ReviewFrontiers in endocrinology2026
A control theoretic primer for systems endocrinology.
Review in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Endocrine systems are characterised by complex dynamic behaviours-oscillations, transient responses, feedback regulation, and noise filtering-that are essential to physiological stability. Despite extensive molecular and clinical research, the quantitative principles governing these dynamics remain incompletely understood. In particular, the mechanistic relationship between the metabolic clearance rates of individual hormones and emergent system-level properties such as oscillatory frequency, damping, and stability has not been systematically integrated into endocrine theory. This paper introduces a control-theoretic framework for systems endocrinology, modelling endocrine networks as cascades of second-order negative feedback systems whose parameters are derived directly from measurable clearance-rate values. Two transfer function architectures are defined-G-type (feed-forward) and H-type (feedback)-which encode a spectrum from rapid, responsive regulation to stable, noise-rejecting maintenance. Frequency-domain analysis via Bode plots extracts biologically interpretable metrics including cutoff frequency, bandwidth, phase margin, and stability margins. The framework is demonstrated using the cortisol-HPA axis as a worked example, where model-predicted timescales are shown to be consistent with experimentally observed ultradian pulsatility (~90-minute period), ACTH-stimulation response kinetics, and dexamethasone suppression dynamics. A reference table of clearance-rate-derived parameters for 36 hormones and substrates is provided, enabling immediate application across major endocrine axes. All computational tools are implemented in R and made freely available. By translating standard pharmacokinetic data into the language of control engineering, the framework provides a candidate, testable account of questions that static endocrine models leave qualitative: why cortisol pulsatility occurs on an approximately ultradian timescale, how stable the HPA axis is, and why the timing-not just the dose-of cortisol replacement determines clinical outcome.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.