Allostatic Load

Most people think about stress wrong. They think it's a feeling. The tight sensation in your chest before a big meeting, the racing thoughts at 2am. But stress is actually an accounting problem. Your body keeps a ledger, and it never forgets.

The ledger has a name: allostatic load. It's the cumulative biological cost of dealing with life. And understanding it might be the most important thing you can do if you care about doing your best work over a long period of time.

The Body's Prediction Machine

Here's something surprising: your body doesn't work the way you were probably taught in biology class.

The textbook story is homeostasis. Your body has set-points (98.6°F, a certain blood sugar level, a certain blood pressure) and when things deviate, negative feedback loops pull them back. Like a thermostat.

That's mostly wrong. In 1988, a neurobiologist named Peter Sterling realized the body works more like a prediction engine [1]. Your blood pressure isn't held at a fixed point. It's low when you're sleeping, surges when you wake up, spikes when you sprint. The brain is constantly adjusting every physiological dial based on what it thinks you'll need next. Sterling called this allostasis, meaning stability through change.

This is a much smarter system than a thermostat. But it has a cost. Every adjustment uses resources. Every prediction that's wrong wastes more. And if the system is chronically activated, if the brain keeps predicting threats that never fully resolve, those costs accumulate.

In 1993, Bruce McEwen at Rockefeller University gave this accumulation a name. He called it allostatic load [2].

What the Load Actually Is

Think of your stress response as a credit card. In an emergency, it's incredibly useful. Cortisol mobilizes energy. Adrenaline sharpens focus. Inflammation fights infection. These are expensive operations, but they're worth it when a lion is chasing you.

The problem is when you never pay off the balance. When the stressor is your job, your relationships, your commute, your financial anxiety. Things that don't end. The credit card stays maxed out. You're paying interest on interest.

McEwen identified four specific ways this goes wrong [3]:

1. Too many hits. You're exposed to one stressor after another, with no recovery between them.

2. No habituation. You keep reacting to the same stressor as if it's new, every time.

3. Can't turn it off. The stressor passes, but your body stays activated.

4. Lopsided response. One system doesn't respond enough, so another has to overcompensate.

McEwen and Wingfield later distinguished two types of allostatic overload [4]. Type 1 occurs when energy demand exceeds supply, like starvation or extreme physical stress. Type 2 occurs in environments of sufficient energy but chronic psychosocial stress. That's the predominant form in modern life. Type 2 overload doesn't trigger escape behaviors. It can only be counteracted through behavioral change and environmental restructuring.

Each of these is a different way the bill gets bigger. And the bill isn't metaphorical. It shows up in your blood work.

What it Looks Like in Your Body

Researchers measure allostatic load using biomarkers. Actual physiological readings. The original index from the MacArthur Studies of Successful Aging [5] used ten: cortisol, adrenaline, noradrenaline, DHEA-S (a repair hormone), blood pressure (systolic and diastolic), waist-hip ratio, cholesterol, HDL, and HbA1c (a measure of blood sugar control over time).

Each marker gets a 1 if it's in the worst quartile, 0 otherwise. Add them up. Higher scores predict worse outcomes. More disease, faster cognitive decline, earlier death. And they predict these things better than any single marker alone [5]. This simple count-based approach has been used in 52.5% of all allostatic load publications through 2021 [6].

The neuroendocrine cascade follows a well-characterized pathway. The HPA axis releases cortisol, which mobilizes energy, suppresses immune function, and reshapes neural circuits. The sympathetic-adrenal-medullary system releases catecholamines (epinephrine and norepinephrine) for immediate fight-or-flight activation. Under chronic stress, cortisol's diurnal rhythm flattens, and inflammatory markers like CRP and IL-6 rise as the immune system shifts toward chronic, sterile inflammation [7].

In 2023, a massive individual participant data meta-analysis across 67,000 people in 13 cohorts found you could get almost the same predictive power from just five markers: CRP, resting heart rate, HDL cholesterol, waist-to-height ratio, and HbA1c [8]. You could get most of these from a standard blood panel and a tape measure. A separate analysis using Item Response Theory found CRP and BMI were the most informationally rich individual biomarkers [9].

Some newer measurement approaches are worth noting. Hair cortisol concentration captures 3-6 months of cumulative HPA axis activity in a single non-invasive sample, overcoming the limitation of saliva or blood cortisol's 24-hour snapshot [10, 11]. Epigenetic clocks based on DNA methylation quantify biological aging; allostatic load correlates with epigenetic age acceleration (r = 0.21 via Levine's PhenoAge clock), though the two measures capture different dimensions of aging [12]. And a 2025 Nature Communications study developed a wearable-derived aging clock from consumer photoplethysmography data that strongly associates with disease and longitudinal physiological changes [13].

At the cellular level, Picard et al. (2023) revealed that chronic glucocorticoid exposure increases cellular energy expenditure by approximately 60%, shifts metabolism toward mitochondrial oxidative phosphorylation, and accelerates aging across multiple epigenetic clocks while shortening telomeres [14]. This provides the first mechanistic cellular evidence for why allostatic load is literally energetically expensive: chronic stress makes every cell in the body work harder and age faster.

But the most telling thing about allostatic load is what it does to your brain.

The Brain Eats Itself

Your brain is both the commander of the stress response and its primary victim. And the parts that get hit hardest are exactly the parts you need most for deep, creative work.

The prefrontal cortex goes first. This is the region responsible for working memory, abstract reasoning, planning, and impulse control. Basically everything that makes your thinking sophisticated rather than reactive. Amy Arnsten at Yale has shown that even moderate stress causes rapid PFC impairment [15]. The mechanism is an inverted U-curve: the neurotransmitters that optimize PFC function at moderate levels (dopamine, norepinephrine) actively shut it down at high levels [16]. Under stress, your brain literally switches from thoughtful mode to reactive mode.

That's fine as a temporary response. The problem is that chronic stress makes it structural. Arnsten documented actual architectural changes, including spine loss and dendritic atrophy, that produce persistent PFC dysfunction [17, 18]. Your prefrontal cortex doesn't just temporarily go offline. Parts of it physically degrade.

The hippocampus shrinks. The hippocampus handles memory consolidation and spatial navigation, but it also inhibits the stress response. It helps turn off cortisol production. Under chronic stress, hippocampal neurons retract their dendrites, neurogenesis slows, and the structure physically shrinks [19]. One landmark study by Lupien et al. found people with prolonged cortisol elevation had hippocampal volumes 14% smaller than controls, with the degree of atrophy correlating with both the duration and magnitude of cortisol elevation [20].

Here's the vicious part: because a smaller hippocampus is worse at suppressing cortisol, damage to it increases further cortisol production, which causes more damage. Sapolsky described this as the glucocorticoid cascade hypothesis [21]. It's a death spiral.

The meta-analytic evidence connecting allostatic load to cognitive outcomes shows modest but significant effect sizes. D'Amico et al.'s 2020 meta-analysis of 18 studies found higher allostatic load associated with poorer global cognition (r = −0.08) and executive function (r = −0.07) [22]. But population-level correlations likely underestimate the impact in individuals with substantially elevated allostatic load. Neuroimaging studies are more compelling: Booth et al. (2015) found allostatic load inversely associated with total brain volume, white matter volume, and both processing speed and general cognitive ability in 658 older adults [23]. Palix et al. (2025) confirmed that allostatic load negatively predicted gray matter volume in the prefrontal cortex and white matter integrity in frontal-temporal regions [24].

A 2025 study found that each one-point increase in allostatic load was associated with a 15% increase in the odds of progressing from mild cognitive impairment to dementia [24]. This isn't abstract. This is your brain's hardware being degraded by software running in the background that you can't see.

Why This Matters for Flow

Now we get to the part that probably brought you here. You want to be in flow. That state of effortless concentration where hours pass like minutes and your output is the best version of what you're capable of. What does allostatic load have to do with it?

Everything, as it turns out. Though almost no study has directly measured allostatic load biomarkers against flow states (a bizarre gap in the literature), the converging evidence is overwhelming.

Flow has specific biological requirements. It's not just a psychological state. It has a physiological signature, and that signature is incompatible with high allostatic load.

Flow needs a specific cortisol window. Peifer et al. (2014) found that flow follows an inverted-U curve with cortisol [25]. Too little and you're bored, too much and you're anxious, and flow peaks at moderate levels. Then a follow-up study gave subjects 20mg exogenous cortisol to push them to the high end. Flow collapsed [26]. You need enough cortisol to be engaged but not so much that you're overwhelmed. Chronic stress, which flattens your cortisol rhythm and keeps baseline levels elevated, destroys the dynamic range needed to hit this sweet spot.

Flow requires parasympathetic tone. This was surprising to me. You'd think flow, which feels energizing and focused, would be a pure sympathetic (fight-or-flight) state. It's not. Multiple studies show that what distinguishes flow from mere stress is that parasympathetic activity (the calming branch) remains high at the same time as sympathetic arousal [25, 27]. It's a co-activation pattern: engaged but composed. High allostatic load suppresses parasympathetic function. Without it, you get effort but not flow.

Flow needs the prefrontal cortex to temporarily step aside. Arne Dietrich's transient hypofrontality theory proposes that flow occurs when the analytical prefrontal cortex temporarily powers down, letting well-practiced implicit systems run without interference [28]. Brain imaging of jazz musicians improvising confirms extensive PFC deactivation during flow [29]. But chronic stress produces prefrontal hyperactivation. Rumination, vigilance, overanalysis [15, 30]. If flow requires your PFC to let go, and chronic stress keeps it gripping harder, you can see why the two are incompatible.

Flow runs on specific neurochemicals that stress depletes. Flow is associated with dopamine, norepinephrine, and likely endorphins and endocannabinoids. De Manzano et al. (2013) used PET imaging to show that flow proneness correlates with D2 receptor availability in the dorsal striatum [31]. Chronic stress degrades all of these systems. It depletes dopamine through accelerated breakdown, shifts the norepinephrine system from adaptive burst-firing to maladaptive constant-drip mode, diverts the raw materials for serotonin into inflammatory pathways, and desensitizes opioid receptors [19]. High allostatic load creates what you might call neurochemical poverty. You're trying to run premium software on depleted hardware.

The single best proxy for all of this is heart rate variability (HRV). High resting HRV means autonomic flexibility, the ability to shift fluidly between activation and recovery. Multiple studies show higher HRV predicts more flow [25, 27]. HRV declines under chronic stress. And it's measurable with a consumer wearable.

If I had to give someone a single number to track as a proxy for both allostatic load and flow readiness, it would be resting HRV.

What Actually Works

Here's where the research gets simultaneously encouraging and frustrating. Encouraging because the interventions are largely things you already know. Frustrating because there are surprisingly few RCTs that measure composite allostatic load as an outcome. Rosemberg et al.'s 2020 scoping review found only six intervention studies specifically measuring composite allostatic load, four of which showed significant reductions within 7 weeks [32]. Most evidence comes from studies on individual biomarkers.

Still, the picture is clear enough.

Exercise is the most evidence-backed intervention, and it's not close. A 2025 meta-review of 25 systematic reviews (30,000+ participants) found exercise significantly reduces CRP (pooled effect −0.38), IL-6 (−0.47), and TNF-α [33]. The mechanism is beautiful: exercising muscle releases IL-6 as a myokine, which, unlike immune-derived IL-6, is actually anti-inflammatory [34]. Exercise also normalizes cortisol rhythms, improves HRV, reduces insulin resistance, and increases hippocampal volume through BDNF upregulation. Erickson et al. (2011) showed a year of daily walking reversed hippocampal shrinkage in older adults [35]. Both aerobic and strength training work. Higher intensity helps more.

The Mediterranean diet has the strongest nutritional evidence. A meta-analysis of 22 RCTs (Koelman et al., 2022) found it reduced IL-6 by 1.07 pg/mL and CRP by 1.00 mg/L, larger effects than DASH or vegetarian diets [36]. One of the most interesting findings: in adolescents following a Mediterranean diet, the normal link between cortisol and inflammation disappeared [37]. The diet specifically seems to buffer stress-induced inflammation, not just lower baseline inflammation.

Sleep is foundational but often discussed too superficially. McEwen (2006) established that even a few days of sleep deprivation increases inflammatory cytokines, evening cortisol, blood pressure, insulin, and blood glucose while tanking parasympathetic tone [38]. Sleep deprivation doesn't just make you feel tired. It activates essentially every pathway that generates allostatic load simultaneously. A 2022 review confirmed that sleep deprivation and circadian disruption function as primary allostatic stressors [39].

Breathwork delivers the most immediate autonomic effects. Slow breathing at about 6 breaths per minute (resonance frequency) maximizes HRV through baroreflex training [40]. A Stanford RCT published in Cell Reports Medicine (2023) found that 5 minutes of daily cyclic sighing, which is extended exhale breathing, beat mindfulness meditation for mood improvement over a month [41]. For someone trying to directly train the autonomic substrate of flow, breathwork has the best ratio of effort to immediate measurable effect.

Mindfulness works, but differently than you might think. Sanada et al.'s 2016 meta-analysis of MBSR RCTs found a moderate effect on salivary cortisol (g = 0.41) [42]. But the more interesting finding is how it works: Rosenkranz et al. (2013) showed that people who completed MBSR had the same cortisol responses to stress as controls but significantly less inflammation afterward [43]. Mindfulness seems to decouple cortisol from its downstream damage. It may work primarily by changing how you appraise stressors, turning threats into challenges, rather than reducing the stress response itself. A 2023 meta-analysis also found small-to-medium effects on telomere length (g = 0.23) and telomerase activity (g = 0.37), consistent with the Epel-Blackburn model linking mindfulness to cellular aging through reduced rumination [44, 45].

Nature, cold exposure, and sauna are hormetic stressors. Brief, controlled stress that strengthens the system. Forest bathing meta-analysis (Antonelli et al., 2019) found cortisol reductions of 12-18% compared to urban environments [46]. Cold water immersion produces a 200-530% spike in norepinephrine with parasympathetic rebound afterward, though long-term RCT evidence for composite allostatic load reduction is lacking [47]. Finnish sauna studies (Laukkanen et al., 2015, JAMA Internal Medicine; >2,000 men, ~20-year follow-up) found that sauna use 4-7 times per week significantly reduced all-cause mortality in a dose-dependent way [48]. These work on the same principle as exercise: strategic, bounded stress that teaches the system to recover faster.

Social connection is a biological buffer, not just a psychological nice-to-have. Loneliness drives allostatic load through sustained HPA and sympathetic activation. Social support reduces cortisol reactivity through oxytocin pathways. In post-COVID-19 populations, social support was associated with reduced allostatic load (OR = 0.90) [49]. This isn't soft science. The effect sizes are comparable to exercise.

Recovery Is the Performance Variable

If I had to distill the entire allostatic load literature into one sentence for a high-performer, it would be this: what limits your output is not your capacity for effort but your capacity for recovery.

This shows up clearly in elite athletics, where it's been independently rediscovered. Overtraining syndrome, which affects 20-60% of athletes at some point [50], is allostatic overload with a sports-medicine label. Angeli et al. (2004) explicitly identified physical training as allostatic load on the HPA axis, with overtraining syndrome representing the transition from adaptive load to overload [51]. The athletes who sustain performance over years are not the ones who train hardest. They're the ones who recover best.

Kellmann's Recovery-Stress Questionnaire (RESTQ-Sport) operationalizes this insight, tracking stress and recovery as independent dimensions rather than opposite ends of a single continuum. Nicolas et al. (2019) validated this framework physiologically, showing significant correlations between RESTQ psychological recovery-stress scores and objective markers including heart rate, heart rate recovery, and HRV in competitive swimmers [52].

HRV-guided recovery monitoring is emerging as a practical tool for managing allostatic load in real time. Pyne et al. (2022) studied Special Operations Forces candidates and found that post-stress parasympathetic rebound (measured by HRV) reliably predicted stress tolerance and cognitive resilience [53]. In military contexts, Andersen et al.'s International Performance Resilience and Efficiency Program (iPREP), a five-module HRV biofeedback protocol, was the only intervention showing effectiveness at improving physiological regulation during high-threat scenarios across 10 years of research [54].

The same principle applies to cognitive work. Bärtl et al. (2022) found significantly higher allostatic load in people with clinical burnout compared to healthy controls, and the relationship wasn't fully explained by depression [55]. Burnout has its own biological signature of multi-system degradation. An earlier study by Hintsa et al. (2016) confirmed an independent association between burnout and allostatic load even after controlling for psychological distress [56].

The practical implication is uncomfortable for people who pride themselves on pushing through: subjective burnout corresponds to measurable physical damage across multiple organ systems. Recovery isn't a luxury or a sign of weakness. It's an active biological process that, when neglected, progressively degrades the machinery you need to do your best work.

Why Some People Break Faster

One thing the research makes clear is that allostatic load accumulates at very different rates for different people, and the reasons are not entirely within your control.

Genetics matter. The FKBP5 gene modulates how sensitive your cortisol receptors are. People with certain variants keep the cortisol tap running longer after each stressor, accumulating damage faster [57]. The same gene variants are overrepresented in depression and PTSD [58]. Hartmann et al.'s 2022 humanized mouse study showed that FKBP5 risk allele carriers exposed to early adversity exhibited attenuated diurnal glucocorticoid rhythms, reduced circadian entrainment, and altered mitochondrial respiration [59].

Early life programs the system. This is probably the most unsettling finding in the entire literature. Weaver et al.'s landmark 2004 rat study showed that low maternal care produces permanent changes in DNA methylation of the glucocorticoid receptor gene, making the HPA axis permanently more reactive [60]. This was confirmed in humans by McGowan et al. (2009). People who experienced childhood maltreatment showed the same epigenetic changes in post-mortem brain tissue [61]. Adverse childhood experiences don't just create psychological scars. They physically reprogram the molecular machinery that controls stress reactivity, potentially for life. Yehuda et al. (2016) even documented transgenerational transmission, finding altered FKBP5 methylation patterns in offspring of Holocaust survivors [62].

ACE scores show a dose-response relationship with allostatic load. Fogelman and Canli's systematic review of 25 studies confirmed this [63], and Jakubowski et al. (2023) found that physical abuse was associated with 9-23% increases in allostatic load with increasing frequency [64].

Personality amplifies or dampens the load. Neuroticism, the tendency to appraise situations as threatening, consistently predicts higher allostatic load. Conscientiousness predicts lower [65]. This works through both direct physiological pathways (threat appraisal drives HPA activation) and indirect behavioral ones (health habits, sleep, exercise). Gallagher et al. (2021) showed that pre-pandemic allostatic load predicted poorer mental health during COVID-19, with neuroticism exacerbating the effect [66].

None of this means you're determined by your history or your genes. But it means that two people doing the same work, sleeping the same hours, and eating the same food may be accumulating allostatic load at very different rates. Knowing your own baseline, through family history, personal health metrics, and honest self-assessment, matters for calibrating how aggressively you need to invest in recovery.

The Practical Stack

If you wanted to turn this research into a personal protocol, here's what the evidence supports, ranked roughly by effect size and quality of evidence:

Track resting HRV daily as your proxy for allostatic load and flow readiness. Use a wearable. Watch for sustained declines. When HRV drops for several days running, that's your body telling you the load is exceeding recovery.

Exercise consistently, with both aerobic and resistance components. This is the single highest-leverage intervention. The anti-inflammatory myokine response, cortisol normalization, HRV improvement, and BDNF-driven hippocampal protection all reduce allostatic load through distinct mechanisms [33, 34, 35].

Eat a Mediterranean-pattern diet. The evidence for its anti-inflammatory and stress-buffering effects is stronger than for any other dietary pattern [36, 37].

Protect sleep ruthlessly. Sleep deprivation activates every allostatic load pathway simultaneously [38, 39]. There is no intervention that compensates for inadequate sleep.

Breathe at resonance frequency (6 breaths/min) daily. Even 5 minutes of extended-exhale breathing measurably increases HRV and trains the autonomic flexibility that flow depends on [40, 41].

Get periodic blood work. CRP, HbA1c, HDL, and resting heart rate, combined with waist-to-height ratio, approximate the new consensus allostatic load index [8]. Track them over time.

Build social connection into your life as a biological intervention, not just a social one [49].

Use nature, cold, and heat as hormetic training. Brief, controlled stressors that build recovery capacity [46, 47, 48].

The Real Insight

The deepest insight from the allostatic load literature isn't any specific intervention. It's a reframe.

Most people who want to be in flow all the time think of it as an optimization problem: find the right task, the right environment, the right playlist, the right stimulant. Maybe learn to meditate. They're trying to hack their way into a state.

But the research says flow isn't something you hack into. It's something that happens when your biology is in the right condition. Moderate cortisol with preserved dynamic range [25, 26]. High parasympathetic tone [27]. Sufficient dopamine and norepinephrine in burst-firing mode [31]. A prefrontal cortex relaxed enough to step aside [28].

All of these conditions are degraded by allostatic load and restored by recovery. You can't access flow through willpower when the underlying hardware is depleted. It's like trying to run a demanding program on a laptop with a dying battery and overheating CPU. No amount of clicking faster will help.

The question isn't "how do I get into flow?" The question is "what is my allostatic load, and what am I doing to reduce it?" Get that right, and flow becomes much less of a mystery. The states you're chasing become available when you stop depleting the biological resources they require.

The tax you didn't know you were paying turns out to have been the bottleneck all along.

References

[1] Sterling, P., & Eyer, J. (1988). Allostasis: A new paradigm to explain arousal pathology. In S. Fisher & J. Reason (Eds.), Handbook of Life Stress, Cognition and Health (pp. 629-649). John Wiley & Sons.

[2] McEwen, B. S., & Stellar, E. (1993). Stress and the individual: Mechanisms leading to disease. Archives of Internal Medicine, 153(18), 2093-2101.

[3] McEwen, B. S. (1998). Protective and damaging effects of stress mediators. New England Journal of Medicine, 338(3), 171-179.

[4] McEwen, B. S., & Wingfield, J. C. (2003). The concept of allostasis in biology and biomedicine. Hormones and Behavior, 43(1), 2-15.

[5] Seeman, T. E., Singer, B. H., Rowe, J. W., Horwitz, R. I., & McEwen, B. S. (2001). Price of adaptation: Allostatic load and its health consequences. Proceedings of the National Academy of Sciences, 98(8), 4770-4775.

[6] Parker, H. W., et al. (2022). Allostatic Load Measurement: A Systematic Review of Reviews. International Journal of Environmental Research and Public Health.

[7] Juster, R.-P., McEwen, B. S., & Lupien, S. J. (2010). Allostatic load biomarkers of chronic stress and impact on health and cognition. Neuroscience & Biobehavioral Reviews, 35(1), 2-16.

[8] McCrory, C., et al. (2023). Towards a consensus definition of allostatic load: A multi-cohort, multi-system, multi-biomarker IPD meta-analysis. Psychoneuroendocrinology, 153, 106117.

[9] Liu, S. R., & Spicer, P. (2022). Allostatic load scoring using item response theory. Comprehensive Psychoneuroendocrinology, 11, 100147.

[10] Stalder, T., et al. (2017). Stress-related and basic determinants of hair cortisol in humans: A meta-analysis. Psychoneuroendocrinology, 77, 261-274.

[11] Russell, E., et al. (2012). Hair cortisol as a biological marker of chronic stress. Psychoneuroendocrinology, 37(5), 589-601.

[12] McCrory, C., et al. (2019). Epigenetic clocks and allostatic load reveal potential sex-specific drivers of biological aging. The Journals of Gerontology: Series A, 75(3), 495-503.

[13] Nature Communications (2025). A wearable-based aging clock associates with disease and behavior.

[14] Picard, M., et al. (2023). Cellular allostatic load is linked to increased energy expenditure and accelerated biological aging. Psychoneuroendocrinology.

[15] Arnsten, A. F. T. (2009). Stress signalling pathways that impair prefrontal cortex structure and function. Nature Reviews Neuroscience, 10(6), 410-422.

[16] Arnsten, A. F. T. (1997). Catecholamine regulation of the prefrontal cortex. Journal of Psychopharmacology, 11(2), 151-162.

[17] Arnsten, A. F. T. (2015). Stress weakens prefrontal networks: Molecular insults to higher cognition. Nature Neuroscience, 18(10), 1376-1385.

[18] Hains, A. B., et al. (2021). Chronic stress weakens connectivity in the prefrontal cortex. Chronic Stress, 5.

[19] McEwen, B. S. (2000). Allostasis and allostatic load: Implications for neuropsychopharmacology. Neuropsychopharmacology, 22(2), 108-124.

[20] Lupien, S. J., et al. (1998). Cortisol levels during human aging predict hippocampal atrophy and memory deficits. Nature Neuroscience, 1(1), 69-73.

[21] Sapolsky, R. M., Krey, L. C., & McEwen, B. S. (1986). The neuroendocrinology of stress and aging: The glucocorticoid cascade hypothesis. Endocrine Reviews, 7(3), 284-301.

[22] D'Amico, D., et al. (2020). The association between allostatic load and cognitive function: A systematic and meta-analytic review. Psychoneuroendocrinology, 121, 104849.

[23] Booth, T., et al. (2015). Association of allostatic load with brain structure and cognitive ability in later life. Neurobiology of Aging, 36(3), 1390-1399.

[24] Palix, C., et al. (2025). Allostatic load impairs brain structure but not β-accumulation in older adults. Frontiers in Aging Neuroscience, 17.

[25] Peifer, C., et al. (2014). The relation of flow-experience and physiological arousal under stress. Journal of Experimental Social Psychology, 53, 62-69.

[26] Peifer, C., et al. (2015). Cortisol effects on flow-experience. Psychopharmacology, 232(6), 1165-1173.

[27] de Manzano, Ö., et al. (2010). The psychophysiology of flow during piano playing. Emotion, 10(3), 301-311.

[28] Dietrich, A. (2004). Neurocognitive mechanisms underlying the experience of flow. Consciousness and Cognition, 13(4), 746-761.

[29] Limb, C. J., & Braun, A. R. (2008). Neural substrates of spontaneous musical performance. PLoS ONE, 3(2), e1679.

[30] Liston, C., McEwen, B. S., & Casey, B. J. (2009). Psychosocial stress reversibly disrupts prefrontal processing. PNAS, 106(3), 912-917.

[31] de Manzano, Ö., et al. (2013). Flow proneness linked to dopamine D2-receptor availability in the dorsal striatum. NeuroImage, 67, 1-6.

[32] Rosemberg, M.-A., et al. (2021). A scoping review of interventions targeting allostatic load. Stress, 24(5), 484-494.

[33] Meta-meta-analysis (2025). The impact of exercise on chronic systemic inflammation. Sport Sciences for Health.

[34] Pedersen, B. K. (2000). Exercise and cytokines. Immunology and Cell Biology, 78(5), 532-535.

[35] Erickson, K. I., et al. (2011). Exercise training increases size of hippocampus and improves memory. PNAS, 108(7), 3017-3022.

[36] Koelman, L., et al. (2022). Effects of dietary patterns on biomarkers of inflammation. Advances in Nutrition, 13(5), 2060-2080.

[37] Navarro, P., et al. (2018). Does the Mediterranean diet protect against stress-induced inflammatory activation? Nutrients, 10(11), 1770.

[38] McEwen, B. S. (2006). Sleep deprivation as a neurobiologic and physiologic stressor. Metabolism, 55(10 Suppl 2), S20-S23.

[39] Szelenberger, W., & Bhatt, R. (2022). Sleep deprivation and circadian disruption. Sleep Medicine Clinics, 17(2), 253-262.

[40] Laborde, S., et al. (2022). Heart rate variability and cardiac vagal tone in psychophysiological research. Frontiers in Psychology, 8, 213.

[41] Balban, M. Y., et al. (2023). Brief structured respiration practices enhance mood. Cell Reports Medicine, 4(1), 100895.

[42] Sanada, K., et al. (2016). Effects of mindfulness-based interventions on salivary cortisol. Frontiers in Physiology, 7, 471.

[43] Rosenkranz, M. A., et al. (2013). MBSR and modulation of neurogenic inflammation. Brain, Behavior, and Immunity, 27(1), 174-184.

[44] Rathore, M., & Abraham, J. (2023). Effects of mindfulness on telomere length and telomerase activity. Mindfulness, 14, 2599-2616.

[45] Epel, E., et al. (2009). Can meditation slow rate of cellular aging? Annals of the New York Academy of Sciences, 1172, 34-53.

[46] Antonelli, M., et al. (2019). Forest bathing and cortisol reduction. International Journal of Environmental Research and Public Health, 16(18), 3371.

[47] Srámek, P., et al. (2000). Human physiological responses to immersion into water of different temperatures. European Journal of Applied Physiology, 81(5), 436-442.

[48] Laukkanen, T., et al. (2015). Association between sauna bathing and fatal cardiovascular and all-cause mortality events. JAMA Internal Medicine, 175(4), 542-548.

[49] Li, X., et al. (2020). Post-COVID-19 epidemic: Allostatic load among medical and nonmedical workers in China. Psychotherapy and Psychosomatics, 90(2), 127-136.

[50] Kreher, J. B., & Schwartz, J. B. (2012). Overtraining syndrome: A practical guide. Sports Health, 4(2), 128-138.

[51] Angeli, A., et al. (2004). The overtraining syndrome in athletes: A stress-related disorder. Journal of Endocrinological Investigation, 27(6), 603-612.

[52] Nicolas, M., et al. (2019). Monitoring stress and recovery states in elite swimmers. Journal of Sport and Health Science, 8(1), 77-88.

[53] Pyne, D. B., et al. (2022). Resting-state HRV after stressful events as a measure of stress tolerance. Frontiers in Physiology, 13, 1070285.

[54] Andersen, J. P., et al. (2024). The iPREP protocol for HRV biofeedback in law enforcement. Applied Psychophysiology and Biofeedback.

[55] Bärtl, C., et al. (2022). Higher allostatic load in work-related burnout. Psychoneuroendocrinology, 143, 105853.

[56] Hintsa, T., et al. (2016). Burnout and increased allostatic load. Journal of Health Psychology, 21(8), 1576-1586.

[57] Zannas, A. S., et al. (2016). Gene-stress-epigenetic regulation of FKBP5. Neuropsychopharmacology, 41(1), 261-274.

[58] Binder, E. B. (2009). The role of FKBP5 in affective and anxiety disorders. Psychoneuroendocrinology, 34(Suppl 1), S186-S195.

[59] Hartmann, J., et al. (2022). FKBP5 risk alleles and early life adversity. Molecular Psychiatry, 27, 5343-5354.

[60] Weaver, I. C., et al. (2004). Epigenetic programming by maternal behavior. Nature Neuroscience, 7(8), 847-854.

[61] McGowan, P. O., et al. (2009). Epigenetic regulation of the glucocorticoid receptor in human brain. Nature Neuroscience, 12(3), 342-348.

[62] Yehuda, R., et al. (2016). Holocaust exposure induced intergenerational effects on FKBP5 methylation. Biological Psychiatry, 80(5), 372-380.

[63] Fogelman, N., & Canli, T. (2018). Early life stress and cortisol: A meta-analysis. Hormones and Behavior, 98, 63-76.

[64] Jakubowski, K. P., et al. (2023). Childhood adversity and allostatic load.

[65] Yoneda, T., et al. (2023). Personality and allostatic load: A meta-analysis.

[66] Gallagher, S., et al. (2021). Allostatic load and mental health during COVID-19. Comprehensive Psychoneuroendocrinology, 8, 100095.