AUTISM SIMPLIFIED
Welcome to Autism Simplified, where we break down complex research papers on autism and make them understandable for everyone! Each episode, we translate the latest studies into everyday language, providing clear insights and explanations that anyone can grasp. Have questions or ideas for future topics? Reach out to us at abaccesscontact@gmail.com and join the conversation in making autism research accessible to all.
At the end of each post, you’ll find a dictionary section, serving as a reference for any unfamiliar terms. If you encounter something you don’t understand, all you need to do is scroll down!
What Is GAPS?
“GAPS” stands for “Gut and Psychology Syndrome,” a concept proposed by Dr. Natasha Campbell-McBride. This theory suggests a link between the health of the gut and various psychological conditions, including autism, ADHD, depression, and more. According to Dr. Campbell-McBride, imbalances in gut flora and integrity can lead to inflammation and dysfunction, affecting not only digestive health but also cognitive and behavioral functioning. The GAPS protocol involves a specific diet and therapeutic interventions aimed at healing the gut lining, rebalancing gut bacteria, and improving overall health.
So, What Is the GAPS diet?
The GAPS diet primarily focuses on removing foods that may contribute to inflammation and gut irritation while emphasizing nutrient-dense, whole foods that support gut healing. The diet consists of:
1.Elimination Phase: This initial phase involves removing potentially inflammatory foods such as grains, refined sugars, processed foods, and certain dairy products. It also eliminates foods that may be difficult to digest, such as starchy vegetables and some fruits.
2.Introduction Phase: During this phase, easily digestible foods are gradually reintroduced, starting with homemade bone broths, fermented foods, and well-cooked vegetables. This phase aims to soothe and heal the gut lining while replenishing beneficial gut bacteria.
3.Full GAPS Diet: Once gut healing progresses and symptoms improve, individuals can transition to the full GAPS diet, which includes a wide variety of nutrient-dense foods such as meats, fish, eggs, non-starchy vegetables, healthy fats, fruits, nuts, and seeds. Grains, legumes, and certain dairy products may still be restricted for some individuals, depending on their tolerance.
The GAPS diet typically bans or restricts the following foods:
1.Grains: Wheat, rice, oats, barley, rye, corn, and other grains are generally avoided due to their potential to irritate the gut lining and contribute to inflammation.
2.Refined Sugars: Foods high in refined sugars, including desserts, candies, sugary beverages, and processed snacks, are eliminated to reduce inflammation and support gut healing.
3.Processed Foods: Processed and packaged foods containing artificial additives, preservatives, and other chemicals are restricted, as they may disrupt gut health and exacerbate symptoms.
4.Starchy Vegetables: Some starchy vegetables, such as potatoes, are limited or avoided during the initial phases of the diet due to their higher carbohydrate content, which can feed harmful gut bacteria.
5.Certain Dairy Products: Dairy products containing lactose (milk sugar) and casein (milk protein), such as cow’s milk, cheese, and yogurt, may be restricted initially. However, homemade fermented dairy products, such as yogurt and kefir, are gradually reintroduced during the protocol.
6.Processed Vegetable Oils: Vegetable oils high in omega-6 fatty acids, such as soybean oil, corn oil, and sunflower oil, are avoided due to their potential to promote inflammation. Instead, healthy fats like olive oil, coconut oil, and animal fats are encouraged.
7.Legumes: Legumes, including beans, lentils, and chickpeas, are often excluded during the initial phases of the diet due to their high carbohydrate and antinutrient content, which can be difficult to digest for some individuals.
It’s important to note that the specific foods banned or restricted on the GAPS diet may vary depending on individual tolerance and progression through the protocol.
Why Does GAPS Ban These foods? Does GAPS work?
To understand why GAPS bans these foods we have to take a step back and compare the guts of neurotypical children to children with autism and understand ‘Whether children with autism spectrum disorder (ASD) have unique gut microbiota profiles or gut dysbiosis compared to neurotypical children’. This comparison can provide valuable insights into how certain dietary components may affect gut health differently in individuals with ASD.
I know you are wondering “Can this extremely-restrictive-diet help my child?” But in order to answer this question we have to first understand what the current literature has to offer.
Exploring the Connection Between Our Gut and Brain: A Comprehensive Analysis
Is There a Connection?
In a recent study Restrepo et al.(2020), researchers evaluated the frequency and severity of gastrointestinal (GI) symptoms (ranging from diarrhea and constipation to gas/bloating and abdominal pain) in preschool‐aged children with ASD compared to children with typical development (TD). They found that children with ASD were almost three times more likely to experience GI symptoms than TD peers. Not only GI symptoms were reported more frequently in children with ASD but children with ASD were also more likely to experience multiple GI symptoms compared to neurotypical children.
Nonetheless, the prevalence of GI symptoms among children with ASD is still unclear as rates vary vastly based on study measures and methodological approaches. Previous research has reported rates ranging from 9% to 91%. It is possible that the differences in frequencies are linked to diverse methodologies used for data collection (parental reports vs. medical records). Meaning that, the true prevalence of these symptoms remain unclear.
Still, there is cumulative data supporting the conclusion that GI symptoms are more frequent and significant in children with ASD than in comparison groups without ASD. The results of the analysis Restrepo et al. (2020), shows that approximately half of the preschool‐aged children with ASD experienced GI symptoms compared to TD children. This percentage is consistent with a literature review of 144 studies dating back to 1980.
While it’s true that there are differences in gastrointestinal (GI) symptoms, this alone isn’t enough to conclusively establish a connection between autism and the gut. However, recent research has shed light on the potential relationship between the two. In 2022, scientists Wan et al. hypothesized that an underdeveloped gut microbiota might be associated with Autism Spectrum Disorder (ASD). The community of microorganisms in the gastrointestinal (GI) tract is known to influence brain physiology and social-behavior via a diverse set of pathways. Given that, this hypothesis suggests that the community of microorganisms in the GI tract can influence brain physiology and social behavior through various pathways.
Wan et al.(2022) found that children with ASD have abnormal development and functional distortions in their gut microbiomes, which are associated with their age and characteristics. They observed an enrichment of potential pathogens, such as Clostridium and Alistipes indistinctus, in the gut microbiomes of children with ASD, while beneficial bacteria such as Faecalibacterium were underrepresented.
In a study conducted by Iglesias-Vázquez et al.(2020), researchers compared the composition of gut microbiota in children with and without Autism Spectrum Disorder (ASD). Interestingly, despite examining 18 studies on gut bacteria in children with and without autism, no significant differences were found in the overall bacterial profiles between the two groups. However, when specifically analyzing the presence of a bacterium called “Clostridium,” it was discovered that 10 out of the 18 studies included in the analysis reported its presence. Remarkably, the percentage difference in the abundance of Clostridium was 4.63 times higher in children with ASD compared to their neurotypical peers.
Suggesting that Clostridium is much more prevalent in the gut microbiota of children with ASD than in neurotypical children.
What is Clostridium?
You might be wondering about Clostridium—it sounds familiar, right? That’s because it was mentioned in the previous study too. If you decide to dive deeper into this topic, you’ll likely encounter the name frequently. But, why?
Because Clostridium has been linked to brain tissue damage and neurological disorders. Spore-forming bacteria like Clostridium release proinflammatory toxins that can reach the brain through blood flow. Similarly, some of the metabolites derived from the activity of Clostridiales have been associated with repetitive behaviors and GI problems in ASD.
Is it Just Clostridiales?
Another fascinating finding of this study, Iglesias-Vázquez et al.(2020), involves short chain fatty acids (SCFAs), produced from fiber fermentation. Short-chain fatty acids play a crucial role in maintaining a healthy gut immune system by controlling gene expression. SCFA can travel to the brain through the bloodstream, where they influence brain development by regulating the production of serotonin and dopamine. Specifically, propionic acid (PPA), produced mainly by Bacteroidetes, is a significant neurotoxic SCFA, especially when its levels are heightened.
This finding is consistent with the findings of Finegold et al. (2002), who observed high levels of PPA in children with ASD who had a high abundance of Bacteroides and Clostridium compared to healthy children. Furthermore, the relationship between high concentrations of PPA and behavioral disorders has been confirmed in various studies on rodents. Considering these researchers, MacFabe DF. et al.(2012) proposed that increased PPA exposure at key neurodevelopmental periods is a major environmental trigger of the brain and behavioral changes observed in ASDs.
PPA is commonly used as a preservative (antifungal) in many processed foods, particularly in refined wheat and dairy products. However, the majority of PPA is produced in the gut lumen by intestinal bacteria.
Lastly, a study conducted by Shultz et al. (2009) comparing rats given PPA to the regular rats. They found cognitive impairments in adult rats given PPA which is consistent with results reported by Trindade et al. (2002) in a study of a rat model of propionic acidemia that involved chronic subcutaneous injections of PPA during early development, followed by water maze testing in adulthood.
Important Note
Clinical findings suggest that inflammation and immune system dysfunction, influenced by the composition of gut bacteria, play crucial roles in the development of gastrointestinal issues and other conditions like Autism Spectrum Disorder (ASD). However, researchers are still investigating whether changes in gut bacteria cause inflammation and immune system imbalances, or if it’s the other way around.
Can the GAPS Diet Help?
While the GAPS diet may benefit some individuals by eliminating foods containing PPA’s such as wheat, dairy, and processed foods, I believe that banning or restricting large food groups, especially in children, may not be advisable in the long run. This is particularly relevant for children with food selectivity issues, as it could further limit their already restricted diet. While reducing processed food consumption is important due to the presence of PPA’s as preservatives, completely cutting out processed foods may severely limit food options, especially if a child’s diet primarily consists of these foods. Especially, again, since there is no research (yet) confirming that there is a correlation between diet and gut microbiota. In fact, the results in research by Wan et al. (2020) showed that diet did not have a statistically significant effect on gut microbiome variation, indicating diet was unlikely to have been a confounding factor. Therefore, a more balanced and individualized approach to dietary interventions may be more appropriate, considering the unique needs and preferences of each child. So, trying an individualized GAPS diet for a short while might be beneficial as many reported!
Dictionary
Inflammation: The body’s response to injury or infection, characterized by redness, swelling, pain, and heat.
Dysfunction: Impaired or abnormal functioning of an organ, system, or process.
Cognitive: Relating to mental processes such as thinking, learning, and memory.
Behavioral: Relating to actions and reactions exhibited by individuals in response to stimuli or situations.
Protocol: A set of rules or guidelines followed in a specific situation or process.
Therapeutic interventions: Treatments or strategies aimed at improving health or relieving symptoms.
Digestive health: The state of well-being of the digestive system, including the stomach, intestines, and associated organs.
Gut lining: The mucous membrane that lines the digestive tract, providing a barrier between the digestive system and the rest of the body.
Rebalancing gut bacteria: Restoring a healthy balance of microorganisms in the digestive tract.
Neurotypical: A term used to describe individuals whose neurological development and function are within the typical range.
Inflammatory foods: Foods that have the potential to cause or exacerbate inflammation in the body.
Nutrient-dense: Foods that provide a high amount of nutrients relative to their calorie content.
Antinutrients: Compounds found in some foods that interfere with the absorption of nutrients or have adverse effects on health.
Microbiota: The community of microorganisms living in a particular environment, such as the gut or skin.
Gastrointestinal (GI) symptoms: Symptoms related to the digestive system, such as diarrhea, constipation, bloating, and abdominal pain.
Neurodevelopmental: Relating to the development of the nervous system, including the brain and spinal cord.
Microbiomes: The collective genomes of microorganisms living in a particular environment.
Pathogens: Microorganisms that cause disease or illness.
Beneficial bacteria: Microorganisms that have a positive impact on health, such as those that aid in digestion or support the immune system.
Clostridium: A genus of bacteria, some species of which can be harmful to humans and are associated with various diseases.
Spore-forming bacteria: Bacteria that have the ability to form dormant spores, allowing them to survive in harsh conditions.
Proinflammatory: Causing or promoting inflammation in the body.
Toxins: Harmful substances produced by living organisms, including bacteria and fungi.
Metabolites: Chemical compounds produced as byproducts of metabolism.
Repetitive behaviors: Behaviors that are repeated in a consistent manner and may be characteristic of certain neurological or psychiatric conditions.
Short-chain fatty acids (SCFAs): Fatty acids with fewer than six carbon atoms, produced by the fermentation of dietary fiber in the gut.
Gene expression: The process by which information from a gene is used to synthesize a functional gene product, such as a protein.
Serotonin and dopamine: Neurotransmitters involved in the regulation of mood, behavior, and other functions in the brain.
Propionic acid (PPA): A short-chain fatty acid produced by the fermentation of dietary fiber in the gut, known for its potential neurotoxic effects.
Preservative: A substance added to foods to prevent spoilage or deterioration.
Omega-6 fatty acids: A type of unsaturated fatty acid found in certain foods, which, when consumed in excess, may contribute to inflammation.
Processed foods: Foods that have been altered from their natural state through cooking, preservation, or other methods.
Neurotoxic: Having the potential to cause harm to the nervous system.
Cognitive impairments: Deficits in cognitive function, such as memory, attention, or problem-solving abilities.
Subcutaneous injections: Injections administered into the fatty tissue layer beneath the skin.
Water maze testing: A behavioral test used to assess spatial learning and memory in animals, typically rodents.
References
Restrepo B, Angkustsiri K, Taylor SL, Rogers SJ, Cabral J, Heath B, Hechtman A, Solomon M, Ashwood P, Amaral DG, Nordahl CW. Developmental-behavioral profiles in children with autism spectrum disorder and co-occurring gastrointestinal symptoms. Autism Res. 2020 Oct;13(10):1778-1789. doi: 10.1002/aur.2354. Epub 2020 Aug 6. PMID: 32767543; PMCID: PMC7689713.
Wan Y, Zuo T, Xu Z, Zhang F, Zhan H, Chan D, Leung TF, Yeoh YK, Chan FKL, Chan R, Ng SC. Underdevelopment of the gut microbiota and bacteria species as non-invasive markers of prediction in children with autism spectrum disorder. Gut. 2022 May;71(5):910-918. doi: 10.1136/gutjnl-2020-324015. Epub 2021 Jul 26. PMID: 34312160.
Iglesias-Vázquez L, Van Ginkel Riba G, Arija V, Canals J. Composition of Gut Microbiota in Children with Autism Spectrum Disorder: A Systematic Review and Meta-Analysis. Nutrients. 2020 Mar 17;12(3):792. doi: 10.3390/nu12030792. PMID: 32192218; PMCID: PMC7146354.
Macfabe DF. Short-chain fatty acid fermentation products of the gut microbiome: implications in autism spectrum disorders. Microb Ecol Health Dis. 2012 Aug 24;23. doi: 10.3402/mehd.v23i0.19260. PMID: 23990817; PMCID: PMC3747729.
Shultz SR, Macfabe DF, Martin S, Jackson J, Taylor R, Boon F, Ossenkopp KP, Cain DP. Intracerebroventricular injections of the enteric bacterial metabolic product propionic acid impair cognition and sensorimotor ability in the Long-Evans rat: further development of a rodent model of autism. Behav Brain Res. 2009 Jun 8;200(1):33-41. doi: 10.1016/j.bbr.2008.12.023. Epub 2008 Dec 30. PMID: 19154758.
Finegold SM, Molitoris D, Song Y, Liu C, Vaisanen ML, Bolte E, McTeague M, Sandler R, Wexler H, Marlowe EM, Collins MD, Lawson PA, Summanen P, Baysallar M, Tomzynski TJ, Read E, Johnson E, Rolfe R, Nasir P, Shah H, Haake DA, Manning P, Kaul A. Gastrointestinal microflora studies in late-onset autism. Clin Infect Dis. 2002 Sep 1;35(Suppl 1):S6-S16. doi: 10.1086/341914. PMID: 12173102.
Trindade VM, Brusque AM, Raasch JR, Pettenuzzo LE, Rocha HP, Wannmacher CM, Wajne M. Ganglioside alterations in the central nervous system of rats chronically injected with methylmalonic and propionic acids. Metab Brain Dis. 2002 Jun;17(2):93-102. doi: 10.1023/a:1015464028616. PMID: 12083341.
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