{
  "snapshot": "44e259f029212318da5739eca7156c9e8cbffc25e5063306c2e960af9795426b",
  "query": "cortisol feedback",
  "passages": [
    {
      "id": "e_5189388d54cb7637f6618812:p00004",
      "entity_id": "e_5189388d54cb7637f6618812",
      "heading": "Interactions & Feedback",
      "text": "Antagonizes insulin (steroid diabetes in excess) and growth hormone's anabolic action; permissive to catecholamines.\n\nSuppresses the reproductive axis — stress-induced amenorrhea is cortisol quieting GnRH.\n\nWeak mineralocorticoid activity at the mineralocorticoid receptor, where 11β-HSD2 protects by deactivating cortisol in the kidney.\n\nAldosterone handles salt; cortisol handles stress — the adrenal cortex's division of labor (see the cortisol compound entry).",
      "source_ids": [
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        "s_1bf6f54a12d48a03a74eb33e"
      ],
      "source_scope": "page",
      "name": "Cortisol",
      "url": "https://teahann.com/human/hormone/cortisol"
    },
    {
      "id": "e_c249457401be6631829b559e:p00002",
      "entity_id": "e_c249457401be6631829b559e",
      "heading": "Pathway Steps",
      "text": "chronic-psychophysical-stress → hpa-axis-dysregulation — via sustained cortisol elevation + reduced negative feedback sensitivity. Chronic physical or psychological stress dysregulates the HPA axis — flattening cortisol rhythms and impairing feedback — a state linked to fatigue and metabolic/mood disturbance. This maladaptive stress response is the target adaptogens are proposed to normalize.\nadaptogen-extract → normalized-hpa-output — via mechanism varies — monoamine modulation + HSP induction + cortisol-curve flattening. Adaptogens (Rhodiola, ashwagandha, Eleutherococcus) are proposed stress-response modulators that nudge a dysregulated HPA axis back toward balance (a hormesis/“eustress” concept) rather than simply stimulating or sedating. Clinical evidence is mixed and mechanisms remain incompletely defined.",
      "source_ids": [
        "s_b6a70491aedbee4418c9e366",
        "s_fa96f24445c5f6003d112fe4"
      ],
      "source_scope": "page",
      "name": "Adaptogen HPA / cortisol stress modulation",
      "url": "https://teahann.com/human/pathway/adaptogen_hpa_stress_modulation"
    },
    {
      "id": "e_0f9b6fba0cfc517adf8622e9:p00001",
      "entity_id": "e_0f9b6fba0cfc517adf8622e9",
      "heading": "Pharmacological Mechanism",
      "text": "Principal human glucocorticoid. Synthesised from cholesterol in the zona fasciculata under HPA-axis control (CRH → ACTH → cortisol). Binds GR → nuclear translocation → transactivation (anti-inflammatory genes) and transrepression (NF-κB, AP-1). Diurnal peak 06:00–08:00, nadir 00:00. Negative feedback at hypothalamus + pituitary.",
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        "s_fabca47588d894c80191959d",
        "s_ffa055f74897147110b300c7"
      ],
      "source_scope": "page",
      "name": "Cortisol",
      "url": "https://teahann.com/human/compound/cortisol"
    },
    {
      "id": "e_5189388d54cb7637f6618812:p00001",
      "entity_id": "e_5189388d54cb7637f6618812",
      "heading": "Secretion & Regulation",
      "text": "Released under ACTH command from the pituitary, itself driven by CRH — the three-tiered HPA axis.\n\nStrong circadian programming: the pre-waking peak prepares glucose for the day; the midnight trough is the body's nightly reset. Losing this rhythm is a hallmark of Cushing syndrome regardless of level.\n\nNegative feedback at hypothalamus and pituitary — the loop dexamethasone suppression testing interrogates.\n\nPhysical stress (surgery, hypoglycemia, pain, fever) overrides the rhythm: in critical illness, cortisol is high at 3 AM if it needs to be.",
      "source_ids": [
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        "s_1bf6f54a12d48a03a74eb33e"
      ],
      "source_scope": "page",
      "name": "Cortisol",
      "url": "https://teahann.com/human/hormone/cortisol"
    },
    {
      "id": "e_04ae60d299ea8b20330d3e7e:p00004",
      "entity_id": "e_04ae60d299ea8b20330d3e7e",
      "heading": "Interactions & Feedback",
      "text": "Sits mid-axis: CRH above, cortisol below; dexamethasone suppression testing reads the loop's integrity.\n\nLost adrenal feedback in primary adrenal failure drives ACTH to extreme levels; an ACTH-secreting pituitary adenoma suppresses the rest of the axis (Cushing disease).\n\nVasopressin synergizes with CRH to amplify release during severe stress.",
      "source_ids": [
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        "s_4ad1487642b0b5cbc9b53f28",
        "s_d9f3874b0ecbd6319674927b"
      ],
      "source_scope": "page",
      "name": "Adrenocorticotropin (ACTH)",
      "url": "https://teahann.com/human/hormone/adrenocorticotropin"
    },
    {
      "id": "e_36e515c032918a3b9820780f:p00004",
      "entity_id": "e_36e515c032918a3b9820780f",
      "heading": "Interactions & Feedback",
      "text": "T4 → T3 → pituitary/hypothalamic feedback is the loop; T4 alone (as levothyroxine) is enough, because the body converts what it needs.\n\nCortisol and starvation lower T4-to-T3 conversion (euthyroid sick syndrome) — the body idles its engine in famine and illness.\n\nSelenium-dependent deiodinases do the conversion — a micronutrient link to thyroid economy.",
      "source_ids": [
        "s_6e3a22b10880867869ef522d",
        "s_4e4501767f002b139ac212c0",
        "s_115419b5d61e6bcf46812f45"
      ],
      "source_scope": "page",
      "name": "Thyroxine (T4)",
      "url": "https://teahann.com/human/hormone/thyroxine"
    },
    {
      "id": "e_065ff1d581497fab1c770da0:p00004",
      "entity_id": "e_065ff1d581497fab1c770da0",
      "heading": "Interactions & Feedback",
      "text": "With somatostatin, forms the accelerator/brake pair; ghrelin is the third input that tilts the balance toward release.\n\nIGF-1 feedback inhibits GHRH and stimulates somatostatin — both ends pushed toward less GH.\n\nGlucocorticoids acutely stimulate but chronically suppress GHRH-GH output — one route by which chronic cortisol excess stunts growth in children.",
      "source_ids": [
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        "s_9996d288384f447cc758eee0",
        "s_a33fec6c1612a1b662e4bf72"
      ],
      "source_scope": "page",
      "name": "Growth Hormone-Releasing Hormone (GHRH)",
      "url": "https://teahann.com/human/hormone/growth_hormone_releasing_hormone"
    },
    {
      "id": "e_ecb1246a69d7a33c1dd8bf86:p00003",
      "entity_id": "e_ecb1246a69d7a33c1dd8bf86",
      "heading": "Regulation",
      "text": "Feedback is the architecture: target-gland hormones throttle their own pituitary drivers.\n\nPulsatility matters — constant GnRH suppresses where pulses stimulate.\n\nCircadian timing gates cortisol and melatonin release.",
      "source_ids": [
        "s_d9c80bb4d21508d41140125f",
        "s_e7eaed23307840ba80df7829"
      ],
      "source_scope": "page",
      "name": "Endocrine System",
      "url": "https://teahann.com/human/system/endocrine"
    },
    {
      "id": "e_deb6033298c48da4e08f7590:p00001",
      "entity_id": "e_deb6033298c48da4e08f7590",
      "heading": "Overview",
      "text": "Stress + circadian cortisol regulation. Hypothalamic CRH → anterior pituitary ACTH → adrenal cortex (zona fasciculata) cortisol. Negative feedback: cortisol → hypothalamus + pituitary (suppresses CRH + ACTH). Exogenous glucocorticoids suppress the entire axis — chronic high-dose Rx (>10-20 mg/d prednisone equivalent for >2-3 weeks) produces tertiary adrenal insufficiency that requires gradual taper. ACTH-stim test diagnoses primary vs secondary AI. Diurnal rhythm: ACTH + cortisol peak in early morning (~6-8am), trough at night (~midnight) — the basis for AM cortisol measurement and dexamethasone suppression test.",
      "source_ids": [
        "s_fa998903e96311b46d4d1c30",
        "s_8c4272f1be46ea455402673d"
      ],
      "source_scope": "page",
      "name": "Hypothalamic-pituitary-adrenal axis",
      "url": "https://teahann.com/human/pathway/hpa_axis"
    },
    {
      "id": "e_b1383b844bd4d55fd60b5425:p00004",
      "entity_id": "e_b1383b844bd4d55fd60b5425",
      "heading": "Interactions & Feedback",
      "text": "Aromatization couples the androgen class to estrogen: male bone and feedback partly run on the estradiol testosterone becomes.\n\nAnabolic-anticatabolic balance with cortisol in muscle — androgen excess builds, glucocorticoid excess wastes.\n\nPharmacology splits at the receptor's co-regulators: SARMs aim for anabolic (muscle/bone) selectivity over prostatic — see SARM androgen modulation.\n\nInsulin and metabolic syndrome lower SHBG, raising free androgen — one thread of PCOS physiology.",
      "source_ids": [
        "s_6dfa17f6bf7006f21b08a837",
        "s_e211be14060a052e02004a1d"
      ],
      "source_scope": "page",
      "name": "Androgen",
      "url": "https://teahann.com/human/hormone/androgen"
    },
    {
      "id": "e_fb009bb5e0a70cbdf4b5f4cb:p00004",
      "entity_id": "e_fb009bb5e0a70cbdf4b5f4cb",
      "heading": "Interactions & Feedback",
      "text": "Excitation-inhibition balance: every glutamate signal is read against a GABA background; shifting the ratio causes seizures or sedation.\n\nStress axis: GABAergic inhibition of the HPA axis is why benzodiazepines dampen cortisol responses to stress.\n\nβ-cells release GABA alongside insulin, where it moderates glucagon release — a paracrine echo of its brain job.",
      "source_ids": [
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        "s_b47efe0024d7c6dcdb414d9e",
        "s_88135713ac8efcadd2e9f686"
      ],
      "source_scope": "page",
      "name": "GABA",
      "url": "https://teahann.com/human/hormone/gaba"
    },
    {
      "id": "e_30f19516d7028f5ceb1a9cd2:p00002",
      "entity_id": "e_30f19516d7028f5ceb1a9cd2",
      "heading": "Hormones & Regulation",
      "text": "ACTH under CRH: drives the adrenal cortex's cortisol.\n\nTSH under TRH: sets the thyroid's tempo; negative feedback by thyroxine.\n\nLH and FSH under GnRH pulses: the reproductive axis to ovary and testis.",
      "source_ids": [
        "s_4f60313e82752d21e5f9a5e3",
        "s_3820be688d46712a432ba0ab"
      ],
      "source_scope": "page",
      "name": "Anterior Pituitary",
      "url": "https://teahann.com/human/endocrine/pituitary_gland_anterior"
    },
    {
      "id": "e_c724e41b53af35453eefc9d1:p00004",
      "entity_id": "e_c724e41b53af35453eefc9d1",
      "heading": "Interactions & Feedback",
      "text": "Structural and functional twin of vasopressin — one ancestral gene duplicated into a social-reproductive pair; their receptors cross-talk at high concentrations.\n\nWorks with prolactin as the lactation duo (production + ejection), and with estrogen, which upregulates its receptor.\n\nOpposes the stress hormones: oxytocin release suppresses cortisol tone and amygdala output.\n\nInteracts with dopamine reward circuits — social reward rides oxytocin-tuned dopamine.",
      "source_ids": [
        "s_c5c7e30a99f4a2e675663ed8",
        "s_8bfbc021411930c55bcdc828",
        "s_20532cd6282a869911dd6e96"
      ],
      "source_scope": "page",
      "name": "Oxytocin",
      "url": "https://teahann.com/human/hormone/oxytocin"
    },
    {
      "id": "e_a68b47e9d86c230ba8f80a3c:p00004",
      "entity_id": "e_a68b47e9d86c230ba8f80a3c",
      "heading": "Interactions & Feedback",
      "text": "Works as the hormonal arm of the autonomic balance, with norepinephrine as its neuronal counterpart — the same receptors, different route of delivery.\n\nCortisol is permissive: it maintains adrenergic receptor density, so adrenal insufficiency blunts the response to epinephrine.\n\nEpinephrine reinforces its own release through the hypothalamic HPA axis stress circuit.\n\nCounter-regulatory teamwork with glucagon and growth hormone against insulin during hypoglycemia.",
      "source_ids": [
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        "s_696ef6bbf7d0f09ab8e0dbd9",
        "s_400fd5c8290c28df63fa0bd6"
      ],
      "source_scope": "page",
      "name": "Epinephrine",
      "url": "https://teahann.com/human/hormone/epinephrine"
    },
    {
      "id": "e_245c046e56ae198cf6734b98:p00004",
      "entity_id": "e_245c046e56ae198cf6734b98",
      "heading": "Interactions",
      "text": "With pituitary TSH and hypothalamic TRH — the thyroid axis is the textbook feedback loop.\n\nPermissive for catecholamine action; interacts with cortisol metabolism.\n\nIts disorders derange every system — the gland that touches everything owns a piece of every clinic.",
      "source_ids": [
        "s_967cf564c872dc0f12a443ef",
        "s_59d2ac2e6531b695b2b9a222"
      ],
      "source_scope": "page",
      "name": "Thyroid Gland",
      "url": "https://teahann.com/human/endocrine/thyroid_gland"
    },
    {
      "id": "e_9732f31df3e31394b2923962:p00004",
      "entity_id": "e_9732f31df3e31394b2923962",
      "heading": "Interactions & Feedback",
      "text": "Member of the steroid cascade: cholesterol → pregnenolone → DHEA → androgens/estrogens — the trunk route through which most sex steroids pass (see pregnenolone and DHEA compound entries).\n\nCompetes pharmacologically at the glucocorticoid axis as a functional antiglucocorticoid in some models — a debated, mild counterweight to cortisol.\n\nIts measurement (usually DHEA-S) marks adrenal androgen status: low in adrenal insufficiency, high in congenital adrenal hyperplasia and PCOS-adjacent states.",
      "source_ids": [
        "s_8504284ae91aac2a1f14ea02",
        "s_92842867580f115859cd6690"
      ],
      "source_scope": "page",
      "name": "Dehydroepiandrosterone (DHEA)",
      "url": "https://teahann.com/human/hormone/dehydroepiandrosterone"
    },
    {
      "id": "e_754d281de801cf3a31794726:p00004",
      "entity_id": "e_754d281de801cf3a31794726",
      "heading": "Interactions & Feedback",
      "text": "Antagonistic duo with glucagon: the insulin:glucagon ratio sets the liver's direction — the full loop in insulin-glucose homeostasis.\n\nEvery counter-regulatory hormone opposes it: glucagon, epinephrine, cortisol, growth hormone — the \"diabetogenic\" club.\n\nInsulin resistance in obesity is aggravated by low adiponectin and high resistin — adipokines set insulin's reception climate.\n\nInsulin and amylin co-secreted from β-cells slow gastric emptying in concert with GLP-1.",
      "source_ids": [
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        "s_5bb6caa3aaa6c26ee1b48018",
        "s_1e6145ba3314a78d3e8ce54d"
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      "source_scope": "page",
      "name": "Insulin",
      "url": "https://teahann.com/human/hormone/insulin"
    },
    {
      "id": "e_806f21be2956bb5f378147d2:p00005",
      "entity_id": "e_806f21be2956bb5f378147d2",
      "heading": "Interactions",
      "text": "The cell pivots the HPA axis: CRH and vasopressin in, ACTH out to the adrenal cortex.\n\nβ-endorphin from the same POMC molecule acts on the peripheral nervous system in pain management.\n\nCortisol's feedback engages glucocorticoid receptor signaling, and mineralocorticoid output extends toward aldosterone.",
      "source_ids": [
        "s_378a0dc59ec4c4baeccb696b",
        "s_48989b0b4c4aaeb5850ebc61"
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      "name": "Corticotrophe",
      "url": "https://teahann.com/human/cell/corticotrophe"
    },
    {
      "id": "e_3946d121e7d41d2a77311858:p00000",
      "entity_id": "e_3946d121e7d41d2a77311858",
      "heading": "Overview",
      "text": "Category\nadaptogen\n\nRoutes\nOral (PO)\n\nHalf-Life (t½)\nPO: 4h\n\nAliases\nEchinacea purpurea / angustifolia",
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      "name": "Echinacea",
      "url": "https://teahann.com/human/compound/echinacea",
      "via": "r_0f17c114990ab6d739503ba5"
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