Tag: wellness

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

NeuroAffective-CBT by Daniel Mirea

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 (Tired–Exercise–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 (Tired–Exercise–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 – Tired: sleep, fatigue, circadian rhythm, and recovery
  • E – Exercise: movement, strength, metabolic resilience, and stress adaptation
  • D – Diet: nutrition, hydration, and gut–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-CBT®, 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 gut–brain communication.

Daniel Mirea (2023 and 2025) articulated the TED model as “Tired, Exercise, and Diet Your Way Out of Trouble,” 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 “biohacking” 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 Doesn’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-CBT® 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 body’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 (3–5 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-CBT®

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-CBT® perspective, insufficient bioenergetic capacity may constrain the brain’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 framework—alongside sleep optimisation, structured movement, and nutrient-dense nutrition—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 brain’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 information—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.

⚠️ Disclaimer

These article (like all other NA-CBT articles) 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.

References:

Allen, P.J., D’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), 13–27. 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, 166–173. https://doi.org/10.1016/j.exger.2018.04.014

Braissant, O., 2012. Creatine and guanidinoacetate transport at the blood–brain and blood–cerebrospinal-fluid barriers. Journal of Inherited Metabolic Disease, 35(4), 655–664. 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 – Regulatory, Integrative and Comparative Physiology, 277(3), R698–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, 2275–2287. https://doi.org/10.1007/s00213-018-4956-2

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), 360–380. 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, 143–172. 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, 525–539. 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), 450–466. 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, 38–44. 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), 937–945. 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), 93–103. 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), 1–8. 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-CBT® 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 “TED” can help you rewire it…). 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), 577–596. https://doi.org/10.1111/bdi.12534

Rae, C. & Bröer, S., 2015. Creatine as a booster for human brain function. Neurochemistry International, 89, 249–259. 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), 719–721. 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. 28–35.

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), 836–845. 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

NeuroAffective-CBT by Daniel Mirea

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 here’s the twist: those preferences aren’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 Body–Brain–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 → how well you rest shapes hunger, hormones, and food choices.
  • Exercise → physical activity resets dopamine and balances stress.
  • Diet → what you eat trains your gut and brain to prefer certain foods.

And now… with TED in mind, let’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 “yum” or “yuck”. But taste alone isn’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 7–14 days (Wise, P. et al., 2016; Turner S et al., 2022).

👉 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. Gut–Brain Signaling (The Sleep & Diet Link)

As food travels down the digestive tract, neurons detect its texture, temperature, and nutrients. Specialised “neuropod cells” 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 Bohórquez 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 here’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 gut–brain communication in healthier ways.

👉 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 “reset” reward associations. People who exercise regularly often find it easier to shift away from addictive food patterns.

👉 TED takeaway: put together, these systems explain why food isn’t just fuel. It’s a constant feedback loop, where your body teaches your brain what to want. You can use movement to retrain your brain’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, it’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 don’t “decide” 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 — 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 don’t raise blood glucose. And at first, dopamine doesn’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 “energy incoming” 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.

👉 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

It’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 “indulgent, high-calorie, rich and satisfying.” Others were told it was “light, low-calorie, and healthy”. The results? The “indulgent” 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

Here’s the good news: your food preferences aren’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 7–14 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 isn’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 today’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. It’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 → Sleep enough to regulate hunger and strengthen decision-making.
  • Exercise → Move daily to reset dopamine and insulin sensitivity.
  • Diet → 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 “indulgent” or “low-calorie”. 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.

✨ In short: TED isn’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 you’d like to explore the science behind food preference and reward systems in more depth, here are a few excellent resources: