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Stress, adverse life events, and risk of pain

PainSci » bibliography » Generaal et al 2015
updated
Tags: etiology, pain, mind, counter-intuitive, pro

Four pages on PainSci cite Generaal 2015: 1. Anxiety & Chronic Pain2. The Complete Guide to Neck Pain & Cricks3. A Rational Guide to Fibromyalgia4. Stress, biology, and pain

PainSci notes on Generaal 2015:

An eyebrow-raiser of a study: it’s a common assumption that stress has biological consequences — like “adrenal fatigue,” say — that drive up the risk of pain later in life, but this study of 2000 Dutch citizens “could not confirm” those biological consequences. Their data affirmed that there’s still a link between having a rough time in life and chronic pain … but this occurs independently of any obvious biological changes. This implies that there is some other mechanism by which stress makes us vulnerable to pain, and the authors suggest that “psychosocial factors play a role in triggering the development of this condition.” In other words, stress may dial up the sensitivity of the brain’s threat-o-meter.

If the study results are reproducible, it’s kind of a big deal. Or the study might have gotten it wrong. 😉

original abstract Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

OBJECTIVES: Dysregulated biological stress systems and adverse life events, independently and in interaction, have been hypothesised to initiate chronic pain. We examine whether (1) function of biological stress systems, (2) adverse life events, and (3) their combination predict the onset of chronic multisite musculoskeletal pain.

METHODS: Subjects (n=2039) of the Netherlands Study of Depression and Anxiety, free from chronic multisite musculoskeletal pain at baseline, were identified using the Chronic Pain Grade Questionnaire and followed up for the onset of chronic multisite musculoskeletal pain over 6 years. Baseline assessment of biological stress systems comprised function of the hypothalamic-pituitary-adrenal axis (1-h cortisol awakening response, evening levels, postdexamethasone levels), the immune system (basal and lipopolysaccharide-stimulated inflammation) and the autonomic nervous system (heart rate, pre-ejection period, SD of the normal-to-normal interval, respiratory sinus arrhythmia). The number of recent adverse life events was assessed at baseline using the List of Threatening Events Questionnaire.

RESULTS: Hypothalamic-pituitary-adrenal axis, immune system and autonomic nervous system functioning was not associated with onset of chronic multisite musculoskeletal pain, either by itself or in interaction with adverse life events. Adverse life events did predict onset of chronic multisite musculoskeletal pain (HR per event=1.14, 95% CI 1.04 to 1.24, p=0.005).

CONCLUSIONS: This longitudinal study could not confirm that dysregulated biological stress systems increase the risk of developing chronic multisite musculoskeletal pain. Adverse life events were a risk factor for the onset of chronic multisite musculoskeletal pain, suggesting that psychosocial factors play a role in triggering the development of this condition.

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