Can working the night shift cause cancers?

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Can working the night shift cause cancers?

Can working the night shift cause cancers?

Chronobiological Disturbance Identified as Human Carcinogen, Facilitating Liver Cancer Onset and Progression.

When asked about potential cancer-causing factors, people might first think of chemicals like tobacco, alcohol, or radiation such as UV rays from the sun. Rarely would one consider chronic jet lag. Yet epidemiological studies have linked chronic jet lag, also known as chronic circadian rhythm disruption, with an increased risk of liver cancer. However, direct evidence linking it to liver cancer has been lacking.

Recently, a study published in the Journal of Hepatology by a team led by Loning Fu from Baylor College of Medicine in the United States sheds light on this matter.

Titled “Circadian dysfunction induces NAFLD-related human liver cancer in a mouse model,” the research provides experimental evidence that chronic jet lag is indeed a human carcinogen.

Moreover, restoring a normal circadian rhythm can inhibit tumor development and metastasis, underscoring the importance of circadian rhythms in the prevention and treatment of liver cancer.

Can working the night shift cause cancers?

Circadian rhythms are our internal 24-hour clocks in the brain, synchronizing with the Earth’s day-night cycle to regulate alertness, sleep, and almost all bodily functions. When this internal clock is disrupted, diseases are more likely to develop.

Chronic circadian disruption increases the risk of non-alcoholic fatty liver disease (NAFLD)-related hepatocellular carcinoma (HCC), but its underlying mechanisms and direct relevance to human liver cancer have remained unclear.

In this study, researchers used a humanized mouse model, containing both human and murine liver cells, to investigate the impact of disrupting circadian rhythms on human cell cancer development.

These humanized mice were exposed to two different conditions: one group was kept synchronized with the natural day-night cycle, while another group had their light-dark cycles altered to mimic the changes experienced by humans flying from San Francisco to London (an 8-hour time difference) and enduring weeks of jet lag.

The study found that compared to mice with normal circadian rhythms, those in the jet lag group had shorter lifespans, higher rates of liver fibrosis and jaundice (yellowing of the skin or eyes), and both their murine and human liver cells underwent carcinogenesis. Importantly, this chronic circadian disruption also induced the metastasis of cancerous cells.

Blood analysis and liver microscopy revealed multiple similarities between the humanized mice and liver cancer patients, including impaired glucose tolerance, abnormal fat accumulation in the liver, inflammation, and fibrosis. This supports the validity of this model for studying the human liver condition. The research team noted that these results indicate changes in biomarkers and gene expression patterns in cells as tumors progress.

Humanized mice with chronic circadian disruption spontaneously developed liver cancer in human cells, with processes and molecular pathways similar to humans. Gene expression studies revealed that in this model, the development of spontaneous liver cancer is driven by changes in the expression of thousands of genes, dependent on cell type, time, and disease stage.

One of the key findings of this study is that once tumors develop spontaneously under chronic circadian disruption, restoring the mice to a normal circadian rhythm slows down tumor development and inhibits tumor metastasis, with gene expression patterns reverting to their previous state.

In summary, this study suggests that chronic circadian disruption is an independent carcinogen for human liver cells and emphasizes the importance of circadian rhythms in the prevention and treatment of liver cancer.

Link to the paper