The 'Neurodiversity' Industry is a Cover for Vaccine Injury

Part I: Two Theories

Introduction

Since the 1990s, the idea of ‘neurodiversity’ has become a cottage industry. The basic tenet of neurodiversity is that autism is a perfectly normal variation of human development that should not be seen as a negative trait. It seeks to highlight the alleged ‘positive’ traits of autism and believes that the struggles of people with autism are largely caused by society not being accepting rather than the inherent downsides of the condition. This article will seek to discuss three parts of this phenomenon by comparing two theories of autism: the neurodiversity theory of autism and the iatrogenic theory of autism i.e. vaccine injury. The first part will discuss the evidence for each theory, concluding that vaccine injury has a large amount of evidence to support it. The second part of this article will look at the individuals and institutions that promote each theory and how the media portrays each group. The third part will draw it together by explaining how the neurodiversity theory is constructed as an alternative to deflect from the vaccine injury theory and to gaslight people suffering with autistic vaccine-injury and their parents about their experiences.

Part I: Two Theories

There are two main theories of autism. The first theory states that autism is genetic, and the second theory states that autism is iatrogenic. The first theory is advocated by both people who think that autism is a good thing, and by those who think it is a bad thing. The latter group of people, who believe that autism is a net negative but who also believe it is genetic, will not be discussed in this article. Instead we will be comparing the ‘autism is a positive, genetic gift’ group (the ‘neurodiversity’ group) to the ‘autism is iatrogenic, largely caused by vaccination’ group (the ‘vaccine-injury theory’ group). Part I will outline these two theories and look at the evidence.

The Neurodiversity Theory of Autism

What is the ‘neurodiversity’ theory of autism? It can be summed up by saying that autism is not a disability, it is a difference that should be celebrated. If you search for ‘neurodiversity’ you can find all sorts of articles advocating for this. Here’s one picked at random:

Neurodiversity is a movement that wants to change the way we think about autism. It rejects the idea that autism is a disorder and sees it instead as a neurological difference: one with a unique way of thinking and experiencing the world.

The movement focuses on celebrating neurological diversity and championing the different world-views and skills that autistic, dyslexic, bipolar, and other neurodiverse people have.

The idea of ‘neurodiversity’ has been increasing in popularity as a paradigm to ‘explain’ autism.

Of course, saying that autism is a positive trait does not explain it. So neurodiversity theorists use genetics to explain autism.

I will argue that both sides of the neurodiversity coin are false: having autism is always a negative thing, and that genetics does not explain autism.

Let’s start with the genetics aspect. One significant piece of evidence that the autism-is-genetic advocates use is twin studies:

Since the first autism twin study in 1977, several teams have compared autism rates in twins and shown that autism is highly heritable. When one identical twin has autism, there is about an 80 percent chance that the other twin has it too. The corresponding rate for fraternal twins is around 40 percent.

On the surface, twin studies look like exceedingly convincing evidence. They have been used to argue for a genetic link for a varying range of problems, including schizophrenia. In reality, though, twin studies are not good evidence that autism is genetic.

The problem that we run into is that twins are likely to have had the same environmental exposure, and this is doubly true when it comes to vaccination. No parent is going to vaccinate one of their twins and not vaccinate the other in some sort of science experiment. Thus both twins will be getting very similar exposure to aluminium, thimerosal, etc. via vaccinations. (Though see this caveat: aluminium levels in vaccination can vary significantly when vials are actually examined). The other major issue with twin studies is that they conclude that interaction between the body and these kinds of exposures is ‘genetic’. A genetic propensity to, say, accumulate certain toxins may well exist in autism cases. But in order for autism to develop, exposure to the toxin is required, and exposure to a toxin is not genetic. The same weakness applies when looking at alleged genes that have been associated with autism – it could be that those genes simply predispose a person to toxin accumulation.

The main weakness in the genetic case for autism is below:

The prevalence rates among children in the United States are now 1-in-30 as of 2020.

It goes without saying that human genes have not radically changed since 1970. So how can the autism rates have changed so drastically? Autism-is-genetic advocates have tried their best to explain this graph, but they have done a bad job of it, because the whole graph screams ‘environmental causes’. But let’s have a look at their explanations for an increase in autism.

The main explanation offered is that the definition of autism has got wider and that is why these numbers have increased so much. Intuitively, this is a really poor explanation, for a number of reasons. For a start, we are looking a massive, massive increase. 1 in 10,000 to 1 in 30 is huge. To explain this simply by stating ‘it’s increased diagnosis’ is intuitively and logically implausible. People who argue this, I think, don’t understand how large a proportion of the population 3% is. That is a very significant chunk of the population. Older people here can employ their common sense. Were 3% or more of your childhood colleagues autistic? If you doubt that you could tell, I assure you that you can with just a little thought. Poor eye contact is a dead giveaway for autism, as is just an obvious awkwardness. The reality is, even ‘high functioning’ autistic people just seem odd, weird and off in particular ways so I would say you could almost always tell. Furthermore, the unemployment rate for people with autism, according to UK government data, is 78%. If we approximate the data, if 1 in 30 people are autistic and 2/3 (being generous) cannot work, this means around 2% of the population cannot work due to autism. The idea that government institutions never noticed 2% of the population being unemployable due to autism is laughably implausible.

This hypothesis also does not fit the shape of the graph very well. It keeps curving upwards, rather than seeing a bump for a change in diagnostic criteria and a levelling. The graph has still not levelled off. At some point, you have to start asking questions.

This issue also becomes more difficult to cover up when you consider severe autism. Autistic people who have a basic level of functioning in the ‘real world’ may just come across to normal people as a bit weird. In these people’s case, it’s more possible that they may not have a diagnosis. This would not be the case with those with severe autistic deficits. Again this is another argument that is just absurd on the face of it:

You can’t have missed 97 percent of the children in the ’80s who had autism. They’re trying to get the public to believe that kids who spin in circles, don’t speak, don’t socialize, can’t go to the bathroom by themselves all existed in our public high schools and elementary schools in the ’80s but only today have gotten a proper diagnosis. It’s incomprehensible.

J.B. HANDLEY

Aside from being intuitively implausible, one study on this issue concluded:

In summary, the incidence of autism rose 7- to 8-fold in California from the early 1990s through the present. Quantitative analysis of the changes in diagnostic criteria, the inclusion of milder cases, and an earlier age at diagnosis during this period suggests that these factors probably contribute 2.2-, 1.56-, and 1.24-fold increases in autism, respectively, and hence cannot fully explain the magnitude of the rise in autism.

THE RISE IN AUTISM AND THE ROLE OF AGE AT DIAGNOSIS

But what about the claim that autism is always a net negative? Surely that’s a little bit fundamentalist? After all, some of the advocates of the neurodiversity theory are autistic themselves, right, and surely they would know? So let’s tackle this thorny question.

The most obvious piece of evidence to start with is life expectancy. The evidence demonstrates that autism significantly decreases life expectancy. This is pretty mainstream evidence that can be found with a quick search.

For example, this article from Psychology Today states that:

One study, published in the American Journal of Public Health in April 2017, finds the life expectancy in the United States of those with ASD to be 36 years old as compared to 72 years old for the general population. 

In other words, according to this study autism halves life expectancy.

The other study was published by the British Journal of Psychiatry in January 2018. This was a Swedish study showing similar results but elaborating on other causes of death as well. This study showed a life expectancy in those with ASD with a cognitive disability (or a learning disability) at 39.5 years versus 70 years for the general population studied. Those with ASD without a learning disability had an average age of death at about 58 years.

Furthermore, most of these causes of death are inherent to autism. For example, being much more likely to die in an accident. Autistic people have poor motor control and are much more likely to have these kinds of accidents such as drowning that lead to death. Horrific anxiety at normal experiences, such as sensory issues around normal noise/light/smell stimuli, also increases mortality as the body becomes overwhelmed with the constant anxiety triggers, meaning that the body’s ability to fight cancers is impaired, and heart attack and stroke risk is increased. People with autism are also unemployed/unemployable, with only about 20% of autistic people even being employed in the UK. This is linked to having awful social skills, having severe anxiety, and in some cases being completely non verbal and non functional. Being perennially unemployable is bad for your health; higher unemployment rates have been well established to be linked to mortality in sociology.

A study that followed autistic people for 20 years showed even more negative outcomes, although most of the participants also had other intellectual disabilities.

The outcome data was grim, showing pervasive inability to live independently, hold a job, or manage money. Few became independent, with 99% unable to live independently. Of those, 70% lived at home with relatives, 21% lived in disability homes in the community, and 8% in residential facilities. A mere 3.7% attained postsecondary education, about half of those representing certificates from college disability programs. While the majority were considered incapable of holding a job in the competitive workspace, some worked in disability workshops or other sheltered positions. Most participants were incapable of handling money, even with caretaker assistance, with only 9.5% considered capable.

NEW STUDY POINTS TO GRIM OUTCOMES FOR ADULTS WITH AUTISM

The neurodiversity paradigm likes to attempt to escape from this reality by claiming that this is purely down to ‘society’ refusing to accept us. That argument is nonsense. The argument is most obviously flawed when it comes to those with severe autism, since any range of accommodations will not fix deficits such as being non verbal, not being able to go to the toilet by yourself, seizures (comorbid with autism), extremely poor motor control, severe gastroenterological issues (linked to autism), sensory issues and meltdowns, etc. If a neurodiversity advocate would like to explain how ‘acceptance’ will fix these problems, the comment section is all theirs. But it is even pretty much nonsense when it comes to ‘high functioning’ autism as well. The reality is ‘acceptance’ and accommodations only really make a difference in edge cases when it comes to solving the issues outlined above. Take for example ability to work. The severely impaired autistic person will never be able to work, you can throw all the accommodations in the world at the issue, it’s not going to happen. Whereas, a high functioning or borderline high functioning autistic person may be able to work if given a few accommodations. I’m not arguing against accommodations. What I am arguing against is the idea that accommodations, or society being more accepting of autism will fix our problems. It won’t.

As for the supposed ‘positive’ aspects of autism, what are they? Usually, it is claimed that many people with autism are more intelligent and analytical than normal people. However, this is likely to confuse correlation and causation. The most plausible explanation here is that brain development is more likely to be disrupted by toxins in the case of intelligent people due to more dense neuron growth in highly intelligent people. And again, severe cases of autism are erased by this view. It glorifies a very narrow spectrum of individuals with autistic injury – the ‘autistic savant’ – while writing off the harms done to the rest.

So what about the people with autism diagnoses who make the claim that autism is a positive thing and that neurodiversity is valid? Well, if someone with an autism diagnosis saying something settles the question, then autism is a devastating vaccine-injury that destroys and obscures the true personality of the individual, rather than reflecting it. Because of course this author has an autism diagnosis. So this kind of argument gets us nowhere.

The Vaccine-Injury Theory of Autism

There is an alternative, ‘underground’ theory of autism which advocates for the view that autism is (at least primarily) caused by vaccination. This article will discuss one cause of autism that the author believes has been comprehensively documented, that is aluminium adjuvants in vaccination entering the brain, disrupting the housekeeping cells of the brain (glia and microglia) and triggering inflammatory reactions such as the il-6 pathway. This is not to say that there are no other problems with vaccination as it relates to autism or no other possible causes (e.g. thimerosal). This article will stick to one cause for reasons of length and clarity.

I will go into a little bit more detail on the basic theory, before discussing the evidence. Aluminium is used in ~80% of vaccines as an adjuvant (substance used to promote an immune response). It is in the vast majority of childhood vaccines, excluding the MMR. However, aluminium is also a neurotoxin that the body cannot filter out effectively when injected, and because of this it can enter the brain. In short, the mechanism of how the injury occurs is like this. The aluminium in a vaccine is injected into the body. Immune cells are stimulated to respond to the site of injection. These immune cells (macrophages) respond and ‘swallow’ the aluminium. But when any inflammatory event in the brain occurs, these cells will be called upon to help, but instead will bring a massive payload of toxic aluminium with them into the brain.

So where’s the evidence? There is a concept in medicine called The Bradford-Hill Criteria.

A set of nine criteria used to determine the strength of an association between a disease and its supposed causative agent. They form the basis of modern medical and dental epidemiological research.

The more of the Bradford-Hill criteria you can demonstrate, the more likely it is that A causes B. Let’s look at these criteria with relevance to the fact that vaccines cause autism.

The first factor we can discuss is coherence. In other words, “does the association fit with other facts?” In the case of the above theory, it fits very well with facts about aluminium.

Aluminium is toxic to the human body. Aluminium has no biological function in human life and so its presence in the human body is always a net negative. The idea than aluminium, at least, can be toxic is widely accepted. Furthermore, it is accepted that aluminium can enter into brain tissue. Even more than this, it is accepted that it can cause harm once it gets into the brain tissue. One form of aluminium toxicity where this occurs has been observed in dialysis patients:

[A]luminium toxicity occurs due to contamination of dialysis solutions, and treatment of the patients with aluminium-containing phosphate binding gels. Aluminium has been shown to be the major contributor to the dialysis encephalopathy [“damage or disease that affects the brain”] syndrome and an osteomalacic component of dialysis osteodystrophy.

In stating this so far, I haven’t deviated from accepted science. Slightly more controversial than this is the idea that Alzheimer’s is caused by aluminium in the brain. This idea has been around since 1965 according to the Alzheimer’s Society. Although some people doubt the correlation-causation relationship (I would argue more for financial reasons than scientific), there is evidence from a wide range of sources.

The Scotsman reported on a study performed by researchers looking at aluminium levels in drinking water that found people in areas with higher levels of aluminium were more likely to die of dementia. The study’s author said:

We still see this well accepted finding that higher levels of aluminium in particular are associated with an increased risk of dementia. It’s confirmatory rather than anything else. [my emphasis]

Dr. Chris Exley has done multiple studies showing high levels of aluminium in the brains of those who died with a diagnosis of Alzheimer’s disease.

Furthermore, infants are at particular risk from aluminium exposure and autism develops in infancy.

Animal studies also provide further evidence for the fact that aluminium in injurious to the brain. Dr. Christopher Exley observed, when he was studying fish, that when the fish were exposed to aluminium, they would start hanging out in the corner of the tank. Another study, performed by a sheep farmer (and shown in the Bert Ehgartner documentary, Under the Skin), showed that sheep injected with aluminium adjuvant (even without an antigen) showed much higher levels of aggressive behaviour and did things like grind their teeth on metal railings. Mice are also negatively affected by aluminium:

Male mice in the “high Al” group showed significant changes in light–dark box tests and in various measures of behaviour in an open field. Female mice showed significant changes in the light–dark box at both doses, but no significant changes in open field behaviours. 

SHAW AND TOMLJENOVIC, 2013.

Thus, aluminium was clearly affecting the neurochemistry of the animals, and these behaviours are decent proxies for autistic symptoms in humans (aggression being analogous to autistic meltdowns and the fish acting strangely being analogous to social avoidance).

All of this evidence is a strong case that the aluminium factor in autism is coherent. We know aluminium is toxic and can harm the brain. Therefore that it can cause the kind of behavioural issues that we observe in autism cannot be prima facie ruled out. This is Criteria 1 on our Bradford Hill list solidly met.

The next criteria we can discuss is dose-response relationship. In short, if we give more aluminium adjuvants to children, do we see an increase in autism? Recall our graph from above – the 1-in-10000 to the 1-in-36 increase in autism prevalence. Now let’s compare this to the increase in aluminium adjuvants and thus exposure.

As is well known, the CDC vaccine schedule has been constantly increasing, particularly since the 1986 National Childhood Vaccine Injury Act (a disingenuous name for a piece of legislation if ever I heard one since the point was to make vaccine manufacturers not financially liable for vaccine injury).

If we take the year 1985, what were the recommended vaccines?

Diphtheria/Tetanus/Pertussis
Measles/Mumps/Rubella
Polio (OPV)
Hib

The MMR does not have any aluminium adjuvant in it. Oral polio vaccine doesn’t have aluminium adjuvant (as it is a live virus vaccine). But DTP vaccine does contain aluminium. Furthermore the research studies on DTP have shown that once healthy user bias is accounted for, the vaccine is very dangerous and significantly increases mortality. A famous study from the 1970s also showed evidence of brain injury from the DTP vaccine.

What are the recommended vaccines in 2020?

Diphtheria/Tetanus/Pertussis (5 doses)
Measles/Mumps/Rubella (2 doses)
Polio (IPV) (4 doses)
Hib (3/4 doses)
Hepatitis B (3 doses)
Varicella (2 doses)
Hepatitis A (2 doses)
Pneumococcal (4 doses)
Influenza (annual vaccination)
Rotavirus (2 doses)

Dose information added from CDC website.

From this information, it is obvious that the amount of aluminium children are exposed to in vaccination has skyrocketed. Most of these jabs contain aluminium and they are being given in more and more doses. This calculation estimates that 3675 mcg aluminium is being given as per the CDC schedule in the first 6 months of life.

Shaw and Tomljenovic wrote a paper addressing this topic:

By applying Hill’s criteria for establishing causality between exposure and outcome we investigated whether exposure to Al from vaccines could be contributing to the rise in ASD prevalence in the Western world. Our results show that: (i) children from countries with the highest ASD prevalence appear to have the highest exposure to Al from vaccines; (ii) the increase in exposure to Al adjuvants significantly correlates with the increase in ASD prevalence in the United States observed over the last two decades (Pearson r=0.92, p<0.0001); and (iii) a significant correlation exists between the amounts of Al administered to preschool children and the current prevalence of ASD in seven Western countries, particularly at 3-4 months of age (Pearson r=0.89-0.94, p=0.0018-0.0248).

DO ALUMINUM VACCINE ADJUVANTS CONTRIBUTE TO THE RISING PREVALENCE OF AUTISM?

The correlation here is strong – more doses, more autism. The dose-response relationship is in this data. Point 2 on the Bradford Hill Criteria list is met.

The third factor that we can discuss is strength of association. Or in other words, how much is the difference in observed rates of autism between the vaccinated and the unvaccinated? This question is not all that easy to answer, mostly because information on this kind of question has been suppressed.

Dr. Paul Thomas has revealing evidence on this question.

Dr. Paul Thomas is the most successful doctor in the world at preventing autism. Data from his practice show:

If zero vaccines, autism rate = 1 in 715;

If alternative vaccine schedule, autism rate = 1 in 440;

If CDC vaccine schedule, autism rate = 1 in 36.

[…]His alternative vaccine schedule reduces autism risk by more than 1200%. However even an alternative vaccine schedule increases autism risk by 160% versus no vaccines at all.

TOBY ROGERS

The difference between 1 in 715 and 1 in 36 is huge. This is evidence of a significant strength of association between two factors. Of course the historical evidence showing fewer cases of autism among older people and more among the young with a strong correlation also matches up with this evidence, since older people are comparatively ‘unvaccinated’. So that’s our third criteria met.

The fourth factor we can discuss is temporal relationship. In other words, the effect must follow, not precede exposure. This factor is difficult to elucidate with vaccines, because exposure is so early on in life, including in the first day of life in the US. This is used by the vaccine cult to argue for the genetic position, but also ensures that it is more difficult to prove that exposure causes the symptoms because the exposure is so early and rampant. However, the simple observation of vaccines preceding autism is almost always true (unless the child is unvaccinated) because if you expose the child at day 1 (US) or 2 months (UK) that is before autistic behaviour is observed. So in a way, their rampant pushing of vaccinations has met this criteria all by itself.

We also have anecdotal evidence for this factor, that is, parents observing their child regressing into autism after vaccination. Of course, anecdotal evidence is automatically dismissed by any Pharma apologist. It is true that when using anecdotal evidence, there are significant pitfalls to consider. People can misremember things, or actively lie. These points are worthy of consideration.

However, both of these risks are minimised in the case of assessing autistic regression after vaccination. In terms of lying, there is simply no motive for a parent to lie about observation of regression into autism after a vaccine. Suggesting to a paediatrician, for example, that a child’s autism was caused by a vaccine will lead to being attacked and dismissed by the doctor. Parents are also attacked in the media if they suggest this idea, such as in the case of Jenny McCarthy, who has been subject to hit pieces because she stated that the MMR vaccine caused her son’s autism. Although vaccine advocates state that parents are likely to fall for the idea that someone is to blame for their child’s autism (such as doctors or Pharma) this is also unlikely. The parents had to consent for the vaccine to be given, and so you would expect to observe the opposite: parents denying that vaccines cause autism, since then they would have to blame themselves for consenting to the vaccine(s) and human beings do not like to acknowledge guilt.

Being mistaken about observation is also less likely in the case of autistic regression. This is because we are talking about parental observation of children and decent parents are highly alert to any signs of illness in a child, particularly a child of the age likely to receive vaccines. I will concede however that it is not impossible for someone to either be mistaken or lie. However it is quite implausible that given the factors weighing against these that all cases are examples of lying or misremembering given the multitude of testimonies that we have.

Thus there is at least some evidence for criteria four on the Bradford-Hill list.

The fifth factor that we can discuss is consistency. In other words, if we introduce aluminium adjuvants to all sorts of different groups, rich, poor, black, white, Asian, male, female, etc, do we see increased levels of autism?

There is a male-female disparity in autism diagnosis, with males being significantly more likely to be diagnosed than females. There is likely some biological reason why boys are more susceptible to this form of aluminium poisoning that is currently unknown (or at least, unknown to me). Nevertheless we see an increase in autism diagnosis in both groups.

Autism diagnoses have also increased across different racial groups, at a similar rate:

Thus factor 5 is met.

The sixth factor we can discuss is experimental evidence. In other words, do we have any hard evidence for aluminium in the brain in autism? The answer to this is yes.

Dr. Exley and his research team examined this question directly. They obtained samples of brain tissue from individuals that had died with a diagnosis of autism. This was the first study of this kind. They examined this brain tissue and found very high levels of aluminium in all samples.

The aluminium content of brain tissue in autism was consistently high. The mean (standard deviation) aluminium content across all 5 individuals for each lobe were 3.82(5.42), 2.30(2.00), 2.79(4.05) and 3.82(5.17) μg/g dry wt. for the occipital, frontal, temporal and parietal lobes respectively. These are some of the highest values for aluminium in human brain tissue yet recorded and one has to question why, for example, the aluminium content of the occipital lobe of a 15 year old boy would be 8.74 (11.59) μg/g dry wt.? 

MOLD, UMAR, KING AND EXLEY, 2018.

We can add another one of Exley’s papers to make this evidence even better. This paper by Exley and Clarkson contains control samples who died with no signs of neurodegenerative disease:

The aluminium content of each lobe (mean and SD) were 1.03 (1.64), 1.02 (1.27), 0.95 (0.88), 0.77 (0.92) and 0.51 (0.51) μg/g dry wt.

EXLEY AND CLARKSON

These samples have much lower levels of aluminium in them than the autism samples, and this is despite the fact that the controls were mostly older than the autism samples – meaning lifelong exposure to aluminium through non-vaccine routes would have been higher and it would have had more time to accumulate in the control tissues.

The main limitation of this evidence as pointed out by its critics is that the study had a small sample size of N=5 when it came to measuring aluminium concentration in the autism samples (and for some aspects of the study N=10). This was for practical reasons (i.e. there isn’t a large amount of samples of autistic brain tissue available).

It is fair to acknowledge this, and obviously it would be better if the sample size was larger. However, it is completely dishonest to dismiss this study because of the small sample size. This study, for example, is completely different from a survey where 5 participants answering would be worthless. We are looking at pathological brains with clear evidence of a high level of a neurotoxin in them. The level of neurotoxin in these brains cannot be explained away by saying that there is only a few of them. To have that level of brain aluminium content and for it to not be pathological and negatively affecting the cells around it is absurd, unless you want to straight up deny that aluminium is neurotoxic.

Furthermore, no-one has tried to either confirm or reject the Aluminium Research Group’s findings (to this author’s knowledge at least). The establishment haven’t done a study where they demonstrate that the levels of aluminium found by the group are overly high. This is another case where the establishment claim the evidence isn’t good enough to support an anti-establishment view and then just ignore the question. So, despite establishment criticisms, this is criteria six on our Bradford-Hill list met.

We can use Exley’s evidence to discuss the seventh criteria, biological plausibility.

The 2018 paper shows that the high levels of aluminium were found associated with glia and microglia:

Discrete deposits of aluminium approximately 1 μm in diameter were clearly visible in both round and amoeboid glial cell bodies (e.g. Fig. 3b). Intracellular aluminium was identified in likely neurones and glia-like cells and often in the vicinity of or co-localised with lipofuscin (Fig. 5). Aluminium-selective fluorescence microscopy was successful in identifying aluminium in extracellular and intracellular locations in neurones and non-neuronal cells and across all brain tissues studied (Fig. 1, Fig. 2, Fig. 3, Fig. 4, Fig. 5). 

This is important because those cells are disrupted in autism. For example, they are responsible for synaptic pruning, which does not occur correctly in autism.

Aluminium-loaded mononuclear white blood cells, probably lymphocytes, were identified in the meninges and possibly in the process of entering brain tissue from the lymphatic system (Fig. 1). 

So we have a) high levels of a neurotoxin in b) an area of the brain known to be disrupted in the disease we suspect of being caused by that neurotoxin and c) evidence of how that neurotoxin enters the brain. This is strong evidence of biological plausibility, meeting criteria seven.

The eighth criteria we can discuss is specificity. The idea of specificity ideally means that one disease has one cause, but this is difficult to apply to reality as Bradford Hill acknowledged. Aluminium adjuvants, in reality, are highly likely to cause more than one disease. However, the argument is not just that aluminium adjuvants cause autism, but that a specific action of aluminium adjuvants causes autism. Our theory offers a specific toxicant (aluminium), a specific route of exposure (injection), a specific method by which that toxin gets into the brain (macrophages), specific cells that are disrupted (glia and microglia), and specific negative cascades that are triggered (excessive IL-6 production due to an inflammatory response). Our argument also does not claim that glial disruption by aluminium adjuvants causes a whole host of problems, but autism specifically (and nothing else). So the theory meets criteria eight on the list.

The last factor we can discuss is analogy. If we can observe similar things happening that makes our own theory more likely to be true. This is easy to demonstrate in the case of aluminium poisoning, as poisoning by different metals, such as mercury, can cause significant impairments in child functioning. One interesting case worthy of discussion here is that of acrodynia. Acrodynia, or ‘Pink disease’ was an early 20th century disease that symptomatically had some overlap with autism although with some differences. It was later proven that pink disease was a form of mercury poisoning caused by mercury teething powders. We know from this case that metal poisoning can cause symptoms with some similarities to autism. There are also examples of aluminium itself causing other forms of poisoning, which were discussed in point 1. So analogy also supports our case and gives us point 9.

Conclusion

As we can see from the above discussion, the idea that vaccines cause autism is strongly evidenced. However, the theory is also opposed by the entire establishment despite this evidence. It is to how these two differing theories of autism are treated that we now turn.