# The Vicious Cycle of Obesity and Low Back Pain: A Comprehensive Review
## 7 Therapeutic Strategies Targeting the Obesity-LBP Connection
### Addressing Obesity as a Pathway to Alleviate LBP
Nevertheless, it is interesting to see that the lack of BMI changes did correspond with the general maintenance of pain scores and the proportion of LBP patients. There was only one study by [PERSON] et al. [220] that was able to directly report a significant correlation between the rate of BMI loss and the alleviation of pain. The direct results are not presented in Table 3, as their findings were reported separately for males and females, and rural- and urban-habituated individuals. The overall lack of BMI changes can likely be explained by two critical features: (i) the general shorter follow-up and intervention duration and (ii) the difficulty of participants to adhere and their compliance to their allocated regimes [219]. As highlighted in the interesting work of [PERSON] et al. [221], adherence to dietary restrictions and other regimes is challenging, in particular through tele-com counselling. Given that obesity often involves complex psychological factors, including an unhealthy relationship with food and self-image, the challenges in adherence are understandable and underscore the need for compassionate and tailored interventions. Additionally, we sought to identify clinical trials investigating the use of pharmacological interventions for managing discogenic LBP in the context of obesity; however, no studies were found testing such approaches directly. There is a rising popularity of agents like Ozempic(r) (i.e., semaglutide), which have shown robust efficacy in promoting weight loss [222]. Semaglutide is a GLP-1 receptor agonist that stimulates insulin secretion, suppresses appetite, and slows gastric emptying. In a randomized controlled trial involving patients with knee osteoarthritis and obesity, once-weekly semaglutide significantly promoted weight loss and led to marked reductions in pain severity [223]. In addition to its metabolic effects, GLP-1 receptor activation has been shown to modulate inflammation and pain pathways by reducing pro-inflammatory cytokine expression, enhancing \(\beta\)-endorphin release, and inhibiting nociceptive signalling within the central nervous system [223; 224]. However, in this trial [223], as with the relationship between obesity and LBP, the interplay between obesity and knee osteoarthritis [225] makes it difficult to fully disentangle weight-dependent effects from direct anti-inflammatory or mental-sate effects. These findings nonetheless suggest that GLP-1 receptor agonists may represent a promising dual-action therapy for obesity-related musculoskeletal pain. In conclusion, it is important to note that the current trials and studies identified are highly heterogeneous and do not uniformly investigate their impact on LBP. Furthermore, the specific sources of back pain were not consistently identified. Only one study, by [PERSON] et al. [110], examined spinal imaging features and reported a significant improvement in disc height with a decrease in overall BMI, suggesting that weight loss can reduce strain on the lumbar region. Additionally, most studies focused solely on recording BMI or weight changes, which can include loss of tissues other than fat. For instance, muscle loss should be avoided, as muscle strength is crucial for maintaining spinal health through supporting the spine and overall posture. We hope that more clinicians and researchers will explore this promising area further, as targeting fat loss represents potentially low-hanging fruit for developing cost-effective methods to alleviate LBP in a significant portion of the LBP patient population. Whether to recommend weight loss for LBP patients remains controversial [43; 219]. While weight loss is generally safe and beneficial for overall health, though its effectiveness in treating LBP remains uncertain.