Malnutrition and muscle loss are among the most underestimated complications of inflammatory bowel disease (IBD).^1-3 Despite guideline recommendations, routine clinical practice still relies heavily on body weight, laboratory markers, and body mass index (BMI).^4-8 The study by Olczyk‑Wieczorkowska et al,⁹ published in the current issue of Polish Archives of Internal Medicine, is a timely and clinically relevant contribution, quantifying the prevalence of sarcopenia, myopenia, and malnutrition in a contemporary cohort of Polish patients with IBD. Importantly, the study uses tools available in everyday clinical practice.⁹

Several clear messages emerge from this work. Firstly, malnutrition and muscle impairment are common and affect relatively young patients, clustering around disease activity, in line with previous evidence.^10,11

One of the most striking findings of the study is that BMI frequently underestimates the true extent of nutritional compromise. While only 22% of the patients were classified as malnourished using BMI, nearly one‑third were identified as at risk of malnutrition using the Nutritional Risk Screening scale. This discrepancy reflects the well‑established phenomenon of malnutrition masked by preserved or increased body weight, often referred to as “malnubesity.”¹² Indeed, in IBD, malnutrition is driven by inflammation, catabolism, malabsorption, and reduced food intake, processes that can coexist with normal or even elevated BMI.¹³ Patients with elevated BMI can nonetheless experience marked muscle loss and deficiencies in essential micronutrients, as excessive adiposity may promote a chronic proinflammatory state that worsens IBD.¹²

The biochemical findings reinforce this message. Hypoalbuminemia was present in almost two‑thirds of the patients, predominantly during active disease.⁹ While albumin is rightly criticized as a nutritional marker because of its acute‑phase behavior, dismissing it entirely is equally misguided. In IBD, low albumin levels reflect the convergence of inflammation, protein loss, and inadequate food intake, precisely the milieu in which adverse outcomes occur.

The most clinically unsettling result is perhaps the prevalence of muscle impairment. Depending on the tool used, sarcopenia affected 18%–24% of the patients, while myopenia, defined by low fat‑free mass index, was present in over one‑third of them.⁹ The median age of the study cohort was just over 30 years. Sarcopenia in IBD is neither an exception nor a geriatric condition, and is not confined to severe disease.^2,14 It is a structural consequence of chronic inflammation.

The study also highlights the methodological challenges of diagnosing sarcopenia in patients with IBD. Variability among diagnostic tools (SARC‑F [Strength, Assistance in walking, Rise from a chair, Climb stairs, and Falls] questionnaire, sit‑to‑stand test, and bioimpedance‑derived indices) should not be interpreted as a methodological weakness of the study. Rather, it highlights the multidimensional nature of sarcopenia and the limitations of tools originally validated in elderly populations. Self‑reported questionnaires and functional tests alone are blunt instruments in young, chronically ill patients.

In this context, the increasing importance of muscle ultrasound warrants attention. Cross‑sectional imaging and magnetic resonance imaging (MRI) are impractical for routine sarcopenia screening, while bioimpedance, although useful, remains underused and methodologically inconsistent across centers. Ultrasound, on the other hand, is a bedside, radiation‑free, repeatable, and environmentally sustainable procedure, already well‑known to gastroenterologists.¹⁵ Importantly, ultrasound measurements showed excellent agreement with the MRI‑derived ones, especially regarding rectus abdominis thickness, effectively bridging the gap between feasibility and accuracy.¹⁰

Olczyk‑Wieczorkowska et al⁹ demonstrated markedly higher rates of sarcopenia and myopenia during active disease phases. This is expected, but the persistence of myopenia and sarcopenia in some patients in remission deserves attention. Clinical remission does not equate to metabolic recovery and may hide subclinical inflammation. As already reported, muscle deficits often persist despite clinical quiescence, suggesting cumulative damage or ongoing subclinical inflammation.¹⁴ This observation supports the argument that nutritional and muscle assessment should be a part of long‑term follow‑up and not be limited to flare‑ups.

The research offers a glimmer of hope regarding biologic therapy. Indeed, the patients receiving biologic therapy had a lower prevalence of malnutrition and a trend toward less sarcopenia.⁹ Biologics reduce inflammation and improve appetite and absorption, which translates into better nutritional risk profiles. However, rebuilding muscle mass likely requires time, adequate protein intake, and physical activity, supported by targeted nutritional interventions; antitumor necrosis factor therapy alone is not sufficient in this regard. Moreover, as recently discussed, muscle health may determine outcomes rather than being a secondary epiphenomenon, particularly in surgery related to Crohn disease.¹⁶

One of the more concerning findings is the lack of association between nutritional knowledge and clinical outcomes. In the Polish study, only 23% of the patients demonstrated good nutritional knowledge, which did not result in better nutritional status or muscle preservation.⁹ This likely reflects fragmented dietary counselling. Dietary advice in IBD is often generic, inconsistent, or fear‑driven, leading to unnecessary restrictions. The data strongly suggest the need for structured, continuous dietetic care integrated into IBD management, rather than an episodic education.

The strengths of the study lie in its pragmatic design and clinical relevance. The authors deliberately avoided sophisticated imaging, instead choosing tools that can be widely implemented. This makes the findings actionable. The limitations are linked to a single‑center design, modest sample size, prevalence of active disease, and use of an unvalidated nutrition questionnaire.

Ultimately, this work shows that muscle failure and malnutrition are prevalent in IBD clinics but often go unnoticed. If clinicians continue to rely solely on BMI and clinical impression, these conditions will remain overlooked.

In conclusion, Olczyk‑Wieczorkowska et al⁹ provide compelling evidence that sarcopenia, myopenia, and malnutrition are frequent, interrelated, and that they are clinically relevant in IBD, even among young adults. Active inflammation is the main driver, BMI is an inadequate screening tool, and nutritional knowledge without structured support is ineffective. Routine IBD care should evolve from weight‑based assessment to continuous, integrated evaluation of nutritional risk and muscle health, supported by multidisciplinary intervention.