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Dr. Michael Cørnwall, 2785 E Desert Inn Road, Suite 280, Las Vegas, NV (2025)

12/06/2025

What Is the Cause of Memory?

Memory comes from the way the brain takes in information, stores it, and brings it back later.

It works a lot like a path that gets deeper the more you walk on it.

Here are the basic parts:

1. Learning makes brain cells connect

When you learn something new, tiny changes happen between your brain cells.

The more you practice or repeat something, the stronger those connections become.

2. Attention and emotion matter

You remember things better when:
• you pay attention
• they mean something to you
• they have an emotional charge (fear, calm, joy, excitement)

This is why you may forget where you put your keys, but you remember your wedding day or where you were on 9/11.

3. Sleep helps memories “stick”

While you sleep, your brain replays and organizes what you experienced during the day so it can be stored long term.

What Does the Hippocampus Do?

The hippocampus is a small part of the brain—shaped like a seahorse—that acts like a memory center.

1. It helps you make new memories

Without the hippocampus, you could have a conversation right now but forget it a few minutes later.
It turns short-term experiences into long-lasting memories.

2. It helps you remember where things happened

The hippocampus helps you remember:
• where you put your keys
• what your house looks like
• what street you turned on
• the layout of a grocery store

It’s your brain’s built-in map and timeline.

3. It helps connect memory and emotion

The hippocampus works closely with the brain area that handles fear, excitement, and strong feelings.
This is why emotional events are easier to remember than ordinary days.

Putting It Simply

Memory forms when:
• brain cells connect
• you pay attention
• the event has meaning or emotion
• sleep helps “lock it in”

And the hippocampus is the part of the brain that:
• makes new memories
• organizes them
• remembers places and context
• links memories with emotions

If the hippocampus is damaged, people can remember old memories but cannot form new ones.

Short-term memories form in the hippocampus and consolidate in the cortex?

The hippocampus is the initial processing center for new memories, and the cerebral cortex becomes the long-term storage system.

Below is the simple breakdown:

1. Short-Term → Hippocampus

When you experience something, the information enters short-term memory through attention.

The hippocampus then:

• receives the new information
• organizes it (time, place, context)
• creates the first version of the memory
• links it with emotion (via the amygdala)

This early version is still fragile and easily disrupted.

2. Consolidation → Cortex

During sleep and quiet rest, the hippocampus “replays” the memory and sends it to the cerebral cortex (especially the temporal, parietal, and frontal association areas).

This process is called systems consolidation (Squire & Kandel, 2009; Diekelmann & Born, 2010).

The cortex then stores the memory long-term.

3. After Consolidation

Once the memory is fully established:
• you no longer need the hippocampus to recall older memories
• the memory becomes more stable and integrated
• details are distributed across multiple cortical areas (sensory, visual, auditory, conceptual)

This is why people with hippocampal damage (like in amnesia) cannot form new memories but can remember old ones.

12/01/2025

The Mask of Emotion — How Words Hide Fear

Most people believe they know what they’re feeling because they can name an emotion. They say “I’m angry,” “I’m frustrated,” “I’m resentful,” “I’m hurt,” or “I’m disappointed.” These labels feel precise, even sophisticated. But the brain’s labels can be misleading. Emotional words are not states. They are stories the cortex quickly constructs to explain what the body is experiencing (Barrett, 2017).

Underneath nearly every imbalancing emotional word lies a core biological state: Fear.

Anger is often fear of vulnerability.
Jealousy is fear of loss.
Resentment is fear of unfairness or insignificance.
Shame is fear of disconnection and exposure.
Hurt is fear of rejection.
Frustration is fear of inefficacy.
Disappointment is fear of unmet expectations and their consequences.

When someone stops at the emotional label, they never discover the fear underneath. And when the fear remains unexamined, the problem cannot be solved.

This happens because the cortex produces emotional words as interpretations, not truths. The limbic system reacts from a biological state of threat long before the cortex has constructed the story (LeDoux, 2012). The person then attempts to regulate the label—the narrative—rather than the fear-based appraisal that generated the reaction.

This is why emotional vocabulary, while culturally valued, can actually distance people from their internal experience. It can make them more articulate but less self-aware. They become fluent in labels but disconnected from their physiological reality.

Emotional intelligence comes not from expanding emotional vocabulary but from simplifying it to the only two states that matter: Fear and Calm.

Once a person identifies the fear underneath the mask, problem-solving becomes possible. They can evaluate the meaning their brain assigned, question the narrative, and regulate the threat response directly. This moves them away from the emotional word and toward the biological truth.

In REBT terms, the emotional label is the “C” (emotional consequence), while the fear is embedded in the “B” (belief). The goal is not to name the emotion better—it is to understand the belief better (Ellis, 1994; Ochsner et al., 2012). Only then can the prefrontal cortex override the limbic response and redirect the system toward calm.

Emotional maturity, then, is the ability to look beneath the emotional mask and ask a single, powerful question: What am I afraid of right now?

References

Barrett, L. F. (2017). How emotions are made: The secret life of the brain. Houghton Mifflin Harcourt.
Ellis, A. (1994). Reason and emotion in psychotherapy (Rev. ed.). Birch Lane Press.
LeDoux, J. (2012). Rethinking the emotional brain. Neuron, 73(4), 653–676.
Ochsner, K. N., Silvers, J. A., & Buhle, J. T. (2012). Functional imaging studies of emotion regulation. Trends in Cognitive Sciences, 16(11), 707–717.

12/01/2025

How the Brain Decides: Fear or Calm

Every moment of human experience begins as something simple: a sight, a sound, a gesture, or a shift in someone’s voice. None of this is emotional yet. It enters the brain as raw sensory data—unclassified, unstamped, and without meaning (Kandel, 2012).

This data first arrives in the cortex, the brain’s vast archive room. Every memory, lesson, belief, emotional pattern, and internalized rule of living is stored there (LeDoux, 2012). The cortex functions like the records office of a courthouse: it pulls whatever files seem relevant based on past learning, trauma, cultural context, and reinforcement (Teicher et al., 2016). It does not judge. It simply provides the evidence—accurate or distorted.

From there, the information travels to the prefrontal cortex, the judge in this internal courtroom. The PFC examines the evidence, applies whatever rules the individual has learned, and determines the meaning of the moment. It compares, inhibits, predicts outcomes, and evaluates context (Miller & Cohen, 2001). But the judge can only use the files stored in the archive. If a person was raised in fear, inconsistency, or chaos, the archive holds distorted records. The judge will still make a ruling, but the ruling will reflect the limitations of the archive (Herman, 2015; Kandel, 2012).

Once meaning is assigned, the ruling passes to the limbic system, the bailiff. The limbic system’s job is not to question the judge. It simply enforces the ruling. If the PFC signals danger, the limbic system activates instantly: the amygdala sounds the alarm, the HPA axis fires, cortisol floods the bloodstream, and the body prepares for defense (Sapolsky, 2004). This is the fear pathway.

If the ruling is "safe," the opposite unfolds. The parasympathetic nervous system engages, breathing steadies, muscles release, and openness, clarity, and connection become available (Porges, 2011). This is the calm pathway.

This internal courtroom metaphor forms only one layer of the brain’s decision-making process. A second metaphor—the 1940s car running out of gas—captures what happens when chronic stress overwhelms the system. The limbic system is the engine, and the HPA axis is the fuel line. When the system is overused, the engine sputters, and the car stalls: this is HPA-axis exhaustion (Nemeroff, 2016). Treating the body alone is like comforting a driver stranded on the roadside. Emotional intelligence, therapy, and reflective practice are the walk to the gas station—repairing the engine, refueling the system, and learning how to prevent future breakdowns (Ochsner et al., 2012).

A third metaphor brings depth to the emotional landscape: the house of the mind. Every belief is a room. Every lesson from childhood is a beam. Every trauma is a locked door. Every safe moment is a window that lets in light. When the brain interprets an event, it walks through this house. The cortex retrieves whichever room the person is most familiar with, and the prefrontal cortex navigates the structure it inherited—not the one it wishes it had (Herman, 2015). The limbic system responds according to the room the person ends up in.

Together, these metaphors illuminate a central principle:
Events do not create emotions. The architecture of the mind does.
The archive, the judge, the engine, the house—these internal systems decide whether the body moves toward fear or calm.

Emotional intelligence reshapes all of these systems. It updates the files in the archive, retrains the judge to pause before ruling, repairs the engine, and rebuilds the house so that more rooms have windows. Through self-awareness and practice, the space between event and reaction expands. The limbic system becomes less reactive. The courtroom grows quieter. The car stays on the road longer. The house grows brighter.

And slowly, the brain learns to choose calm over fear.

References

Herman, J. L. (2015). Trauma and recovery (Rev. ed.). Basic Books.
Kandel, E. R. (2012). Principles of neural science (5th ed.). McGraw–Hill.
LeDoux, J. (2012). Rethinking the emotional brain. Neuron, 73(4), 653–676.
Miller, E. K., & Cohen, J. D. (2001). An integrative theory of prefrontal cortex function. Annual Review of Neuroscience, 24, 167–202.
Nemeroff, C. B. (2016). Paradise lost: Neurobiological consequences of child abuse. Neuron, 89(5), 892–909.
Ochsner, K. N., Silvers, J. A., & Buhle, J. T. (2012). Functional imaging studies of emotion regulation. Trends in Cognitive Sciences, 16(11), 707–717.
Porges, S. W. (2011). The polyvagal theory. W. W. Norton.
Sapolsky, R. M. (2004). Why zebras don’t get ulcers (3rd ed.). Henry Holt.
Teicher, M. H., Samson, J. A., Anderson, C. M., & Ohashi, K. (2016). Childhood maltreatment effects on brain structure. Nature Reviews Neuroscience, 17(10), 652–666.

11/27/2025

When Anxiety Looks Like Depression: Understanding HPA Axis Exhaustion Through REBT and Emotional Intelligence

Why treating the “exhaust” instead of the “engine” keeps people stuck.

Introduction: When Depression Isn’t Depression

Many people are diagnosed and treated for depression when, in reality, their symptoms arise from a stress system pushed far beyond its limits. What looks like depression—the exhaustion, slowed thinking, low motivation, irritability, flat mood, and cognitive fatigue—is often the final stage of chronic anxiety, not a separate disorder. Anxiety is the engine that runs too hot for too long; depression is the exhaust that appears when the engine begins to fail (McEwen, 2007; Sapolsky, 2004).

This essay explores how an exhausted hypothalamic–pituitary–adrenal (HPA) axis can mimic depression, why SSRIs may be ineffective when anxiety is the true driver, and how a treatment model informed by Rational Emotive Behavior Therapy (REBT) and Emotional Intelligence (EI) can restore stability. I also examine why misdiagnosis is common and what clinicians can do to recognize when “depression” is actually anxiety-driven burnout.

Understanding the HPA Axis and Stress Activation

The HPA axis—the hypothalamic, pituitary, and adrenal system—is the body’s primary stress-regulation network. It governs the release of cortisol, the hormone responsible for energy mobilization, alertness, metabolic readiness, morning arousal, and the capacity for motivation and goal-directed behavior (Chrousos, 2009; McEwen, 2007).

Under normal circumstances:
• cortisol rises in the morning to help us get up, think clearly, and initiate action
• it declines throughout the day to allow the body to rest and reset

But chronic anxiety, fear-based thinking, and sympathetic overactivation cause the HPA axis to fire repeatedly. What should be a temporary adaptive response becomes the individual’s daily baseline.

Over time, this sustained activation produces allostatic load, a biological wear-and-tear process that leads to depletion and exhaustion (McEwen, 2007). The individual begins to experience:
• slowed cognition
• low mood
• irritability
• emotional flatness
• diminished motivation
• chronic fatigue

These symptoms look like classic depression—but the cause lies in physiological burnout, not mood dysregulation (Sapolsky, 2004).

Why Anxiety So Often Gets Misdiagnosed as Depression

In everyday clinical practice, individuals with HPA exhaustion are frequently diagnosed with depression and placed on SSRIs. While SSRIs help many people, they often fall short when the root issue is chronic anxiety depleting the stress system (Stahl, 2013). In some cases, SSRIs may blunt affect or leave the core anxiety untreated, prolonging recovery.

Here is the key clinical point:

Anxiety is the engine. Depression is the exhaust.
If we treat the exhaust without repairing the engine, the person remains stuck.

Diagnostic Subjectivity: Why This Mistake Happens

Mental health diagnosis is inherently subjective. Two clinicians can reasonably diagnose the same individual differently, depending on their experience, theoretical orientation, and time spent with the client (APA, 2022). Many clinicians simply accept the diagnosis a person arrives with—either because they agree with it or because they do not have time to reassess.

Yet good clinical practice requires a new evaluation. When depression emerges as a symptom of chronic anxiety, treating it as a primary disorder is ineffective. We must identify the system driving the distress, not the surface-level appearance.

How REBT and Emotional Intelligence Explain the Exhaustion

REBT: Beliefs Drive Emotional Disturbance

Rational Emotive Behavior Therapy (Ellis, 1994) teaches that emotional disturbance arises not from events but from the beliefs about those events. Catastrophizing, rigid demands, worst-case assumptions, and global self-criticism keep the stress system activated long after the triggering event has passed.

These dysfunctional beliefs repeatedly stimulate the HPA axis, contributing directly to chronic hyperarousal.

Emotional Intelligence: Regulating Internal States

Emotional Intelligence theory (Goleman, 1995) emphasizes:
• identifying emotions early
• labeling them accurately
• regulating internal states
• maintaining adaptive responses

Low EI—especially poor self-awareness—allows chronic anxiety to go unnoticed until the exhaustion stage appears as “depression.”

Both REBT and EI intervene early in the stress cycle, reducing unnecessary limbic activation and giving the HPA axis room to recover.

The Lawnmower Metaphor: Clearing the Debris Before Starting the Engine

Imagine walking into a field and finding a lawnmower buried under grass clippings, sticks, and debris. The machine cannot start—not because the engine is broken, but because it is suffocating.
• depression = the exhaust
• anxiety = the engine
• chronic stress = the debris

Before pulling the starter cord, you remove the debris. In treatment, that debris is addressed through:
• talking therapy
• cognitive restructuring
• emotional regulation skills
• psychoeducation
• structured recovery

Only then do you use the right tools—medication targeting both serotonin and norepinephrine (such as SNRIs), combined with therapy—to help the engine catch and begin to run smoothly again (Stahl, 2013).

The Car-With-No-Gas Metaphor: Treating the Engine, Not the Driver

When the HPA axis is depleted, it is also like a car that has run out of gas and is stranded on the side of the road. The driver—the emotional self—may feel frustrated, overwhelmed, or ashamed, but the car is not moving because the tank is empty.

Treating the driver alone—soothing him while he remains stranded—is the equivalent of treating only the emotional distress without refueling the stress system.

Talking therapy is the process of sitting with the driver, helping him understand what happened, regain clarity, and reorient himself.
Medication and targeted anxiety treatment are the fuel and mechanical support required to refill the tank, restore the engine, and get the car moving again.

Comforting the driver without refueling the engine leaves the person stranded.
We must repair the system—not merely soothe the distress created by its exhaustion.

Once the HPA axis is restored, the depressive “exhaust” clears naturally.

Conclusion: Repair the Engine and the Exhaust Clears

When depression presents as a symptom of chronic anxiety and HPA axis exhaustion, treating it as a primary disorder misses the mark. By understanding the biology of the HPA axis, the motivational role of cortisol, and the draining effects of sympathetic overactivation, we can see that depression often reflects a deeper system imbalance.

REBT and EI strengthen the person’s ability to regulate internal states, restructure fear-based beliefs, and reduce unnecessary stress activation. Together with targeted pharmacology, they repair the engine rather than chasing the exhaust.

Treating depression alone is like polishing a lawnmower whose engine is clogged with debris—or comforting a stranded driver without refueling the tank. Only by addressing the true source of the problem can energy return, mood stabilize, and meaningful recovery begin.

References

American Psychiatric Association. (2022). Diagnostic and statistical manual of mental disorders (5th ed., text rev.).
Chrousos, G. P. (2009). Stress and disorders of the stress system. Nature Reviews Endocrinology, 5(7), 374–381.
Ellis, A. (1994). Reason and emotion in psychotherapy.
Goleman, D. (1995). Emotional intelligence.
McEwen, B. S. (2007). Physiology and neurobiology of stress and adaptation: Central role of the brain.
Sapolsky, R. M. (2004). Why zebras don’t get ulcers.
Stahl, S. M. (2013). Stahl’s essential psychopharmacology.

11/01/2025

. . . before you heal someone, ask him if he's willing to give up the things that made him sick - Hippocrates

10/30/2025

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10/29/2025

The Limits of Transcranial Magnetic Stimulation: Why Brain Complexity Defies Magnetic Intervention

Michael Robert Cornwall, PhD, PsyD
Cornwall Counseling Group – Las Vegas, Nevada

Abstract

Transcranial Magnetic Stimulation (TMS) has been promoted as a non-invasive intervention for treatment-resistant depression. Despite its clinical popularity, the scientific rationale underlying TMS remains limited by the oversimplified assumption that depression can be localized to discrete brain regions. The human brain is a dynamic, distributed network whose emotional processes emerge from complex, individualized interactions across neural, cognitive, and experiential systems. This paper argues that the reductionist premise of TMS neglects the heterogeneous and phenomenological nature of depression, the idiosyncratic architecture of the brain, and the ethical implications of applying external electromagnetic modulation to an organ we still only partially understand.

Introduction

In recent years, Transcranial Magnetic Stimulation (TMS) has gained approval as a treatment for major depressive disorder, particularly in individuals unresponsive to pharmacotherapy. The treatment’s appeal rests on its claim to target specific cortical regions associated with mood regulation through focused magnetic fields (George & Post, 2011). However, this mechanistic approach to a profoundly human condition risks reducing the complexity of emotional suffering to a matter of neural circuitry. Depression, rather than being confined to one neural locus, represents a convergence of biological, psychological, and social processes—each embedded within the individual’s lived experience (Mayberg, 2003).

The Reductionist Assumption of Localized Dysfunction

Central to TMS is the presumption that depressive symptoms originate in hypoactivity of the dorsolateral prefrontal cortex (DLPFC), and that stimulating this region can restore normative function. Yet, extensive neuroimaging literature reveals that depression involves distributed network dysfunctions encompassing limbic, cortical, and subcortical systems (Mulders et al., 2015). Connectivity between the prefrontal cortex, amygdala, anterior cingulate, hippocampus, and default mode network dynamically fluctuates across individuals and states of mind (Pessoa, 2017). Consequently, to assume that stimulating one cortical region will produce uniform clinical benefit contradicts the empirical evidence for depression’s neurobiological heterogeneity.

Depression as a Distributed Phenomenon

Depression is not a monolithic disorder but a constellation of symptoms shaped by personal history, cognitive style, and environmental context. Neurobiological studies indicate that emotional regulation involves multiple feedback loops integrating affective, cognitive, and sensory processes (DeRubeis et al., 2008). The unique organization of these circuits in each person reflects genetic predisposition, developmental experience, and learned appraisal systems. Attempting to alter mood through external magnetic pulses neglects the adaptive and plastic nature of these interdependent networks. As such, TMS offers an illusion of mechanistic precision unsupported by the brain’s intrinsic variability and interconnectivity.

The Ethical and Clinical Uncertainty of Magnetic Modulation

Although TMS is often described as non-invasive, the ethical implications of altering neuronal activity without fully understanding long-term consequences remain considerable. The brain’s self-organizing complexity means that modulation of one region inevitably influences others in unpredictable ways (Fitzgerald & Daskalakis, 2012). Longitudinal studies assessing cognitive, affective, and neurophysiological changes beyond the acute treatment phase are limited. Furthermore, TMS’s commercial expansion raises concerns about accessibility, informed consent, and therapeutic marketing that may exaggerate efficacy while minimizing uncertainty. The promise of a “neural reset” risks appealing to patient desperation rather than evidence-based understanding.

Individual Experience and Neurobiological Diversity

Human emotion cannot be reduced to cortical activation maps. The subjective experience of depression—its meaning, context, and psychological narrative—is inseparable from its neurobiological expression. Each individual’s brain represents a unique synthesis of experience, perception, and adaptation. Therefore, therapeutic interventions must integrate subjective and relational dimensions rather than rely solely on mechanical stimulation. Psychotherapeutic and cognitive-behavioral approaches recognize this individuality by emphasizing meaning-making, insight, and personal agency (Beck, 2011). In contrast, TMS operates under a biomedical paradigm that privileges physiology while neglecting phenomenology.

Conclusion

The complexity of the human brain and the distributed nature of depression challenge the conceptual foundations of Transcranial Magnetic Stimulation. The assumption that targeted magnetic pulses can recalibrate mood circuits disregards the emergent and individualized character of emotional life. Until neuroscience develops the capacity to map and interpret the full range of interconnected neural dynamics underlying affective experience, TMS should remain a cautiously experimental modality rather than a standardized clinical solution. Depression demands understanding, not magnetization. Its healing arises through human insight, relational depth, and self-awareness—dimensions that no magnetic field can meaningfully reproduce.

References

Beck, A. T. (2011). Cognitive therapy of depression. Guilford Press.

DeRubeis, R. J., Siegle, G. J., & Hollon, S. D. (2008). Cognitive therapy versus medication for depression: Treatment outcomes and neural mechanisms. Nature Reviews Neuroscience, 9(10), 788–796. https://doi.org/10.1038/nrn2345

Fitzgerald, P. B., & Daskalakis, Z. J. (2012). The evolving use of transcranial magnetic stimulation in the treatment of psychiatric disorders. The Journal of Clinical Psychiatry, 73(8), 1097–1103. https://doi.org/10.4088/JCP.10r06556

George, M. S., & Post, R. M. (2011). Daily left prefrontal repetitive transcranial magnetic stimulation for acute treatment of medication-resistant depression. American Journal of Psychiatry, 168(4), 356–364. https://doi.org/10.1176/appi.ajp.2010.10060864

Mayberg, H. S. (2003). Modulating dysfunctional limbic–cortical circuits in depression: Towards development of brain-based algorithms for diagnosis and optimized treatment. British Medical Bulletin, 65(1), 193–207. https://doi.org/10.1093/bmb/65.1.193

Mulders, P. C., van Eijndhoven, P. F., Schene, A. H., Beckmann, C. F., & Tendolkar, I. (2015). Resting-state functional connectivity in major depressive disorder: A review. Neuroscience & Biobehavioral Reviews, 56, 330–344. https://doi.org/10.1016/j.neubiorev.2015.07.014

Pessoa, L. (2017). Understanding brain networks and brain organization. Physics of Life Reviews, 11(3), 400–435. https://doi.org/10.1016/j.plrev.2014.12.009

10/19/2025

The Influence of Sleep Timing on Aggression and Emotional Regulation

Abstract

Michael Cornwall, PsyD, PhD
Cornwall Counseling, Las Vegas, Nevada

This paper explores the relationship between sleep timing—specifically, evening chronotype tendencies—and aggressive or irritable behaviors in humans. Research indicates that individuals who habitually stay up late and sleep late into the day may exhibit higher levels of aggression, impulsivity, and emotional reactivity compared to those with earlier sleep patterns. The phenomenon appears to be mediated by circadian misalignment, impaired sleep quality, and neurobiological processes involving dopamine and serotonin regulation. While causation cannot be established, evidence supports a significant association between delayed sleep schedules and reduced emotional control.

Introduction

Sleep and aggression have long been recognized as interconnected aspects of human functioning. Chronotype, or an individual’s preferred timing of sleep and wakefulness, influences both cognitive and emotional regulation (Hood & Amir, 2020). People classified as “evening types”—those who stay awake late into the night and sleep later in the day—often report higher irritability, reduced impulse control, and increased aggression compared to “morning types,” who wake and retire earlier (Wang et al., 2023).

Literature Review

Wang et al. (2023) examined adolescents and found that those with evening chronotypes demonstrated significantly higher levels of both verbal and physical aggression than morning chronotypes, even after controlling for gender, age, and personality factors. Similar results have been observed in adult and clinical populations, where later bedtimes and reduced total sleep duration correlate with greater hostility and impulsivity (Kamphuis et al., 2012; Ksinan & Spada, 2020).

Discussion

The accumulated evidence supports a consistent association between evening chronotype and elevated aggression, though the relationship appears to be indirect. Sleep quality, circadian misalignment, and neurobiological regulation function as mediating factors. Chronic misalignment may act as a subtle but persistent stressor, leading to reduced emotional control and increased irritability.

Conclusion

Staying up late and sleeping late into the day does not inherently cause aggression, but it may contribute to physiological and psychological conditions that make emotional regulation more difficult. Circadian misalignment, poor sleep quality, and neurochemical imbalance collectively appear to lower emotional thresholds, resulting in more reactive interpersonal interactions. Addressing these sleep-related vulnerabilities through behavioral and therapeutic interventions offers a promising avenue for improving emotional resilience and reducing aggression in both clinical and community settings.

References

Hood, S., & Amir, S. (2020). Are owls and larks different when it comes to aggression? Frontiers in Behavioral Neuroscience, 14, 39. https://doi.org/10.3389/fnbeh.2020.00039

Kamphuis, J., Meerlo, P., Koolhaas, J. M., & Lancel, M. (2012). Poor sleep as a potential causal factor in aggression and violence. Sleep Medicine, 13(4), 327–334. https://doi.org/10.1016/j.sleep.2011.12.006

Ksinan, A. J., & Spada, M. M. (2020). Sleep and aggression: A systematic review. Aggression and Violent Behavior, 51, 101382. https://doi.org/10.1016/j.avb.2020.101382

Tassi, P., & Muzet, A. (2000). Sleep inertia. Sleep Medicine Reviews, 4(4), 341–353. https://doi.org/10.1053/smrv.2000.0098

Taylor, D. J., Lichstein, K. L., Durrence, H. H., Reidel, B. W., & Bush, A. J. (2011). Epidemiology of insomnia, depression, and anxiety. Sleep, 28(11), 1457–1464. https://doi.org/10.1093/sleep/28.11.1457

Wang, Y., Liu, H., Wang, Y.-R., Wei, J., Zhao, R.-R., & Fang, J.-Q. (2023). Relationship between chronotypes and aggression in adolescents. BMC Psychology, 11, 34. https://doi.org/10.1186/s40359-023-01045-8

Dr. Michael Cørnwall

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