Another study causally linking PUFA with a chronic, debilitating disease. Namely, it appears that PUFA is capable of causing autism in both humans and animals, which suggests that the detrimental effects of PUFA is generic and likely applies not only to other species, but to other diseases as well. More specifically, the study below demonstrated that a dihydroxy-metabolite of the PUFA arachidonic acid (itself highly inflammatory even when intact) can reliably cause autism symptoms in animals and is causally linked to autism development and severity in humans. While the study implicated only one PUFA metabolite so far, there are other studies demonstrating that arachidonic acid, and even its precursor linoleic acid, are also linked to autism development. As such, the best option is to avoid dietary PUFA altogether instead of trying to modulate/block its downstream metabolites (which is what the study below is suggesting as therapy), of which undoubtedly there are many yet to be discovered. Finally, considering that inflammation has already been confirmed to be a major component in both autism and virtually all other chronic disease, I think it would not be far-fetched to conclude that PUFA is a major causal factor for all chronic diseases known to medicine so far, so its avoidance becomes that much more important.
https://www.thelancet.com/journals/ebiom/article/PIIS2352-3964(20)30292-9/fulltext
https://onlinelibrary.wiley.com/doi/10.1002/aur.2365
http://dx.doi.org/10.1111/pcn.13710
https://www.sciencedaily.com/releases/2024/07/240729104241.htm
“…Although the exact causes of ASD are unclear, currently available evidence points to neuroinflammation as a major factor. Several studies in mouse models of ASD have hinted at the importance of polyunsaturated fatty acids (PUFA) and their metabolites during pregnancy in playing a key role in ASD development. PUFA metabolites regulated by the cytochrome P450 (CYP) affect fetal development in mice causing impairments closely linked to ASD symptoms. However, it is still unclear if the same is true for humans and needs further investigation.”
“…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. “The levels of diHETrE, an arachidonic acid-derived diol, in cord blood at birth significantly impacted subsequent ASD symptoms in children and were also associated with impaired adaptive functioning. These findings suggest that the dynamics of diHETrE during the fetal period is important in the developmental trajectory of children after birth,” highlights Prof. Matsuzaki.”
“…”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.”
