HPA axis
The hypothalamic-pituitary-adrenal axis: the neuroendocrine arm of the stress response, terminating in cortisol release. Its relevance here is mechanistic — it is the most concrete pathway offered for how a social variable (attachment-style) could produce a physiological difference in interoception.
The architectural argument
Oldroyd et al. (2019) note that stress and interoception traverse the same brain-body pathways in opposite directions: the stress response is the descending brain-body connection, interoception the ascending one (citing Seth 2013). Anything that chronically dysregulates the descending arm should therefore be expected to leave marks on the ascending one. And individual differences in attachment are reliably characterized by differential HPA reactivity to stress across the lifespan (Allen & Miga 2010; Diamond & Fagundes 2010; Lovallo 2013).
Two proposed routes to altered interoception
1. Signal strength. HPA activation releases epinephrine, which increases cardiac contractility, heart rate and depolarization — and thus stroke volume. Schandry et al. (1993) found stroke volume predicts heartbeat-detection performance: the more blood pumped per beat, the better people estimate their own heart rate. Higher stroke volume is therefore a literally stronger interoceptive signal, and chronically increased sympathetic outflow has been proposed as one route to high interoceptive accuracy (Paulus & Stein 2010).
This is a notable point for the heartbeat-detection-task: it implies heartbeat-detection scores partly index cardiodynamics, not only perceptual skill. A person with a more forceful heartbeat has an easier signal to detect. Any interpretation of heartbeat-detection differences as differences in perceptual ability inherits this confound.
2. Signal processing. Cortisol appears to lower the threshold for interoceptive signal processing centrally — the brain becomes more attuned to interoceptive signals in its presence (Rief et al. 1998). Intravenous cortisol (4 mg) improves interoceptive accuracy (Schulz et al. 2013), and the regions responsible for attentional processing of interoceptive signals — ACC and OFC — show greater activation under cortisol (Cameron 2002; Critchley et al. 2004; Pollatos et al. 2007). Chronic HPA dysregulation may therefore permanently alter perception of bodily cues (Schulz & Vögele 2015).
Interpretive tension
Both routes predict that stress increases interoceptive accuracy — stronger signal, lower processing threshold. But the developmental thesis of oldroyd-2019-attachment-interoception is that insecure attachment (and hence HPA dysregulation) yields worse or distorted interoception. The paper does not reconcile these, and the mechanism section is never tested against its own data: no cortisol, stroke volume, or HPA measure was collected in either study.
A charitable reading is that the anxious profile is where the mechanism fits — heightened noticing plus heightened worry (attachment-style) is what “stronger signal + lower threshold” should produce, and the term the authors reach for is distorted rather than diminished interoception. It does not obviously explain the avoidant profile, which the paper attributes to attentional strategy and neural architecture instead. Worth holding loosely: this is a plausible mechanism sketch, not a result.
What drives the axis, and why the timing matters
LeDoux (2012) supplies the upstream half this page previously left implicit. Central amygdala outputs target neurons activating the sympathetic division of the ANS (releasing adrenergic hormones from the adrenal medulla) and the HPA axis (releasing cortisol from the adrenal cortex) — so the axis is an output limb of a survival circuit, triggered by threat detection rather than free-standing.
His timing observation bears on the wiki’s mechanism discussion above: central neuromodulator effects are rapid, whereas peripheral hormone effects are “considerably slower, allowing the prolongation of the survival state for extended periods of time.” Cortisol crosses the blood-brain barrier and binds receptors widely; adrenergic hormones affect the CNS indirectly (McGaugh 2000). This is a concrete route by which a brief trigger yields a sustained state — and it matters for the chronic-dysregulation claims Oldroyd et al. rest on, since it is the slow limb that would plausibly leave lasting marks.
Also relevant: arousal signals feed back to facilitate the very circuit that triggered them, and facilitate sensory and memory areas — a loop, not a one-way output. See global-organismic-state.
Related
Sits alongside homeostasis and allostasis as the endocrine face of the body-regulation story that interoception senses.