Tag: diet

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.

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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.

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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?

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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.

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“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.

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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.

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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.

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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.

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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.

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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.

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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

Daniel Mirea (October, 2025)
NeuroAffective-CBT® | https://neuroaffectivecbt.com

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Abstract

The TED (Tired–Exercise–Diet) model is not a peripheral wellness add-on but a formally articulated component of the NeuroAffective-CBT framework. Daniel Mirea introduced TED in NeuroAffective-CBT publications such as Tired, Exercise and Diet Your Way Out of Trouble, where it is presented as a core regulatory module linking body, brain, and affect within the broader NA-CBT schema (Mirea, 2023; Mirea, 2025).

Within the six-module NeuroAffective-CBT programme, TED provides a structured way of translating insights from neuroscience, nutritional psychiatry, psychophysiology, and behavioural science into clinically usable lifestyle interventions. By organising these domains—sleep, movement, and diet—under a single conceptual umbrella, TED offers clinicians and clients a flexible, evidence-informed scaffold for addressing biological factors that interact with emotional learning and self-regulation.

A central assumption of the TED model is that lifestyle-related physiological states meaningfully shape affective capacity, motivational tone, and cognitive flexibility. In clinical populations characterised by chronic internalised shame, self-loathing, affective instability, or low self-regulatory capacity, metabolic strain, sleep disruption, and sedentary behaviour frequently coexist with psychological distress. TED provides a framework for recognising and working with these interactions alongside, rather than instead of, psychotherapeutic processes.

If Part I of the TED series examined creatine as a bioenergetic substrate relevant to brain energy and mood regulation, Part II turns to a more prevalent and system-wide metabolic challenge: insulin resistance. The sections that follow explore how insulin dysregulation intersects with emotional and cognitive functioning, and how TED-aligned lifestyle levers may be used to address these dynamics within an integrated psychotherapeutic context.

Keywords: NeuroAffective-CBT, TED model, insulin resistance, psychometabolic health, affect regulation, depression, fatigue, gut–brain axis, lifestyle interventions, psychotherapy augmentation

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Introducing TED in the NeuroAffective-CBT Framework

The TED (Tired–Exercise–Diet) model is not a peripheral wellness concept but a formally articulated component of the NeuroAffective-CBT framework. Daniel Mirea first introduced TED in NeuroAffective-CBT publications such as Tired, Exercise and Diet Your Way Out of Trouble, where it is presented as a core module linking body, brain, and affect within the NA-CBT schema (Mirea, 2023; Mirea, 2025).

Within the broader NeuroAffective-CBT programme, which comprises six interrelated modules, TED is embedded early in treatment to support psychotherapeutic work targeting chronic internalised shame, self-loathing, affect dysregulation, and self-regulatory vulnerabilities (Mirea, 2023). The underlying clinical rationale is that lifestyle-related physiological states meaningfully influence emotional stability, motivational capacity, and responsiveness to affect-focused and cognitive interventions. Consistent with findings from lifestyle psychiatry, modifying sleep, movement, and nutritional patterns may therefore enhance and stabilise psychotherapeutic gains (Firth et al., 2020; Lopresti, 2019).

TED integrates insights from multiple domains, including neuroscience (e.g., gut–brain signalling and reward pathways), nutritional psychiatry, psychophysiology (e.g., the effects of sleep deprivation and fatigue), and behavioural science (e.g., habit formation and conditioning). By framing sleep, movement, and diet within a single, coherent model, TED provides clinicians and clients with a flexible, evidence-informed scaffold for lifestyle-oriented intervention that can be integrated alongside standard psychotherapeutic techniques.

If Part I of the TED series examined creatine as a bioenergetic substrate relevant to brain energy availability and mood regulation (Candow et al., 2022; Allen et al., 2024), Part II turns to a more prevalent and system-wide metabolic challenge: insulin resistance. The sections that follow explore its links to emotional and cognitive functioning, and consider how TED-aligned lifestyle levers may be used to address psychometabolic constraints within an integrated NeuroAffective-CBT® framework.

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Insulin Resistance & Mental Health: Why It Matters

Epidemiology & Hidden Burden

The World Health Organization estimates over one billion people globally live with diabetes or prediabetes, conditions rooted in chronic insulin resistance. Though early stages may lack dramatic physical symptoms, substantial evidence ties insulin resistance to mood disturbances: irritability, poor sleep, low motivation, brain fog, diminished self-confidence, depression, and anxiety.

Clinically, many mental health practitioners begin treatment for depression or anxiety without ordering metabolic labs, thereby potentially missing a root driver. Treating symptoms without addressing underlying insulin dysregulation may limit long-term efficacy.

Dietary Drivers & Dopamine Links

Modern diets, usually rich in refined sugars, starches, and processed carbohydrates, easily produce repeated glucose spikes. These not only tax metabolic systems but elicit strong dopamine responses, reinforcing cravings and behaviours analogous to substance addiction (Smith & Robbins, 2020). Sugar “addiction” is increasingly framed as a real phenomenon, with parallels to addictive substances in neurobiology and behaviour (Kempton et al., 2024).

Excess glucose that is not immediately utilised is stored as fat, contributing to chronic inflammation, glycation (a form of molecular “aging”), and metabolic stress. Over time, these processes damage organs, accelerate aging, and intersect with psychiatric vulnerability.

Mechanistic Cascade: From Glucose Spikes to Neural Dysregulation

When glucose surges, the pancreas secretes insulin to clear it from the bloodstream into liver, muscle, and fat tissue. In insulin resistance, muscle and liver cells become less responsive, so insulin must work harder. Over time, insulin’s compensatory drive fails, and fat accumulation accelerates, especially visceral adiposity. Because skeletal muscle has high metabolic demand, individuals who train or have greater lean mass may buffer this process somewhat, but they are not immune.

In insulin resistance, cells degrade signalling pathways. One key culprit is diacylglycerol (DAG): metabolic overflow in muscle and liver leads to DAG accumulation, which impairs insulin receptor signalling (Schulman et al., 2019). Imagine an insulin “key” (insulin molecule) trying to unlock a blocked “car door” (GLUT4 transporter) but the signal pathway is jammed by DAG sludge.

From a TED viewpoint, knowingly or unknowingly, many people live in this metabolic state: they feel fatigue or fogginess after meals, gain “stubborn” fat, crave sweets, and feel stuck. Their cells are refusing insulin’s “key”, causing chronic internal stress that can manifest in mood, cognition, and energy dysregulation.

Prevalence & Clinical Relevance

In a striking study of 18 to 44-year-olds, 44.8 % were estimated to have insulin resistance; notably, half of them were not obese, demonstrating the “thin-outside, fat-inside” phenotype. That means many lean individuals may silently carry metabolic dysfunction. Importantly, several studies suggest insulin resistance is a stronger predictor of cardiovascular disease than LDL cholesterol (Reaven, 2011; Wang et al., 2022).

As insulin resistance worsens, elevated glycation, oxidative stress, inflammatory markers, and microvascular dysfunction set in. In the brain, these intersect with neuroinflammation, microglial activation, and compromised mitochondrial function, pathways implicated in depression and cognitive decline (Morris et al., 2017; Louie et al., 2023).

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Intervention Levers: What TED Can Do (and What the Research Suggests)

Below is a revised structure of actionable insights, rooted in emerging metabolic neuroscience, that align well with the TED domains.

1. Postprandial Movement: The Manual “Tesla Door” Activation

A 10 to 20 minute walk after meals activates AMPK signalling. Adenosine monophosphate-activated protein kinase – an enzyme that helps your body use energy more efficiently and draw sugar from the blood into muscles, thus allowing glucose to enter muscle cells independently of insulin. In this metaphor, walking acts as a manual opener of the automatic Tesla door, granting access when the remote control (or the insulin) fails. This simple, low-risk strategy is well supported by metabolic research (Hawley & Holloszy, 2009; Richter & Hargreaves, 2013).

2. Carbohydrate Timing & Contextual Use

Use fast-digesting carbohydrates selectively (e.g. white rice or ripe bananas) during periods of high energy demand, such as intra-workout or immediately post-exercise, when insulin sensitivity is highest. This ensures glucose is directed into active muscle tissue rather than exacerbating systemic dysregulation. In other words, this refers to rare, strategic use in small amounts, only when the body can efficiently utilise glucose for fuel.

Two good examples of fast-digesting carbohydrates, often called high-glycaemic index carbs, are:

1. White rice – breaks down quickly into glucose, providing a rapid spike in blood sugar and energy.
2. Bananas (ripe) – contain simple sugars like glucose and fructose that are quickly absorbed, making them ideal before or during exercise.

Other common examples include white bread, honey, dextrose, sports drinks, or small amounts of fruit juice. This guidance, however, does not apply to individuals on a strict weight-loss programme. In such cases, the goal is to reduce overall glucose exposure and promote fat metabolism, meaning fast-digesting carbohydrates are best avoided.

Emerging evidence suggests that consuming a small amount of vinegar, around one teaspoon diluted in water, before a high-carbohydrate or sweet meal can help moderate postprandial (after-meal) glucose spikes by slowing gastric emptying and improving insulin sensitivity (Johnston et al., 2004; Mitrou et al., 2010). This simple intervention, often highlighted by metabolic educators such as “Jesse the Glucose Goddess”, aligns with the TED model’s focus on practical, low-cost strategies to stabilise energy and mood through metabolic regulation.

3. Rate-limiting Absorption: Protein + Soluble Fibre

By combining carbs with protein and soluble fibre (e.g. psyllium, chia, pectin), you slow the influx of glucose, turning a firehose into a gentle stream. This helps prevent peaks and DAG formation. This method is well supported in glycaemic control literature (Wolever et al., 2008; Jenkins et al., 2018).

Example: Oatmeal Power Bowl

Carbohydrate: Rolled oats (complex carbs that digest steadily)

Protein: Greek yoghurt or a scoop of whey protein mixed in

Soluble fibre: Chia seeds or ground flaxseeds (both rich in soluble fibre)

Healthy fats (optional): A few almonds or a teaspoon of nut butter

Extras: Add sliced banana or berries for natural sweetness

Alternative savoury example

• Carbohydrate: Quinoa or sweet potato
• Protein: Grilled salmon, chicken, or tofu
• Soluble fibre: Steamed vegetables (broccoli, carrots) + half an avocado or lentils

TED perspective: this combo reduces post-meal glucose peaks, supports satiety, and keeps insulin responses smooth, exactly what TED aims for.

4. Sludge Clearance & Mitochondrial Support

• Trimethylglycine (TMG): May enhance methylation, support mitochondrial function, and assist in DAG clearance pathways (Ueland et al., 2019).
• Cinnamon: Contains insulin mimetic compounds; small trials suggest improved glycaemic control and insulin sensitivity when used judiciously (Khan et al., 2003).
• Carnosine: Serves as a buffer and antiglycation agent, intercepting reactive sugar moieties before they damage tissues (Hipkiss, 2009).

5. Master Reset: Intermittent Fasting / Time-Restricted Eating

Caloric restriction or “fasting” regimes although not always recommended if one suffers from high-blood pressure (e.g. 16:8, 24-h fasts) can however flip metabolic switches: lower insulin, upregulate autophagy (cellular cleanup), and reduce DAG accumulation. Animal and human studies show fasting improves insulin sensitivity, clears metabolic “sludge,” and supports mitochondrial health (Longo & Panda, 2016; de Cabo & Mattson, 2019).

6. Synergy of TED: Sleep, Exercise, Diet & Metabolic Hygiene

• Sleep deprivation impairs insulin sensitivity and raises cortisol, further dysregulating glucose control (Spiegel et al., 1999).
• Resistance and aerobic exercise enhance insulin receptivity and mitochondrial density (Hawley & Lessard, 2008).
• Diet quality (minimally processed foods, low glycaemic load) is central to preventing glucose surges.

7. Gut–Brain Signalling & Cravings

Emerging research identifies neuropod cells in the gut lining that respond to nutrients (e.g. glucose, amino acids) and send electrical signals to the brain, influencing cravings, reward, and hedonic experience (Kaelberer et al., 2020). This offers a mechanistic bridge: diet choices influence not only metabolism but “what feels good” and how the brain interprets internal states.

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Implications for Clinical Practice & Research

From a clinical standpoint, incorporating metabolic screening into the psychological assessment process may help identify psychometabolic contributors to fatigue, irritability, mood instability, and depressive symptoms that might otherwise be attributed solely to psychosocial factors. Measures such as fasting insulin, HbA1c, lipid profiles, and inflammatory markers can provide valuable contextual data when affective symptoms appear treatment-resistant, cyclical, or disproportionate to identifiable stressors. Recognising insulin resistance as a contributor to emotional and cognitive dysregulation also carries implications for clinician training and interdisciplinary collaboration within mental health care.

Within treatment, TED-aligned behavioural strategies—such as post-meal movement, carbohydrate pacing, fibre pairing, time-restricted eating, and structured exercise—may be introduced early as adjunctive supports to psychotherapy. When individualised, ethically applied, and appropriately monitored, these interventions may help stabilise metabolic and neuroenergetic conditions that facilitate emotional regulation, motivation, and engagement with affect-focused and cognitive interventions.

From a research perspective, controlled clinical trials are needed to determine whether improving insulin sensitivity enhances outcomes in depression and anxiety, how metabolic change interacts with established psychotherapeutic approaches, and whether emerging mechanisms such as gut–brain signalling via neuropod cells mediate changes in craving, reward processing, and motivation. Addressing these questions is essential for establishing the clinical relevance and mechanistic validity of TED-informed metabolic interventions.

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Summary & Outlook

Insulin resistance extends beyond a purely metabolic condition and likely contributes to mood dysregulation, fatigue, cravings, and cognitive impairment through its effects on cellular energy availability, inflammatory signalling, and reward-related neurocircuitry. Within the TED framework, these psychological manifestations are understood as downstream consequences of impaired metabolic regulation that constrains affect tolerance and emotional learning.

Rather than advocating rigid dietary prescriptions, this article frames lifestyle-based metabolic regulation as a clinically meaningful adjunct to psychotherapy. By improving insulin sensitivity and stabilising metabolic flux, interventions such as movement, meal pacing, fibre intake, and strategically applied fasting may help restore the physiological conditions necessary for sustained therapeutic engagement and neuroplastic change.

At a mechanistic level, pathways involving the gut–brain axis, intracellular signalling disruptions such as diacylglycerol accumulation, and mitochondrial dysfunction provide a coherent bridge between metabolic state and mental health. Together, these processes illustrate how metabolic inputs shape not only physical health, but also motivation, affective stability, and cognitive clarity.

Future research should evaluate TED-driven metabolic interventions in clinical populations using controlled designs and objective biomarker endpoints—including measures of insulin sensitivity, inflammatory markers, and neuroimaging indices such as magnetic resonance spectroscopy—to clarify causal pathways and clinical utility.

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Biochemical Terms with Plain-Language Clarifications

AMPK adenosine monophosphate-activated protein kinase (an enzyme that acts as the body’s “energy switch,” helping cells burn fuel efficiently and move sugar from the bloodstream into muscles)

GLUT4 glucose transporter type 4 – a “doorway” protein that opens to let glucose enter muscle and fat cells when activated by insulin or exercise

DAG diacylglycerol – a fat-like molecule that builds up inside cells and “jams” insulin signals, making it harder for the body to use glucose properly

Autophagy – a natural “cellular recycling” process where old or damaged cell parts are broken down and reused to keep cells healthy

Glycation – a chemical process where excess sugar sticks to proteins and tissues, accelerating ageing and inflammation)

Mitochondria – tiny “power stations” inside cells that turn food into usable energy and are essential for brain and muscle function)

Neuropod cells – specialised sensory cells in the gut lining that communicate directly with the brain via electrical signals, influencing hunger, cravings, and mood

Carnosine – a naturally occurring compound found in muscle and brain tissue that helps protect cells from sugar-related damage and oxidative stress

TMG (Trimethylglycine) – a compound derived from beets that supports liver and mitochondrial function, helping cells process fats and sugars more effectively

⚠️ Disclaimer

This article is not a substitute for professional medical or psychological assessment and care. Regular health checks and blood tests with your GP or family physician are essential, including from adolescence onward given rising rates of metabolic conditions (e.g., pre-diabetes, diabetes). Where appropriate, seek guidance from qualified professionals such as a GP, psychiatrist, registered nurse or nutritionist, or indeed a NeuroAffective-CBT® therapist, who can interpret your health data and support sustainable lifestyle changes. Supplements and behavioural strategies discussed here cannot and should not replace prescribed psychiatric or medical treatments; they function as potential adjuncts within a supervised care plan. Used responsibly, TED-aligned interventions may enhance wellbeing and resilience, but responses vary and should always be monitored by a healthcare professional.

Series context: next article will target Omega-3 (fatty acid): TED Series, Part III: “Omega-3 Fatty Acids and Emotional Stabilisation”

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