No association between stress at work and prostate, other cancers

In another article in the British Medical Journal this week, the authors conclude that “work related stress, measured and defined as job strain, at baseline is unlikely to be an important risk factor for colorectal, lung, breast, or prostate cancers” (at least in a large database of Europeans).

The conclusion is based on a meta-analysis of prospective individual participant data from 12 European cohort studies that included 116,056 men and women aged between 17 and 70 years of age, all of whom were free from cancer at study baseline and were followed-up for a median of 12 years.

The full text of this article by Heikkilä et al. is available on line. With respect to prostate cancer specifically, the authors demonstrate, based on the available data, that the hazard ratio (HR) for any association between job strain and a diagnosis of prostate cancer is 0.86 and is not statistically significant.

3 Responses

  1. Though stress may not be considered a risk factor “for the development” of cancers, it certainly becomes a risk factor for those diagnosed with cancer.

    The paper titled “Stress hormones may play new role in speeding up cancer growth” is quite contrary to the conclusions of the British paper, and I tend to side with the conclusions of the researchers from the Institute of Behavioral Health at Ohio State University.

  2. Dear Chuck:

    The paper you refer to addresses a study in cell lines of a relatively rare and aggressive type of cancer (nasopharengeal cancer). As you know, the ability to demonstrate biological effects in the laboratory is by no means the same thing as being able to document a comparable clinical effect in humans. The title of their paper includes that famous word “may”.

    Having said that, having cancer of any type is or at least can be very stressful; stress can impact the efficiency of the immune system; and so it is perfectly reasonable to believe that stress can and does play a role in the progression of cancers in some people (after they know that they have cancer).

    By contrast, the paper above is addressing a very different issue, which is whether stress has a early, and potentially causative, role in the development of cancer (before diagnosis). There is a fine line here, because if people under stress are at risk for sub-optimal immune response to disease (of any type), then are they (hypothetically) at greater risk that their bodies are less able to fight off the very earliest stages of development of specific types of cancer. Heikkilä and her colleagues would probably argue that they have shown that this is not the case in the patients for whom they had data … but then just how “stressed” were the patients in the studies on which their meta-analysis was based?

  3. Seems that this is another example of “more study is needed”. Here is a link to a Forbes article about a study about men already diagnosed who are being treated. Quote from the article:

    ‘ “We are at the very beginning of understanding complex stress-cancer interactions with multifaceted responses to stress that affect cancer cells, tumor microenvironment, and the organism overall,” he said. “We hope that components of this signaling pathway could be used as biomarkers to predict whether and how a given tumor will respond to stress and anti-stress therapies.” ‘

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