Insomnia cortisol: What the evidence shows

The relationship between insomnia and cortisol runs in both directions. Elevated cortisol may disrupt sleep onset and architecture, and poor sleep may dysregulate cortisol rhythms further. Passos et al. (2023) found that insomnia severity scores correlated significantly with morning cortisol levels in a clinical sample — not a massive effect, but a consistent one. That bidirectionality is what makes this worth understanding properly.

What the evidence actually shows

The cortisol-insomnia link is not a new hypothesis. It has been studied in clinical populations for over two decades. But the quality of that evidence varies a lot, and I think it is worth being precise about what we actually know versus what gets repeated as fact.

Passos et al. (2023) published a study examining whether insomnia severity — measured using the Insomnia Severity Index — was associated with morning cortisol in adults. It was. Higher ISI scores correlated with elevated morning cortisol, and the association held after controlling for psychological health variables. The sample was relatively modest, which limits how far you can generalise, but the direction of the finding is consistent with the broader literature.

Vargas et al. (2018) took a different angle. Rather than looking at single morning cortisol readings, they examined ultradian cortisol rhythmicity — the pulsatile pattern of cortisol release across the 24-hour cycle — in people with chronic insomnia versus good sleepers. They found that the normal pulsatile pattern was altered in the insomnia group. This is a more mechanistically interesting finding than a simple "cortisol is high" headline, because it suggests the problem is not just elevated levels but disrupted timing.

Ahabrach et al. (2023) looked at hair cortisol concentration — a marker of cumulative cortisol exposure over weeks rather than a single-point snapshot — in breast cancer survivors with insomnia. Hair cortisol was significantly associated with insomnia symptoms and perceived stress. Hair cortisol is a methodologically useful measure precisely because it is not subject to the acute variability of serum or salivary sampling. The population here is specific, so I would not extrapolate too broadly, but the finding adds weight to the idea that chronic insomnia and sustained cortisol dysregulation tend to co-occur.

My honest read: the evidence is consistent enough that I take the cortisol-insomnia relationship seriously. But the effect sizes are moderate, the directionality is often unclear, and most studies are observational. This is not a simple "stress hormone causes insomnia" story.

The biology: what is actually happening in the body

Cortisol is produced by the adrenal cortex in response to signals from the hypothalamic-pituitary-adrenal (HPA) axis. Under normal conditions, cortisol follows a diurnal pattern: it peaks sharply in the 30–45 minutes after waking — the cortisol awakening response — then declines across the day, reaching its lowest point in the first half of the night to allow sleep onset and maintenance.

The problem with chronic insomnia is that the HPA axis appears to remain in a state of relative activation at times when it should be quiet. Agorastos et al. (2021) describe how stress-related disruption to the circadian system can dysregulate the normal cortisol rhythm, with downstream effects on sleep architecture, particularly slow-wave and REM sleep. Cortisol is arousing — it promotes wakefulness by activating the locus coeruleus and increasing noradrenergic tone. Elevated cortisol in the evening or early night is, broadly speaking, incompatible with the neurological conditions required for sleep onset.

There is also a feedback loop worth understanding. Poor sleep may itself drive HPA activation. If you sleep badly, the brain registers this as a physiological stressor, and cortisol output the following day may be elevated. That elevated cortisol then makes the next night harder. This is one reason chronic insomnia can feel so self-sustaining. If you want to go deeper on the sleep-deprivation side of this equation, I have written separately about lack of sleep cortisol and what the data shows there.

Blake et al. (2019) examined the mechanisms linking insomnia, anxiety, and depression in adolescents, identifying HPA dysregulation as a shared pathway. The finding that cortisol dysregulation sits at the intersection of sleep and mood disorders is not surprising, but it does reinforce why treating insomnia purely as a behavioural problem — without acknowledging the underlying physiology — is often insufficient.

Is a dysregulated cortisol response a risk factor for insomnia?

This is a question I find genuinely interesting, partly because it inverts the usual framing. Most people think of stress causing poor sleep. But could a blunted or dysregulated cortisol stress response actually predispose someone to developing insomnia?

Reffi et al. (2022) explored exactly this. They examined whether a blunted cortisol awakening response — a flattened morning cortisol peak — might represent a premorbid vulnerability for insomnia rather than simply a consequence of it. Their data suggested that a blunted response may precede insomnia onset in some individuals, which would imply that cortisol dysregulation is not just a downstream effect of poor sleep but potentially a contributing factor upstream. The human data here is still fairly thin and I would be overstating it to treat this as settled, but it is a plausible mechanistic hypothesis that deserves attention as the research matures.

What the cardiovascular data tells us about long-term insomnia

Khan et al. (2022) reviewed the cardiovascular consequences of insomnia and sleep loss. Chronically elevated cortisol is one of the proposed mechanisms linking poor sleep to cardiovascular risk — via effects on blood pressure, inflammatory signalling, and metabolic function. The review does not establish cortisol as the sole driver, and it is worth noting that the cardiovascular literature on insomnia involves multiple overlapping pathways. But it contextualises why the insomnia-cortisol relationship matters beyond just feeling tired. If you are curious about the broader picture of what elevated cortisol during sleep disruption looks like symptomatically, the article on high cortisol symptoms sleep covers that in more detail.

What the supplement evidence actually supports

I want to be careful here. There is no supplement that has been shown to directly normalise cortisol rhythms in people with insomnia. Anyone telling you otherwise is selling something harder than I am. What the evidence does support — in varying degrees — is a handful of ingredients that have been studied in the context of sleep quality, stress physiology, or both.

Magnesium

Abbasi et al. (2013) conducted a double-blind, placebo-controlled trial of magnesium supplementation in elderly adults with primary insomnia. The magnesium group showed statistically significant improvements in sleep time, sleep efficiency, and early morning awakening compared to placebo (p < 0.05 across most measures). They also observed that serum cortisol levels were significantly lower in the magnesium group post-intervention. Sample size was 46 — small, and specific to an elderly population — so I would not overextend this finding. But it is one of the more methodologically solid pieces of evidence in this space.

Khalid et al. (2024) examined magnesium and potassium supplementation in patients with diabetes mellitus and insomnia. Sleep hormone profiles, including melatonin and cortisol-adjacent markers, may show some response to combined mineral supplementation, though the study population is specific and the data should not be generalised to healthy adults without caution.

Ashwagandha

Wiciński et al. (2023) reviewed ashwagandha's potential effects on the endocrine system, including the HPA axis. Some studies suggest it may help modulate cortisol output, with one RCT reporting reductions in serum cortisol of approximately 27–30% versus placebo in stressed adults. The mechanistic picture — involving withanolides and their interaction with glucocorticoid receptors — is plausible. But I want to be honest: the trials are often small, industry-funded, and conducted in stressed rather than clinically insomniac populations. The human data is more promising than many adaptogens but still early-stage.

Glycine and Taurine

Both glycine (2000mg) and taurine (2000mg) are included in the KōJō Daily Formula. Glycine has been studied for its potential role in sleep quality — some small trials suggest it may help with subjective sleep satisfaction and morning alertness — but large-scale, well-controlled human trials are limited, and I would not make strong claims about its effects on cortisol specifically. Taurine has been studied in the context of neurological function and stress physiology in animal models, but the human data relevant to insomnia or cortisol is thin, and I would be overstating it to suggest otherwise. Research on both is ongoing.

Vitamin C

Vitamin C contributes to the reduction of tiredness and fatigue, and Vitamin C contributes to the protection of cells from oxidative stress — both registered claims with a reasonable evidence base. Whether it directly affects cortisol or sleep is a different question. Some research suggests that ascorbic acid may help attenuate the cortisol response to acute physiological stress, but the human evidence in an insomnia context specifically is limited. I include 500mg in the formula primarily for its established roles in immune function and energy metabolism, not as a sleep ingredient per se.

Behavioural interventions: the evidence base is stronger than any supplement

I feel obliged to say this clearly: cognitive behavioural therapy for insomnia (CBT-I) has the strongest evidence base of anything in this space. Brückner et al. (2025) published results from a digital CBT-I trial in nurses with shift work sleep disorder, finding meaningful reductions in insomnia severity. CBT-I addresses the hyperarousal and cognitive patterns that sustain insomnia — which are closely tied to HPA activation — in a way that no supplement currently can. If your insomnia is chronic and significantly affecting your life, the evidence points to CBT-I as a first-line approach, not a pill or powder. Supplements may play a supporting role, but they are not the foundation.

For context on how a daily supplement powder fits into a broader health routine, I have written about that separately — including the evidence hierarchy and where supplementation genuinely adds value versus where it does not.

Frequently asked questions

My honest take

I started paying attention to the cortisol-insomnia literature partly because I noticed my own sleep was worst during high-pressure periods — not just in terms of time available, but in terms of how long it took to actually fall asleep and how often I woke between two and four in the morning. That pattern, I later learned, is fairly consistent with elevated evening cortisol interfering with normal sleep architecture. Whether that is what was actually happening in my case, I genuinely do not know.

What I do know is that the evidence supports a real, bidirectional relationship between insomnia and cortisol dysregulation. It is not a dramatic story — the effect sizes are moderate, the mechanisms are complex, and there is no single intervention that reliably fixes it. Magnesium has the most credible RCT data in this space, specifically in elderly populations. Ashwagandha has some promising but still limited human data. CBT-I has the strongest overall evidence base for chronic insomnia, and I think it is worth being honest that no supplement comes close to matching it.

The ingredients I have included in the formula — glycine, taurine, Vitamin C — are there because I think the broader evidence justifies them for daily health support, not because I am claiming they will fix cortisol-driven insomnia. I am wary of the supplement industry's tendency to attach sleep claims to anything vaguely calming. The honest answer is that the human data on most of these ingredients, in the context of insomnia and cortisol specifically, is still developing. I would rather say that plainly than dress it up.

If your insomnia is persistent and affecting your quality of life, talk to a GP or a sleep specialist. That is not a disclaimer I am adding reluctantly — it is what the evidence actually supports.

This article is for informational purposes only and does not constitute medical advice. Consult your healthcare provider before starting any supplement regimen.