Aluminum in Vaccines is a likely cause of Autism

Summary

  • Autism is defined behaviourally, and classified as neurodevelopmental disorder
  • Autism rates are increasing, and technical changes to definitions, diagnosis, or awareness cannot fully explain the increase
  • Genetics plays a role, but there must be environmental factors that cause autism, and there may be multiple factors
  • Aluminum is a neurotoxin that can have subtle neurological effects
  • Aluminum from infant vaccines exceeds the WHO safety level
  • No large-scale epidemiological studies have been carried out looking for an association between aluminum-containing vaccines and autism.
  • Several small-scale epidemiological studies found an association.

Autism is neurological

Autism is defined behaviourally by the two characteristics: 1) Persistent deficits in social communication and social interaction across multiple contexts, and 2) Restricted, repetitive patterns of behavior, interests, or activities. This definition comes from DSM-5 (2013), which classifies autism as a neurodevelopmental disorder, a type of mental disorder. There are three levels of severity on each characteristic, based on the extent of support required.

Something is causing children’s brains to be altered during neurodevelopment, resulting in autistic behaviours. Shouldn’t we try and find out what is causing that? An investigation into cause does not require any judgement about whether more autistic children is “good” or “bad”, or whether being autistic is a strength or a weakness. It is merely an attempt to explain the observation that autism occurs and is increasing.

The autism rise is real

The number of people diagnosed with autism has increased dramatically since 1985, from 1-in-10000 to 1-in-35, and the number is still increasing rapidly (Nevison, 2014). This dramatic rise cannot be explained by changes to the definition of autism or to improved diagnosis and awareness. Something is causing more children to develop autism. The increase is real, not technical (Nevison, 2017).

Autism has an environmental cause

The increase is too rapid to be explained as genetic, so the cause must be environmental. We know from twin studies that autism is partly genetic and partly caused by environmental factors (Hallmayer, 2011).

Autism has been linked to multiple environmental toxins, including glyphosate, electro-magnetic frequencies, and vaccine ingredients such as aluminum and thimerasol (Mercola, 2018). Environmental toxins activate the innate immune system and initiate the inflammatory process. Inflammation is excessive in the brains of autistic people, demonstrating neurotoxicity (Tsilioni, 2019).

Maternal immune activation (MIA) has been identified as a cause of autism, through both epidemiological and animal studies. A severe infection during pregnancy is associated with autism (Zerbo, 2015). Autistic behaviours can be induced in animals by activating the immune system during pregnancy (Malkova, 2012). Post-natal immune activation has also been found to cause autistic behaviours in animals (Missig, 2018).

The particular toxin or pathogen appears to be less important than the strength and timing of the immune activation during early neurodevelopment. This is why any or all of the above-mentioned environmental toxins could be a cause of autism. Since the focus of this website is vaccines in general, and aluminum toxicity in particular, I will explain specifically why aluminum in vaccines is a likely cause of autism.

Aluminum is a neurotoxin that can have subtle neurological effects

Aluminum toxicity has been recognised as a major cause of encephalopathy (brain damage) in uremic patients, whose kidneys are less effective at eliminating aluminum (Alfrey, 1993).

Aluminum can have more subtle neurological effects, only detected through behavioural tests, even when the kidneys are healthy. Subtle neurological effects have been observed in workers chronically exposed to aluminum dust or fumes (ATSDR, 2008). Preterm babies exposed to high levels of aluminum through Total Parenteral Nutrition (TPN) scored lower in mental development tests (Bishop 1997), leading the FDA to place a limit on aluminum content in TPN products (FDA, 21CFR201.323).

In animal models, aluminum at sufficient doses in the diet induces: neuroinflammation (Viezeliene, 2013); loss of neuronal dendritic spine and cognition impairment (Cao, 2016); memory impairment (Martinez, 2017); adverse reproductive effects (Hirata-Koizumi, 2011); learning delay (Bilkei-Gorzo, 1993); decreased limb strength (Poirier, 2011); and decreased motor performance (Golub, 2001).

Based on these animal studies, health agencies such as the WHO (JECFA, 2011) have established safety limits for oral intake of aluminum. The current WHO oral intake safety limit is 0.3 mg/kgbw/day.

High levels of aluminum have been observed in the brains of individuals who had neurological conditions, including Alzheimer’s disease (Mirza, 2017) and autism (Mold, 2018). A meta-analysis showed that excessive aluminum in blood, urine, and hair is associated with autism (Sulaiman, 2020).

Given all this, we ought to be deeply concerned with the possibility that aluminum toxicity may be altering the neurodevelopment of children, resulting in autism.

Aluminum from infant vaccines exceeds the WHO safety level

The primary source of exposure to aluminum during infancy is from vaccines. Exposure through diet and air is limited by very low permeability of the gut and lung linings to aluminum. The aluminum in vaccines on the other hand all enters systemic circulation, since it has no other way of leaving the injection site. Over the whole of infancy, uptake of aluminum from vaccines is around 50x higher than uptake from breast milk and air, as I demonstrated here.

The WHO oral intake safety level of 0.3 mg/kgbw/day can be converted into an uptake safety level by multiplying the oral intake safety level by the gut bioavailability of ingested aluminum. When this is done, it can be seen that aluminum uptake from vaccines exceeds the implied WHO uptake safety level, as I demonstrated here.

The only evidence cited by the CDC that the amount of aluminum in infant vaccines is safe is a pharmacokinetic model (Mitkus, 2011) which has many critical errors and weaknesses; I wrote about one of them here.

No large-scale epidemiological studies

No large-scale epidemiological studies have been carried out looking for an association between aluminum-containing vaccines and autism (IOM, 2012). The vaccine schedule as a whole has not been tested (IOM, 2013)

This is despite the existence of an extensive database called the Vaccine Safety Datalink (VSD), controlled by the CDC. The Institute of Medicine described the VSD as the most feasible way to conduct large scale-studies comparing health outcomes of vaccinated and unvaccinated children (IOM, 2013), but still no such studies have been done.

Small-scale epidemiological studies found an association

Some independently-funded small-scale epidemiological studies have been conducted:

  • an ecological study that found that autism rates are higher in countries with schedules where aluminum-containing vaccines are given earlier, and that 8 of 9 of Hill’s criteria for establishing causality are satisfied in the case of aluminum and autism (Tomljenovic, 2011)
  • a pair of cross-sectional studies that found an association between the aluminum-containing Hepatitis B vaccine and developmental disability and autism (Gallagher, 2008 and Gallagher, 2010)
  • a survey of parents of 666 homeschooled children that found an association between vaccinations and neurodevelopmental disorders, allergies, and eczema (Mawson, 2017)
  • a retrospective cohort study of 2,047 children across three paediatric practices found an association between vaccines and developmental delay, ear infections, and asthma (Hooker, 2020).

Finally, mice vaccinated to mimic the CDC recommended schedule were found to exhibit autistic behaviour (Sheth, 2018).

Conclusion

Given this abundance of evidence implicating aluminum in vaccines as a likely cause of autism, it is urgent that large-scale epidemiological studies are carried out to test this highly-plausible hypothesis. Parents need to be informed about the evidence that the aluminum in vaccines can alter the neurodevelopment of their children.

CDC removes “Vaccines Do Not Cause Autism” claim from their website

The CDC has changed the title of their webpage giving information about vaccines and autism from “Vaccines Do Not Cause Autism” to simply “Autism and Vaccines”.

Why did they change it? It could be due to the legal action of ICAN, or it could be an innocent “reformatting” of the website, as CDC defenders are claiming.

As both sides acknowledge, the text of the page is unchanged and still says that “vaccines do not cause ASD”, and that “there is no link between receiving vaccines and developing ASD” and “no links have been found between any vaccine ingredients and ASD”.

ICAN intend to pressure the CDC to remove these statements, too, because they say they are not supported by the scientific evidence.

Let us assess whether ICAN are right by looking at each of the sources cited by the CDC on this page to support their claim that vaccines do not cause autism.

Institute of Medicine, 2012

Under the heading “There is no link between vaccines and autism”, the CDC writes that:

Some people have had concerns that ASD might be linked to the vaccines children receive, but studies have shown that there is no link between receiving vaccines and developing ASD. In 2011, an Institute of Medicine (IOM) report on eight vaccines given to children and adults found that with rare exceptions, these vaccines are very safe.

That Institute of Medicine (IOM) report was called “Adverse Effects of Vaccines: Evidence and Causality” (2012) and is a systematic review of all the scientific literature looking adverse effects of vaccines. The eight vaccines included in the study were MMR, Varicella, Influenza, Hepatitis A, Hepatitis B, HPV, DTaP, and Meningococcal. An impressive 76 different health outcomes were included in the study, one of which was autism.

Vaccine Autism Studies Inadequate

However, only two vaccines – MMR and DTaP – were even examined in relation to the autism health outcome. Presumably, this is because there are no studies to examine. This alone makes the report insufficient evidence to claim that vaccines don’t cause autism. For all but two vaccines, according to the IOM, there have been no studies looking at associations to autism.

Regarding DTaP, the IOM concluded that:

The evidence is inadequate to accept or reject a causal relationship between DTaP and autism.

Their epidemiological assessment found the evidence “insufficient” (just one single study, rejected due to being based on data from a passive reporting system). Their mechanistic assessment found the evidence “lacking” (no studies at all).

The MMR is the only vaccine where the IOM made a conclusive statement:

The evidence favors rejection of a causal relationship between MMR and autism.

At best, therefore, this report supports the claim that the MMR does not cause autism. It cannot possibly support the bigger claim that vaccines do not cause autism.

MMR-Autism Studies

In their epidemiological assessment, the IOM reviewed an impressive 22 studies looking for an association between MMR and autism. 12 of them were dismissed for being based on data from a passive surveillance system lacking an unvaccinated comparison population, or for being an ecological comparison study lacking individual-level data. A further 5 were dismissed as having “very serious methodological limitations”.

In their mechanistic assessment, the IOM reviewed 6 studies, but dismissed them all for not providing evidence beyond temporality, concluding that the mechanistic evidence is “lacking” when it comes to assessing a causal association between MMR and autism.

This left just 5 epidemiological studies that the IOM considered good enough to be used to conclude the lack of a causal association between MMR and autism. These were the studies by Taylor 1999, Farrington 2001, Madsen 2002, Smeeth 2004, and Mrozek-Budzyn 2010. The Mrozek-Budzyn study was acknowledged by the IOM as having “serious limitations”, and the Farrington study is based on the same data as the Taylor study.

I will review each of these MMR-autism studies in a future post.

Antigens-Autism Study

The CDC writes that:

A 2013 CDC study added to the research showing that vaccines do not cause ASD. The study looked at the number of antigens (substances in vaccines that cause the body’s immune system to produce disease-fighting antibodies) from vaccines during the first two years of life. The results showed that the total amount of antigen from vaccines received was the same between children with ASD and those that did not have ASD.

The De Stefano study is a helpful addition to the research, in that it looks at the cumulative effects of multiple vaccines, rather than at vaccines in isolation as in the IOM report.

However, the study is deeply flawed, because no one who claims that vaccines cause autism says that it should be related to the number of antigens received. It is the other ingredients of vaccines that are of greater concern, especially the aluminum salts used as adjuvants. Nevertheless, grouping by number of antigens has the potential to act as a proxy for distinguishing fully vaccinated, partially vaccinated, and unvaccinated, so it may not be an entirely worthless measurement.

Unfortunately, the results in the study are skewed by the presence of three vaccines with 3000 antigens (DTP, DTP-Hib, and Typhoid), and then a large drop down to vaccines with 69 antigens (Varicella), 24 antigens (MMR), and all other vaccines having less than 15 antigens. Total number of antigens is therefore merely a proxy for number of doses of high-antigenic vaccines. From the chart below it can be seen that most subjects had either zero, three, or four doses of these high-antigenic vaccines, and this alone determines the groups used in the analysis.

The chart also shows that there were no unvaccinated subjects in the study. Nobody received less than 50 antigens. The group that received zero high-antigenic vaccines received many other vaccines, because most of them had between 151 and 311 antigens. During the study period, the high-antigenic DTP vaccines were replaced by low-antigentic DTaP vaccines, so most of those in the “low antigens” group were fully vaccinated, just like most of the subjects in all the other groups.

At best, this study can be used to support the claim that high-antigenic vaccines do not cause autism any more than low-antigenic vaccines do. Since there are no high-antigenic vaccines used anymore, this is a moot conclusion. This study certainly cannot be used to support the claim that vaccines do not cause autism, because there were no unvaccinated subjects in the study.

Thimerosal-Autism Studies

The CDC then has a heading of “Vaccine ingredients do not cause autism” and writes that:

One vaccine ingredient that has been studied specifically is thimerosal, a mercury-based preservative used to prevent contamination of multidose vials of vaccines. Research shows that thimerosal does not cause ASD. In fact, a 2004 scientific review by the IOM concluded that “the evidence favors rejection of a causal relationship between thimerosal–containing vaccines and autism.” Since 2003, there have been nine CDC-funded or conducted studies that have found no link between thimerosal-containing vaccines and ASD, as well as no link between the measles, mumps, and rubella (MMR) vaccine and ASD in children.

That Institute of Medicine (IOM) report was called “Immunization Safety Review: Vaccines and Autism” (2004) and is a systematic review of all the epidemiology studies looking at associations between vaccines and autism. The report only examines studies of thimerosal-containing vaccines (TCVs) and the MMR vaccine (superceded by their 2012 review).

The IOM reviewed 12 studies looking for an association between TCVs and autism. 6 of them were dismissed for being based on data from a passive surveillance system lacking an unvaccinated comparison population, or for being an ecological comparison study lacking individual-level data. One study based on Vaccine Safety Datalink (VSD) data was dismissed as “uninterpretable”.

This left 5 studies on which the IOM relied for their conclusion that TCVs do not cause autism: Hviid 2003, Miller 2004, Verstraeten 2003, Madsen 2003, Stehr-Green 2003.

The CDC cites a two-page PDF that lists and briefly summarises eight further studies to support their claim TCVs do not cause autism: Barile 2011, Price 2010, Tozzi 2009, DeStefano 2009, McMahon 2008, Thompson 2007, Verstraeten 2003, Stehr-Green 2003 (included twice).

I will review each of these TCV-autism studies in a future post.

Thimerosal Removed From Vaccines

The CDC writes that:

Between 1999 and 2001, thimerosal was removed or reduced to trace amounts in all childhood vaccines except for some flu vaccines. This was done as part of a broader national effort to reduce all types of mercury exposure in children before studies were conducted that determined that thimerosal was not harmful. It was done as a precaution. Currently, the only childhood vaccines that contain thimerosal are flu vaccines packaged in multidose vials. Thimerosal-free alternatives are also available for flu vaccine.

Thus, the question of whether TCVs cause autism is now only of historical interest within the wider context of the question of whether vaccines cause autism. The studies cited to support that the claim that TCVs do not cause autism have significant weaknesses, and there is considerable evidence suggesting that TCVs do cause autism.

Since they are now rarely used, TCVs are clearly not an ingredient of concern to those who claim that vaccines cause autism today. Therefore, whether TCVs do cause autism is a moot point in respect of this present-tense claim.

“Other Ingredients”

Besides thimerosal, no other vaccine ingredients are named. All the ingredients in vaccines today are addressed by the CDC with a single sentence:

Besides thimerosal, some people have had concerns about other vaccine ingredients in relation to ASD as well. However, no links have been found between any vaccine ingredients and ASD.

No studies at all are cited to support this claim. The link goes to a page merely listing types of vaccine ingredients and their purpose:

Aluminum salts are the vaccine ingredient of biggest concern when it comes to autism, because aluminum is a neurotoxin that has been observed to induce subtle neurological effects and autism-like behaviour in animals exposed to it. The toxic nature of aluminum is why aluminum salt works as a vaccine adjuvant, ensuring that the activation of the immune system is strong enough to result in immunological memory.

There have also been health concerns raised about formaldehyde, glutamate, polysorbate-80, antibiotics, animal cells and fetal cells.

No studies are cited on this page to support the claim that vaccine ingredients do not cause autism.

“More Information”

The CDC provides a list of five links:

Facts About Autism Spectrum Disorders

Fact Sheet: Understanding Thimerosal, Mercury, and Vaccine Safety

IOM Report: Adverse Effects of Vaccines: Evidence and Causality, 2011

Timeline: Thimerosal in Vaccines (1999-2010)

Frequently Asked Questions about Thimerosal

The first link has information about autism but not about vaccines. The second, fourth and fifth links are about TCVs. The third link is to the IOM 2011 Report cited above.

“Related Scientific Articles”

The CDC provides a list of seven links:

Taylor LE, Swerdfeger AL, Eslick GD. Vaccines are not associated with autism: An evidence-based meta-analysis of case-control and cohort studiesexternal iconexternal iconVaccine. 2014 June;32(29):3623–3629.

Schechter R, Grether JK. Continuing increases in autism reported to California’s developmental services system: Mercury in retrogradeexternal iconArch Gen Psychiatry. 2008;65:19-24.

Institute of Medicine. Immunization Safety Review. Vaccines and Autismexternal icon Board of Health Promotion and Disease Prevention, Institute of Medicine (National Academy Press, Washington, DC, 2004).

Hviid A, Stellfeld M, Wohlfahrt J, Melbye M. Association between thimerosal-containing vaccine and autism pdf icon[PDF – 5 pages]external iconJAMA. 2003;290:1763–6.

Madsen KM, Hviid A, Vestergaard M, Schendel D, Wohlfahrt J, et al. A population-based study of measles, mumps, and rubella vaccination and autismexternal iconN Engl J Med. 2002;347 (19):1477–1482.

Ball L, Ball R, Pratt RD.An assessment of thimerosal in childhood vaccinesexternal iconPediatrics. 2001;107:1147–1154.

Joint statement of the American Academy of Pediatrics (AAP) and the United States Public Health Service (USPHS)external iconPediatrics. 1999;104:568–9.

The first link is to a meta-analysis that combined the results of five MMR-autism studies, and five TCV-autism studies, all of which individually found no associations. Most of the studies in this Taylor 2014 meta-analysis are the same papers reviewed by the IOM, cited above (including some they rejected for having serious methodological limitations); there is one new TCV study (Andrews 2004) and one new MMR study (Uno 2012).

The second link is to an ecological study, Schechter 2008, showing the removal of TCVs did not coincide with any reduction of cases of autism in California. The third link is to the IOM 2004 Report cited above. The fourth link is to the Hviid 2003 study of TCVs-autism. The fifth link is to the Madsen 2002 study of MMR-autism, both in the IOM Reports cited above. The sixth link is to an outdated review of TCVs that does not reference autism. The seventh link is to a statement by the AAP regarding removing thimerosal from vaccines.

Conclusion

There is no evidence cited on the CDC’s “Autism and Vaccines” page to support their claim that vaccines do not cause autism. The only evidence cited relates either to one single vaccine: the MMR, or to one single vaccine ingredient: thimerosal. Even if this evidence is accepted, it does not follow that vaccines do not cause autism.

More studies are needed in order to determine whether vaccines cause autism, starting with the most basic kind: epidemiological studies that compare health outcomes in vaccinated and unvaccinated children.

Interestingly, this was pointed out by the IOM itself in their 2013 report “The Childhood Immunization Schedule and Safety”:

Vaccine Schedule Not Tested

Without any studies looking at autism as a health outcome and comparing vaccinated and unvaccinated groups, there is no support for the CDC’s claim that vaccines do not cause autism. They were right to change the title of their page. They now need to correct the rest of it.

The Vaccine-Autism Hypothesis

This infographic presents some of what we know about immune activation events causing autism and states the vaccine-autism hypothesis.

Given the close association between the immune system activations and autism, supported by animal testing, the vaccine-autism hypothesis is highly plausible.

After all, the purpose of vaccines is to activate the immune system, which is something we know can trigger autism.

Sources are listed and linked below, and I have copied a line from the abstract of each study for the convenience of the reader.

Sources

  1. Hallmeyer, 2015: Autism heritability was estimated to be 38% and the shared environmental component to be 58% https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4440679/
  2. Atladottir, 2010: admission to hospital due to maternal viral infection in the first trimester and maternal bacterial infection in the second trimester were found to be associated with diagnosis of ASDs in the offspring https://www.ncbi.nlm.nih.gov/pubmed/20414802
  3. Zerbo, 2015: women with infections diagnosed during a hospital admission, particularly bacterial infections, were at increased risk of delivering a child with ASD https://europepmc.org/articles/pmc4108569
  4. Vargas, 2005: The brains of people with ASD show a marked activation of microglia and astroglia, and cytokine profiling indicated that MCP-1 and TGF- β1, derived from neuroglia, were the most prevalent cytokines. Cerebrospinal fluid showed a unique proinflammatory profile of cytokines, including a marked increase in MCP-1. https://www.ncbi.nlm.nih.gov/pubmed/15546155
  5. Li, 2015: Neonatal vaccination of rats with bacillus Calmette-Guérin and hepatitis B vaccines modulates hippocampal synaptic plasticity https://www.ncbi.nlm.nih.gov/pubmed/26531688
  6. Wei, 2011: The cerebellum of the brains of people with ASD has increased IL-6, which alters neural cell adhesion, migration and synaptic formation https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3114764/
  7. Abdallah, 2013: The amniotic fluid of mothers of children with ASD showed elevated levels of inflammatory cytokines https://www.ncbi.nlm.nih.gov/pubmed/22175527
  8. Suzuki, 2013: In multiple brain regions in people with ASD there is excessive microglial activation https://www.ncbi.nlm.nih.gov/pubmed/23404112
  9. Jones, 2017: The serum of mothers of children with ASD with ID showed increased levels of maternal cytokines and chemokines during gestation https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5122473/
  10. Tsilioni, 2019: The brains of children with ASD have increase inflammatory cytokines https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6027314/
  11. Smith, 2007: Maternal immune activation (MIA) in mice alters fetal brain development through interleukin-6 https://www.ncbi.nlm.nih.gov/pubmed/17913903
  12. Malkova, 2012: MIA in mice results in offspring that show more autism-like behaviours https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3322300/
  13. Bauman, 2014: MIA in rhesus monkeys yields offspring with abnormal repetitive behaviors, communication, and social interactionshttps://www.ncbi.nlm.nih.gov/pubmed/24011823
  14. Choi, 2016: Either MIA or direct administration to the fetal brain of mice of inflammatory cytokine IL-17a promotes abnormal cortical development and ASD-like behaviors in offspring https://www.ncbi.nlm.nih.gov/pubmed/26822608
  15. Missig, 2018: Early-life immune activation in mice can lead to long-lasting physiologic perturbations that resemble medical comorbidities often seen in ASD and other neuropsychiatric conditions https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5770773/

MMR-Autism Association in DeStefano 2004 Study

William Thompson is the CDC whistleblower who revealed that he had been involved in a cover-up of a key result in the vaccine-autism debate.

He was referring to the DeStefano 2004 study of MMR and autism, on which Thompson was a co-author, conducting the statistical analysis. Thompson claimed that an association between MMR and autism in African American boys was identified in the data, but that the finding was omitted from the final paper. He cited the pressure to show no association between MMR and autism, and explained how they tried various statistical techniques to try to hide the association.

The infographic above presents the data behind the debate. Brian Hooker’s 2014 re-analysis of the data shows there is indeed an association between MMR and autism in African American boys in the data.

Forget the politics; the science here is telling us there is an association between a vaccine and autism.

Sources:

Vaccine Autism Studies are Inadequate

In 2012, the Institute of Medicine (IOM) released a comprehensive evidence review entitled “Adverse Effects of Vaccines: Evidence and Causality”.

They looked at 8 different vaccines and 76 different adverse events. One of these adverse events was autism.

  • For 1 vaccine (MMR), the IOM favored rejection of a causal relationship.
  • For 1 vaccine (DTaP), the IOM declared the evidence inadequate to accept or reject a causal relationship.
  • For the other 6 vaccines in the review, the IOM did not look for any evidence regarding a causal relationship.

Clearly then, the correct conclusion of this evidence is NOT that “vaccines do not cause autism”. There is not enough evidence to make that conclusion.

Even if a causal relationship between MMR and autism is rejected, it does not follow that “vaccine do not cause autism” because MMR is only one of 8 or more vaccines, and the evidence is inadequate to accept or reject a causal relationship for them. There have also been no studies looking for associations between cumulative vaccinations, or different timings, or different combinations of vaccines, and autism.

The CDC cites this IOM report for its claim that “vaccines do not cause autism” and yet this report does not support this claim.

Maternal Immune Activation causes Autism

The diagram in the infographic above comes from:

The CDC Vaccine-Autism Studies

The studies cited by the CDC on their “Vaccine Do Not Cause Autism” page cannot possibly support that claim. The CDC’s conclusion is invalid.

See the infographic above for details about why that is.

Autism Defined

Our understanding and conception of autism has changed considerably over the years, as shown in the infographic above.  

Autism Before 1980

The first recognition of autism only occurred in 1943, and for decades it was believed to be very rare, affecting only 1-in-10,000 children.  The first time the American Psychiatric Association (APA) published their list of all known mental disorders, the prestigious Diagnostic and Statistical Manual of Mental Disorders or DSM-1 (1952), it did not include autism.  It used the word autistic only in reference to one of the behaviours associated with childhood-onset schizophrenia.  Autism was also not listed in the second edition, DSM-2 (1968).

Autism in DSM-3

Autism was first listed as a known mental disorder in DSM-3 in 1980.  A category of neurodevelopmental (early onset) disorders was created called the Pervasive Development Disorders (PDDs), which contained infantile autism for when autistic behaviours appeared before 30 months of age and childhood onset PDD for when they appear after 30 months of age. 

These autistic behaviors include lack of responsiveness to other people, deficits in language development and social relationships, resistance to change, attachment to inanimate objects, anxiety and panic attacks, inappropriate fear or rage reactions, oddities of motor movement, and speech and hyper-sensitivity to sensory stimulation. 

A third PDD was atypical autism, a catch-all for when there were impairments in social skills and language but the criteria for a specific PDD cannot be met.

Autism in DSM-4

The DSM-4 in 1994 introduced three areas of diagnosis for the PDDs: impairments in social interaction, impairments in communication, and restricted, repetitive and stereotyped patterns of behavior, interests and activities.  It also renamed and reformulated the PDDs.

Autistic Disorder required onset before 36 months of age and at least 6 of the 12 impairments listed across the three areas of diagnosis.  Those previously diagnosed with infantile autism would in the new system likely be diagnosed with autistic disorder.  Those previously diagnosed with childhood onset PDD or atypical autism would likely be diagnosed with PDD-NOS (for Not Otherwise Specified), the new catch-all for where there are severe deficits in one of the three areas of diagnosis but the criteria are not met for any of the specific PDDs. 

Three new PDDs were added: Asperger’s Disorder was created for those with impairments in social interaction and restricted behaviours, but no impairments in communication, cognition or language skills, and it was considered “mild autism” or “high-functioning autism”.  The other two new additions were Childhood Disintegrative Disorder (CDD), a sudden and severe regressive disorder in multiple areas of functioning with subsequent onset of autistic behaviors, and Rett’s Disorder, a regressive disorder affecting head growth, motor skills, gait and trunk movements, as well as autistic behaviours.  These are both very rare disorders, and Rett’s Disorder is now considered a genetic brain disorder rather than an autism spectrum disorder or PDD.

Asperger’s makes up 17% of cases of PDD, autistic disorder is 31%, but the largest group is PDD-NOS at 53% (Hviid, 2019).  The addition of Asperger’s Disorder (and to a much lesser extent, CDD and Rett’s) would thus have caused only a small step change – ceteris paribus – in the number of people diagnosed with a PDD, as DSM-4 replaced DSM-3.

Autism in DSM-5

The DSM-5 in 2013 replaced the PDD category entirely and replaced it with Autism Spectrum Disorder (ASD).  The PDDs were already considered a spectrum widely known as the autism spectrum, ranging from the most severe (Autistic Disorder) to the less severe (PDD-NOS and Asperger’s).  Autism was no longer the name of one type of PDD, but the whole category, and it was defined as a single spectrum disorder rather than a category of related disorders with distinct names, as PDD had been.

Within ASD, there is a classification by severity in two dimensions: 1) deficits in social interaction and communication, and 2) restricted, repetitive behavior, interests, or activities.  Three severity levels (mild, moderate and severe) are defined by how much support the individual requires.  Most of those previously diagnosed with autistic disorder would now be diagnosed with moderate or severe ASD (aka autism), while most of those previously diagnosed with Asperger’s disorder would now be diagnosed with mild or moderate autism.  It is possible to be diagnosed as having one severity level for social deficits and a different severity level for restricted behaviors, giving nine possible severity level combinations within the spectrum.

The DSM-5 also created a new neurodevelopmental disorder called Social (Pragmatic) Communication Disorder (SCD) for cases that meet the social deficits criteria for ASD but not the restricted behaviors criteria.   According to one study (Kim, 2014), only 63% of those with a previous diagnosis of PDD-NOS meet the DSM-5 criteria for ASD, with 32% lacking the restrictive behaviours criteria and so would now be diagnosed with SCD, not ASD.  Those previously diagnosed with PDD-NOS who do meet the ASD criteria are likely to have either a mild or moderate DSM-5 severity level (Walker, 2004). 

The impact of a third of those with PDD-NOS (the largest PDD disorder) being taken out of the umbrella of ASD should have a noticeable decrease – ceteris paribus – in autism diagnoses as DSM-5 replaces DSM-4.  The definition of ASD in DSM-5 is tighter than the definition of PDD in DSM-4 and may be tighter than the definition of PDD in DSM-3 as well.

Autism in ICD-10 Codes

The World Health Organisation (WHO) maintains a comprehensive medical coding system known as the International Classification of Diseases (ICD).  The current iteration of this system is ICD-10, which has been used since 1994.  Chapter 5 contains the codes for mental and behavioural disorders (F00-F99) and it has codes for “childhood autism” (F84.0), “atypical autism” (F84.1) and Asperger’s disorder (F84.5), “Other PDD” (F84.8) and “Unspecified PDD” (F84.9) all within the category of pervasive development disorders (F84). 

These five ICD-10 codes are considered to cover the whole autism spectrum and epidemiological studies of autism generally define an outcome of autism as a diagnosis with one of these five ICD-10 codes (for example, Hviid 2019). 

These codes map easily to the disorders in DSM-4 and DSM-3: childhood autism is the same as infantile autism (DSM-3) and autistic disorder (DSM-4); Asperger’s Disorder is defined the same way as in DSM-4; PDD-NOS (DSM-4) is split between ICD codes for atypical autism, other PDD and unspecified PDD, with atypical autism being defined in a way similar to the DSM-3 definition.

Autism Diagnostic Criteria

Despite the many taxonomical changes within the PDD / ASD category of disorders over the years, the diagnostic criteria have been refined and elaborated with each iteration of the DSM, but the basic idea has always been the same.  Autism has always been defined as a disorder with two fundamental defining elements: deficits in social communication and social interaction, and restricted, repetitive patterns of behavior, interests and activities. 

DSM-5 gives the clearest diagnostic criteria for each of these two elements.  It provides three illustrative examples of social deficits, all of which must be met for a diagnosis, and four illustrative examples of restricted behaviors, two of which must be met for a diagnosis.  The examples are:

Persistent deficits in social communication and social interaction across multiple contexts, as manifested by ALL OF the following, currently or by history:

  • Deficits in social-emotional reciprocity, ranging, for example, from abnormal social approach and failure of normal back-and-forth conversation; to reduced sharing of interests, emotions, or affect; to failure to initiate or respond to social interactions.
  • Deficits in nonverbal communicative behaviors used for social interaction, ranging, for example, from poorly integrated verbal and nonverbal communication; to abnormalities in eye contact and body language or deficits in understanding and use of gestures: to a total lack of facial expressions and nonverbal communication.
  • Deficits in developing, maintaining, and understanding relationships, ranging, for example, from difficulties adjusting behavior to suit various social contexts; to difficulties in sharing imaginative play or in making friends; to absence of interest in peers.

Restricted, repetitive patterns of behavior, interests, or activities as manifested by AT LEAST TWO of the following, currently or by history:

  • Stereotyped or repetitive motor movements, use of objects, or speech (e.g., simple motor stereotypies, lining up toys or flipping objects, echolalia, idiosyncratic phrases).
  • Insistence on sameness, inflexible adherence to routines, or ritualized patterns of verbal or nonverbal behavior (e.g., extreme distress at small changes, difficulties with transitions, rigid thinking patterns, greeting rituals, need to take same route or eat same food every day).
  • Highly restricted, fixated interests that are abnormal in intensity or focus (e.g., strong attachment to or preoccupation with unusual objects, excessively circumscribed or perseverative interests).
  • Hyper- or hyporeactivity to sensory input or unusual interest in sensory aspects of the environment (e.g., apparent indifference to pain/temperature, adverse response to specific sounds or textures, excessive smelling or touching of objects, visual fascination with lights or movement).

For a diagnosis of ASD, symptoms must also be present in the early developmental period (but may not become fully manifest until social demands exceed limited capacities, or may be masked by learned strategies in later life), they must cause clinically significant impairment in social, occupational, or other important areas of current functioning, and these disturbances are not better explained by intellectual disability or global developmental delay. 

Clinical Significance

The requirement for onset during the “early developmental period,” meaning early childhood, obviously means that adults cannot develop autism.  However, adults can be and are diagnosed with autism if they are impaired significantly enough by their social deficits and repetitive behaviors today to warrant a diagnosis, without any evidence that their autistic behavior started in the early developmental period.  The age of onset diagnosis criteria is essentially ignored as it is assumed that any adult that meets the criteria for autism today must have been autistic their whole life.

The requirement for “clinically significant impairment” is standard wording throughout the DSM-5 for all mental disorders.  It means that it is left entirely at the discretion of clinicians to judge whether a child (or adult) is impaired *significantly enough* by his social deficits and repetitive behaviors to get a diagnosis of ASD.  Clinicians get to draw the line between marginal cases of mild ASD and no ASD, and where they draw that line is flexible and may have changed over time to include more people: an adult previously considered merely as having autistic-like traits (perhaps an introvert with restricted interests, a geek or an eccentric) may now get a diagnosis of ASD, if he seeks one.  There are incentives for adults to get a diagnosis, for parents and schools to have their children diagnosed, and for clinicians to give diagnoses in marginal cases.  There is a clear danger of over-diagnosis of autism due to the flexibility of the clinical significance requirement, and this must be borne in mind when looking at historical statistics of autism prevalence and incidence.

Conclusion

Clear and well-understood definitions are essential for productive discussion and good science.  When discussing autism, it is important that all the participants understand whether the term is being used:

  • in the wider sense of anyone on the autism spectrum in the DSM-5 conception, roughly equivalent to what DSM-4 called PDDs
  • in the narrower sense of autistic disorder (only 31% of PDDs) in the DSM-4 conception, roughly equivalent to severe autism in the DSM-5 conception. 

The wider sense includes those with Asperger’s (17%) and PDD-NOS (53%), which are likely mild or moderate autism in the DSM-5 conception. 

When discussing autism, when reviewing data from epidemiological studies, comorbidity studies, historical trends, independence surveys, and so on, it is crucial to understand if the data refers to the whole autism spectrum or just those with severe autism, or those with autism and some other condition comorbid with autism, such as a language disorder or intellectual disability.