# The Vicious Cycle of Obesity and Low Back Pain: A Comprehensive Review
## 5 The Biomechanical Impact of Obesity on the Spine  
Overweight and obesity have long been recognized as major contributors to IDD and disogenic LBP, primarily due to the biomechanical overloading they place on the IVDs and spinal structures, particularly in the lumbar spine [3; 6]. Studies indicate that individuals with excess weight have a significantly higher risk of developing chronic LBP, surpassing the influence of age and sex [107]. Furthermore, obesity increases the likelihood of developing IDD by up to 1.8 times [108], and raises the risk of lumbar disc herninations that may require surgical intervention [30]. Notably, weight loss after bariatric surgery has been suggested to improve LBP intensity and related disability [109], as well as L4-L5 disc height [110]. The biomechanical factors associated with increased IDD in overweight and obese individuals are related to a combination of the following factors: (1) overloading that exceeds the strength threshold of IVD tissues, (2) spinal joint instability caused by hypermobility under increased loads, and (3) cyclic loading under repetitive conditions exceeding the inherent tissue healing capacity [111]. Importantly, not only BMI, but also body shape and fat distribution may differentially affect spinal loading. Central obesity, characterized by accumulation of abdominal fat and a higher waist-to-hip ratio, is particularly associated with greater spinal forces, possibly causing damage to the IVDs and vertebrae [111]. These observations were confirmed by a recent meta-analysis, which showed that waist circumference and waist-to-hip ratio were associated with an increased risk of chronic LBP [112]. Obesity-related postural changes also affect spinal biomechanics. A recent study by [PERSON] et al. [113] demonstrated that adults with obesity are characterized by increased thoracic kyphosis and decreased thoracic and lumbar flexion-extension ROM, a pattern previously noted in obese children and adolescents with and without idiopathic scoliosis [114]. On the other hand, reduced spine mobility in obese individuals may be attributed to several factors, including the increased soft tissue mass and more severe osteoarthritic changes. In a cadaveric study, [PERSON] and coauthors [115] found that L4-L5 specimens from obese subjects exhibited greater facet joint degeneration and a higher prevalence of disc herninations. Additionally, a negative correlation between BMI and both flexion-extension ROM and axial compressive stiffness was noted, although significant only in female specimens [115]. Apart from postural features, overweight status has been shown to also impact dynamic activities. A finite-element study demonstrated that obese individuals experience around 40% higher compression and shear stress at the L5-S1 level during lifting activities, independent of hand position [116]. This finding implies that even postural adjustments (e.g., use of braces) may not effectively counterbalance the increased spinal loads in obese individuals [116]. Increased segmental overloading in distal lumbar segments has also been confirmed in vivo. In a recent study, [PERSON] et al. [117] compared lumbar IVD deformation before and after treadmill walking. Intriguingly, the authors demonstrated that post-exercise magnetic resonance imaging (MRI) showed that increasing BMI was associated with significantly higher strain in the L5-S1 disc. Increased IDD in overweight and obese individuals may also be partly attributed to poor PSM quality due to fatty infiltration, as mentioned above. In physiological conditions,PSMs are essential for a balanced load distribution across the spine and proper postural control. Therefore, muscle imbalances and/or a reduction in functional muscle mass (e.g., loss of fibres due to atrophy or fatty substitution) diminish the net capacity of the muscle tissues to stabilize the spine and resist displacement forces [118].