This cross-sectional study investigated the association between WWI and chronic pain, revealing a significant positive linear relationship. Subgroup analyses and interaction evaluations showed that this positive correlation remained consistent across most subgroups, including age, gender, physical activity, alcohol consumption, smoking status, and diabetes status, except for race. Furthermore, saturation effect analysis identified an inflection point at WWI 11.88 cm/\(\:\sqrt{\text{k}\text{g}}\). Above this threshold, no significant association with chronic pain was observed.
Chronic pain presents a substantial challenge for individuals with obesity, with reports indicating that obese individuals experience clinically significant pain three times higher than the general population [21]. Studies have shown that across increasing BMI categories, there is an elevated likelihood of reporting daily pain [22]. A meta-analysis suggested that obesity (BMI ≥ 30.0) correlates with higher self-reported pain intensity and pain interference in daily life among adults [23, 24]. Conversely, experiencing pain can exacerbate obesity by promoting sedentary behavior and increasing food intake due to fear of exercise or physical limitations [25].
Obesity contributes to chronic pain through various mechanisms, primarily due to its proinflammatory status. Adipose, metabolically active tissue releases proinflammatory cytokine such as IL-6, TNF, and prostaglandins [26]. These cytokines play a crucial role in sensitizing nociceptors, increasing nociceptive input to the central nervous system, and sustaining sensitization of the nociceptive system [27, 28]. This inflammatory response likely intensifies pain symptoms experienced by individuals with obesity. The second mechanism involves excessive mechanical stress on the skeletal system and joints [8, 29]. Excessive stress on joint tissue may also lead to joint cartilage rupture, triggering local inflammation and pain [7]. Thirdly, obesity can also have psychological effects. Contributing to increased rates of depression, decreased self-esteem, and reduced physical activity levels, all of which can worsen chronic pain [30].
In terms of dietary habits, obesity-related dietary patterns can exacerbate nociceptive stimuli by promoting inflammation and recruiting M1 macrophages that trigger immune responses [31]. Among chronic pain patients receiving long-term opioid therapy, there is a tendency to consume diets high in sugar, fat, sodium, and caffeine, which further aggravates obesity [32]. Therefore, various treatment methods for obesity offer benefits for improving pain outcomes. For example, physical exercise has a positive impact on both weight loss and pain relief [33]. In addition, pain experiences and syndromes ameliorate significantly after weight loss surgery [34].
Traditionally, obesity has been assessed using BMI, but BMI fails to differentiate between fat and muscle mass or distinguish between fat and muscle mass or abdominal visceral fat and peripheral fat [35]. Abdominal visceral fat has distinct metabolic properties and is increasingly recognized as an independent risk factor for medical complications and chronic pain [36, 37]. In chronic pain conditions, abdominal obesity may be critical as visceral fat releases various systemic inflammatory markers implicated in pain pathophysiology [38].
To address this issue, WWI was used to evaluate the relationship between obesity and chronic pain. WWI was designed to reflect the composition of abdominal tissue, significantly positively correlated with abdominal fat mass and negatively correlated with muscle mass and bone mass [39]. It is found that metabolic syndrome is physiologically associated with chronic pain, with abdominal obesity being the strongest predictor of pain over the past three months [40]. Another research suggested that body fat, rather than lean weight, is associated with lower back pain and disability [41]. Our study findings also suggested a positive association between WWI, which better represents abdominal obesity and chronic pain. Meanwhile, evidence has shown a positive correlation between WWI and depression, diabetes, and cognitive function, which were important factors in the weight-pain relationship [42–45].
Subgroup analysis revealed notable differences in the relationship between WWI and chronic pain across racial and gender groups. Non-Hispanic whites and individuals of other racial backgrounds showed a stronger association between WWI and chronic pain compared to non-Hispanic blacks or Mexican Americans, possibly influenced by body size and fat composition differences [46]. Additionally, our analysis highlighted gender disparities in the relationship between WWI and chronic pain, particularly noting a significant threshold effect among females. Studies suggested that gender differences in BMI and pain may be attributed to metabolic factors associated with obesity [47, 48, 40]. Variations in body composition and fat mass distribution likely contribute to these gender differences in the association between WWI and chronic pain.
Our study has several limitations. Firstly, cross-sectional design prevents establishing a causal relationship between WWI and chronic pain. Secondly, chronic pain status was based on self-reported recall, which may introduce recall bias. Further prospective research is necessary to validate our findings and explore causality.