Your body makes melatonin in the pineal gland, a pea-sized organ near the centre of your brain, and only when your eyes stop registering light. The darkness signal leaves the retina, reaches the suprachiasmatic nucleus, runs down the spinal cord and arrives back at the pineal gland, where four enzymes turn tryptophan into melatonin.
Melatonin is a hormone that the pineal gland releases into the blood at night to tell every other tissue in your body that the dark phase of the day has started. It does not sedate you. It time-stamps you.
Written by The Oak Age research desk. We formulate and sell third-party-tested longevity supplements in India. Our writing draws on primary literature indexed by PubMed and the National Library of Medicine, not on secondary blog summaries, and every statistic on this page carries a link to the study behind it.
Published: 21 September 2026. Last updated: 21 September 2026.
Key takeaways
- Dietary tryptophan becomes 5-hydroxytryptophan, then serotonin, then N-acetylserotonin, then melatonin. Four enzymes, one direction, no shortcuts.
- The switch is darkness, not tiredness. Norepinephrine released onto the pineal gland at night turns on the enzyme AA-NAT, which sets the production rate.
- Ordinary indoor lighting is enough to interfere. Room light below 200 lux delayed melatonin onset in 99 percent of people in a Harvard study, and cut the nightly melatonin window by roughly 90 minutes.
- Alcohol, evening caffeine, some blood pressure medicines and ordinary ageing all shrink the nocturnal melatonin peak through different routes.
- India runs a single clock across roughly 30 degrees of longitude, so the gap between your bedtime and your actual sunset is far wider in Ahmedabad than in Guwahati.
- A melatonin supplement adds a timing signal from outside. It does not repair the pineal gland's own output, which is why light behaviour matters more than the capsule.
What is melatonin, and what does it actually do in the body?
Melatonin is a small molecule, N-acetyl-5-methoxytryptamine, made mainly by cells called pinealocytes that account for about 95 percent of the pineal gland. According to Physiology of the Pineal Gland and Melatonin, the Endotext chapter hosted by the National Library of Medicine, the pineal gland weighs only 100 to 150 milligrams and sits outside the blood brain barrier, attached to the roof of the third ventricle.
Its job is narrow and specific. It reports the length of the night. When melatonin is high in your blood, your tissues read that as night. When it is low, they read that as day. Body temperature, blood pressure, hormone release and sleep pressure all take their cue from that signal.
This is worth separating from a common assumption. Melatonin is not a sedative in the way a sleeping pill is. A person with a healthy melatonin rhythm can still lie awake with a racing mind, and a person taking a melatonin capsule can still fail to fall asleep. The hormone tells the body what time it is. What you do with that information is a separate question.
Small amounts of melatonin are also made in the skin, gut, retina, bone marrow and placenta, where it acts locally. The Endotext chapter notes that after the pineal gland is removed, circulating melatonin becomes mostly undetectable, so these other sites contribute little to what shows up in a blood test.
How does your body produce melatonin, step by step?
Melatonin production starts with an amino acid you eat and ends with a hormone that sets your clock. Five stages, in order:
- Tryptophan enters the pinealocyte. Tryptophan is an essential amino acid, meaning your body cannot make it and has to get it from food. Dal, paneer, eggs, chicken, soya and pumpkin seeds all supply it. If you are considering it in supplement form, our guide on what to check on an L-tryptophan label in India covers the purity questions worth asking.
- Tryptophan becomes 5-hydroxytryptophan (5-HTP). The enzyme tryptophan hydroxylase adds a hydroxyl group.
- 5-HTP becomes serotonin. A decarboxylase enzyme strips off a carboxyl group. Serotonin sits at the centre of this pathway, which is why melatonin and mood chemistry share a common raw material.
- Serotonin becomes N-acetylserotonin (NAS). The enzyme arylalkylamine N-acetyltransferase, abbreviated AA-NAT, does this. This is the rate-limiting step, meaning the whole pathway runs only as fast as this one enzyme allows.
- NAS becomes melatonin. The enzyme acetylserotonin O-methyltransferase adds a methyl group, and the finished hormone is released straight into the bloodstream without being stored.
That last detail matters more than it sounds. The pineal gland has no melatonin reservoir. Every molecule in your blood at 2 am was made minutes earlier. Interrupt production and the level drops almost immediately, because there is no buffer to draw down.
What actually switches melatonin production on?
Light, or rather the absence of it. A subset of retinal ganglion cells contain a pigment called melanopsin and respond to light directly, independently of the rods and cones you see with. These cells project along the retinohypothalamic tract to the suprachiasmatic nucleus (SCN) in the hypothalamus, the body's master clock.
The Endotext chapter describes the relay in detail. When light hits those melanopsin cells, the SCN releases gamma-aminobutyric acid, which inhibits the neurons in the paraventricular nucleus and cuts the signal to the pineal gland. Melatonin production stops. In darkness, the SCN releases glutamate instead, the signal travels down to the upper thoracic spinal cord, out to the superior cervical ganglion, and up sympathetic fibres to the pineal gland, where norepinephrine is released.
Norepinephrine acting on beta-1 and alpha-1 adrenergic receptors is what turns on transcription of the AA-NAT gene. That is the molecular on switch. It is also why beta blockers, which sit on those same receptors, reduce melatonin output as a side effect.
How long does melatonin stay in the blood?
Not long. Melatonin's half-life in blood is around 40 minutes. The liver clears it using the enzyme CYP1A2, converting it to 6-hydroxymelatonin and then to 6-sulfatoxymelatonin, which leaves in urine. Researchers measure urinary 6-sulfatoxymelatonin as a proxy for overnight production, since it tracks the blood pattern with roughly a two hour lag.
What time does melatonin production start and peak?
Melatonin production begins in the evening once light levels fall, usually a couple of hours before habitual sleep onset. Researchers call this the dim light melatonin onset, or DLMO, and use it as the single cleanest marker of where your internal clock sits.
Levels then climb through the first half of the night. The Endotext chapter reports that peak plasma melatonin in adults occurs between 2 am and 4 am and averages roughly 60 to 70 picograms per millilitre when measured with high-specificity assays. Saliva concentrations run about three times lower than plasma, which is why saliva testing is convenient but uses different reference ranges. Daytime minimums sit below 1 picogram per millilitre.
Two details often get missed. First, secretion lasts about as long as the night does, which is why the pattern shifts across seasons. Second, the rhythm is internally generated. Put someone in constant darkness and melatonin keeps cycling, on a period that drifts slightly away from 24 hours. Light does not create the rhythm. Light anchors it against the solar day.
What disrupts melatonin production?
Most of what suppresses melatonin production is ordinary. Here is what the evidence shows, with the size of the effect where researchers measured one.
| Disruptor | What happens to melatonin | What the research found |
|---|---|---|
| Evening room light | Onset delayed, nightly window shortened | Room light before bed delayed onset in 99 percent of participants and shortened melatonin duration by about 90 minutes (Gooley et al., JCEM 2011) |
| Screens at night | Suppressed, clock pushed later | Light-emitting e-readers before bed reduced melatonin, delayed circadian timing and cut next-morning alertness against print books (Chang et al., PNAS 2015) |
| Alcohol in the evening | Nocturnal secretion reduced, dose dependent | Ethanol taken around 7 pm lowered melatonin by 41 percent at midnight versus control (Rojdmark et al., JCEM 1993) |
| Late caffeine | Rhythm pushed later | Caffeine equal to a double espresso three hours before bed delayed the melatonin rhythm by about 40 minutes, roughly half the shift produced by three hours of evening bright light (Burke et al., Science Translational Medicine 2015) |
| Beta blockers | Synthesis reduced | Beta-adrenoceptor antagonists block the receptor that switches on AA-NAT (Endotext, National Library of Medicine) |
| Regular NSAID use | Reduced | Aspirin and ibuprofen are both listed as lowering melatonin (Endotext, National Library of Medicine) |
| Ageing | Peak height falls, timing preserved | Nocturnal peak levels decline in older adults while the circadian pattern itself stays intact (Chronobiology International 2022 review) |
How much light does it take to suppress melatonin?
This is where two credible sources point in different directions, and the gap is worth naming rather than smoothing over.
The Endotext chapter states that completely shutting down nighttime melatonin in humans takes around 2,500 lux of full spectrum light, with domestic lighting sitting somewhere between 100 and 500 lux. Read alone, that sounds reassuring. Your bedroom lamp is nowhere near 2,500 lux.
The same chapter then notes that intensities below 200 lux still suppress secretion and shift the rhythm, and that wavelengths in the blue range of 460 to 480 nanometres do the most damage at the lowest intensity, with a suppression threshold above roughly 30 lux.
The Harvard work by Gooley and colleagues lands squarely on the second reading. In 116 healthy adults living under controlled conditions, ordinary room light in the hours before bed was enough to delay melatonin onset in nearly everyone tested.
The two claims are not in conflict once you notice they answer different questions. Total suppression needs bright light. Meaningful disruption does not. Your living room is almost never bright enough to abolish melatonin, and that is the wrong thing to be asking about. What matters is whether it is bright enough to push your onset later, and at typical Indian household lighting levels combined with a phone held close to the face, the answer is usually yes.
Does the colour of light matter more than the brightness?
Yes, within limits. Melanopsin responds most strongly to short wavelength light, the blue-cyan band around 460 to 480 nanometres. White LED lighting and phone screens are rich in exactly that band, which is why a modest amount of screen light at close range can outperform a much brighter warm bulb across the room.
One nuance the marketing around blue-light glasses tends to skip: your recent light history changes your sensitivity. The Endotext chapter notes that people living in dim conditions become more sensitive to light at night. Someone who spends the whole day indoors under office lighting is likely to react more strongly to evening light than someone who got an hour of direct sun in the morning.
Why does melatonin production fall with age?
The nocturnal melatonin peak gets smaller with age. The timing largely does not.
The systematic review published in Chronobiology International examined melatonin profiles in healthy older adults and found the circadian pattern preserved, with a nocturnal peak still occurring in the small hours, but a lower peak concentration in the oldest groups. An earlier review in the Journal of Psychosomatic Research reached a similar conclusion for people aged 65 and above.
Several mechanisms are proposed. The pineal gland calcifies progressively with age, visible on brain imaging. Its sympathetic input may weaken. And older eyes transmit less light to the retina, which means the daytime signal that anchors the rhythm arrives attenuated. Research cited in the ageing literature has attributed diminished melatonin in older people partly to insufficient environmental light rather than to the gland alone, which is a more hopeful framing than pure glandular decline.
There is also the matter of what happens before adulthood. Newborns do not make their own melatonin and develop a rhythm at roughly three to four months of age. Levels peak in childhood and fall through puberty, then stay broadly stable until around 40.
Why does India's single time zone change when your melatonin rises?
Here is a piece of the picture that international articles on melatonin never cover, because it is specific to countries with one clock and a wide footprint.
India uses a single time zone, Indian Standard Time at UTC plus 5:30, across a country spanning roughly 30 degrees of longitude. Economist Maulik Jagnani's research on sunset timing and schooling, covered by the Proceedings of the National Academy of Sciences, puts the annual average sunset difference between the eastern and western edges of the country at around two hours.
Melatonin onset follows darkness. Office hours, school bells and television schedules follow the clock. In the northeast, darkness arrives well before the evening is socially over, so people spend several hours under artificial light during a window when their melatonin would otherwise be climbing. In the far west, the sun is still up when the working day ends, and bedtime arrives soon after darkness does.
That is an inference from the physiology rather than a finding from a melatonin study, and it should be read as one. What Jagnani's data does show empirically is that later sunset is associated with later bedtimes and shorter sleep among Indian children, without a compensating later wake time, since wake times are set by school rather than by the sun.
The practical implication is the same either way. Evening light discipline is not a uniform prescription across India. A 10 pm routine sits at very different points on the melatonin curve depending on which end of the country you are in.
What lowers melatonin that people rarely suspect?
- Late, heavy dinners under bright kitchen lights. The issue is less the food than the hour of light exposure that goes with a 10 pm meal.
- Evening chai and coffee. The Burke study used a double espresso equivalent, roughly 200 milligrams of caffeine. A strong evening filter coffee is in the same territory.
- Beta blockers taken for blood pressure. These are common after 40 and act directly on the receptor that starts melatonin synthesis. This is not a reason to stop a prescription. It is a reason to ask your doctor about it.
- Routine painkiller use. Aspirin and ibuprofen both appear on the list of melatonin-lowering agents.
- Shift work and long-haul travel. Both decouple the light schedule from the social one, which is the core of the problem in a different form. Our breakdown of how to time melatonin for east-west travel out of India deals with the travel case specifically.
- Waking unrefreshed despite eight hours in bed. This is often a timing problem rather than a duration problem, which we unpack in the cortisol and REM sleep connection behind waking up tired.
How do you protect your own melatonin production?
Protecting melatonin production needs no equipment. It needs a decision that the last two hours of the day belong to the dark.
- Get bright light early. Morning daylight anchors the clock and reduces your sensitivity to light later in the evening. Fifteen to thirty minutes outdoors, without sunglasses, is the simplest version.
- Drop indoor light levels about two hours before bed. Switch off overhead lights and use lamps at eye level or lower. Warm bulbs over cool white.
- Move screens away from your face. Distance works as well as filters, because light intensity at the eye falls sharply with distance. A laptop at arm's length delivers far less to the retina than a phone at 25 centimetres.
- Shift caffeine earlier. If your bedtime is 11 pm, the Burke data suggests the evening cup sitting closest to 8 pm is the one doing the most to your rhythm.
- Treat alcohol as a clock disruptor, not a sleep aid. It shortens time to sleep onset and reduces melatonin at the same time.
- Keep the sleep window consistent. The rhythm is generated internally and entrained by regular light and dark. Erratic timing gives it nothing to lock onto.
Where do melatonin supplements fit, and who should skip them?
An honest answer about melatonin supplements requires separating two things that get conflated.
A melatonin supplement does not restore your pineal gland's production. It adds an external dose of the same molecule, which your tissues read as a night signal. That is genuinely useful when the problem is a misaligned clock, such as jet lag or a delayed sleep schedule. It does nothing to fix the light environment that suppressed your own output in the first place.
The case is reasonable when the clock itself has moved: crossing time zones, a sleep schedule that has drifted very late, or shift patterns that force sleep at biologically wrong hours. The case gets much weaker when someone takes it every night to paper over an evening routine spent under bright light with a phone in hand, because the underlying signal problem stays exactly where it was.
Caution applies to anyone on blood pressure medication, blood thinners, sedatives or antidepressants, anyone pregnant or breastfeeding, and anyone with an autoimmune condition. Those are conversations for a doctor, not for a product page.
If you do use one, the things worth checking on an Indian label are whether the brand publishes third-party test reports, whether the melatonin content is stated per serving rather than per blend, and what else is in the capsule. We wrote a longer version of those checks in our guide to choosing a melatonin supplement in India, including the FSSAI position on permitted amounts.
The Oak Age Sleep Support formula combines melatonin with L-theanine and L-tryptophan, the same amino acid that sits at the head of the biosynthesis pathway described above, and every batch has third-party lab reports you can read before you buy. L-theanine is in there for a different reason than melatonin, which we explain in our piece on L-theanine and daytime anxiety. We also think Sleep Support is the wrong purchase for someone whose real problem is a bright bedroom and a 1 am scroll, and we would rather say so than sell into that.
This page sits inside our larger reference on sleep and recovery for Indians, which covers sleep architecture, shift work and recovery beyond the melatonin question.
What the evidence does not settle yet
- Whether long-term nightly supplementation suppresses the body's own melatonin production is still debated, and the studies are shorter than the way people actually use these products.
- The claimed antioxidant and anti-ageing effects of melatonin come largely from cell and animal work. Human outcome data is thin.
- Blue-light-blocking glasses have plausible mechanics but inconsistent trial results, especially compared against simply dimming the room.
- Individual sensitivity to evening light varies by a wide margin between people, and there is no practical way to test where you fall.
The short answer
Your pineal gland builds melatonin out of tryptophan using four enzymes, and it starts only when darkness signals reaching your retina trigger norepinephrine release onto the gland. Light in the hours before bed is what interrupts that, at intensities far lower than most people assume. The supplement aisle addresses the symptom. The light switch addresses the cause.
Melatonin production: frequently asked questions
The pineal gland produces almost all the melatonin that circulates in your blood. It is a gland of roughly 100 to 150 milligrams sitting near the centre of the brain, attached to the roof of the third ventricle. Cells inside it called pinealocytes make up about 95 percent of the gland and do the actual synthesis. Small amounts of melatonin are also produced in the skin, gut, retina and bone marrow, but these act locally and contribute little to blood levels.
Melatonin is made from tryptophan, an essential amino acid you get from food such as dal, paneer, eggs, chicken, soya and pumpkin seeds. Inside the pineal cell, tryptophan becomes 5-hydroxytryptophan, then serotonin, then N-acetylserotonin, then melatonin. The enzyme AA-NAT controls the fourth step and sets the speed of the whole pathway.
Production usually begins a couple of hours before your habitual sleep time, once ambient light falls. Researchers call this the dim light melatonin onset. Levels then climb and peak between roughly 2 am and 4 am, averaging about 60 to 70 picograms per millilitre of plasma in adults, before falling back to under 1 picogram per millilitre during the day.
It reduces and delays it rather than stopping it outright. Complete suppression takes very bright light, around 2,500 lux. But light below 200 lux already shifts the rhythm, and blue-range wavelengths around 460 to 480 nanometres suppress melatonin at intensities above roughly 30 lux. A Harvard study found ordinary room light before bed delayed melatonin onset in 99 percent of participants and shortened the nightly melatonin window by about 90 minutes.
The height of the nighttime peak declines with age, while the timing of the rhythm is largely preserved. Proposed reasons include progressive calcification of the pineal gland, weakening sympathetic input to it, and older eyes transmitting less daytime light to the retina. Melatonin levels peak in childhood, drop through puberty, and stay broadly stable until around age 40.
Whether long-term nightly supplementation suppresses the body's own production is still debated, and most trials are shorter than the way people actually use these products. What is clearer is that a supplement adds an external timing signal rather than repairing the pineal gland's own output. If evening light is what shrank your production, the capsule does not address that.
Food supplies the raw material rather than the trigger. Tryptophan-containing foods provide the starting amino acid, but the pathway runs on the darkness signal, not on how much tryptophan you ate. Eating more protein at dinner does not push melatonin higher if you then sit under bright light until midnight.
Yes, and the effect is dose dependent. In a randomised crossover study published in the Journal of Clinical Endocrinology and Metabolism, ethanol taken in the early evening reduced nocturnal melatonin by 41 percent at midnight compared with control. Alcohol shortens the time it takes to fall asleep while simultaneously suppressing the hormone that organises the night, which is part of why sleep after drinking tends to be fragmented.
Citations
Arendt, Josephine, and Anna Aulinas. "Physiology of the Pineal Gland and Melatonin." Endotext, edited by Kenneth R. Feingold et al., MDText.com, 30 Oct. 2022, www.ncbi.nlm.nih.gov/books/NBK550972/.
Burke, Tina M., et al. "Effects of Caffeine on the Human Circadian Clock in Vivo and in Vitro." Science Translational Medicine, vol. 7, no. 305, 2015, pubmed.ncbi.nlm.nih.gov/26378246/.
Chang, Anne-Marie, et al. "Evening Use of Light-Emitting eReaders Negatively Affects Sleep, Circadian Timing, and Next-Morning Alertness." Proceedings of the National Academy of Sciences, vol. 112, no. 4, 2015, pp. 1232-37, www.pnas.org/doi/10.1073/pnas.1418490112.
Gooley, Joshua J., et al. "Exposure to Room Light before Bedtime Suppresses Melatonin Onset and Shortens Melatonin Duration in Humans." The Journal of Clinical Endocrinology and Metabolism, vol. 96, no. 3, 2011, pp. E463-72, pubmed.ncbi.nlm.nih.gov/21193540/.
"Melatonin: What It Is, What It Does and How It Works." Cleveland Clinic, 28 Apr. 2025, my.clevelandclinic.org/health/articles/23411-melatonin.
"Melatonin Profile in Healthy, Elderly Subjects: A Systematic Literature Review." Chronobiology International, vol. 39, no. 4, 2022, pubmed.ncbi.nlm.nih.gov/34983254/.
"Poor Sleep Leads to Worse Test Scores for Kids, More School Attrition in the Developing World." PNAS Journal Club, Proceedings of the National Academy of Sciences, www.pnas.org/post/journal-club/poor-sleep-leads-worse-test-scores-kids-more-school-attrition-developing-world.
Rojdmark, S., et al. "Ethanol Inhibits Melatonin Secretion in Healthy Volunteers in a Dose-Dependent Randomized Double Blind Cross-over Study." The Journal of Clinical Endocrinology and Metabolism, vol. 77, no. 3, 1993, pp. 780-83, pubmed.ncbi.nlm.nih.gov/8370699/.
Savage, Rachel A., et al. "Melatonin." StatPearls, StatPearls Publishing, 2024, www.ncbi.nlm.nih.gov/books/NBK534823/.
Scholtens, Rikie M., et al. "Physiological Melatonin Levels in Healthy Older People: A Systematic Review." Journal of Psychosomatic Research, vol. 86, 2016, pp. 20-27, pubmed.ncbi.nlm.nih.gov/27306853/.
Disclosure and disclaimer
Conflict of interest: The Oak Age sells supplements discussed in this article, including melatonin. The recommendations here are drawn from published research rather than from sponsorship, and we have named the situations where our own product is the wrong purchase.
The information on this page is for educational purposes only. It is not intended to diagnose, treat, cure, or prevent any disease. Consult a healthcare professional before making changes to your supplement routine. Statements on this page have not been evaluated by the Food Safety and Standards Authority of India (FSSAI).
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