When Melatonin Works for Insomnia (And When It Doesn’t): The Dosing Truth That Changes Everything

Story-at-a-Glance

• Melatonin’s effectiveness for insomnia depends entirely on the type – it works well for circadian rhythm disorders like delayed sleep phase syndrome and jet lag, but shows limited benefit for garden-variety adult insomnia

• The most commonly available melatonin doses (3-10mg) may actually be too high to work properly – MIT research reveals that 0.3mg is often more effective, as higher doses cause receptors to become unresponsive after just a few days

• Melatonin is a circadian regulator, not a sleeping pill – it signals to your body when it’s time for sleep rather than directly inducing drowsiness, which explains why timing matters more than dose for many people

• Long-term safety data remains surprisingly limited – while melatonin shows no signs of physical addiction, most studies last only weeks to months, leaving questions about extended use unanswered

• The global sleep crisis has driven melatonin use to record highs – yet many users don’t realize that addressing underlying sleep hygiene and stress may be more effective than supplementation alone

• Age and insomnia type dramatically affect outcomes – children and adolescents show better results than adults, and people with comorbid conditions may respond differently than those with primary insomnia

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The bottle sits on countless nightstands across America: melatonin, the hormone supplement that promises natural, restorative sleep. A 2024 global survey revealed a staggering reality – nearly 40% of people get no more than three nights of good sleep each week. Personal anxiety and insomnia topped the list of sleep disruptors. With melatonin use increasing dramatically over the past decade, it’s become the go-to solution for millions seeking relief.

But here’s what keeps me up at night (pun intended): most people using melatonin for insomnia treatment don’t realize they may be taking the wrong dose at the wrong time. They’re also using it for the wrong type of sleep problem. The disconnect between how melatonin actually works and how it’s commonly used represents one of the most widespread misunderstandings in self-directed health management.

The Circadian Truth: Melatonin Isn’t What You Think It Is

Let me start with a confession that might surprise you: melatonin isn’t actually a sleeping pill. I know, I know – every supplement aisle markets it that way. But melatonin functions primarily as a circadian rhythm regulator, not a direct sedative.

As Johns Hopkins sleep expert Luis F. Buenaver, Ph.D. explains it: “Your body produces melatonin naturally. It doesn’t make you sleep, but as melatonin levels rise in the evening it puts you into a state of quiet wakefulness that helps promote sleep.” This distinction matters enormously when we’re trying to understand when melatonin works for insomnia and when it doesn’t.

Your pineal gland begins secreting melatonin around 9 PM each evening. Levels rise tenfold and peak between 2-4 AM. This natural rhythm serves as a biological “time giver” – what researchers call a zeitgeber. It synchronizes your sleep-wake cycle with the 24-hour day. When you take supplemental melatonin, you’re essentially trying to either boost this natural signal or shift its timing.

This is precisely why melatonin shines for certain conditions but disappoints for others. Research published in PLOS Medicine showed remarkable success with melatonin for delayed sleep-wake phase disorder (DSWPD). This is a condition where people’s natural sleep timing is shifted later. When participants with confirmed circadian misalignment took just 0.5mg of melatonin one hour before their desired bedtime, they experienced earlier sleep onset and improved sleep quality. They also reported reduced daytime impairment.

The Great Melatonin Dosing Paradox

Here’s where things get interesting – and frustrating. Walk into any pharmacy, and you’ll find melatonin supplements ranging from 3mg to 10mg or even higher. Yet groundbreaking research from MIT tells us this could be exactly the wrong approach.

Professor Richard Wurtman, the pioneering MIT researcher who literally patented melatonin’s use for sleep, discovered something that should have revolutionized how we use this supplement. Doses as low as 0.3 milligrams are often more effective than the typical 3-10mg supplements. In his research, a 0.3mg dose not only helped elderly insomniacs fall asleep. It actually restored their plasma melatonin levels to the normal range. The 3mg dose? It stopped working after just a few days.

Why does this happen? When melatonin receptors in the brain are exposed to supraphysiological doses, they become downregulated. Essentially, they become unresponsive to the hormone. As Wurtman explained, “many people don’t think melatonin works at all” precisely because they’re taking doses that are far too high. The irony is almost painful. The supplement industry, unable to patent these tiny effective doses, manufactures pills with 10 to 30 times more melatonin than research suggests we need.

A comprehensive 2024 meta-analysis in the Journal of Pineal Research confirmed the complexity of melatonin dosing. The research team, led by Francy Cruz-Sanabria at the University of Pisa, found that timing mattered more than dose for many patients. The sweet spot for sleep-promoting effects occurred with doses administered 2-3 hours before the intended sleep episode – not the 30 minutes commonly recommended on supplement labels.

Additionally, research has shown concerning quality control issues. Studies have found that melatonin supplements can contain anywhere from 83% less to 478% more melatonin than what’s listed on the label. Some samples even contained no melatonin at all, while others included serotonin – an entirely different neurotransmitter. This variability makes it nearly impossible to know what dose you’re actually taking.

When Melatonin Actually Works: The Clinical Evidence

Let’s cut through the marketing and look at what the science actually tells us about melatonin for insomnia treatment. The evidence isn’t nearly as universally positive as supplement advertising would suggest.

A particularly revealing 2022 systematic review published in Sleep Medicine Reviews analyzed multiple randomized controlled trials and reached a sobering conclusion: in adults with non-comorbid chronic insomnia, melatonin was not significantly effective in improving sleep onset latency, total sleep time, or sleep efficiency. Read that again – for the most common type of adult insomnia (the kind where you’re otherwise healthy but just can’t sleep), melatonin didn’t move the needle in a statistically meaningful way.

However, the picture changes dramatically for specific populations and conditions. Here’s where melatonin truly shines:

Circadian Rhythm Disorders: Melatonin demonstrates robust efficacy for conditions involving misaligned biological clocks. This includes delayed sleep-wake phase disorder (common in teenagers and young adults who are natural “night owls”). It also helps with non-24-hour sleep-wake disorder (particularly in blind individuals) and shift work sleep disorder. A review of melatonin for delayed sleep phase syndrome found it helped people fall asleep earlier and wake up earlier when taken strategically.

Jet Lag: Research strongly supports melatonin’s effectiveness for jet lag, particularly after eastward flights across multiple time zones. The key is timing: taking melatonin at the bedtime of your destination, beginning before travel and continuing for a few days after arrival.

Children and Adolescents: One of the most striking findings in melatonin research is the age difference in response. The same 2022 systematic review found that children and adolescents with chronic insomnia showed significant improvements in sleep onset latency and total sleep time – the exact outcomes that didn’t budge for adults. Another comprehensive 2023 study in eClinicalMedicine found that children with chronic insomnia due to underlying neurodevelopmental disorders experienced an average reduction of nearly 15 minutes in sleep latency. They also got almost 19 minutes more total sleep time.

Comorbid Insomnia: People whose insomnia exists alongside other medical or psychiatric conditions may respond better to melatonin than those with primary insomnia. The mechanisms here likely involve melatonin’s broader effects on inflammation, mood regulation, and circadian system restoration.

But here’s what research from University of Missouri neuroscientist Mahesh Thakkar helps us understand at a mechanistic level: melatonin promotes sleep by suppressing specific neurons that keep you awake and alert. Specifically, it suppresses orexin neurons in the lateral hypothalamus. This explains why melatonin works better for disorders involving circadian misalignment (where the wake signal needs to be shifted) rather than for people whose circadian rhythm is fine but who simply can’t turn off their racing thoughts at bedtime.

What About Primary Insomnia? The Uncomfortable Truth

This is where I need to share what might be disappointing news for many people using melatonin for insomnia: if you’re an adult with primary insomnia – meaning you have trouble sleeping but no clear circadian rhythm disorder or underlying medical condition – the evidence for melatonin’s effectiveness is surprisingly weak.

A 2022 CADTH review examining the evidence for melatonin in treating adult insomnia found “modest favourable effects” on some sleep outcomes. However, it also noted that one influential guideline by the Department of Veterans Affairs and Department of Defense actually recommends against the use of melatonin for chronic insomnia disorder. Their reasoning? Insufficient evidence of benefit.

The American Academy of Sleep Medicine’s position is similarly cautious. They note there’s “not enough strong evidence on the effectiveness or safety of melatonin supplementation for chronic insomnia to recommend its use.” Instead, they strongly recommend cognitive behavioral therapy for insomnia (CBT-I) as the first-line treatment.

Why doesn’t melatonin work better for primary insomnia? The issue likely comes down to what’s actually causing the sleep problem. If your insomnia stems from anxiety, racing thoughts, chronic pain, or conditioned arousal (where your bed has become associated with wakefulness), simply boosting melatonin levels won’t address these root causes. As one research review noted, melatonin’s sleep-promoting effects work through its role as a circadian signal and its ability to promote “sleep anticipation” in certain brain networks. However, this may not be sufficient to overcome the hyperarousal or cognitive factors driving primary insomnia.

Does this mean melatonin is useless for primary insomnia? Not necessarily. Individual responses vary widely, and some people do report subjective improvements. But it does mean we should temper our expectations and consider melatonin as one tool in a comprehensive sleep improvement strategy rather than a standalone solution.

The Timing Factor: When You Take It Matters More Than You Think

One of the most overlooked aspects of melatonin use is timing – and this might explain why many people don’t see results despite taking appropriate doses. The relationship between melatonin timing and effectiveness follows a surprisingly complex curve.

The 2024 dose-response meta-analysis I mentioned earlier revealed fascinating insights. For sleep onset, the optimal administration time appears to be 2-3 hours before your intended bedtime, not the 30 minutes typically recommended on bottles. This earlier timing aligns with when your body naturally begins its melatonin ramp-up, essentially giving the signal a head start.

However – and here’s where it gets tricky – the optimal timing shifts depending on what you’re trying to achieve:

For phase-shifting (moving your sleep schedule earlier): Take lower doses (0.5-3mg) in the late afternoon or early evening, roughly 3-4 hours before your desired bedtime. This approach works well for delayed sleep phase syndrome. It also helps when preparing for eastward travel.

For direct sleep-promoting effects: Take melatonin 60-90 minutes before bed. This timing may work better with slightly higher doses, though remember that “higher” in research terms often means 3-5mg, not the 10mg megadoses available at stores.

For jet lag: The timing shifts based on your destination. Generally, you’d take melatonin at the bedtime of your destination timezone, beginning before travel.

There’s also an intriguing interaction with light exposure. As research shows, melatonin’s circadian effects work in concert with light cues. Taking melatonin while simultaneously exposing yourself to bright lights (especially blue light from screens) can blunt its effectiveness. This is one reason why sleep hygiene practices may be just as important as the supplement itself. Dimming lights in the evening and avoiding screens before bed can enhance melatonin’s effects.

The Extended-Release Question: Does Formulation Matter?

Walk down the supplement aisle and you’ll notice something: melatonin now comes in multiple formulations – immediate release, extended release, and even sublingual (under the tongue) varieties. Does it matter which you choose?

The answer appears to be yes, depending on your sleep problem. Prolonged-release melatonin (PRM), which releases melatonin gradually over 8-10 hours, was specifically designed to mimic the body’s natural overnight melatonin production curve. A landmark study published in BMC Medicine followed participants taking 2mg PRM nightly for six months. The study found sustained improvements in sleep quality, particularly in adults aged 65 and older.

The key difference: immediate-release melatonin may help you fall asleep faster (sleep onset latency) but does less for staying asleep. Extended-release formulations, by maintaining melatonin levels throughout the night, may better address sleep maintenance – the problem of waking up in the middle of the night and struggling to fall back asleep.

That said, most research on circadian phase-shifting and jet lag has used immediate-release formulations, suggesting that for these applications, you want the quick spike in melatonin levels rather than the sustained release.

The sublingual (under-tongue) formulations claim faster absorption, bypassing first-pass metabolism in the liver. While this theoretically makes sense, I haven’t found robust clinical trials comparing sublingual to oral melatonin head-to-head for insomnia outcomes. The absorption difference exists, but whether it translates to meaningfully better sleep remains unclear.

Long-Term Use: The Questions We Still Can’t Fully Answer

Here’s where I wish I could give you more definitive guidance: we simply don’t have sufficient long-term safety data on extended melatonin use. Most clinical trials run for weeks to a few months, with one notable exception being a 6-month study of prolonged-release melatonin that found no concerning adverse effects.

What we do know is reassuring in some ways: melatonin doesn’t appear to cause physical dependence or withdrawal symptoms in the way that traditional sleep medications do. Multiple reviews have noted that melatonin can be stopped abruptly without the rebound insomnia that plagues users of benzodiazepines or Z-drugs like Ambien.

The most common side effects reported in studies include headaches (affecting less than 1% of users more than placebo), dizziness, and next-day grogginess. These are generally mild. One systematic review of randomized controlled trials found adverse effects occurred at similar rates to placebo, suggesting melatonin is remarkably well-tolerated for short-term use.

However, several concerns warrant caution:

Hormonal effects: Melatonin is, after all, a hormone. Some researchers worry about potential effects on sex hormones, particularly with long-term use in children and adolescents. Research notes that in some cases, long-term high-dose melatonin use might suppress the hypothalamic-gonadal axis. While rare, sudden discontinuation could theoretically trigger early puberty.

Psychological dependence: While melatonin isn’t physically addictive, some experts note the possibility of psychological dependence. This is where people feel anxious about sleeping without it, which paradoxically interferes with sleep. This isn’t addiction in the clinical sense, but it represents a form of reliance that might make it harder to develop natural sleep regulation.

Unknown unknowns: As a 2023 review in the journal Pharmaceuticals pointed out, we lack data on what happens with years or decades of melatonin use. Most people treat it as utterly benign. However, we’re essentially conducting an uncontrolled experiment.

Quality control concerns: Since melatonin is classified as a dietary supplement in the United States, it escapes the stringent oversight applied to pharmaceuticals. Studies have repeatedly found significant variability in actual melatonin content compared to label claims. This problem makes even dose-response research challenging.

My personal take? I think short-term strategic use of melatonin – for jet lag, adjusting to shift work, or managing a temporary circadian disruption – represents a relatively low-risk intervention. Extended daily use for months or years without medical supervision makes me more uneasy, particularly given the lack of long-term safety data and the possibility that it may mask underlying sleep disorders that warrant proper diagnosis and treatment.

Melatonin as Part of a Comprehensive Approach

Let me be direct about something: if you’re taking melatonin every night for months or years and still struggling with insomnia, melatonin probably isn’t your solution. This is where I’d encourage you to zoom out and look at the bigger picture.

Sleep is influenced by a complex web of factors. These include stress, light exposure, exercise timing, caffeine consumption, bedroom environment, underlying medical conditions, and psychological factors like anxiety or depression. As highlighted by Johns Hopkins experts, melatonin works best when combined with good sleep hygiene practices.

What does this actually look like in practice? Consider someone dealing with what they think is simple insomnia. They’ve been taking 5mg of melatonin nightly for six months with marginal improvement. A more comprehensive evaluation might reveal:

• Circadian misalignment: Their natural sleep drive doesn’t kick in until 1 AM, but they’re trying to sleep at 10 PM because of work demands. This is delayed sleep phase disorder. While melatonin can help, it needs to be timed strategically (4-5 hours before the desired bedtime) and combined with morning light exposure.

• Sleep hygiene issues: They’re scrolling social media in bed, which creates both cognitive arousal and blue light exposure that suppresses their own melatonin production. The supplement can’t override this physiological disruption.

• Stress and rumination: Work stress has them lying awake mentally composing emails. This is a cognitive arousal problem that cognitive behavioral therapy for insomnia (CBT-I) addresses far more effectively than any supplement.

• Sleep state misperception: They actually sleep more than they think they do, but their perception of sleep quality is poor – a phenomenon that won’t respond to melatonin at all.

Research consistently shows that cognitive behavioral therapy for insomnia outperforms melatonin for chronic insomnia, with effects that persist long after treatment ends. The American College of Physicians actually recommends CBT-I as the first-line treatment for chronic insomnia. This isn’t because melatonin is dangerous, but because addressing the behavioral and cognitive factors driving insomnia tends to work better.

This doesn’t mean you shouldn’t use melatonin. It means melatonin works best as one tool among several in a thoughtful approach to sleep improvement. Think of it like this: if you’re building a house, a hammer is an excellent tool – but you also need saws, levels, and a solid foundation. Melatonin might be your hammer, but sleep hygiene, stress management, and properly timed light exposure are equally important parts of the construction project.

There’s also the question of absorption and bioavailability – something we think about extensively with all supplements. Just as liposomal delivery systems can dramatically improve vitamin C absorption, the formulation of melatonin may affect how much actually reaches your bloodstream. This is yet another variable that makes it challenging to know if you’re getting an effective dose.

What a Top Sleep Researcher Would Say

If you could sit down with someone like Richard Wurtman, the MIT neuroscientist who pioneered much of our understanding of melatonin’s role in sleep, I suspect the conversation would challenge many mainstream assumptions about this hormone.

First, he’d probably emphasize that less is genuinely more when it comes to melatonin dosing. His research consistently showed that physiologic doses (0.3-1mg) that mimic the body’s natural nighttime levels work better than pharmacologic megadoses. He’d likely express frustration that the supplement industry largely ignored this finding. They favored higher-dose products that generate more profit but may actually work worse.

Second, he’d stress that melatonin is fundamentally a chronobiotic agent – a substance that affects the timing of biological rhythms – rather than a hypnotic sleeping pill. Understanding this distinction is crucial for using it effectively. You’re not trying to knock yourself out; you’re trying to signal to your body when it’s nighttime.

Third, Wurtman and his colleagues documented that melatonin’s effectiveness depends heavily on an individual’s baseline endogenous melatonin production. People whose natural melatonin production has declined (particularly older adults) tend to respond better to supplementation. Young, healthy adults with robust nighttime melatonin secretion may see minimal benefit from adding more.

Finally, I think he’d caution against the notion that melatonin is a panacea for all sleep complaints. His research showed that even among elderly insomniacs with low melatonin levels, the supplement improved sleep in some individuals but not others. This suggests that melatonin deficiency isn’t the sole driver of insomnia for most people. Other factors – psychological stress, poor sleep habits, underlying sleep disorders like apnea – often play larger roles.

Other leading researchers echo similar themes. The work from University of Pisa’s research team emphasized that individual variability in response is enormous. They also stressed that personalization of both dose and timing is crucial. One-size-fits-all recommendations miss the point.

The Bottom Line: A More Nuanced View of Melatonin

After diving deep into the research, my perspective on melatonin for insomnia treatment has evolved considerably. It’s not the universal sleep solution it’s marketed to be, but it’s also not useless when used appropriately.

Here’s what I think represents a balanced, evidence-based view:

Melatonin works best for: • Circadian rhythm disorders (delayed sleep phase, jet lag, shift work)
• Children and adolescents with insomnia
• Older adults with documented low melatonin production
• People with insomnia secondary to other medical conditions

Melatonin shows limited effectiveness for: • Primary insomnia in healthy adults
• Insomnia driven by anxiety, stress, or racing thoughts
• Sleep maintenance problems (unless using extended-release)

Key factors for success: • Start with low doses (0.3-1mg) rather than megadoses
• Time administration 2-3 hours before target bedtime for circadian effects
• Combine with sleep hygiene practices and light management
• Use strategically and intermittently rather than as chronic daily therapy
• Consider extended-release formulations for sleep maintenance issues

Red flags that suggest you need more than melatonin: • You’ve been using it nightly for months without lasting improvement
• Your sleep problem started after a major life stressor or trauma
• You have symptoms of sleep apnea (snoring, gasping, excessive daytime sleepiness)
• Your insomnia is accompanied by significant anxiety or depression
• You sleep fine on weekends but poorly during work weeks

Perhaps the most important insight from all this research is that sleep is too important and too complex to approach simplistically. Yes, melatonin can play a valuable role – but it’s most powerful when combined with a broader understanding of what drives healthy sleep: appropriate light exposure, consistent sleep-wake timing, stress management, and addressing whatever underlying factors might be disrupting your rest.

If you’re currently taking melatonin for insomnia, I’d encourage you to evaluate whether it’s actually helping. Try keeping a sleep diary for two weeks while using it, then two weeks without it (after checking with your healthcare provider if you have underlying conditions). The difference – or lack thereof – might surprise you and guide you toward strategies that work better for your unique situation.

What questions do you have about your own sleep struggles? Have you found melatonin helpful, or did it leave you disappointed? The more we can share honest observations about what actually works in real-world conditions, the better we can all support each other in this perpetual quest for restorative sleep.

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FAQ Section

Q: What is melatonin and how does it differ from a sleeping pill?

A: Melatonin is a naturally occurring hormone produced by your pineal gland that regulates your circadian rhythm – your body’s 24-hour internal clock. Unlike sleeping pills (sedative-hypnotics like benzodiazepines or Z-drugs) that directly induce drowsiness by affecting brain receptors associated with consciousness, melatonin works by signaling to your body that it’s nighttime and helping prepare you for sleep. It promotes “quiet wakefulness” that facilitates sleep onset rather than forcing unconsciousness. This is why melatonin is classified as a chronobiotic (time-regulating) agent rather than a traditional hypnotic sleeping medication.

Q: What is sleep onset latency?

A: Sleep onset latency (SOL) is the technical term for how long it takes you to fall asleep after you turn out the lights and intend to sleep. It’s measured from “lights out” to the beginning of the first sleep stage. A normal sleep onset latency is generally considered to be 10-20 minutes. Much shorter than this might indicate sleep deprivation, while consistently taking 30 minutes or longer might suggest insomnia or other sleep disorders.

Q: What does “physiologic dose” mean for melatonin?

A: A physiologic dose refers to an amount of a hormone that mimics what your body naturally produces, as opposed to a pharmacologic dose that exceeds natural levels. For melatonin, a physiologic dose is approximately 0.3-1mg, which raises blood melatonin levels to what you’d normally experience at night. Doses above 3mg are considered pharmacologic – they produce melatonin levels far higher than the body naturally creates, which can cause receptor downregulation where the receptors become less responsive to melatonin.

Q: What are circadian rhythm sleep-wake disorders?

A: These are conditions where your body’s internal clock (circadian rhythm) is misaligned with the external 24-hour day or your desired sleep-wake schedule. Common types include: delayed sleep-wake phase disorder (DSWPD), where you naturally feel sleepy very late and wake very late; advanced sleep-wake phase disorder, the opposite pattern with very early sleep and wake times; non-24-hour sleep-wake rhythm disorder, where sleep timing drifts later each day; shift work sleep disorder, involving disruption from rotating or night shifts; and jet lag disorder from rapid travel across time zones.

Q: What is the suprachiasmatic nucleus (SCN)?

A: The suprachiasmatic nucleus is a tiny region in your hypothalamus (part of your brain) that serves as your master circadian clock. It contains about 20,000 neurons that maintain your 24-hour biological rhythms. The SCN receives direct input from your eyes about light and darkness, and it controls the timing of melatonin release from your pineal gland. Essentially, it’s the conductor orchestrating your body’s daily rhythm, influencing sleep-wake cycles, body temperature, hormone release, and metabolism.

Q: What does “receptor downregulation” mean?

A: Receptor downregulation is a process where cells reduce the number or sensitivity of receptors on their surface in response to prolonged or excessive exposure to a particular substance. When you take high doses of melatonin repeatedly, the melatonin receptors in your brain can become less numerous or less responsive – essentially the cells are saying “there’s too much of this hormone, so we’re going to ignore some of it.” This is why very high doses of melatonin often stop working after a few days, even though lower doses might continue to be effective.

Q: What is comorbid insomnia?

A: Comorbid insomnia means insomnia that occurs alongside (comorbid with) another medical condition, psychiatric disorder, or sleep disorder. For example, insomnia associated with depression, anxiety, chronic pain, Parkinson’s disease, or sleep apnea would be considered comorbid insomnia. This contrasts with primary insomnia, where sleep difficulty is the main problem without another clearly identifiable cause. The distinction matters because treatment approaches often need to address both the insomnia and the coexisting condition.

Q: What is delayed sleep-wake phase disorder (DSWPD)?

A: Delayed sleep-wake phase disorder is a circadian rhythm disorder where a person’s sleep-wake cycle is delayed by two or more hours compared to desired or socially acceptable times. People with DSWPD typically can’t fall asleep until 2-6 AM and struggle to wake before 10 AM to 1 PM. When they do sleep, the sleep itself is normal quality – the problem is purely one of timing. This is not the same as insomnia (difficulty sleeping even when trying at an appropriate time) or simple preference for staying up late. DSWPD involves a genuine physiological delay in the circadian clock that makes earlier sleep and wake times extremely difficult or impossible without intervention.

Q: What does it mean for melatonin to be a dietary supplement versus a medication?

A: In the United States, melatonin is classified as a dietary supplement rather than a drug, which has significant regulatory implications. Unlike FDA-approved medications, dietary supplements don’t require proof of efficacy or safety before being sold, don’t need FDA approval before hitting the market, aren’t subject to the same manufacturing quality standards, and may not contain the amount or purity of ingredients claimed on the label. This classification means supplement companies can sell melatonin without proving it works for insomnia, and studies have found wide variability in actual melatonin content in commercial products (ranging from 83% less to 478% more than labeled amounts). In many other countries, melatonin is available only by prescription and regulated as a drug.

Q: What is cognitive behavioral therapy for insomnia (CBT-I)?

A: Cognitive behavioral therapy for insomnia is a structured program that helps identify and replace thoughts and behaviors that cause or worsen sleep problems with habits that promote sound sleep. It typically involves components like sleep restriction therapy (limiting time in bed to match actual sleep time), stimulus control (reassociating the bed with sleep rather than wakefulness), relaxation training, and addressing unhelpful beliefs about sleep. Unlike sleeping pills or supplements that you take indefinitely, CBT-I teaches you skills that continue working long after treatment ends. Major medical organizations recommend it as the first-line treatment for chronic insomnia because it’s been shown to be as effective as sleep medications in the short term and more effective in the long term, without side effects.

Q: What is sleep efficiency?

A: Sleep efficiency is the ratio of actual sleep time to time spent in bed, expressed as a percentage. For example, if you’re in bed for 8 hours but only actually sleep for 6 hours (with the other 2 hours spent trying to fall asleep or lying awake), your sleep efficiency is 75% (6÷8 × 100). Sleep efficiency above 85% is generally considered normal, while below 85% may indicate a sleep disorder. It’s a useful measure because it captures not just how much you sleep, but how efficiently you’re using your time in bed. Poor sleep efficiency often responds better to behavioral interventions (like sleep restriction therapy) than to medications or supplements.

Q: What is the HPA axis that’s mentioned in stress and sleep research?

A: The HPA axis (hypothalamic-pituitary-adrenal axis) is your body’s central stress response system. When you encounter a stressor, your hypothalamus releases a hormone that signals your pituitary gland, which then releases ACTH (adrenocorticotropic hormone) that tells your adrenal glands to produce cortisol and other stress hormones. This cascade helps you respond to challenges, but chronic activation of the HPA axis (from ongoing stress) can disrupt sleep, suppress immune function, and contribute to various health problems. The HPA axis and the circadian system (which includes melatonin) normally work in coordinated rhythms, which is why stress and sleep problems so often go hand-in-hand.

Q: What is primary insomnia?

A: Primary insomnia (also called idiopathic insomnia) is difficulty falling asleep, staying asleep, or poor sleep quality that isn’t directly caused by another medical condition, medication, substance use, or psychiatric disorder. It’s insomnia as the main problem, not as a symptom of something else. Diagnosis requires ruling out other causes like sleep apnea, circadian rhythm disorders, anxiety, depression, or medication effects. Primary insomnia often involves hyperarousal (increased physiological and cognitive activation) and may be maintained by conditioned responses where the bed becomes associated with wakefulness rather than sleep.

Q: Why is timing more important than dose for melatonin’s effects?

A: Melatonin’s dual action – both as a chronobiotic (phase-shifting agent) and a sleep-promoting substance – means timing determines which effect you get and how strong it is. Taking melatonin in the late afternoon or early evening (3-5 hours before bed) produces strong circadian phase-shifting effects, helping move your sleep schedule earlier. Taking it closer to bedtime (1-2 hours before) produces more immediate sleep-promoting effects but less phase-shifting. Additionally, your natural melatonin production begins rising about 2 hours before your usual bedtime (called dim light melatonin onset or DLMO), so supplementing before this window works with your body’s rhythm, while taking it too late may miss the critical timing window. This is why the same dose taken at different times can produce very different results.