Abstract
BACKGROUND:
Pain sensitization may be one of the mechanisms contributing to chronic low back pain (CLBP).
OBJECTIVE:
To evaluate the association between visceral fat, CLBP, and central sensitization (CS); describe the relationship between low back pain (LBP) intensity and CS; and identify possible correlation between visceral fat and LBP intensity.
METHODS:
Patients with CLBP were divided using their CS inventory (CSI) scores into low- (CSI
RESULTS:
The low-CSI and the high-CSI groups had 47 patients (67.1%; 21 men, 26 women) and 23 patients (32.9%; 11 men and 12 women), respectively. The high-CSI group had a significantly higher mean VAS score (
CONCLUSIONS:
Visceral fat is associated with CLBP, regardless of sex or age, and may be a potential therapeutic target for CLBP with CS.
Background
Low back pain (LBP) is a frequently observed condition and one of the most common physiological issues worldwide [1]. LBP can be caused by a variety of problems in any part of the interconnected network of spinal muscles, bones, discs, nerves, or tendons of the lumbar spine. Some underlying mechanisms of LBP have been elucidated in previous studies using, for example, quantitative magnetic resonance imaging (MRI) of the lumbar spine [2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13]; however, further evidence and association with treatment outcomes remain unclear. Recently, visceral fat has been reported to be associated with musculoskeletal and widespread pain, providing a rationale for future research [14].
Obesity, smoking, lack of exercise, advancing age, lifestyle variables, and comorbid factors including psychological illnesses and various medical conditions have all been identified as risk factors for LBP [15]. Recent meta-analysis research has identified obesity and being overweight as potential risk factors for LBP [16, 17]. However, other reviews and meta-analyses report that weight or body mass index (BMI) were not significant predictors of LBP [18, 19, 20]. The conflicting results regarding the association between obesity and LBP indicate the need for further investigation.
Obesity is commonly associated with large amounts of visceral fat, subcutaneous fat, and abdominal circumference. Among these, visceral fat can induce systemic inflammation [21] and is associated with an increased risk of musculoskeletal and widespread pain [14]. However, there are few reports on the association between visceral fat and chronic LBP (CLBP). Central sensitisation (CS) has recently been recognised as a possible pathophysiological cause of several chronic pain disorders, including CLBP, chronic neck pain, myofascial pain syndrome, fibromyalgia, temporomandibular joint disorder, irritable bowel syndrome, interstitial cystitis, and tension-type headache [22, 23, 24, 25, 26, 27]. These disorders have been classified on the mental-physical health spectrum as psychosomatic, medically unexplained, or arising due to functional or somatic factors [22, 25, 26]. CS involves the increased responsiveness of the central and/or peripheral nervous system circuits [22] and has been associated with the development of CLBP [23, 24], although the association between CLBP and CS remains unknown. Since the association between symptoms and imaging results has been consistently weak in patients with CLBP [28], there is a need for further investigation of contributing and underlying mechanisms, such as CS. Recent studies have suggested that CS is improved after weight loss following bariatric surgery [29, 30], which indicates an association between obesity and CS. Thus, we hypothesised that visceral fat may be associated with both CS and pain intensity in patients with CLBP.
This study aimed to determine whether there are differences according to a CS inventory (CSI) in individuals with CLBP; in LBP intensity and the amount of visceral fat area, subcutaneous fat area, and abdominal circumference.
Methods
The Institutional Review Board of Sapporo Medical University approved this study (IRB approval no. 302-1203). All participants were provided with written and verbal explanations of the study, and their consent was obtained prior to participation.
Participants
This study initially included all patients with lumbar spinal stenosis (aged 41–79 years) who had CLBP for at least 3 months. All patients had intermittent claudication with lower extremity symptoms of cauda equina syndrome. The exclusion criteria were as follows: (i) systemic inflammatory disease, (ii) prior spine surgery, (iii) neoplasm, infection, or acute trauma, and (iv) complications of fibromyalgia.
After applying the exclusion criteria, 70 patients were enrolled in the study (32 men, 38 women; mean age: 61.2
Central sensitization evaluation
The CSI measures the extent to which an individual’s symptoms are likely attributable to CS [33, 34]. Part A was used, which has 25 symptom-related items scored on a Likert scale (0–4 for each item; total score range of 0–100). Part B was used to identify patients with concurrent fibromyalgia. The CSI has been established as valid and reliable [33] with test-retest reliability of 0.82, Cronbach’s alpha of 0.88, sensitivity of 81%, and specificity of 75% [34]. The CSI has also been translated into Japanese and validated [35]. Neblett et al. [34] investigated patients referred to a multidisciplinary pain centre, which specialises in the assessment and treatment of chronic pain, including central sensitivity syndromes (CSSs) such as fibromyalgia, chronic fatigue, and irritable bowel, for which CS may be a common aetiology. A receiver operating characteristic analysis determined that a CSI score of 40 out of 100 best distinguished the CSS patient group from a non-patient comparison sample (area under the curve
Computed tomography imaging
Cross-sectional areas of the visceral and subcutaneous fat were calculated semiautomatically using tissue-specific attenuation thresholds including adipose tissue (
Abdominal CT images showing fat measurements (red: visceral fat; green: subcutaneous fat) in patients with low-CSI scores (a) and high-CSI scores (b). CT, computed tomography; CSI, central sensitisation inventory.
The difference in men and women was analysed using the chi-square test. Differences among the groups regarding age, BMI, and VAS scores were compared using the Mann-Whitney U test. Analysis of covariance (ANCOVA) was used to compare the CT measurements between the low- and high-CSI groups adjusted for age and sex. Multiple linear regression analysis adjusted for age and sex was performed for the VAS and CT measurements in the low- and high-CSI groups. All statistical analyses were performed using SPSS (version 27.0; IBM Corp., Armonk, NY, USA). Differences were considered statistically significant at
Patient demographic data with regard to the sex, age, BMI, and VAS in the low- and high-CSI groups
Patient demographic data with regard to the sex, age, BMI, and VAS in the low- and high-CSI groups
Data are expressed as the mean
As shown in Table 1, the low-CSI group had 47 patients (67.1%; 21 men, 26 women), and the high-CSI group had 23 patients (32.9%; 11 men, 12 women). The difference in mean BMI between the two groups was not statistically significant (
Comparisons of CT measurements in the low- and high-CSI groups using analysis of covariance adjusted for age and sex
Comparisons of CT measurements in the low- and high-CSI groups using analysis of covariance adjusted for age and sex
Data are expressed as the estimated mean
Multiple linear regression analysis adjusted for age and sex with VAS as the dependent variable
VAS: visual analog scale, CSI: central sensitization inventory.
This study aimed to determine whether there are differences in LBP intensity and the amount of visceral fat area, subcutaneous fat area, and abdominal circumference according to CSI score in individuals with CLBP. We hypothesized that visceral fat may be associated with both CS and pain intensity in patients with CLBP. Our results confirm the hypothesis since the high-CSI group had significantly higher visceral fat than the low-CSI group and a moderate positive correlation was found between VAS score and visceral fat in the high-CSI group.
In the present study, the prevalence of high-CSI was 32.9% (high-CSI,
There were two important findings concerning the VAS score in this study. First, the high-CSI group had significantly higher VAS scores than the low-CSI group, suggesting that high-CSI patients had more severe LBP. In a previous report, severity based on CSI score was significantly related to other types of pain intensity, pain-related anxiety, depressive symptoms, somatisation symptoms, perceived disability, and sleep disturbance [41]. Patients with CLBP experienced more severe pain at equal pressure levels, and functional MRIs revealed more widespread patterns of neuronal activation in pain-related cortical areas [44]. Mibu et al. [43] found that patients with CLBP showed more pronounced CS-related symptoms than patients with knee osteoarthritis, and the CSI scores in patients with CLBP were associated with pain-related disability and health-related quality of life. In addition, there was a correlation between pain intensity and CSI scores in patients with CLBP. These previous findings support our results and suggest that CS, as diagnosed by the CSI, is involved in CLBP pain pathology, thus implying a relationship between LBP intensity and CS. Second, the visceral fat area had a significant positive correlation with the VAS score only in the high-CSI group. Previously, Li et al. [14] found that visceral fat was associated with knee pain, suggesting that the inflammatory environment created by the accumulation of visceral fat may aggravate pain independent of the loading effect of weight. Tarabeih et al. [45] showed the positive correlation between the visceral fat-derived serine protease inhibitor (vaspin) and LBP disability scores (odds ratio, 1.33; 95% CI, 1.07–1.64) with the multiple logistic regression analyses. Tanaka et al. [46] categorized Japanese males aged between 35 and 59 years into four groups according to the amount of visceral fat (high vs. low) and trunk skeletal muscle (high vs. low) and showed that individuals with the combination of high visceral fat and low trunk skeletal muscle had a significantly higher prevalence of LBP which caused an increase in intramuscular adipose tissue. These findings showed that CLBP should be included in the list of diseases associated with visceral fat accumulation; however, the association with CS was not mentioned in the study. To our knowledge, no previous studies have analysed the association of visceral fat and CS, which may contribute to LBP intensity. Thus, we believe our study may provide new insights into the cause of CLBP.
In a previous study using CSI score as a treatment outcome, Neblett et al. [41] reported that the percentage of patients in the high-CSI group decreased from 67% to 40% after a functional restoration treatment program, which included a quantitatively directed and medically supervised exercise process, as well as a multimodal psychosocial disability management component. The study concluded that CSI may have important clinical utility, both for screening and as an outcome measure for treatment results in patients with chronic spinal pain disorder.
Stefanik et al. [29] showed that patients with obesity and overweight who underwent bariatric surgery experienced an improvement in CS symptoms. Tanaka et al. [46] reported that preventing visceral fat accumulation and trunk skeletal muscle loss are important methods of intervention for CLBP. However, there is currently no evidence that decreasing visceral fat improves CS. We believe that our findings provide evidence for targeting visceral fat reduction as a treatment for CLBP with CS.
Our results also show that BMI was not significantly different between the low- and high-CSI groups. Similarly, there was no evidence of BMI with CS involvement. However, even among patients with similar BMIs, visceral and subcutaneous fat distribution may vary [48]. Abdominal circumference had a stronger correlation with the subcutaneous fat area than with the visceral fat area, suggesting that abdominal circumference is predominantly an index of the subcutaneous fat area [49]. Visceral fat might be specifically associated with CLBP and CS, unlike BMI, subcutaneous fat, and abdominal circumference. We believe that our results reveal an unexplored topic for future research on CS, visceral fat, and CLBP.
This study has some limitations. First, the sample size was small. Power analysis using G*Power 3.1 required 37 patients per group to obtain a sufficient power of approximately 0.8, an effect size of 0.33 (squared multiple correlation of 0.25), three predictors, and an error probability of 0.05. Therefore, the number of patients in the high-CSI group was insufficient for robust statistical analysis, and thus, a larger number of cases is needed in future studies. Second, the cross-sectional study design has limitations regarding the timing of the association between visceral fat accumulation and CLBP onset. Future longitudinal studies are needed to confirm whether the visceral fat is associated with CLBP in patients with lumbar spinal stenosis and CS using CT myelography as well as plain CT or abdominal MRI. Third, the CSI is a self-reported inventory and therefore cannot be physiologically equated with central nervous system sensitivity changes. The best measure of the physiological changes is quantitative sensory testing which may be an avenue for future research. Moreover, CSI scores of
Conclusion
This study evaluated the association of visceral fat with CLBP according to CS severity, analyzed the relationship between LBP intensity and CS, and identified possible correlations between visceral fat and LBP intensity. Patients in the high-CSI group had significantly higher visceral fat and VAS scores (i.e., more severe LBP intensity) than those in the low-CSI group. Moreover, the visceral fat area had a moderately positive correlation with VAS scores among patients with high-CSI scores. Thus, visceral fat is associated with CLBP according to CS severity. We believe that these results elucidate one of the causes of CLBP, as well as provide evidence that visceral fat should be a therapeutic target for CLBP with CS.
Footnotes
Acknowledgments
The authors have no acknowledgments.
Conflict of interest
The authors declare that they have no conflict of interest.
