Analysis of Human
Recall Behavior
and Cognitive Rumination

01Introduction: Why Humans Repeatedly Recall

Over the long course of evolution, the human brain developed a powerful capability — mental time travel. We can consciously revisit past scenes and imagine futures that have not yet occurred. This ability confers unique learning and planning advantages, but it also produces a byproduct: when this temporal traversal loses control, it becomes rumination — a repetitive, passive, negatively-focused thought cycle.

Rumination is not simply “overthinking.” It is a specific cognitive mode with identifiable neural circuits, measurable physiological signatures, and predictable circadian fluctuation patterns. Understanding these mechanisms is not merely academic exploration — it is practical knowledge from which anyone who tosses and turns in the early morning hours can benefit.

02Definition and Theoretical Frameworks of Rumination

2.1 Response Styles Theory (RST)

In 1991, Susan Nolen-Hoeksema proposed what remains the most widely used conceptual model of rumination — Response Styles Theory (RST). She defined rumination as repetitive, passive focus on the symptoms, causes, and consequences of one’s negative emotions. The theory predicted that individuals who tend to ruminate are more likely than those who tend toward distraction to experience depressive episodes within 18 months. This prediction was subsequently confirmed in prospective studies.

In 1993, Nolen-Hoeksema and Morrow published a landmark experiment using an induction paradigm demonstrating that participants guided into rumination experienced deeper depressive moods, while distraction strategies effectively alleviated naturally occurring depressed mood.

2.2 Goal Progress Theory

In 1996, Martin and Tesser proposed a different framework, redefining rumination as “conscious thought that recurs around a common theme in the absence of immediate environmental demands.” They argued that rumination arises not from reactions to emotions but from blocked goal progress — when individuals perceive insufficient progress toward a goal, goal-related rumination is triggered, with intensity proportional to the goal’s subjective importance.

2.3 The Critical Distinction Between Brooding and Reflection

In 2003, Treynor, Gonzalez, and Nolen-Hoeksema discovered through factor analysis that rumination contains two sub-dimensions: brooding and reflection. While both correlate positively with current depression levels, longitudinal tracking revealed markedly different trajectories — brooding predicted higher future depression, while reflection was associated with lower long-term depression.

2.4 Transdiagnostic Unification: Repetitive Negative Thinking (RNT)

In 2008, Ehring and Watkins proposed “Repetitive Negative Thinking” (RNT) as a transdiagnostic superordinate concept, arguing that various disorder-specific definitions — depressive rumination, anxious worry, obsessive intrusive thoughts — all describe the same core process: repetitive, passive or relatively uncontrollable thinking focused on negative content. In 2025, Moulds and McEvoy’s review in Nature Reviews Psychology further consolidated this framework’s standing.

03Timeline of Research History

04Neurobiological Mechanisms of Early-Morning Rumination Eruption

A widespread but previously under-explained phenomenon is that ruminative behavior may be more prone to eruption during the early morning hours — especially when insomnia, sleep deprivation, stress, and emotional arousal coexist. In 2022, Tubbs et al. proposed the “Mind After Midnight” hypothesis in Frontiers in Network Physiology. It must be emphasized that this is a theoretical framework awaiting experimental verification, not an established conclusion — but it integrates multiple lines of existing evidence to provide the most coherent explanation currently available for this phenomenon.

4.1 Medial Prefrontal Cortex (mPFC) “Going Offline” and Amygdala “Coming Online”

The medial prefrontal cortex (mPFC) exerts top-down inhibitory control over the amygdala — a function distinct from the dorsolateral prefrontal cortex (dlPFC), which handles working memory and executive control, and from the ventromedial prefrontal cortex (vmPFC), which handles value assessment and fear extinction. Sleep deprivation disrupts the negative coupling between mPFC and amygdala, leading to heightened limbic system sensitivity while weakening functional connectivity between prefrontal subregions and the limbic system. In short: during the early morning hours, the brain’s “brake pedal” (mPFC) function declines while the amygdala — responsible for fear and emotional responses — becomes abnormally active.

4.2 Quadruple Superposition Effect

The Tubbs model proposes that during post-midnight wakefulness, attention bias (focus on negative stimuli), negative emotion (at peak), altered reward processing (enhanced immediate rumination impulses), and prefrontal disinhibition (reduced executive control) interact to collectively promote nocturnal behavioral dysregulation. Indirect evidence supporting this hypothesis includes: epidemiological data showing that after adjusting for population wakefulness proportions, suicide risk is significantly elevated during nocturnal waking hours; an analysis encompassing over 78,000 suicides and 50,000 homicides found that nocturnal wakefulness is a shared risk characteristic for both categories of events.

4.3 The Pre-Dawn Cortisol Climb

In healthy individuals, cortisol drops to its lowest point around midnight, then gradually rises during the early morning hours, peaking in the cortisol awakening response (CAR) 30–45 minutes after waking. Research has found that individuals with high trait rumination tendency show significantly elevated cortisol concentrations during the nighttime/pre-sleep period, and this association is independent of daily negative emotions and depressive states — though the generalizability of this finding requires further verification across additional populations.

4.4 Sensory Deprivation Creates the “Perfect Greenhouse”

During insomnia, individuals are awake, frustrated, and lying still in a dark, quiet room — an environment with virtually no distractors to interrupt ruminative thinking. During the day, work, conversations, and environmental stimuli continuously break the thought chain; the sensory deprivation of the early morning removes all external “circuit breakers.” The brain’s default mode network becomes hyperactive during a period when it should be transitioning from wakefulness to rest.

4.5 Overlooked Biochemical Variables: Melatonin and Serotonin

The early-morning neurochemical environment involves more than cortisol. Melatonin reaches its secretion peak between 2:00–4:00 AM; beyond promoting sleep, it exerts direct modulatory effects on the amygdala — animal studies show melatonin can influence limbic system response thresholds. When an individual is abnormally awake during the melatonin peak, the conflict between sleep-promoting signals and the waking state may exacerbate cognitive confusion and emotional dysregulation.

Furthermore, the serotonin (5-HT) system also undergoes significant fluctuations at night. As a core neurotransmitter in emotion regulation, 5-HT has complex interactive relationships with tryptophan metabolism, light exposure, and circadian rhythms. Attributing early-morning emotional dysregulation solely to “absence of light” and “prefrontal metabolic vulnerability” would overlook these important biochemical regulatory variables.

05The Dual Vulnerability of the Prefrontal Cortex: Light and Oxygen

5.1 The Light Pathway: Retina Direct to Prefrontal Cortex

In 2018, Fernandez et al. published a key finding (mouse model) in Cell: intrinsically photosensitive retinal ganglion cells (ipRGCs) on the retina transmit light intensity information to the perihabenular nucleus (PHb) of the thalamus, which then projects to emotional regulation centers including the ventromedial prefrontal cortex (vmPFC) and nucleus accumbens. This pathway is entirely independent of the visual pathway — it conveys not image information but pure ambient light intensity signals. In 2024, Lazzerini Ospri et al. in Science Advances further demonstrated (still in mouse models): absence of ipRGC signaling leads to vmPFC dendritic degeneration, synaptic plasticity gene dysregulation, and neural activity suppression — meaning ipRGCs have direct effects on prefrontal structural integrity and function.

At the human level, brain imaging studies have found that light can proportionally modulate prefrontal activity, with response characteristics highly consistent with ipRGC melanopsin spectral properties. Moreover, melanopsin-expressing cells in ipRGCs project axons densely to the suprachiasmatic nucleus (SCN) — the mammalian central circadian pacemaker. It should be noted that inference from the mouse PHb-vmPFC pathway to human prefrontal function still requires further cross-species validation.

The key finding is that light can directly modulate emotion through an independent ipRGC-dependent mechanism without going through the circadian system. However, a critical species difference must be noted: mice are nocturnal animals, and in experiments, what caused their emotional dysregulation was “abnormal light” (light given during the dark period when they should be active). Humans are diurnal, and the absence of light in the early morning is our biological norm. Therefore, how the ipRGC pathway actually operates in humans during the night — whether it simply “powers down” or switches to another regulatory mode — remains an open question. Directly equating the mouse finding of “abnormal light causes emotional disturbance” with human “early-morning absence of light causes rumination” carries the risk of cross-species polarity reversal in the logic.

5.2 Metabolic Strategy: Evolution’s Double-Edged Bet

The prefrontal cortex is the most recently evolved, highest-functioning region of the human brain. A critical fact: even under conditions of fully adequate oxygen supply, the prefrontal cortex still elects to use substantial amounts of non-oxidative glycolysis — termed “aerobic glycolysis.”

What does this mean? The prefrontal cortex’s high glycolytic rate is an evolutionary “bet”: sacrificing energy efficiency for faster synaptic remodeling capability — the very foundation of learning, memory consolidation, and cognitive flexibility. But this strategy has a cost: when oxygen supply truly declines (as in hypoventilation, hypoperfusion, or high altitude), the prefrontal cortex, because it already depends on large metabolic substrate supplies, is affected earlier and more severely than other brain regions. Systematic reviews suggest that hypoxic impairments to attention, response inhibition, and working memory are highly correlated with prefrontal function. Furthermore, after moderate-intensity aerobic exercise, dorsolateral prefrontal cortex (dlPFC) oxyhemoglobin concentrations rise significantly, and activation levels during equivalent tasks decrease — indicating improved neural efficiency.

06Anticipatory Anxiety Before Major Events

6.1 Uncertainty Is More Tormenting Than Bad News

In 2006, Gregory Berns published a landmark experiment in Science: using fMRI to measure brain responses during the anticipation of electric shocks, he found that some individuals were so fearful of the outcome that they preferred to receive higher voltage rather than wait. The distinction between extreme and mild fearers lay in the rate of neural activity increase in the posterior cortical pain matrix. This suggests that dread derives partly from attentional investment in anticipated bodily responses, not merely from fear or anxiety per se.

When you try to rationally persuade yourself out of anticipatory anxiety, the ventromedial prefrontal cortex (vmPFC) — the key region for integrating emotional signals in decision-making — cannot provide the corrective feedback the emotional brain needs, because the dreaded event has not yet occurred: there is no evidence to process, no outcome to evaluate. When the dreaded event finally arrives, the relief is not just psychological but neural — the brain finally has something real to process, and the neural network switches from rumination to action.

6.2 Intolerance of Uncertainty (IU)

The Dugas and Ladouceur series of studies (1997–2007) established the Intolerance of Uncertainty model, defining it as perceiving uncertainty itself as threatening regardless of the actual probability of threat. A 2025 study found that individual differences in this trait are primarily associated with brain structure in the inferior frontal regions, and IU has been confirmed as a transdiagnostic feature of internalizing disorders.

6.3 Systematic Biases in Affective Forecasting

Daniel Gilbert and Timothy Wilson’s series of studies (1998–2006) systematically revealed the “impact bias”: people universally overestimate the emotional intensity and duration of future events’ impact. Whether college students predicting the emotional impact of exam results, sports fans predicting the psychological shock of their team winning or losing, or voters predicting the emotional consequences of election results, this bias is robustly present.

07Emotion as Memory Amplifier: Why Anxious Memories Are Especially Deep

Emotional arousal enhancing memory storage is not a metaphor — it is a fact supported by clear biochemical mechanisms. Adrenal stress hormones released during emotional arousal modulate the consolidation of long-term memory. The amygdala plays a critical role in mediating these stress hormones’ effects on memory.

The amygdala supports “item-emotion” binding — due to enhanced consolidation, these emotional memories are forgotten more slowly over time, possessing higher vividness and a greater sense of recollection. The latest intracranial EEG studies have found that after encoding more arousing experiences, the amygdala triggers more prominent hippocampal sharp-wave ripples, which are believed to play a key role in memory consolidation.

This constitutes a self-reinforcing closed loop across temporal scales. On the short timescale (seconds to minutes): facing major environmental change → uncertainty activates anticipatory anxiety → amygdala tags as “high importance.” On the medium timescale (hours to days): emotional memories are enhanced in storage during the hours after encoding — especially during the consolidation phase of sleep. On the long timescale (days to weeks): if emotions are not processed into a coherent narrative, they remain in an “unfinished” state → the brain continuously expends resources suppressing them → suppression paradoxically makes them more intrusive (Wegner’s Ironic Process Theory) → prefrontal resources are occupied → cognitive capacity for new decisions declines → more anxiety → stronger memory imprinting. These processes across different timescales nest within one another rather than occurring in linear sequence.

08Release Mechanisms: From Catharsis to Narrativization

8.1 Pennebaker’s Expressive Writing Paradigm

In 1986, James Pennebaker first published experiments showing that brief emotional writing can produce physical and mental health benefits. In the classic paradigm, participants write for 15–20 minutes per day over 3–4 consecutive days, exploring their “deepest thoughts and feelings.”

The most important and counterintuitive finding from three decades of research: the people who showed the greatest health improvements were not those who expressed the most emotion. They were those whose writing evolved over the four days from fragmented emotional catharsis into structured, coherent narrative. The linguistic markers that predicted health improvement included increasing use of causal words (“because,” “reason,” “led to”).

8.2 Ironic Process Theory: Why “Don’t Think About It” Backfires

Daniel Wegner’s (1994) “Ironic Process Theory” published in Psychological Review explains a paradox: actively suppressing unwanted thoughts requires sustained mental effort, depletes executive function, increases physiological stress markers, and makes the suppressed thoughts more intrusive.

This is why “don’t think about it” is not only ineffective but counterproductive. Emotions do not disappear because they are suppressed — they merely retreat from the foreground to the background of consciousness, where they continue to consume cognitive resources and re-emerge when the prefrontal cortex is at its weakest (early morning).

8.3 The Autonomic Nervous System’s Immediate Response

When individuals talk or write about deeply personal topics, immediate physiological responses are consistent with those during relaxation: skin conductance levels drop significantly, and systolic blood pressure and heart rate fall below baseline. The implication: narrativization of emotions is not merely cognitive-level restructuring — it is immediate stress reduction at the autonomic nervous system level.

8.4 Metacognitive Awareness and Self-Distancing

Beyond narrative writing, two other intervention pathways deserve attention. Adrian Wells’s (1995–2009) metacognitive model (S-REF) holds that what maintains rumination is not the thought content itself, but the individual’s metacognitive beliefs about rumination — for example, “I need to keep thinking to find the answer” (positive meta-belief) or “I cannot control my thoughts” (negative meta-belief). Clinical trials of Metacognitive Therapy (MCT) have shown that changing these beliefs about thinking is more effective than changing the thought content itself.

Ethan Kross and Ozlem Ayduk’s series of studies (2005–2017) took a different approach: when people re-examine rumination-triggering events from a third-person (“he”/”she”) or external observer perspective — i.e., “self-distancing” — they experience reduced emotional intensity and extract more meaningful understanding from the event. This mechanism corresponds precisely to Treynor’s brooding-reflection dimensional shift: self-distancing helps individuals switch from the immersive “why me” (brooding) to the observational “what does this event mean” (reflection).

09Integrated Model: Multi-Level Mechanisms of Human Recall Behavior

10Evidence Levels and Causal Boundaries

This paper integrates research at different evidence levels. To help readers assess the reliability of each layer of argumentation, the following annotates the evidence level for core propositions.

11Limitations and Unresolved Questions

This paper is an interdisciplinary integrative thought paper that does not contain original experimental data. Its limitations should be explicitly stated:

First, the inferential chain from animal models to human experience is long. The ipRGC-PHb-vmPFC pathway, aerobic glycolysis metabolic strategy, melatonin modulation of the amygdala, and other findings derive primarily from rodent models, and cross-species functional mapping has not been fully established — especially given that nocturnal animals and diurnal humans may have fundamental differences in light response polarity.

Second, the causal chain spans different timescales and levels of analysis (second-level autonomic responses, hour-level memory consolidation, day-level cognitive patterns, week-level emotional states). While each level has individual research support, when stringing them together into a single causal sequence, the evidence strength is not the sum of each link.

Third, this paper does not address cultural variation in rumination behavior. Existing research suggests that the manifestation forms, functional evaluations, and clinical significance of rumination may differ significantly between collectivist and individualist cultures.

Fourth, prefrontal subregions (mPFC, dlPFC, vmPFC) play different roles in different mechanisms. While this paper has partially differentiated these, the integrative discussion inevitably uses “prefrontal cortex” as a collective term, which may obscure functional dissociations between subregions.

12Conclusion: Answers at Three Levels

This paper attempts to answer a specific question about human experience: Why do we repeatedly recall the past on the eve of major change? The answer can be given at three levels.

Phenomenological Level: Why We Recall the Past Before Change

When a future goal is highly important yet its outcome remains unknown, the brain’s default mode network automatically initiates self-referential processing. But the future offers no material to process, so it turns to the past — those already settled experiences with detail and emotional texture — as simulation material. This is not a malfunction; it is a factory default. It is precisely that past self — the one with “only half the wisdom and courage of now” — who accumulated, step by step, the cognitive resources of the present.

Mechanistic Level: Why the Early Morning Is More Prone to Loss of Control

The early morning may constitute a multi-factor susceptibility window: mPFC inhibition of the amygdala is at its nadir, the melatonin peak conflicts with abnormal wakefulness, cortisol begins climbing but the prefrontal cortex has not yet fully come online, and sensory deprivation removes all external “circuit breakers.” But it must be emphasized: this integrated model is currently supported primarily by the Tubbs hypothesis framework and multiple lines of indirect evidence, and still awaits direct experimental verification. Early-morning thoughts are not more “true” than daytime thoughts — they may simply be amplified in the space between the weakest control and the strongest emotional drive.

Methodological Level: How to Shift from Brooding to Reflection

The key to breaking the rumination cycle is not “not thinking about it” (Wegner’s Ironic Process Theory explains why this backfires), but switching thinking modes: from the passive “why me” to the active “what is the structure of this event.” Narrative writing, metacognitive awareness, and self-distancing offer three pathways — their shared mechanism is reactivating the prefrontal cortex’s organizing and contextualizing functions, transforming fragmented emotional experience into archivable, coherent narrative.

Perhaps, as one insight born at the early morning moment when this paper came into being: the future me is looking down at the present me from above, just as the present me looks down at the past me — each layer sees further than the last. The only constant is the person who keeps walking forward.