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Autism spectrum disorder (ASD) is a complex neurodevelopmental condition affecting approximately 1 in 44 children by age 8. Emerging research suggests a link between ASD and abnormal lipid metabolism, particularly involving polyunsaturated fatty acids (PUFAs). This study, part of the Hamamatsu Birth Cohort for Mothers and Children (HBC Study), investigates the relationship between PUFA metabolites in neonatal cord blood and subsequent ASD symptoms and adaptive functioning in children.

Methods

This prospective cohort study utilized cord blood samples from 200 children to quantify PUFA metabolites processed by the cytochrome P450 (CYP) pathway. The study focused on the Autism Diagnostic Observation Schedule (ADOS-2) for assessing ASD symptoms and the Vineland Adaptive Behaviors Scales, Second Edition (VABS-II) for evaluating adaptive functioning at age 6.

Key Findings

Association with ASD Symptoms:

High levels of 11,12-dihydroxyeicosatrienoic acid (11,12-diHETrE), a diol derived from arachidonic acid, were significantly associated with increased ASD symptom severity (P = 0.0003) and impairments in socialization (P = 0.004).

Specific impacts were noted in the social affect domain of ASD symptoms with high 11,12-diHETrE levels (P = 0.002), while low levels of 8,9-diHETrE correlated with repetitive/restrictive behavior (P = 0.003).

Gender-Specific Findings:

The associations between diHETrE levels and ASD symptoms showed notable specificity, particularly among female participants.

Discussion

These results highlight the critical role of dihydroxy fatty acids, specifically diHETrE, during the fetal period in influencing the developmental trajectory of ASD. The study's findings underscore the importance of understanding the metabolic pathways and their products, such as CYP-PUFA metabolites, in neurodevelopment and ASD pathophysiology.

Broader Implications

ASD has been previously linked to immune dysfunction and neuroinflammation. Studies have shown that maternal immune activation (MIA) during pregnancy, including exposure to inflammatory cytokines, can lead to ASD-like behaviors in offspring. The current study's findings align with this body of research, suggesting that maternal and fetal inflammatory states, mediated by metabolites like diHETrE, play a significant role in ASD development.

The metabolism of PUFAs via the CYP pathway results in both anti-inflammatory epoxy fatty acids (EpFAs) and pro-inflammatory dihydroxy fatty acids (diols). This balance between EpFAs and diols could influence neurodevelopmental outcomes. For instance, EpFAs have been shown to prevent inflammatory cytokine transcription, while diols promote inflammatory responses through monocyte motility.

Future Research

Further research is necessary to explore the therapeutic potential of modulating sEH activity and PUFA metabolites in preventing or mitigating ASD symptoms. The findings from this study open avenues for exploring the biochemical underpinnings of ASD and highlight the importance of early biomarkers for predicting neurodevelopmental outcomes.

In Closing

The HBC Study provides compelling evidence that the dynamics of PUFA metabolites, specifically diHETrE, during the fetal period are crucial in the developmental trajectory of ASD. These insights pave the way for future research into targeted interventions and underscore the importance of prenatal health in preventing ASD.

By AUTISM LATINO MAGAZINE in Association with BLOCK WORK MEDIA GROUP

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DATA SOURCE: Arachidonic acid‐derived dihydroxy fatty acids in neonatal cord blood relate symptoms of autism spectrum disorders and social adaptive functioning: Hamamatsu Birth Cohort for Mothers and Children (HBC Study) - Hirai - Psychiatry and Clinical Neurosciences - Wiley Online Library