A neurodevelopmental disease that impacts people’s capacity to learn and their social behaviour is known as autism spectrum disorder (ASD).
The last several decades have seen a rise in understanding of ASD, particularly in relation to its prevalence and impact on the lives of those who have been diagnosed with it.
There is still more research to be done on a number of ASD-related issues, though.
Though the precise origins of ASD remain unknown, the information that is now available suggests that neuroinflammation plays a significant role.
Pregnancy-related exposure to polyunsaturated fatty acids (PUFA) and their metabolites may have a significant impact on the development of ASD, according to several research using mice models of the disorder.
In mice, PUFA metabolites controlled by cytochrome P450 (CYP) impact foetal development, leading to deficits strongly associated with symptoms of ASD. Further research is necessary to determine whether the same holds true for humans, as it is currently uncertain.
In an effort to close this knowledge gap, a Japanese research team led by Professor Hideo Matsuzaki of the University of Fukui’s Research Centre for Child Mental Development, Dr. Takaharu Hirai of the department of psychiatric and mental health nursing at the school of nursing, and Dr. Naoko Umeda of the department of maternal and child health nursing at the same university examined the levels of CYP-PUFA in neonatal umbilical cord blood samples.
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Their research illuminates potential origins of ASD and was published in Psychiatry and Clinical Neurosciences.
Sharing the motivation behind their study, Prof. Matsuzaki explains, “CYP metabolism forms both epoxy fatty acids (EpFAs), which have anti-inflammatory effects, and dihydroxy fatty acids, or ‘diols,’ which have inflammatory properties.
We hypothesized that the dynamics of CYP-PUFA metabolites during the fetal period, that is, lower EpFA levels, higher diol levels, and/or increased EpFA metabolic enzymes would influence ASD symptoms and difficulties with daily functioning in children after birth.”
To test this hypothesis, the researchers investigated the link between PUFA metabolites in umbilical cord blood and ASD scores in 200 children. The cord blood samples had been collected immediately after birth and preserved appropriately, whereas ASD symptoms and adaptive functioning were assessed when the same children were six years old, with the help of their mothers.
After careful statistical analyses of the results, the researchers identified one compound in cord blood that may have strong implications for ASD severity, namely 11,12- dihydroxyeicosatrienoic acids (diHETrE), a dihydroxy fatty acid derived from arachidonic acid.
More specifically, the researchers found that higher levels of the molecule 11,12-diHETrE had an impact on social interactions, whereas low levels of 8,9-diHETrE impacted repetitive and restrictive behaviors. Moreover, this correlation was more specific for girls than for boys.
This newfound knowledge could be crucial in understanding, diagnosing, and potentially preventing ASD. By measuring diHETrE levels at birth, it may be possible to predict the likelihood of ASD development in children
“The effectiveness of early intervention for children with ASD is well established and detecting it at birth could enhance intervention and support for children with ASD,” muses Prof. Matsuzaki. He also adds that inhibiting diHETrE metabolism during pregnancy might be a promising avenue for preventing ASD traits in children, although more research will be needed in this regard.
In conclusion, these findings open a promising avenue for researchers unraveling the mysteries surrounding ASD. We hope that enhanced understanding and early diagnostics will be able to improve the lives of people with ASD and their families.
WITH INPUTS FROM ANI
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