Hormesis¶
Calabrese, E. J., & Baldwin, L. A. (2003). Hormesis: The Dose-Response Revolution. Annual Review of Pharmacology and Toxicology, 43, 175-197.
Cited by¶
5 citations across 5 artifacts.
Each citation links to the sentence it supports in the citing article.
Primes¶
- Antifragility
- The property is strictly dose-bounded: hormesis, its biological prototype, describes a biphasic curve in which a low dose of a stressor stimulates overcompensation while a high dose of the same stressor is toxic, a dose-response shape Calabrese and Baldwin (2003) documented across thousands of toxicological studies.
This sourceDocuments the biphasic hormetic dose-response curve — low-dose stimulation, high-dose inhibition — as broadly generalizable across agents, models, and endpoints; the biological prototype for dose-bounded overcompensation and for the controlled-dose transfer to training, immune education, and fault-injection; supports markers 066, 067, 075.
- The property is strictly dose-bounded: hormesis, its biological prototype, describes a biphasic curve in which a low dose of a stressor stimulates overcompensation while a high dose of the same stressor is toxic, a dose-response shape Calabrese and Baldwin (2003) documented across thousands of toxicological studies.
- Dose-Response Relationship
- Not a linear relationship: while "dose-response" is sometimes colloquially equated with linearity, the canonical pharmacological form is sigmoidal on log-dose, and U-shaped (hormetic) and biphasic relationships are well-documented in specific contexts—a point Calabrese and Baldwin (2003) marshal in their argument that hormesis represents a generalizable, biologically based dose-response signature rather than an exceptional curve type.
This sourceDocuments the biphasic hormetic dose-response curve (low-dose stimulation, high-dose inhibition) as broadly generalizable; supports D47-022 (hormesis as a generalizable dose-response signature, not an exceptional curve type).
- Not a linear relationship: while "dose-response" is sometimes colloquially equated with linearity, the canonical pharmacological form is sigmoidal on log-dose, and U-shaped (hormetic) and biphasic relationships are well-documented in specific contexts—a point Calabrese and Baldwin (2003) marshal in their argument that hormesis represents a generalizable, biologically based dose-response signature rather than an exceptional curve type.
- Inverted-U Response
- Pharmacology and toxicology: hormesis — low doses of certain agents stimulate while high doses suppress the same response; the therapeutic window is the inverted-U of clinical effect minus toxicity.
This sourceReviews hormesis as the biphasic (inverted-U) dose-response where low doses stimulate and high doses suppress the same response.
- Pharmacology and toxicology: hormesis — low doses of certain agents stimulate while high doses suppress the same response; the therapeutic window is the inverted-U of clinical effect minus toxicity.
- Selectivity Window
- And the inversion-edge inference: some windows have an edge at which the process reverses sign — hormesis, where very low doses are neutral, low doses beneficial, and high doses harmful, is the canonical inverting window — and spotting it changes the predicted failure from "less effective" to "actively harmful."
This sourceDescribes the biphasic (hormetic) dose-response in which low doses are beneficial and high doses harmful — the canonical inverting window where an edge crosses into opposite-signed effect.
- And the inversion-edge inference: some windows have an edge at which the process reverses sign — hormesis, where very low doses are neutral, low doses beneficial, and high doses harmful, is the canonical inverting window — and spotting it changes the predicted failure from "less effective" to "actively harmful."
- Threshold
- Every threshold articulation specifies four core components, as the toxicological-threshold framework articulated by Calabrese and Baldwin (2003) makes explicit: (1) the input variable (dose, concentration, stimulus intensity, temperature, duration, load); (2) the response whose presence or absence delimits the regimes (detection, response, failure, phase change, activation); (3) the specific threshold value—fixed (e.g., a receptor's activation threshold) or population-distributed (each individual has a threshold, with population-level distribution); and (4) the mechanism underlying the threshold—receptor activation cooperativity, nucleation energy, neuron firing, material yield, critical mass.
This sourceDocuments the biphasic hormetic dose-response curve — low-dose stimulation and high-dose inhibition — as broadly generalizable across chemical/physical agents, biological models, and endpoints in toxicology; the biological prototype for dose-bounded overcompensation (exercise, fasting, low-dose radiation; bone, muscle, and immune remodeling) and for the controlled-dose transfer to training, immune education, and fault-injection.
- Every threshold articulation specifies four core components, as the toxicological-threshold framework articulated by Calabrese and Baldwin (2003) makes explicit: (1) the input variable (dose, concentration, stimulus intensity, temperature, duration, load); (2) the response whose presence or absence delimits the regimes (detection, response, failure, phase change, activation); (3) the specific threshold value—fixed (e.g., a receptor's activation threshold) or population-distributed (each individual has a threshold, with population-level distribution); and (4) the mechanism underlying the threshold—receptor activation cooperativity, nucleation energy, neuron firing, material yield, critical mass.
Verification¶
This reference passed the adversarial substantiation pipeline: it was checked to exist and to support the claim it is attached to. See how references were verified.
Registry ID ref:56d94895dd09 · see in the full table