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HPA axis dysfunction and chronic pain risk

PainSci » bibliography » McBeth et al 2007
Tags: etiology, chronic pain, mind, psychology, pro, pain problems

One article on PainSci cites McBeth 2007: Anxiety & Chronic Pain

PainSci notes on McBeth 2007:

This unusual study showed that dysfunction of the hypothalamic–pituitary–adrenal (HPA) axis helps to distinguish those who will and will not develop new-onset chronic widespread pain. Many studies have shown that people with chronic widespread pain (CWP) show biological evidence of stress (hypercortisolic states), but such studies have generally been

unable to determine whether the observed HPA axis alterations preceded or were a consequence of having CWP. Neither did they account for the effects of anxiety, depression, life stresses, and sleep disturbance, all of which are associated with HPA axis dysfunction and may explain the observed relationship. The only way to establish the nature of the relationship is to conduct a prospective cohort study in which subjects who are free of CWP but are at risk of developing CWP are identified, their HPA axis function assessed, and their courses are followed over time in order to establish who develops pain. We conducted the first such study to test the hypothesis that among a group of subjects free of CWP, altered HPA function would mediate the relationship between psychosocial risk factors indicative of the process of somatization and the onset of symptoms of CWP. We further hypothesized that this relationship would be independent of the effect of concomitant psychosocial factors that may be confounding the relationship, including depressive symptoms and sleep disturbances.

This study is far from the last word on this topic, but it is intriguing evidence on one side of the debate.

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.

OBJECTIVE: To test the hypothesis that abnormalities in the hypothalamic-pituitary-adrenal (HPA) stress-response system would act as an effect moderator between HPA function and the onset of chronic widespread pain (CWP).

METHODS: We conducted a population-based prospective cohort study. Current pain and psychosocial status were ascertained in 11,000 subjects. Of the 768 eligible subjects free of CWP but at future risk based on their psychosocial profile, 463 were randomly selected, and 267 (57.7%) consented to assessment of their HPA axis function. Diurnal function was measured by assessing levels of salivary cortisol in the morning (9:00 AM) and evening (10:00 PM). Serum cortisol levels were measured after an overnight low-dose (0.25 mg) dexamethasone suppression test and a potentially stressful clinical examination. All subjects were followed up 15 months later to identify cases of new-onset CWP.

RESULTS: A total of 241 subjects (94.9%) completed the followup study, and 28 (11.6%) reported the new onset of CWP. High levels of cortisol post-dexamethasone (odds ratio [OR] 3.53, 95% confidence interval [95% CI] 1.17-10.65), low levels in morning saliva (OR 1.43, 95% CI 0.52-3.94), and high levels in evening saliva (OR 2.32, 95% CI 0.64-8.42) were all associated with CWP. These 3 factors were found to be independent and additive predictors of CWP (OR for all 3 factors 8.5, 95% CI 1.5-47.9) in analyses controlling for age, sex, depression, sleep disturbance, recent traumatic life events, and pain status. One or more of these 3 HPA factors identified 26 (92.9%) cases of new-onset CWP.

CONCLUSION: Among a group of psychologically at-risk subjects, dysfunction of the HPA axis helps to distinguish those who will and will not develop new-onset CWP.

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