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Why “Resting” Doesn’t Make You Better──Allostatic Overload and the Three Self-Sustaining Loops

A note to English-language readers: This article was originally written in Japanese and is the sequel to “You Can’t ‘Blow Off’ Stress──The ‘Stress’ You Think You Know Doesn’t Exist.” While it draws on Japan’s medical and welfare systems as concrete examples, the physiological mechanisms it describes──allostatic overload, the failure of rest to halt self-sustaining stress loops, and the structural mismatch between individual recovery models and socially generated damage──are universal. If you’ve ever been told “just take some time off and you’ll get better,” this article is about you, too.

In the previous article, “You Can’t ‘Blow Off’ Stress──The ‘Stress’ You Think You Know Doesn’t Exist,” we examined what the word “stress” actually refers to as a physiological phenomenon.

The conclusion of that article was: the stress response is a physiological process occurring inside the body, and it cannot be “blown off” or expelled.

That was still a story for people who hadn’t broken down yet.

This article is written for those who are already on the broken side.

You took leave. You entered recovery. The stressor was supposed to be gone. And yet──you’re not getting better. Every time someone says “You’re resting, so you should be improving,” you think so too, but your body won’t cooperate.

If that’s where you are right now──what you’re experiencing has a name. And the reason it’s not your fault has a proper physiological explanation.

This is a long article, but there’s no rush. Close it partway through and come back whenever you’re ready.

TruResearch™

🧬 Allostasis and Allostatic Load──How the Body “Adapts”

First, let me lay out what happened in your body. The things we called “stress responses” in the previous article──elevated heart rate, cortisol release, blood pressure changes──have a formal name in physiology.

Stability Through Change──Allostasis

Allostasis. A concept proposed by Sterling and Eyer in 1988, meaning “maintaining stability through change” [1:sciencedirect.com]. If homeostasis is about “keeping things the same,” allostasis is the process of “changing your state to ultimately maintain stability” [1:sciencedirect.com].

For example, when you encounter danger, your heart rate increases──not because something is wrong, but because your body has determined “raising the heart rate right now improves my chances of survival.” This is the basic idea of allostasis: the brain predicts environmental demands and shifts the body’s set points to adapt [2:wikipedia.org].

Up to this point, the body is doing its job properly.

The Cost of Adaptation──Allostatic Load

But this “stability through change” system comes at a cost.

McEwen and Stellar (1993) named the cumulative wear and tear on the body from repeated allostasis allostatic load [3:pubmed.ncbi.nlm.nih.gov].

Think of it like a car engine. Repeated hard acceleration and sudden braking won’t stop the car from running, but the engine and brake pads are steadily accumulating damage. Allostatic load is the body’s version of that.

When stress is repeated, prolonged, or poorly managed, this load──the body’s wear──keeps building [3:pubmed.ncbi.nlm.nih.gov].

The Breaking Point──Allostatic Overload

And when this wear exceeds a certain threshold, the body’s systems actually break down. McEwen and Wingfield (2003) called this allostatic overload [4:sciencedirect.com].

To summarize the progression so far:

This three-stage framework is the theoretical backbone behind the “mild → moderate → severe → chronic” progression outlined in the previous article.

allostasis_hierarchy_en.drawio.svg

⚙️ How the Body Gets Cornered──Four Patterns

McEwen (1998) identified four patterns by which allostatic load accumulates [5:nejm.org]. This shows that the story isn’t simply “you had too much stress, so you broke.” And among these patterns, you’ll almost certainly recognize what happened to your own body.

Pattern 1: Repeated hits

Repeated exposure to multiple stressors. Work pressure, family problems, financial anxiety──when these all converge simultaneously, the body’s stress response fires again and again. Each one may be small, but they add up, and the load keeps growing [5:nejm.org].

Pattern 2: Lack of adaptation

Normally, when you’re repeatedly exposed to the same stressor, the body’s response gradually weakens (habituation). But when this habituation fails, you end up responding at full intensity every single time [5:nejm.org]. ──This “failure of habituation” will come back later when we discuss the “rumination loop.”

Pattern 3: Prolonged response

Even after the stressor is gone, the body can’t shut off the stress response. Cortisol keeps flowing. Heart rate stays elevated. It’s like a car with broken brakes [5:nejm.org].

Pattern 4: Inadequate response

The body fails to mount a sufficient stress response, and as a result, other systems compensate by becoming hyperactive. For instance, if cortisol secretion is insufficient, the inflammatory responses that cortisol normally suppresses run unchecked [5:nejm.org].

These four patterns don’t typically apply one at a time──under chronic stress, multiple patterns tend to progress simultaneously.

🔥 “Overloaded”──Two Types of Allostatic Overload

This is the most important part of this article.

McEwen and Wingfield (2003) divided allostatic overload into two types [4:sciencedirect.com].

Type 1: Energy Deficit

When energy demand exceeds supply. The body enters “emergency survival mode,” reducing allostatic load to restore energy balance [4:sciencedirect.com].

This is the type where the normal escape response works. Starvation, hibernation, severe acute illness──these fall into this category. Once the stressor passes, you can return to normal life [6:wikipedia.org].

Type 2: Social-Structural

This is the problem.

Type 2 occurs when energy is sufficient──or even in excess──but is accompanied by social conflict or other social dysfunction [4:sciencedirect.com].

The defining feature of this type is that the escape response does not activate. In Type 1, the body automatically issues the command “run.” In Type 2, that mechanism doesn’t fire. Because the problem isn’t a lack of energy──it’s the structure of society [6:wikipedia.org].

In McEwen and Wingfield’s original text, Type 2 overload “can only be counteracted by learning and changes in social structure” [6:wikipedia.org].

Let’s pause here, because this is critical.

“Can only be counteracted by changes in social structure.”

In other words, no amount of individual rest, meditation, or medication will resolve Type 2 overload on its own. It’s not enough for the individual to change──the social structure must change. This is built into the very definition of the theory.

If you’re in the middle of recovery, thinking “I need to try harder” or “I need to get back sooner”──there’s one thing I want you to know. The reason you can’t go back isn’t that you’re not trying hard enough. It’s that the structure you’d be going back to hasn’t changed. The theory says so.

This connects directly to what was described in the previous article: “the structure where those who generate stressors offload the coping onto the individual.”

🔄 “Resting but Not Recovering”──Three Self-Sustaining Loops

This is the core of this article. And probably the part you’ve been most wanting to hear.

You left work. The stressor was supposed to be removed. And yet──you’re not getting better.

“Maybe I’m just being lazy.” “Maybe I just want a break.” ──Those voices come from outside, or from inside your own head.

That’s not what’s happening. Inside your body, loops that keep running on their own even after the stressor is gone are in motion. At least three of them.

Important note: Each individual component of these three loops has supporting evidence, but no study to date has tested this three-loop integration as a unified model. The integration presented here is the author’s structural synthesis.

Loop A: The Rumination Loop

At night, lying in bed wide awake, memories replaying in your head. In the morning, a tightness in your chest for no apparent reason. ──Many people will recognize this.

Leave work → lose contact with people → spend more time alone → rumination begins.

Rumination is the involuntary, repetitive mental replay of painful past events. “What my boss said that time.” “That question in the interview.” ──These memories keep spinning in your head, around and around.

The crucial point here is that rumination is not just “overthinking.”

According to the Perseverative Cognition Hypothesis proposed by Brosschot, Gerin, and Thayer (2006), even after a stressor has been removed, rumination maintains the cognitive representation of the stressor──the mental images and memories──thereby prolonging the physiological stress response (cardiovascular, endocrine, immune) [7:pubmed.ncbi.nlm.nih.gov].

To put it more plainly: for the body, “actually being in front of a hostile boss” and “repeatedly reliving the hostile boss in your mind” are physiologically almost indistinguishable. As long as rumination continues, the HPA axis──the system that produces cortisol──remains activated [7:pubmed.ncbi.nlm.nih.gov].

This was demonstrated empirically by Gianferante et al. (2014). People with high post-stress rumination showed no decrease in cortisol response even with repeated stress exposure──confirming that “Pattern 2: failure of habituation” actually occurs [8:pmc.ncbi.nlm.nih.gov].

This means: if you’re at home on medical leave, ruminating about work, your body is still responding to work stress despite the fact that you’ve left work.

“Stop thinking about it,” people say. Of course you can’t stop. Rumination isn’t a matter of willpower──it’s a physiological phenomenon linked to failed HPA axis habituation.

This is the first mechanism behind “resting but not recovering.”

Loop B: The BDNF Loop

Leave work → go out less → lose contact with people → physical activity decreases → BDNF (Brain-Derived Neurotrophic Factor) declines → hippocampal neuroplasticity (the brain’s ability to change in response to use and retain those changes──like clay holding its shape after being molded) fails to recover.

Why does it matter so much that the hippocampus doesn’t recover? Let’s pause to look at what the hippocampus actually does.

The hippocampus is known as the “memory center,” but that’s not all it does. The hippocampus has a close, bidirectional relationship with the amygdala──the region that governs fear and anxiety responses. The amygdala reacts with “this is dangerous,” and the hippocampus processes the contextual memory of that experience. The interaction between these two regions underpins the formation and regulation of emotional memory. When hippocampal function declines, the ability to contextually suppress amygdala responses──to judge “I’m safe right now, there’s no need to be afraid”──deteriorates.

And it’s important to note that chronic stress doesn’t damage only the hippocampus. A review by McEwen et al. (2016) showed that chronic stress causes dendritic atrophy and reduced neurogenesis in the hippocampus, while simultaneously causing dendritic shortening in the prefrontal cortex and, conversely, promoting dendritic growth in the amygdala [23:pmc.ncbi.nlm.nih.gov]. In other words, stress simultaneously shrinks the regions responsible for “contextual memory processing” and “emotional regulation” while enlarging the region responsible for “fear and anxiety”──at a structural level, the brain becomes locked into “threat mode” [23:pmc.ncbi.nlm.nih.gov].

Returning to the context of Loop B: when hippocampal plasticity fails to recover, it’s not just memory processing that stalls──the neural circuits involved in prefrontal emotional regulation and amygdala suppression also stagnate. The inability to stop past memories from replaying (Loop A) and the continued autonomic dysregulation (Loop C) are not unrelated to these structural changes in the hippocampus-prefrontal cortex-amygdala circuit.

BDNF is a protein that supports the growth and repair of neurons. It is essential for hippocampal neurogenesis and plasticity in particular [9:dovepress.com].

In animal studies, socially isolated rats showed significantly lower BDNF and dramatically reduced hippocampal neurogenesis compared to group-housed rats (10 vs. 232 cells per 400× field) [9:dovepress.com]. A 2017 systematic review also showed that chronic social isolation downregulates hippocampal BDNF protein and mRNA across multiple studies [10:frontiersin.org].

Furthermore, physical inactivity itself acutely reduces BDNF. A 2024 human study by Duderstadt et al. demonstrated that just 30 minutes of sedentary rest was enough to significantly decrease serum BDNF [11:ncbi.nlm.nih.gov].

So when you stay home and don’t move during recovery──even though you’re technically “resting”──BDNF declines, hippocampal neuroplasticity needed for recovery is impaired, and the nervous system deformed by allostatic overload loses its chance to return to normal.

Let me be clear about one thing here.

This is not a “you’re bad for not exercising” story.

“Just exercise” is easy to say. But a body in allostatic overload can’t move precisely because it’s in that state. The lack of motivation, the fatigue, the heaviness──all of these are results of the loops, not results of laziness.

But the inability to move itself causes BDNF to decline, pushing recovery further away. ──The cruelty of this loop is something those living it know better than anyone.

Loop C: The Circadian Rhythm Loop

Waking up at 4 AM. Unable to get out of bed until past noon. Meals at random times. ──This is what recovery tends to look like.

Leave work → no need to wake at a fixed time → wake, eat, and activity times become irregular → the diurnal cortisol rhythm collapses → the HPA axis remains in a hyperactivated state.

Cortisol has a diurnal rhythm: it peaks in the morning and declines toward evening. This rhythm is regulated not only by the circadian clock (internal body clock) but also by social time structures──zeitgebers (literally “time givers”) [12:ncbi.nlm.nih.gov].

Commuting time, mealtimes, scheduled meetings with people──these function as zeitgebers, stabilizing the diurnal cortisol rhythm. But when you leave work for medical recovery, most of these zeitgebers disappear.

According to a review by Balbo et al. (2010), abrupt changes in sleep schedule cause significant disruption to the diurnal cortisol rhythm, and reduced sleep quality leads to HPA axis activation [12:ncbi.nlm.nih.gov]. Regarding irregular eating patterns, reviews have shown that late-night eating disrupts circadian rhythms via HPA axis dysregulation, and sustained cortisol elevation amplifies stress responses and mood instability [13:pmc.ncbi.nlm.nih.gov].

Early morning awakening──waking at 3-5 AM and being unable to fall back asleep──is also deeply linked to circadian rhythm disruption. A review by Boyce and Barriball (2010) identifies early morning awakening, diurnal mood variation, changes in sleep architecture, and shifts in cortisol peak timing as features of circadian rhythm disturbance in depression [14:pubmed.ncbi.nlm.nih.gov].

The Mutual Amplification of the Three Loops

Reading this far, you may be thinking “I recognize all of this.” Yes──these three loops don’t run independently. They amplify each other.

The three loops mesh like gears: when one turns, the other two start spinning. And once they start, simply removing the stressor (work) is not enough to stop them.

And Now, About Alcohol

There’s one topic we can’t avoid here.

Drinking during recovery. “Alcohol is a no-no,” the doctor says, and that’s that. ──Many people have had this experience.

But for someone caught inside these three loops, reaching for alcohol is structurally inevitable.

The Self-Medication Hypothesis proposed by psychiatrist Khantzian (1997) frames substance use not as “weakness of will” but as an adaptive coping behavior in response to unbearable internal suffering [19:wikipedia.org]. People suffering from anxiety and depression turn to alcohol because its CNS-depressant sedative effect temporarily alleviates their pain [19:wikipedia.org].

Mapped onto the three loops:

None of these are about “being too weak to resist.” In every case, alcohol is the only analgesic the body has found for the pain generated by the three loops.

The problem is that alcohol worsens all three loops.

Regarding sleep: while alcohol accelerates sleep onset, it causes REM sleep suppression and rebound in the second half of the night, increasing sleep fragmentation and middle-of-the-night awakening [20:pmc.ncbi.nlm.nih.gov]. Regarding BDNF: a systematic review has shown that chronic alcohol consumption affects blood BDNF levels [21:nature.com]. Regarding the HPA axis: chronic alcohol exposure has been reported to significantly impair HPA axis function [22:pmc.ncbi.nlm.nih.gov].

The result: you feel relief the moment you drink, but all three loops accelerate. The next morning is worse. So you drink again.

Medicine that ends at “don’t do that” is not seeing this structure.

It’s easy to prohibit. But if you prohibit it without providing an alternative means of pain relief, you’re just leaving a person inside their pain. As long as the three loops keep running, the pain doesn’t stop. As long as the pain doesn’t stop, the person will seek analgesics. If you take away alcohol, you must intervene in the loops themselves, or it’s meaningless.

20260628-2013-three_loops_integration_en.drawio.svg

Structural note: This three-loop integration model and the positioning of alcohol within it are composed from a combination of individual pieces of evidence; the integrated model itself has not yet been empirically validated. However, each individual connection──rumination and cortisol, social isolation and BDNF, sleep and the HPA axis, the self-medication hypothesis and alcohol use──has solid evidence behind it.

🏥 Three Misconceptions That Produce “Not Getting Better”

Having read this far, you may be thinking: “Okay, I get that it’s not my fault. But the people around me don’t think so.”

That’s not because the people around you are wrong as individuals. It’s because the model they believe in is wrong. Let’s look at three.

The Disease Model Misconception

“Depression is caused by a serotonin deficiency in the brain.” ──Most people have heard this explanation. And the “serotonin hypothesis” that underpins it was addressed in a comprehensive umbrella review published by Moncrieff et al. in Molecular Psychiatry in 2022, which concluded that there is no consistent evidence supporting it [15:nature.com].

However, methodological criticisms of this review have also been raised. In 2023, Jauhar et al. (36 experts) published a comment in Molecular Psychiatry pointing out methodological inconsistencies──noting that unlike conventional umbrella reviews, it conducted no new data analyses, selectively cited studies, and misinterpreted serotonin receptor pharmacology [24:doi.org]. Moncrieff et al. responded by acknowledging the serotonin system’s complex role in emotion and behavior, but arguing that the core issue is the absence of evidence for the specific claim that “depression is caused by low serotonin”──the explanation frequently communicated to patients [25:psychiatrist.com].

Of course, this doesn’t mean serotonin has nothing to do with depression at all. But the simplistic model of “serotonin is low → supplement it with medication → cured” makes it impossible to see the deeper mechanisms we’ve been examining: chronic HPA axis activation and the accumulation of allostatic load.

The Medical Model Misconception

“Treatment will cure it.” ──The idea that with the right medication at the right dose, depression should improve.

But in reality, a significant number of patients have treatment-resistant depression (TRD) that doesn’t respond to antidepressants. And at the center of TRD’s pathology lies HPA axis dysregulation, glucocorticoid receptor (GR) resistance, and persistent hypercortisolemia [16:springer.com].

In other words, as long as the allostatic overload loops keep running, medication may fail to normalize the HPA axis, and systemic recovery may not be achieved.

To anyone who has cycled through multiple medications without improvement, thinking “I just don’t respond to drugs”: it’s not you that doesn’t fit. It’s a structural problem with the pathology──that medication alone can’t stop the loops.

The Welfare Model Misconception

“Rest and you’ll recover.” “Once recovered, you’ll return to society.” ──Japan’s welfare system is designed on these assumptions.

Research on Japan’s Re-Work programs also shows that the shared objective of these programs is shortening the period of leave, with the primary outcome measure being days until return to work [17:ncbi.nlm.nih.gov].

But if you’ve read this far, you already know. By the definition of Type 2 overload, the escape response does not activate. Even if the individual takes leave, the social structure they’d return to hasn’t changed. Return to the same structure, and the same loops will start spinning again.

Cohen (2024) critiques this problem through the concept of “neorecovery”──the phenomenon by which neoliberalism distorts the recovery movement, centering it on the individual and minimizing the influence of social structure [18:springer.com]. The word “recovery” has been quietly redefined to mean “the individual makes an effort to re-adapt to society” [18:springer.com].

But Type 2 allostatic overload, by its very theoretical definition, states that it “can only be counteracted by changes in social structure.” For this population, the “recovery → return” model is structurally nonfunctional.

The feeling of being cornered every time someone asks “When can you go back to work?” That’s not weakness or self-indulgence. It’s a legitimate sense that the model is wrong.

⛈ Closing

This article does not offer a prescription for “how to get better.” It can’t, because the theory presented here demonstrates that this is not a problem solvable by individual prescription.

But if there is one thing that can be said: the reason you’re “resting but not recovering” is not because you are broken, but because your body is responding honestly.

The reason you broke lies on the side of the structure. But the structure won’t help you, and it won’t take responsibility. In the end, the only one who can tend to your body is you──and that is a cruel fact.

However, there is a world of difference between trying to repair yourself while believing “I broke because of me” and tending to your body while knowing “I broke because of the structure.” The actions may be the same, but their meaning is entirely different.

If this article can do anything in place of a prescription, it’s to change that meaning.

📚 References

#allostatic-load #depression #mental-health #social-structure #stress #recovery #welfare