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Melatonin

/ˌmɛləˈtoʊnɪn/

Definition

Melatonin is a hormone secreted by the pineal gland that signals darkness to every cell in the body, cueing the onset of sleep and anchoring the 24-hour circadian clock. It does not generate sleep — it opens the gate. Levels rise after dusk, peak around 2–3 a.m., and are suppressed within minutes by light.

How it works#

The engine of melatonin production is a feedback loop running from the eyes to the brain's master clock. Light detected by retinal intrinsically photosensitive retinal ganglion cells (ipRGCs) — especially at the ~480 nm blue-light wavelength — travels via the retinohypothalamic tract to the suprachiasmatic nucleus (SCN), which gates pineal activity. Remove the light signal and the SCN releases its inhibition; the pineal begins converting serotonin to melatonin within roughly two hours. The resulting rise in plasma melatonin — the dim light melatonin onset (DLMO) — is the gold-standard biomarker for an individual's circadian phase position.1

Once released, melatonin binds MT1 and MT2 receptors throughout the brain and body, promoting sleep propensity and lowering core body temperature in a complementary move that deepens slow-wave sleep. Because the SCN is exquisitely sensitive to short-wavelength light, the modern environment is chronobiologically hostile: ordinary indoor room lighting (~200 lux) is sufficient to delay the DLMO and compress the biological night — the window during which the body's repair and consolidation programs run. Chronic compression of this window degrades cognitive recovery even when total sleep time appears adequate.2

In action#

Scenario

A surgeon finishes a late case, debriefs with the team under fluorescent overheads, and spends 40 minutes reviewing notes on a tablet in bed. She's in bed by midnight and wakes at 6 a.m. — a respectable six hours. But her reaction time the next morning is sluggish, her fine-motor precision subtly off. She attributes it to the case load. The real mechanism: the light exposure before and during sleep has delayed her DLMO by over an hour, compressing her biological night and attenuating the slow-wave sleep window during which procedural memory consolidates.

Analysis Sleep duration is not the same as sleep timing. The surgeon's circadian clock was running 60–90 minutes late relative to her social schedule, truncating the restorative architecture at the front end — the part she can't buy back by sleeping longer.4

Why it matters#

Melatonin is the body's darkness signal and the circadian system's most direct performance lever. Every cognitive process that depends on overnight consolidation — procedural skill, declarative memory, emotional regulation — runs on a schedule gated by melatonin's nightly release. Modern screen environments, travel across time zones, and irregular shift patterns all attack the same upstream variable. Understanding melatonin means understanding why protecting the two hours before sleep matters more than almost any other recovery intervention a high-performer can make.5

The principle
Melatonin doesn't put you to sleep. It tells your body that darkness has arrived — and darkness is when repair begins.

Frequently asked

What does melatonin actually do in the body?

Melatonin signals the onset of biological night to every organ system. It lowers core body temperature, promotes sleep propensity, and sets the timing of hormone cascades — including growth hormone release — that govern overnight repair. It does not directly cause unconsciousness; it opens the circadian window in which sleep architecture deepens.

Does blue light really suppress melatonin?

Yes, and the sensitivity is striking. The retina's ipRGCs peak in sensitivity around 480 nm — the wavelength dominant in LED screens and fluorescent lighting. Cajochen et al. demonstrated that 460 nm monochromatic light suppresses melatonin significantly more than longer wavelengths, and Gooley et al. showed that ordinary room light delays the DLMO in 99% of individuals tested.

Should I take melatonin supplements to sleep better?

Melatonin supplements are most evidence-supported for phase-shifting — combating jet lag or adjusting shift-work schedules — rather than treating primary insomnia. Low doses (0.5–1 mg) timed to the target phase are more effective than the 5–10 mg doses common in retail. Protecting endogenous melatonin through light management is generally more powerful than supplementation.

What is DLMO and why do sleep clinicians measure it?

Dim light melatonin onset (DLMO) is the time at which salivary or plasma melatonin first rises above threshold under dim-light conditions, typically 2–3 hours before habitual sleep onset. Established by Lewy and Sack, it is the most reliable biomarker of an individual's circadian phase — far more precise than subjective sleep timing — and guides light and melatonin dosing in clinical chronotherapy.

Related terms

Go deeper
Sleep Architecture & Recovery
The complete optimisation system · 14 min · 78 sources

Sources

  1. Lewy, A.J., & Sack, R.L. 1989 Journal
    The dim light melatonin onset as a marker for circadian phase position.
    Chronobiology International, 6(1), 93-102.
    DOI 10.3109/07420528909059144
  2. Cajochen, C., Münch, M., Kobialka, S., Kräuchi, K., Steiner, R., Oelhafen, P., Orgül, S., & Wirz-Justice, A. 2005 Journal
    High sensitivity of human melatonin, alertness, thermoregulation, and heart rate to short wavelength light.
    Journal of Clinical Endocrinology & Metabolism, 90(3), 1311-1316.
    DOI 10.1210/jc.2004-0957
  3. Gooley, J.J., Chamberlain, K., Smith, K.A., Khalsa, S.B.S., Rajaratnam, S.M.W., Van Reen, E., Zeitzer, J.M., Czeisler, C.A., & Lockley, S.W. 2011 Journal
    Exposure to room light before bedtime suppresses melatonin onset and shortens melatonin duration in humans.
    Journal of Clinical Endocrinology & Metabolism, 96(3), E463-E472.
    DOI 10.1210/jc.2010-2098
  4. Lockley, S.W., Brainard, G.C., & Czeisler, C.A. 2003 Journal
    High sensitivity of the human circadian melatonin rhythm to resetting by short wavelength light.
    Journal of Clinical Endocrinology & Metabolism, 88(9), 4502-4505.
    DOI 10.1210/jc.2003-030570
  5. Walker, M. 2017 Book
    Why We Sleep.
    Scribner, New York.

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