Obesity and Osteoporosis

Introduction

Obesity is a well-known major global comorbidity, with a prevalence rising steadily over the last few decades. The most recent global data indicate that in 2021, 2.11 billion adults aged 25 years and older were affected by overweight and obesity, representing 45.1% of the global adult population. Of these, approximately 867 million adults (18.5% of women and 14.0% of men) were living with obesity (1). While obesity is widely recognised for its association with increased morbidity and mortality, including several cancers, type 2 diabetes, cardiovascular disease, and stroke, its impact on skeletal health has become an area of growing interest in the last decade (2).

Effects of obesity on bone density and bone quality

The relationship between obesity and bone health is complex. Individuals with obesity generally exhibit higher bone mineral density (BMD) than non-obese individuals (3). However, this does not translate into higher bone quality or lower fracture risk. Several studies have shown that obesity may impair bone quality, with alterations in microarchitecture and reduced bone formation (4).

Site-specific fracture risk patterns

Obesity influences fracture patterns in a site-specific manner. Patients affected with obesity have a lower risk of osteoporotic fractures at the hip and wrist, attributed to higher BMD from increased mechanical loading and greater estrogen production by adipose tissue, as well as cushioning from soft tissue during falls (5). However, obesity is associated with a higher risk of fractures at the proximal humerus, ankle, and lower leg, due to altered fall biomechanics in obesity (e.g., increased instability, different fall directions), impaired mobility, and greater impact forces due to higher body mass contribute to more frequent and severe trauma at these locations (6).

Beyond BMD: mechanisms underlying obesity-related fractures

Obesity’s effect on fracture risk cannot be explained by BMD alone. Factors such as the amount and distribution of adipose tissue, altered mechanical loading, and changes in fall dynamics all contribute to fracture susceptibility (2). Mobility impairment, poorer muscle quality, and postural instability, particularly in individuals with sarcopenic obesity, further amplify fracture risk at specific anatomical sites. Moreover, bone marrow adipose tissue (BMAT) has recently gained attention as a potential mediator of obesity-related bone fragility. Higher BMAT levels have been associated with adverse effects on bone strength and quality (7). Individuals with obesity and substantial visceral adiposity often exhibit greater BMAT accumulation, and consistent inverse relationships between BMAT and BMD have been reported in this population.

The impact of weight-loss interventions on bone health

Although a range of weight-loss approaches, such as dietary restriction, exercise, bariatric procedures, and GLP-1 receptor agonists, provide important health benefits, they may simultaneously lead to adverse effects on bone, including accelerated bone loss and higher fracture risk (8). The severity of skeletal complications is closely tied to the extent of weight loss and is particularly marked after bariatric procedures with a malabsorptive component (e.g., Roux-en-Y gastric bypass). The European Calcified Tissue Society recommends correcting vitamin D deficiency, ensuring adequate daily calcium and protein intake, and promoting physical activity before and after bariatric surgery to mitigate these risks. GLP-1 receptor agonists induce weight loss but may cause modest reductions in BMD and promote bone remodelling, favouring resorption, similar to calorie restriction. Current data suggest a neutral or slightly negative effect on bone turnover markers and BMD, but no clinically significant increase in fracture risk at approved doses. Preclinical data indicate possible bone-protective effects at higher concentrations, and dual/triple agonists (GLP-1/GIP/glucagon) may have positive effects, but robust human data are lacking (9). The Obesity Society advises that rapid, substantial weight loss (≥14% over 3–4 months) with GLP-1 therapy is associated with significant bone loss, and recommends combining GLP-1s with structured exercise and adequate nutrition to preserve bone and muscle mass.

Conclusion

Obesity is associated with a distinctive skeletal phenotype marked by higher BMD but reduced bone quality, altered fall dynamics, and a characteristic distribution of fracture sites. Because people with obesity typically present with higher BMD values, a smaller proportion of those who fracture meet the traditional densitometric threshold for osteoporosis, making diagnosis and subsequent treatment decisions more challenging. In 2023, new recommendations were introduced to address the particular considerations required for managing and treating osteoporosis in this population. As the use of obesity treatments continues to expand, there is a growing need for strategies that not only optimise weight-loss outcomes but also proactively protect bone health in individuals living with obesity.

Figure 1 – Obesity-specific features of osteoporosis (10)

References

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