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 โTired, 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., gutโbrain 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 creatineโs 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 TEDโs 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 โaddictionโ 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 โagingโ), 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, insulinโs compensatory drive fails, and fat accumulation acceleratesโespecially 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 โkeyโ (insulin molecule) trying to unlock a blocked โcar 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 โstubbornโ fat, crave sweets, and feel stuck. Their cells are refusing insulinโs โkey,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 โthin-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 โTesla 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:
- White rice โ breaks down quickly into glucose, providing a rapid spike in blood sugar and energy.
- Bananas (ripe) โ contain simple sugars like glucose and fructose that are quickly absorbed, making them ideal before or during exercise.
๐ 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.
๐Emerging 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 โJesse the Glucose Goddessโ, aligns with the TED modelโs 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).
๐ฅฃ 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
๐ฅ 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
๐ก 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 โsludge,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. GutโBrain 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 โwhat 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 gutโbrain 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).
๐Biochemical Terms with Plain-Language Clarifications
AMPK adenosine monophosphate-activated protein kinase (an enzyme that acts as the bodyโs โenergy switch,โ helping cells burn fuel efficiently and move sugar from the bloodstream into muscles)
GLUT4 glucose transporter type 4 – a โdoorwayโ 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 โjamsโ insulin signals, making it harder for the body to use glucose properly
Autophagy – a natural โcellular 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 โpower 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
โ ๏ธDisclaimer
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.
๐งพReferences
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