Evidence map›Paper›PMID 42220619›Full record

ArticleInternational journal of tryptophan research : IJTR2026

Potential Treatment for ADHD Based on Recovery from Tryptophan-Induced Central Fatigue by Powerful Competitive Inhibition of L-System Amino Acid Transporter.

Takanobu Yamamoto, Bianca Koleda-Yamamoto

Abstract read
In one paragraph

Article in International journal of tryptophan research : IJTR, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Takanobu YamamotoDepartment of Psychology, Neurophysiology Section, Tezukayama University, Nara, Japan.ORCID https://orcid.org/0000-0002-6194-537X
Bianca Koleda-YamamotoDepartment of Biomedicine, Auckland University, New Zealand.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fatigability in attention deficit hyperactivity disorder (ADHD) is associated with the characteristic inattention behavior. Evidence has indicated that the administration of branched-chain amino acids (BCAAs) to Nagase analbuminemic rats (NARs), a fatigue-prone animal model of ADHD, diminishes central fatigue. This effect is accompanied by competitive inhibition at the L-system amino acid transporter (LAT), which takes tryptophan into the brain. We investigated whether dietary supplementation with BCAAs plus phenylalanine and methionine (BPM) or BCAAs plus 2-amino-2-norbornanecarboxylic acid (BCAAs + BCH) has the effect of synergistically improving central fatigue in rats and humans compared with BCAAs alone. NAR performed exercise duration for 420 minutes (5 out of 5 rats; n = 5/5) using BPM and 542 minutes (n = 5/5) using BCAA + BCH. These were significantly longer than when saline or BCAA alone were administered to rats. When administering BPM supplements to human subjects, they found an efficacy rate of 50% in reducing fatigue compared to a placebo, compared to 38% for BCAA alone. Central fatigue in rats and humans was caused by a common mechanism involving tryptophan as an inducing trigger, and BPM supplementation contributed to the strong amplification effect of competitive inhibition at the LAT, the addition of phenylalanine and methionine. These powerful nutritional strategies improved exercise performance and mood beyond the physiological limits of fatigue. BPM, the natural nutrients, can promote the improvement of ADHD symptoms in humans. Prior to treatment with conventional monoamine reuptake inhibitors, it is necessary to eliminate fatigue by BPM treatment, which is the causative basis of ADHD.

Indexed as

ADHDbranched-chain amino acidscentral fatigueL-system amino acid transportermethionineNagase analbuminemic ratsphenylalanine

Identifiers

PMID42220619
PMCPMC13219888

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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 OpenQuestion graph.