The Science™ on Vaccines Causing Autism in Primates

Hewitson et al. (2010) injected the US childhood vaccine schedule of the 1990s into a small group of macaques--and looks like gave the poor monkeys autism

For about a year, ever since RFK Jr. joined the MAGA-MAHA-Trump bruahahaha, calls to do something™, preferably 3 days ago, abounded.

But. There was so much we once knew, it would seem, to warrant a brief look before diving deeper into these waters.

The other day, I came across the following study: ‘Influence of pediatric vaccines on amygdala growth and opioid ligand binding in rhesus macaque infants: A pilot study’ by Laure Hewitson et al., which appeared in Acta Neurobiol Exp (Wars). 2010;70(2):147-64. doi: 10.55782/ane-2010-1787. In case you can’t find the study quickly, click here.

Here’s the abstract

This longitudinal, case-control pilot study examined amygdala growth in rhesus macaque infants receiving the complete US childhood vaccine schedule (1994-1999). Longitudinal structural and functional neuroimaging was undertaken to examine central effects of the vaccine regimen on the developing brain. Vaccine-exposed and saline-injected control infants underwent MRI and PET imaging at approximately 4 and 6 months of age, representing two specific timeframes within the vaccination schedule. Volumetric analyses showed that exposed animals did not undergo the maturational changes over time in amygdala volume that was observed in unexposed animals. After controlling for left amygdala volume, the binding of the opioid antagonist [(11)C]diprenorphine (DPN) in exposed animals remained relatively constant over time, compared with unexposed animals, in which a significant decrease in [(11)C]DPN binding occurred. These results suggest that maturational changes in amygdala volume and the binding capacity of [(11)C]DPN in the amygdala was significantly altered in infant macaques receiving the vaccine schedule. The macaque infant is a relevant animal model in which to investigate specific environmental exposures and structural/functional neuroimaging during neurodevelopment.

Basically, what the authors have been asking is—does exposure to the US childhood vaccine schedule (1994-99) trigger problems associated with the development of neurological problems called ‘autism’ in humans.

You can clearly see how much of a hot potato this one is, eh?

Longitudinal studies of non-human primates pro-vides a complementary approach to clinical studies since their environment can be selectively manipulated and tightly controlled, and pre-and post-exposure testing enables the detection of deviations from normal biological and behavioral trajectories. Non-human primates are particularly useful for studying aspects of vaccine safety (Kennedy et al. 1997). In the 1990’s, the majority of approved pediatric vaccines contained the preservative thimerosal an organic mercury compound [i.e., highly toxic heavy metal] with bactericidal and fungicidal properties (Ball et al. 2001). During this time, the cumulative exposure to mercury from thimerosal in infants under-going immunization during the first 6 months of life could exceed U.S. Environmental Protection Agency guidelines (Clements et al. 2000). Thimerosal was removed from most pediatric vaccines in the United States in 2001 (Ball et al. 2001), based on the risk assessment assumption that the dose-effect and dose-response relationships of ethylmercury, the presumed metabolite of thimerosal (Tan and Parkin 2000, Wu et al. 2008), and methylmercury were the same [that’s why they have different names and properties, right?]. The safety of the combined vaccine regimen per se, rather than that of individual vaccines or vaccine components, is an important aspect of vaccine safety that has not been examined. In order to more directly investigate the neurodevelopmental impact of the complete US pediatric vaccine schedule (1994-1999), our model examined structural and functional changes in the amygdala before and after vaccination in the developing infant primate brain.

Aren’t you excited (yet)? MDs who raised these issues at the time—hi, Andy Wakefield—were pilloried.

As regards study design and approach, this is what was done:

For this pilot study, a total of sixteen male infant rhesus macaques (Macaca mulatta) were randomly allocated to either the exposed or unexposed study group in order to complete peer groups (Ruppenthal and Sackett 1992) such that each peer group contained animals from either the unexposed or exposed study group.

I’ll say this out loud: that’s twice the number of mice (8) that sufficed to get the poison/death juice boosters™ approved.

Four infants were assigned to the unexposed study group and received saline injections according to the schedule…The remaining 12 infants were allocated to the exposed study group and received the complete, age-adjusted childhood vaccine regimen.

Here’s the summary in form of table 1:

Neuroimaging studies (MR and PET) were under-taken for both exposed and unexposed animals at two time points: Time One (T1) at approximately 4 months of age and Time Two (T2) at approximately 6 months of age. At T1 exposed animals had received only thimerosal-containing vaccines equivalent to those given up to 6 months of age (Table I). At T2, vaccine exposure also included the primary MMR vaccine and an additional DTaP and Hib booster, equivalent to those vaccines given between 12-18 months of age for children following the recommended pediatric schedule (Centers for Disease Control, 1995)…

A complete set of MRI data at both T1 and T2 were obtained from 9 exposed and 2 unexposed animals [still more than 8 mice]. The MR images were used for volumetric analyses, as well as for anatomical co-registration to the PET images of [11C]DPN and anatomical guidance of volume-of-interest (VOI) definition.

Results of these investigations included:

There was a statistically significant interaction between exposure [to the US paediatric vaccine schedule] and time on total amygdala volume…

Data indicate that there was a statistically significant interaction between time and exposure on left amygdala volume, such that the pattern of change over time differed according to exposure…

[11C]DPN binding is influenced by vaccine exposure and amygdala volume

GEE analyses evaluating the impact of vaccine exposure on overall [11C]DPN-binding over time, whilst controlling for amygdala volume, revealed a number of significant observations. In exposed animals, mean [11C]DPN binding remained relatively stable over time compared with unexposed animals, which exhibited a maturational decrease in [11C]DPN binding [i.e., your amygdala is supposed to shrink as you age]…

In summary, at T1 there was a significant effect of exposure on total brain volume (exposed > unexposed), but no difference in amygdala volume between groups. Changes occurring between T1 and T2 include a differential change in total amygdala volume between groups (a significant decrease in unexposed animals compared with a non-significant increase in exposed animals) after adjustment for total brain volume, and an increase in [11C]DPN binding in left amygdala compared with a decrease in binding in unexposed animals, after adjusting for amygdala volume.

From the Discussion by Hewitson et al. 2010

The structural and functional CNS alterations identified here provide a model to study the impact of early environmental exposures on primate neurodevelopment…Volumetric analyses identified significantly greater total brain volume in exposed compared with unexposed animals at both measured time points. These results raise the possibility that multiple vaccine exposures during the previous 3-4 months may have had a significant impact on brain growth and development [read that again, if needed]. However, for the amygdala, volumetric and [11C]DPN binding differences between groups appeared to be a function of more recent vaccine exposures, the primary MMR vaccine and the DTaP and Hib boosters given between T1 and T2…

Interestingly, a rapid increase in total brain volume between 6 and 14 months is generally considered to be a consistent finding for many children with an Autism Spectrum Disorder (ASD) ( Piven et al. 1995, Courchesne et al. 2001, Sparks et al. 2002), although this effect may be age-related ( Courchesne et al. 2001, Aylward et al. 2002) and cannot be used as a biomarker for the disorder (Herbert 2005). An enlarged brain volume may be due to a failure in programmed cell death or ‘neuronal pruning’, a process which rids the brain of abnormally functioning neural connections and optimizes coordinated neural functioning (Huttenlocher and Dabholkar 1997). When pruning fails to function, as may be the case in ASD, brain size will increase and neural connectivity will be decreased (Hill and Frith 2003).

This is what happened to these poor primates—scientists injected them with the 1994-99 US childhood vaccine recommendations and the macaques developed (sic) in a way that resembles autism in humans.

Cross-sectional studies that have stratified individuals with ASD by age and behavioral phenotype have shown that the amygdala is enlarged in younger children compared with neurotypical controls, rapidly achieves adult size in childhood, and therefore does not undergo the growth pattern observed during normal male adolescence (Schumann et al. 2004). Several studies have also demonstrated an increase in amygdala volume in young children, with the amygdala typically enlarged by approximately 15% relative to age-matched control subjects (Sparks et al. 2002, Schumann et al. 2004, Mosconi et al. 2009, Schumann et al. 2009). In the present study, amygdala volumes were significantly increased in the vaccine exposed animals relative to the unexposed animals at T2.

I’m not an MD, but this reads like: the more injections esp. in the first year of a baby’s life—significantly increases the risk of the baby developing autism.

The data suggest that vaccine exposure may be associated with significant disturbances in central opioidergic pathways in this model…

With respect to maturational changes in the amygdala, there is substantial evidence of a central role for endogenous opioid systems in regulating the structural development of the nervous system, with reported effects upon cellular proliferation, migration, differentiation, and growth (reviewed by Zagon et al. 1982)…

And now for the conclusions, shall we?

Infant macaques receiving the recommended pediatric vaccine regimen from the 1990’s displayed a different pattern of maturational changes in amygdala volume and differences in amygdala-binding of [11C]DPN following the MMR/DTaP/Hib vaccinations between T1 and T2 compared with non-exposed animals. There was also evidence of greater total brain volume in the exposed group prior to these vaccinations suggesting a possible effect of previous vaccinations to which these animals had been exposed. Because primate testing is an important aspect of pre-clinical vaccine safety assessment prior to approval for human use (Kennedy et al. 1997), the results of this pilot study warrant additional research into the potential impact of an interaction between the MMR and thimerosal-containing vaccines on brain structure and function.

The Science™ Rebutted

Needless to say, the Science™ quickly responded—and I shall quote from the response by Steven Novella and Terence Hines in the ‘Letters to the Editors Acta Neurobiol Exp 2011, 71: 178–179’, which I found here, to ensure we’re letting everyone speak here:

In their recent paper in this journal Hewitson and coauthors (2010) reported that exposing infant macaques to the standard US vaccine regimen resulted in increased amygdalae growth, based on neuroimaging results, in the exposed animals compared to control animals. The paper also reported the effects of vaccination on binding of opioids in the amygdala. This claim that vaccination led to increased amygdala volume has attracted considerable attention in the autism media [note the professional, matter-of-fact tone]. Unfortunately, there are several serious problems with the methods and analyses used in the study [wait for it]. Further, the results reported by the authors are directly contradicted by their own earlier published findings and the findings of other researchers. These problems render the conclusions drawn by Hewitson and coworkers invalid [you see, if you do the Science™ and get different results, your findings are ‘invalid’].

The most obvious problem with the Hewitson and others (2010) study is the number of animals used. A total of 16 animals was enrolled in the study, the plan being to have 12 in the exposed group and four in the unexposed, control, group. However, one animal in the control group was “withdrawn due to a scheduling error” (p. 149). That should have left 12 animals in the exposed and three in the non-exposed group. Even had this been the case, only three animals in the control group would have been inadequate and it would be problematic at best to base any firm conclusions on results from such a small sample [do we talk about the 8 mice for the Covid boosters here?]. But, it transpires, that, for reasons unstated in the paper, the amygdala volumes of only nine exposed and two unexposed animals were measured. Even in a pilot study, such tiny numbers, especially in the control group, render any results meaningless [to be fair, the 8 mice for the Covid boosters had no control group; speaking of a control group, do we remember that the original trial™ of the poison/death juices was terminated by injecting the control group after a few months?]. The unexplained missing data is a cause for serious concern. While the authors correctly point out that this is a pilot study and only conclude that further research is necessary, the statistical and other limitations of this study do not meet even that low standard [what does this verdict say about the Covid shenanigans, then?].

Another problem…is the fact that, while Hewitson and her coworkers make much of this interaction, and it was widely discussed as evidence for the harmful effects of vaccination on the internet, it is just the opposite of what Hewitson and coauthors (2008) has reported previously. Specifically, “compared with unexposed animals, exposed animals showed attenuation of amygdala growth”. So, which is it? Reading the results of the current study, especially in light of previous publications, gives an overall impression of a random scatter of data with cherry picking in order to make the argument that there are any meaningful results at all.

Kinda a fair thing to point out—until you notice that the 2008 presentation is a conference paper and not a refereed study.

Yet another problem with the paper is its serious lack of scholarship. The authors neither mentioned nor discussed a previous paper, the results of which directly contradict their own [looks like a he said-she said argument to me]. Payne with his group (2009) studied the size of both the hippocampus and the amygdala in rhesus macaques, the same species used by Hewitson and others (2010). Payne and colleagues found that the amygdala (and hippocampus) enlarged from infancy to adulthood. This matches what Hewitson found in their vaccinated animals while their “control” or unvaccinated animals (both of them) showed a shrinkage of the amygdala over time. This combination of results suggests that the differences between the vaccinated and unvaccinated animals in the Hewitson and coworkers study is due to the anomalous shrinkage seen in the tiny control group [maybe, maybe not, but I submit we may agree on the notion that two qualitative studies are too little to be certain]. It is, of course, difficult to compare across different studies, but it appears that the vaccinated animals in the Hewitson and her group study showed normal amygdala development [so, did it or didn’t? I mean, ‘it appears’ is way too weak to allege ‘serious lack of scholarship’].

I’m skipping over the notion that Hewitson et al. omitted the paper by Payne and colleagues, which appeared a few months before the former was submitted. That doesn’t look well, granted, but let’s face it—to note this would have been the task of the referees (which Novella and Thines acknowledge in their comment, yet they place the blame squarely on Hewitson et al.):

In summary, the several serious methodological, logical, and scholarly problems with the Hewitson and coauthors (2010) paper make any conclusions about the effect of vaccination on amygdala development totally [sic] unwarranted.

Bottom Lines

So, what do we make of this?

It’s a no-brainer that heavy metals, such as mercury, are not healthy. We know this.

There’s also kinda no way that by looking at certain ingredients in childhood injections and one part of the brain (amygdala) is going to ‘splain’ all of the issues related to autism.

But the association is both interesting and certainly raises a lot of questions, in particular as the number of injections on said US childhood vaccine schedule has risen significantly since the 1990s.

I suppose that it would be interesting to look at the pharmacokinetics of all the ingredients, i.e., where’s all the stuff from the injections going.

Yet we don’t know, and neither do we know if thimerosal (mercury) is the only problematic compound—it’s the same with the Covid injections, too, where the modRNA is a big deal, but so are the pseudouridine parts, the possible DNA contamination, and the electric charge of the lipid nano particles.

I suppose that looking at labels and product inserts is the least anyone can do; if there’s stuff you wouldn’t otherwise ingest, you should likely not get injected with it either.