A multistable slow-fast model of affective state switching under circadian drive.

Rhythmic mood fluctuations are often associated with circadian timing, but it remains unclear how daily rhythms that normally organize physiological affective variation also shape transitions into longer pathological episodes in bipolar disorder. We introduce a phenomenological slow-fast model of affective dynamics inspired by hypothalamic-pituitary-adrenal-axis homeostatic feedback. A fast affective coordinate evolves on a multistable landscape whose geometry is shaped by a slow homeostatic variable, producing four stable wells: depression-like, physiological low, physiological high, and mania-like. Circadian input acts not as a local forcing term but as a periodic tilt of the global affective landscape. With intact barriers, this tilt entrains physiological low-high cycling; when outer barriers are weakened, it creates phase-dependent windows for stochastic escape into pathological wells, where prolonged occupancy can produce episode-like infradian cycling. Modeling persistent perturbations as an Ornstein-Uhlenbeck process, we derive a Kramers-type escape criterion linking pathological transitions to phase-dependent barrier height and perturbation strength. One-year simulations and scans over the parameter governing landscape geometry show that preserved circadian amplitude stabilizes physiological cycling, whereas reduced amplitude combined with stronger perturbations promotes entry into and occupancy within depression-like or mania-like wells. The model provides a dynamical framework for studying how circadian disruption, landscape geometry, and perturbation sensitivity jointly shape transitions between physiological mood cycling and episode-like pathological states.