Tag: wellness

The NeuroAffective-CBT® Formulation of Pain: Understanding the Body–Brain–Affect Connection

NeuroAffective-CBT

Pain is not simply a signal travelling from the body to the brain. It is a neuroaffective experience emerging from the continuous interaction between physiology, emotion, cognition, and context.

Daniel Mirea (June, 2026)
NeuroAffective-CBT® | https://neuroaffectivecbt.com

Abstract

Pain has traditionally been conceptualised as a direct consequence of tissue damage, whereby nociceptive signals travel from the body to the brain and are subsequently perceived as pain. However, contemporary neuroscience suggests that this explanation is incomplete. Modern pain science increasingly recognises pain as a multidimensional neurobiological and psychological experience that emerges from the continuous interaction between sensory information, emotional states, memory, learning, expectation, context, and prediction. This article explores the distinction between nociception and pain, reviews the role of spinal gating and descending modulation pathways, and examines how affective and cognitive processes contribute to the conscious experience of pain. Drawing upon developments in affective neuroscience, cognitive neuroscience, and contemporary pain research, the article proposes that pain is best understood as a neuroaffective phenomenon rather than a simple sensory event. A NeuroAffective-CBT® (NA-CBT®) perspective is presented, conceptualising pain as the product of an ongoing interaction between the body, brain, and affective systems. Understanding pain through this integrative framework may help clinicians and individuals alike appreciate why pain can persist in the absence of ongoing tissue damage and why effective treatment often requires a biopsychosocial and neuroaffective approach.

Keywords: Pain, Nociception, NeuroAffective-CBT®, Chronic Pain, Affective Neuroscience, Central Sensitisation, Predictive Processing, Pain Perception, Cognitive Behavioural Therapy, Neuroaffective Formulation

The Traditional View of Pain

Although pain has been extensively studied within medicine, neuroscience, and rehabilitation disciplines, discussions within psychotherapy have often focused primarily on symptom management rather than on understanding pain as a complex neuroaffective experience. From a NeuroAffective-CBT perspective, this distinction is important because many of the emotional difficulties presented in therapy involve physiological distress that is experienced, interpreted, and responded to in ways that closely resemble the mechanisms observed in pain itself.

Therefore, pain is not simply something we detect. It is something we experience. And experiences emerge from the continuous conversation between the body, the brain, and affect.

Most of us have been taught a relatively simple explanation of pain. You step on a nail. The injured tissue sends a pain signal through the nerves. The signal travels up the spinal cord.

The brain receives the message. You feel pain.

Simple. Logical. Intuitive.

And yet, although this explanation contains some truth, it is only part of the story.

Over the last several decades, advances in neuroscience, psychology, pain medicine, and affective neuroscience have fundamentally changed our understanding of pain. What we once believed to be a straightforward sensory process is now understood to be a far more complex interaction between the body, brain, emotions, memories, beliefs, expectations, and context.

In many ways, pain provides one of the clearest examples of how the body, brain, and affective systems continuously interact to shape our lived experience.

Most educational diagrams describe pain as a four-step process:

1. Detection of Potential Harm

Specialised nerve endings known as nociceptors detect potentially harmful stimuli such as:

  • Extreme heat
  • Excessive pressure
  • Tissue injury
  • Chemical irritation

These receptors are often described as “pain receptors,” although this is not entirely accurate.

Their actual role is to detect potential danger.

When activated, they send electrical signals through peripheral nerves toward the spinal cord.

2. The Spinal Gate

The signal reaches the spinal cord, where information is filtered before continuing toward the brain.

This concept originates from the famous Gate Control Theory of Pain, proposed by Ronald Melzack and Patrick Wall in 1965.

According to this theory, the spinal cord functions somewhat like a gatekeeper.

Some signals are allowed through. Others are dampened. Others may be amplified.

This explains why rubbing an injured area often reduces discomfort. Touch signals can partially compete with and inhibit nociceptive input at spinal cord level.

3. Modulation

Signals reaching higher centres of the nervous system can be increased or decreased by descending pathways from the brainstem.

In some situations, pain can be dramatically suppressed.

Examples include:

  • Soldiers injured in battle
  • Athletes finishing a race despite serious injuries
  • Emergency situations where survival is prioritised

Conversely, pain can also be amplified by stress, anxiety, fear, sleep deprivation, inflammation, or sensitisation.

4. Conscious Perception

If sufficient information reaches the brain, pain becomes consciously experienced.

This is where most simplified diagrams end.

However, this is also where the most interesting part of the story begins.

The Biggest Misunderstanding About Pain

Perhaps the most important discovery in modern pain science is this:

Pain signals are not actually pain.

The nerves do not carry pain itself.

They carry information.

They carry evidence.

They carry warning signals.

What travels through the nervous system is better described as:

Nociception

Nociception refers to the detection and transmission of potentially harmful stimuli.

Pain, however, is something different.

Pain is an experience.

And experiences are generated by the brain.

This distinction may sound subtle, but it changes everything.

Nociception Without Pain

Consider the following examples.

A footballer breaks a bone during an important match and continues playing.

A soldier is shot in combat and reports little or no pain until reaching safety.

An individual involved in a car accident walks around helping others before realising they are injured.

In all these situations:

The injury exists.

The nociceptive signals exist.

Yet the pain experience is significantly reduced or absent. The nervous system has decided that survival is currently more important than suffering.

Pain Without Injury

Now consider the opposite situation.

An individual experiences severe chronic pain despite normal scans and medical investigations.

Someone develops phantom limb pain after amputation.

A person with fibromyalgia experiences widespread pain despite no obvious tissue damage.

An individual suffers debilitating migraines despite no visible injury.

In these situations, pain exists. Yet tissue damage may be minimal or absent. Again, pain cannot simply be explained as a direct readout of injury.

Something else is happening.

The Brain Is Not Reading Pain

A common misconception is that the brain acts like a computer reading incoming messages. The reality is far more sophisticated.

Modern neuroscience increasingly supports the idea that the brain functions as a prediction machine. Rather than passively waiting for information, the brain continuously asks:

“What is happening?”

“How dangerous is it?”

“What should I do about it?”

Pain appears to emerge from the brain’s attempt to answer these questions.

The human brain rapidly combines incoming sensory information with previous experiences, memory, learning, expectations, emotional state, beliefs, current stress levels, and environmental context before constructing the experience we call pain.

Pain is therefore not merely detected. Pain is actively constructed by the brain based upon incoming information, prior learning, emotional state, and context.

Why Context Matters

Imagine stepping on the same object under different circumstances.

Scenario One:

You are walking barefoot through your garden.

You step on a sharp object unexpectedly.

Pain is immediate.

Scenario Two:

You are undergoing a medical procedure.

You know discomfort is expected.

You trust the clinician.

The same level of stimulation may feel significantly less painful.

Scenario Three:

You are highly anxious, exhausted, sleep deprived, and worried about your health.

The exact same physical stimulus may feel dramatically worse.

The tissue has not changed.

The brain’s interpretation has changed.

The Emotional Brain and Pain

One of the greatest limitations of many pain models is that they largely ignore emotion. Pain is not simply sensory. Pain is profoundly emotional. Several brain regions contribute to the experience.

Somatosensory Cortex

Helps determine (1) Where the pain is (2) How intense it is

Insula

Processes bodily awareness and internal sensations.

Anterior Cingulate Cortex

Contributes to suffering and distress.

Amygdala

Assesses threat and danger.

Generates fear responses.

Prefrontal Cortex

Adds meaning, interpretation, planning, and decision making.

Pain emerges through the interaction of all these systems rather than from a single pain centre.

There is no single location in the brain where pain exists.

Pain is a network phenomenon.

Fear Can Increase Pain

Imagine touching a hot stove.

The immediate pain serves an adaptive purpose.

You withdraw your hand.

Problem solved.

However, if the nervous system begins associating many harmless experiences with danger, pain can become amplified.

The more fearful we become of pain:

  • The more we monitor it
  • The more we anticipate it
  • The more attention we give it

The more significant it can become.

This does not mean the pain is imaginary.

It means the nervous system is becoming increasingly protective.

In many chronic pain conditions, the alarm system becomes overly sensitive.

The danger detector becomes too good at its job.

What Chronic Pain Teaches Us

Acute pain protects us.

Chronic pain often reflects protection that has become excessive.

The nervous system learns.

The brain learns.

The body learns.

Neural pathways become strengthened through repetition.

Eventually the system may begin generating pain responses disproportionate to actual tissue damage.

This process is often referred to as:

  • Central sensitisation
  • Neural amplification
  • Pain sensitisation

The pain remains real.

The suffering remains real.

The underlying mechanisms, however, are different from those involved in acute injury.

A NeuroAffective-CBT Perspective

Within NeuroAffective-CBT, pain can be understood through the interaction between three continuously communicating systems:

Body

The body provides physiological information.

This includes:

  • Injury
  • Inflammation
  • Hormonal changes
  • Sleep quality
  • Nutrition
  • Energy availability
  • Physical conditioning

Brain

The brain interprets incoming information.

It generates predictions based upon:

  • Previous experiences
  • Memory
  • Learning
  • Core beliefs
  • Expectations

Affect

Affective systems shape emotional meaning.

These include:

  • Fear
  • Shame
  • Anxiety
  • Helplessness
  • Anger
  • Grief

Together these systems create the subjective experience we call pain.

Within NeuroAffective-CBT, emotional pain and physical pain are not viewed as entirely separate phenomena. Both involve physiological activation, affective meaning-making, cognitive interpretation, and behavioural responses. Clients frequently describe emotional suffering using physical language: a heavy chest, a knot in the stomach, emotional exhaustion, pressure, tension, emptiness, or feeling broken. Understanding pain therefore provides an important framework for understanding emotional suffering itself.

The Core Principle of NeuroAffective-CBT

The Body influences the Brain.

The Brain influences Affect.

Affect influences Behaviour.

Behaviour influences Physiology.

When any part of this system becomes dysregulated, suffering may emerge.

When all parts of the system are addressed together, healing becomes possible.

Why This Matters Clinically

Understanding pain differently changes how we approach treatment.

Rather than asking only:

“Where is the damage?”

We might also ask:

  • What is the nervous system trying to protect?
  • What role is stress playing?
  • What role is sleep playing?
  • What role is fear playing?
  • What role is emotional suppression playing?
  • What role is avoidance playing?
  • What role is physical deconditioning playing?
  • What role is chronic activation of threat systems playing?

These questions do not invalidate physical explanations.

They expand them.

Pain Is Real, Even When Scans Are Normal

One of the most harmful misconceptions encountered in clinical practice is the belief that normal scans mean symptoms are “all in the mind.”

Nothing could be further from the truth.

Modern neuroscience demonstrates that:

  • Pain is real.
  • The nervous system is real.
  • Brain-based processing is real.
  • Emotional amplification is real.
  • Sensitisation is real.

The absence of visible tissue damage does not invalidate suffering.

It simply means the explanation may be more complex than originally assumed.

The Future of Pain Science

Pain science continues to evolve.

Increasingly, researchers are recognising the importance of integrating:

  • Neuroscience
  • Psychology
  • Physiology
  • Immunology
  • Lifestyle medicine
  • Sleep science
  • Exercise science
  • Nutritional psychiatry
  • Metabolic psychiatry

into a more comprehensive understanding of human suffering.

Pain cannot be fully understood through tissue damage alone.

Nor can it be fully understood through psychology alone.

The future almost certainly lies in integration.

A NeuroAffective-CBT Formulation of Pain

From a NeuroAffective-CBT perspective, pain cannot be fully understood through a purely biomedical model, nor can it be adequately explained through a purely psychological framework. Rather, pain emerges from the dynamic interaction between physiological processes, affective systems, and cognitive interpretation. This perspective is consistent with the NA-CBT Body–Brain–Affect Triangle, which proposes that emotional and behavioural experiences arise from the continuous bidirectional communication between bodily states, brain-based processing, and affective meaning-making systems.

Within this framework, the body provides ongoing physiological information regarding injury, inflammation, fatigue, energy availability, sleep quality, nutrition, hormonal changes, and physical conditioning. The brain continuously interprets this information through the lens of prior learning, autobiographical memory, expectations, beliefs, and threat predictions. Simultaneously, affective systems assign emotional meaning to incoming experiences, influencing whether bodily sensations are perceived as manageable, threatening, overwhelming, or catastrophic.

Consequently, pain is not viewed as a simple readout of tissue damage but rather as a neuroaffective experience generated by the interaction of these multiple systems.

The Role of Threat Perception

One of the central assumptions within NA-CBT is that the nervous system is fundamentally organised around safety and survival. The brain continuously evaluates internal and external information to determine the level of threat present in any given situation.

When a stimulus is interpreted as dangerous, the nervous system may increase vigilance, muscular tension, autonomic arousal, and pain sensitivity. Conversely, when safety cues are present, physiological regulation improves, threat responses diminish, and pain intensity may decrease.

Importantly, threat perception is not determined solely by objective reality. It is influenced by previous experiences, trauma histories, attachment experiences, health beliefs, social context, and emotional states.

Two individuals may therefore experience the same physical injury in dramatically different ways depending upon how their nervous systems interpret and respond to the event.

Trauma, Emotional Learning, and Pain Amplification

Traumatic experiences can significantly alter the way the nervous system responds to future threats. Individuals who have experienced chronic adversity, abuse, neglect, medical trauma, bullying, or emotionally invalidating environments may develop heightened sensitivity within threat-detection systems.

Over time, the nervous system may become increasingly efficient at detecting danger, sometimes responding to relatively minor stimuli as though they represent significant threats.

Within the NA-CBT model, unresolved trauma memories may continue to influence present-day physiological and emotional reactions long after the original event has passed. Pain can therefore become linked not only to tissue-based signals but also to fear networks, emotional memories, learned associations, and protective behavioural patterns.

This perspective aligns with contemporary research demonstrating the involvement of the amygdala, anterior cingulate cortex, insula, hippocampus, and prefrontal regions in both pain processing and emotional regulation.

The Influence of Shame and Anxiety

NA-CBT places particular emphasis on the role of shame-based emotional schemas and chronic anxiety in maintaining emotional distress and self-sabotaging patterns.

Shame frequently operates as a hidden amplifier of suffering.

Individuals who carry longstanding beliefs such as:

  • “I am weak.”
  • “I should be coping better.”
  • “There must be something seriously wrong with me.”
  • “Nobody understands what I am going through.”

may experience increased emotional distress alongside physical symptoms.

Similarly, chronic anxiety can maintain heightened physiological arousal, increased muscle tension, sleep disruption, hypervigilance, and persistent monitoring of bodily sensations. These processes may inadvertently reinforce pain pathways and increase the perceived intensity of symptoms.

From a neuroaffective perspective, emotional suffering and physical suffering often become intertwined, creating self-reinforcing cycles that can be difficult to break without targeted intervention.

The Original TED Model: Tired, Exercise, and Diet

A central component of the NeuroAffective-CBT framework is the original TED model, which focuses on three fundamental physiological domains that frequently influence emotional wellbeing, stress tolerance, cognitive functioning, and pain perception:

Tiredness, Exercise, and Diet.

Within NA-CBT, TED is often conceptualised as an individual’s internal physiological coach. Before attempting to understand complex emotional reactions, trauma responses, self-sabotaging behaviours, or chronic distress, clinicians are encouraged to assess the extent to which these three biological domains may be influencing the individual’s current functioning.

Tiredness

Sleep deprivation and chronic fatigue can significantly alter the way the nervous system processes both emotional and physical experiences.

Research consistently demonstrates that insufficient sleep is associated with:

  • Increased pain sensitivity
  • Reduced emotional regulation
  • Heightened threat perception
  • Increased anxiety and irritability
  • Poorer stress tolerance
  • Reduced cognitive flexibility
  • Greater physiological arousal

From a neuroaffective perspective, an exhausted nervous system is often a more reactive nervous system.

Individuals experiencing chronic pain frequently report poor sleep quality, whilst poor sleep itself can increase pain intensity, creating a self-perpetuating cycle of distress and physiological dysregulation.

For this reason, improving sleep and recovery is often considered a foundational intervention within the NA-CBT model before attempting more intensive emotional processing work.

Exercise

Physical activity plays a critical role in both emotional and physiological regulation.

Regular movement influences multiple systems associated with pain modulation, including:

  • Endorphin release
  • Stress regulation
  • Neuroplasticity
  • Cardiovascular health
  • Inflammatory processes
  • Mood regulation
  • Self-efficacy and resilience

Importantly, exercise may also help challenge fear-avoidance patterns commonly observed in chronic pain conditions.

Many individuals gradually reduce activity levels because movement becomes associated with discomfort or fear of injury. Whilst avoidance may provide short-term relief, prolonged inactivity can contribute to deconditioning, increased vulnerability, reduced confidence, and further sensitisation of the nervous system.

Within NA-CBT, exercise is therefore viewed not simply as a physical intervention but also as a psychological and neurobiological regulator capable of influencing both mood and pain perception.

Diet

Nutrition provides the biological foundation upon which the brain and body operate.

Emerging evidence from nutritional psychiatry, metabolic psychiatry, and neuroscience increasingly suggests that dietary factors may influence emotional wellbeing, inflammation, energy production, cognitive functioning, and stress resilience.

Poor nutritional habits may contribute to:

  • Fatigue
  • Metabolic dysfunction
  • Increased inflammation
  • Blood sugar instability
  • Reduced concentration
  • Mood fluctuations
  • Poor recovery capacity

From an NA-CBT perspective, diet is not viewed through a restrictive or purely weight-focused lens. Rather, it is considered a crucial component of physiological regulation that may influence how effectively the nervous system responds to both emotional and physical stressors.

TED and Pain Perception

The relevance of the TED model to pain becomes increasingly apparent when viewed through a neuroaffective lens.

An individual who is:

  • Chronically sleep deprived,
  • Physically deconditioned,
  • Nutritionally dysregulated,

may experience a nervous system that is more reactive, more vigilant, and more sensitive to both internal and external stressors.

Consequently, pain intensity may increase even when tissue damage remains unchanged.

Conversely, improvements in sleep, physical conditioning, and nutritional stability may help reduce physiological stress, improve emotional regulation, increase resilience, and support healthier pain modulation pathways.

Within the NeuroAffective-CBT framework, TED therefore represents far more than a lifestyle intervention.

It represents a foundational physiological platform upon which emotional regulation, cognitive flexibility, behavioural change, trauma processing, and recovery can occur.

When individuals begin addressing tiredness, exercise, and diet simultaneously, they are often not simply improving their physical health. They are creating the biological conditions necessary for the nervous system to feel safer, more regulated, and less protective.

From this perspective, the TED model becomes directly relevant to understanding why some individuals remain trapped within cycles of chronic pain, emotional distress, and physiological dysregulation, whilst others gradually move towards recovery and resilience.

Metabolic Health, Ketogenic Therapies and Pain

Over recent years, growing attention has been directed towards the relationship between metabolic health, inflammation, brain function, emotional wellbeing, and chronic illness. Whilst traditionally associated with weight management or epilepsy treatment, ketogenic therapies are increasingly being investigated for their potential effects on neurological, psychiatric, and inflammatory conditions.

As discussed in a recent NeuroAffective-CBT article exploring ketogenic therapies and mental health, emerging research suggests that metabolic dysfunction may influence psychological wellbeing through mechanisms involving inflammation, mitochondrial function, oxidative stress, insulin resistance, and energy metabolism within the brain.

This perspective aligns closely with one of the central assumptions of the NA-CBT model: the brain does not function independently from the body. Physiological dysregulation may influence emotional wellbeing, whilst emotional distress may simultaneously influence physiological functioning.

The relevance of this emerging field to pain should not be underestimated.

Many chronic pain conditions are now recognised to involve not only structural or tissue-based factors but also inflammatory processes, autonomic dysregulation, altered stress responses, sleep disturbance, and changes in central nervous system functioning. Increasingly, researchers are exploring whether metabolic interventions may influence some of these mechanisms.

As stated in the recent NeuroAffective-CBT review of ketogenic therapies:

“The question is not whether ketogenic therapies represent a miracle cure. The question is whether some of the benefits reported by patients may be explained by improvements in physiological regulation, inflammation, energy metabolism, sleep, cognition, and emotional stability.”

This is an important distinction.

Within NA-CBT, ketogenic diets are not conceptualised as psychological treatments. Rather, they may represent one example of how physiological interventions can potentially influence the Body–Brain–Affect system.

For some individuals, improvements in metabolic health may be associated with:

  • Reduced systemic inflammation
  • Improved energy regulation
  • Enhanced cognitive clarity
  • Better sleep quality
  • Reduced emotional volatility
  • Improved stress tolerance

All of which may indirectly influence the experience of pain.

Further research is required before definitive conclusions can be reached. However, the growing field of metabolic psychiatry reinforces a principle that sits at the heart of NeuroAffective-CBT®:

The body influences the brain. The brain influences affect. Affect influences behaviour. Behaviour influences physiology.

Understanding pain therefore requires us to look beyond symptoms alone and consider the broader physiological and emotional ecosystem within which those symptoms occur.

Towards an Integrated Understanding of Pain

The clinical implications of this model are significant.

Rather than asking solely:

“Where is the injury?“

NA-CBT® encourages clinicians and individuals to also ask:

  • What is the nervous system trying to protect?
  • What emotional meanings have become attached to the symptoms?
  • What role is fear playing?
  • What role is shame playing?
  • What role is avoidance playing?
  • What role is trauma playing?
  • What role are sleep, nutrition, and physical conditioning playing?
  • What factors are maintaining the brain’s prediction that danger remains present?

These questions do not deny the reality of pain.

Instead, they acknowledge the complexity of human suffering and provide a broader framework for understanding why pain may persist long after tissue healing has occurred.

Ultimately, the NeuroAffective-CBT® model views pain as a whole-person experience emerging from the continuous interaction between the body, brain, and affective systems. By addressing all three domains simultaneously, clinicians may be better positioned to help individuals reduce suffering, improve functioning, and develop a more integrated relationship with their physical and emotional experiences.

Final Thoughts

Perhaps the most important lesson from modern pain science is this:

Pain is not simply a signal travelling from the body to the brain.

Pain is a dynamic neurobiological experience emerging from the continuous interaction between bodily information, emotional states, prior learning, memory, beliefs, context, and prediction.

The body provides information.

The brain evaluates that information.

The affective system gives it meaning.

Together they create the conscious experience we call pain.

Understanding this complexity does not make pain less real.

If anything, it helps explain why pain can sometimes persist long after tissue healing has occurred, why emotions can influence symptoms, why stress can worsen discomfort, and why genuinely effective treatment often requires us to address the whole person rather than a single body part.

In many respects, pain may be one of the clearest demonstrations that human beings cannot be reduced to either mind or body alone.

We are, and always have been, an integrated neuroaffective system.

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Ketogenic Diet and Mental Health

NeuroAffective-CBT

Could Altering Brain Metabolism Improve Emotional Wellbeing?

Daniel Mirea (May, 2026)
NeuroAffective-CBT® | https://neuroaffectivecbt.com

Abstract

This article explores the emerging fields of metabolic psychiatry and nutritional psychiatry, two rapidly developing areas of research investigating how metabolism, inflammation, insulin resistance, mitochondrial function, and nutrition may influence mental health and brain functioning. It examines the growing interest in ketogenic diets, originally developed in the 1920s as a treatment for epilepsy, as potential interventions capable of affecting mood, cognition, emotional regulation, and psychiatric symptoms through changes in brain energy metabolism.

The article also considers an important conceptual question: why are these developments increasingly discussed within psychiatry and medicine, yet far less frequently within mainstream psychology and psychotherapy? While nutritional psychiatry focuses upon the biological and medical relationship between diet and mental illness, psychological models have historically placed greater emphasis upon cognition, behaviour, trauma, attachment, and emotional learning. Emerging integrative approaches such as NeuroAffective-CBT® (NA-CBT®) attempt to bridge this divide by recognising that psychological functioning and physiological regulation continuously interact within the Body–Brain–Affect system.

Although research in this area remains in its early stages, increasing evidence suggests that mental health and metabolic health may be far more interconnected than previously understood.

The relationship between nutrition, metabolism, and mental health is increasingly recognised as one of the most important discussions within modern psychiatry and integrative psychotherapy.

Keywords:
Ketogenic diet; mental health; metabolic psychiatry; nutritional psychiatry; NeuroAffective-CBT; NA-CBT; brain metabolism; insulin resistance; mitochondrial dysfunction; emotional regulation; nutritional ketosis; psychotherapy; metabolism and mental health; inflammation; neuroplasticity; brain energy; metabolic health; depression; anxiety; bipolar disorder; ADHD; trauma; Body–Brain–Affect model.

Introduction: Exploring the Emerging Science of Metabolic Psychiatry

For decades, mental health treatment has focused primarily on psychotherapy and medication. These approaches remain incredibly important and, for many people, life-changing. However, a growing body of research is beginning to suggest that another major factor may have been underestimated for far too long:

Metabolic health.

Researchers working within the emerging field of metabolic psychiatry are increasingly exploring how brain energy, inflammation, insulin resistance, diet, and mitochondrial function may influence emotional wellbeing and psychiatric symptoms.

One of the most discussed interventions within this field is the ketogenic diet — not simply as a weight-loss strategy, but as a possible way of improving how the brain produces and uses energy.

At its core, the idea is surprisingly simple:

Mental health and physical metabolism may be far more interconnected than we once believed.

What Is the Ketogenic Diet?

The ketogenic diet was originally developed in the 1920s as a medical treatment for severe epilepsy in children. Physicians had noticed that periods of fasting sometimes dramatically reduced seizures, but prolonged fasting was obviously not sustainable. Researchers therefore attempted to create a diet that could reproduce the metabolic effects of fasting while still allowing people to eat normally.

The result became known as the ketogenic diet.

A ketogenic diet significantly reduces carbohydrates while increasing fat intake and maintaining moderate protein levels. This shifts the body away from relying primarily on glucose (sugar) for energy and toward burning fat and producing molecules called ketones.

This metabolic state is known as nutritional ketosis.

Ketones can act as an alternative fuel source for the brain, and many researchers now believe that this change in fuel supply may affect not only physical health, but also emotional and cognitive functioning.

In simple terms, a ketogenic diet is a low-carbohydrate, moderate-protein, high-fat nutritional approach designed to shift the body away from relying primarily on glucose (sugar) for energy and toward producing ketones as an alternative fuel source. Ketones are molecules produced by the liver through the breakdown of fat and can be used by the brain and body for energy.

In practical terms, ketogenic diets typically encourage foods such as oily fish, eggs, olive oil, avocado, nuts, seeds, natural full-fat dairy products, and unprocessed meats, while reducing foods high in sugar and refined carbohydrates such as sweets, sugary drinks, white bread, pastries, ultra-processed snacks, and heavily processed fast foods. Many clinicians and researchers also emphasise the importance of prioritising healthier fats and minimally processed foods rather than simply consuming large amounts of fat indiscriminately.

The Forgotten Medical History of Keto

Although ketogenic diets have become fashionable in recent years, their origins are deeply medical rather than commercial.

The ketogenic diet was first formally introduced in 1921 at the Mayo Clinic by Dr. Russell Wilder. At the time, it was considered a serious neurological treatment rather than a lifestyle trend.

Throughout the 1920s and 1930s, ketogenic diets were widely used in hospitals to treat epilepsy, often with remarkable results. Interest later declined after anti-seizure medications became available in the 1940s and 1950s, largely because medication was easier to prescribe and commercially scalable.

For decades, ketogenic therapy remained mostly confined to treatment-resistant epilepsy.

Only in the past twenty years has scientific interest expanded again. Researchers are now exploring ketogenic and low-carbohydrate approaches in relation to obesity, insulin resistance, type 2 diabetes, Alzheimer’s disease, Parkinson’s disease, migraine disorders, inflammation, and increasingly, mental health conditions such as depression, bipolar disorder, schizophrenia, anxiety disorders, and ADHD.

This newer field, more established in the United States than in the United Kingdom, is often referred to as metabolic psychiatry, a field that has emerged more recently than nutritional psychiatry. Using modern neuroscience and advances in brain metabolism research, it is beginning to revisit an old question:

Could changing brain metabolism influence mental health outcomes?

The Brain Is an Energy-Hungry Organ

The human brain represents only around 2% of total body weight, yet it consumes roughly 20% of the body’s energy at rest.

In simple terms, the brain is extraordinarily energy-demanding.

Increasingly, researchers suspect that many psychiatric and neurological conditions may involve problems with how the brain produces, accesses, or regulates energy. Scientists are investigating links between mental illness and insulin resistance, inflammation, oxidative stress, mitochondrial dysfunction, and disrupted neurotransmitter regulation.

This has led to an important question:

What happens when the brain is not being fuelled efficiently?

Some researchers now believe that certain psychiatric symptoms may partly reflect a “brain energy crisis” occurring at the cellular level.

“Changing the Brain’s Operating System”

Harvard psychiatrist Chris Palmer has described the ketogenic diet as potentially changing the brain’s “operating system.”

When the body moves away from a high-carbohydrate, high-insulin state and begins using ketones for fuel, brain cells appear to function differently. Researchers believe this metabolic shift may influence inflammation, neurotransmitter balance, oxidative stress, hormone regulation, and mitochondrial function.

Some scientists hypothesise that ketones may provide a more stable and efficient fuel source for certain brain cells, potentially improving energy production while reducing inflammatory stress.

Although the science is still evolving, this may help explain why some individuals report improvements not only in weight or energy levels, but also in mood stability, concentration, emotional regulation, and mental clarity.

Mental Health and Metabolic Dysfunction

Modern psychiatry is increasingly recognising that mental health difficulties are not always “just psychological.”

Large studies have repeatedly found strong associations between psychiatric conditions and metabolic problems such as obesity, insulin resistance, metabolic syndrome, inflammation, and type 2 diabetes.

This does not mean that depression, anxiety, bipolar disorder, ADHD, PTSD, or schizophrenia are “caused by diet.” Mental health is always complex and multi-layered. Trauma, relationships, stress, genetics, attachment history, and social environment all matter enormously.

However, biology matters too.

In fact, poor metabolic health may sometimes worsen emotional regulation, cognitive function, fatigue, motivation, sleep quality, and stress resilience. To complicate matters further, many psychiatric medications themselves can contribute to weight gain, insulin resistance, and metabolic dysfunction.

Whilst much of the emerging ketogenic psychiatry literature has focused upon symptom reduction, an equally important question may be whether metabolic interventions influence a person’s ability to engage with psychotherapy itself. This issue is particularly relevant within NeuroAffective-CBT (NA-CBT), where emotional regulation, cognitive flexibility, behavioural activation, and trauma processing are understood as dependent upon the ongoing interaction between physiology, affect, and cognition within the Body–Brain–Affect system.

Ketogenic Diets and Psychotherapy Engagement: A NeuroAffective-CBT Perspective

Recent work by Laurent (2026) has proposed an important conceptual shift in how ketogenic metabolic therapy (KMT) may be understood within mental health services. Rather than focusing solely on whether ketogenic interventions directly reduce psychiatric symptoms, Laurent suggests that an equally important question is whether metabolic stabilisation may improve a person’s capacity to engage with psychotherapy itself.

Writing specifically about Cognitive Behavioural Therapy for Psychosis (CBTp), Laurent highlights that many individuals struggle to fully participate in treatment because of factors such as sleep disturbance, cognitive overload, emotional reactivity, poor concentration, low distress tolerance, fluctuating motivation, and difficulties completing between-session therapeutic tasks. These barriers often interfere with treatment initiation, retention, and successful completion.

As Laurent explains:

“The question of this paper is not whether ketogenic therapies are an effective treatment for schizophrenia spectrum disorders. The question is whether this can improve the ability for these patients to utilise CBTp.“

This distinction is clinically significant because it shifts attention from symptom reduction alone towards the broader issue of therapeutic readiness and engagement. Rather than asking whether ketogenic metabolic therapy directly treats psychosis, Laurent asks whether improvements in physiological functioning may help individuals engage more effectively in the psychological work required for meaningful change.

During discussion of the paper, Laurent further observed:

“Could some of the treatment benefits that people are reporting map onto what patients talk about when they discuss having difficulty using CBT?“

This question closely mirrors one of the central assumptions underpinning NeuroAffective-CBT: that psychological change is influenced not only by what individuals think, but also by the physiological state from which those thoughts emerge. Improvements in sleep quality, energy regulation, metabolic functioning, emotional stability, and cognitive clarity may influence therapeutic outcomes not merely through symptom reduction, but by enhancing a person’s capacity to engage in emotional learning, behavioural change, cognitive restructuring, trauma processing, and the development of an integrated sense of self.

Within NA-CBT, therapeutic progress is not viewed solely as a product of cognitive insight. Psychological functioning is understood as emerging from the continuous interaction between physiological regulation, emotional processing, and cognitive interpretation, as illustrated within the Body–Brain–Affect Triangle. From this perspective, interventions that improve physiological stability may indirectly strengthen psychotherapy by creating the conditions necessary for reflective thinking, emotional regulation, behavioural activation, and psychological resilience.

Laurent identifies several domains repeatedly reported within the ketogenic psychiatry literature that are also recognised barriers to successful psychotherapy engagement:

  • Sleep disturbance
  • Cognitive burden and “brain fog”
  • Emotional distress reactivity
  • Mood instability
  • Reduced resilience
  • Functional impairment in everyday life

These domains overlap considerably with those addressed within the original NeuroAffective-CBT® TED model (Tiredness–Exercise–Diet), where physiological regulation is viewed as a prerequisite for optimal emotional and cognitive functioning.

This observation is particularly noteworthy because the original TED model was developed long before the recent emergence of metabolic psychiatry. TED was originally conceived as a practical psychoeducational framework helping clients understand how tiredness, physical activity, nutrition, and lifestyle behaviours continuously influence emotional regulation, cognitive functioning, decision-making, and psychological resilience. From an NA-CBT® perspective, physiological dysregulation frequently manifests as emotional volatility, cognitive overload, reduced distress tolerance, motivational difficulties, and increased vulnerability to shame-based coping patterns. The emerging ketogenic psychiatry literature may therefore be viewed as supporting a broader principle already embedded within the TED framework: when physiology becomes more stable, emotional regulation improves, cognitive flexibility increases, and psychological change often becomes more accessible.

From an NA-CBT perspective, ketogenic interventions should not be viewed as replacements for psychotherapy. Rather, where clinically appropriate and medically supervised, they may function as adjunctive interventions that enhance readiness for psychological treatment. In other words, metabolic interventions may help prepare the psychological and physiological conditions in which psychotherapy can take root and flourish.

This perspective is consistent with a broader biopsychosocial understanding of mental health. When physiological dysregulation is reduced, individuals often experience improved concentration, greater emotional tolerance, increased motivation, enhanced self-reflective capacity, and greater resilience in the face of distress. These changes may allow them to engage more effectively with cognitive restructuring, behavioural experiments, trauma processing, emotional regulation work, and other psychotherapy interventions.

Future research will be needed to determine the extent to which ketogenic metabolic therapy improves psychotherapy engagement across a range of mental health conditions. Nevertheless, the emerging evidence reinforces an important principle already embedded within the NeuroAffective-CBT framework: sustainable psychological change is often easier to achieve when physiological regulation is addressed alongside emotional and cognitive processes. Put simply, when the body functions more effectively, the mind is often better positioned to learn, adapt, regulate, and heal.

Within the NeuroAffective-CBT Body–Brain–Affect Triangle, physiological regulation, emotional experience, and cognitive processing are viewed as continuously interacting components of a single integrated system. Changes in sleep quality, nutrition, inflammation, insulin sensitivity, hormonal balance, physical activity, and energy metabolism do not simply affect the body; they may also influence how emotions are experienced, how meaning is constructed, and how individuals respond to psychological challenges.

From this perspective, ketogenic metabolic therapy represents one example of a broader principle that has long been embedded within the NA-CBT framework: psychological functioning cannot be fully separated from physiological functioning. The way we think, feel, regulate emotions, tolerate distress, and engage in psychotherapy is influenced not only by our beliefs, learning history, and relationships, but also by the biological state of the nervous system from which those experiences emerge.

Consequently, interventions that improve physiological regulation may indirectly enhance emotional resilience, cognitive flexibility, distress tolerance, self-reflective capacity, and therapeutic engagement. From a NeuroAffective-CBT perspective, physiology and psychology are not separate domains competing for explanatory power; rather, they represent different levels of the same interconnected human system. The Body–Brain–Affect Triangle therefore provides a framework for understanding how changes in metabolism, sleep, nutrition, physical activity, emotional regulation, cognition, behaviour, and relationships continuously influence one another. In this context, ketogenic metabolic therapy may be viewed not simply as a dietary intervention, but as one potential pathway through which physiological stabilisation may facilitate emotional regulation, psychological growth, and meaningful therapeutic change.

Clinical Implications for NeuroAffective-CBT

As discussed previously in the article TED Series, Part II: Insulin Resistance and Mental Health, insulin resistance may influence far more than blood sugar alone. Emerging evidence suggests it may also contribute to fatigue, emotional instability, cognitive slowing, cravings, depressive symptoms, and motivational collapse.

Within the NeuroAffective-CBT framework, these physiological states are understood as directly influencing the Body–Brain–Affect system central to emotional functioning.

From this perspective, ketogenic diets may hold psychotherapeutic relevance because they target metabolic flexibility and glucose regulation. By reducing glucose volatility and lowering insulin demand, ketogenic interventions may help stabilise energy availability within the brain and nervous system.

In everyday clinical terms, this may mean that some individuals feel calmer, clearer, less reactive, more emotionally stable, and more capable of engaging in therapeutic work.

Within NA-CBT, TED interventions (Tired–Exercise–Diet) are not presented as rigid dietary rules or wellness ideology. Rather, they are viewed as biologically informed interventions that may improve emotional regulation capacity and psychotherapy responsiveness.

When individuals experience chronic fatigue, emotional dysregulation, shame-driven eating, unstable sleep, poor concentration, or constant cravings, psychotherapy itself may become significantly more difficult because the nervous system remains physiologically overwhelmed.

Chronic physiological dysregulation may also increase vulnerability to shame-based interpretations of failure, weakness, inadequacy, and self-criticism, further reinforcing the maladaptive cycles described within the Pendulum Effect model of NeuroAffective-CBT.

Improving metabolic stability may therefore increase a person’s ability to tolerate emotions, engage in trauma processing, participate in behavioural activation, and benefit from cognitive restructuring.

Importantly, NA-CBT does not present ketogenic diets as a miracle cure or replacement for psychotherapy, psychiatric care, or medication. Rather, the model proposes that psychological functioning and physiological functioning continuously interact.

The brain does not operate separately from the body.

Emotional suffering is often both psychological and physiological at the same time.

Final Thoughts

The ketogenic diet is not a universal solution, and the science surrounding metabolic psychiatry remains in its early stages. Much more high-quality research is still needed, particularly regarding long-term outcomes, individual differences, and the interaction between nutrition, metabolism, psychotherapy, and psychiatric care.

However, one of the most important developments emerging from both metabolic psychiatry and nutritional psychiatry may be the growing recognition that mental health cannot be fully separated from physical health.

What we eat influences how we think, feel, regulate emotion, tolerate stress, and engage with the world around us. Brain metabolism, inflammation, insulin resistance, sleep, trauma, lifestyle, and emotional learning may all interact far more dynamically than traditional models once assumed.

At the same time, these developments raise important questions for psychology and psychotherapy. If nutrition and metabolism can influence mood, cognition, motivation, emotional regulation, and neuroplasticity, then psychological therapies may also benefit from greater integration with physiology and lifestyle medicine.

Approaches such as NeuroAffective-CBT (NA-CBT) attempt to bridge this divide by recognising that the brain does not operate separately from the body, and emotional suffering is often simultaneously psychological, neurological, behavioural, and physiological.

Rather than viewing biology and psychology as competing explanations, emerging integrative models increasingly suggest they may represent different levels of the same human system.

The future of mental health treatment may therefore lie not in choosing between biology or psychology, but in understanding how physiology, emotion, cognition, behaviour, relationships, trauma, and meaning continuously interact within one integrated human system. From a NeuroAffective-CBT perspective, lasting psychological change becomes most achievable when the Body, Brain, and Affect are understood not as separate domains, but as interconnected components of the same human experience.

Disclaimer

This article is for educational purposes only and does not constitute medical advice, diagnosis, or treatment. Ketogenic diets and therapeutic nutritional ketosis may significantly affect metabolism, medications, blood sugar, blood pressure, and psychiatric symptoms. Individuals considering significant dietary changes, particularly those with mental health conditions, eating disorders, diabetes, or those taking medication, should consult appropriately qualified healthcare professionals before making changes to diet or treatment plans.

References

Chris Palmer (2022). Brain Energy: A Revolutionary Breakthrough in Understanding Mental Health — and Improving Treatment for Anxiety, Depression, OCD, PTSD, and More. BenBella Books.

Georgia Ede (2024). Change Your Diet, Change Your Mind. London: Hodder & Stoughton.

Laurent, N. (2026) ‘Ketogenic metabolic therapy as a candidate adjunct for CBTp delivery in schizophrenia spectrum disorders’, Frontiers in Psychology, 17, 1775511. doi:10.3389/fpsyg.2026.1775511.

Mirea, D. (2025) TED in NeuroAffective-CBT®: An applied self-regulation framework for enhancing emotional well-being through sleep, movement and nutrition. NeuroAffective-CBT®. Available at: https://neuroaffectivecbt.com/2025/12/10/ted-in-neuroaffective-cbt-an-applied-self-regulation-framework-for-enhancing-emotional-well-being-through-sleep-movement-and-nutrition/ (Accessed: 2026).

Russell Wilder (1921). Original work introducing the ketogenic diet as a treatment for epilepsy at the Mayo Clinic.

Further Reading

Articles exploring NeuroAffective-CBT®, emotional regulation, trauma, neuroplasticity, and the Body–Brain–Affect model. And additional perspectives integrating physiology and psychotherapy can be found at NeuroAffective-CBT® Articles including: TED Series, Part II: Insulin Resistance and Mental Health

Research literature within Metabolic Psychiatry exploring the relationship between brain energy metabolism, insulin resistance, inflammation, and psychiatric disorders.

Mitochondrial Psychiatry literature investigating the role of mitochondrial dysfunction in depression, bipolar disorder, schizophrenia, and neurodegenerative conditions.

Research into insulin resistance and mental health increasingly suggests associations between impaired glucose metabolism, inflammation, depression, cognitive dysfunction, and emotional dysregulation.

Studies investigating ketogenic therapy in epilepsy continue to demonstrate the long-established neurological effects of nutritional ketosis, particularly in treatment-resistant epilepsy.

Evidence supporting ketogenic diet as an adjunct therapy in the treatment for chronic mental illness: 

MetabolicMind.org

Frontiers | Ketogenic metabolic therapy as a candidate adjunct for CBTp delivery in schizophrenia spectrum disorders

A NeuroAffective-CBT Perspective on Perimenopause: Multi-System Recalibration of Brain, Body, and Behaviour

NeuroAffective-CBT

Defining Perimenopause and Menopause

Perimenopause is often approached primarily as a hormonal issue and is typically managed within general medical practice. While this is appropriate, it may underrepresent the broader impact of this transition across neural, behavioural, and regulatory systems. As a result, the condition is not consistently addressed within the field of psychotherapy. From a NeuroAffective-CBT perspective, perimenopause can be understood as a multi-system recalibration involving the brain, body, and behaviour, with direct implications for clinical formulation and support.

Perimenopause refers to the transitional period leading up to menopause, during which ovarian hormone production becomes increasingly variable. This phase may begin several years before the final menstrual period and is characterised by fluctuations in estrogen and progesterone levels, often accompanied by changes in menstrual regularity, sleep, mood, and physiological stability.

Menopause is clinically defined as the point at which menstruation has ceased for twelve consecutive months, marking the end of reproductive function (National Institute for Health and Care Excellence, 2024). Postmenopause refers to the phase following this transition, during which hormone levels stabilise at a lower baseline.

From a physiological perspective, perimenopause represents a continuous process of endocrine adjustment rather than a discrete event. It is characterised by fluctuating hormone levels and associated changes in sleep, mood, and cognitive function (National Institute for Health and Care Excellence, 2024). From a NeuroAffective-CBT perspective, this transition can be understood as a biopsychophysiological process in which these changes increase regulatory load across multiple interacting systems.

The transition from the reproductive years into this phase involves a significant endocrine shift, characterised primarily by declining estrogen and progesterone levels (Mirea and Popa, 2026). These hormonal changes do not affect a single system in isolation. Estrogen receptors are widely distributed across the brain, cardiovascular tissue, skeletal muscle, bone, and immune structures, meaning that changes in estrogen signalling influence multiple interconnected physiological systems simultaneously (Strasser, 2015; Mennitti et al., 2024).

Brain and Neurochemical Regulation

The central nervous system is directly involved in this transition. Estrogen crosses the blood–brain barrier and modulates neural function through its effects on receptor expression, synaptic plasticity, and neurotransmitter dynamics. In particular, estrogen interacts with serotonergic pathways, influencing serotonin synthesis, receptor sensitivity, and reuptake processes.

Fluctuations or sustained reductions in estrogen during perimenopause and menopause have been associated with changes in mood stability, increased vulnerability to anxiety, reduced cognitive clarity, and the commonly reported experience of “brain fog.” These outcomes are multifactorial; however, altered stress responsivity and changes in neuroplastic processes are recognised contributors to emotional and cognitive shifts (Davidson and McEwen, 2012; Deslandes, 2014).

Gut–Brain–Immune Interactions

Serotonin regulation is not confined to the brain. Approximately 90% of serotonin is synthesised in the gastrointestinal tract. Although peripheral serotonin does not directly cross the blood–brain barrier, the gut microbiome influences central nervous system function through immune signalling, vagal pathways, and metabolite production, a bidirectional system often described as the gut–brain axis.

Emerging evidence suggests further interaction between estrogen metabolism and the gut microbiome via the estrobolome, the collection of microbial genes capable of metabolising estrogens (Plottel and Blaser, 2011). After hepatic processing, conjugated estrogens enter the intestinal tract, where microbial enzymes may influence their reactivation and recirculation.

In parallel, short-chain fatty acids (SCFAs), produced by specific bacterial populations, contribute to gut barrier integrity, immune modulation, and metabolic regulation. During perimenopause, shifts in estrogen levels may coincide with changes in microbiome composition, with potential downstream effects on inflammatory tone and stress-related physiology (Gleeson et al., 2011; Nieman, 2018).

A System in Ongoing Dialogue

Taken together, endocrine, neural, immune, and microbial systems operate in continuous interaction. When estrogen signalling declines, the balance of regulatory processes across these systems may shift, influencing metabolic health, mood stability, energy regulation, and cognitive clarity.

From this perspective, the experience of perimenopause is not reducible to a single mechanism. Rather, it reflects the convergence of multiple regulatory changes occurring simultaneously across the organism.

NA-CBT Implications: Supporting Regulation During Transition

The day-to-day manifestations of this recalibration are both physiological and psychological. Changes in sleep quality, stress tolerance, digestion, appetite, mood stability, and cognitive function may reflect underlying shifts in hormonal, neural, and gut–brain signalling; presenting complaints are common across a range of psychiatric conditions therefore diagnosis and mental health assessment is difficult.

Within the NA-CBT framework, these changes are understood not simply as symptoms to be eliminated, but as indicators of altered regulatory load within the system.

This perspective reinforces the importance of stabilising core regulatory domains:

  • Sleep: maintaining consistent timing and protecting recovery
  • Exercise: particularly resistance training, to support neuromuscular and metabolic stability
  • Nutrition: ensuring adequate protein, fibre, alcohol reduction and energy availability
  • Stress regulation: supporting transitions between activation and recovery

These are not quick fixes. They function as foundational supports for a system undergoing biological recalibration.

The Body–Brain–Affect Relationship

As outlined above, the body–brain–affect connection is central to how the organism functions as an integrated system. Early work by Charles Darwin (1872) recognised that affective expression is a core feature of emotional states and contributes to subjective experience. More recent research, including work by David J. Anderson (2014 and 2016), has further explored the neural circuits underlying behavioural responses, demonstrating how hormones and neuromodulators shape contextual affective states through signals experienced as feelings, imagery, and automatic behavioural tendencies.

From this perspective, the perimenopausal transition can be understood as a complex interaction of hormonal change, affective fluctuation, and behavioural shifts. Translating these processes into psychotherapy highlights the importance of understanding how to support exposure, regulation, and recovery in a safe and compassionate manner, with the aim of improving quality of life.

As illustrated in the Body–Brain–Affect model, this relationship provides a clinically useful framework for formulation:

  • Physiological states shape emotional and cognitive processes
  • Emotions influence thoughts and behaviour
  • Thoughts and behaviours, in turn, reshape physiology

Within this system, the TED model (Tired – Exercise – Diet) functions as the physiological regulation arm of NA-CBT, reducing background volatility so that deeper psychological learning can occur.

A central therapeutic aim is supporting clients in distinguishing between:

  • Raw affect — the body’s immediate signal of threat or discomfort
  • Interpretation — the meaning the mind assigns to that signal

When these become fused, emotions may be experienced as overwhelming, self-defining, or difficult to regulate. Stabilising physiological state first helps create the conditions for more flexible interpretation and response.

Why Lifestyle Interventions Belong Inside Psychotherapy

When sleep is disrupted, movement is limited, or metabolic stability is compromised, individuals often experience:

  • heightened anxiety or irritability
  • increased emotional reactivity and rumination
  • intensified self-criticism or shame
  • reduced tolerance for uncertainty, stress, or interpersonal challenge

From an NA-CBT perspective, these are not failures of insight or willpower. They reflect a system operating under strain and psychotherapeutic intervention without emotional recalibration is difficult. The TED model aims for sufficiency rather than optimisation. The goal is not perfect habits, but a stable internal environment that reduces threat sensitivity and supports emotional regulation.

Illustrative Case Example

A 47-year-old woman presented with anxiety and work-related stress, without initial awareness of potential perimenopausal influences. A previous contact with mental health services had led to a referral for attention-deficit/hyperactivity disorder (ADHD), which was not subsequently supported. During assessment, she noted that her most intense episodes of worry occurred in the late morning, typically following poor sleep, skipped breakfast, and increased caffeine and sugar intake.

Using a TED-informed framework, these episodes were reformulated as reflecting not only psychological stress but also fatigue and metabolic instability. Initial intervention focused on stabilising these domains: sleep training, reducing caffeine and sugar intake, improving nutritional adequacy (including micronutrient support where indicated), and introducing a consistent routine of exercise, relaxation, and recovery practices.

As physiological stability improved, the client was better able to engage in psychological work, including exploring beliefs related to menopause, health, and identity. Subsequent consultation with her GP led to the initiation of hormone replacement therapy (HRT), which further contributed to improvements in overall quality of life. What initially felt overwhelming became more manageable as the underlying regulatory load was reduced. This case illustrates how addressing physiological load may facilitate engagement with psychological processes during the perimenopausal transition

Common Negative Beliefs and Associated Behavioural Patterns

The menopausal transition is often accompanied by shifts in the interpretation of internal states and significant alterations to self-image. A long history of mental illness complicates the picture even more. The following belief–affect–behaviour patterns are commonly observed:

  1. “Something is wrong with me”
    Affect: anxiety, confusion, hypervigilance
    Behaviour: symptom checking, excessive reassurance seeking, or avoidance of medical consultation
  2. “I’m losing control of my body and mind”
    Affect: fear, helplessness
    Behaviour: withdrawal from demands, reduced decision-making, disengagement from responsibilities
  3. “I can’t cope like I used to. This is embarrassing; Sex is not the same. I will end up alone”
    Affect: shame, frustration
    Behaviour: avoidance of challenge, argumentative, over-reliance on others, reduced role engagement
  4. “This is permanent and will only get worse”
    Affect: hopelessness
    Behaviour: reduced help-seeking, disengagement from treatment or behavioural change
  5. “I’m becoming less capable”
    Affect: self-doubt, embarrassment
    Behaviour: avoidance of cognitively demanding or evaluative situations
  6. “I’m not myself anymore”
    Affect: identity disturbance, grief
    Behaviour: social withdrawal, loss of engagement in valued activities
  7. “Other people will notice and judge me”
    Affect: social anxiety
    Behaviour: avoidance of visibility (meetings, presentations, social interaction)
  8. “Exercise will make things worse. I’m too exhausted”
    Affect: fatigue, apprehension
    Behaviour: inactivity, loss of routine, reduced exposure to beneficial physiological stress
  9. “I just need to push through this”
    Affect: internal pressure
    Behaviour: paradoxical avoidance of rest and recovery, leading to further dysregulation
  10. “I should be able to handle this on my own”
    Affect: isolation, self-criticism
    Behaviour: reduced help-seeking (medical, psychological, or social)

NA-CBT Formulation

From a NeuroAffective-CBT perspective, these patterns often emerge when physiological signals (raw affect) become fused with cognitive interpretation.

For example:

Physiological load →
Fatigue and hormonal fluctuation →
Increased limbic (amygdala) reactivity →
Threat-focused attention and cognitive interpretation (“I’m losing control”) →
Avoidance / compensatory / capitulatory behaviours →
Reduced regulatory capacity →
Increased instability →
Increased physiological load

This sequence operates as a self-reinforcing loop. Behavioural responses such as avoidance, overcompensation, or capitulation may reduce distress in the short term, but they contribute to the maintenance of the problem through several interacting mechanisms.

First, they reinforce threat perception and amplify raw affect. When internal states are repeatedly interpreted as dangerous or unmanageable, the nervous system becomes increasingly sensitised, heightening vigilance toward bodily sensations and emotional shifts.

Second, they reduce exposure to corrective experiences. Avoiding situations, sensations, or demands limits opportunities to learn that these internal states are tolerable, transient, and manageable. As a result, threat-based interpretations remain unchallenged.

Third, these behaviours constrain opportunities for physiological regulation. Reduced movement, disrupted routines, poor sleep, and inconsistent nutrition can increase physiological load, narrowing the system’s capacity to recover from activation.

Over time, these processes interact to maintain both physiological and psychological dysregulation. Increased instability feeds back into elevated physiological load, perpetuating the cycle and increasing the likelihood that future internal states will again be interpreted as threatening.

Intervention within this framework focuses on interrupting this loop by stabilising physiological load, modifying threat-based interpretation, and reintroducing corrective behavioural experience.

Clinical Implications

The therapeutic aim is not the immediate elimination of these beliefs, but the creation of conditions in which they can be re-evaluated more flexibly.

This involves:

  • differentiating physiological state from interpretation
  • stabilising underlying regulatory systems (TED: sleep, exercise, nutrition)
  • gradually reintroducing avoided or restricted behaviours

As regulatory stability improves, interpretation becomes less rigid and more context-sensitive. This supports a shift from:

“Something is wrong with me”
to
“My system is under load, and can be supported”

Plain-Language Summary

Perimenopause is not just hormonal; it affects the whole system — brain, body, and behaviour.

Hormonal changes influence mood, sleep, stress sensitivity, and cognitive clarity. At the same time, the brain, immune system, and gut interact in ways that shape how these changes are experienced.

From a NeuroAffective-CBT perspective, these are not simply “symptoms”, but signals that the system is operating under increased regulatory load. By supporting sleep, movement, and nutrition, individuals can reduce this load and improve emotional regulation. These lifestyle interventions can then be complemented by targeted cognitive and behavioural strategies.

Rather than being only a period of disruption, perimenopause can also represent an opportunity to develop more stable and adaptive patterns of functioning, adjust expectations, and strengthen coping and self-efficacy in preparation for the next stage of transition.

Conclusion

Perimenopause can be understood as a period of multi-system adjustment involving endocrine, neural, immune, and metabolic processes. The variability in individual experience reflects the complexity of these interacting systems rather than a single causal pathway.

From a NeuroAffective-CBT perspective, this transition highlights the importance of integrating physiological regulation into psychological formulation. Changes in mood, cognition, and behaviour are not solely psychological in origin, but often reflect shifts in underlying regulatory systems operating under increased load.

This perspective has practical implications. Interventions that stabilise sleep, support nutritional adequacy, and maintain appropriate levels of physical activity may help reduce background physiological volatility, creating conditions in which emotional regulation and cognitive flexibility can be more effectively supported.

Within this framework, the aim is not to eliminate distress, but to improve the system’s capacity to move between states of activation and recovery with greater stability and predictability. As regulatory capacity improves, individuals are better able to differentiate between physiological signals and their interpretation, reducing the likelihood that transient internal states are experienced as overwhelming or self-defining.

In this way, perimenopause can be understood not only as a period of challenge, but also as an opportunity for recalibration. When supported appropriately, this transition may facilitate the development of more stable regulatory patterns across physiological and psychological domains, contributing to long-term resilience and adaptive functioning.

Perimenopause is not merely an endocrine event but a biopsychophysiological transition with implications for affect regulation, cognition, sleep, and behaviour. A NeuroAffective-CBT formulation may be clinically useful insofar as it integrates physiological state, emotional processing, and behavioural adaptation. Within this framework, interventions targeting sleep regularity, movement, nutrition, stress recovery, and cognitive appraisal may help reduce regulatory load and support more flexible functioning during the menopausal transition. However, the specific contribution of NA-CBT remains a clinical formulation model rather than an established evidence-based treatment protocol for perimenopausal distress.

Glossary of Key Terms

Perimenopause
The transitional phase before menopause, characterised by fluctuating levels of estrogen and progesterone, often accompanied by changes in mood, sleep, and physiological stability.

Menopause
The point at which menstruation has ceased for twelve consecutive months, marking the end of reproductive function.

Estrogen
A primary female sex hormone involved in reproductive function, but also influencing brain activity, mood regulation, bone health, and metabolic processes.

Serotonergic signalling
The activity of serotonin (a neurotransmitter) in the brain, involved in mood, emotional regulation, sleep, and cognition.

Synaptic plasticity
The brain’s ability to change and adapt by strengthening or weakening connections between neurons, supporting learning, memory, and emotional regulation.

Stress responsivity
The way the body and brain respond to stress, including activation of hormonal and nervous system pathways.

Gut–brain axis
The bidirectional communication system between the gastrointestinal tract and the brain, involving neural, immune, and metabolic pathways.

Estrobolome
The collection of gut bacteria capable of metabolising estrogen, influencing how estrogen is processed and recirculated in the body.

Short-chain fatty acids (SCFAs)
Metabolic by-products produced by gut bacteria that support immune function, gut integrity, and metabolic regulation.

Physiological load
The overall burden placed on the body’s regulatory systems, influenced by factors such as sleep, stress, nutrition, hormonal changes, and physical activity.

Raw affect
Immediate, pre-cognitive bodily signals of emotional or physiological states (e.g., tension, fatigue, heat, agitation).

Cognitive interpretation
The meaning or explanation the mind assigns to internal or external experiences (e.g., “something is wrong with me”).

Limbic (amygdala) reactivity
Increased activity in brain regions involved in threat detection and emotional processing, particularly the amygdala.

Threat-focused attention
A cognitive bias in which attention is directed toward perceived threats, including bodily sensations or emotional states.

Avoidance behaviours
Actions aimed at reducing distress by withdrawing from or avoiding perceived threats, often maintaining anxiety over time.

Compensatory behaviours
Actions intended to counteract or control perceived problems (e.g., overworking, excessive reassurance seeking), which may inadvertently maintain distress.

Capitulatory behaviours
Patterns of giving up or disengaging in response to perceived inability to cope, often associated with withdrawal or reduced functioning.

Regulatory capacity
The ability of the body and mind to return to a stable baseline following stress or activation.

Autonomic flexibility
The capacity of the nervous system to shift effectively between states of activation (stress) and recovery (rest).

Neuroplasticity
The brain’s ability to reorganise and adapt in response to experience, learning, and environmental demands.

NeuroAffective-CBT (NA-CBT)
An integrative cognitive-behavioural framework that incorporates physiological regulation (sleep, exercise, nutrition) into psychological formulation and intervention.

TED Framework (Tired–Exercise–Diet)
A model within NA-CBT focusing on three core regulatory domains: sleep/fatigue, physical activity, and nutrition.

Regulatory load
The cumulative demand placed on physiological and psychological systems, influencing emotional stability and cognitive function.

References

Anderson, D.J. (2016) Circuit modules linking internal states and social behaviour in flies and mice. Nature Reviews Neuroscience, 17(11), pp. 692–704.

Anderson, D.J. and Adolphs, R. (2014) A framework for studying emotions across species, Cell, 157(1), pp. 187–200.

Cortez, M. and Mirea, D. (2026) The transdiagnostic application of NeuroAffective-CBT: A case study of chronic stress and burnout. NeuroAffective-CBT®, London. Available at: ResearchGate.

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