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.