Isla M. Goldie is an independent researcher exploring cortisol as the organising principle of neurobiology. Her Cortisol Signal Fidelity framework redefines cortisol as the body’s central translator and foreman — the signal that directs development, repair, and adaptive action across systems. Through her papers Unmasking Neurodivergence - Cortisol and the HPA Axis and Don’t Shoot the Messenger - Cortisol and the Rhythm of Repair, she proposes a transformative view of the HPA axis: not as a pathway of stress, but as the command network that builds, coordinates, and sustains the mind–body system. Her work invites a new understanding of neurodivergence and human variation through the lens of endocrine intelligence and signal coherence.

CORTISOL - UNMASKING NEURODIVERGENCE, 2025

This working paper proposes that neurodivergence arises from differences in physiological calibration established prenatally by the sequential development of the autonomic nervous system (ANS) and the hypothalamic–pituitary–adrenal (HPA) axis. Within genetically susceptible templates, maternal–foetal cortisol rhythms, placental buffering, foetal placement, and timing of exposure set the developmental tone for stress responsivity, attention, and sensory processing. Cortisol functions as a developmental signal that shapes neuronal growth, synaptic pruning, and myelination. These early rhythms leave durable imprints on limbic and prefrontal circuits, and on connective-tissue biology through modulation of collagen synthesis. The framework integrates established findings in endocrine regulation, immune and oxidative balance, and dopaminergic function. It positions sex hormones as modulators that buffer or amplify stress-axis calibration and treats connective-tissue phenotype as a somatic expression of the same regulatory history. The paper concludes with testing models focused on genetically predisposed populations and invites empirical collaboration to evaluate this integrative hypothesis. This framework presents neurodivergence as an outcome of adaptive developmental calibration rather than deficit, encouraging biological precision and clinical respect for human variation. By situating neurodivergence within a physiological calibration spectrum, this paper encourages research that distinguishes adaptive diversity from pathology. The proposed Cortisol Signal Fidelity framework offers a foundation for empirical investigation into how temporal hormone dynamics shape neurodevelopmental diversity.  Full paper below.

CORTISOL-DONT SHOOT THE MESSENGER, 2025

The second paper in the series discusses how cortisol has long been characterised as the "stress hormone," a marker of threat and dysfunction. Yet across evolution, development, and recovery, cortisol appears not as an agent of damage but as a coordinator of adaptive work. This paper reframes cortisol as a dynamic communication signal-one whose quantity enables action and whose rhythm gives that action meaning. We propose the Cortisol Signal Fidelity (CSF) framework, which defines cortisol as a temporal regulator of adaptation rather than a static measure of stress. The model posits that biological resilience depends on the fidelity of cortisol's timing, amplitude, and coherence-not its mean level alone. A new composite metric, the Cortisol Signal Fidelity Index (CSFI), integrates five measurable domains: circadian alignment, phasic gain, recovery offset, ultradian regularity, and cross-system coupling. Review of the literature shows that disorders of fatigue, metabolic inefficiency, and maladaptive mood correspond to timing distortion rather than absolute deficiency or excess. The CSFI framework predicts that health arises when cortisol's concentration and timing interact precisely to direct energy, repair, and behaviour. Recasting cortisol as the language of adaptation unifies disparate clinical conditions under a single physiological principle: that the body's success depends not only on how much cortisol is made, but on how clearly and coherently it speaks through time. The proposed Cortisol Signal Fidelity framework offers a foundation for empirical investigation into how temporal hormone dynamics shape neurodevelopmental diversity.