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

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

Abstract

Creatine, long associated with skeletal muscle performance, has attracted growing interest within neuroscience and psychiatry due to its role in cerebral energy metabolism, mitochondrial function, and stress resilience. Evidence from animal models, neuroimaging studies, and early-stage human trials suggests that creatine supplementation may enhance brain bioenergetics, buffer cognitive and emotional functioning under metabolic stress, and augment established treatments for depression when used adjunctively. Preliminary randomised controlled data indicate greater reductions in depressive symptoms when creatine supplementation is combined with cognitive-behavioural therapy compared to psychotherapy alone.

Although findings remain heterogeneous and exploratory, they support a neuroaffective perspective in which cellular energy availability may enable, or constrain, emotional regulation, learning, and psychotherapeutic change. This first instalment of the TED (Tiredโ€“Exerciseโ€“Diet) series examines creatine as a foundational metabolic substrate within a broader lifestyle neuroscience framework relevant to affect regulation, fatigue, and motivation. The article reviews what creatine is, why it may matter for the emotional brain, and what the current evidence does, and does not, support, while underscoring the need for larger, well-controlled clinical trials prior to routine clinical implementation.

More broadly, this article aims to bridge psychotherapy and lifestyle neuroscience in a grounded, theory-integrative manner, offering relevance to mental health clinicians, researchers, and advanced readers interested in biologically informed approaches to emotional regulation.


Keywords

NeuroAffective-CBT, TED model, creatine supplementation, lifestyle interventions, affect regulation, shame-based disorders, depression, psychotherapy augmentation, brain energy metabolism, mitochondrial function, fatigue, affect dysregulation


The TED Series: Rationale, Order, and Structure

This article opens the TED (Tiredโ€“Exerciseโ€“Diet) series, an eight-part examination of how lifestyle-related variables shape emotional regulation, cognitive performance, and mental health. The series addresses not only supplements, but also behavioural and physiological regulators that operate largely outside conscious awareness while exerting significant influence over mood, motivation, self-control, and learning capacity.

TED is organised around three interdependent pillars:

  • T โ€“ Tired: sleep, fatigue, circadian rhythm, and recovery
  • E โ€“ Exercise: movement, strength, metabolic resilience, and stress adaptation
  • D โ€“ Diet: nutrition, hydration, and gutโ€“brain biochemical signalling

Although conceptually simple, each pillar encompasses multiple interacting neurobiological mechanisms. For this reason, the series both begins and ends with “Diet”. Nutrition supplies the molecular substrates required for neural energy production, neurotransmission, immune balance, and plasticity. Sleep restores and exercise activates; diet sustains the biochemical conditions upon which both depend.

Rather than opening with dietary patterns or prescriptive guidance, Part I focuses on a single, well-characterised nutritional compound central to cellular energy availability. This establishes a physiological foundation upon which subsequent instalments progressively address broader metabolic, neurochemical, behavioural, and restorative processes.

The sequence of the TED series is as follows:


Introducing TED within the NeuroAffective-CBT Framework

Within NeuroAffective-CBT (NA-CBT), TED functions as a biologically grounded scaffold of self-regulation that supports emotional learning, affect tolerance, and therapeutic engagement. Rather than serving as an adjunctive wellness strategy, TED is embedded as a core regulatory module designed to stabilise the physiological conditions upon which affective and cognitive interventions depend.

A central clinical observation underpinning the TED model is that shame-based and affect-dysregulated presentations, characterised by self-loathing, entrenched self-criticism, fatigue, and motivational collapse, frequently co-occur with sleep disruption, metabolic strain, low physical activity, and dysregulated eating. These states are associated with reduced neural flexibility, impaired stress tolerance, and diminished capacity for emotional integration. When such physiological constraints remain unaddressed, engagement with psychotherapy may be limited regardless of insight or motivation.

TED targets three interdependent domains that operate largely outside conscious awareness yet exert powerful influence over mood, motivation, self-control, and learning capacity. Its aim is not optimisation or performance enhancement, but regulation: establishing sufficient physiological stability to widen the window for emotional regulation and psychotherapeutic change.

In NA-CBTยฎ, TED is introduced early in treatment, following assessment and case conceptualisation. Addressing sleep, movement, and nutritional regulation at this stage helps establish the metabolic and neurophysiological conditions necessary for deeper affective and cognitive work. Lifestyle variables are therefore treated as modifiable neuro-behavioural levers capable of influencing dopamine signalling, serotonin synthesis, immune activity, circadian rhythm, and vagus-mediated gutโ€“brain communication.

Daniel Mirea (2023 and 2025) articulated the TED model as โ€œTired, Exercise, and Diet Your Way Out of Trouble,โ€ positioning it as a bridge between neuroscience, nutritional psychiatry, psychophysiology, and behavioural science. Within this framework, psychological change is constrained, but not determined, by metabolic capacity. TED thus supports, rather than replaces, affect-focused psychotherapy.

In this context, it is important to distinguish the TED framework from performance-first lifestyle or โ€œbiohackingโ€ models that prioritise optimisation, productivity, or symptom elimination. Whereas performance-oriented approaches often aim to push cognitive, emotional, or physical output beyond baseline, TED is explicitly regulatory rather than augmentative. Its goal is not to enhance performance, resilience, or motivation per se (although these could be byproducts) but to stabilise the physiological conditions required for emotional tolerance, learning, and self-regulation. Within TED, sleep, movement, and nutrition are not leveraged to maximise efficiency or willpower, but to reduce background physiological noise that constrains affective processing and psychotherapeutic change. In this sense, TED operates as a constraint-reducing framework rather than a performance-enhancing one, supporting psychological work without reframing distress as a failure of optimisation or effort.


What Does the Evidence Suggest.. and What Doesnโ€™t

Creatine has traditionally been viewed as a sports supplement valued for muscular performance. More recently, neuroscience research has examined creatine as a neurometabolic compound relevant under conditions of cerebral stress. Although the liver and brain synthesise small endogenous amounts, supplementation appears most relevant during periods of elevated cognitive demand, sleep deprivation, depression, or neurodegenerative vulnerability, states characterised by energetic strain, inflammation, and oxidative stress.

Animal models, neuroimaging studies, and early-stage human trials suggest that creatine supplementation may enhance brain bioenergetics, buffer cognitive performance under metabolic stress, and support emotional functioning. However, the evidence base remains emergent and heterogeneous, with effects varying by population, dose, and context. Current findings therefore support cautious optimism rather than clinical certainty.

From a NeuroAffective-CBTยฎ perspective, these findings raise the possibility that cellular energy availability may function as a permissive factor for emotional regulation and psychotherapeutic learning, rather than as a direct treatment mechanism.


The Rationale: Bioenergetics, Oxidative Stress, and Brain Demand

Creatine functions as a rapid energy-buffering system, maintaining cellular ATP availability during periods of high demand via the phosphocreatine system. Although commonly associated with muscle tissue, the brain consumes approximately 20% of the bodyโ€™s resting energy expenditure.

In depression, anxiety, and chronic stress, mitochondrial inefficiency and elevated oxidative stress are frequently observed. These processes are associated with impaired neural signalling, reduced synaptic efficiency, and diminished capacity for affect regulation. By supporting mitochondrial efficiency and stabilising cellular energy availability, creatine supplementation may mitigate some of these constraints.

Animal models demonstrate reduced stress markers and depression-like behaviours following creatine administration, while early human findings remain cautiously promising. Together, these mechanisms suggest a plausible link between bioenergetic support and emotional regulation, although causal pathways remain under investigation.

TED summary: Creatine may help stabilise cerebral energy supply under stress, reducing metabolic interference with emotional regulation and learning.


Human Evidence: Mood, Cognition, and Stress Conditions

Mood and Depression

Controlled trials indicate that creatine may accelerate and potentiate antidepressant effects when used adjunctively. Studies combining creatine with selective serotonin reuptake inhibitors, as well as a recent randomised pilot trial combining creatine with cognitive-behavioural therapy, report greater reductions in depressive symptoms compared to treatment alone, without increased adverse events.

Neuroimaging studies demonstrate increased cerebral phosphocreatine following supplementation, potentially addressing reduced brain-energy states observed in mood disorders. Reviews consistently conclude that creatine shows greatest promise as an adjunct rather than a stand-alone intervention.

TED perspective: By supporting metabolic stability, creatine may enhance engagement with psychotherapy and emotional learning.


Cognition, Memory, and Sleep Deprivation

Systematic reviews suggest that creatine can improve memory, processing speed, and cognitive endurance under conditions of metabolic stress, including sleep deprivation and sustained mental effort. Benefits are most consistently observed in older adults or individuals with compromised energy regulation, while effects in young, well-rested populations are minimal.

Experimental sleep-deprivation models indicate that acute high-dose creatine can reverse cognitive deficits and, in some paradigms, restore performance to near baseline levels. These findings point to relatively rapid effects on cerebral energy metabolism rather than slow structural adaptation.

TED perspective: Creatine may support cognitively and emotionally tired brains under pressure, bridging the Tired and Diet domains.


Key Questions and Practical Considerations

Dose and Brain Uptake

While low-dose creatine (3โ€“5 g/day) effectively supports muscular performance, evidence suggests higher doses may be required to meaningfully elevate brain creatine levels once muscular stores are saturated. Brain uptake appears slower and more variable, which may explain why cognitive and mood effects often emerge gradually. These observations are mechanistic rather than prescriptive.

Electrolytes and Hydration

Creatine transport relies on sodium- and chloride-dependent transporters. Adequate hydration and electrolyte intake may facilitate cellular uptake, although brain-specific effects remain under investigation.

Safety

Extensive evidence supports the safety of creatine monohydrate at standard doses. Rare reports of manic switching underscore the need for monitoring in vulnerable populations, particularly individuals with bipolar spectrum conditions.


Implications for TED and NeuroAffective-CBTยฎ

Creatine should be understood as a supportive metabolic adjunct rather than a substitute for psychotherapy or pharmacotherapy. Its potential value lies in stabilising bioenergetic foundations that may enhance emotional learning, affect regulation, and therapeutic engagement.

From a NeuroAffective-CBTยฎ perspective, insufficient bioenergetic capacity may constrain the brainโ€™s ability to tolerate affect, regulate emotion, and engage in self-reflection. Addressing such constraints may widen the therapeutic window within which affect-focused and cognitive interventions can operate. When integrated within the TED frameworkโ€”alongside sleep optimisation, structured movement, and nutrient-dense nutritionโ€”creatine may contribute to synergistic effects that support psychological change.


Summary and Outlook

Taken together, current evidence suggests that creatine could play a limited but meaningful role in mental health, not as a stand-alone intervention, but as a metabolic support that may enhance emotional regulation and psychotherapeutic change under conditions of fatigue and stress. Within the TED model, this reflects a broader principle: psychological change is constrained by metabolic capacity. When bioenergetic resources are insufficient, the brainโ€™s ability to tolerate affect, sustain motivation, and engage in emotional learning may be reduced.

By examining creatine in the first instalment of the TED series, this article establishes a physiological foundation for understanding how lifestyle-related variables shape mental health outcomes. Creatine emerges as a scientifically plausible example of how targeted metabolic support may stabilise cerebral energy availability, thereby widening the window within which affect-focused and cognitive interventions can operate. Its value lies in facilitation rather than substitution.

Subsequent instalments examine insulin sensitivity, fatty acid composition, micronutrient sufficiency, sleep architecture, and movement, progressively outlining how lifestyle regulation can support emotional regulation, cognitive flexibility, and neuroplastic change. The final instalment returns to Diet as a whole, reframing nutrition not merely as fuel but as informationโ€”a continuous stream of biochemical signals shaping emotional states, cognition, and behaviour. Within this framework, creatine is best understood not as a cure, but as a metabolic ally supporting tired brains so psychotherapy can work more effectively.

โš ๏ธ Disclaimer

This article is not intended to replace professional medical or psychological assessment or treatment. Lifestyle or supplement changes should always be discussed with qualified health professionals, including a GP, psychiatrist, registered nutritionist, particularly when managing mental health or metabolic conditions.

Series context:ย next article will focus on insulin resistance and explore beyond the obvious connection with diabetes: TED Series, Part II: โ€œInsulin Resistance and Mental Health .. โ€œ


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Why Your Brain Makes You Crave Certain Foods

and How ‘TED’ can Help You Rewire It…

Why do some foods feel irresistible, while others barely tempt you? It is tempting to think cravings are just about taste, sweet, salty, sour, bitter, but the truth runs much deeper. Your brain and gut are in constant conversation, sending signals that shape not only what you like to eat, but what you want to eat again and again. But hereโ€™s the twist: those preferences arenโ€™t fixed! With the right strategies, you can actually retrain your brain to crave healthier foods. One of the most practical tools for doing this is ‘TED‘ short for Tired, Exercise, Diet. Within the NeuroAffective-CBT approach, TED is one of the most compelling self-regulation frameworks. It uses the idea of an ‘imaginal friend‘, a life-coach or inner guide that can help you stay focused on daily choices which support meaningful lifestyle changes. These changes strengthen both physical health and immunity while also building psychological resilience, self-appreciation, and self-love.

Each component of TED – Tiredness (sleep), Exercise, and Diet, has strong empirical links to emotional and cognitive wellbeing. First introduced to the psychotherapy world nearly 20 years ago by behaviourist Daniel Mirea (Mirea, 2023), TED has become a cornerstone of the NA-CBT approach. At its core, TED highlights the Bodyโ€“Brainโ€“Affect triangle, showing how rest, movement, and nutrition work together to regulate cravings, balance mood, and improve overall health.

So, let’s think of TED as your inner coach and personal trainer, totally on your side but tough and fair, a voice you can hear all the time:

  • Tired โ†’ how well you rest shapes hunger, hormones, and food choices.
  • Exercise โ†’ physical activity resets dopamine and balances stress.
  • Diet โ†’ what you eat trains your gut and brain to prefer certain foods.

And now… with TED in mind, letโ€™s examine how cravings really work and how to rewire them.

The Three Layers of Food Preference

Scientists generally point to three systems that explain why we like certain foods:

1. Taste Buds (Diet in Action)

The tongue is the first gatekeeper of food preference. It detects sweet, salty, sour, bitter and, umami (savory, meaty flavour), behaviourally guiding us toward energy-rich or protein-rich foods. This happens because specialised neurons on the tongue can detect sweetness, saltiness, sourness, bitterness, and umami. They give us that instant โ€œyumโ€ or โ€œyuckโ€. But taste alone isnโ€™t the full story. What you repeatedly eat conditions your taste buds. A diet heavy in ultra-processed foods can dull sensitivity to natural flavors, while a shift to whole foods can make simple tastes more rewarding within 7โ€“14 days (Wise, P. et al., 2016; Turner S et al., 2022).

๐Ÿ‘‰ What does TED say? This is where D for Diet comes in: by choosing nourishing foods consistently, you retrain both your taste buds and your reward circuits. But also, E for Exercise: by changing habits and replacing eating with exercise rewiring occurs even faster and the brain is much more likely to ‘demand and accept’ protein-based products useful for muscle development.


2. Gutโ€“Brain Signaling (The Sleep & Diet Link)

As food travels down the digestive tract, neurons detect its texture, temperature, and nutrients. Specialised โ€œneuropod cellsโ€ are tuned to sense amino acids, sugars, and fats. These cells send electrical signals through the nodose ganglion straight into the brain, triggering dopamine, the neurotransmitter of motivation and reward Bohรณrquez et al., 2015. In other words, when sugar, fat, or amino acids hit the gut, they trigger dopamine release, shaping cravings at a subconscious level.

And hereโ€™s the worse news: poor sleep (The T from TED – Tired) makes these signals even stronger. Lack of rest ramps up ghrelin (the hunger hormone) and dampens leptin (the satiety hormone), pushing you toward high-calorie foods. At the same time, a diet rich in fiber, protein, and complex carbs strengthens gutโ€“brain communication in healthier ways.

๐Ÿ‘‰ TED takeaway: better sleep and diet quality work hand in hand to keep cravings in check.


3. Learned Associations (Exercise as a Reset Button)

The brain is able to link the flavour of food with its aftereffects, like blood sugar rise and dopamine rise after a sweet snack. Over time, these associations become powerful drivers of preference de Araujo et al., 2008.

As such, our brain learns fast to link specific flavours with specific metabolic outcomes. As in the earlier example, sweet taste plus a rise in blood glucose teaches the brain to crave sugar.

And even though artificial sweeteners and many fruits contain little or no glucose, when paired with high-carbohydrate foods (e.g., low-sugar jam with a croissant or fruit with cornflakes), the brain links their sweet taste to the subsequent glucose surge. Over time, this conditioning strengthens the craving pathway at both behavioural and neural levels.

However, regular and intensive Exercise (The E out of TED) helps break this loop. Movement not only burns energy but also improves insulin sensitivity and modulates dopamine pathways, making it easier to โ€œresetโ€ reward associations. People who exercise regularly often find it easier to shift away from addictive food patterns.

๐Ÿ‘‰ TED takeaway: put together, these systems explain why food isnโ€™t just fuel. Itโ€™s a constant feedback loop, where your body teaches your brain what to want. You can use movement to retrain your brainโ€™s learned food-reward pathways.


Your Gut Is Training You

We tend to think of the gut as just a digestion machine. But in reality, itโ€™s a sensory system. As food moves through the stomach and intestines, neurons are watching closely. They respond to stretch (how full your gut is), texture, spiciness, and even temperature.

The most fascinating players are those neuropod cells. They act like food sensors, tuned to the chemistry of whatever you eat. The moment they detect sugars, fats, or amino acids, they send electrical signals to the brain in milliseconds Kaelberer et al., 2018. The brain responds by releasing dopamine, making you feel motivated to seek out more of that food.

This whole process is subconscious. You donโ€™t โ€œdecideโ€ that chocolate cake is rewarding. Your gut tells your brain before you even realize it.


Sweetness and the Dopamine Trap

Sweet taste gives us the clearest example of how these systems interact. Humans are naturally wired to like sweet things โ€” especially children. Sweetness signals calories, which the brain rewards with dopamine.

So what about artificial sweeteners? Why are those still problematic? As explained earlier, sugar reliably increases blood glucose and dopamine. Non-caloric sweeteners taste sweet but donโ€™t raise blood glucose. And at first, dopamine doesnโ€™t budge. But here is the twist: with repeated exposure, artificial sweeteners do start to trigger dopamine. Why? Because your brain learns to expect that sweet taste to mean โ€œenergy incomingโ€ Tellez et al., 2016.

And as already mentioned things get even more complicated when you pair diet drinks (sweet but calorie-free) with a burger and fries (calorie-dense). Over time, your brain begins to link the sweet taste with a metabolic effect. Later, even diet fizzy drink alone can change your insulin response, as if it contained sugar Swithers, 2013.

๐Ÿ‘‰ A practical tip from TED? If you enjoy a diet or low-calorie drink, it is probably better to drink it separately from high-carb meals. Otherwise, you may condition your body to release insulin in ways that throw off blood sugar control. But of course, it would be ideal to avoid sugar or sweetener rich drinks all together especially if your meal is equally rich in carbs and instead… simply replace it with water!


The Psychology of Belief

Itโ€™s not just biology at play. Your mindset about food can literally change how your body reacts. Stanford University professor Alia Crum ran a striking study: participants were given the exact same milkshake but told two different stories about it. Some were told it was โ€œindulgent, high-calorie, rich and satisfying.โ€ Others were told it was โ€œlight, low-calorie, and healthyโ€. The results? The โ€œindulgentโ€ shake produced bigger rises in insulin, ghrelin (a hunger hormone), and blood glucose. People also reported feeling more satisfied Crum et al., 2011. The same drink or shake but a totally different body response, based only on belief.

This is not the classic placebo effect. It is a belief effect: our expectations about food shape our physiology!


Rewiring Your Cravings

Hereโ€™s the good news: your food preferences arenโ€™t set in stone. Scientists describe them as soft-wired, flexible and open to change. Studies show that if you consistently eat a food for 7โ€“14 days, especially when paired with enjoyable or energizing foods, your brain starts to assign more value to it. Translation: it literally tastes better over time (Wise, P. et al., 2016; Turner S et al., 2022; Small et al., 2019).

This is why people in different dietary war-camps like keto, vegan, Mediterranean, etc. Often feel so passionate about their way of eating and fight each other in research facts. Their brains have been conditioned to find their chosen foods the most rewarding.

And you can use the same principle to your advantage. Want to enjoy more leafy greens? Pair them with foods that give you a metabolic boost. Over time, your brain will start rewarding you for those choices.


The Bigger Picture

At the deepest level, your brain isnโ€™t chasing sweetness, salt, or even dopamine. What it really wants is energy for neurons. Food preference is just the surface expression of this survival mechanism.

The catch? In todayโ€™s food environment, ultra-processed and hyper-palatable foods hijack this system. They deliver intense dopamine spikes that make ordinary, healthier foods seem bland by comparison Johnson & Kenny, 2010.

But the opposite is also true: by gradually shifting your diet toward whole, nutrient-rich foods, your dopamine system adapts, and those foods become genuinely more rewarding.


Final Thoughts

Food is far more than fuel. Itโ€™s a dialogue between taste buds, gut neurons, brain chemistry, and even your beliefs. Together, these systems decide what you crave, what satisfies you, and what you keep reaching for.

Perhaps a useful analogy would be to view food preferences as being both hard-wired and soft-wired. Hard-wired circuits push us toward energy-rich foods. Soft-wired associations, however, can be reshaped through repeated exposure and lifestyle choices. And this is where TED truly shines:

  • Tired โ†’ Sleep enough to regulate hunger and strengthen decision-making.
  • Exercise โ†’ Move daily to reset dopamine and insulin sensitivity.
  • Diet โ†’ Feed your gut and brain with nutrient-rich foods that train cravings. Add products like vinegar, lemon, kefir to your diet in order to keep the glucose spike down.

Modern processed foods hijack dopamine pathways, but TED offers a counterweight. With small, consistent shifts, better rest, regular movement, and smarter eating, you can rewire your cravings and restore balance. In a well-known study, participants drank the same milkshake but were told it was either โ€œindulgentโ€ or โ€œlow-calorieโ€. The indulgent version triggered stronger hormonal and metabolic responses, showing that belief changes physiology – so the mindset matters.

This is where TED would demand from you a renewed and improved attitude and mindset:

Diet: Choosing whole foods builds a narrative of self-care that strengthens psychological reward.

Tired: A good sleep and regular rest bites improve emotional regulation, making you less vulnerable to comfort eating and in general emotions are more manageable due to a less reactive amygdala.

Exercise: This list is very long – builds muscle, burns fat, deals with insuline resistance and overall boosts confidence and reinforces positive self-beliefs about health.


โœจ In short: TED isnโ€™t just a checklist; it is a neuroscience-backed guide for aligning your lifestyle with the way your brain and gut actually work. By honoring the ‘big three‘, sleep, exercise, and diet, you can gradually teach your brain to want specific activities and foods that fuel health and wellbeing.

Recommended Reading

If youโ€™d like to explore the science behind food preference and reward systems in more depth, here are a few excellent resources:

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/