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Chronic Stress and Obesity May Promote Pancreatic Cancer Growth via CREB Activation, Study Suggests

Key Takeaways

Stress and obesity may contribute to pancreatic cancer – Both factors activate biological pathways that may accelerate tumor growth.

Women may be more vulnerable – Hormonal differences could heighten stress-related cancer risks, but human studies are needed.

Beta-blockers show promise – These medications might counteract stress-driven tumor growth, but clinical trials are required.

A study by UCLA Health Sciences, published in Molecular Cancer Research (March 1, 2025), found that chronic stress and obesity may promote pancreatic cancer development.

Pancreas Image Courtesy of Blausen Medical

The prognosis for pancreatic cancer is particularly grim, with a five-year survival rate of just 11%. Two factors may fuel its progression. Chronic stress and obesity may possibly speed up the growth of this deadly tumor, according to the study published in Molecular Cancer Research on March 1, 2025.

Stress and Obesity Linked to Tumor Growth

In a study on human cells, researchers discovered that stress and obesity trigger changes in pancreatic cells that can lead to cancer. This builds on prior research linking stress and obesity to cancer progression. “Specifically, it was found that stress-related neurotransmitters and obesity-related hormones activate a protein called CREB, which is linked to the growth of cancer cells through different biological pathways. “Stress hormones activate the beta-adrenergic receptor/PKA pathway, while obesity-related signals primarily use the PKD pathway,” the study authors wrote in their report.

Researchers observed that both lifestyle-related factors may contribute to pancreatic cancer progression through similar mechanisms. However, further studies are needed to confirm direct causation in humans.

The team confirmed their discovery through experiments on mice. The mice were fed a high-fat diet to induce obesity. Analysis showed that this diet promoted the growth of precancerous pancreatic lesions. However, when the rodents were also subjected to the stress of social isolation, they developed even more advanced lesions.

Women More Sensitive to Stress and Obesity

The study observed that female mice showed a stronger response to stress-related cancer progression. Researchers hypothesize this may be due to differences in hormone activity, particularly estrogen and beta-adrenergic receptor signaling. However, additional human studies are needed to confirm this effect.

To counteract the impact of stress and obesity-related hormones on pancreatic cancer risk, the researchers suggest that medications targeting beta-adrenergic receptors—such as beta-blockers commonly used for high blood pressure—could be a potential solution. Further studies are needed to explore this possibility.

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FAQs

How do stress and obesity accelerate pancreatic cancer?

They activate biological pathways (PKA and PKD) that promote tumor growth.

Are women more at risk for stress-related pancreatic cancer?

Possibly. Hormonal differences may increase vulnerability, but more human research is needed.

Can beta-blockers help prevent pancreatic cancer?

Maybe. They block stress-related signals, but clinical trials are needed to confirm effectiveness.

Does this study prove stress and obesity cause pancreatic cancer?

No. It shows a correlation, but causation in humans is not yet confirmed.

What’s missing from the study?

Human trials, genetic factors, and other biological pathways need further exploration.

Bottom Line

While the study offers compelling insights, it has several limitations. First, it relies heavily on mouse models, which don’t always translate directly to human biology. Second, it focuses on two specific pathways (PKA and PKD), but cancer is influenced by multiple complex mechanisms—did the researchers overlook other key contributors? Additionally, the study doesn’t account for real-world variables like genetics, diet quality beyond fat intake, or pre-existing conditions. Finally, while beta-blockers show promise, the research doesn’t establish causation between their use and reduced pancreatic cancer risk in humans—are there existing studies on beta-blocker users with cancer outcomes? Addressing these gaps in future research will be essential to validate these findings.

References

Sun, X., Teper, Y., Sinnett-Smith, J., Markarian, M., Hines, O. J., Li, G., Eibl, G., & Rozengurt, E. (2025, March 3). Stress and obesity signaling converge on CREB phosphorylation to promote pancreatic cancer. Molecular Cancer Research, 23(3), 236–249. https://doi.org/10.1158/1541-7786.MCR-24-0785

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