High cortisol insomnia: what the evidence shows

Cortisol and sleep have an inverse relationship by design — cortisol peaks roughly 30 minutes after waking and is supposed to be near its lowest point when you go to bed. When that rhythm breaks down, falling and staying asleep becomes genuinely difficult. One study found that men with poor sleep quality had measurably higher evening cortisol concentrations than good sleepers, suggesting the association is real — though the direction of causation is harder to untangle than most articles admit. Hirokawa et al. (2022)

What the evidence actually shows

The relationship between cortisol and insomnia is well-documented but frequently oversimplified. Most popular coverage frames it as: stress raises cortisol, cortisol causes insomnia, fix your cortisol and you fix your sleep. The reality is messier.

Reffi et al. (2022) published a genuinely interesting paper asking whether a blunted cortisol stress response — not an elevated one — might be a premorbid risk factor for insomnia. Their argument is that people who don't mount an adequate cortisol response to acute stress may fail to properly consolidate threat-memory extinction, keeping the nervous system in a low-grade state of vigilance at night. It's a counterintuitive hypothesis and the evidence is still preliminary, but it complicates the simple "high cortisol = insomnia" narrative.

On the more established side, Kater et al. (2022) looked at stress reactivity in adolescents and found associations between salivary cortisol stress responses and sleep disturbance, though effect sizes were modest and the causal pathway wasn't established. What I take from this: cortisol dysregulation — whether elevated or blunted — appears to be linked to poor sleep. The direction matters, and it likely varies between individuals.

The HPA axis work from Elder et al. (2023), reviewing stress and hypothalamic-pituitary-adrenal function, reinforces that chronic stress exposure may alter the diurnal cortisol pattern in ways that are slow to reverse. That's the mechanism most relevant to people who feel wired at 11pm despite being exhausted.

The biology: why elevated evening cortisol disrupts sleep

Cortisol is produced by the adrenal cortex in response to signals from the hypothalamus and pituitary — the HPA axis. Under normal conditions, cortisol follows a diurnal rhythm: high in the morning, declining across the day, reaching its nadir in the first few hours of sleep. This rhythm is partly entrained by light exposure and partly by the circadian clock in the suprachiasmatic nucleus.

When cortisol is elevated in the evening — whether from chronic psychological stress, disrupted sleep itself, or HPA dysregulation — it directly antagonises the physiological conditions required for sleep onset. Cortisol promotes arousal, raises core body temperature, and may suppress melatonin production. It also appears to interact with interleukin-6, a cytokine with its own circadian secretion pattern. Vgontzas et al. (2005) noted that IL-6 and cortisol dysregulation co-occur in chronic insomnia, though disentangling cause from effect in that relationship is difficult.

There's also a feedback problem. Poor sleep itself may raise cortisol the following day — a point I've written about separately when looking at lack of sleep cortisol research. Once you're in that loop, the question of which came first becomes somewhat academic. You need to interrupt the cycle from multiple angles.

Menopause is a relevant context here. Eichling et al. (2007) documented how the hormonal shifts of menopause — declining oestrogen and progesterone — interact with HPA axis function in ways that may disrupt sleep architecture. Elevated nocturnal cortisol is one proposed mechanism for the sleep difficulties that are disproportionately reported by women in perimenopause and beyond.

The cortisol-sleep feedback loop

One thing that rarely gets discussed honestly: the relationship between high cortisol levels and sleep is bidirectional, and the feedback loop can be self-sustaining. Sleep deprivation activates the HPA axis. HPA activation disrupts sleep. Both directions have reasonable mechanistic support.

Hirokawa et al. (2022) found in their cohort of Japanese male workers that higher cortisol concentrations were associated with worse sleep quality scores, but the cross-sectional design means it's not possible to say which came first. This is an honest limitation most supplement marketing conveniently ignores.

What this means practically: if your sleep has been poor for months, your cortisol rhythm may have shifted as a consequence of that poor sleep — not only as a cause. Addressing only the cortisol side of the equation may be insufficient. Sleep hygiene, light exposure, and consistent wake times all play a role in re-entraining the diurnal cortisol curve, independent of any supplement.

Lifestyle factors with the strongest evidence

Before I get to ingredients, I want to be direct about where the strongest evidence sits. No supplement has the effect size of the following:

• Consistent wake time: Anchoring your wake time — even after a poor night — is one of the most reliable ways to stabilise circadian rhythms and, by extension, the diurnal cortisol pattern.
• Morning light exposure: Bright light in the first hour after waking helps entrain the cortisol awakening response to an appropriate time, which may make it less likely to peak at night.
• Evening temperature: Core body temperature needs to drop for sleep onset. Hot rooms, hot baths immediately before bed, and high-intensity evening exercise all work against this.
• Alcohol: Widely misunderstood as a sleep aid. It may reduce sleep onset latency but disrupts sleep architecture in the second half of the night and appears to alter cortisol secretion patterns. The human data on this is fairly consistent.

I'm not listing these to be preachy. I'm listing them because if you're spending money on supplements while ignoring these, you're likely wasting your money.

Ingredients studied in the context of cortisol and sleep

Glycine

Glycine is an amino acid that some research suggests may help with sleep quality, possibly by lowering core body temperature through peripheral vasodilation. The human data is thin and I'd be overstating it to claim otherwise — the most-cited trial had a small sample. The KōJō Daily Formula includes 2000mg of crystalline glycine, which aligns with the doses used in preliminary research, though large-scale RCTs are still limited and I'm not going to tell you this is settled science.

Taurine

Taurine is an amino acid with some preliminary research suggesting it may interact with GABA receptors, which are involved in the neurological transition to sleep. The animal data is more extensive than the human data. Research is ongoing and I wouldn't lean heavily on taurine as a primary sleep intervention based on current evidence. The formula includes 2000mg.

Aged Garlic Extract

Aged Garlic Extract has been studied for its potential effects on the stress response and cardiovascular markers. The direct evidence linking it to cortisol or sleep in humans is limited, and large-scale trials are lacking. I include it for other reasons; I wouldn't position it as a sleep ingredient.

Olive Leaf Extract and Grape Seed Extract

Both have been studied for their polyphenol content and potential effects on oxidative stress. Vitamin C contributes to the protection of cells from oxidative stress — that's a registered claim — but for olive leaf and grape seed specifically, the human evidence on sleep or cortisol is preliminary and I'd be doing you a disservice to overstate it.

Vitamin C

Vitamin C contributes to the reduction of tiredness and fatigue — that's a registered UK/EU health claim and I'm comfortable stating it. There's also some evidence that the adrenal glands have among the highest concentrations of vitamin C of any tissue, and that cortisol synthesis may place demands on vitamin C status, though the clinical relevance of this in people who aren't deficient is uncertain.

What the HPA axis research tells us about chronic stress

Elder et al. (2023) used the COVID-19 pandemic as a lens for understanding HPA dysregulation under sustained stress — a useful natural experiment. Their review found that prolonged psychosocial stress may alter both the amplitude and timing of the diurnal cortisol curve, and that these changes are slow to reverse even when the stressor is removed. This has practical implications: if you've been under sustained stress for months or years, a single week of better sleep hygiene probably won't reset your cortisol rhythm. The timeline is longer than most people expect.

Kiani et al. (2021) reviewed neurobiological mechanisms relevant to stress and mood, noting the interplay between HPA axis function and neurotransmitter systems. The evidence points to a system with multiple feedback loops — which is why interventions that target only one node (say, a single adaptogen) often produce modest effects in isolation.

A note on altitude and sleep disruption

This is a bit niche, but worth mentioning for completeness. Li et al. (2025) studied sleep architecture under hypobaric hypoxia — low-oxygen conditions at altitude — and found significant disruptions to sleep stages. The relevance here is that hypoxia activates the HPA axis, and elevated cortisol is part of the altitude stress response. If you've ever slept badly in the mountains, this is part of the reason. It's also a useful reminder that cortisol-driven insomnia isn't always psychological in origin.

Frequently asked questions

My honest take

I started looking into high cortisol insomnia because I was experiencing it. Wired at midnight, exhausted at 7am, that specific feeling of a brain that won't stop running even when the body is clearly done. I wanted a clean answer. I didn't find one.

What I found instead is a literature full of associations, modest effect sizes, and genuinely unresolved questions about causation. Reffi et al. (2022) arguing that a blunted cortisol response might be a risk factor for insomnia was particularly humbling — it reminded me that the "high cortisol = bad" framing I'd absorbed from popular science writing was incomplete.

The ingredients in the KōJō formula were chosen because they have at least some credible evidence behind them and a reasonable safety profile — not because I think any single one of them is going to fix a broken sleep pattern. Glycine and taurine have interesting mechanistic hypotheses. Vitamin C contributes to the reduction of tiredness and fatigue — that's a registered claim I'm comfortable making. But if your sleep is genuinely disrupted, a supplement is at best a supporting player.

What actually made the biggest difference for me: a consistent wake time regardless of how badly I'd slept the night before, no screens in the bedroom, and being more honest about how much work stress I was carrying into the evening. Boring advice. Genuinely effective.

The cortisol-sleep relationship is real. The evidence that you can meaningfully alter it with supplements alone is thin. I'd rather tell you that directly than sell you a story.

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

References (9 studies)

1. Hirokawa et al. (2022) — Associations of testosterone and cortisol concentrations with sleep quality in Japanese male workers. PMID 36148025.
2. Reffi et al. (2022) — Is a blunted cortisol response to stress a premorbid risk for insomnia? PMID 35905512.
3. Kater et al. (2022) — Stress reactivity in salivary cortisol and electrocardiogram in adolescents: Investigating sleep disturbances and insomnia. PMID 35843709.
4. Elder et al. (2023) — Stress and the hypothalamic-pituitary-adrenal axis: How can the COVID-19 pandemic inform our understanding and treatment. PMID 36748346.
5. Vgontzas et al. (2005) — IL-6 and its circadian secretion in humans. PMID 15905620.
6. Eichling et al. (2007) — Menopause related sleep disorders. PMID 17566192.
7. Kiani et al. (2021) — Neurobiological basis of chiropractic manipulative treatment of the spine in the care of major depression. PMID 33170171.
8. Li et al. (2025) — The Effects and Mechanisms of Continuous 7-Day Hypobaric Hypoxia Exposure on Sleep Architecture in Rats. PMID 40507808.
9. Moon et al. (2022) — Effects of antipsychotics on circadian rhythms in humans: a systematic review and meta-analysis. PMID 33152385.

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