Sciatica is one of the most common forms of neuropathic pain, typically resulting from compression or inflammation of the lumbosacral nerve roots, often due to intervertebral disk herniation or spinal stenosis (1, 2). It is characterized by radiating pain along the sciatic nerve distribution, frequently accompanied by numbness, muscle weakness, and functional limitations (3). The global prevalence of sciatica ranges between 1.6 and 43%, depending on the population studied and diagnostic criteria used (4). In addition to its high burden on individual patients, sciatica imposes significant societal costs through increased healthcare utilization, reduced work capacity, and long-term disability (5).

While conventional treatments such as nonsteroidal anti-inflammatory drugs (NSAIDs), physical therapy, and epidural steroid injections are widely used, their effectiveness is often suboptimal and recurrence rates remain high (6). This has led to growing interest in identifying modifiable lifestyle factors—particularly those influencing systemic inflammation—that may contribute to the onset, maintenance, or exacerbation of sciatic pain. In this context, diet has emerged as a potential contributor, with accumulating evidence linking unhealthy dietary patterns to increased levels of low-grade systemic inflammation and heightened pain sensitivity (7).

Recent advances in nutritional epidemiology have led to the development of the Dietary Inflammatory Index (DII), a literature-based tool designed to quantify the inflammatory potential of an individual’s diet (8). Higher DII scores reflect a more pro-inflammatory dietary pattern, typically characterized by excessive consumption of saturated fats, refined carbohydrates, and low intake of fiber, antioxidants, and polyunsaturated fatty acids. Numerous studies have demonstrated that high DII scores are positively associated with elevated levels of inflammatory biomarkers such as C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α), all of which play key roles in the pathophysiology of pain and neuroinflammation (9, 10).

Importantly, emerging evidence has linked DII with a variety of pain-related conditions, including rheumatoid arthritis, migraine, fibromyalgia, and chronic low back pain (11–13). Emerging evidence suggests that diet-induced inflammation exacerbates chronic neuropathic pain through neuro-immune mechanisms, including cytokine-mediated sensitization, glial activation, and dysregulation of the gut–spine axis. Pro-inflammatory dietary patterns have been shown to alter the microbiome, increase oxidative stress, and potentiate central sensitization. In parallel, non-pharmacological therapies such as physiotherapy and chiropractic care—which can reduce mechanical and inflammatory drivers of sciatic pain—have demonstrated meaningful benefits, underscoring the need for integrative management approaches (14). Despite these advances, the role of dietary inflammatory potential in sciatica remains largely unexplored, and no study to date has systematically examined its association with pain or disability in this population. Furthermore, current evidence is predominantly observational, highlighting a critical translational gap and the need for randomized dietary interventions. Although the present study focuses on Chinese clinical populations, sciatica and pro-inflammatory dietary patterns are prevalent worldwide, underscoring the global relevance of this work.

We therefore hypothesized that higher Dietary Inflammatory Index scores would be associated with greater pain intensity and functional disability in patients with sciatica, and that systemic inflammation may contribute to—but not fully explain—these associations.

A total of 598 patients with clinically diagnosed sciatica were included in the analysis. The mean age was 55.6 years, and 47.5% were male. The mean BMI was 26.3 kg/m², with 29.0% of participants identified as current smokers and 18.5% diagnosed with type 2 diabetes. Participants were stratified into tertiles based on their DII: low (≤1.43), medium (1.44–2.60), and high (>2.60).

Across the DII tertiles, there was a clear increasing trend in pain severity and disability. The mean VAS increased from 2.5 ± 1.2 in the low-DII group to 3.2 ± 1.1 in the medium-DII group and further to 3.9 ± 1.3 in the high-DII group (p for trend < 0.001). Similarly, the ODI rose from 24.5 ± 8.3 to 31.8 ± 9.0 and 39.8 ± 10.2 across the three groups (p < 0.001). Depression scores were comparable across the three groups, with no significant differences observed between low (7.1 ± 4.1), medium (7.1 ± 4.8), and high (6.7 ± 4.3) DII tertiles (p = 0.624), while sleep quality showed a up trend across DII groups.

Nutritional variables exhibited partially consistent differences across DII tertiles. Energy intake demonstrated a clear upward trend, increasing from 1849.7 ± 359.5 kcal in the low-DII group to 2070.4 ± 336.2 kcal in the medium group and 2404.4 ± 342.3 kcal in the high-DII group (p < 0.001). In contrast, fiber intake decreased progressively from 18.4 ± 5.2 g/day in the low-DII group to 16.8 ± 5.5 g/day in the high-DII group (p = 0.002). However, protein and fat intake showed no consistent linear trend across the tertiles, and changes in iron and vitamin E intake were modest without a clear directional pattern.

Interestingly, no significant differences were found in serum CRP levels across DII tertiles (p = 0.892), despite the marked increase in pain and disability scores. These findings are summarized in Table 1, highlighting that a more pro-inflammatory dietary profile is associated with worse physical, emotional, and behavioral outcomes among patients with sciatica.

This study investigated the association between dietary inflammatory potential, as quantified by the DII, and pain severity and functional disability in patients with sciatica. Our findings demonstrated that a higher DII score was significantly associated with both increased pain intensity and greater functional impairment, even after adjusting for demographic, clinical, and psychological covariates. Furthermore, dose–response analyses revealed nonlinear relationships, indicating that individuals with highly pro-inflammatory diets may be disproportionately affected. Mediation analysis further suggested that systemic inflammation, as indicated by CRP, partially explains the observed association between DII and pain. These results underscore the potential importance of dietary inflammatory load in the multidimensional experience of sciatica and support the integration of dietary assessment into routine pain management strategies.

Several previous studies have demonstrated that pro-inflammatory dietary patterns, as reflected by higher DII scores, are associated with increased pain symptoms in various chronic conditions, including osteoarthritis, rheumatoid arthritis, and fibromyalgia (15, 16). For example, Shivappa et al. reported that a higher DII was associated with greater osteoarthritis-related knee pain and functional limitation (15). Similarly, a cross-sectional study of 84 women with fibromyalgia found that higher DII scores correlated significantly with increased VAS, disease severity (FIQR), and biochemical markers of inflammation, even after adjusting for confounders (17). However, limited evidence exists regarding the role of DII in neuropathic pain disorders such as sciatica. Our findings contribute novel data in this area, demonstrating that DII is positively associated with both VAS and ODI in patients with sciatica, even after controlling for psychological and metabolic covariates.

Importantly, the observed nonlinear dose–response relationships between DII and both VAS and ODI further emphasize the clinical relevance of dietary inflammation. This curvilinear pattern suggests that small increases in DII may have negligible effects at lower ranges but can lead to disproportionate increases in symptom severity once a certain inflammatory threshold is exceeded. Similar threshold effects of dietary patterns have been observed in Cardiovascular Disease and psychological disorders (18–20), reinforcing the hypothesis that highly pro-inflammatory diets may trigger synergistic interactions with systemic or neurogenic inflammation pathways in vulnerable populations.

Furthermore, our study expands the clinical utility of the DII from being a predictive marker in systemic diseases to a potentially modifiable risk factor in pain-related disability. Unlike many fixed non-modifiable factors such as age or sex, dietary inflammation can be targeted through nutritional interventions, offering a promising avenue for integrative pain management.

The biological plausibility of the relationship between dietary inflammatory potential and pain outcomes in sciatica may be explained through several interrelated pathways. First, pro-inflammatory diets characterized by high intakes of saturated fats, refined carbohydrates, and low levels of antioxidants, fiber, and omega-3 fatty acids are known to promote systemic low-grade inflammation (8, 21). Inflammatory cytokines such as IL-6, TNF-α, and CRP play a pivotal role in the pathogenesis of neuropathic pain. They do so by sensitizing nociceptors at the peripheral level and by facilitating central sensitization in the spinal cord through modulation of synaptic activity and long-term plasticity (22–25).

In our study, the mediating role of CRP in the association between DII and pain severity provides empirical support for inflammation as a key mechanistic link. Prior research suggests that systemic inflammation can intensify pain by disrupting the homeostatic cytokine balance in the spinal cord and dorsal root ganglia, leading to nociceptor sensitization and central sensitization. These immune-neural interactions underscore the importance of inflammatory signaling in chronic pain development and maintenance (26–29). Furthermore, animal models of nerve root compression demonstrate that inflammation contributes to both nociceptive and neuropathic components of pain, partially via the activation of microglia and astrocytes (30, 31).

Another potential pathway involves oxidative stress, which is closely intertwined with inflammation. There is compelling evidence that oxidative stress and neuroinflammation are co-regulated processes, and that antioxidant-rich diets, particularly those with vitamin C, vitamin E, polyphenols, and flavonoids, can attenuate these pathologies. These compounds modulate inflammatory cytokines, reduce reactive oxygen species (ROS), and protect neuronal integrity, providing a potential non-pharmacological avenue for neuroinflammatory condition management (32–34). Conversely, pro-inflammatory diets can promote mitochondrial dysfunction and neuronal injury through increased ROS generation, which may further aggravate sciatic nerve damage and delay recovery.

Moreover, emerging evidence supports a neuro-immune-endocrine interface in chronic pain conditions, where psychological comorbidities such as depression and poor sleep may interact with dietary inflammation to exacerbate symptom burden (35, 36). Although we adjusted for these factors in our models, their potential to modulate inflammatory processes and pain sensitivity suggests that future studies should explore these multidimensional pathways using longitudinal and interventional designs.

These findings highlight the potential role of anti-inflammatory diets in the integrative management of sciatica. Non-pharmacological therapies such as physiotherapy have demonstrated meaningful improvements in VAS and ODI scores and are known to reduce pro-inflammatory cytokines in patients with lumbar radiculopathy (37). These benefits suggest that nutritional strategies aimed at lowering DII may synergize with rehabilitation-based interventions to enhance pain relief and functional recovery. Incorporating dietary assessment and DII-targeted counseling into routine clinical pathways may therefore strengthen multidisciplinary protocols for sciatica management.

This study has several limitations. First, the cross-sectional design does not permit causal inference, and reverse causation is possible—patients experiencing more severe pain may adopt less healthy dietary habits. Second, dietary intake was assessed using an FFQ, which is subject to recall bias despite standardized training and quality control procedures. Third, we measured only CRP as an inflammatory biomarker, which may not fully capture the complexity of systemic and neuroimmune inflammation. Finally, participants were recruited from two hospitals within a single region, which may limit generalizability to other populations with different dietary profiles. Future longitudinal cohorts and randomized controlled trials are needed to determine whether lowering DII can causally improve pain and disability and to evaluate the therapeutic potential of anti-inflammatory dietary interventions in sciatica.

The higher DII scores were strongly associated with increased pain intensity and greater functional disability in patients with sciatica, with effect sizes that were both statistically robust and clinically meaningful. Although CRP did not significantly mediate these associations, the findings point toward broader inflammation-related pathways linking diet and neuropathic pain. As one of the first studies to examine dietary inflammatory potential specifically in sciatica, our results highlight the need for prospective and randomized intervention trials to determine whether reducing DII can improve pain and function and support precision dietary strategies in integrative pain management.