnormalities prior to regression, i.e. during the “normal” developmental months. We propose here that the risk of developing the sensory and behavioral changes characteristic of autism – along with the concurrent pathophysiology described in this paper - lies on a continuum. Differing levels ofin utero , neonatal, and postnatal glyphosate exposure, against a background of other risk factors, helps explain this chronological gradient of autism symptom onset.
We strongly suggest that glyphosate may be playing a significant (and possibly central) role in contributing to the autistic phenotype. Current CDC recommendation regarding COVID-19 vaccination is that infants should be vaccinated beginning at 6 months of age [275] Furthermore, prenatal and postnatal exposure to the constituents of COVID-19 mRNA vaccines via maternal, neonatal and early-postnatal periods is potentially an additional strong push toward that same phenotype for the reasons we have explained above. For children manifesting as regressive autism, we are concerned that mRNA vaccination may contribute the spark of neuroinflammation that is the tipping point for an infant with excessive prior exposure to glyphosate and/or other environmental factors, particularly when combined with risk genes. In this regard, we agree with the letter published by Mawson (2019) regarding the finding of increased autism following MMR vaccination: “Many factors, including receiving the MMR vaccine and other vaccines, may be combining with as-yet unidentified host and environmental factors to cause [autism].” [276]. We believe this paper makes a compelling case that one of those environmental factors has now been identified.