Dietary Inflammatory Index (DII) is Associated with Movement-Evoked Pain Severity in Adults with Chronic Low Back Pain: Sociodemographic Differences.

Chronic low back pain (CLBP) is one of the leading causes of pain and disability in adults in the United States and disproportionately burdens non-Hispanic Black (NHB) individuals and females. Approximately 90% of CLBP cases are of unknown cause, and it is imperative that potential causes be explored. It has been reported that diet quality can influence pain state via diet-induced inflammation. The present study assessed the relationship between Dietary Inflammatory Index (DII) and movement evoked-pain severity in people with CLBP and investigated whether race/sex moderated the relationship between DII and movement-evoked pain. Results revealed no significant differences in DII scores between males and females, or between NHB and non-Hispanic White (NHW) participants. Participant sex significantly modified the relationship between DII and movement-evoked pain severity (P = .0155), such that movement-evoked pain severity was significantly impacted by DII scores in females, but not males. Participant race did not significantly moderate the DII - movement-evoked pain severity relationship. These results suggest that diet-induced inflammation may impact the CLBP experiences of females to a greater degree than males. Further research is needed to determine whether dietary interventions that reduce inflammation improve CLBP outcomes and whether these interventions may be differentially-beneficial based on sex. PERSPECTIVE: This article highlights the impact of diet-induced inflammation in a community-based sample as a whole, as well as stratified in various sociodemographic groups. This work expands our understanding of the influence of diet on pain experience and suggests that modifications to diet may be efficacious treatments for reducing chronic pain.

Epigenome-wide DNA methylation profiling of conditioned pain modulation in individuals with non-specific chronic low back pain.

BACKGROUND: The pathoanatomic cause of chronic low back pain (cLBP) cannot be identified for up to 90% of individuals. However, dysfunctional processing of endogenous nociceptive input, measured as conditioned pain modulation (CPM), has been associated with cLBP and may involve changes in neuronal gene expression. Epigenetic-induced changes such as DNA methylation (DNAm) have been associated with cLBP. METHODS: In the present study, the relationship between CPM and DNAm changes in a sample of community-dwelling adults with nonspecific cLBP (n = 48) and pain-free controls (PFC; n = 50) was examined using reduced representation bisulfite sequencing. Gene ontology (GO) term enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were applied to identify key pathways involved in efficient versus deficient CPM. RESULTS: Based on CPM efficiency, we identified 6006 and 18,305 differentially methylated CpG sites (DMCs) with q values < 0.01 among individuals with cLBP and PFCs, respectively. Most of the DMCs were hypomethylated and annotated to genes of relevance to pain, including OPRM1, ADRB2, CACNA2D3, GNA12, LPL, NAXD, and ASPHD1. In both cLBP and PFC groups, the DMCs annotated genes enriched many GO terms relevant to pain processing, including transcription regulation by RNA polymerase II, nervous system development, generation of neurons, neuron differentiation, and neurogenesis. Both groups also enriched the pathways involved in Rap1-signaling, cancer, and dopaminergic neurogenesis. However, MAPK-Ras signaling pathways were enriched in the cLBP, not the PFC group. CONCLUSIONS: This is the first study to investigate the genome-scale DNA methylation profiles of CPM phenotype in adults with cLBP and PFCs. Based on CPM efficiency, fewer DMC enrichment pathways were unique to the cLBP than the PFCs group. Our results suggest that epigenetically induced modification of neuronal development/differentiation pathways may affect CPM efficiency, suggesting novel potential therapeutic targets for central sensitization. However, CPM efficiency and the experience of nonspecific cLBP may be independent. Further mechanistic studies are required to confirm the relationship between CPM, central sensitization, and nonspecific cLBP.