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Stress, biology, and pain

 •  • by Paul Ingraham
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Weekly nuggets of pain science news and insight, usually 100-300 words, with the occasional longer post. The blog is the “director’s commentary” on the core content of a library of major articles and books about common painful problems and popular treatments. See the blog archives or updates for the whole site.

There’s a widespread assumption about stress, based on all kinds of educating guessing and some hard data (e.g. McBeth et al): we assume that harsh stress has biological consequences which in turn drives up the risk of chronic pain later.

That’s a chain of reasoning with three links: stress > biological consequences > pain. A > B > C. It seems strong.

But here’s an eyebrow-raiser of a new study that “could not confirm” those connections: Generaal et al, 2015. The researchers looked for and failed to confirm “that dysregulated biological stress systems increase the risk of developing chronic multisite musculoskeletal pain.”

And yet they did confirm that “adverse life events” are a risk factor for pain. A causes C (or at least one follows the other). But the B-for-biology middleman may not be required.

If those results are reproducible, it implies that severe stresses might ultimately lead to chronic pain without any obvious biological effects — no endocrine system “burnout” (which is a real thing in itself, see Kakiashvili et al). In other words, the connection might be entirely psychological. For instance, adverse life events may dial up the sensitivity of the brain’s threat-o-meter, which is plausible.

Or the study might have gotten it wrong, of course. Stress might have biological effects these researchers didn’t examine (for instance, functional connectivity in the brain is altered with stress and predicts chronification of pain — hat tip to Tony Ingram for this suggestion).

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