Published in the journal Cancer Cell, their study found that the body's “master clock,” which regulates the circadian rhythms in both tissues and organs throughout the body, basically stops functioning when normal sleep patterns are disrupted. This master clock regulates not only restful sleeping patterns, but also metabolic function.
To come to this conclusion, the team evaluated the effects of chronic sleep disruption, or what they termed “social jet lag,” on a group of mice. These mice were exposed to abnormal light and dark cycles for nearly two years, which resulted in many of them developing a range of health conditions including various skin disorders, neurodegeneration, and cancer. Control mice, on the other hand, developed none of these adverse effects.
The life-cycle of mice is much greater than that of humans, and by age 78 weeks – roughly 67-72 years old in human equivalency – many of the sleep-deprived mice developed hepatocellular carcinoma, the most common form of liver cancer. By 90 weeks, a shocking 96 percent of jet-lagged mice also developed nonalcoholic fatty liver disease, or NAFLD, which experts say is a major cause of HCC.
Sleep deprivation negatively alters gene expression, scientists discover
Lack of sleep, it turns out, has a direct effect on gene expression throughout the body, including genes that regulate circadian rhythm – Bmal1, Clock, Per1, Per2, and Nr1d1 being among these. Genes that regulate cholesterol and bile acid pathways, both of which are essential for normal liver function, were also disrupted.
The nuclear receptor CAR gene, which is responsible for sensing toxic compounds, was found to activate as a result of sleep deprivation, while the FXR gene, also known as the bile acid receptor, was correspondingly suppressed. This pattern, say experts, is very similar to what happens in humans when HCC develops.
“To us, our results are consistent with what we already knew about these receptors, but they definitely show that chronic circadian disruption alone leads to malfunction of these receptors,” stated Loning Fu, senior author of the study. “And thus, maintaining internal physiological homeostasis is really important for liver tumor suppression.”
As to how this all translates to humans, data from these types of mice models often extrapolates directly, hence why they're conducted in the first place. Based on the findings, it's apparent that humans have a similar risk of liver damage and potentially liver cancer when their sleep patterns are routinely disrupted, which helps explain why rates of liver cancer have escalated so dramatically in recent years.
“Recent studies have shown that more than 80 percent of the population in the United States adopt a lifestyle that leads to chronic disruption in their sleep schedules,” Fu added. “This has also reached an epidemic level in other developed countries, which is coupled with the increase in obesity and liver cancer risk.”
Adding to this sentiment in a more direct way, co-lead study author David Moore, a professor of molecular and cellular biology at Baylor, explained how simple it is for sleep deprivation to turn into full-blown chronic disease.
“Liver cancer is on the rise worldwide, and in human studies we've now seen that patients can progress from fatty liver disease to liver cancer without any middle steps such as cirrhosis,” he's quoted as saying.
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