The circadian system plays a critical role in maintaining internal homeostasis by regulating daily rhythms of hormone secretion (e.g., melatonin and cortisol), body temperature, and metabolism. When this finely tuned system is disrupted—by inappropriate light exposure, irregular sleep timing, or social desynchrony—it may act as an anti-physiological or anti-homeostatic stimulus. Over time, such misalignment can break down biological equilibrium due to a loss of temporal coordination in the internal processes.

Importantly, these disruptions may not be consciously perceived as stress. Yet, they still provoke neuroendocrine responses, such as elevated cortisol levels—a widely recognized biomarker of psychological strain. This perspective helps explain why individuals with DSWPD frequently report depressive symptoms even without identifiable psychological triggers [3]. Their chronic circadian misalignment results in persistent dysregulation of the HPA axis, as evidenced by both elevated cortisol levels and phase-delayed cortisol rhythms—a pattern where cortisol secretion peaks later than normal and remains elevated into the evening [4,5].

Findings from individuals with DSWPD provide compelling support for the view that circadian misalignment acts as an anti-physiological stressor with emotional consequences. In our previous study, we found that despite no significant differences in total sleep time or architecture, DSWPD patients exhibited chronically elevated cortisol levels, amplified mood fluctuations, and phase delays in both melatonin and cortisol rhythms [6].

Time-lagged analyses further revealed that increases in negative mood were followed by cortisol elevations, indicating that the HPA axis in DSWPD patients may be hypersensitive to affective changes [6]. These results support a model in which emotional dysregulation arises from physiological rhythm disruption, rather than from cognitive processes or environmental stressors. Notably, this feedback loop—wherein emotional distress intensifies physiological stress responses—was absent in healthy controls, suggesting a unique vulnerability in circadian-disrupted individuals.

The broader implication is that not all stress is consciously experienced. A patient with DSWPD may not report feeling “stressed,” yet their limbic system and HPA axis react as if under biological threat. This aligns with Joseph LeDoux’s theory of unconscious emotional pathways [7], which posits that subcortical brain structures can initiate affective responses before cortical awareness emerges. In this light, circadian misalignment functions as a silent stressor—disrupting physiology and mood prior to conscious recognition. This framework helps reconcile discrepancies between patients’ subjective reports (“I don’t feel stressed”) and their biological profiles (e.g., elevated cortisol, delayed melatonin, and low mood). This perspective aligns with neurobiological models of emotion, such as those proposed by Dalgleish [8], which emphasize that affective responses can emerge from physiological disruptions independent of conscious appraisal.

Given these findings, clinicians should begin to recognize circadian misalignment as a primary physiological insult—capable of triggering depressive symptoms even in the absence of psychological causes. DSWPD, in particular, should be understood not merely as a sleep-timing issue, but as a chronobiological disorder affecting mood, endocrine regulation, and stress resilience.

Therapeutic approaches for depression should therefore move beyond behavioral strategies alone (e.g., cognitive behavioral therapy for insomnia), and include interventions aimed at circadian realignment—such as timed light exposure [9], melatonin therapy, chronotherapy, and personalized sleep hygiene based on chronotype. By targeting both the stimulus (circadian misalignment) and its anti-homeostatic effects, we can more effectively address the depressive risks inherent in circadian rhythm disorders [1].