Obesity in Axial Spondyloarthritis: what are we missing beyond the scale? Save

Obesity in axial spondyloarthritis (axSpA) is not a minor comorbidity. 

While obesity is more often discussed in psoriatic arthritis (PsA) due to the psoriasis-adipose tissue link which is mechanistically better studied and publicised, the prevalence of obesity in axSpA is comparable to that of PsA. In the Groningen Leeuwarden Axial SpA (GLAS) cohort, 37% of patients were overweight and 22% were obese, roughly 59% above normal weight combined, well above matched general-population rates (1). The EuroSpA collaboration, pooling 14 European registries and nearly 15,000 patients, found almost identical figures with 37% overweight and 21% obese (2). 

Beyond the scale, there are several factors that need to be considered with obesity in axSpA. The first practical problem is the disease activity measurement. Both ASDAS and BASDAI lean heavily on patient-reported pain, stiffness and fatigue. In the GLAS cohort, obesity was independently associated with higher ASDAS, BASDAI, and even CRP, alongside central sensitisation and illness perception. Put together, this explained the 35–47% of the variance in these scores (3). In practice, this means a high composite score in an obese patient may reflect pain burden and functional limitation as much as active inflammation. Before escalating therapy on the strength of a borderline ASDAS and BASDAI, it's worth reviewing whether CRP and imaging correlate with the composite score.

Fatigue is one of the most burdensome symptoms in axSpA, and obstructive sleep apnoea (OSA) is a major, correctable contributor. OSA prevalence is elevated in axSpA compared with the general population (4). The relationship appears bidirectional with intermittent hypoxia and inflammatory pathways (TNF-α, IL-17/IL-23) plausibly interact in both directions. OSA prevalence is not only higher in axSpA cohorts than expected but it has been directly implicated as a cause of otherwise unexplained fatigue in AS. Restricted chest expansion which itself is a feature of more advanced axial disease appears to compound this risk (5).

A validated screening tool that can be used to screen for OSA is  STOP-BANG (score ≥5 = high OSA risk). It considers measurements such as BMI, neck circumference, hypertension. Using this with the Epworth Sleepiness Scale (score >10 = clinically significant daytime sleepiness) can help separate sleep-driven fatigue from disease-driven fatigue. In a patient with obesity, axSpA and disproportionate fatigue it is worth screening for OSA this way, not just BASDAI or ASDAS scoring.

Depression and anxiety are common in axSpA and are linked to both worse disease activity and quality of life. A systematic review and meta-analysis found a pooled prevalence of at least moderate depression around 15% using HADS ≥11, with individual study estimates ranging from 11–64% depending on the tool used. Patients with depression scored significantly higher on BASDAI and ASDAS (6). None of this is obesity-specific, but the overlap matters clinically as obesity, chronic pain, fatigue and mood symptoms occur together. Disentangling which one is driving  the high BASDAI is impossible without asking about all of them.

Two studies now quantify what obesity does to biologic response in axSpA. The Swiss SCQM registry found obese patients had substantially lower odds of achieving ASAS40 response to a first TNF inhibitor at one year than normal-weight patients (adjusted OR 0.27) (7). The EuroSpA analysis of 14 registries confirmed this at scale: overweight and obese patients had 24–47% lower odds of meeting treatment response criteria at 12 months, a dose-dependent relationship that held after adjusting for baseline disease activity and other lifestyle factors (2). Their conclusion is that clinicians should consider referral to weight-management services at the point of starting therapy, not after a biologic appears to have failed.

From a practical point of view, before or shortly after diagnosing axSpA in a patient with obesity, consider screening for inflammatory back pain features on history and not to assume mechanical pain because of raised BMI. The STOP-BANG and Epworth Sleepiness Scale can help differentiate sleep-driven from disease-driven fatigue, with formal sleep study referral if positive. A brief validated mood screen (HADS, PHQ-9/GAD-7) alongside routine disease activity assessment can help identify associated anxiety or depression. Cross-checking ASDAS/BASDAI against CRP and imaging when scores and clinical impression diverge will be important to avoid unnecessary escalation of biologic therapy. Counselling on the likely impact of obesity on TNFi response before starting therapy, with a weight-management referral offered proactively ensures a holistic approach to care. None of this replaces treating the underlying inflammatory disease but axSpA management built purely around escalating biologics without addressing what obesity is doing to both the disease and our ability to measure it may lead us to miss out beyond the scale.

References

1. Maas F, Arends S, van der Veer E, Wink F, Efde M, Bootsma H, et al. Obesity is common in axial spondyloarthritis and is associated with poor clinical outcome. The Journal of Rheumatology. 2016;43(2):383-7.

2. Jones GT, Rotariu O, MacDonald R, Michelsen B, Glintborg B, van der Horst-Bruinsma I, et al. The relationship between lifestyle factors and outcome of treatment with TNFα inhibitors in axial spondyloarthritis – results from 14 European countries. BMC Rheumatology. 2025;9:88.

3. Kieskamp SC, Paap D, Carbo MJG, Wink F, Bos R, Bootsma H, et al. Central sensitization, illness perception and obesity should be considered when interpreting disease activity in axial spondyloarthritis. Rheumatology (Oxford). 2021;60(10):4476-85.

4. Erb N, Karokis D, Delamere JP, Cushley MJ, Kitas GD. Obstructive sleep apnoea as a cause of fatigue in ankylosing spondylitis. Annals of Rheumatic Diseases. 2003;62(2):183-4.

5. Wiginder A, Sahlin-Ingridsson C, Geijer M, Blomberg A, Franklin KA, Forsblad-d'Elia H. Prevalence and factors related to sleep apnoea in ankylosing spondylitis. Clinical Rheumatology. 2022;41(2):491-8.

6. Zhao S, Thong D, Miller N, Duffield SJ, Hughes DM, Chadwick L, et al. The prevalence of depression in axial spondyloarthritis and its association with disease activity: a systematic review and meta-analysis. Arthritis Res Ther. 2018;20(1):140.

7. Micheroli R, Hebeisen M, Wildi LM, Exer P, Tamborrini G, Bernhard J, et al. Impact of obesity on the response to tumor necrosis factor inhibitors in axial spondyloarthritis. Arthritis Research & Therapy. 2017;19:164.