Stress 'helps cancer spread' and 'increases risk of heart attack,', scientists warn

Experiencing occasional bursts of stress is a common part of life - whether it's due to running late for an appointment, going through a job interview, or worrying about a friend. However, persistent long-term stress, which seems to be a constant presence in your life, can significantly impact your overall health.

Studies have consistently linked chronic stress to an increased risk of heart disease and stroke. For instance, a study published in The Lancet in 2017 established a correlation between stress and episodes of cardiovascular disease. Similarly, a 2022 publication revealed that undergoing a major stressful life event could elevate the risk of a first stroke by 17 percent.

While there's no direct evidence indicating that stress directly causes cancer, according to Cancer Research UK, it can exacerbate unhealthy behaviors during stressful periods, potentially raising the risk of developing cancer indirectly.

Recent research has unveiled that stress can exacerbate cancer progression in individuals already battling the disease, shedding light on the underlying mechanisms involved. Xue-Yan He, a former postdoctoral researcher at Cold Spring Harbor Laboratory (CSHL), emphasized the inevitability of stress in cancer patients, highlighting the importance of understanding its effects.

The CSHL team's findings revealed that stress prompts the formation of sticky web-like structures by certain white blood cells known as neutrophils. These structures render body tissues more susceptible to metastasis, the spread of cancer cells from their original site to other parts of the body. This discovery holds promise for developing novel treatment strategies to halt the spread of cancer.

In their study using mice, the CSHL researchers simulated the effects of chronic stress to observe its impact on cancer progression. They observed a significant increase in metastatic lesions in mice exposed to stress, indicating a fourfold rise in metastasis. Stress hormones, specifically glucocorticoids, were found to influence neutrophils, triggering the formation of these metastasis-promoting structures called NETs (neutrophil extracellular traps).

Further experiments confirmed the role of stress in triggering NET formation and subsequent metastasis. Removing neutrophils from mice using antibodies, injecting a NET-disrupting drug, and utilizing mice with neutrophils resistant to glucocorticoids all yielded similar results, halting the development of metastasis in stressed mice.

Moreover, the team discovered that chronic stress-induced NET formation could alter lung tissue, even in mice without cancer, potentially predisposing the tissue to cancer development.

These findings underscore the complex interplay between stress and cancer progression, opening avenues for developing targeted therapies to mitigate the detrimental effects of stress on cancer patients.