New study shows chronic jet lag increases risk of liver cancer

February 23, 2024
A photo of Professor David Moore smiling at the camera against a blurry backdrop.

When you think about what causes cancer, you might be quick to name chemicals like tobacco and asbestos or sources of radiation such as ultraviolet light. But a new Journal of Hepatology study co-authored by Nutritional Science and Toxicology professor and chair David Moore identifies a surprising new carcinogen: chronic jet lag.

Jet lag affects your body’s circadian rhythm: the natural, automatic clock that governs multiple bodily processes including alertness or sleepiness, appetite, and body temperature. When that rhythm is disrupted, people tend to exhibit extreme daytime sleepiness, decreased alertness, and problems with memory and decision-making. More serious complications can emerge when jet lag becomes chronic

To test the disorder’s long-term impacts, Moore and co-authors from the Baylor College of Medicine examined how a mouse with both human and rodent liver cells responded to changes in periods of light and darkness. One group of mice was kept in sync with the natural day-and-night cycle, while the other was exposed to conditions that mimicked the jet lag associated with many weeks of round-trip flights between San Francisco and London.

“We found that, compared to mice kept in normal light/dark cycles, mice in the jet-lagged group had a shorter lifespan as well as increased cirrhosis, jaundice, and also developed cancer in both mouse and human liver cells,” said Baylor College of Medicine professor and lead corresponding author Loning Fu. “Importantly, chronic jet lag also induced metastasis from humanized livers.”

Results of blood analyses and microscopy studies of the mice's livers revealed multiple similarities with human liver cancer patients. Moore, who served as co-corresponding author, said the spontaneous cancer development in jet-lagged mice followed the same process and molecular pathways as liver cancer in humans. The authors also reported similar levels of glucose intolerance, abnormal fat accumulation in the liver, inflammation, and fibrosis between mice and humans.

“One of the important findings of the paper is that, once the tumors spontaneously develop in response to chronic circadian disruption, returning the mice to a normal circadian clock slows tumor development, prevents metastasis, and restores their gene expression pattern,” said Moore. “Our work shows that circadian influences in cancer cannot be underestimated: chronic circadian dysfunction is a human carcinogen.”

This article was adapted from a press release by the Baylor College of Medicine.