Although estimates vary widely, some studies have concluded that up to 90 percent of autistic children suffer from gut related problems with new research revealing that the same gene mutations that are found both in the brain and the gut — could be the cause.
Research confirms gut-brain connection in autism — Science Daily
The following recent findings have provided a basic summary of gut-related issues in ASD and the Gut-Brain Connection in ASD:
Gastrointestinal symptoms are very common in people with ASD. These include constipation, diarrhea, gas, bloating, reflux, and abdominal pain. These symptoms are connected to the severity of ASD symptoms, with more severely impaired children exhibiting more GI-related issues. The term “gut microbiome” refers to the community of microorganisms that inhabit the gut, and includes both helpful and harmful bacteria. Kids with autism who have GI symptoms seem to have less diversity of bacteria in their gut, higher levels of harmful bacteria, and lower levels of specific beneficial bacteria.
Gut microbiota has become an issue of great importance recently due to its major role in autism spectrum disorder (ASD). Over the past three decades, there has been a sustained research activity focused to explain the actual mechanism by which gut microbiota triggers/develops autism.
Several genetic and epigenetic factors are involved in this disorder, with epigenetics being the most active area of research. Although the constant investigation and advancements, epigenetic implications in ASD still need a deeper functional/causal analysis.
The following review (Gut microbiota metabolites in autistic children: An epigenetic perspective), describes the major gut microbiota metabolites and how they induce epigenetic changes in ASD along with interactions through the gut-brain axis.
In addition, the role for DNA methylation in autism spectrum disorder has been supported by evidence from different research studies. The mechanism of such epigenetic changes is still mysterious and likely to be heterogeneous in nature; it could be due to changes in transcription levels of critical gene products during certain stages of brain development, caused by genetic and/or environmental factors.
Further studies in identification of loci of promoters, miRNA or other genetic signatures affected by such epigenetic changes would help in better prevention of the recent epidemics of autism spectrum disorder.
https://www.sciencedirect.com/science/article/pii/S2405844021002103
Further Reading
The Gut Microbiota and Autism Spectrum Disorders
https://www.frontiersin.org/articles/10.3389/fncel.2017.00120/full
Gut Microbiota & Olive Oil
Modulation of the Gut Microbiota by Olive Oil Phenolic Compounds: Implications for Lipid Metabolism, Immune System, and Obesity
There is extensive information of the beneficial effects of virgin olive oil (VOO), especially on cardiovascular diseases. Some VOO healthy properties have been attributed to their phenolic-compounds (PCs).
The aim of this review is to present updated data on the effects of olive oil (OO) PCs on the gut microbiota, lipid metabolism, immune system, and obesity, as well as on the crosstalk among them. We summarize experiments and clinical trials which assessed the specific effects of the olive oil phenolic-compounds (OOPCs) without the synergy with OO-fats. Several studies have demonstrated that OOPC consumption increases Bacteroidetes and/or reduces the Firmicutes/Bacteroidetes ratio, which have both been related to atheroprotection. OOPCs also increase certain beneficial bacteria and gut-bacteria diversity which can be therapeutic for lipid-immune disorders and obesity. Furthermore, some of the mechanisms implicated in the crosstalk between OOPCs and these disorders include antimicrobial-activity, cholesterol microbial metabolism, and metabolites produced by bacteria. Specifically, OOPCs modulate short-chain fatty-acids produced by gut-microbiota, which can affect cholesterol metabolism and the immune system, and may play a role in weight gain through promoting satiety. Since data in humans are scarce, there is a necessity for more clinical trials designed to assess the specific role of the OOPCs in this crosstalk.
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