In a small but carefully controlled trial, melatonin supplements boosted the body's ability to repair DNA damage by 80% during daytime sleep among night shift workers—a finding that hints at one way to counter the hidden biological toll of working through the night.
The discovery matters because night shift work disrupts the natural rhythm of melatonin production, the hormone that normally rises in darkness to signal the body it's time to rest. When that signal fails, the body's capacity to repair oxidative DNA damage—the cellular wear and tear that accumulates during normal metabolism—appears to weaken. This impaired repair may be one pathway linking persistent night work with higher risk for certain cancers, a concern serious enough that the International Agency for Research on Cancer has classified night shift work as probably carcinogenic to humans.
To test whether melatonin could restore that lost repair capacity, researchers conducted a randomized placebo-controlled trial with 40 night shift workers, all of whom had worked at least two consecutive night shifts weekly for at least six months, with each shift lasting at least seven hours. Half took a 3 milligram melatonin pill once daily for four weeks, timing it about one hour before daytime sleep. The other half took an identical placebo on the same schedule.
The researchers measured urinary levels of 8-OHdG, a biomarker that signals oxidative DNA damage repair activity. Higher urinary levels during sleep suggest greater repair work happening in the body. Among workers who took melatonin, 8-OHdG levels rose 80% during daytime sleep compared with the placebo group—a substantial increase that suggests melatonin may help restore the body's repair signals even when sleep happens during the day. The effect did not appear during the subsequent night shift, however, which indicates melatonin's benefit may be specific to restoring the circadian conditions of daytime recovery.
The findings offer a plausible biological mechanism: the body normally uses sleep and circadian timing to coordinate repair processes. When night shift workers sleep during daylight hours instead, that system falters. Melatonin may help reactivate part of that lost signaling, at least temporarily.
Yet the researchers are careful to frame their work as preliminary. The trial was small and ran for only four weeks. It measured a biomarker related to DNA repair, not actual cancer outcomes. Most participants worked in healthcare, so the results may not apply to all night shift workers across different industries. The team also could not account for natural light exposure, which affects melatonin levels independently.
The broader research landscape supports the need for caution and further study. Recent scientific reviews have identified multiple pathways through which night shift work may harm health: circadian disruption, altered hormone signaling, changes in immune function, metabolic disruption, and impaired DNA repair. The National Toxicology Program has similarly reviewed evidence linking persistent night work and light exposure with cancer risk.
What the researchers have not done—and what they emphasize cannot be claimed—is prove that melatonin prevents cancer. Instead, their work strengthens the scientific case for studying whether restoring melatonin signaling could help reduce some of the biological strain of long-term night work. Larger trials with different doses and longer follow-up periods now lie ahead.