Assessment & Research

Metabolomic Profiles in Jamaican Children With and Without Autism Spectrum Disorder.

Yazdani et al. (2025) · Journal of autism and developmental disorders 2025
★ The Verdict

Jamaican kids with ASD carry a clear blood signature—three fatty acids and sarcosine—that echoes earlier urine and adult data and may soon guide diagnosis or diet.

✓ Read this if BCBAs who work with autistic children in medical partnership clinics.
✗ Skip if RBTs looking solely for behavior-reduction protocols.

01Research in Context

01

What this study did

Yazdani et al. (2025) compared blood chemicals in Jamaican children with and without autism.

They drew one tube of plasma from each child and ran a metabolomics screen.

The lab hunted for small molecules that differed between the two groups.

02

What they found

Four plasma chemicals stood out.

Three were fatty acids; the fourth was the amino acid sarcosine.

All four levels were shifted in the ASD group, giving a possible fingerprint for the diagnosis.

03

How this fits with other research

Lussu et al. (2017) saw a similar pattern in Italian kids, but they used urine instead of blood.

The body fluids differ, yet both studies point to the same metabolic disruption—an apparent contradiction that actually strengthens the signal.

Nickel et al. (2023) moved the lens to adults and again found odd fatty-acid profiles, showing the pattern may last across the lifespan.

Burack et al. (2004) first flagged low carnitine in ASD; Akram’s fatty-acid shifts now give the modern, detailed update.

04

Why it matters

You can’t run metabolomics in clinic tomorrow, but you can watch for signs of mitochondrial or fatty-acid issues.

If a child shows fatigue, low muscle tone, or picky eating heavy on carbs, mention the Akram findings when you refer to the pediatrician.

Tracking these subtle chemistry clues may soon give BCBAs and doctors a joint biomarker to confirm diagnosis or guide diet choices.

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Flag any child on your caseload with chronic fatigue or dairy refusal and share the Akram paper with the supervising physician.

02At a glance

Intervention
not applicable
Design
quasi experimental
Sample size
400
Population
autism spectrum disorder, neurotypical
Finding
positive

03Original abstract

Autism spectrum disorder (ASD) is a complex neurodevelopmental condition with a wide range of behavioral and cognitive impairments. While genetic and environmental factors are known to contribute to its etiology, metabolic perturbations associated with ASD, which can potentially connect genetic and environmental factors, remain poorly understood. Therefore, we conducted a metabolomic case-control study and performed a comprehensive analysis to identify significant alterations in metabolite profiles between children with ASD and typically developing (TD) controls in order to identify specific metabolites that may serve as biomarkers for the disorder. We conducted metabolomic profiling on plasma samples from participants in the second phase of Epidemiological Research on Autism in Jamaica, an age and sex-matched cohort of 200 children with ASD and 200 TD controls (2-8 years old). Using high-throughput liquid chromatography-mass spectrometry techniques, we performed a targeted metabolite analysis, encompassing amino acids, lipids, carbohydrates, and other key metabolic compounds. After quality control and missing data imputation, we performed univariable and multivariable analysis using normalized metabolites while adjusting for covariates, age, sex, socioeconomic status, and child's parish of birth. Our findings revealed unique metabolic patterns in children with ASD for four metabolites compared to TD controls. Notably, three metabolites were fatty acids, including myristoleic acid, eicosatetraenoic acid, and octadecenoic acid. The amino acid sarcosine exhibited a significant association with ASD. These findings highlight the role of metabolites in the etiology of ASD and suggest opportunities for the development of targeted interventions.

Journal of autism and developmental disorders, 2025 · doi:10.1016/j.jbi.2016.01.012