The past several decades have been met with a roaring increase in the discussions surrounding autism and related disorders that fall within the Autism Spectrum. And with good reason.
First coined in 1910, autism quickly emerged as a notoriously difficult condition to diagnose, given its eerie similarity to other neurodevelopment disorders, specifically childhood schizophrenia. Indeed, it took nearly 70 years of intense research for autism to be diagnosed as a separate disorder (2). Since then, autism prevalence has skyrocketed in Western society; prior to 1980, 1 in 5000 children were diagnosed with autism. Today, an astounding 1 in 68 children possess autism-like symptoms, which include limited social interactions, a tendency for repetitive behaviour and reduced overall communication (3).
Which begs us to ask the question: why?
An enormous array of controversial explanations have been put forward to explain the worrying increase in autism prevalence. The most notorious of which is Andrew Wakefield’s “vaccine hypothesis”, which singled-out the MMR vaccine (Measles, Mumps & Rubella) as the cause of rising autism prevalence (note: Wakefield’s findings have since proven to be falsified and have been retracted from the scientific literature. Read more here: (4))
It was only in the mid 1980s that researchers uncovered that autism had a strong genetic component, wherein certain gene mutations were found to associated with autism (5). The genetic basis became even more clear by the 1990s, when it was discovered that a child was 25-times more likely to be diagnosed with autism if one of their siblings was also diagnosed (6). Since then, an impressive amount of research, made possible by advances in genetic technologies, has identified numerous genes linked to autism (which are summarized in this article: (7)).
While genetics undoubtedly play a role in the development of autism, the last decade saw scientists explore an alternative hypothesis — one that included the microbiome. For years, researchers couldn’t explain the seemingly-odd data that showed — quite conclusively — that women who suffered a high, prolonged fever during pregnancy were seven times more likely to have a child with autism. In 2007, Paul Patterson was able to reproduce this result in mice, such that if he induced a prolonged fever in pregnant mice, then their offspring would display all three features of human autism, including limited social interactions, a tendency for repetitive behaviour and reduced overall communication (8). Patterson also showed that the offsprings also had leaky intestines, which is a critical detail here because anywhere from 40 to 90% of human children with autism also suffer gastrointestinal issues (9).
Then, in 2013, Dr. Sarkis Mazmanian and his research team made the remarkable discovery that these mice had abnormal microbiomes compared to non-autistic mice (10). This finding suggested that the autistic-like behaviour of these mice — and perhaps by extension autistic behaviour in humans — might be partially rooted in the gut rather than entirely in the brain.
If this is true, then treating the gut bacteria should also treat the autism-like symptoms. And indeed, Mazmanian’s research team was able to show that by simply restoring a normal microbiota, the mice also displayed better communication and a decreased tendency towards repetitive behaviour. This heavily implicates our gut bacteria as one of the culprits of autism, and — at least in mice — shows that some features of autism can be reversed by treating an abnormal gut microbiome.
There remains one more twist to this story. Earlier, it was mentioned that a sharp rise in autism prevalence was observed at the end of the 1970s. It turns out that the same can be said for obesity. That is, the rates of both autism and obesity among Westerners seem to have taken off around the same time — the end of the 1970s. This may seem like a simple coincidence (and it very well might be) but consider this: it was during the 1970s that Westerns began to adopt a diet rich in processed foods, sugar-sweetened drinks and a mostly sedentary lifestyle (11). That’s important here because, as we have spoken about in previous blogs, it’s already very well appreciated that our gut bacteria influence our weight (You can read that blog here: http://www.thegutguys.com/myhealth/category/obesity).
Given that our gut bacteria have already been shown to influence weight, and given that autism prevalence spiked once the Western diet was introduced in the late 1970s, is it too far-fetched to assume that they also contribute to autism? Has our adoption of the Western diet molded a “bad” microbiome conducive to both obesity and autism? Although further research is required to fully understand the answer to that question, it definitely deserves its fair share of discussion, as autism prevalence among our children continues to increase at an alarming rate.
1. Muir, H. 2003. Einstein and Newton showed signs of autism. In New Scientist.
2. Wilson, M. 1993. DSM-III and the transformation of American psychiatry: a history. Am. J. Psychiatry 150: 399-410.
3. Centers for Disease Control and Prevention. 2012. Autism Spectrum Disorder — Data & Statistics.
4. Rao, T. S. S., and C. Andrade. 2011. The MMR vaccine and autism: Sensation, refutation, retraction, and fraud. Indian J. Psychiatry 53: 95-96.
5. Blomquist, H. K., M. Bohman, S. O. Edvinsson, C. Gillberg, K. H. Gustavson, G. Holmgren, and J. Wahlstrom. 1985. Frequency of the fragile X syndrome in infantile autism. A Swedish multicenter study. Clin. Genet. 27: 113-117.
6. Jorde, L. B., S. J. Hasstedt, E. R. Ritvo, A. Mason-Brothers, B. J. Freeman, C. Pingree, W. M. McMahon, B. Petersen, W. R. Jenson, and A. Mo. 1991. Complex segregation analysis of autism. Am. J. Hum. Genet. 49: 932-938.
7. Miles, J. H. 2011. Autism spectrum disorders--a genetics review. Genet. Med. 13: 278-294.
8. Malkova, N. V., C. Z. Yu, E. Y. Hsiao, M. J. Moore, and P. H. Patterson. 2012. Maternal immune activation yields offspring displaying mouse versions of the three core symptoms of autism. Brain. Behav. Immun. 26: 607-616.
9. Erickson, C. A., K. A. Stigler, M. R. Corkins, D. J. Posey, J. F. Fitzgerald, and C. J. McDougle. 2005. Gastrointestinal factors in autistic disorder: a critical review. J. Autism Dev. Disord. 35: 713-727.
10. Hsiao, E. Y., S. W. McBride, S. Hsien, G. Sharon, E. R. Hyde, T. McCue, J. A. Codelli, J. Chow, S. E. Reisman, J. F. Petrosino, P. H. Patterson, and S. K. Mazmanian. 2013. Microbiota modulate behavioral and physiological abnormalities associated with neurodevelopmental disorders. Cell 155: 1451-1463.
11. Popkin, B. M., L. S. Adair, and S. W. Ng. 2012. NOW AND THEN: The Global Nutrition Transition: The Pandemic of Obesity in Developing Countries. Nutr. Rev. 70: 3-21.