Adverse Childhood Experiences and Chronic Low Back Pain in Adulthood: The Role of Emotion Regulation.

Chronic low back pain (cLBP) is characterized by biopsychosocial determinants that collectively result in a substantial burden at the individual, community, and health care system levels. A growing body of literature suggests that childhood adversity is longitudinally associated with the development and maintenance of various chronic pain conditions in adulthood. Little research has investigated the psychological processes that might underlie the association between adverse childhood experiences (ACEs) and cLBP. Emotion regulation comprises a substantive part of the subjective experience of pain and may be a potential mechanism through which ACEs contribute to cLBP etiology and maintenance. Thus, the current study examined the extent to which emotion dysregulation mediated the relationship between ACEs and pain severity (pain at rest and movement-evoked pain) in adults with cLBP. Participants included 183 adults (53.0% female, 62.5% non-Hispanic Black) between the ages of 18 and 85 with cLBP. Participants self-reported on ACEs, pain, difficulties in emotion regulation (DER), depression, and completed brief physical function tasks. In data analytic models, sociodemographic variables were included as covariates. Analyses revealed that emotion regulation mediated the relationship between ACEs and cLBP severity at rest (indirect effect = .15 [95% CI {.06-.25}]) and with movement (indirect effect = 1.50 [95% CI {.69-2.57}]). Findings suggest ACEs are linked to cLBP severity in adulthood through DER. This aligns with research demonstrating that childhood maltreatment can lead to DER, which perpetuate over the lifespan to impact adult health outcomes. PERSPECTIVE: This study presents emotion dysregulation as a psychological pathway through which childhood adversity may contribute to cLBP in adulthood. This work may bolster our understanding of social experiences as risk factors for chronic pain, while identifying targets for clinical intervention. TRIAL REGISTRATION: This study utilized baseline data collected as part of a parent trial titled "Examining Racial and SocioEconomic Disparities in Chronic Low Back Pain" (ClinicalTrials.gov ID: NCT03338192).

Race-specific associations: inflammatory mediators and chronic low back pain.

ABSTRACT: Chronic low back pain (cLBP) is a global health crisis that disproportionately burdens non-Hispanic Black (NHB) individuals, compared with those who identify as non-Hispanic White (NHW). Despite the growing personal and societal impact of cLBP, its biological underpinnings remain poorly understood. To elucidate the biological factors that underlie the racial disparities in cLBP, this study sought to determine whether inflammatory mediators associated with pain interference (PI), pain at rest (PAR), and movement-evoked pain (MEP) differ as a function of racial identity. Blood samples were collected from 156 individuals with cLBP (n = 98 NHB participants, n = 58 NHW participants). Enzyme-linked immunosorbent assay and multiplex assays were used to quantify concentrations of proinflammatory (fibrinogen, C-reactive protein [CRP], serum amyloid A, tumor necrosis factor α [TNF-α], and interleukin [IL]-1α, IL-1ß, and IL-6) and anti-inflammatory markers (IL-4 and IL-13). Spearman rho correlations were used to assess associations among markers of inflammation and PI, PAR, and MEP using the Brief Pain Inventory-Short Form. Analyses revealed that for NHW patients, CRP, serum amyloid A, and IL-6 were positively associated with cLBP outcomes and IL-4 was inversely associated with PAR and MEP. However, for NHB patients, only IL-1α was positively associated with PAR. Our findings suggest that, while there are associations between inflammation and cLBP outcomes, the biomarkers that underlie the inflammation could very well differ as a function of racialized minority group. However, more research with racially inclusive samples is needed to elucidate the mechanisms that may contribute to racial disparities in cLBP.

The Pace of Biological Aging Predicts Nonspecific Chronic Low Back Pain Severity.

This study aimed to determine if and how the pace of biological aging was associated with nonspecific chronic low back pain (cLBP) and compare what measure of epigenetic age acceleration most strongly predicts cLBP outcomes. We used the Dunedin Pace of Aging from the Epigenome (DunedinPACE), Horvath's, Hannum's, and PhenoAge clocks to determine the pace of biological aging in 69 cLBP, and 49 pain-free controls (PFCs) adults, ages 18 to 85 years. On average, participants with cLBP had higher DunedinPACE (P < .001) but lower Horvath (P = .04) and Hannum (P = .02) accelerated epigenetic age than PFCs. There was no significant difference in PhenoAge acceleration between the cLBP and PFC groups (P = .97). DunedinPACE had the largest effect size (Cohen's d = .78) on group differences. In univariate regressions, a unit increase in DunedinPACE score was associated with 265.98 times higher odds of cLBP than the PFC group (P < .001). After controlling for sex, race, and body mass index (BMI), the odds ratio of cLBP to PFC group was 149.62 (P < .001). Furthermore, among participants with cLBP, DunedinPACE scores positively correlated with pain severity (rs = .385, P = .001) and interference (rs = .338, P = .005). Epigenetic age acceleration from Horvath, Hannum, and PhenoAge clocks were not significant predictors of cLBP. The odds of a faster pace of biological aging are higher among adults with cLBP, and this was associated with greater pain severity and disability. Future interventions to slow the pace of biological aging may improve cLBP outcomes. PERSPECTIVE: Accelerated epigenetic aging is common among adults with nonspecific cLBP. Higher DunedinPACE scores positively correlate with pain severity and interference, and better predict cLBP than other DNA methylation clocks. Interventions to slow the pace of biological aging may be viable targets for improving pain outcomes.

The pace of biological aging helps explain the association between insomnia and chronic low back pain.

Chronic low back pain (cLBP) is associated with insomnia and advanced age. Emerging evidence suggests that the severity of both sleep disorders (like insomnia) and chronic pain are associated with a faster pace of biological aging. We aimed to determine whether the pace of biological age mediates the relationship between insomnia and the impact of cLBP in a sample of community-dwelling adults ages 19 to 85 years. Participants (49 with no pain, 32 with low-impact pain, and 37 with high-impact pain) completed sociodemographic, pain, insomnia, and short physical performance battery assessments. We calculated the pace of biological aging using DunedinPACE from blood leukocyte DNA. On average, individuals with high-impact cLBP had significantly faster biological aging than those with low-impact and no chronic pain (p < .001). Bivariate associations of DunedinPACE scores with insomnia severity and functional performance were significant at p < .01 (rs = 0.324 and -0.502, respectively). After adjusting for race and sex, the association of insomnia severity and the impact of cLBP was partially mediated by the pace of biological aging (ß = 0.070, p < .001). Also, the association of insomnia severity with functional performance was partially mediated by the pace of biological aging (ß = -0.105, p < .001). Thus, insomnia remains strongly predictive of cLBP outcomes, and the pace of biological aging helps explain this association. Future prospective studies with repeated assessments are needed to uncover the directionality of these complex relationships and ultimately develop interventions to manage cLBP.

The Negative Effect of Social Discrimination on Pain Tolerance and the Moderating Role of Pain Catastrophizing.

This study examined the negative impact of social discrimination on the time to pain tolerance during experimentally induced cold pressor pain among healthy individuals. It was hypothesized that the degree to which one catastrophized about pain would exacerbate the negative impact of a history discriminatory experiences on pain tolerance, and that this interaction would be different between individuals of a racial and ethnic minority and non-Hispanic white individuals (thus testing catastrophizing as a moderated moderator). Higher levels of discrimination were positively related to catastrophic thinking about pain, and there was a significant negative relationship between the level of experienced discrimination and time to pain tolerance. Pain catastrophizing emerged as a significant moderator in that when pain catastrophizing levels were high, there was no association between social discrimination and pain tolerance. A history of social discrimination was significantly associated with reduced pain tolerance at low and moderate levels of pain catastrophizing. Racial minority status did not significantly alter this moderating relationship. Implications for the importance of assessing sociocultural variables, such as experiencing social discrimination in the clinical assessment of the individual with pain are outlined.

Racial Differences in 25-Hydroxy Vitamin D and Self-Reported Pain Severity in a Sample of Individuals Living with Non-Specific Chronic Low Back Pain.

Introduction: Considerable evidence suggests that there are significant ethnic/racial differences in the experience of pain among individuals suffering from chronic musculoskeletal conditions. Additionally, low levels of vitamin D have been associated with pain severity. Further, vitamin D deficiency is more prevalent in Non-Hispanic Black (NHB) individuals compared to Non-Hispanic Whites (NHW). Objective: The aim of this study was to investigate the associations among race, pain severity, and serum levels of vitamin D in a sample of patients with chronic low back pain (cLBP). Methods: All study participants (n = 155) self-identified their race/ethnicity as either NHB or NHW. Blood samples were collected to assess circulating levels of serum 25- hydroxy vitamin D. Vitamin D levels were categorized as optimal (≥20 ng/mL), insufficient (12-19 ng/mL) or deficient (<12 ng/mL). Participants then self-reported their pain severity using the Brief Pain Inventory - Short Form. Results: Results showed that a greater proportion of NHB versus NHW participants were categorized as Vitamin D deficient (χ 2 (2, N = 155) = 16.79, p < 0.001). An analysis of covariance (ANCOVA) revealed that NHBs reported significantly greater pain severity relative to NHWs (F(1150) = 6.45) p = 0.012. Further, self-reported pain severity significantly differed according to Vitamin D clinical categories (F(2150) = 4.19, p = 0.013). Participants with deficient vitamin D reported significantly greater pain severity in comparison to participants with optimal vitamin D (F(1101) = 7.28, p = 0.008). Conclusion: The findings suggest that Vitamin D deficiency may be linked to greater pain severity in a sample of individuals with cLBP, especially for those who identify as NHB.

An improved model of type 2 diabetes with effects on glucose tolerance, neuropathy and retinopathy with and without obesity.

RATIONALE: Type 2 diabetes (T2D) costs billions of dollars annually, is also associated with pain (diabetic neuropathy), as well as retinopathy, lower urinary tract/urinary bladder dysfunction, depression, and systemic inflammation, affecting quality of life for patients. To that end, animal models are utilized to explore potential treatments, but may not reflect the complexity of the condition. OBJECTIVE: We aimed to test an improved model of T2D that more closely mimics the clinical mechanisms and symptoms in an outbred strain of mouse. FINDINGS: Male and female CD-1 mice (n = 72) were fed one of four diets: regular chow (REG), our Standard American Diet (SAD), a revised SAD (SAD2), or the commonly-used high-fat diet (HFD). Overall, HFD- and SAD-fed mice had significant weight gain and increased fat mass. Following injury, the SAD- and SAD2-fed mice showed protracted recovery, but the HFD-fed mice did not. Similarly, SAD- and SAD2-fed mice showed impaired retinal function compared to REG-fed mice, but the HFD-fed mice did not. CONCLUSIONS: The SAD and SAD2 more closely model the problematic dietary intake and subsequent clinical symptoms associated with T2D. POTENTIAL IMPACT OF STUDY: The adjusted SAD2 may be a better representation of a human-translatable diet than the SAD and HFD, and may allow for increased advances in the investigation of T2D-related symptoms.