Search

Purpose: Childhood lead exposure is linked to poorer neurobehavioral function in adolescence, but the relationship between lead and adolescent sleep health remains inconsistent. This study aimed to investigate concurrent and longitudinal associations between lead exposure and multiple sleep health domains in adolescents. Methods: A total of 972 adolescents from China Jintan Child Cohort were included in analyses. The Blood lead levels (BLLs) were assessed in two Waves, at ages 3–5 years (mean 6.50 ± 2.76 μg/dL) and 11–13 years (mean 3.12 ± 1.17 μg/dL). Sleep problems at age 11–13 were parent-reported via the Child Sleep Health Questionnaire (CSHQ) and self-reported by adolescents using the Pittsburgh Sleep Quality Index (PSQI). Results: Both early and later BLLs were associated positively with parental reported sleep problems, including sleep onset delay, night waking, short duration, parasomnias, and disordered breathing. Sex-stratified analyzes showed that most adjusted associations between two-Wave BLLs and sleep outcomes (CSHQ and PSQI) remained statistically significant in males, with a minor increase in the magnitude of these associations. The association between Wave II BLLs and shorter self-reported sleep duration was only statistically significant in female adolescents. Compared to children with consistently low BLLs at both ages, those with persistently high BLLs at both ages had significantly shorter parental-reported sleep duration and worse sleep onset delay. Conclusion: Findings suggest that both early and later childhood lead exposures link to more adolescent sleep problems, with recent BLLs showing stronger associations with poor adolescent sleep health reported by their parents. [ABSTRACT FROM AUTHOR]

Introduction: The degree to which opioid-induced hyperalgesia contributes to the pain experience of patients with chronic pain remains relatively undescribed. The objective of this pilot study was to determine if experimental pain responses improve in patients with chronic pain as they undergo a planned opioid taper. Methods: This was a prospective observational study. Seven patients with chronic neuropathic pain on at least 120 mg morphine equivalents/day were enrolled. The participants were followed over the course of an individualized opioid taper to a lower dose. Measures of experimental pain sensitivity, including indicators of central pain modulation, were collected on a biweekly basis; in addition, measures of function and quality of life were collected monthly. The effect of opioid taper on pain responses and functional outcomes over time were examined using longitudinal mixed-effects regression modeling and general linear regression modeling with regularization as a function of baseline dose, end dose, and taper rate. Results: In this small sample of patients undergoing highly individualized and variable opioid taper, the opioid taper was significantly associated with improved pain responses to the cold-pressor test, with the pain threshold on average increasing by 1.14 s every 6 weeks (p = 0.0084, 95% confidence interval [CI] for 6-week change 0.3039–2.0178) and pain tolerance on average increasing by 2.87 s every 6 weeks (p = 0.0026, 95% CI for 6-week change 1.02–4.7277). Taper-related changes in central pain modulation were not observed, although conditioned modulation trended toward improvement by the completion of opioid taper. Similarly, no declines in function and quality of life were observed with the opioid taper, suggesting stability despite decreased opioid dose. Conclusions: Opioid taper was associated with improvements in experimental pain responses without a decline in function and quality of life, suggestive of diminished opioid-induced hyperalgesia in this clinical sample. Trial Registration: ClinicalTrials.gov identifier, NCT03912298. [ABSTRACT FROM AUTHOR]