Melatonin is produced at night (or in conditions of darkness) and nocturnal light disrupts melatonin synthesis. When women work at night or are otherwise exposed to light at night, their risks of breast cancer and its recurrence increase. Habitually sleeping in the presence of artificial light also appears to promote breast cancer by inhibiting melatonin production. Blue light wavelengths appear to have a far greater suppressive effect on melatonin production than red wavelengths. Melatonin is a hormone known primarily for its involvement in the regulation of circadian rhythms (the body clock). However, melatonin has also been shown to have antioxidant, anti-inflammatory, and anti-carcinogenic properties, especially in breast cancer.
In one Israeli study, 1,679 breast cancer patients were interviewed regarding bedroom light levels, including light coming in the room outside the bedroom and sleeping with the television on. "Sleeping habitat" light intensity was also found to be linked to breast cancer risk. Now a new study has reported that circadian/melatonin disruption by exposure to dim light at night is able to drive progression in a mouse model of hormone receptor positive (ER+/PR+) breast cancer, resulting in lung, liver, and brain metastatic lesions.
Women can maintain their melatonin levels by getting enough sleep, avoiding night shift work and any regular light exposure (including power light indicators, electronic clock faces and visual displays) at night, and consuming melatonin-rich foods. The foods below are good sources of melatonin and have also been found to be associated with reduced breast cancer risk or recurrence:Sweet corn and rolled oats also contain melatonin. On the other hand, red meat consumption has been shown reduce circulating melatonin.
Latest research finds dim light at night can hasten metastasis
The study referenced at the beginning of this news story was designed to investigate whether dim light at night-induced circadian/melatonin disruption can promote epithelial-to-mesenchymal transition (EMT) of mammary tumor xenografts in a mouse model of ER+/PR+ breast cancer. EMT is a crucial event in the tumor invasion process. An EMT enables an epithelial cell to undergo a variety of changes that empowers it to assume a mesenchymal cell phenotype, thereby acquiring enhanced migratory capacity and invasiveness, as well as elevated resistance to apoptosis (programmed cell death). Inhibition of EMT-related signaling appears to play a central role in the anticancer activity of some micronutrients.
The authors previously reported that circadian/melatonin disruption by exposure to dim light at night promoted resistance to both tamoxifen and Adriamycin (doxorubicin) in mouse mammary tumor xenografts (grafts of human breast cancer cells). Since chemoresistant breast cancer is often metastatic, the authors decided to investigate whether dim light at night-induced circadian/melatonin disruption can lead to the development of metastases in the lungs, livers, and brains of female rats and mice. Female rats with ER+ breast cancer xenografts were housed in various light at night conditions with or without supplemental melatonin (0.05 µg/ml) administered at night in the in the drinking water. Blood samples collected from the animals showed significantly lowered melatonin in the dim light at night group compared to the night darkness group.
Tumor xenografts of rats housed in dim light at night conditions had decreased latency-to-onset and increased growth compared to those of rats in housed in dim light at night and given supplemental melatonin. Tumor signaling pathways involved in promoting EMT and metastasis had increased expression at in response to dim light at night but reduced expression in tumors from rats in dim light at night plus melatonin. Additional experiments using mice implanted with non-metastatic ER+/PR+ breast cancer cells demonstrated that exposure to dim light at night reduced nighttime levels of melatonin by 93% compared to those in a 12 hour light/12 hour dark schedule. Mice exposed to dim light at night experienced rapid growth of ER+/PR+ xenografts—after five weeks all of the animals had identifiable metastases in their lungs, livers, and brains. On the other hand, ER+/PR+ xenografts in mice exposed to dim light at night but supplemented with melatonin had less tumor development and 3-fold slower tumor growth—in fact, only one of these mice developed a metastatic lesion. The authors conclude that circadian/melatonin disruption by exposure to dim light at night is able to drive EMT in ER+/PR+ breast cancer xenografts, resulting in lung, liver, and brain metastatic lesions.