Digital information overload and ageing: physiological evidence, an abiotic-stressor analogy, and competing dose–response hypotheses

Digital information overload (DIO) is increasingly considered an environmentally mediated stress exposure, yet its physiological consequences and relevance to biological ageing remain uncertain. This critical narrative review evaluates evidence for sustained allostatic strain, adaptation and alternative exposure–response patterns, distinguishing content-defined overload from occupational technostress, general screen use, screen-emitted light and broader stress biology. The literature was collected between 4 March and 20 August 2026 and appraised according to exposure specificity, study design and measured endpoints. Occupational studies reported an inverse prospective association between technostress and hair cortisol, without significant associations with C-reactive protein, challenging assumptions of uniform hypercortisolism or inflammation. Acute autonomic responses varied with task conditions, while experimental screen-light research demonstrated circadian effects without isolating informational content. A short randomised screen-reduction study reported favourable changes in selected physiological measures, although its broad exposure definition and co-interventions prevent attribution to DIO. In a cross-sectional study, an association between social-media duration and DunedinPACE was attenuated after adjustment for body mass index, while GrimAge2 was not associated with exposure duration. Current research does not establish that objectively quantified DIO causes cellular senescence, mitochondrial dysfunction or accelerated biological ageing. We propose the unvalidated Digital Information Stress Dose (DISD) framework, encompassing exposure duration and frequency, arousal, cognitive load, attentional capture, circadian displacement and perceived controllability. Null or weak, monotonic adverse, threshold and biphasic hormesis-like relationships remain plausible but untested alternatives. Future investigations should combine passive exposure logs and ecological momentary assessment with repeated physiological measurements, neutral and supportive digital comparators, longitudinal follow-up and controlled exposure modifications. DISD is intended as a falsifiable research framework, not an established biomarker, clinical threshold or demonstration of harm.