ArticleBMC psychiatry2025
Exploring causal associations between plasma metabolites and attention-deficit/hyperactivity disorder.
Article in BMC psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundObservational studies reported altered levels of plasma metabolites in attention-deficit/hyperactivity disorder (ADHD). We aim to explore the causal link between plasma metabolites and ADHD.
methodsWe utilized Mendelian randomization (MR) analysis to assess the causal relationship between plasma metabolites and ADHD and the Genome-wide association study (GWAS) summary datasets were sourced from public databases. GWAS summary datasets were used in the study, including ADHD (n = 292,548) and 871 plasma metabolites (n = 8,299). Moreover, we used DrugBank and ChEMBL to evaluate whether the identified metabolites are potential therapeutic targets, and in addition, Bayesian colocalization analyses were conducted to assess the shared genetic signals between these metabolites and ADHD.
resultsOur MR analysis identified 20 plasma metabolites that conferred protective effects against the risk of ADHD, including dimethylglycine, 3-methoxytyramine sulfate, and adenosine 3',5'-cyclic monophosphate (OR: 0.97-0.98). Additionally, 22 metabolites were associated with an increased risk of ADHD, including N-acetylneuraminate and 3-indoleglyoxylic acid (OR:1.01-1.03). Druggability evaluation showed that 12 of the ADHD-related metabolites have been targeted by pharmacological interventions. For example, doconexent has been used to increase the levels of docosahexaenoic acid. Our reverse MR analysis showed that genetic liability to ADHD may affect the abundance of 91 metabolites. Notably, several plasma metabolites had bidirectional causal associations with ADHD, including docosahexaenoate (DHA; 22:6n3), docosatrienoate (22:3n3), N1-methyladenosine, S-adenosylhomocysteine, and 4-allylcatechol sulfate.
conclusionsOur study supported a causal role of plasma metabolites in the susceptibility to ADHD, and the identified metabolites may provide a new avenue for the prevention and treatment of ADHD. CLINICAL TRIAL NUMBER: Not applicable.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.