Dear Editor, We read with great interest the recent article by Chen et al1, which investigated the roles of BMI, body fat distribution, and grip strength in rotator cuff calcific tendonitis (RCCT) through a combination of retrospective analysis and Mendelian randomization (MR). Chen et al should be recognized for combining retrospective analysis with Mendelian randomization – a design that does more than confirm BMI as a risk factor. By using genetic instruments, they disentangle adiposity from diabetes, two variables that often travel together in clinical datasets and are easily conflated. Their finding that trunk and limb fat percentages, but not hip circumference, are causally linked to RCCT adds specificity: not all fat is equal when it comes to tendon health. That said, what this means at the tissue level remains unclear. Adipose tissue is metabolically active, and adipokines like leptin and adiponectin are known to influence bone and cartilage2. Whether these systemic signals directly promote chondroid metaplasia and hydroxyapatite deposition within the rotator cuff – or whether their effect is mediated by low-grade inflammation – is not addressed by the current data. The study establishes a statistical association, but the biological bridge from fat depot to calcific tendon is still speculative. Moreover, the MR analysis utilized GWAS data for fat percentages derived from bioelectrical impedance, which cannot distinguish between subcutaneous and visceral adipose depots. Visceral fat, with its pro-inflammatory profile, may be more relevant than subcutaneous fat in driving tendon pathology3. Future studies should incorporate imaging-based body composition measures (e.g., CT/MRI) to dissect the specific contributions of visceral adiposity and intramuscular fat infiltration – a known feature of rotator cuff muscle degeneration – to RCCT risk. Grip strength as a surrogate: what does it truly represent? The finding that greater grip strength is protective against RCCT is consistent with the well-established link between muscle function and tendon health. That grip strength is protective makes sense – but it is also a coarse measure. Handgrip dynamometry primarily captures forearm and hand function, not the rotator cuff itself. While grip strength correlates with overall physical capacity and may reflect general muscle health, it tells us little about whether the supraspinatus or infraspinatus is strong, coordinated, or resilient to calcific change. Targeted rotator cuff training improves shoulder-specific outcomes4; whether grip strength training alone does the same for RCCT is another question. Future studies might move beyond grip strength to more precise traits – isometric shoulder strength, or muscle cross-sectional area on imaging – if GWAS data for such phenotypes become available. The unresolved role of sex and age The retrospective analysis identified female sex and older age as independent risk factors, yet these variables were not examined in the MR framework. Sex-stratified MR is challenging due to limited sample sizes in publicly available GWAS, but the striking female predominance in RCCT (61 of 71 cases in this cohort) suggests that sex-specific biological mechanisms – such as hormonal influences on calcium metabolism or tendon composition – may interact with adiposity5. Similarly, age-related changes in tendon structure and fat distribution could modify causal effects. We encourage the authors or future investigators to explore whether the causal estimates for adiposity and grip strength differ by sex or age when sufficiently powered datasets become available. Clinical translation: from population-level evidence to individual guidance Chen et al conclude that weight management and maintaining muscular strength are central to RCCT primary prevention. But “sound” is not the same as “actionable.” If the goal is prevention, the question becomes: what should clinicians actually do? For patients with elevated BMI or unfavorable fat distribution – increased waist circumference in particular – caloric restriction and aerobic exercise remain the logical first step. These interventions target total and visceral adiposity, which the data implicate most consistently. For those with low grip strength or suspected sarcopenia, the focus shifts to resistance training, not just for the upper limb generally but for the rotator cuff specifically: external rotation, prone rowing, exercises that enhance local tendon resilience. Whether such training prevents RCCT directly is unproven, but the logic is plausible. A third point follows from the dissociation the authors demonstrate between diabetes and RCCT. In clinical practice, these two often cluster; the data suggest that when RCCT risk is the specific concern, obesity – not glycemic status – should be the priority. Diabetes control matters, of course, but for different reasons. Chen et al have clarified that adiposity and muscle strength are not proxies for each other, and that neither reduces to diabetes. Their work underscores the need to move beyond BMI: fat distribution matters, muscle function matters, and they may matter through different pathways. What comes next? Mechanistic studies that trace how systemic adiposity translates to local calcification, and trials testing whether interventions aimed at body composition – not just weight – can actually reduce RCCT incidence. For now, the authors have given us a sharper set of questions to ask.
Jing et al. (Mon,) studied this question.