Hyperarousal: why chronic insomnia is not a sleep problem but an arousal problem

“It makes no sense. All day I’m so tired I could fall asleep in a meeting — and in the evening, when I finally lie down, I’m completely awake.” I hear this sentence in the therapy room again and again, and every time the same question echoes in it: what’s wrong with me that my body can’t do the most natural thing in the world?

Science’s answer is unexpected, and for many people freeing: in chronic insomnia the mechanism of sleep is usually not broken. What’s broken is the switch for wakefulness — it stays on. We call this state hyperarousal, and it is today the best supported model for understanding chronic insomnia. I’ve already sketched the basic mechanism — how the sympathetic nervous system drowns out sleep — in my piece on insomnia and the nervous system; this time we go deeper. We’ll look at what researchers have actually measured in people with insomnia — in the blood, the heart, the metabolism and the brain — why insomnia is really a 24-hour disorder rather than a night-time one, and why sleeping pills therefore so often disappoint.

What they measured in the body: a body on permanent standby

When Dieter Riemann and colleagues reviewed decades of hyperarousal research in 2010, a surprisingly consistent picture emerged: people with chronic insomnia differ measurably from good sleepers across a range of physical markers — and not only at night.

• The stress hormone axis. Alexandros Vgontzas and colleagues showed in 2001 that people with insomnia have elevated secretion of cortisol and ACTH — the hormones of the stress axis — across the full 24 hours, with the most pronounced difference in the evening and the first half of the night, that is, precisely when the body should be settling. An important detail: the more objectively disturbed the sleep, the higher the cortisol. The stress system and insomnia are measurably intertwined.
• The heart and autonomic balance. Research consistently measures a somewhat higher heart rate and, above all, lower heart rate variability (HRV) — during sleep as well. Low HRV means the sympathetic branch, the accelerator, is dominant and the parasympathetic branch, the brake, isn’t getting the wheel. Even at two in the morning, the heart of someone with insomnia beats like the heart of someone who is slightly on guard.
• Metabolism. Back in the 1990s, Michael Bonnet and Donna Arand measured elevated whole-body oxygen consumption — a faster metabolism — in people with insomnia, both by day and by night. The body literally burns more fuel than it should at rest; it idles at raised revs.
• Body temperature. In insomnia this too is often slightly elevated at the time when it should be falling — and a drop in core body temperature is one of the physiological signals for falling asleep.

All these measurements point in the same direction: this isn’t a person who “doesn’t know how to sleep”. This is a body stuck in a state of readiness — and in a state of readiness no mammalian body sleeps deeply. From an evolutionary point of view this even makes sense: an organism that senses threat makes sleep shallow and fragmented, because it has to stay capable of a rapid response.

What they measured in the brain: an “awake” brain during sleep

What shows up in the brain is even more telling. Michael Perlis and colleagues found elevated fast, so-called beta activity in the EEG recordings of people with insomnia — brain waves characteristic of focused, analytical wakefulness — during sleep itself, especially around sleep onset and in non-REM sleep. Part of the brain, in other words, goes on “thinking” during sleep.

In 2004 Eric Nofzinger and colleagues showed this in images for the first time: using positron emission tomography they compared brain metabolism during wakefulness and non-REM sleep. In good sleepers, activity in the arousal structures — the brainstem, the hypothalamus, the thalamus — and in the emotional and self-referential networks drops markedly on the transition into sleep. In people with insomnia this switching-off didn’t happen to the same degree: it was precisely the systems for wakefulness, emotion and thinking about oneself that stayed more active during sleep. To put it vividly: the body was lying in bed while part of the brain stayed at the office.

This finding explains two experiences people with insomnia often describe, and which make them doubt themselves. First, the feeling of “I didn’t shut an eye all night” even though the measuring devices show several hours of sleep — if the arousal networks keep smouldering, sleep simply isn’t experienced as sleep; science calls this sleep state misperception, and it isn’t an invention but the consequence of a half-awake brain. And second, the feeling that sleep doesn’t quench: even when the hours aren’t few, the restoration is shallow, because the system never really switches off.

Insomnia is a 24-hour disorder — and that’s actually good news

Taken together, these findings lead to a conclusion that turns the view on its head: chronic insomnia isn’t a disorder that happens at night. It’s a 24-hour state of heightened arousal that simply shows up most at night — because night is the only part of the day when excessive revs collide directly with the need to switch off.

So hyperarousal shows itself differently by day, but it does show itself: as an inability to really rest (sitting with nothing to do is uncomfortable), as constant mild tension in the shoulders and jaw, as shallow breathing, as being startled by small stimuli, as a head that compiles lists even on holiday. The “tired but wired” paradox isn’t a quirk of character — it’s an accurate description of physiology: sleep pressure is high, but the arousal system drowns it out.

Why is that good news? Because it moves the target. If insomnia is a night-time problem, then every measure is confined to those few hours of darkness — and night is exactly when you have the least influence. But if insomnia is a 24-hour disorder, then it is also — and above all — treated by day. Every hour of the day becomes an opportunity to bring the system’s revs down.

Where it comes from: a system that learned to keep watch

The logical question in all this is: why does it happen to me? Research shows that we differ from one another from the outset — psychology calls this sleep reactivity to stress. Christopher Drake and colleagues even developed a measure for it (the FIRST scale) and showed that people with high reactivity — those whose sleep is quickly disrupted by stress — go on to develop chronic insomnia significantly more often. Part of this sensitivity is probably inborn, part of it learned: a nervous system that grew up, or lived for a long time, in an environment where you had to stay on guard remembers high readiness as its default setting.

On top of that comes conditioning: if enough evenings pass in tension, struggle and counting the hours, the bed and the darkness themselves become triggers of arousal — the body eventually learns the alarm so well that it fires automatically, before a single worry has appeared. That’s how the cruel reversal so many people describe comes about: you doze on the sofa, and in bed you’re as awake as an owl. Not because there’s anything special about the bed — but because your system has stored the wrong association with it. The good news: what is learned can be rewritten, and this is exactly what the behavioural part of therapy builds on.

Why sleeping pills don’t solve arousal

This also shows why sleeping pills so often disappoint in chronic insomnia. Classic sedatives and hypnotics mostly work by strengthening the inhibitory transmitter GABA — chemically damping the brain, in other words. That can shorten sleep onset and get you through the night after a fashion, but it changes nothing in the mechanism driving the insomnia: the stress axis stays overheated, the autonomic balance stays tilted towards the sympathetic, the daytime sources of tension stay untouched. The extinguisher, then, is putting out the smoke rather than the fire.

This is why clinical guidelines — the European ones (Riemann et al., 2017) and the American ones — recommend sleeping pills at most short-term, in an acute crisis, and cognitive behavioural treatment as the first choice for chronic insomnia. Not out of moralism, but out of mechanism: a medication that doesn’t address the arousal can even entrench the insomnia — you start to believe you can’t sleep without the pill, and every attempt to stop sets off a fresh wave of fear and with it of arousal. If you’re taking sleeping pills, of course don’t stop them on your own — that’s a conversation for your doctor. But do know that there is a path that aims at the cause.

How hyperarousal comes down: three levers

If the core of the problem is a system running at too high a rev count, then the logical question is: what reliably brings the revs down? Research and clinical practice point to three levers, which work best together.

The first lever: end the night-time fight. A large part of the arousal in chronic insomnia is produced by your relationship with sleep itself — the effort, the fear, the counting of hours, lying awake in a bed that becomes a proving ground for tension. This is exactly what cognitive behavioural therapy for insomnia takes apart: it condenses sleep, reconnects the bed with sleeping and dismantles catastrophic thoughts; I’ve described it in detail in my piece on CBT-I. It’s important to understand: CBT-I doesn’t “teach you to sleep” — it removes the arousal that blocks sleep, and sleep returns on its own.

The second lever: through the body. Because hyperarousal is a bodily state, you can’t simply think your way out of it. But you can influence it from the bottom up — through the breath (a lengthened out-breath directly activates the parasympathetic system), progressive muscle relaxation, a warm bath a few hours before bed (the subsequent drop in body temperature supports falling asleep), regular movement during the day. For people who no longer notice tension in the body at all — and there are many of them in chronic insomnia — therapeutic work that puts the body at the centre is also valuable; how that works I’ve described in my piece on body psychotherapy.

The third lever: the day, not the night. If the body has accumulated twelve hours of uninterrupted activation by evening, one cup of camomile tea at ten won’t switch it over. Lowering the revs is a daytime practice: micro-pauses between commitments (two minutes of breathing between meetings), screen-free breaks, a lunch that isn’t eaten standing up, boundaries at work, movement, daylight. And, at a deeper level: a conversation about what is keeping your system on standby in the first place — an overheated working day, a relationship under strain, an old story you were never allowed to give room to. In chronic insomnia it almost always turns out that the night is only the last link in a chain that is woven during the day.

So am I “too sensitive”? No — your system can learn

Many people then ask: if my body is set this way, is it a permanent fixture? It’s true that some of us inherit a more excitable nervous system, and that prolonged stress — especially early stress — teaches the system higher readiness. But the key word is teaches: what the system has learned it can also unlearn. That’s exactly what research on the effectiveness of CBT-I and related approaches shows — after treatment it isn’t only hours of sleep that improve, but arousal markers that come down too, and the effects persist for years after therapy ends, which no sleeping pill achieves.

In my work I see something else as well: people with chronic insomnia are often people who learned long ago to be attentive, responsible, on the lookout for other people’s needs. Their system isn’t broken — it’s overtrained in vigilance and undernourished in letting go. So working with hyperarousal is almost never just technique; it’s also learning that it’s safe to release. I know this at close range — my own insomnia didn’t retreat either, as long as I was only trying to fix the nights.

Where to start tonight — and where it really starts

If you take one single thing away from this piece, let it be this: your wakefulness isn’t a fault in you but a measurable bodily state — and states change. Tonight you can start with something small: when you’re lying awake, instead of fighting the thought “I have to fall asleep”, try lengthening your out-breath and telling yourself “my system is at high revs — I can’t force the revs down, but I can stop pouring in fuel”. The real beginning, though, is by day: with pauses, with movement, with boundaries and — if the nights have already gone on for months — with professional support. For what a structured path out of chronic insomnia looks like, read my piece on CBT-I; and if you suspect that something deeper is keeping your system on standby, you’re welcome to get in touch and we can look at it together.