TED Series, Part II: Insulin Resistance and Mental Health

Introducing TED in the NeuroAffective-CBTยฎ Framework

The TED (Tired-Exercise-Diet) model is more than just theory. Daniel Mirea first introduced TED in NeuroAffective-CBTยฎ publications such as โ€œTired, Exercise and Diet Your Way Out of Troubleโ€, where it is presented as a core module within the NA-CBT schema linking body, brain, and affect (Mirea, 2023; Mirea, 2025).

Within the broader NeuroAffective-CBTยฎ programme, comprising of six modules, TED is embedded early, supporting psychotherapeutic work targeting chronic internalised shame, self-loathing, self-regulation, and affective vulnerabilities (Mirea, 2023). The underlying principle is that lifestyle modification can enhance and stabilise psychotherapeutic gains (Firth et al., 2020; Lopresti, 2019).

TED integrates insights from neuroscience (e.g., gutโ€“brain signalling, reward pathways), nutritional psychiatry, psychophysiology (e.g., sleep deprivation), and behavioural science (habit formation, conditioning). By framing these domains, sleep, movement, and diet, under one umbrella, TED provides clinicians and clients with a flexible, evidence-informed scaffold for lifestyle-oriented intervention.

If Part I of the TED series explored creatineโ€™s interface with brain energetics and mood (Candow et al., 2022; Allen et al., 2024), Part II turns to a more widespread metabolic challenge: insulin resistance. What are its links to mental health, and how might TEDโ€™s lifestyle levers help?


Insulin Resistance & Mental Health: Why It Matters

Epidemiology & Hidden Burden

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

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

Dietary Drivers & Dopamine Links

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

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

Mechanistic Cascade: From Glucose Spikes to Neural Dysregulation

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

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

From a TED viewpoint, knowingly or unknowingly, many people live in this metabolic state: they feel fatigue or fogginess after meals, gain โ€œstubbornโ€ fat, crave sweets, and feel stuck. Their cells are refusing insulinโ€™s โ€œkey,โ€ causing chronic internal stress that can manifest in mood, cognition, and energy dysregulation.

Prevalence & Clinical Relevance

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

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


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

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

1. Postprandial Movement: The Manual โ€œTesla Doorโ€ Activation

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

2. Carbohydrate Timing & Contextual Use

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

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

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

๐Ÿ‘‰ Other common examples include white bread, honey, dextrose, sports drinks, or small amounts of fruit juice. This guidance, however, does not apply to individuals on a strict weight-loss programme. In such cases, the goal is to reduce overall glucose exposure and promote fat metabolism, meaning fast-digesting carbohydrates are best avoided.

๐Ÿ‘‰Emerging evidence suggests that consuming a small amount of vinegar, around one teaspoon diluted in water, before a high-carbohydrate or sweet meal can help moderate postprandial (after-meal) glucose spikes by slowing gastric emptying and improving insulin sensitivity (Johnston et al., 2004; Mitrou et al., 2010). This simple intervention, often highlighted by metabolic educators such as โ€œJesse the Glucose Goddessโ€, aligns with the TED modelโ€™s focus on practical, low-cost strategies to stabilise energy and mood through metabolic regulation.

3. Rate-limiting Absorption: Protein + Soluble Fibre

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

๐Ÿฅฃ Example: Oatmeal Power Bowl

Carbohydrate: Rolled oats (complex carbs that digest steadily)

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

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

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

Extras: Add sliced banana or berries for natural sweetness

๐Ÿฅ— Alternative savoury example

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

๐Ÿ’ก TED says: his combo reduces post-meal glucose peaks, supports satiety, and keeps insulin responses smooth, exactly what TED aims for.

4. Sludge Clearance & Mitochondrial Support

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

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

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

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

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

7. Gutโ€“Brain Signalling & Cravings

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


Implications for Clinical Practice & Research

  • Incorporate full blood works and/or metabolic screening including fasting insulin, HbA1c, lipid profile, and inflammatory markers into the psychological assessment process to identify underlying metabolic dysfunctions that may contribute to fatigue, irritability, or mood instability. Recognise insulin resistance as a psychometabolic driver of fatigue, irritability, and depressive symptoms. Training implications for education providers.
  • Integrate TED-aligned behavioural tools post-meal walks, fibre pairing, fasting or other nutritional protocols early in therapy.
  • TED-based interventions (post-meal movement, dietary pacing, fibre, cyclical fasting) could be integrated early in therapy, personalised, and monitored.
  • Controlled clinical trials are needed:
    • Does metabolic correction improve mood/anxiety outcomes?
    • What is the interaction between metabolic change and CBT efficacy?
    • Can neuropod modulation mediate craving reduction?

Summary & Outlook

  • Insulin resistance is more than a metabolic disease, it likely contributes to mood dysregulation, fatigue, cravings, and cognitive dysfunction.
  • Within the TED lens, lifestyle levers (movement, meal pacing, fibre, fasting) offer promising adjuncts to psychotherapeutic work.
  • The gutโ€“brain axis, cellular signalling (e.g. DAG accumulation), and mitochondrial health form mechanistic bridges between metabolism and mental health.
  • Future work should test TED-driven metabolic interventions in clinical populations, ideally with objective biomarker endpoints (insulin, inflammatory markers, MRS imaging).

๐Ÿ’ŠBiochemical Terms with Plain-Language Clarifications

AMPK adenosine monophosphate-activated protein kinase (an enzyme that acts as the bodyโ€™s โ€œenergy switch,โ€ helping cells burn fuel efficiently and move sugar from the bloodstream into muscles)

GLUT4 glucose transporter type 4 – a โ€œdoorwayโ€ protein that opens to let glucose enter muscle and fat cells when activated by insulin or exercise

DAG diacylglycerol – a fat-like molecule that builds up inside cells and โ€œjamsโ€ insulin signals, making it harder for the body to use glucose properly

Autophagy – a natural โ€œcellular recyclingโ€ process where old or damaged cell parts are broken down and reused to keep cells healthy

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

Mitochondria – tiny โ€œpower stationsโ€ inside cells that turn food into usable energy and are essential for brain and muscle function)

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

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

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

โš ๏ธDisclaimer

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

๐ŸงพReferences

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

Candow, D.G., Forbes, S.C., Chiang, E., Farthing, J.P. & Johnson, P., 2022. Creatine supplementation and aging: physiological responses, safety, and potential benefits. Nutrients, 14(6), 1218. https://doi.org/10.3390/nu14061218

de Cabo, R. & Mattson, M.P., 2019. Effects of intermittent fasting on health, aging, and disease. New England Journal of Medicine, 381(26), 2541โ€“2551. https://doi.org/10.1056/NEJMra1905136

Firth, J. et al., 2020. A meta-review of lifestyle psychiatry: the role of exercise, smoking, diet and sleep in mental disorders. World Psychiatry, 19(3), 360โ€“380. https://doi.org/10.1002/wps.20773

Hawley, J.A. & Holloszy, J.O., 2009. Exercise: itโ€™s the real thing! Nutrition Reviews, 67(Suppl 2), S172โ€“S178. https://doi.org/10.1111/j.1753-4887.2009.00170.x

Hawley, J.A. & Lessard, S.J., 2008. Exercise training-induced improvements in insulin action. Acta Physiologica, 192(1), 127โ€“135. https://doi.org/10.1111/j.1748-1716.2007.01783.x

Hipkiss, A.R., 2009. Carnosine and its possible roles in nutrition and health. Advances in Food and Nutrition Research, 57, 87โ€“154. https://doi.org/10.1016/S1043-4526(09)57003-1

Jenkins, D.J.A. et al., 2018. Effects of high-fibre foods on glycaemic control. Lancet Diabetes & Endocrinology, 6(10), 794โ€“807. https://doi.org/10.1016/S2213-8587(18)30135-0

Johnston, C.S., Kim, C.M. & Buller, A.J., 2004. Vinegar improves insulin sensitivity to a high-carbohydrate meal in subjects with insulin resistance or type 2 diabetes. Diabetes Care, 27(1), pp.281โ€“282.

https://doi.org/10.2337/diacare.27.1.281Kaelberer, M.M. et al., 2020. Gut neuropod cells: sensory transducers that couple the gut to the brain. Cell, 182(4), 947โ€“949. https://doi.org/10.1016/j.cell.2020.07.035

Khan, A. et al., 2003. Cinnamon improves glucose and lipids of people with type 2 diabetes. Diabetes Care, 26(12), 3215โ€“3218. https://doi.org/10.2337/diacare.26.12.3215

Kempton, M.J., Fusar-Poli, P. & Allen, P., 2024. Neurobiology of food reward and addiction. Trends in Neurosciences, 47(2), 112โ€“126. https://doi.org/10.1016/j.tins.2023.11.003

Longo, V.D. & Panda, S., 2016. Fasting, circadian rhythms, and time-restricted feeding in healthy lifespan. Cell Metabolism, 23(6), 1048โ€“1059. https://doi.org/10.1016/j.cmet.2016.05.001

Lopresti, A.L., 2019. A review of lifestyle factors that contribute to important pathways in depression: diet, sleep and exercise. Journal of Affective Disorders, 256, 38โ€“44. https://doi.org/10.1016/j.jad.2019.05.066

Louie, A.M., Ramos-Loyo, J. & Ketter, T.A., 2023. Insulin resistance and depression: shared pathways and implications. Frontiers in Psychiatry, 14, 1123657. https://doi.org/10.3389/fpsyt.2023.1123657

Mirea, D., 2023. Tired, Exercise and Diet Your Way Out of Trouble (T.E.D.) model. NeuroAffective-CBTยฎ. Available at: https://www.researchgate.net/publication/382274002_Tired_Exercise_and_Diet_Your_Way_Out_of_Trouble_T_E_D_model_by_Mirea [Accessed 17 Oct 2025].

Mirea, D., 2025. Why your brain makes you crave certain foods (and how โ€œTEDโ€ can help you rewire itโ€ฆ). NeuroAffective-CBTยฎ, 17 September. Available at: https://neuroaffectivecbt.com/2025/09/17/why-your-brain-makes-you-crave-certain-foods/ [Accessed 17 Oct 2025].

Mitrou, P., Petsiou, E., Papakonstantinou, E., Maratou, E., Lambadiari, V., Dimitriadis, P. & Raptis, S.A., 2010. Vinegar consumption increases insulin-stimulated glucose uptake by the forearm muscle in humans with type 2 diabetes. European Journal of Clinical Nutrition, 64(8), pp.871โ€“877. https://doi.org/10.1038/ejcn.2010.102

Morris, G., Berk, M., Carvalho, A.F. et al., 2017. The role of mitochondria in mood disorders. Bipolar Disorders, 19(7), 577โ€“596. https://doi.org/10.1111/bdi.12534

Reaven, G.M., 2011. Insulin resistance: the link between obesity and cardiovascular disease. Medical Clinics of North America, 95(5), 875โ€“892. https://doi.org/10.1016/j.mcna.2011.06.002

Richter, E.A. & Hargreaves, M., 2013. Exercise, GLUT4, and skeletal muscle glucose uptake. Physiological Reviews, 93(3), 993โ€“1017. https://doi.org/10.1152/physrev.00038.2012

Schulman, G.I. et al., 2019. Diacylglycerol activation of PKCฮต mediates hepatic insulin resistance. Physiological Reviews, 99(2), 511โ€“536. https://doi.org/10.1152/physrev.00061.2017

Smith, D.G. & Robbins, T.W., 2020. The neurobiological basis of obesity and binge eating. Physiology & Behavior, 222, 112978. https://doi.org/10.1016/j.physbeh.2020.112978

Spiegel, K., Leproult, R. & Van Cauter, E., 1999. Impact of sleep debt on metabolic and endocrine function. Lancet, 354(9188), 1435โ€“1439. https://doi.org/10.1016/S0140-6736(99)01376-8

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

Antonio, J. et al., 2021. Common questions and misconceptions about creatine supplementation: what does the scientific evidence really show? Journal of the International Society of Sports Nutrition, 18(1), 13โ€“27. https://doi.org/10.1186/s12970-021-00412-z

Avgerinos, K.I., Spyrou, N., Bougioukas, K.I. & Kapogiannis, D., 2018. Effects of creatine supplementation on cognitive function of healthy individuals: a systematic review of randomized controlled trials. Experimental Gerontology, 108, 166โ€“173. https://doi.org/10.1016/j.exger.2018.04.014

Braissant, O., 2012. Creatine and guanidinoacetate transport at the bloodโ€“brain and bloodโ€“cerebrospinal-fluid barriers. Journal of Inherited Metabolic Disease, 35(4), 655โ€“664. https://doi.org/10.1007/s10545-011-9415-6

Candow, D.G., Forbes, S.C., Chiang, E., Farthing, J.P. & Johnson, P., 2022. Creatine supplementation and aging: physiological responses, safety, and potential benefits. Nutrients, 14(6), 1218. https://doi.org/10.3390/nu14061218

Dechent, P., Pouwels, P.J.W., Wilken, B., Hanefeld, F. & Frahm, J., 1999. Increase of total creatine in human brain after oral supplementation of creatine monohydrate. American Journal of Physiology โ€“ Regulatory, Integrative and Comparative Physiology, 277(3), R698โ€“R704. https://doi.org/10.1152/ajpregu.1999.277.3.R698

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

Firth, J. et al., 2020. A meta-review of โ€œlifestyle psychiatryโ€: the role of exercise, smoking, diet and sleep in mental disorders. World Psychiatry, 19(3), 360โ€“380. https://doi.org/10.1002/wps.20773

Harvard Health Publishing, 2024. What is creatine? Harvard Medical School. Available at: https://www.health.harvard.edu/staying-healthy/what-is-creatine

Irwin, M.R., 2015. Why sleep is important for health: a psychoneuroimmunology perspective. Annual Review of Psychology, 66, 143โ€“172. https://doi.org/10.1146/annurev-psych-010213-115205

Kandola, A., Ashdown-Franks, G., Hendrikse, J., Sabiston, C.M. & Stubbs, B., 2019. Physical activity and depression: toward understanding the antidepressant mechanisms of physical activity. Neuroscience & Biobehavioral Reviews, 107, 525โ€“539. https://doi.org/10.1016/j.neubiorev.2019.09.040

Kreider, R.B. et al., 2017. ISSN position stand: safety and efficacy of creatine supplementation in exercise, sport, and medicine. Journal of the International Society of Sports Nutrition, 14, 18. https://doi.org/10.1186/s12970-017-0173-z

L-Kiaux, A., Brachet, P. & Gilloteaux, J., 2024. Creatine for the treatment of depression: preclinical and clinical evidence. Current Neuropharmacology, 22(4), 450โ€“466. https://doi.org/10.2174/1570159X22666230314101523

Lopresti, A.L., 2019. A review of lifestyle factors that contribute to important pathways in depression: diet, sleep and exercise. Journal of Affective Disorders, 256, 38โ€“44. https://doi.org/10.1016/j.jad.2019.05.066

Lyoo, I.K. et al., 2012. A randomized, double-blind clinical trial of creatine monohydrate augmentation for major depressive disorder in women. American

Journal of Psychiatry, 169(9), 937โ€“945. https://doi.org/10.1176/appi.ajp.2012.11081259

McMorris, T. et al., 2006. Creatine supplementation and cognitive performance during sleep deprivation. Psychopharmacology, 185(1), 93โ€“103. https://doi.org/10.1007/s00213-005-0269-8

McMorris, T., Harris, R.C., Howard, A. & Jones, M., 2017. Creatine, sleep deprivation, oxygen deprivation and cognition: a review. Journal of Sports Sciences, 35(1), 1โ€“8. https://doi.org/10.1080/02640414.2016.1156723

Mirea, D., 2023. Tired, Exercise and Diet Your Way Out of Trouble (T.E.D.) model. NeuroAffective-CBTยฎ Publication. Available at: https://www.researchgate.net/publication/382274002_Tired_Exercise_and_Diet_Your_Way_Out_of_Trouble_T_E_D_model_by_Mirea [Accessed 17 October 2025]

Mirea, D., 2025. Why your brain makes you crave certain foods (and how โ€œTEDโ€ can help you rewire itโ€ฆ). NeuroAffective-CBT, 17 September. [online] Available at: https://neuroaffectivecbt.com/2025/09/17/why-your-brain-makes-you-crave-certain-foods/ [Accessed 17 October 2025].

Morris, G., Berk, M., Carvalho, A.F. et al., 2017. The role of mitochondria in mood disorders: from pathophysiology to novel therapeutics. Bipolar Disorders, 19(7), 577โ€“596. https://doi.org/10.1111/bdi.12534

Rae, C. & Brรถer, S., 2015. Creatine as a booster for human brain function. Neurochemistry International, 89, 249โ€“259. https://doi.org/10.1016/j.neuint.2015.07.009

Silva, R. et al., 2013. Mania induced by creatine supplementation in bipolar disorder: case report. Journal of Clinical Psychopharmacology, 33(5), 719โ€“721. https://doi.org/10.1097/JCP.0b013e3182a60792

Simpson, E.J. & Rawson, E.S., 2021. Creatine supplementation and cognitive performance: a critical appraisal. Nutrients, 13(5), 1505. https://doi.org/10.3390/nu13051505

Sherpa, N.N., De Giorgi, R., Ostinelli, E.G. et al. (2025). Efficacy and safety profile of oral creatine monohydrate as an add-on to cognitive-behavioural therapy in depression: an 8-week pilot, double-blind, randomized, placebo-controlled feasibility and exploratory trial in an under-resourced area. European Neuropsychopharmacology, 90, pp. 28โ€“35.

Tachikawa, M., Fukaya, M., Terasaki, T. & Ohtsuki, S., 2013. Distinct cellular expression of creatine transporter (SLC6A8) in mouse brain. Journal of Cerebral Blood Flow & Metabolism, 33(5), 836โ€“845. https://doi.org/10.1038/jcbfm.2013.6

Zhang, Y., Li, X., Chen, S. & Wang, J., 2023. Creatine and brain health: mechanisms and therapeutic prospects. Frontiers in Neuroscience, 17, 1176542. https://doi.org/10.3389/fnins.2023.1176542

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: