Melatonin

SAD is closely linked to seasonal/light-driven changes in circadian timing. In winter the timing (phase) of people’s internal clock can shift relative to the sleep/wake cycle; that circadian misalignment is a leading explanation for SAD symptoms. Studies and reviews call this the phase-shift hypothesis (Lewy et al.). Taylor & Francis Online

Melatonin is the body’s “night” signal and a strong circadian phase-shifter. Exogenous (taken) melatonin can shift circadian rhythms (advance or delay them) depending on dose and timing, so it can be used to correct the phase misalignment thought to underlie SAD. This is the principal rationale for using melatonin to treat or prevent winter depression. Taylor & Francis Online

How that translates to clinical benefit: early pilot and experimental work showed that timed, low-dose melatonin given in the afternoon/evening (to produce a phase advance) reduced depressive scores in small SAD samples — supporting the idea that correcting circadian phase can improve mood in SAD. However, subsequent larger reviews find the clinical picture is mixed. Gwern

Key principle: Dose + timing determine whether melatonin advances or delays the circadian clock. For SAD the therapeutic goal in many studies is a phase advance (make internal rhythms earlier), which is achieved by low doses given in the afternoon/early evening.

Practical points derived from the literature and clinician guidance:

• Dose: clinical chronobiology work recommends low doses — often ≤ 0.5 mg (some authors discuss 0.1–0.5 mg for phase shifting). Trials labelled “low-dose” melatonin (Lewy and colleagues) showed phase-shifting effects without sedation. Many consumer guides and clinics (for sleep disorders) recommend starting low (e.g., 0.5–1 mg) for circadian effects and increasing only if needed for sleep problems (but SAD-phase studies used the lower range). Taylor & Francis Online
• Timing: to advance circadian phase (the usual aim in winter SAD), melatonin is given in the afternoon or early evening (several hours before habitual bedtime) rather than right at bedtime or in the morning. Clinical papers describe afternoon/evening administration vs morning (which causes delays). Exact timing in experimental protocols is often set relative to each subject’s circadian marker (DLMO — dim light melatonin onset) or habitual sleep time; in practical (non-lab) use clinicians typically prescribe a timed dose a few hours before desired sleep time. Gwern
• Duration: trials testing prophylaxis used repeated daily dosing through the at-risk season; other studies used multi-week courses (e.g., weeks). There is no universally accepted single “standard” regimen for SAD — protocols vary. The Cochrane review concluded evidence is insufficient to definitively recommend a standard preventive melatonin regimen for SAD. Cochrane

How clinicians typically approach this in practice

• If melatonin is considered for SAD, many sleep/circadian experts recommend:

1. Evaluate and prioritize first-line treatments (see section 4 below).
2. If using melatonin to target circadian phase, use a low dose (commonly 0.1–0.5 mg or up to 1 mg in some clinics) given in the afternoon/early evening to induce a phase advance — ideally timed relative to assessment of circadian phase (DLMO) if available; otherwise timed by experienced clinician guidance. Taylor & Francis Online

Note: Over-the-counter melatonin tablets are often much larger (1–5 mg or more). For circadian phase effects, smaller, accurately-measured doses (and sometimes compounded preparations) were used in the chronobiology trials. If you or a patient consider this, ask a clinician/pharmacist about low-dose formulations or splitting tablets only if the product and formulation make that safe and accurate.

Supportive experimental/clinical work (mechanistic / small trials):

• Lewy et al. pilot and controlled studies showed that timed, low-dose melatonin could produce phase advances and reduce depressive symptoms in small samples of winter-depressed patients (pilot RCT and chronobiology experiments). These studies are frequently cited in support of the phase-shift mechanism. Gwern
• Other trials exploring melatonin for circadian disorders (delayed sleep phase, etc.) also show clear phase-shifting effects of low doses when properly timed (useful mechanistic support). SAGE Journals

Larger systematic reviews / major evidence summaries:

• Cochrane review (melatonin and agomelatine for preventing winter depression / SAD): concluded that methodologically sound evidence is lacking to determine whether melatonin prevents SAD — trials are heterogeneous and insufficient to make a clear recommendation. The review calls for larger, well-designed trials comparing melatonin to established treatments. In short: evidence is inconclusive for routine use as prevention. Cochrane
• NCCIH / NIH summary and other authoritative overviews note the same: biological plausibility and small trials exist, but high-quality evidence for melatonin as a proven preventive treatment for SAD is not established. NCCIH

How melatonin compares to established treatments:

• Bright-light therapy and antidepressants (e.g., SSRIs) have stronger, more consistent evidence for treating winter SAD; many meta-analyses and treatment guidelines list bright light therapy as first-line non-pharmacologic therapy. Melatonin is best characterized as a circadian-targeted intervention with plausible benefit for some patients but weaker proof of clinical benefit in larger trials. ScienceDirect

Summary on evidence: melatonin has a strong mechanistic rationale and positive signals from small/experimental studies, but larger randomized trials and systematic reviews do not yet provide high-certainty evidence that melatonin is a reliably effective, standalone preventive or primary treatment for SAD. Clinicians sometimes use it as an adjunct or when targeting circadian phase, but light therapy/SSRIs remain better-supported first-line options. Gwern