Component

Epinephrine

Independent small molecule record; interpretation is limited by each linked claim and its study context.

6 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 it acts on

  1. Heat produced by the thermogenic action of adrenaline may represent more than a quarter of total cold thermogenesis, and in winter swimmers shivering was induced later during cooling, after 40 minutes, suggesting an important contribution of non-shivering thermogenesis to the early thermogenic response.

    Epinephrine → Catecholamine-driven cold thermogenesis source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/cold-research/10825419.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "df5b07f571e51ae21572ac56aa97d1a9dffcd44fe8f5ead4c929086cbbd37e62", "start_char": 0, "end_char": 2308, "text_sha256": "df5b07f571e51ae21572ac56aa97d1a9dffcd44fe8f5ead4c929086cbbd37e62"}
    experimental_model
    Cold-adapted winter swimmers and controls during one hour of immersion at 13 degrees C
    exposure
    One hour of cold water immersion at 13 degrees C
    limitations
    A comparison of adapted and unadapted people. The adrenaline contribution to thermogenesis is the authors’ estimate from their thermoregulation data, not a direct measurement of a hormone-driven heat fraction.
    nutrient_topic
    Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Cold water immersion
    organism
    Human
    plain_language
    A quarter of the heat may come from a hormone rather than from muscle shaking.
    primary_references
    [cold-p10825419] Thermoregulation in winter swimmers and physiological significance of human catecholamine thermogenesis. (2000). https://pubmed.ncbi.nlm.nih.gov/10825419/ DOI: 10.1111/j.1469-445x.2000.01909.x
    tissue_or_cell_type
    Whole body thermoregulation

    Cold water immersion: cold sensing, heat production, the catecholamine axis and what repeated exposure changes (2026-09-19) · lines 624–635

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cold-adapted winter swimmers and controls during one hour of immersion at 13 degrees C · source_derived_draft · unverified_draft

    ### cold-catecholamine-thermogenesis-share Heat produced by the thermogenic action of adrenaline may represent more than a quarter of total cold thermogenesis, and in winter swimmers shivering was induced later during cooling, after 40 minutes, suggesting an important contribution of non-shivering thermogenesis to the early thermogenic response. Condition category: normal nutrient_topic: Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: A quarter of the heat may come from a hormone rather than from muscle shaking. organism: Human tissue_or_cell_type: Whole body thermoregulation experimental_model: Cold-adapted winter swimmers and controls during one hour of immersion at 13 degrees C limitations: A comparison of adapted and unadapted people. The adrenaline contribution to thermogenesis is the authors’ estimate from their thermoregulation data, not a direct measurement of a hormone-driven heat fraction. exposure: One hour of cold water immersion at 13 degrees C evidence_span: {"source_cache": "artifacts/cold-research/10825419.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "df5b07f571e51ae21572ac56aa97d1a9dffcd44fe8f5ead4c929086cbbd37e62", "start_char": 0, "end_char": 2308, "text_sha256": "df5b07f571e51ae21572ac56aa97d1a9dffcd44fe8f5ead4c929086cbbd37e62"} [cold-p10825419] Thermoregulation in winter swimmers and physiological significance of human catecholamine thermogenesis. (2000). https://pubmed.ncbi.nlm.nih.gov/10825419/ DOI: 10.1111/j.1469-445x.2000.01909.x
    Complete structured claim and evidence

What acts on it

  1. Human PNMT transfers a methyl group from SAM to norepinephrine during epinephrine synthesis.

    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human enzyme transition-state and inhibitor kinetics; structural analysis.
    limitations
    Shared SAM use does not prove that tyrosine supplementation drains folate, B12 or methionine.
    nutrient_topic
    L-Tyrosine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Tyrosine
    plain_language
    A downstream branch uses a methyl donor from methionine metabolism.
    primary_references
    Transition-State Analogues of Phenylethanolamine N-Methyltransferase. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32702980/ · DOI 10.1021/jacs.0c05446

    L-Tyrosine: catecholamines, thyroid chemistry, pigment, metabolism and cross-nutrient mechanisms (2026-09-19) · lines 44–50

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human enzyme transition-state and inhibitor kinetics; structural analysis. · source_derived_draft · unverified_draft

    ## l-tyrosine-pnmt-methyl A downstream branch uses a methyl donor from methionine metabolism. Human PNMT transfers a methyl group from SAM to norepinephrine during epinephrine synthesis. Model: Human enzyme transition-state and inhibitor kinetics; structural analysis. Limitations: Shared SAM use does not prove that tyrosine supplementation drains folate, B12 or methionine. Evidence access: Primary abstract Transition-State Analogues of Phenylethanolamine N-Methyltransferase. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32702980/ · DOI 10.1021/jacs.0c05446
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Pathogenic CYB561 variants in four patients accompanied very low norepinephrine and epinephrine despite normal plasma DBH activity; impaired intravesicular ascorbate support was the proposed functional block.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Two human families; genetic analysis with supporting Cyb561 knockout mouse results.
    limitations
    The human defect and mouse corroboration are distinct evidence; ordinary dietary vitamin C deficiency was not the intervention.
    nutrient_topic
    L-Tyrosine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Tyrosine
    plain_language
    A normal blood enzyme test can miss a cofactor problem inside a vesicle.
    primary_references
    Mutations in CYB561 Causing a Novel Orthostatic Hypotension Syndrome. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29343526/ · DOI 10.1161/CIRCRESAHA.117.311949
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Tyrosine: catecholamines, thyroid chemistry, pigment, metabolism and cross-nutrient mechanisms (2026-09-19) · lines 52–58

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Two human families; genetic analysis with supporting Cyb561 knockout mouse results. · source_derived_draft · unverified_draft

    ## l-tyrosine-cyb-vesicle A normal blood enzyme test can miss a cofactor problem inside a vesicle. Pathogenic CYB561 variants in four patients accompanied very low norepinephrine and epinephrine despite normal plasma DBH activity; impaired intravesicular ascorbate support was the proposed functional block. Model: Two human families; genetic analysis with supporting Cyb561 knockout mouse results. Limitations: The human defect and mouse corroboration are distinct evidence; ordinary dietary vitamin C deficiency was not the intervention. Evidence access: Primary abstract Mutations in CYB561 Causing a Novel Orthostatic Hypotension Syndrome. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29343526/ · DOI 10.1161/CIRCRESAHA.117.311949
    Complete structured claim and evidence
  2. In 29 high-trait-anxiety participants, lysine plus arginine increased stress-evoked ACTH, cortisol, adrenaline, and noradrenaline responses without changing heart-rate or blood-pressure responses.

    L-Lysine → Neuroendocrine stress response source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Ten-day randomized trial; 3 g/day of each amino acid, followed by public-speaking stress
    limitations
    Small combination trial; authors' proposed normalization is an interpretation, not a proven lysine-specific mechanism.
    organism
    Homo sapiens
    plain_language
    The mixture did not simply suppress all stress hormones.
    primary_references
    [jezova2005] Subchronic treatment with amino acid mixture of L-lysine and L-arginine modifies neuroendocrine activation during psychosocial stress in subjects with high trait anxiety (2005). https://pubmed.ncbi.nlm.nih.gov/16117182/ DOI: 10.1080/10284150500162937
    tissue_or_cell_type
    Blood stress hormones and cardiovascular measurements

    L-Lysine: mechanism-first literature curation (2026-09-17) · lines 739–747

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ten-day randomized trial; 3 g/day of each amino acid, followed by public-speaking stress · source_derived_draft · unverified_draft

    ### lysine-arginine-stress-hormones In 29 high-trait-anxiety participants, lysine plus arginine increased stress-evoked ACTH, cortisol, adrenaline, and noradrenaline responses without changing heart-rate or blood-pressure responses. Plain language: The mixture did not simply suppress all stress hormones. Condition category: normal organism: Homo sapiens tissue_or_cell_type: Blood stress hormones and cardiovascular measurements experimental_model: Ten-day randomized trial; 3 g/day of each amino acid, followed by public-speaking stress limitations: Small combination trial; authors' proposed normalization is an interpretation, not a proven lysine-specific mechanism. [jezova2005] Subchronic treatment with amino acid mixture of L-lysine and L-arginine modifies neuroendocrine activation during psychosocial stress in subjects with high trait anxiety (2005). https://pubmed.ncbi.nlm.nih.gov/16117182/ DOI: 10.1080/10284150500162937
    Complete structured claim and evidence
  3. With propranolol, caffeine-associated insulin and C-peptide responses resembled placebo.

    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Seven healthy men; 5 mg/kg caffeine, 80 mg propranolol, combination or placebo before an oral glucose tolerance test.
    limitations
    Small acute experiment. Beta blockade supports an adrenergic contribution, not proof that it is the only mechanism or that a blocker should be used to counter caffeine.
    nutrient_topic
    Caffeine collection; salts, coffee, species and coexposure contexts retain their identities. · Caffeine
    plain_language
    Blocking beta-adrenergic signaling removed the response in this test.
    primary_references
    Caffeine-induced impairment of glucose tolerance is abolished by beta-adrenergic receptor blockade in humans. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12015346/ · DOI 10.1152/japplphysiol.01229.2001

    Caffeine: receptors, metabolism, nutrient interactions, adaptation and discovery questions (2026-09-18) · lines 500–506

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Seven healthy men; 5 mg/kg caffeine, 80 mg propranolol, combination or placebo before an oral glucose tolerance test. · source_derived_draft · unverified_draft

    ## caf-beta-block Blocking beta-adrenergic signaling removed the response in this test. With propranolol, caffeine-associated insulin and C-peptide responses resembled placebo. Model: Seven healthy men; 5 mg/kg caffeine, 80 mg propranolol, combination or placebo before an oral glucose tolerance test. Limitations: Small acute experiment. Beta blockade supports an adrenergic contribution, not proof that it is the only mechanism or that a blocker should be used to counter caffeine. Evidence access: Primary abstract Caffeine-induced impairment of glucose tolerance is abolished by beta-adrenergic receptor blockade in humans. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12015346/ · DOI 10.1152/japplphysiol.01229.2001
    Complete structured claim and evidence
  4. Caffeine increased plasma epinephrine with or without propranolol.

    Caffeine → Plasma epinephrine concentration source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Seven healthy men; 5 mg/kg caffeine, 80 mg propranolol, combination or placebo before an oral glucose tolerance test.
    limitations
    Small acute experiment. Beta blockade supports an adrenergic contribution, not proof that it is the only mechanism or that a blocker should be used to counter caffeine.
    nutrient_topic
    Caffeine collection; salts, coffee, species and coexposure contexts retain their identities. · Caffeine
    plain_language
    Caffeine changed an adrenergic hormone measurement.
    primary_references
    Caffeine-induced impairment of glucose tolerance is abolished by beta-adrenergic receptor blockade in humans. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12015346/ · DOI 10.1152/japplphysiol.01229.2001

    Caffeine: receptors, metabolism, nutrient interactions, adaptation and discovery questions (2026-09-18) · lines 484–490

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Seven healthy men; 5 mg/kg caffeine, 80 mg propranolol, combination or placebo before an oral glucose tolerance test. · source_derived_draft · unverified_draft

    ## caf-epinephrine Caffeine changed an adrenergic hormone measurement. Caffeine increased plasma epinephrine with or without propranolol. Model: Seven healthy men; 5 mg/kg caffeine, 80 mg propranolol, combination or placebo before an oral glucose tolerance test. Limitations: Small acute experiment. Beta blockade supports an adrenergic contribution, not proof that it is the only mechanism or that a blocker should be used to counter caffeine. Evidence access: Primary abstract Caffeine-induced impairment of glucose tolerance is abolished by beta-adrenergic receptor blockade in humans. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12015346/ · DOI 10.1152/japplphysiol.01229.2001
    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