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Chronic low back pain (LBP) is among the most prevalent musculoskeletal disorders globally and has significant socioeconomic costs associated with disability, healthcare, and loss of quality of life. Epidemiological data indicate that 7–10% of adults report LBP globally, with lifetime prevalence sometimes reaching 84%1. It is most common in low/middle-income countries, where work-related factors, poor access to health services, and socio-economic inequity increase risk, with prevalence often exceeding 20% among working-age adults2. Adolescents and the elderly, particularly, are more vulnerable to structural and degenerative changes such as intervertebral disc degeneration and osteoporosis3.
LBP is a multifactorial disease influenced by biomechanical, psychosocial, genetic, and nutritional factors, necessitating analytical methods capable of simultaneously capturing the complex interactions among these diverse variables. Recent systematic reviews continue to highlight that the etiology of LBP remains enigmatic, influenced by biomechanical, psychosocial, and genetic factors, and that it is thus difficult to pinpoint with specificity. More than 85% of cases of ‘LBP are nonspecific’ - making the development of targeted prevention and treatment challenging4,5. Although multimodal therapies encompassing a combination of physical and pharmacological methods tend to provide symptomatic relief, many patients remain recurrent, a sign that points to an urgent need for new, preventable, and modifiable risk factors for LBP6.
Traditional statistical methods are limited in addressing this complexity, as they often rely on linear assumptions and fail to adequately model high-dimensional interactions and nonlinear relationships inherent in multifactorial data such as NHANES dietary profiles. In contrast, machine learning approaches offer superior utility by handling large numbers of variables concurrently, detecting subtle patterns and interactions, and providing robust predictions for diseases like LBP where multiple factors converge.
Dietary micronutrients, including vitamins, minerals, and trace elements, are necessary for physiological balance and help reduce the risk of chronic disease. The antioxidant vitamins E (α-tocopherol) and C reduce oxidative damage present in cardiovascular and neurodegenerative diseases7,8. B-complex vitamins, such as thiamine (vitamin B1), pyridoxine (vitamin B6), folate, and cobalamin (vitamin B12), are also immunoregulatory and facilitate cellular energy metabolism; deficiencies of which have been linked to cancer, infertility, and depressed mood9,10,11. Minerals, particularly magnesium, zinc, copper, and selenium, participate in enzymatic and anti-inflammatory pathways that prevent sarcopenia, endometriosis, and postoperative nutritional discharge after bariatric surgery12. Narrative reviews highlight their importance in preventing obesity-related comorbidities and skin conditions such as seborrheic dermatitis and alopecia areata via lipid modulation and immunologic roles13,14. Overall, a signal that the best approach to community health may be adequate micronutrient intake, though interventional trials largely show heterogeneous outcomes based on contextual factors15,16.
Furthermore, machine learning applications incorporating nutritional data have shown efficacy in elucidating risk factors for other musculoskeletal diseases, such as predicting arthritis risk from survey data17 and identifying lifestyle (including dietary) contributors to LBP and related conditions in population-based cohorts18.
Despite a wealth of links between micronutrients and chronic disease, the relationship between micronutrients in food and LBP risk remains poorly defined, and the mechanisms of action are uncertain. While observational studies frequently report deficiencies in vitamin D, magnesium, and antioxidants among individuals with LBP, meta-analyses of supplementation trials—particularly those involving vitamin D—have yielded limited and inconsistent evidence of pain relief19,20.
A systematic examination of existing literature reveals key limitations: reliance on cross-sectional and case-control designs that cannot establish causality21; inadequate control for confounders, including demographics, lifestyle, and comorbidities20,22; small and non-representative samples; variable definitions of micronutrient status and pain outcomes; and a focus on isolated nutrients without considering dietary synergies or antagonisms23. These shortcomings have hindered the development of clear, actionable insights into nutritional modulation of LBP.
For a more explicit hypothesis structure, it is proposed that micronutrients exert protective effects against LBP through a triad of mechanistically linked pathways: antioxidant and anti-inflammatory actions that attenuate oxidative stress and neuroinflammation (vitamins C, E, selenium, zinc, magnesium); support for neural repair and mitigation of homocysteine-induced damage (B-complex vitamins); and enhancement of bone and muscle homeostasis via mineral signaling and vitamin D-mediated calcium regulation (vitamin D, magnesium, calcium). Such a framework highlights the bidirectional interplay between micronutrient status, systemic inflammation, and pain chronicity, as evidenced by associations with pro-inflammatory diets24.
Cross-sectional studies indicate that pro-inflammatory diets lacking micronutrients produce greater levels of abdominal or chronic pain, suggesting a bidirectional association in which a lack of micronutrient inputs aggravates systemic inflammation and pain24.
To address these issues, the developed multiple ML models that incorporate a wide array of diet micronutrients (vitamins (E, A, B1, B6, B12, C, K), minerals (calcium, magnesium, iron, zinc, copper, selenium) and other dietary elements including fiber, polyunsaturated fatty acids, potassium and caffeine) with NHANES data for predicting LBP risk. This ML-based strategy is particularly suited to the multifactorial nature of LBP, as it overcomes the limitations of traditional statistics by modeling complex, nonlinear associations among nutritional and other risk factors simultaneously. This more exhaustive exploration can handle nonlinear associations and provides a robust equation for key LBP predictors. Using SHAP values for global interpretability, they can see how combinations of nutrients affect LBP risk, which opens the door to personalized interventions and nutrigenomic studies.