According to findings published in Pain Medicine, sulfated dehydroepiandrosterone (DHEA-S) concentrations in blood serum were reduced among women with chronic pain.
For this study, participants (N=1216) provided blood samples between 6:00 and 8:00 AM following an overnight fast and were surveyed about symptoms of chronic pain.
Of the participants, 57% were women; 43.6% of the men and 44.0% of the women were aged 50 to 64 years; 79.0% of the men and 71.4% of the women were white, and 47.4% of the men and 38.2% of the women had a bachelor’s degree or higher. More of the women – 37% – reported chronic pain than the men, 34%.
Among men, serum DHEA concentrations did not differ on the basis of chronic pain status (4.83 vs 4.79 ng/mL; P =.87), and neither did DHEA-S levels (107.7 vs 110.0 mg/dL; P =.74). Women with chronic pain had DHEA levels of 4.23 ng/mL and DHEA-S levels of 54.6 mg/dL which were significantly lower than women without chronic pain (5.04 ng/mL; P =.002; 68.6 mg/dL; P <.001).
DHEA-S was significantly associated with pain status among women (b, -0.072; 95% CI, -0.127 to -0.017; P =.010) and remained significant after adjusting for medication use, lag time, and symptoms of depression (b, -0.076; 95% CI, -0.132 to -0.021; P =.007). DHEA was not significantly associated with pain status among women (b, -0.038; 95% CI, -0.086 to 0.011; P =.13).
With a continuous linear analysis, number of pain locations (DHEA: b, -0.046; 95% CI, -0.078 to -0.014; P =.0005; DHEA-S: b, -0.059; 95% CI, -0.095 to -0.022; P =.002) and degree of interference (DHEA: b, -0.014; 95% CI, -0.027 to -0.001; P =.034; DHEA-S: b, -0.026; 95% CI, -0.041 to -0.012; P <.001) were significantly associated among women.
Chronic pain explained 29.3% of the variance observed for DHEA among women and 28.9% of the DHEA-S variance. Additional predictors for DHEA among women were age (b, -0.010; P <.001), use of opioid medication (b, -0.149; P <.001), black race (b, -0.094; P =.002), use of lipid-lowering medication (b, -0.067; P =.013), and constipation (b, -0.083; P =.050).
Additional predictors for DHEA-S among were age (b, -0.010; P <.001), black race (b, -0.108; P =.001), use of opioid medication (b, -0.145; P =.002), current use of female hormone (b, -0.083; P =.013), thyroid hormone levels (b, -0.092; P =.014), use of antihypertensive medication (b, -0.066; P =.022), autoimmune disorder (b, -0.228; P =.026), moderate alcohol consumption (b, 0.057; P =.030), and use of antidiabetic medication (b, 0.097; P =.039).
Comparing sexes, the sex-specific coefficients differed significantly (DHEA:b, -0.062; P =.046; DHEA-S: b, -0.073; P =.041).
This study was limited by its cross-sectional design, in which causal relationships could not be tested.
These data indicated that DHEA or DHEA-S may be biomarkers for chronic pain among women. Future studies are needed to determine whether DHEA supplementation could provide an effective pain therapeutic.
Reference
Li R, Chapman BP, Smith SM. Blood dehydroepiandrosterone and dehydroepiandrosterone sulfate as pathophysiological correlates of chronic pain: analyses using a national sample of midlife adults in the United States. Pain Med. 2020;pnaa345. doi:10.1093/pm/pnaa345.