Reduced hypothalamic-pituitary-adrenal axis activity in chronic multi-site musculoskeletal pain : partly masked by depressive and anxiety disorders

Peer reviewedPublisher PD

Biological Stress Systems, Adverse Life Events, and the Improvement of Chronic Multisite Musculoskeletal Pain Across a 6-Year Follow-Up

Peer reviewedPostprin

Insomnia, Sleep Duration, Depressive Symptoms, and the Onset of Chronic Multisite Musculoskeletal Pain

Study objective: The temporal relationships among sleep, depressive symptoms, and pain are unclear. This longitudinal study examines whether insomnia and sleep duration predict the onset of chronic multisite musculoskeletal pain over 6 years and whether this association is mediated by depressive symptoms. Methods: 1860 subjects of the Netherlands Study of Depression and Anxiety, free from chronic multisite musculoskeletal pain at baseline, were followed up for the onset of chronic multisite musculoskeletal pain over 6 years (Chronic Pain Grade Questionnaire). We determined baseline insomnia (Women's Health Initiative Insomnia Rating Scale ≥9) and sleep duration (short: ≤6 hr, normal: 7-9 hr, long: ≥10 hr). Depressive symptoms were assessed at baseline and as a change score over time (Inventory of Depressive Symptomatology). Results: Insomnia (hazard ratio [HR] [95% confidence interval, 95%CI] = 1.60 [1.30-1.96], p < .001) and short sleep duration (HR [95%CI] = 1.52 [1.22-1.90], p < .001) were associated with chronic pain onset. Adding baseline depressive symptoms as a mediator attenuated the associations for insomnia and short sleep with chronic pain onset (∆B = 40% and 26%, respectively). Adding the change score of depressive symptoms further weakened the association for insomnia (∆B = 16%) but not for short sleep. All direct effects for sleep measures with chronic pain onset remained statistically significant (p < .05). Conclusions: This longitudinal study shows that insomnia and short sleep duration are risk factors for developing chronic pain. Depressive symptoms partially mediate the effect for insomnia and short sleep with developing chronic pain

The association between road traffic noise and depressed mood among different ethnic and socioeconomic groups. The HELIUS study

Background: Although there is growing evidence that depressed mood is affected by road traffic noise, previous results are not fully consistent. Furthermore, to our knowledge, no previous research has assessed ethnic and socioeconomic inequalities in the association of noise exposure with depressed mood. Objective: To investigate the association between road traffic noise with depressed mood and to determine to what extent this association varies between ethnic and socioeconomic groups. Method: We investigated cross-sectional data collected between 2011 and 2015 from 23,293 HELIUS participants (18–70 years) living in Amsterdam. Our study included five different ethnic groups (Dutch, Moroccan, Turkish, South-Asian Surinamese and African Surinamese origin). All respondents were linked by their residential postal code to geographic data on road traffic noise levels (24 h noise average in A-weighted decibels [dB(A)]). Noise was categorized into five categories (45–54 dB(A), 55–59 dB(A), 60–64 dB(A), 65–69 dB(A), ≥70 dB(A)) and high noise exposure was defined as noise levels ≥65 dB(A). Depressed mood was defined as a sum-score of ≥10 on the 9-item Patient Health Questionnaire (PHQ-9). Logistic regression was performed to assess the relationship between road traffic noise and depressed mood. Multilevel analyses were used to take into account the clustering of observations within neighbourhoods. Lastly, logistic regression analyses were applied to estimate relative risks for depressed mood per different ethnic and socioeconomic groups exposed to high noise exposure ≥65 dB(A) compared to <65 dB(A). Analyses were adjusted for individual- and neighbourhood-level confounders. Results: Exposure to ≥70 dB(A) compared to the reference group of 45–54 dB(A) showed a significant positive association with depressed mood (OR: 1.65, 95% CI 1.10, 2.48). Participants exposed to 60–64 dB(A) showed a significantly lower odds ratio of 0.82 (95% CI 0.70, 0.97) compared to the reference group. We observed no differences between ethnic groups in the association of high noise exposure ≥65 dB(A) with depressed mood. Regarding socioeconomic groups, results were different for the medium-low educated group and unemployed group only. Conclusion: This study adds new evidence regarding a positive association between high road traffic noise exposure and depressed mood in residential settings. We found no evidence for systematic ethnic or socioeconomic inequalities regarding this association

The brain-derived neurotrophic factor pathway, life stress, and chronic multi-site musculoskeletal pain

INTRODUCTION: Brain-derived neurotrophic factor (BDNF) disturbances and life stress, both independently and in interaction, have been hypothesized to induce chronic pain. We examined whether (a) the BDNF pathway (val(66)met genotype, gene expression, and serum levels), (b) early and recent life stress, and (c) their interaction are associated with the presence and severity of chronic multi-site musculoskeletal pain. METHODS: Cross-sectional data are from 1646 subjects of the Netherlands Study of Depression and Anxiety. The presence and severity of chronic multi-site musculoskeletal pain were determined using the Chronic Pain Grade (CPG) questionnaire. The BDNF val(66)met polymorphism, BDNF gene expression, and BDNF serum levels were measured. Early life stress before the age of 16 was assessed by calculating a childhood trauma index using the Childhood Trauma Interview. Recent life stress was assessed as the number of recent adverse life events using the List of Threatening Events Questionnaire. RESULTS: Compared to val(66)val, BDNF met carriers more often had chronic pain, whereas no differences were found for BDNF gene expression and serum levels. Higher levels of early and recent stress were both associated with the presence and severity of chronic pain (p < 0.001). No interaction effect was found for the BDNF pathway with life stress in the associations with chronic pain presence and severity. CONCLUSIONS: This study suggests that the BDNF gene marks vulnerability for chronic pain. Although life stress did not alter the impact of BDNF on chronic pain, it seems an independent factor in the onset and persistence of chronic pain

A Feasibility Study to Increase Chronic Hepatitis C Virus RNA Testing and Linkage to Care among Clients Attending Homeless Services in Amsterdam, The Netherlands

People who inject drugs (PWID) are disproportionately affected by hepatitis C virus (HCV) infections and are frequently homeless. To improve HCV case finding in these individuals, we examined the feasibility of rapid HCV RNA testing in homeless services in Amsterdam. In 2020, we provided a comprehensive service to homeless facilities, which included workshops on HCV for personnel, a “hepatitis ambassador” at each facility, a rapid, onsite HCV RNA fingerstick test service, and assistance with linkage to care. Risk factors for HCV RNA-positive status were examined using Bayesian logistic regression. Of the 152 participants enrolled, 150 (87% men; median age: 47 years) accepted rapid HCV testing. Seven tested HCV RNA positive (4.7%, 95%CrI = 1.31–8.09; 7/150). Of these, five (71%) were linked to care, of whom four (57%, 4/7) initiated treatment and one (14%, 1/7) delayed treatment due to a drug–drug interaction. Of these four people, two completed treatment (50%), of whom one (25%) achieved sustained virologic response after 12 weeks. HCV RNA-positive individuals were more likely to originate from Eastern Europe (posterior-odds ratio (OR) = 3.59 (95% credible interval (CrI) = 1.27–10.04)) and to inject drugs (ever: posterior-OR = 3.89 (95% CrI = 1.37–11.09); recent: posterior-OR = 3.94 (95% CrI = 1.29–11.71)). We identified HCV RNA-positive individuals and linkage to care was relatively high. Screening in homeless services with rapid testing is feasible and could improve HCV case finding for PWID who do not regularly attend primary care or other harm reduction services for people who use drugs

Exercise interventions for the prevention of depression: a systematic review of meta-analyses

BACKGROUND: Exercise may be a promising target for depression interventions. However, evidence for a beneficial effect of exercise interventions on the prevention of depression differs substantially across different studies. METHODS: A systematic search was performed up to July 2018 using PubMed, Embase, PsycINFO, and Cochrane. Articles were included if a meta-analysis of randomized controlled trials was performed that examined the effect of exercise interventions on the onset of depression or depressive symptoms in the general population. Meta-analyses focusing on treatment of diagnosed depression were excluded. Two authors independently screened the articles and graded the quality of included meta-analyses using AMSTAR 2. RESULTS: Eight meta-analyses were included that showed little overlap in 134 included studies. All meta-analyses reported on depressive symptoms rather than onset of depression. Five of these were rated as moderate quality and three of low quality. Six meta-analyses found significant effects, and two found non-significant effects of exercise interventions in reducing depressive symptoms in children, adolescents, adults and the elderly (effect sizes ranging from - 0.10 to - 0.81). Scarce evidence did not allow to draw conclusions about the role of sex and characteristics of exercise on depression. However, some findings suggest that low intensity exercise was as effective as high intensity exercise. Heterogeneity among primary studies was high, likely caused by differences in study quality and exercise characteristics. CONCLUSIONS: The evidence from this study suggests that exercise interventions have a beneficial effect on depressive symptoms in the general population across a wide age-range

Biological stress systems, adverse life events and the onset of chronic multisite musculoskeletal pain : a 6-year cohort study

Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.Peer reviewedPostprintPostprin