Component

Human depressive relapse during acute tryptophan depletion

Context-specific entity; species, compartment and exposure are stated on each claim.

1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. During depletion, 8/15 fluoxetine responders relapsed versus 1/15 desipramine responders; significant depressive symptoms did not occur in control sessions.

    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Randomized antidepressant assignment followed by crossover depletion testing of responders.
    limitations
    Does not prove that depression generally results from low dietary tryptophan or that supplementation treats it.
    nutrient_topic
    Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
    plain_language
    The response depended on which treatment had produced remission.
    primary_references
    Tryptophan-depletion challenge in depressed patients treated with desipramine or fluoxetine: implications for the role of serotonin in the mechanism of antidepressant action. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10418696/ · DOI 10.1016/s0006-3223(99)00014-1
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 154–160

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Randomized antidepressant assignment followed by crossover depletion testing of responders. · source_derived_draft · unverified_draft

    ## tryptophan-antidepressant-context The response depended on which treatment had produced remission. During depletion, 8/15 fluoxetine responders relapsed versus 1/15 desipramine responders; significant depressive symptoms did not occur in control sessions. Model: Randomized antidepressant assignment followed by crossover depletion testing of responders. Limitations: Does not prove that depression generally results from low dietary tryptophan or that supplementation treats it. Evidence access: Primary abstract Tryptophan-depletion challenge in depressed patients treated with desipramine or fluoxetine: implications for the role of serotonin in the mechanism of antidepressant action. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10418696/ · DOI 10.1016/s0006-3223(99)00014-1
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards