TED Series, Part III: Omega-3 and Mental Health.

New Research Findings and NeuroAffective-CBTยฎ Implications

In this third instalment of the TED (Tiredโ€“Exerciseโ€“Diet) Series, we explore how omega-3 fatty acids, particularly EPA and DHA, influence mood, cognition, and emotional regulation. Drawing from neuroscience, nutritional psychiatry, and the NeuroAffective-CBTยฎ framework, this article examines the growing evidence that dietary fats do more than protect the heart, they also nourish the mind. Blending practical TED applications with current clinical research, it offers clinicians and readers accessible strategies for integrating omega-3s into a new lifestyle-based approach to mental health.

Introducing TED in the NeuroAffective-CBTยฎ Framework

The TED (Tiredโ€“Exerciseโ€“Diet) model brings neuroscience, nutritional psychiatry, psychophysiology, and behavioural science into an integrated framework for emotional regulation and mental health. Within the broader NeuroAffective-CBTยฎ (NA-CBT) programme, TED is introduced early to support self-regulation and biological stability, the โ€œBodyโ€“Brainโ€“Affectโ€ triangle that underpins shame-based and affective disorders (Mirea, 2023; Mirea, 2025).

Earlier parts of this series explored the roles of creatine and insulin regulation in mood and cognition. This third instalment turns to omega-3 fatty acids, essential nutrients that play a central role in brain health, mood regulation, and anti-inflammatory balance.


Why Omega-3s Matter: The Brainโ€™s Structural Fat

When people hear the word โ€œfat,โ€ they often think of storage fat the kind that accumulates around the waist or organs. But the brain depends on an entirely different type: structural fat, which makes up the cell membranes of neurons. These membranes control how signals and chemicals move between brain cells, and their flexibility directly affects how efficiently neurons communicate (Huberman, 2023).

Omega-3 fatty acids, primarily EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid) are the building blocks of these membranes. DHA maintains the structure of neurons, while EPA modulates inflammation and neurotransmission, influencing serotonin and dopamine signalling (Freeman et al., 2006; Mocking et al., 2020).

From a TED perspective, this is where Diet meets Affect: better membrane health and lower inflammation translate into improved emotional regulation, resilience to stress, and more stable mood patterns.

๐Ÿงฌ What Are EPA and DHA? (In Simple Terms)

When we talk about omega-3 fatty acids, weโ€™re mostly referring to two main types that the body uses for brain and heart health:

  • EPA (Eicosapentaenoic Acid): Think of EPA as the firefighter in your system. It helps reduce inflammation, calm overactive stress responses, and balance the brainโ€™s chemical messengers that affect mood. Studies show that getting enough EPA can help lift low mood and reduce symptoms of depression.
  • DHA (Docosahexaenoic Acid): DHA is more like the architect of your brain. It builds and maintains the structure of your brain cells, especially in areas responsible for memory, focus, and emotional stability. Itโ€™s crucial for brain development, but also for keeping adult brains flexible and resilient under stress.

Both EPA and DHA work together , EPA helps your brain feel better, and DHA helps it work better. You can get them from oily fish like salmon, sardines, and mackerel, or from algal oil if you follow a plant-based diet.

๐Ÿ’ก TED Translation:
EPA supports the Diet part of TED by reducing emotional inflammation, those biochemical โ€œstormsโ€ that make you feel tense or flat. DHA supports the Tired part, helping your brain stay sharp and recover faster when youโ€™re mentally drained. Together, they strengthen the brainโ€“body connection that TED and NeuroAffective-CBTยฎ aim to restore. It is important to note that these supplements do not cure mental health conditions but can operate as adjuncts to therapy and medication, supporting recovery and prevention.


๐Ÿ”ฌ Evidence from Research: Depression, Focus, and Emotional Health

EPA and Depression – What Research Shows

A growing number of studies show that omega-3 supplements rich in EPA (about 1 gram per day) can noticeably reduce symptoms of depression. In some cases, the improvements are similar to those seen with common antidepressant medications in people with mild to moderate depression (Peet & Horrobin, 2002; Martins, 2009; Mocking et al., 2020).

One major study compared 1 gram of EPA to fluoxetine (Prozac), a widely used SSRI antidepressant and found that both worked equally well in improving mood. The group that combined EPA and fluoxetine together did even better, suggesting that omega-3s may enhance the effects of antidepressant treatment (Nemets et al., 2006).

Scientists believe EPA helps mood in several ways. It reduces inflammation in the body and brain (which can interfere with mood-regulating chemicals like serotonin) and keeps brain cell membranes flexible, allowing signals to travel more efficiently between neurons (Su et al., 2018).

๐Ÿ’ก TED Translation:
In TED terms, EPA acts like a โ€œmood stabiliserโ€ for the bodyโ€“brain system, calming internal inflammation, improving brain energy flow, and helping emotions move more smoothly through the day.

DHA and Cognition – The Brainโ€™s Structural Support

While EPA helps regulate mood and inflammation, DHA focuses more on the structure and performance of brain cells. Itโ€™s especially concentrated in brain areas responsible for memory, focus, and emotional balance, such as the prefrontal cortex and hippocampus.

Research shows that people who get enough DHA perform better on memory and attention tasks, particularly older adults or those who normally eat little fish or other omega-3 sources (Yurko-Mauro et al., 2010). DHA helps brain cells maintain flexible outer membranes, allowing them to communicate efficiently and adapt to new information, a process linked to learning and resilience.

When DHA levels are low, brain signalling can become sluggish, affecting concentration, motivation, and even emotional stability. Regular intake through food (like oily fish) or supplements can help restore this โ€œneural flexibility.โ€

๐Ÿ’ก TED Translation:
In TED language, DHA supports the Tired and Diet domains, it helps the brain stay sharp, focused, and emotionally steady, especially under mental fatigue or stress. Think of it as giving your neurons the healthy fat insulation they need to keep your thoughts and emotions running smoothly.


โš–๏ธ Dosage, Ratios, and Practical Guidance

Most research suggests that taking between 1,000 and 2,000 mg per day of omega-3 fatty acids, especially formulations higher in EPA, can noticeably improve mood, focus, and general wellbeing (Martins, 2009; Mocking et al., 2020). For depression and emotional balance, experts often recommend that EPA make up at least 60% of the total omega-3 blend.

You can get these healthy fats from both food and supplements:

  • ๐ŸŸ Natural sources: oily fish such as salmon, sardines, mackerel, and anchovies.
  • ๐ŸŒฑ Plant-based options: chia seeds, flaxseed, walnuts, and algal oil (a vegan source rich in DHA).
  • ๐Ÿ’Š Supplements: choose products that are molecularly distilled or third-party tested for purity and heavy-metal safety.

Because omega-3s are fat-soluble, they are best absorbed when taken with meals that include some healthy fat, such as avocado, eggs, or olive oil.

๐Ÿ’ก TED Translation:
Omega-3s are like the high-quality oil in your brainโ€™s engine, helping neurons glide, communicate, and self-repair. For best results, pair consistent intake with the other TED elements: regular sleep (Tired), sports (Exercise), and nutrient-dense meals (Diet).


TED Practical Layer: Combining Nutrition with Behaviour

The TED approach is about how we live, not just what we take. Omega-3s work best when integrated into daily habits that support absorption, brain function, and emotional balance.

Here are a few practical ways to make that happen:

  1. Take omega-3s with meals that contain healthy fats.
    These fats, like those from eggs, olive oil, or avocado, help your body absorb EPA and DHA more efficiently.
  2. Pair with regular movement.
    Exercise increases enzymes that help omega-3s get into brain cells (Dyall, 2014). Even short daily walks or light strength training enhance this process.
  3. Balance omega-6 intake.
    Many modern diets contain too much omega-6 (from seed oils and processed foods), which can block omega-3 benefits. Aim for a lower omega-6 to omega-3 ratio (around 3:1) to reduce inflammation and support mood regulation (Simopoulos, 2016).
  4. Track mood and focus.
    Keep a brief weekly log of your energy, sleep, and emotional stability. Over a month or two, most people notice more mental clarity and steadier mood.

๐Ÿ’ก TED Translation:
Small, consistent actions matter. Taking omega-3s in the morning, walking regularly, and eating real, unprocessed foods all work together to open up the bodyโ€“brainโ€“affect loop, the very system TED aims to strengthen.

TED and NeuroAffective-CBTยฎ Integration

In the NeuroAffective-CBTยฎ (NA-CBT) framework, the TED model (Tired, Exercise, Diet) bridges the gap between the mind and body. Omega-3 supplementation fits naturally within the Diet domain, but its effects ripple across all three.

Low omega-3 levels have been linked to mood dysregulation, impulsivity, and emotional reactivity โ€” all central features of the bodyโ€“brainโ€“affect triangle that NA-CBT helps regulate (Mirea, 2025). Supporting neuronal health through dietary means therefore complements core CBT processes such as emotional awareness, behavioural activation, and self-compassion.

For clinicians, this integration can be structured through a few evidence-informed steps:

  1. Screen for dietary insufficiency or inflammation markers (e.g., high omega-6 intake, poor diet quality).
  2. Psychoeducate clients on the bodyโ€“mind connection โ€” explain how stabilising the bodyโ€™s biochemistry supports cognitive flexibility.
  3. Encourage gradual habit stacking, introducing omega-3s alongside TED routines (sleep hygiene, consistent exercise).
  4. Monitor outcomes, tracking not just mood changes, but energy, focus, and emotional resilience.

๐Ÿ’ก TED Translation:
Think of omega-3s as emotional lubricants, subtle but powerful agents that help the brainโ€™s communication systems run smoothly, making it easier for CBT tools to โ€œclick.โ€ Combined with good sleep and movement, they form part of a whole-person therapy that builds physiological and psychological balance from the inside out.


Summary & Outlook

The evidence around omega-3 fatty acids, particularly EPA and DHA, continues to grow, positioning them as safe, low-cost, and biologically plausible adjuncts for improving mood, cognition, and emotional regulation. In depression, EPA-dominant formulations (~1 g/day) have demonstrated antidepressant effects comparable to SSRIs in mild-to-moderate cases (Nemets et al., 2006; Mocking et al., 2020). DHA, on the other hand, plays a structural and neuroprotective role, supporting long-term cognitive resilience.

From the TED viewpoint, omega-3s bridge physiology and psychology. They not only support neuronal efficiency but also improve the emotional flexibility required for therapeutic change โ€” embodying TEDโ€™s principle that lifestyle science and psychotherapy are most effective when integrated.

Within the TED (Tiredโ€“Exerciseโ€“Diet) framework, omega-3s exemplify how dietary micro-interventions can amplify psychotherapeutic outcomes. Combined with good sleep, consistent exercise, and emotional processing, the three TED pillars, they help restore the physiological stability necessary for deeper psychological change.

For clinicians, the takeaway is practical:

  • Screen for dietary quality and omega-3 intake early in assessment.
  • Encourage balanced omega-3 to omega-6 ratios.
  • Integrate nutritional strategies alongside CBT interventions.
  • Track progress using both subjective (mood, focus) and objective (diet logs) measures.

๐Ÿ’ก Final Thought (TED Translation):
Omega-3s donโ€™t just feed the body, they fuel the brain. When woven into the TED lifestyle and NeuroAffective-CBTยฎ framework, they help restore energy, sharpen thinking, and smooth the emotional landscape, supporting the long-term goal of mindโ€“body regulation.


โš ๏ธ Disclaimer

These articles do not replace medical or psychological assessment. Regular health checks, including blood lipid and inflammatory markers, are recommended. Always consult your GP or prescribing clinician before starting supplementation, particularly if taking psychiatric medication or anticoagulants.


๐Ÿงพ References

Allen, P.J., Dโ€™Anci, K.E. & Kanarek, R.B. (2024) โ€˜Creatine supplementation in depression: bioenergetic mechanisms and clinical prospectsโ€™, Neuroscience & Biobehavioral Reviews, 158, 105308.
Dyall, S.C. (2014) โ€˜Long-chain omega-3 fatty acids and the brain: A review of the independent and shared effects of EPA, DHA and ALAโ€™, Frontiers in Aging Neuroscience, 6, 52.
Freeman, M.P. et al. (2006) โ€˜Omega-3 fatty acids: Evidence basis for treatment and future research in psychiatryโ€™, Journal of Clinical Psychiatry, 67(12), pp. 1954โ€“1967.
Huberman, A. (2023) Food and Supplements for Mental Health. The Huberman Lab Podcast, Stanford University.
Martins, J.G. (2009) โ€˜EPA but not DHA appears to be responsible for the efficacy of omega-3 supplementation in depressionโ€™, Journal of Affective Disorders, 116(1โ€“2), pp. 137โ€“143.
Mirea, D. (2023) Tired, Exercise and Diet Your Way Out of Trouble (TED Model). NeuroAffective-CBTยฎ. ResearchGate.
Mirea, D. (2025) TED Series, Part III: Omega-3 and Mental Health. NeuroAffective-CBTยฎ. Available at: https://neuroaffectivecbt.com/2025/10/18/ted-series-part-iii-omega-3-and-mental-health/ [Accessed 18 October 2025].
Mocking, R.J.T. et al. (2020) โ€˜Meta-analysis and meta-regression of omega-3 polyunsaturated fatty acid supplementation for major depressive disorderโ€™, Translational Psychiatry, 10, 190.
Nemets, B., Stahl, Z. & Belmaker, R.H. (2006) โ€˜Addition of omega-3 fatty acid to maintenance medication treatment for recurrent unipolar depressive disorderโ€™, American Journal of Psychiatry, 163(6), pp. 1098โ€“1100.
Simopoulos, A.P. (2016) โ€˜An increase in the omega-6/omega-3 fatty acid ratio increases the risk for obesity and metabolic syndromeโ€™, Nutrients, 8(3), 128.
Su, K.P. et al. (2018) โ€˜Omega-3 fatty acids in major depressive disorder: A preliminary double-blind, placebo-controlled trialโ€™, European Neuropsychopharmacology, 28(4), pp. 502โ€“510.
Yurko-Mauro, K. et al. (2010) โ€˜Beneficial effects of docosahexaenoic acid on cognition in age-related cognitive declineโ€™, Alzheimerโ€™s & Dementia, 6(6), pp. 456โ€“464.

TED Series, Part I: Could Creatine Play an Important Role to Mental Health?

Abstract

The TED (Tiredโ€“Exerciseโ€“Diet) model within the NeuroAffective-CBTยฎ (NA-CBT) framework integrates lifestyle-based interventions with affect-focused psychotherapy to support emotional regulation, particularly in shame-based and affect-dysregulated disorders. This article presents a narrative, theory-integrative review exploring the emerging role of creatine supplementation as a potential neurometabolic adjunct within this model. Traditionally associated with muscular performance, creatine has gained neuroscientific attention for its role in cerebral energy metabolism, mitochondrial function, and stress resilience. Evidence from animal studies, neuroimaging research, and early-stage human trials suggests that creatine supplementation may enhance brain bioenergetics, attenuate cognitive deficits under metabolic stress, and augment established treatments for depression when used adjunctively. Of particular relevance, a recent randomized, double-blind, placebo-controlled pilot trial reported greater reductions in depressive symptoms when creatine was combined with cognitive-behavioural therapy compared to therapy alone. While findings remain preliminary and heterogeneous, they support a neuroaffective perspective in which metabolic support may enhance the brainโ€™s capacity for emotional learning and regulation. The article situates creatine within the TED framework, emphasising its potential as a supportive, individualised, and ethically integrated lifestyle intervention, while underscoring the need for larger, well-controlled clinical trials before routine clinical implementation.

Keywords: NeuroAffective-CBTยฎ, TED model, creatine supplementation, lifestyle interventions, affect regulation, shame-based disorders, depression, cognitive-behavioural therapy, brain energy metabolism, mitochondrial function, sleep deprivation, affect dysregulation

The TED Series: Introduction

This article forms part of a TED (Tiredโ€“Exerciseโ€“Diet) series comprising eight articles examining supplements and lifestyle-related factors that may influence mental health. Across the series, each instalment focuses on a specific nutritional compound, behavioural factor, or physiological mechanism relevant to mental health, emotional regulation, nutrition, exercise, and sleep, with the overarching aim of clarifying how these elements interact to define practical, evidence-informed lifestyle interventions.

In this first instalment of the TED series, the article explores the intriguing possibility that creatine supplementation, long associated with sports performance, may also play a role in mental healthโ€”particularly in disorders rooted in shame, self-hatred, self-criticism, and broader affect dysregulation. Subsequent articles will extend this framework to other supplements and lifestyle variables, progressively building an integrated model of how sleep, movement, and nutrition can be leveraged to support psychotherapeutic change within the NeuroAffective-CBTยฎ framework.

Introducing TED in the NeuroAffective-CBTยฎ Framework – Mireaโ€™s Contribution

The TED model (Tired-Exercise-Diet) synthesises insights from neuroscience (e.g., gutโ€“brain signalling, reward pathways), nutritional psychiatry, psychophysiology (e.g., sleep deprivation), and behavioural science (habit formation, conditioning). By organising these findings into three core domains, sleep, exercise, and diet, TED provides an accessible, flexible, and evidence-informed structure for lifestyle-oriented intervention.

But TED is not just theoretical: it is publicly presented and described by Daniel Mirea in the NeuroAffective-CBTยฎ literature. Mireaโ€™s โ€œTired, Exercise and Diet Your Way Out of Troubleโ€ (TED model) is available via ResearchGate, Academia, and the NA-CBT site as a leaflet and white-paper introduction to emotional regulation through lifestyle (Mirea, 2023). In his description, the TED module is positioned centrally within the NA-CBT method, linking body, brain, and affect, the Bodyโ€“Brainโ€“Affect triangle (Mirea, 2025).

Within the larger NeuroAffective-CBTยฎ programme (comprising six modules), TED is introduced early, immediately after assessment and conceptualisation. NA-CBT specifically targets shame-based disorders such as self-loathing, self-disgust, and low self-esteem, which often underpin psychopathologies like major depressive disorder and anorexia (Mirea, 2023). Addressing lifestyle factors may augment traditional CBT approaches (Firth et al., 2020; Lopresti, 2019).

Empirical evidence shows that improving sleep, increasing physical activity, and enhancing diet quality yield synergistic benefits for emotional regulation, reduction of maladaptive cravings, and improvement of self-esteem (Kandola et al., 2019; Irwin, 2015).

For clinicians, TED offers a concrete tool: integrate lifestyle domains early, personalise interventions, and use TED to amplify CBT. For researchers, it highlights testable mechanisms and opportunities for controlled trials.

This first part focuses on a lesser-known nutritional agent now attracting neuroscientific attention: creatine, a compound with emerging evidence linking it to neuroenergetics and mental health (Candow et al., 2022; Allen et al., 2024).

Why Creatine? What the Evidence Suggests (and Doesnโ€™t..)

Drawing on emerging neuroscience and clinical psychology research, Dr Wendy Suzuki has highlighted creatineโ€™s shift from a narrowly defined โ€œgym supplementโ€ to a promising neurometabolic support under conditions of brain stress. Although the liver and brain synthesize small endogenous amounts of creatine, supplementation appears most relevant during periods of elevated cognitive demand, sleep deprivation, depression, or neurodegenerative vulnerability, states marked by energetic strain, inflammation, and oxidative stress. While low-dose creatine (โ‰ˆ5 g/day) effectively supports muscular performance, studies from European and North American laboratories indicate that higher doses (โ‰ˆ10 g/day or more) may be required to meaningfully elevate brain creatine levels once muscular stores are saturated. Experimental sleep-deprivation models further suggest that acute high-dose creatine can reverse cognitive deficits, and in some cases restore performance beyond well-rested baselines, pointing to rapid effects on cerebral energy metabolism rather than slow structural adaptation. Of particular relevance to NeuroAffective-CBT, a recent Harvard-affiliated randomised, double-blind, placebo-controlled pilot trial found that individuals with depressive symptoms who received creatine monohydrate (5 g/day) alongside cognitive-behavioural therapy experienced significantly greater reductions in PHQ-9 depression scores than those receiving CBT alone, without increased adverse events (Sherpa NN et al., 2025). While preliminary animal and early human studies also suggest anti-inflammatory and neuroprotective effects, along with small pilot signals in conditions such as Alzheimerโ€™s disease, the evidence base remains emergent. Taken together, current findings support a neuroaffective framework in which creatine may enhance the brainโ€™s energetic resilience, potentially amplifying psychotherapeutic efficacy under stress, while underscoring the need for larger, well-controlled trials before broad clinical recommendations are made.

The Rationale: Bioenergetics, Oxidative Stress, and Brain Demand

Creatine helps the body make and recycle energy quickly. It acts like a backup battery for your cells, keeping them charged when energy demand is high. While we often think of creatine as something that helps muscles perform better, the brain also uses a huge amount of energy, about one-fifth of everything the body burns at rest.

In people experiencing depression or anxiety, studies suggest that the brainโ€™s mitochondria (the cellโ€™s โ€œpower stationsโ€ that turn food into usable energy) often donโ€™t work as efficiently. This can lead to higher levels of oxidative stressa kind of cellular โ€œwear and tearโ€ caused by unstable oxygen molecules that damage cells over time (Morris et al., 2017).

Taking creatine as a supplement may help the brainโ€™s mitochondria work more efficiently, reduce oxidative stress, and stabilise the brainโ€™s energy balance (Allen et al., 2024). Animal studies show that creatine can reduce stress in brain cells and even decrease depression-like behaviours (Zhang et al., 2023). Research in humans is still early, but the results so far are promising.


๐Ÿ’ก In simple TED terms:
Why Creatine Might Help the Brain: Energy and Stress Balance! Creatine may help the brain produce cleaner, steadier energy, while reducing the internal โ€œrustโ€ that builds up from stress and poor metabolism, both of which are key targets in emotional regulation.

Human Evidence: Mood, Cognition, and Stress Conditions

Mood and Depression

Early studies suggest that creatine may help boost the effects of antidepressant medication. In one carefully controlled trial, women who took 5 grams of creatine monohydrate per day alongside their usual SSRI antidepressant showed faster and stronger improvements in mood than those taking a placebo (Lyoo et al., 2012).

Several reviews of this research confirm that creatine seems most effective as an add-on rather than a stand-alone treatment (Allen et al., 2024; L-Kiaux et al., 2024). In other words, creatine may make existing treatments work better, but it is not yet proven to work on its own.

Although there have been no large human trials testing creatine by itself for depression or PTSD, brain-imaging studies show that creatine supplementation increases the brainโ€™s phosphocreatine levels (the stored form of cellular energy). This may help restore low brain-energy levels often found in people with mood disorders (Dechent et al., 1999; Rae & Brรถer, 2015).

๐Ÿ’ก TED translation: Creatine may act like an energy booster for the brain, helping antidepressants โ€œcatchโ€ faster and work more effectively. Within the TED framework, this fits the Diet domain, using nutrition to support energy stability and emotional regulation and, complements therapeutic work in the Affect domain.

Cognition, Memory, and Sleep Deprivation

Research also shows that creatine can help the brain think and react more effectively, especially when it is under pressure. Systematic reviews indicate that creatine can enhance memory, focus, and processing speed in conditions of metabolic stress, such as sleep deprivation, oxygen deprivation, or prolonged mental effort (Avgerinos et al., 2018; McMorris et al., 2017).

In one notable experiment, people who stayed awake all night performed better on reaction-time tasks and reported less mental fatigue after taking creatine (McMorris et al., 2006). These benefits appear strongest in older adults or individuals whose brains are already energy-challenged, for example, due to stress, ageing, or poor sleep (Dolan et al., 2018). In contrast, young, well-rested participants often show little or no change (Simpson & Rawson, 2021).

๐Ÿ’ก TED translation: Creatine seems to protect the brain when energy is low during exhaustion, stress, or lack of sleep. This is what we call a reactive emtional state (reactive amygdala). It doesnโ€™t make a healthy, rested brain โ€œsmarter,โ€ but it helps a tired brain function more efficiently. In TED terms, it bridges the Tired and Diet domains: improving sleep quality indirectly and supporting cognitive endurance under pressure.

Key Questions & Considerations

Dose, Duration, and Uptake

A few muscle studies, led by Dr. Darren Candow, show that taking 3โ€“5 grams of creatine monohydrate per day is enough to maintain muscle levels once stores are full. To load the system faster, some use about 20 grams per day for 5โ€“7 days, which quickly saturates muscle tissue (Candow et al., 2022; Kreider et al., 2017).

However, the brain takes longer to absorb creatine. Imaging studies suggest that at least 10 grams per day for several weeks may be needed to raise brain levels meaningfully (Dechent et al., 1999; Rae & Brรถer, 2015). Because around 95% of the bodyโ€™s creatine is stored in muscle, the brain receives its share more slowly, which may explain why mood or cognitive effects sometimes take weeks to appear.

๐Ÿ’ก TED translation: Creatine needs time to โ€œcharge the systemโ€. Like building savings in a bank, the longer and more consistently you invest, the better the returns. Within TED, this reflects the Tired and Diet domains, combining steady supplementation with sleep and nutrition for sustained brain energy.

Sodium and Electrolyte Co-Ingestion

Creatine is carried into cells by a sodium-chloride transporter (called SLC6A8) (Tachikawa et al., 2013). This means that electrolytes, especially sodium, help creatine get where it needs to go. While not yet proven for brain outcomes, pairing creatine with a small amount of electrolyte water or a balanced meal containing sodium may improve absorption.

๐Ÿ’ก TED translation: Think of sodium as a helper molecule, like a key that lets creatine into the cell. In TED language, this links Diet with Physiology: hydration, electrolytes, and nutrition work together to optimise energy flow.

Dietary Status

People who eat little or no animal protein, such as vegetarians or vegans, often start with lower creatine stores and therefore show a greater response to supplementation (Candow et al., 2022; Antonio et al., 2021). Interestingly, brain creatine levels appear to stay relatively stable across diet types, which suggests the brain has its own built-in regulation system (Rae & Brรถer, 2015).

๐Ÿ’ก TED translation: Your baseline diet changes how quickly you benefit from creatine. If you avoid animal foods, your muscles may โ€œfill upโ€ faster when you supplement but the brain keeps itself balanced. This reflects TEDโ€™s Diet principle: individualisation matters.

Safety and Misconceptions

Decades of studies confirm that creatine monohydrate is safe for healthy adults. No evidence links standard doses (3โ€“5 g/day) to kidney or liver problems (Kreider et al., 2017; Harvard Health Publishing, 2024). Increases in serum creatinine after supplementation simply reflect higher turnover, not kidney damage.

The often-mentioned hair-loss claim remains unsupported (Antonio et al., 2021). However, clinicians should note that in rare cases, individuals with bipolar disorder have reported manic switching after starting creatine (Silva et al., 2013). These cases are very uncommon but worth monitoring in sensitive populations.

๐Ÿ’ก TED translation: Creatine is one of the safest, best-studied supplements in both sport and health science. Still, as with all lifestyle tools, TED encourages personalisation and medical oversight, particularly in those with complex mental-health or metabolic conditions.

Implications for TED and NeuroAffective-CBTยฎ

In clinical contexts, creatine should be understood as a supportive, adjunctive tool rather than a substitute for established psychotherapeutic or pharmacological treatments. Its value lies in its potential to stabilise metabolic and energetic foundations that may facilitate emotional learning and regulation. Accordingly, creatine supplementation should be implemented thoughtfully, within a broader clinical formulation, and under appropriate medical supervision.

Practical Guidelines

Screen and personalise
Prior to supplementation, assess renal function, dietary patterns, and potential interactions with prescribed medications. Additional caution is warranted in individuals with pre-existing renal, metabolic, or psychiatric vulnerabilities.

Adjunctive use only
Creatine should complementโ€”not replaceโ€”psychotherapy or pharmacological treatment. Supplementation is best undertaken with oversight from a GP or psychiatrist, particularly when active mental health treatment is required.

Dosing strategy
A short loading phase of approximately 20 g/day for 5โ€“7 days, or a more gradual titration of 10โ€“20 g/day over four weeks, may be followed by a maintenance dose of 3โ€“5 g/day, depending on tolerance and clinical response (Candow et al., 2022).

Timing considerations
Creatine may be most beneficial during periods of sleep disruption, sustained cognitive demand, or emotional exhaustion, when cerebral energy requirements are elevated.

Integration within TED
For optimal benefit, supplementation should be integrated with the other TED domainsโ€”sleep hygiene, structured physical activity, and a nutrient-dense dietโ€”to support synergistic effects on emotional regulation and cognitive resilience (Firth et al., 2020).

Monitoring and documentation
Clinicians and clients are encouraged to systematically monitor mood, cognitive clarity, sleep quality, and physical functioning. Dosing may be adjusted empirically, and anonymised observations can contribute to practice-based evidence and future research.

๐Ÿ’ก TED translation: Creatine fits naturally within the Tiredโ€“Exerciseโ€“Diet framework as a form of metabolic support for emotional regulation. Rather than functioning as a โ€œpill for a problem,โ€ it is best conceptualised as one component of a whole-lifestyle system in which sleep, movement, and nutrition work together to reinforce psychological recovery.


Summary & Outlook

  • The TED model (sleep, exercise, diet) offers a practical bridge between psychotherapy and lifestyle science, especially for conditions rooted in shame, self-criticism, and affect dysregulation (Firth et al., 2020; Lopresti, 2019).
  • Creatine demonstrates strong scientific plausibility and early clinical promise for improving mood, cognition, and resilience under metabolic stress (Allen et al., 2024; Candow et al., 2022).
  • The next step for researchers is to conduct large, placebo-controlled clinical trials testing creatine as an adjunct to CBT for depression and anxiety โ€” ideally with neuroimaging to confirm its effects on brain energy metabolism.

๐Ÿ’ก TED translation: Creatine may one day become a recognised โ€œnutritional allyโ€ for the brain, enhancing therapy outcomes by helping clients feel less tired, more focused, and more emotionally stable. For now, it serves as a valuable prototype of how lifestyle science can empower both clinicians and clients to target emotional health from the body upward.

โš ๏ธ Disclaimer:
A final and important reminder: these articles are not intended to replace professional medical or psychological assessment and/or treatment. Regular blood tests and health check-ups with your GP or a private family doctor are essential throughout adult life, in fact increasingly relevant from adolescence onward, given the rising incidence of metabolic and endocrine conditions such as diabetes among young people. It is strongly recommended to seek guidance from qualified professionals, for example, a GP or a psychiatrist, depending on your personal goals and needs a registered nutritionist, indeed a certified NeuroAffective-CBTยฎ practitioner, who can help interpret your health data (including blood work) and help you understand how your lifestyle, daily habits, and nutritional choices influence your mental and emotional wellbeing.

References:

Allen, P.J., Dโ€™Anci, K.E. & Kanarek, R.B., 2024. Creatine supplementation in depression: bioenergetic mechanisms and clinical prospects. Neuroscience & Biobehavioral Reviews, 158, 105308. https://doi.org/10.1016/j.neubiorev.2024.105308

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Dolan, E., Gualano, B., Rawson, E.S. & Phillips, S.M., 2018. Creatine supplementation and brain function: a systematic review. Psychopharmacology, 235, 2275โ€“2287. https://doi.org/10.1007/s00213-018-4956-2

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Shame: The Central Mechanism in Chronic Low Self-Esteem, a NeuroAffective-CBTยฎ perspective

How Early Life Experiences Shape Our Sense of Self

From the moment we are born, our earliest interactions with caregivers begin shaping the lens through which we view ourselves and the world. While overt mistreatment, such as physical punishment, neglect, or abuse, is widely recognised, subtler forms of emotional harm can leave equally lasting psychological imprints. Persistent criticism, emotional invalidation, or unspoken parental expectations may quietly distort a childโ€™s emerging sense of self.

Donald Meichenbaumโ€™s early work on narrative-constructivism (Meichenbaum Free Publications, 2024) offers a powerful framework for understanding how early experiences form the foundation of identity. According to his model, children unconsciously develop internal narratives, or life scripts, based on the emotional messages they receive from caregivers. Behaviourist Daniel Mirea (2018) refers to these internalisations as โ€œnarrow lensesโ€ through which we learn to interpret ourselves and our world. These scripts often hinge on perceived conditions for acceptance: โ€œBe perfect,โ€ โ€œDonโ€™t disappoint,โ€ or โ€œAlways succeedโ€. They become internal blueprints for behaviour and identity.

When individuals deviate from these internalised rules, whether intentionally or not, it can evoke intense psychological distress. For instance, someone who grew up believing they must always please others may feel overwhelming shame and guilt when attempting to assert a boundary. Others might experience anxiety or self-sabotage when success feels incompatible with early messages that achievement would lead to rejection or disapproval. In these moments, the distress often doesnโ€™t arise from the external situation itself, but from the unconscious violation of internal survival strategies. Breaking the script can feel like a betrayal of self, evoking shame, guilt, confusion, or resurfaced emotional pain. Therapeutic work that brings these early narratives to light, and helps individuals examine and reframe them, is often essential for healing and for the development of a more authentic, self-compassionate identity.

Just as overt mistreatment leaves scars, subtle emotional neglect and persistent invalidation can be just as damaging. Environments that emphasise a childโ€™s flaws while ignoring their strengths, repeating phrases like โ€œYou couldโ€™ve done betterโ€, or comparing them to siblings or peers, can lead to internalised shame. Over time, such experiences may cultivate what is often referred to as core shame: a deep, embodied sense of being defective, unworthy, or inherently unacceptable (Mirea, 2018). This shame can become embedded within the self-concept, reinforced by experiences of ridicule, teasing, or belittlement.

As children grow, the role of peer relationships becomes increasingly central to their self-esteem. During late childhood and adolescence, physical appearance, popularity, and social belonging rise in importance. Children who feel different, due to body image, skin conditions, or social exclusion, are especially vulnerable to shame-based beliefs such as โ€œIโ€™m uglyโ€, โ€œIโ€™m weirdโ€ or โ€œNo one likes meโ€. These beliefs are often intensified by social media, which promotes narrow, unrealistic standards of attractiveness and worth.

Social identity also plays a critical role. How society views and treats the communities we belong to, our culture, class, or ethnicity, shapes how we come to view ourselves. If oneโ€™s cultural group is marginalised or discriminated against, societal messages of inferiority or invisibility can deeply seep into the personal identity, compounding feelings of shame or self-doubt.

Importantly, not all harm stems from overt abuse or criticism. Sometimes itโ€™s the absence of nurturing experiences, affection, praise, encouragement, or emotional presence that causes the most damage. Children with caregivers who are physically present but emotionally disengaged may grow up feeling unloved or unseen. Even when their material needs are met, the emotional void can lead to a persistent sense of being fundamentally flawed. Later in life, comparisons with peers who received emotional warmth can deepen this sense of inadequacy.

Such was the case with James. Throughout his childhood, he endured chronic emotional abuse, marked by relentless criticism, verbal attacks, and public humiliation, most often at the hands of his father during family gatherings or in front of peers. Over time, James internalised the belief that he could never measure up, that he would always fall short of his fatherโ€™s expectations. To cope, he began to rely heavily on external validation and constant reassurance, grasping for fleeting moments of feeling โ€œgood enoughโ€.

This emotional backdrop seeded a chronic sense of internalised shame, a deep โ€œfelt-senseโ€ that he was fundamentally flawed. To emotionally survive this environment, James developed a set of coping strategies, what we might call life strategies, to navigate social situations and relationships where he felt undeserving or defective. These strategies helped him appear functional and even successful on the outside, but internally, they were rooted in fear, shame, and emotional self-protection.

Even minor interpersonal situations could trigger his shame. For example, if a university acquaintance asked him for a loan, even someone he barely knew or trusted, James felt unable to say “no,” even when his financial situation was precarious. Embarrassed and afraid of being disliked, he would give away money he couldnโ€™t afford to lose. Despite sensing the relationship was one-sided or exploitative, he was unable to assert his needs.

After such encounters, James would spiral into self-criticism. He would replay the event, berating himself for not setting a boundary. In the days that followed, he felt guilt, sadness, and depression, compounded by the recognition that the money would likely never be returned. These episodes only reinforced his internal narrative of unworthiness and deepened his shame.

Jamesโ€™s patterns of behaviour reflected three common shame-based coping strategies: overcompensation, avoidance, and capitulation. He would overcompensate by being excessively generous and accommodating, often at the expense of his own wellbeing. He avoided assertiveness and confrontation, fearing rejection. And ultimately, he capitulated, silently accepting that betrayal of his own needs was the price of being liked. โ€œIf even my own father didnโ€™t accept meโ€, he often thought, โ€œwhy would anyone else?โ€

Over time, these strategies would become automatic, like an emotional autopilot. Through repeated use, they formed an internalised maintenance program, a hidden operating system, that reinforced his shame and shaped his sense of self across time. What began as a useful defence – a way to survive childhood, ended up as the foundation for chronic low self-esteem and shame, manifesting in symptoms that spanned both anxiety and depression.

Shame as a Core Mechanism

Shame often lies beneath overt symptoms of emotional distress. While clients frequently seek help for anxiety or depression, it is often shame that quietly drives much of their inner turmoil. In this light, chronic low self-esteem may be best understood as a shame-based condition.

Despite its central role, shame is often overlooked in psychotherapy, not out of neglect, but because it tends to remain hidden beneath more visible symptoms that feel immediate to the client. Clients typically tend to present symptoms of anxiety and depression, while the deeper, silent driver, shame, goes unaddressed. Yet neuroaffective research identifies shame as a core emotion, evolutionarily essential for social survival. Without the capacity for shame, early humans would have struggled to understand social hierarchies, maintain group cohesion, or follow communal norms. In this sense, shame originally served an adaptive purpose: to guide behaviour in socially acceptable ways (Matos, Pinto-Gouveia & Duarte, 2013).

Like all other core emotions, shame functions as a sudden “call to action“. It generates immediate internal distress, a state of hyper or hypo-arousal, which demands urgent behavioural regulation. People may respond with submission, withdrawal, compliance, or people-pleasing. These reactions serve as social survival mechanisms, especially for those raised in emotionally unsafe environments.

It is only natural that, when adaptive regulation is lacking, individuals revert to maladaptive strategies like lying, substance use, excessive niceness, or self-betrayal, often learned in childhood through repeated exposure to shame and invalidation.

And so, in a perceived social crisis when emotionally overwhelmed (i.e., activating event), individuals often unconsciously revert to coping mechanisms such as overcompensation, avoidance, or capitulation (i.e., surrendering to shame) in no particular order. These strategies may feel protective in the moment, offering a temporary sense of control or relief. However, they are often subtle forms of self-sabotage and ironically, they end up reinforcing the very shame they were unconsciously trying to manage or escape.

For instance, overcompensation may manifest as perfectionism, over-working to exhaustion, clinging to abusive relationships, giving away money one cannot afford to lose, pretending to like people one inwardly distrusts, or engaging in overly self-sacrificing behaviour, all in a desperate effort to gain acceptance or avoid perceived rejection. These actions may appear altruistic or generous on the surface but are often driven by deep fears of abandonment or worthlessness.

Capitulation occurs when a person begins to behave in ways that conflict with their true self, often to fit in or fulfil internalised narratives of inadequacy. In some cases, this leads to acting out beliefs like: โ€œSince Iโ€™m already bad, I might as well be bad and show everyone just how bad I really amโ€. This distorted logic can result in self-destructive behaviours like compulsive gambling, excessive drinking, drug use, not necessarily driven by desire, but by hopelessness, self-punishment, or a deep yearning to belong. These behaviours serve as powerful, if maladaptive, emotional regulation tools. They may temporarily ease anxiety or internal chaos, but in the long term, they reinforce the painful identity narrative the person is trying to escape: the belief that they are defective, unworthy, or beyond help.

Avoidance strategies may involve a chronic inability to say “no”, withdrawing from social settings, procrastinating, or avoiding interactions that risk judgment or criticism. These behaviours offer immediate emotional relief but are rarely sustainable. Over time, their short-term success becomes neurologically reinforced, because they โ€œworkedโ€ once, the brain learns to default to them automatically, even when they are no longer adaptive or helpful.

After the triggering event passes and the individual is left alone and reflective, a second emotional wave often emerges. Long episodes of rumination characterised by intrusive thoughts such as โ€œWhy am I like this?โ€, โ€œIโ€™m uselessโ€, โ€œI always give money I donโ€™t have,โ€ or โ€œNo one ever helps me in returnโ€ begin to surface. This cascade of self-criticism and self-blame induces a temporary hypo-aroused state of guilt, thus reinforcing the shame cycle.

In this way, individuals can become trapped in recurring emotional loops, cycles of shame, anxiety, guilt, and depression, that are externally triggered, internally reinforced, and sustained by long-standing behavioural and neurobiological patterns. Over time, these behaviours cease to be mere reactions to isolated stressors; they evolve into a default operating system through which the individual interprets and navigates daily life. The underlying core shame remains unexamined, silently shaping emotional responses, relationship dynamics, and everyday decision-making.

Conclusion

Chronic low self-esteem is not merely a collection of negative thoughts or surface-level insecurities, it may be the visible tip of a deeper, shame-based emotional system. Often hidden beneath symptoms of anxiety or depression, shame fuels emotional dysregulation, self-sabotaging behaviours, and entrenched beliefs of unworthiness. Left unexamined, it becomes a silent architect of identity, shaping how one sees themselves, relates to others, and makes daily decisions.

Bringing shame into therapeutic awareness is rarely straightforward, yet it is essential. One of the challenges lies in the confusion that surrounds this complex and often misunderstood emotion. Shame is frequently mistaken for guilt, though the two serve distinct psychological functions. Guilt is behaviour-focused, โ€œI did something wrongโ€, whereas shame is identity-based, โ€œI am something wrong.โ€ According to the NeuroAffective-CBT developmental model, guilt tends to emerge later in development, while shame takes root earlier, forming a foundational layer of the emotional system.



To loosen shameโ€™s grip, it must be called out and named, explored, and brought into conscious awareness. Only then can individuals begin to interrupt its influence and develop more compassionate, flexible ways of relating to themselves and others.

Crucially, shame should not be demonised. It is part of an adaptive emotional system that evolved over thousands of years, to promote social cohesion and survival. The problem arises when shame becomes chronic and dominant, distorting self-perception, shaping behaviour, and stalling emotional growth. Shame is only painful when it governs the internal world unchecked. The goal in therapy is not to eliminate shame, but to understand its origins, normalise its presence, and dismantle the reinforcing patterns that keep it active.

In doing so, individuals begin to reclaim agency, authenticity, and emotional resilience. Despite its power, shame is not immutable. Through compassionate therapeutic inquiry and reflective self-awareness, people can challenge the narratives that shaped their inner world. By uncovering the roots of shame and gradually rewriting these internal scripts, individuals like James can move from survival toward authenticity, from emotional self-protection to genuine self-acceptance.

Glossary:

Adaptive vs. Maladaptive Behaviours
Adaptive behaviours are healthy coping mechanisms that support resilience, the ability to adapt constructively to difficult or stressful situations. They promote long-term emotional growth and psychological flexibility. In contrast, maladaptive coping mechanisms may offer short-term relief but ultimately reinforce avoidance, overcompensation, or capitulation. These strategies are unproductive and often harmful, preventing individuals from developing more adaptive ways of relating to themselves and others.

Core Emotions
In this article, core emotions (or core affects) are defined as primary emotional systems essential to survival, shared by most mammals. According to neuroaffective research and the work of neuroscientist Jaak Panksepp (2012), these include SEEKING (expectancy/curiosity), FEAR (anxiety), RAGE (anger), LUST (sexual excitement), CARE (nurturance), PANIC/GRIEF (sadness/loss), and PLAY (social joy). Clinical theorist Mirea proposes that SHAME, while derivative of FEAR, also functions as a core affect in humans, distinct yet equally vital for social survival. For example, the behaviour of a shamed or embarrassed dog illustrates how shame functions as a primitive, embodied emotional state.

Deeply-Rooted Beliefs (DRBs)
DRBs first mentioned by Mirea (2018) when describing the fundamentals of NeuroAffective-CBT, refer to early internalised felt-senses accompanied by corresponding beliefs and affective responses. These experiences are typically nonverbal and rooted in emotionally charged moments, often occurring before the individual has the language to articulate them. Originating in childhood, DRBs shape a rigid sense of identity and self-perception. As language develops, these implicit emotional experiences may later be verbalised, often for the first time in adulthood, particularly within a therapeutic setting. DRBs are resistant to change without external support, as individuals frequently dismiss conflicting evidence through cognitive distortions such as mental filtering, a mechanism explored in detail in Mirea’s approach NeuroAffective-CBT.

Felt-Sense / Gut-Sense / Gut-Feelings
These terms are used interchangeably throughout the paper to describe internal sensory experiences that arise in response to perceived threats or rewards. A felt-sense serves as an embodied memory of prior emotional events, functioning as an internal alarm system. It can manifest as a subtle tension, discomfort, or intuitive knowing, guiding decisions and emotional reactions even before conscious thought occurs.

References:

Panksepp, J. & Biven, L. (2012).โ€ฏThe Archaeology of Mind: Neuroevolutionary Origins of Human Emotion. W. W. Norton & Company.

Matos, M., Pinto-Gouveia, J. and Duarte, C., 2013. Shame as a functional and adaptive emotion: A biopsychosocial perspective. Journal for the Theory of Social Behaviour, 43(3), pp.358-379. https://doi.org/10.1111/jtsb.12016

Meichenbaum D (2024). Don Meichenbaum Publications. URL: https://www.donaldmeichenbaum.com/publications (accessed 26.06.2025)

Mirea D (2024). If my gut could talk to me, what would it say? URL: https://www.researchgate.net/publication/382218761_If_My_Gut_Could_Talk_To_Me_What_Would_It_Say (accessed 26.06.2025)

Mirea D (2018). The underlayers of NeuroAffective-CBT. URL: https://neuroaffectivecbt.com/2018/10/19/the-underlayers-of-neuroaffective-cbt/ (accessed 26.06.2025)

Edited and supported by:

Dr Mark Paget URL: https://www.drmarkpaget.com/