Objective: In the present study we examined the potential association between age, gender, the genetic variant FKBP5 rs9470080 and subjective health complaints. Methods: The data were collected through a three-wave nationally representative survey of 1060 Norwegian employees drawn from the Norwegian Central Employee Register by Statistics Norway. The follow-up period was six months. Subjective health complaints were scored by eight items reflecting; headache, neck pain, mid and low back pain, stomach cramps or intestinal discomfort, problems with sleep onset or maintenance and early morning awakening. Genotyping with regard to FKBP5 rs9470080, previously linked to cortisol sensitivity, was carried out using Taqman assay. Results: The baseline data showed that in women, levels of subjective health complaints were highest among those above 50 years of age. Moreover, in women the rs9470080 CC variant at baseline was associated with higher levels of subjective health complaints. However, the effect size was not large, and no relationships were demonstrated between age or genotype and subjective health complaints in men. Also, the study variables were not related to any changes in the levels of subjective health complaints during the follow-up period. Conclusion: We conclude that our biology such as age and sex, but also single genetic variants found in non-sex chromosomes, may be important in understanding the mechanisms underlying subjective health complaints in the general working population.

Despite most episodes of low back pain (LBP) being short-lasting, some transition into persistent long-lasting problems. Hence, the need for a deeper understanding of the physiological mechanisms of this is pertinent. Therefore, the aims of the present study are (1) to map pain-induced changes in brain activity and blood gene expression associated with persistent LBP, and (2) to explore whether these brain and gene expression signatures show promise as predictive biomarkers for the development of persistent LBP. The participants will be allocated into three different pain groups (no pain, mild short-lasting, or moderate long-term). One in-person visit, where two blood samples will be collected and sent for RNA sequencing, along with resting 64-channel electro-encephalography measurements before, during, and after a cold pressor test, will be conducted. Thereafter, follow-up questionnaires will be distributed at 2 weeks, 3 months, and 6 months. Recruitment will start during the second quarter of 2024, with expected completion by the last quarter of 2024. The results are expected to provide insight into the relationship between central nervous system activity, gene expression profiles, and LBP. If successful, this study has the potential to provide physiological indicators that are sensitive to the transition from mild, short-term LBP to more problematic, long-term LBP.

Objectives: The objective was to develop, internally and externally validate a prognostic model for symptom dissatisfaction, assessed by the patient acceptable symptom state (PASS), for older adults (≥55 years) seeking primary care for a new episode of back pain. Design: Development, internal and external validation of a prognostic model using data from two prospective cohort studies with a 1-year follow-up was conducted. Participants and setting: The Norwegian cohort (n=452) was used for model development and internal validation. External validation was conducted using the Dutch cohort (n=675). Outcome measures and method: The outcome was defined as symptom dissatisfaction based on the PASS at 12 months follow-up. A logistic regression model was developed using backward selection and internally validated using 200 bootstrap samples. External validation included recalibration of the model intercept and slope. Model performance was measured using Nagelkerke-R², area under the curve (AUC) and calibration slope, calibration in-the-large (CITL) and calibration plots. Results: At 12 months, ~55% reported dissatisfaction in both cohorts. The final model included disability, catastrophising, recent back pain episode, spinal rotation pain, baseline symptom satisfaction, symptom duration and recovery expectation as predictors. The internally validated model showed acceptable discrimination (AUC 0.75, 95% CI 0.71 to 0.78), R² was 0.23, the calibration slope and CITL being 0.89 (95% CI 0.73 to 1.08) and 0.01 (95% CI −0.16 to 0.15), respectively. External validation performance after recalibration yielded AUC 0.68 (95% CI 0.65 to 0.70), slope 0.86 (95% CI 0.67 to 1.05) and CITL 0.08 (95% CI −0.01 to 0.16). Conclusions: This prognostic model could be a useful tool for predicting PASS outcomes among older adults with back pain. The external validation results imply that more research is needed to optimise predictions. Trial registration number: NCT04261309.

Previous reports suggest that the progression from subacute to chronic non-specific low back pain (nsLBP) involves functional changes in both the nervous and immune systems. The purpose of the present study was to characterize the gene expression profiles of circulating immune cells that affect the interaction between these two systems when subacute nsLBP turns into chronic nsLBP. Participants aged 18–55 were included based on the presence or duration of LBP, with peripheral blood mononuclear cells collected for RNA sequencing from 20 healthy controls (no nsLBP), 20 subclinical patients (intermittent nsLBP), and 19 chronic patients (long-term nsLBP). The data revealed that chronic nsLBP is linked to a distinct gene expression profile, with 139 uniquely differentially expressed genes (DEGs), differing from those in the subclinical and control groups. Interestingly, comparing chronic and subclinical groups showed minimal overlap in DEGs, indicating a clear inflammatory distinction between subclinical nsLBP and chronic nsLBP. The findings also indicated that patients with chronic nsLBP were different from other individuals regarding axon guidance, indicating neuroplastic changes when intermittent nsLBP turns into chronic nsLBP. Hence, early recognition of the transition from subclinical to chronic nsLBP using RNA profiling may pave the way for more precise therapeutic strategies targeting neuroplastic changes and inflammatory processes.

Objectives: Previous findings suggest that abusive supervision, i.e., subordinates’ perceptions of their supervisor’s behaviours as hostile (excluding physical aggression), may increase the risk of health complaints. In addition, recent data suggest that the FKBP5 genotype rs9470080 important in the regulation of cortisol release, influences the same outcome. Adding to this complexity, different health complaints often co-occur. The present study aimed to (1) uncover patterns of pain complaints and insomnia symptoms by using latent class analysis, (2) determine whether abusive supervision or FKBP5 rs9470080 was associated with these patterns, and (3) examine the interaction between abusive supervision and FKBP5 genotype regarding pain and insomnia symptoms. Methods: The data was collected through a national probability survey of 5,000 employees drawn from the National Central Employee Register by Statistics Norway. Abusive supervision was measured by a 5-item version of the Tepper’s 2000 scale. Pain and insomnia symptoms were measured by 5 items reflecting pain and 3 items reflecting insomnia. The FKBP5 rs9470080 genotyping was carried out using TaqMan assay. Results: A total of 1,226 participants returned the questionnaire and the saliva kit sample. Based on these the latent class analyses revealed four classes based on response patterns of pain and insomnia symptoms. In the regression analysis, abusive supervision was a significant predictor for the response patterns. However, neither the FKBP5 nor the interaction between abusive supervision and FKBP5 showed significant contributions. Conclusions: In conclusion, awareness of the association between abusive supervision and the revealed four pain- and insomnia subgroups, and what separates them, may be important for prognosis and an optimal follow-up for those affected.