Where does hormesis collide?

In psychology the Yerkes–Dodson law describes a non-monotonic, inverted-U relation between arousal and performance: too little arousal leaves performance slack, moderate arousal sharpens it to a peak, and excessive arousal degrades it, with the optimum lower for harder tasks. Robert Yerkes and John Dodson's 1908 The Relation of Strength of Stimulus to Rapidity of Habit-Formation first reported this curved dose–response in learning. The referent is a stimulus whose intensity helps up to a point and then harms, a biphasic response with an interior optimum. It is the same inverted-U shape that toxicology would name hormesis and that risk theory would call antifragility, expressed in arousal and performance rather than dose and biological effect.[1]

Unit

Performance as a function of the intensity of arousal or stimulation

Recovery means

Not applicable

Measured by

Traced as an inverted-U curve of performance against arousal, with the peak shifting by task difficulty

In toxicology and pharmacology, hormesis is a biphasic dose–response in which a low dose of an agent that is harmful at high dose instead stimulates or benefits the organism, because a mild stressor provokes an over-compensating repair and defence response. Edward Calabrese and Linda Baldwin's 2003 Hormesis: The Dose–Response Revolution assembled thousands of cases and argued that this low-dose stimulation, not the standard threshold or linear model, is the more general shape of the dose–response. The referent is a stressor that is beneficial in moderation and toxic in excess, an interior optimum in the dose–effect curve. It is the same non-monotonic response that psychology observed as the Yerkes–Dodson law and that risk theory generalised as antifragility.[2]

Unit

Biological effect as a function of the dose of a stressor

Recovery means

The over-compensation subsides as the stressor is cleared and the system returns to baseline

Measured by

Identified by a biphasic (J- or U-shaped) dose–response with low-dose stimulation below the toxic threshold

In risk theory, antifragility is the property of a system that gains from disorder: within limits, exposure to volatility, stressors, randomness, and errors makes it stronger rather than merely resistant, because a convex response lets small harms trigger over-compensating improvements while large shocks are avoided. Nassim Taleb's 2012 Antifragile: Things That Gain from Disorder named the property and explicitly grounded it in biological hormesis, contrasting it with fragility and with mere robustness. The referent is a system that benefits from moderate stressors and is harmed only by extremes, the same biphasic, interior-optimum response as hormesis and the Yerkes–Dodson law, generalised from a single dose curve to a system's whole response to volatility.[3]

Unit

A system's change in performance as a function of exposure to volatility or stressors

Recovery means

Not applicable

Measured by

Diagnosed by a convex (accelerating-benefit, bounded-harm) response to increasing variability