The word “autism” conjures up a number of different images, which vary widely depending on the person. Traditionally thought of as a very debilitating disorder of neural development, the public awareness of autism has grown and expanded with time.1 With the elimination of Asperger’s from the DSM-5, and its replacement with just ‘autism’ (with accompanying degrees of severity);2 patients now vary widely, from barely functioning to highly functioning. This fascinating condition has no cure, and its causation, and/or mechanism of action, remains a mystery.3 Humans with autism typically exhibit impaired social skills, apparent lack of empathy for others, and repetitive movement patterns. Depending on the severity, altered cognitive function is also observed.4 It is important to note that autism is diagnosed on a spectrum, meaning that someone with high functioning autism may have a near-genius level IQ, but someone lower on the spectrum may not.
As we look into the science behind autism, we see that nerve cells and synapses are altered, both in organization and connectivity.5 How exactly these are altered, is not well understood. One interesting fact regarding prevalence of autism, is that males are four times as likely to be diagnosed as females.6 The underlying cause of this discrepancy is not understood or agreed upon. Within the first 3 years of a child’s life, autism symptoms are usually observed, and hopefully diagnosed. With proper forms of therapy, quality of life can improve. However, heartbreakingly, oftentimes people with autism cannot live alone in adulthood.7 The social aspects of autism are heartbreaking and frustrating, both for those suffering from it, and those related to them. As reported in a study8 by Audrey F. Burgess and Steven E. Gutstein “children with high-functioning autism suffer from more intense and frequent loneliness compared to non-autistic peers, despite the common belief that children with autism prefer to be alone. Making and maintaining friendships often proves to be difficult for those with autism. For them, the quality of friendships, not the number of friends, predicts how lonely they feel.” Keep in mind that this quote refers to HIGH functioning forms of autism. Imagine how a child lower on the spectrum may feel.
But what does diet have to do with a neurological development disorder? Well, as is becoming increasingly well known in the scientific community,9 important neurotransmitters like serotonin are all altered by dietary choices.10 So what does the scientific literature say about autism and diet? In short, quite a bit.11 The anti-inflammatory effects of a diet based on real, whole foods, such as the Paleo Diet, will certainly help many biomarkers related to autism12, 13 To what degree, is still being debated.
Via what mechanism can food alter brain activity? Well, exorphins from grains and dairy can cross the blood-brain barrier and act as opioids in the brain.14 Yes, you read that correctly. Since sufferers of autism typically exhibit ‘leaky gut,’15 the proposed mechanism of action is that these exorphins make their way to the brain, and cause developmental delays.16 This is backed up by different studies,17 and is linked with celiac disease and other conditions like schizophrenia.18 The same mechanism, albeit with addiction-like properties, can be implicated in those suffering from binge eating and obesity, as well.19
There are even more interesting theories, such as the one proposed by John Cannell, M.D., relating low vitamin D levels and damage to the brain.20 As Cannell writes “if your genetics deal you low numbers of VDRs and you have to deal with vitamin D deficiency as well, your developing brain loses. The autism geneticists have been looking for mutations. It is not a mutation; the small de novo mutations they do find (in all 23 pairs of chromosomes) are effects, not causes, of autism because vitamin D deficiency impairs DNA repair mechanisms.”21 This is particularly ground breaking research that deserves more recognition. As Emily Deans, M.D., has also excellently pointed out,22 autism and schizophrenia both exhibit similar gene deletion syndromes, like 1q21.1 deletion syndrome.23 Coincidence? Maybe. But this is certainly an interesting hypothesis.
While no doubt autism and diet are still somewhat controversially linked, it is definitely worth a families’ time and effort to try out a Paleo Diet, because the results can be life-changing. Someone suffering with this disorder deserves the best quality of life possible.
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2. Huerta M, Bishop SL, Duncan A, Hus V, Lord C. Application of DSM-5 criteria for autism spectrum disorder to three samples of children with DSM-IV diagnoses of pervasive developmental disorders. Am J Psychiatry. 2012;169(10):1056-64.
3. Shelton JF, Hertz-picciotto I, Pessah IN. Tipping the balance of autism risk: potential mechanisms linking pesticides and autism. Environ Health Perspect. 2012;120(7):944-51.
4. Dawson G, Webb SJ, Wijsman E, et al. Neurocognitive and electrophysiological evidence of altered face processing in parents of children with autism: implications for a model of abnormal development of social brain circuitry in autism. Dev Psychopathol. 2005;17(3):679-97.
5. Gutierrez RC, Hung J, Zhang Y, Kertesz AC, Espina FJ, Colicos MA. Altered synchrony and connectivity in neuronal networks expressing an autism-related mutation of neuroligin 3. Neuroscience. 2009;162(1):208-21.
6. Newschaffer CJ, Croen LA, Daniels J, et al. The epidemiology of autism spectrum disorders. Annu Rev Public Health. 2007;28:235-58.
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8. Quality of Life for People with Autism: Raising the Standard for Evaluating Successful Outcomes. Child and Adolescent Mental Health. 12(2):80.
9. Available at: http://www.washingtonpost.com/national/health-science/can-what-you-eat-affect-your-mental-health-new-research-links-diet-and-the-mind/2014/03/24/c6b40876-abc0-11e3-af5f-4c56b834c4bf_story.html. Accessed May 16, 2014.
10. Young SN. How to increase serotonin in the human brain without drugs. J Psychiatry Neurosci. 2007;32(6):394-9.
11. Available at: http://www.ncbi.nlm.nih.gov/pmc/?term=autism diet. Accessed May 16, 2014.
12. Herbert MR, Buckley JA. Autism and dietary therapy: case report and review of the literature. J Child Neurol. 2013;28(8):975-82.
13. Nadon G, Feldman DE, Dunn W, Gisel E. Association of sensory processing and eating problems in children with autism spectrum disorders. Autism Res Treat. 2011;2011:541926.
14. Available at: http://www.childrensdisabilities.info/allergies/developmentaldisordersprotein7.html. Accessed May 16, 2014.
15. De magistris L, Familiari V, Pascotto A, et al. Alterations of the intestinal barrier in patients with autism spectrum disorders and in their first-degree relatives. J Pediatr Gastroenterol Nutr. 2010;51(4):418-24.
16. Elder JH. The gluten-free, casein-free diet in autism: an overview with clinical implications. Nutr Clin Pract. 2008;23(6):583-8.
17. Dubynin VA, Malinovskaia IV, Beliaeva IuA, et al. [Delayed effect of exorphins on learning of albino rat pups]. Izv Akad Nauk Ser Biol. 2008;(1):53-60.
18. Severance EG, Alaedini A, Yang S, et al. Gastrointestinal inflammation and associated immune activation in schizophrenia. Schizophr Res. 2012;138(1):48-53.
19. Drewnowski A, Krahn DD, Demitrack MA, Nairn K, Gosnell BA. Naloxone, an opiate blocker, reduces the consumption of sweet high-fat foods in obese and lean female binge eaters. Am J Clin Nutr. 1995;61(6):1206-12.
20. Cannell JJ, Grant WB. What is the role of vitamin D in autism?. Dermatoendocrinol. 2013;5(1):199-204.
21. John Cannell, M. (2014). Mechanism of action in autism? | Vitamin D Council. [online] Vitamindcouncil.org. Available at: https://www.vitamindcouncil.org/the-paleo-diet-blog/mechanism-of-action-in-autism/ [Accessed 16 May. 2014].
22. Available at: http://www.psychologytoday.com/the-paleo-diet-blog/evolutionary-psychiatry/201104/diet-and-autism-newer-studies-and-intriguing-links. Accessed May 16, 2014.
23. Bottillo I, Castori M, De bernardo C, et al. Prenatal diagnosis and post-mortem examination in a fetus with thrombocytopenia-absent radius (TAR) syndrome due to compound heterozygosity for a 1q21.1 microdeletion and a RBM8A hypomorphic allele: a case report. BMC Res Notes. 2013;6:376.