Ketogenic Diet and Mental Health

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.

This can create a vicious cycle in which worsening physical health and worsening mental health begin reinforcing one another.


Keto, Insulin Resistance, and 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.

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, NeuroAffective-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 metabolism, neuroscience, relationships, trauma, behaviour, and meaning continuously interact within one integrated human system.


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.


Further Reading and References

Articles exploring NeuroAffective-CBT®, emotional regulation, trauma, neuroplasticity, and the Body–Brain–Affect model.

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

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

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

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.

Additional psychoeducational perspectives integrating physiology and psychotherapy can be found at NeuroAffective-CBT® Articles including: TED Series, Part II: Insulin Resistance and Mental Health

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

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.


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Peluso, M.A.M. and Guerra de Andrade, L.H.S. (2005) ‘Physical activity and mental health: the association between exercise and mood’, Clinics, 60(1), pp. 61–70.

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When Panic Attacks Go Beyond Panic Disorder: A NeuroAffective-CBT Perspective

A clinical story about how panic, shame, and physiological dysregulation interact and why stabilising physiological regulation can be the first step toward recovery.

Co-author: Ioana Dulcu (Clinical Psychology, Hypno-CBT)
www.neuroaffectivecbt.com
March 2026


Jenna’s story

When Jenna, a 26-year-old married woman, first arrived for therapy after the sudden onset of panic attacks, she dreaded that the conversation would revolve around her anxiety symptoms.

Naturally, she thought there would be questions about panic, about the frightening episode that had sent her to the emergency department, about what she had been thinking and feeling when the dizziness first appeared. In fact, she later admitted that she even anticipated she might throw up again.

What Jenna did not anticipate was that the assessment would begin somewhere more fundamental: examining the biological foundations that shape how the body responds to stress.

Sleep. Daily routines. Caffeine intake. Hydration. Movement. Even blood tests.

Like many people seeking help for panic attacks, Jenna assumed therapy would focus mainly on her thoughts, behaviours, and fears. Many people now research treatment options online before beginning therapy, and when they do, cognitive-behavioural methods such as interoceptive exposure are often presented as key evidence-based interventions, though they can also appear challenging at first.

What Jenna did not expect was that we would begin somewhere safer and more stabilising.

In the early sessions, rather than immediately exploring painful memories or emotional narratives, the work focused on regulation, restoring physiological balance through better sleep, movement, and nutritional habits.

The deeper personal stories would come later. Timing in NA-CBT is everything.

This approach reflects a core principle of NeuroAffective-CBT: when physiological arousal remains chronically elevated, emotional processing becomes far more difficult. Stabilising the body first often creates the conditions necessary for deeper psychological work to emerge safely.

Jenna had self-referred for therapy after a sudden episode of dizziness that appeared without warning two months earlier. The sensation was intense and frightening, accompanied by nausea, weakness in her knees, and a powerful fear that she might collapse or lose control. She went to the emergency department, where a full medical assessment was carried out. Neurological and vestibular causes were investigated, but no medical explanation was found.

Although the doctors reassured her that nothing serious had been detected, Jenna did not feel reassured. If anything, the uncertainty intensified her distress.

In the weeks that followed, panic attacks began to occur repeatedly. She developed a growing mistrust of her own body. Ordinary sensations—dizziness, nausea, shifts in breathing—began to feel unpredictable and dangerous. Her attention became increasingly focused inward, scanning constantly for signs that another episode might occur.

Soon the panic spread into daily life. Jenna began avoiding leaving the house alone. Shopping trips felt unsafe unless her husband accompanied her. Her world gradually narrowed as the fear of bodily sensations expanded.

Vomiting episodes also began to appear, usually during periods of intense anticipatory anxiety. These episodes seemed to provide temporary relief from the overwhelming sensations in her body, but they reinforced her belief that something was fundamentally wrong internally.

At the same time, sleep became disrupted. Fatigue increased. The body’s resilience decreased. The more exhausted she became, the more reactive her internal regulation felt.

During one of the early sessions, Jenna used a phrase that captured the essence of her distress:

“My body doesn’t feel safe anymore”.

At first glance, this presentation might seem like a relatively typical panic disorder with agoraphobic avoidance. But as the assessment unfolded, a deeper pattern began to emerge.

Jenna had been raised by a single mother together with three siblings. One memory stood out vividly. She was eight years old when her father left to work abroad and never returned. From that point forward, the emotional and practical responsibilities within the family shifted dramatically. Her mother, struggling with depression, found it difficult to maintain stability at home.

Jenna stepped in.

Even as a child, she assumed responsibilities that extended far beyond ordinary expectations. Helping her siblings became part of daily life, preparing lunches, supporting routines like cleaning and cooking and managing various responsibilities within the household.

Failure was not an option.

Getting things wrong felt dangerous. Someone might suffer if she did.

Looking back, Jenna described that period not as a conscious decision but as something she simply had to do. Over time, a quiet internal rule formed: if she remained alert enough, responsible enough, and careful enough, she could prevent things from going wrong.

The NeuroAffective-CBT formulation known as the Pendulum-Effect helps explain how such internal rules can shape coping patterns across many years.

At the centre of this pendulum system typically lies a powerful core affect—often shame, guilt, or the fear of failing others. Around this core experience, a set of self-protective strategies gradually develops in an attempt to manage the internal threat it creates.

In Jenna’s case, these strategies took three familiar forms. What once began as adaptive coping gradually evolved into self-sabotaging patterns that maintained the very distress they were originally designed to regulate.

One was overcompensation. She became highly vigilant, attentive to details, and constantly alert to potential problems. Missing something important felt unacceptable. Remaining on guard all the time seemed like the safest option.

Another strategy was avoidance. Situations that might create additional stress or draw attention toward her own needs were often postponed or abandoned. Investing time in herself, hobbies, rest, or personal interests, rarely felt justified.

Eventually, these cycles led to capitulation, moments when exhaustion and self-criticism took over. When she could not meet the impossible standards she had set for herself, the internal response was harsh: self-blame, guilt, and a sense that she was failing.

These strategies oscillated continuously—overcompensation, avoidance, and capitulation—like the movement of a pendulum. Each provided temporary relief from the underlying fear of getting things wrong, yet each also reinforced the deeper shame driving the system.

For many years, this pattern functioned quietly in the background of Jenna’s life.

Until her body interrupted it.

When panic attacks appeared, the same pendulum dynamics intensified. Hypervigilance shifted toward internal sensations. Avoidance expanded into everyday life. Exhaustion and self-criticism deepened when symptoms seemed uncontrollable.

This was one of the reasons the therapist introduced the TED framework (Tired–Exercise–Diet) early in the treatment process. Lifestyle interventions in NeuroAffective-CBT are not simply recommendations for general wellbeing. They function as direct interventions within the pendulum system itself.

For someone whose life has been dominated by overcompensation and self-neglect, improving sleep, eating regularly, or creating space for physical movement becomes more than self-care. It becomes a challenge to the internal rule that personal needs must always come last.

In Jenna’s case, stabilising her daily rhythms began to soften the relentless cycle of hypervigilance and exhaustion. Less fatigue meant less physiological reactivity. More predictable routines meant her internal regulation no longer had to remain constantly on guard.

Only once this stabilisation began did the deeper emotional narratives gradually come into view.

And only then did it become clear that Jenna’s panic attacks were not simply about panic.

They were about a system that had spent many years trying not to fail anyone, until eventually the pendulum could no longer keep swinging.

To understand why this happens, we need to look more closely at how panic attacks actually develop inside the body.

Why Panic Attacks Are Sometimes Not Just About Panic

When people experience their first panic attack, it often feels as though something in the body has suddenly gone wrong.

The heart races. Breathing changes. The body may tremble or feel weak. Dizziness appears without warning. Nausea, heat, or a sense of losing control can follow within seconds. Because these sensations are so intense and unfamiliar, many people understandably assume they are experiencing a serious medical emergency.

Jenna’s experience began in exactly this way.

The sudden dizziness that sent her to the emergency department felt like something catastrophic was happening inside her body. Even after medical tests ruled out neurological or vestibular causes, the feeling of danger did not disappear. The absence of a medical explanation did not bring relief, it created uncertainty.

And uncertainty is something the body’s regulatory system does not tolerate well.

From the outside, panic attacks can appear sudden and unpredictable. Yet when we look more closely, they often emerge from an internal system that has been under pressure for a long time.

NeuroAffective-CBT approaches panic from the understanding that emotional distress rarely originates in thoughts alone. Instead, it arises from the interaction between three continuously communicating systems: the body, the brain, and affect, our emotional signalling system.

The body constantly sends signals about internal states, fatigue, hunger, hormonal shifts, blood sugar levels, sleep deprivation, muscle tension, and breathing patterns. The brain interprets these signals and attempts to predict whether the environment is safe or threatening. Affect provides the emotional tone that guides behaviour: fear, shame, anger, safety, and relief.

When these systems are balanced, signals move smoothly between them. The body senses changes, the brain interprets them accurately, and emotions guide appropriate responses.

But when the system becomes dysregulated, those signals can begin to amplify one another.

Fatigue may increase physiological sensitivity. Increased sensitivity can heighten attention toward bodily sensations. Heightened attention can make normal sensations feel unusual or threatening. Once the brain interprets those sensations as danger, the body responds with a rapid stress reaction.

At that point, the panic attack is already underway.

In Jenna’s case, the first episode of dizziness acted like a spark in a system that was already vulnerable. Her autonomic state had spent many years in heightened vigilance, trying to anticipate problems, trying not to miss anything important, trying not to fail the responsibilities she had carried since childhood.

Hypervigilance can be a powerful survival strategy. It helps people remain alert, organised, and prepared. But when the body remains in this state for too long, it becomes increasingly sensitive to internal signals.

Even small fluctuations in breathing, blood pressure, or balance can suddenly feel alarming.

The body begins sending signals of danger not because there is a real external threat, but because the regulatory system has become overly reactive.

Once that cycle begins, panic attacks can develop quickly. The body senses something unusual, the brain interprets it as threat, and the emotional system amplifies the response.

This is why panic attacks often persist even when people know intellectually that nothing medically dangerous is happening.

The mind may understand that the body is safe, but the body’s internal regulation has not yet learned that lesson.

And this is also why treatment that focuses only on thoughts may not always be sufficient.

If the body remains exhausted, overstimulated, sleep deprived, or metabolically unstable, it will continue sending signals that the brain interprets as danger. The emotional system then reacts accordingly.

In other words, the panic attack may be the final expression of a much larger regulatory imbalance.

This was the case for Jenna.

Her panic attacks were not simply the result of catastrophic thinking about bodily sensations. They were emerging from a system that had been operating under prolonged pressure, physiologically, emotionally, and psychologically.

Before the deeper emotional narratives could be explored, her body first needed something much more basic. It needed stabilisation.

And that is why, in the early sessions of therapy, the focus turned toward something Jenna had not expected to discuss at all, how she slept, how she ate, how she moved, and how her body had been carrying the weight of many years of responsibility.

The next step was learning something much harder: how to experience safety again inside her own body.

Learning to Trust the Body Again

Understanding the pendulum was an important step for Jenna.

But understanding alone was not enough.

Her mind could now see the pattern, how vigilance, avoidance, and self-criticism had reinforced one another for years, but her body was still reacting as if danger could appear at any moment. The dizziness, the nausea, the waves of anxiety still felt unpredictable.

And unpredictability is exactly what keeps the nervous system on guard. So the next phase of therapy focused on something very practical: helping Jenna experience safety again inside her own body. This required gently reversing several habits that had developed since the panic attacks began.

One of the most powerful of those habits was constant monitoring of internal sensations. Jenna had become extremely attentive to what was happening inside her body. Small changes in balance, breathing, or stomach sensations immediately triggered concern.

Ironically, this kind of monitoring often intensifies the very sensations people fear. The more attention we place on internal signals, the louder those signals can become.

Part of the work therefore involved gradually shifting Jenna’s attention outward again—toward activities, environments, and everyday experiences—rather than constantly scanning for signs of danger within her body.

At the same time, we began introducing graded exposure.

This did not mean forcing Jenna into overwhelming situations. Instead, it meant carefully testing the predictions her anxiety was making.

For example, one of Jenna’s fears was leaving the house alone. Her mind predicted that if she went out without her husband, she might experience dizziness, lose control, or be unable to cope with panic. Rather than arguing with those predictions, therapy focused on gently testing them.

The first step was simply stepping outside alone for a short walk. Then walking a little farther. Then entering a shop independently. Each step was small enough to remain manageable, but meaningful enough to challenge the belief that she could not cope.

Each successful experience quietly sent a new message to her nervous system:

The body can feel uncomfortable and still be safe.

Another important part of this process involved what psychologists call interoceptive exposure—learning to tolerate bodily sensations that had previously triggered panic.

For Jenna, sensations like dizziness or nausea had become signals of danger. The immediate instinct was to escape them as quickly as possible. In the past, vomiting had sometimes served as a way to relieve the sensation temporarily.

But the relief was short-lived. And each time the behaviour occurred, it reinforced the belief that the sensation itself was intolerable.

Instead, Jenna gradually practiced allowing these sensations to rise and fall without reacting to them. She noticed the dizziness, the changes in breathing, the slight waves of nausea, and remained with them long enough to observe that they eventually passed on their own.

This was not easy at first. But over time something important began to shift. The sensations that once felt catastrophic began to feel simply uncomfortable.

And uncomfortable is very different from dangerous.

The stabilising routines introduced earlier through the TED framework also played an important role during this phase. Better sleep meant her nervous system was less reactive. Regular meals and hydration helped prevent energy fluctuations that could mimic anxiety symptoms. Daily walking continued to strengthen her confidence in movement and balance.

Together, these changes created a more stable physiological foundation against which exposure could work effectively.

Little by little, Jenna began to experience something she had not felt in months. Moments of ordinary life. A walk outside without scanning for danger. A shopping trip completed alone.
An evening of sleep without waking in panic.

These were small victories, but they carried enormous meaning. Each one helped recalibrate a system that had been locked in fear. Gradually, the pendulum that once swung wildly between vigilance, avoidance, and collapse began to slow.

And with that slowing came something else Jenna had not felt in a long time: the sense that her body might once again be a place she could trust.

But the most important change was not simply the disappearance of panic.

The Moment Therapy Almost Changed Direction

Recovery from anxiety rarely follows a straight line.

For Jenna, the first months of therapy had already brought meaningful changes. The panic attacks had stopped. Vomiting episodes had reduced significantly. She was sleeping better, moving more, and gradually testing situations that had once felt impossible.

From the outside, it might have looked as though the hardest part was over.

But around the fifteenth session, something shifted.

During that week Jenna arrived at therapy noticeably distressed. The anxiety had intensified again, and the familiar sensations, dizziness, internal tension, waves of fear, felt closer to the surface than they had for several weeks. Although the panic attacks themselves had not returned, the emotional pressure she was experiencing was unmistakable.

Moments like this can be unsettling in therapy.

When symptoms reappear after progress has been made, it is easy for both therapist and client to wonder whether the improvement was temporary. The mind quickly begins asking uncomfortable questions: Is this working? Should something else be tried?

During that session we discussed the possibility of returning to her psychiatrist for a medication review. Jenna had already been taking escitalopram, and adjusting the medication was a reasonable option to consider if her distress continued to increase.

At first, the suggestion seemed as though it might signal a setback.

But something unexpected happened.

Instead of experiencing the conversation as a sign that therapy was failing, Jenna responded differently. The possibility of adjusting medication appeared to sharpen her awareness of how much progress she had already made. She realised that she did not want to retreat from the work she had been doing.

In that moment, something subtle but important shifted.

Rather than relying solely on external solutions, medication, reassurance, or avoidance, Jenna began to recognise her own role in the recovery process. The exposure exercises, the lifestyle changes, the effort to tolerate difficult sensations: these were not things being done to her. They were actions she had been taking herself.

Paradoxically, the conversation about medication strengthened her sense of responsibility and commitment.

In the sessions that followed, her engagement with the therapeutic work deepened noticeably. Exposure exercises became more consistent. She approached situations with greater confidence, even when anxiety appeared.

Instead of interpreting discomfort as a signal that something had gone wrong, she began to see it as part of the process of retraining her nervous system.

This is an important moment in many therapeutic journeys.

Recovery often accelerates when people move from seeing themselves as passive recipients of treatment to active participants in change. The focus shifts from “How do I make the anxiety disappear?” to “How do I respond differently when anxiety appears?”

For Jenna, this shift marked the beginning of a more stable phase of recovery.

The pendulum that had once swung violently between vigilance, avoidance, and collapse was slowing. The sensations that once felt catastrophic were becoming manageable.

And perhaps most importantly, the sense that her body had betrayed her was gradually being replaced by something new: a quiet but growing confidence that she could handle what her body was feeling.

Closing Reflection

Jenna’s story is not unusual. Many people who experience panic attacks assume the problem lies entirely in anxiety itself. They focus on the frightening sensations in the moment, the racing heart, the dizziness, and the feeling that something is about to go terribly wrong.

But panic often emerges at the intersection of several interacting systems: a body that has become physiologically over-reactive, an emotional system shaped by years of responsibility or vulnerability, and a mind that tries to make sense of sensations that suddenly feel unfamiliar.

When these systems fall out of balance, panic can become the language through which the nervous system signals distress. What Jenna’s journey reminds us is that recovery does not always begin where people expect. Sometimes it begins with sleep, with nourishment, and with learning to move again without fear. Sometimes it begins with understanding the patterns that quietly shaped our responses to stress long before anxiety appeared.

And sometimes, as the pendulum slows, people discover something they had not realised they had lost: the ability to trust their own body again.

For clinicians, Jenna’s case also illustrates an important point. Panic disorder can rarely be understood purely as a cognitive problem. When physiological instability, shame-based self-evaluation, and behavioural avoidance interact, treatment may need to address all three systems simultaneously.

For those experiencing panic themselves, the message is equally important.

The sensations may feel overwhelming. They may feel unpredictable. They may even feel dangerous.

But very often, they are the nervous system’s attempt to adapt.

And with the right support, the same system that once generated panic can learn something new: how to settle, how to rebalance, and how to move forward again.

This article does not aim to redefine the established understanding of panic disorder. Instead, it suggests that in some cases panic attacks may represent the final expression of earlier experiences marked by emotional neglect, which can contribute to broader regulatory imbalances involving physiological arousal, emotional signalling, and cognitive interpretation.

Traditional CBT offers well-established and effective models for the treatment of panic disorder. However, Jenna’s story illustrates how panic symptoms can sometimes emerge from earlier life experiences marked by prolonged stress, hypervigilance, and role reversal within the family. Standard CBT approaches typically focus on the maintenance of panic symptoms in the present and may explore early experiences only when they are directly linked to current beliefs or behaviours.

Contemporary CBT protocols for panic disorder commonly incorporate excellent techniques such as cognitive restructuring and interoceptive exposure, originally developed within the Panic Control Treatment model of David H. Barlow and colleagues, alongside cognitive approaches such as the catastrophic misinterpretation model proposed by David M. Clark.

Over time, however, prolonged patterns of stress and self-regulation can contribute to dysregulation across physiological, affective, and cognitive systems. Restoring balance within this body–brain–affect network can gradually transform how anxiety is experienced and regulated.

In this sense, treating panic may sometimes require more than addressing fear itself, it may require accepting a painful history and helping the body, the mind, and the emotional system learn how to work together again.

Further reading:

Barlow, D.H. (2002) Anxiety and its disorders: The nature and treatment of anxiety and panic. 2nd edn. New York: Guilford Press.

Barlow, D.H., Craske, M.G. and Meadows, E.A. (2000) ‘Mastery of your anxiety and panic: Therapist guide’, 3rd edn. New York: Oxford University Press.

Barlow, D.H., Gorman, J.M., Shear, M.K. and Woods, S.W. (2000) ‘Cognitive-behavioral therapy, imipramine, or their combination for panic disorder: A randomized controlled trial’, Journal of the American Medical Association, 283(19), pp. 2529–2536.

Barrett, L.F. (2017) ‘The theory of constructed emotion: An active inference account of interoception and categorization’, Social Cognitive and Affective Neuroscience, 12(1), pp. 1–23.

Clark, D.M. (1986) ‘A cognitive approach to panic’, Behaviour Research and Therapy, 24(4), pp. 461–470.

Clark, D.M. (1997) ‘Panic disorder and social phobia’, in Clark, D.M. and Fairburn, C.G. (eds.) Science and practice of cognitive behaviour therapy. Oxford: Oxford University Press, pp. 121–153.

Craske, M.G. and Barlow, D.H. (2007) ‘Mastery of your anxiety and panic: Therapist guide’, 4th edn. New York: Oxford University Press.

Hirsch, C.R. and Mathews, A. (2019) ‘Approaching cognitive behaviour therapy for generalized anxiety disorder from a cognitive process perspective’, Frontiers in Psychiatry, 10, p. 796.

McEwen, B.S. (2007) ‘Physiology and neurobiology of stress and adaptation: Central role of the brain’, Physiological Reviews, 87(3), pp. 873–904.

Mirea, D. (2018) NeuroAffective-CBT®: Advancing the frontiers of cognitive-behavioural therapy. Available at: https://neuroaffectivecbt.com/2018/07/24/describing-na-cbt/ (Accessed: March 2026).

Mirea, D. (2019) The underlayers of NeuroAffective-CBT®. Available at: https://neuroaffectivecbt.com/2018/10/19/the-underlayers-of-neuroaffective-cbt/ (Accessed: March 2026).

Mirea, D. (2025) The transdiagnostic application of NeuroAffective-CBT®: A case study of chronic stress and burnout. Available at: https://neuroaffectivecbt.com (Accessed: March 2026).

National Institute for Health and Care Excellence (2020) Generalised anxiety disorder and panic disorder in adults: Management (CG113). London: NICE.

Confidentiality note: Jenna is a composite clinical vignette based on several cases. Identifying details have been altered to protect confidentiality.