Is the gut microbiome involved in autism spectrum disorder?

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By: Dr. Shaina Cahill, Ph.D. (Director Medical Communications & Affairs)

The prevalence of Autism Spectrum Disorder (ASD) diagnosis has increased in recent years, currently reported as 1 in 54 children today compared to 1 in 150 children over 20 years ago, in 2000, by the US Centers for Disease Control and Prevention 1–4. This increase in ASD diagnosis is not specific to the US, with ASD diagnosis in China also being reported to have increased from 2.80 per 10 000 in 2000 to 63 per 10 000 in 2015 5–7. As we look to better understand ASD and its core symptom presentation, the connection between the gut (gut microbiome) and autism has become a focus. This is partly fueled by increasing evidence indicating that children with neurodevelopmental disorders, including ASD, suffer from increased gastrointestinal problems and dysbiosis of the gut microbiota, which significantly impacts quality of life 8–10.

Our microbiome is unique and is vital for many functions within the human body, including protection against pathogens, production of essential vitamins, maintenance of intestinal homeostasis, influencing gut-brain communications and modulation of the immune system 11–13. The gut microbiome is host to approximately 100 trillion bacteria, has been linked to many acute and chronic conditions and is critical to our health and wellbeing 11–18. Dysfunction of the gut microbiome (or gut dysbiosis) can trigger infections and has been associated with the development of diseases like inflammatory bowel disease, neuropsychiatric-related diseases, metabolic conditions or even cancer 11,19–24. Research on neuropsychiatric-related diseases shows that gut dysbiosis can lead to neurological changes such as autism, schizophrenia or Parkinson’s disease and can impact the severity of psychiatric disorders, including depression, stress or anxiety 25–33 (Learn more about the gut microbiome HERE).

The link between ASD and the gut microbiome has been highlighted by many recent studies 31,34–41. These findings have motivated an exploration into the connection between the gut microbiome and ASD presentation, with multiple studies supporting a strong relationship between GI symptoms and ASD 2,9,14,42–55. Below are some highlights from the research on the relationship between ASD and GI issues:

1. Gut microbiome development during childhood plays an important role.

Early childhood is a period of significant behavioural, immune and biological development, where a relationship between the gut microbiome and the brain is thought to play an instrumental role 56–60. Gut microbiota are thought to play an essential role in development by assisting in energy metabolism and modulating and programming the immune system 5,60–62. In addition, gut microbiota development is thought to have a close relationship with cognitive development 5,37,63. Abnormal gut development, gut dysbiosis, in childhood may disrupt these critical physiological processes, which may have a long-lasting effect on overall health and the development of various disorders. 5 56,60,61.

Several external factors are thought to impact early gut microbiome development, including mode of delivery, gestational age, infant feeding mode, and antibiotic use 60,64–70. Interestingly, clinical research has shown that children diagnosed with ASD are more likely to have been born by cesarean section, have ear infections, and been exposed to antibiotics 60,71–78.

2. Children diagnosed with ASD have increased GI issues.

Several studies report that children with ASD present with more GI problems, including abdominal pain, constipation, diarrhea, bloating, and/or gastroesophageal reflux, than typically developing (TD) peers 2,9,30,38,43,55,79. Restrepo et al. report that children with ASD were almost three times more likely to experience GI symptoms than typically developing peers, which is in line with others who have reported that the prevalence of GI symptoms ranges from 9% to 96.8% in children diagnosed with ASD 9,38,44,80–82.

In addition, research indicates that children with ASD are more likely to experience multiple GI symptoms presenting with a significantly higher number of GI symptoms than their TD peers (30.6% vs 5.4%) 9. Overall, research shows that GI symptoms are more frequent and significant in children with ASD, significantly reducing the quality of life 9,10,30,43,83,84.

3. The gut microbiome is altered in children diagnosed with ASD.

A large body of research demonstrates that the gut microbiota of children with ASD significantly differs from TD peers 5,8,29,30,38,41,47,53,85–95. Wan et al. also found that children diagnosed with ASD have impaired gut microbiome development, such that the gut microbiota is abnormally developed and underdeveloped compared to age-matched peers 5. While strong evidence indicates that the gut microbiome is altered in children diagnosed with ASD, a link between the specific composition of gut microbiota and ASD susceptibility is not well established 30,87,96,97.

4. There appears to be a connection between GI issues and ASD-related behaviours.

GI symptoms have been reported to be strongly correlated with the severity of autistic-related behaviours 2,8,30,42,45,47,51,53. Multiple studies support a relationship between behavioural and GI symptoms in ASD, such that those with significant GI symptoms tend to exhibit higher levels of repetitive behaviour, sensory hyperreactivity, social withdrawal, lethargy, irritability, aggressive behaviours, self-injurious behaviours, sleep problems, maladaptive behaviours and inappropriate speech 2,9,30,42–44,47–52,54,55,83,98. In addition, the number of GI symptoms is also associated with increased self-injurious behaviours, somatic complaints, reduced sleep duration, and increased sleep problems 9,42,43,46,53,55,98.

Associations between GI symptoms and psychiatric problems, including somatic complaints, internalizing and externalizing problems, oppositional defiant behaviours, and affective disorders, in children diagnosed with ASD, have also been reported 9,45,48,50,54,98

In summary, while it is unknown to what extent autistic-related behaviours correlate with, predict, or are predicted by the gut microbiome, current clinical research provides significant evidence for a relationship between the gut microbiome and ASD. There is also a growing clinical interest in understanding what role the gut microbiome may play in ASD and how modulation of the gut microbiome via Fecal Microbiota Transplant (FMT) may be a promising therapeutic strategy for children diagnosed with ASD.

Our focus at Novel Biome is on supporting autistic children who suffer from digestive symptoms and significant microbiome imbalance to restore their microbiome through Fecal Microbiota Transplantation (FMT).

In health,

Team Novel Biome

References: 1. Baio, J. et al. 2018, 2. Fouquier, J. et al. 2021, , 3. Lombardi, M. & Troisi, J. 2021, 4. Sabit, H. et al. 2021, 5. Wan, Y. et al. 2021, 6. Wang, F. et al. 2018, 7. Zheng, Y. & Zheng, X. 2015, 8. Ding, X. et al. 2020, 9. Restrepo, B. et al. 2020, 10. Yang, Y. et al. 2018, 11. Choi, H. H. & Cho, Y.-S. 2016, 12. Hooper, L. V. et al. 2012, 13. Sommer, F. & Bäckhed, F. 2013, 14. Bresalier, R. S. & Chapkin, R. S. 2020, 15. Chung, H.-J. et al. 2018, 16. Fan, Y. & Pedersen, O. 2021, 17. Perez-Muñoz, M. E. et al. 2017, 18. Wilson, B. C. et al. 2019, 19. Johnson, D. et al. 2020, 20. Lee, L.-H. et al. 2019, 21. Lee, M. & Chang, E. B. 2021, 22. Ser, H.-L. et al. 2021, 23. Ternes, D. et al. 2020, 24. Xu, M.-Q. 2015, 25. Allegretti, J. R. et al. 2019, 26. Dinan, T. G. & Cryan, J. F. 2015, 27. Dinan, T. G. & Cryan, J. F. 2017, 28. Foster, J. A. & McVey Neufeld, K. A. 2013, 29. Huang, H. et al. 2019, 30. Jendraszak, M. et al. 2021, 31. Kang, D.-W. et al. 2017, 32. Luna, R. A. & Foster, J. A. 2015, 33. Vuong, H. E. et al. 2017, 34. Hsiao, E. Y. 2014, 35. Hsiao, E. Y. et al. 2013, 36. Kang, D.-W. et al. 2020, 37. Li, N. et al. 2019, 38. Liu, Z. et al. 2021, 39. Malkki, H. 2014, 40. Sharon, G. et al. 2019, 41. Wang, M. et al. 2019, 42. Adams, J. B. et al. 2011, 43. Chaidez, V. et al. 2014, 44. Ferguson, B. J. et al. 2019, 45. Fulceri, F. et al. 2016, 46. Gorrindo, P. et al. 2012, 47. Huang, M. et al. 2021, 48. Maenner, M. J. et al. 2012, 49. Marler, S. et al. 2017, 50. Mazefsky, C. A. et al. 2014, 51. Nikolov, R. N. et al. 2009, 52. Peeters, B. et al. 2013, 53. Tomova, A. et al. 2015, 54. Valicent-McDermott, M. et al. 2006, 55. Wang, L. W. et al. 2011, 56. Clarke, G. et al. 2014, 57. Diaz Heijtz, R. 2016, 58. Diaz Heijtz, R. et al. 2011, 59. Manco, M. 2012, 60. Milani, C. et al. 2017, 61. Houghteling, P. D. & Walker, W. A. 2015, 62. Zhuang, L. et al. 2019, 63. Mulle, J. G. et al. 2013, 64. Ho, N. T. et al. 2018, 65. Kim, G. et al. 2020, 66. Pannaraj, P. S. et al. 2017, 67. Rodríguez, J. M. et al. 2015, 68. Shao, X. et al. 2017, 69. Shao, Y. et al. 2019, 70. Yang, I. et al. 2016, 71. Bilder, D. et al. 2009, 72. Cryan, J. F. & Dinan, T. G. 2012, 73. Glasson, E. J. et al. 2004, 74. Guinchat, V. et al. 2012, 75. Kolevzon, A. et al. 2007, 76. Lee, E., Cho, J. & Kim, K. Y. 2019, 77. Niehus, R. & Lord, C. 2006, 78. Vargason, T. et al. 2019, 79. Coury, D. L. et al. 2012, 80. Buie, T. et al. 2010, 81. Holingue, C. et al. 2018, 82. Johnson, C. R. et al. 2014, 83. Mazurek, M. O. et al. 2013, 84. Valicenti-McDermott, M. D. et al. 2008, 85. Coretti, L. et al. 2018, 86. De Angelis, M. et al. 2013, 87. De Angelis, M. et al. 2015, 88. Finegold, S. M. et al. 2010, 89. Kang, D.-W. et al. 2013, 90. Liu, S. et al. 2019, 91. Ma, B. et al. 2019, 92. Plaza-Díaz, J. et al. 2019, 93. Pulikkan, J. et al. 2018, 94. Wang, L. et al. 2011, 95. Zhang, M. et al. 2018, 96. Hughes, H. K. et al. 2018, 97. Srikantha, P. & Mohajeri, M. H. 2019, 98. Neuhaus, E. et al. 2018.
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