Could Melatonin Protect Night Shift Workers From DNA Damage?

Night shift work is a necessity in many industries, but its long-term health effects remain a concern.

Researchers from the BC Cancer Research Institute and the University of British Columbia recently published a study in Occupational & Environmental Medicine examining whether melatonin supplementation could help repair DNA damage caused by circadian disruption. Their findings suggest that taking a 3 mg melatonin supplement before daytime sleep can lead to an increase in DNA repair markers.

The hidden toll of night shift work

Night shift work, while essential in our 24-hour society, has been linked to various health risks – notably an increased likelihood of certain cancers. The International Agency for Research on Cancer classifies "shift work that involves circadian disruption" as a probable human carcinogen. This classification stems from studies indicating that women engaged in long-term night shift work may face a slightly elevated risk of breast cancer.

The underlying mechanism involves the disruption of the body's circadian rhythm – our internal clock that regulates sleep-wake cycles. Exposure to light during nighttime hours suppresses the production of melatonin, a hormone predominantly produced at night that regulates sleep. Reduced melatonin levels can impair the body's ability to repair oxidative DNA damage, potentially leading to increased cancer risk.

Melatonin supplements are widely used to address sleep disturbances, such as those caused by jet lag or shift work. However, their availability varies by country. In the United States and Canada, melatonin is available over the counter as a dietary supplement. In contrast, the United Kingdom classifies melatonin as a prescription-only medication, restricting its sale without proper medical authorization. This regulatory approach aims to ensure appropriate use under medical supervision, given potential side effects and the need for correct dosing.

Despite the widespread use of melatonin supplements, there is a notable gap in research regarding their efficacy in repairing oxidative DNA damage among night shift workers. Prior to this latest study, no clinical trials had specifically examined whether melatonin supplementation could enhance the DNA repair mechanisms that are often compromised by circadian disruption in this population.

Investigating melatonin’s role in DNA repair

The team conducted a randomized, placebo-controlled trial involving 40 night shift workers. Participants were randomly assigned to receive either a 3 mg melatonin supplement or a placebo for 4 weeks. The supplements were taken with food, an hour before daytime sleep, following a night shift. Participants were required to work at least two consecutive night shifts per week, lasting at least seven hours per night, for at least six months. To ensure the study's validity, individuals with sleep disorders or chronic conditions were excluded.

Participants collected all urine excreted during two key periods: daytime sleep and the following night shift. This was done twice – once before starting the intervention and once near the end of the four-week study – resulting in four total urine collection periods per participant. The study measured levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG) in urine, a widely recognized biomarker for oxidative DNA damage and repair capacity. Higher urinary levels of 8-OHdG indicate better DNA repair, as this means the body is effectively identifying and removing damaged DNA.

Participants wore activity trackers to monitor their sleep patterns and their subjective sleepiness levels were recorded using the Karolinska Sleepiness Scale.

Melatonin supplementation increased DNA repair markers by 80% during daytime sleep compared to the placebo group, a result that was found to be borderline statistically significant.

Two participants in the melatonin group did not show an increase in DNA repair, possibly due to differences in melatonin metabolism or absorption. The researchers ran a secondary analysis excluding those with the lowest circulating melatonin levels, which then showed a statistically significant increase in DNA repair markers.

No significant difference in DNA repair markers was observed during the subsequent night shift, suggesting melatonin’s effect was limited to the sleep period.

Sleep duration and alertness remained largely unchanged between the melatonin and placebo groups.

“Increased oxidative DNA damage due to diminished DNA repair capacity is a compelling mechanism that may contribute to the carcinogenicity of night shift work,” the authors wrote. "Our randomized placebo-controlled trial suggested melatonin supplementation may improve oxidative DNA damage repair capacity among night shift workers.” 

Could melatonin reduce cancer risk for night shift workers?

While the results are promising, the study has several key limitations that must be addressed in future research. Most participants worked in healthcare, meaning the results may not apply to workers in other industries. Since light is a major factor in melatonin suppression, variations in the participant's light exposure outside of work could have influenced the results, and with only 40 participants, the study also lacks the statistical power to draw broad conclusions.

“Our findings warrant future larger-scale studies that examine varying doses of melatonin supplements and longer-term impacts of melatonin use,” the authors wrote. “Assessing long-term efficacy is critical since those who work night shifts for many years would need to consistently consume melatonin supplements over that time frame to maximize the potential cancer prevention benefits.”

“Pending the outcome of such studies, melatonin supplementation may prove to be a viable intervention strategy to reduce the burden of cancer among night shift workers.” 

Reference: Zanif U, Lai AS, Parks J, et al. Melatonin supplementation and oxidative DNA damage repair capacity among night shift workers: a randomised placebo-controlled trial. Occup Environ Med. 2025. doi: 10.1136/oemed-2024-109824

This article is a rework of a press release issued by the BMJ. Material has been edited for length and content.