The association between gastric cancer and sarcopenia: a scoping review

Aim: To explore the relationship between gastric cancer and sarcopenia and review the underlying mechanisms.

Method: A systematic search was conducted across the Web of Science, PubMed, Cochrane, CNKI, Wanfang, and VIP databases following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) guidelines. Literature describing the relationship between gastric cancer and sarcopenia was included in this study, with methodological quality assessed using the Joanna Briggs Institute (JBI) Critical Appraisal Tools.

Results: Among the 1,518 identified publications, 33 cohort studies involving 10,679 participants were ultimately included. The results revealed a sarcopenia prevalence ranging from 6.8% to 72.22% in gastric cancer patients. Most studies indicated that reduced muscle mass—potentially attributable to fat infiltration, immunosuppression, cachexia-associated metabolic disturbances, and protein reserve depletion—serves as an independent predictor of postoperative complications, overall survival, and disease-free survival in gastric cancer patients. However, due to heterogeneity in assessment criteria and measurement tools, only two studies demonstrated that sarcopenia did not significantly impact survival or prognosis in this population.

Conclusion: Postoperative sarcopenia exhibits a high prevalence after gastric cancer surgery and is a significant predictor of adverse clinical outcomes. This underscores the importance of prioritizing muscle mass preservation in postoperative management and integrating its assessment into preoperative risk stratification. However, the current body of evidence is limited by inconsistent diagnostic criteria and a lack of mechanistic studies. Future research should focus on establishing standardized diagnostic frameworks through multidisciplinary collaboration and developing targeted interventions to improve patient prognosis.

1 Introduction

Gastric cancer, a malignancy originating from the gastric mucosal epithelium, represents a significant global health burden. Data indicate that an estimated 19.3 million new cancer cases occurred worldwide in 2020, with gastric cancer accounting for approximately 1.09 million cases (1). Cancer-related deaths approached 10 million, including roughly 769,000 gastric cancer fatalities, underscoring its persistent status as a major public health challenge globally (2). Patients with gastric cancer frequently experience persistent digestive dysfunction due to anatomical alterations, manifesting as chronic eating difficulties, vomiting, diarrhea, and malabsorption. Sarcopenia—a syndrome characterized by progressive loss of muscle mass and function—exhibits multifactorial pathogenesis involving chronic inflammation, malnutrition, mitochondrial dysfunction, prolonged disuse, neuromuscular degeneration, and insufficient physical activity (3).

Research demonstrates that tumor-associated inflammatory metabolic dysregulation and hypercatabolic states significantly contribute to sarcopenia pathogenesis in gastric cancer, with prevalence rates ranging from 10.0% to 57.7% (4). The underlying mechanisms involve proinflammatory cytokine-mediated enhancement of proteolytic pathways, where excessive IL-6 and TNF-α in the tumor microenvironment persistently activate both ubiquitin-proteasome and autophagy-lysosomal systems, accelerating muscle protein catabolism (5). Concurrently, tumor-induced insulin resistance and dysregulated lipid metabolism compromise bioenergetic supply to muscle tissue (6), while gastrointestinal obstruction and malabsorption further exacerbate protein-energy malnutrition, establishing a self-perpetuating vicious cycle (7). Notably, aberrant myokine secretion resulting from muscle atrophy modulates critical signaling pathways, including JAK/STAT and mTOR, thereby altering the tumor microenvironment to promote cancer proliferation and metastasis (8).

Despite accumulating evidence supporting the association between gastric cancer and sarcopenia, research on their bidirectional mechanisms remains fragmented due to methodological heterogeneity, population diversity, and lack of standardized interventions, precluding comprehensive systematic synthesis. This review, therefore, aims to consolidate existing evidence by integrating findings across study designs, analyzing how population characteristics modulate association strength, evaluating comparative merits of sarcopenia assessment tools, and elucidating the clinical implications of their interplay—ultimately informing the development of integrated management strategies encompassing screening, assessment, and targeted interventions for gastric cancer patients.

2 Materials and methods

This scoping review consolidates current knowledge on the sarcopenia-gastric cancer relationship through a five-phase methodology comprising research question development, systematic literature screening, rigorous study selection, standardized data extraction, and critical evidence synthesis (9), with all results reported in strict adherence to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Extension for Scoping Reviews (PRISMA-ScR) guidelines (10). The study protocol was registered on the Open Science Framework with the registration number https://doi.org/10.17605/OSF.IO/JC9VD.

2.1 Research questions

This review addresses three core research questions: 1. What is the reported prevalence range of sarcopenia among gastric cancer patients in existing studies? 2. How does sarcopenia affect survival and prognosis in gastric cancer patients? 3. What are the underlying biological mechanisms governing the bidirectional relationship between gastric cancer and sarcopenia?

2.2 Search strategy

This study conducted a systematic literature search under the guidance of a professional librarian, encompassing records from database inception to 1 July 2025, across PubMed, Web of Science, Embase, Cochrane Library, CNKI, Wanfang, and VIP databases, utilizing the key terms “gastric cancer” and “sarcopenia” as primary search parameters (Table 1).

Table 1

Table 1. Medical subject headings (MeSH) and keywords used in searches.

2.3 Study selection

Literature management and screening were performed using Zotero software. Inclusion criteria comprised (1) POS framework adherence: P (Participants)—adults (≥18 years) with clinically confirmed gastric cancer and sarcopenia; O (Outcomes)—gastric cancer-related complications, survival outcomes, and prognosis; S (Study design)—empirical human studies (randomized controlled trials, cohort studies, case-control studies, cross-sectional studies); (2) no restrictions on demographic characteristics or geographical regions. Exclusion criteria included (1) non-empirical studies (e.g., reviews, editorials, theoretical articles), (2) secondary data analyses, (3) non-English literature, and (4) studies failing to report outcomes examining the gastric cancer-sarcopenia relationship.

2.4 Data extraction

This study implemented a standardized data extraction protocol whereby two researchers independently extracted literature information using predefined Excel templates, with discrepancies resolved by a third reviewer. Extracted variables included first author, publication year, study design, country, gastric cancer staging, sample size, patient age, sarcopenia diagnostic criteria, assessment metrics, gastric cancer patient outcomes, and their interrelationship.

2.5 Evidence synthesis

Data were categorized according to research context, sample characteristics, assessment tools, metrics, outcome presentations, and key findings, with this review specifically centering on elucidating the bidirectional relationship between gastric cancer and sarcopenia.

2.6 Critical appraisal of included studies

The methodological quality of included studies was assessed using the Joanna Briggs Institute (JBI) Critical Appraisal Tools (11). As all incorporated studies were cohort designs, the corresponding checklist containing 11 appraisal items was applied.

3 Results

3.1 Search results and literature characteristics

A comprehensive search identified 1,518 publications. Following deduplication (n = 468 excluded), title/abstract screening eliminated 673 records, yielding 377 articles for full-text assessment. Ultimately, 33 studies met the inclusion criteria and were incorporated into this review. The selection process is detailed in Figure 1. Quality appraisal confirmed that all eligible studies were retained for analysis (Appendix 1).

Figure 1

Figure 1. PRISMA-ScR flow diagram.

Geographically, 25 studies originated from Asian countries, including 13 from China (14, 18–21, 23, 24, 27, 34, 35, 38, 42, 43), 8 from Japan (12, 16, 25, 29–33), 2 from South Korea (26, 36), and 2 from India (39, 41). European contributions comprised eight studies: Spain (n = 2) (15, 44), Italy (n = 2) (22, 38), with single studies from Turkey (13), Poland (17), Ireland (37), and Romania (40). Publications spanned 2016–2025, encompassing 10,679 participants aged 26–89 years. All studies employed cohort designs, with 23 retrospective cohorts (12, 14–18, 21, 22, 24–26, 28–37, 40, 44) and 10 prospective cohorts (13, 19, 20, 23, 27, 38, 39, 41–43). Regarding therapeutic approaches, surgery was reported as the primary gastric cancer treatment in most studies, while only three investigations incorporated chemotherapy (28, 31, 36)—including one combining surgical and chemotherapeutic approaches (31) (Tables 2, 3).

Table 2

Table 2. Characteristics and analytics of included studies (N = 33).

Table 3

Table 3. The relationship between GC and sarcopenia (N = 33).

3.2 Prevalence and assessment of sarcopenia in gastric cancer patients

This systematic review synthesizes evidence of a 6.8%–72.22% sarcopenia prevalence in gastric cancer patients, with assessment metrics including SMI (12, 14–24, 26–28, 30–32, 34–44), IMAC (12, 30), VFA (21, 30, 42, 44), VAT (15), PMI (29), BMI (26), physical performance (13, 14, 19, 20, 23, 38, 39, 41), body composition (25), SMD (23, 43), muscle strength (13, 14, 19, 20, 23, 38, 39, 41), and muscle-specific strength (38), where CT emerged as the predominant diagnostic modality implemented alongside criteria from the EWGSOP (13, 14, 19, 20, 23, 25, 38, 43), AWGS (19, 20, 38, 39), KNHANES (38), WHO (26), and international consensus definitions (17), while VAT specifically serves as a biomarker for sarcopenic obesity with thresholds at −150 to −50 HU measured through volumetric analysis (12), dynamometry (13, 14, 19, 20, 38, 39), multifrequency BIA (25), and handheld dynamometer (41), revealing significant heterogeneity in threshold definitions across instruments and inconsistent cutoffs for identical tools (Table 3).

3.3 Survival and prognosis of gastric cancer

Analysis of gastric cancer outcomes in the included literature primarily focused on postoperative complications, encompassing overall complications (24, 27, 38) and major complications (24, 37); survival metrics including OS (16–18, 21, 22, 24, 26, 28, 29, 32–36, 42), DFS (24, 34, 42), and RFS (18, 21, 22, 34); as well as hospitalization duration and costs (17, 18, 20, 23, 43). Two additional studies evaluated sarcopenia’s impact on chemotherapy delays (43) and treatment-related toxicities (31) in gastric cancer patients. Evidence indicates significantly elevated overall complication rates among sarcopenic patients, with major complication rates reaching 12.9%–43.8% in this subgroup. Regarding survival outcomes, sarcopenia substantially reduced long-term survival rates and increased recurrence risk. Sarcopenic patients incurred higher hospitalization costs with prolonged hospital stays. Follow-up durations varied considerably across studies: short-term (30-day) assessments (12–14, 20, 25, 39, 40, 43), intermediate term (3–5 years) (15–17, 21, 23, 24, 26, 28, 32–38, 42, 44), and long term (18, 22). Regarding short-term outcomes, sarcopenia substantially increases postoperative complication risks, including infectious complications (12, 25, 30), anastomotic leakage (12, 30), and major complications (19, 24); prolongs hospital stays (17, 20, 23); and elevates healthcare costs (20, 23). Sarcopenia independently predicts reduced survival, significantly diminishing 5-year overall survival (16, 18, 42) and disease-free survival (18, 24), with particularly pronounced effects in metastatic/advanced disease (33, 36). Concurrent evidence indicates sarcopenia correlates with higher chemotherapy-related toxicities (31) and treatment delay risks (34). However, two studies reported no significant impact of sarcopenia or body composition alterations on postoperative complications or survival outcomes (39, 44) (Table 3).

3.4 Insights into the mechanism of action between gastric cancer and sarcopenia

Through a review of the included literature, we have preliminarily summarized that the core mechanisms underlying the interaction between sarcopenia and gastric cancer may encompass four key aspects. First, sarcopenia exacerbates postoperative risks in gastric cancer patients through disordered nutritional metabolism (12, 14, 16, 19). Second, inflammation and immune suppression mediate bidirectional adverse effects (12, 16, 18, 20). Third, surgical stress and tumor progression act synergistically to cause harm (13, 17, 18, 21). Finally, the fourth aspect may involve the compounded risk resulting from altered body composition, such as sarcopenic obesity (12, 15, 18, 19). Please refer to the schematic diagram of the mechanism of action for specific details (Figure 2).

Figure 2

Figure 2. Diagram of the mechanism of action. PNI, Prognostic Nutritional Index; SMI, Skeletal Muscle Index; IMAC, intramuscular adipose tissue content.

4 Discussion

Gastric cancer treatment risks increase with advancing age, while the prevalence of sarcopenia is notably higher in older populations (45). Therefore, precise nutritional risk assessment and careful selection of management strategies are clinically essential for elderly patients. Multiple studies have confirmed that sarcopenia is a significant risk factor for survival following curative surgery for gastric cancer (46, 47), although the exact relationship between sarcopenia and gastric cancer remains incompletely understood. Consistent with the majority of existing evidence, this review confirms that sarcopenia significantly increases the risk of postoperative complications, reduces overall survival (OS) and disease-free survival (DFS), and is associated with prolonged hospitalization and higher medical costs (37, 43). Notably, one study reported a fivefold increase in the risk of major complications among sarcopenic patients compared to non-sarcopenic patients after adjusting for covariates (19). Li et al. (35) identified both preoperative and postoperative sarcopenia as independent risk factors for OS in gastric cancer patients (35). However, conflicting evidence exists regarding the effect of sarcopenia on OS (48). There is growing research interest in the impact of sarcopenic obesity on gastric cancer outcomes (20, 21). Due to the complexity of screening procedures, clinicians often rely excessively on BMI for nutritional assessment, which may lead to underrecognition of nutritional risks in overweight or obese patients (49).

However, several limitations persist in current research, including the absence of standardized diagnostic criteria for sarcopenia—particularly in the systematic assessment of muscle strength and physical performance—which contributes to substantial discrepancies in reported prevalence rates. Most existing studies depend on preoperative imaging for muscle mass evaluation, with CT being the most widely used modality, despite ongoing debate regarding its validity in accurately reflecting whole-body musculature (25). Bioelectrical impedance analysis (BIA), although radiation-free and cost-effective, has not been routinely incorporated into preoperative assessment protocols (50). Moreover, muscle strength evaluations such as grip dynamometry can be influenced by subjects’ volitional effort or preexisting hand pathologies, potentially affecting measurement accuracy (51). Current sarcopenia diagnosis predominantly relies on SMI cutoffs; however, conventional definitions often overlook age as a critical modifier of muscle quality. Excessive reliance on SMI alone may therefore introduce bias into research outcomes (52). The revised 2018 EWGSOP guidelines explicitly incorporated “reduced muscle quality” as a core diagnostic criterion (53), underscoring the inadequacy of muscle quantity alone in predicting gastric cancer prognosis and highlighting the necessity of incorporating comprehensive functional assessments. A recent multicenter study integrating CT imaging and clinical data from three prospective gastric cancer cohorts proposed a composite metric known as the SMG, which synergistically evaluates both muscle mass and quality and may outperform single-parameter indices (54). This approach is conceptually analogous to diamond valuation, which considers both carat weight and clarity; nevertheless, the utility of SMG remains underexplored in gastric oncology. Concurrently, IMAC has emerged as a quantifiable biomarker of muscle quality, with emerging evidence indicating that IMAC-guided prehabilitation programs may contribute to improved surgical outcomes (12).

The pathophysiological interplay between gastric cancer and sarcopenia involves complex mechanisms, with no definitive causal relationship yet established. Current evidence indicates that gastric cancer patients exhibit heightened susceptibility to sarcopenia, primarily mediated through accelerated protein catabolism, systemic inflammatory responses, metabolic dysregulation, and reduced nutritional intake—processes intrinsically linked to cancer cachexia (55). Cachexia further impairs skeletal muscle regenerative capacity (56), while the concomitant loss of muscle-derived myokines, which exert anti-inflammatory and anti-tumor effects, may facilitate cancer progression (57). The immunometabolic imbalance hypothesis posits that fat-infiltrated skeletal muscle secretes aberrant adipokines that suppress NK cell function, thereby exacerbating postoperative immunosuppression and predisposing patients to infectious complications (58). Notably, males with sarcopenic obesity demonstrate elevated perioperative risk, largely attributable to increased adipose tissue friability that compromises surgical exposure (59). Concurrently, inadequate protein reserves in sarcopenic patients impair postoperative tissue repair under hypercatabolic stress, leading to delayed wound healing and prolonged hospitalization (60, 61). Skeletal muscle serves as an amino acid reservoir that mobilizes substrates for biosynthetic defense during surgical trauma; sarcopenia-induced amino acid deficiency restricts this reparative capacity, thereby increasing infection susceptibility (62). Importantly, most available studies do not adequately evaluate post-gastrectomy dietary intake patterns, which precludes definitive attribution of muscle loss to either surgical sequelae or underlying cancer pathophysiology (29).

This review synthesizes current evidence regarding the association between gastric cancer and sarcopenia, delineating the prevalence of sarcopenia among gastric cancer patients and evaluating its prognostic implications. While consolidating key insights, several limitations must be acknowledged. First, the predominance of retrospective study designs inherently constrains the assessment of core diagnostic parameters for sarcopenia—such as muscle strength and physical performance—which are frequently unavailable in archival datasets. Second, a geographical selection bias is evident, with studies predominantly involving East Asian populations and a notable scarcity of data from Western demographics. Furthermore, the use of heterogeneous assessment metrics across studies complicates comparative analysis. To address these issues, future efforts should focus on establishing integrated diagnostic criteria that combine artificial intelligence—enhanced imaging with validated biomarkers. Such advances would improve diagnostic accuracy and facilitate the identification of patients who may benefit from early nutritional and therapeutic interventions aimed at increasing muscle mass and improving clinical outcomes. Additionally, mechanistic studies are needed to elucidate the role of muscle density in gastric cancer progression, alongside randomized controlled trials to determine whether targeted interventions for sarcopenia significantly improve long-term survival.

5 Conclusion

This study demonstrates that sarcopenia is highly prevalent after gastric cancer surgery and serves as a significant predictor of adverse postoperative outcomes. However, its underlying mechanisms and standardized diagnostic criteria require further elucidation. Methodological variations and the lack of uniform assessment metrics across existing studies have contributed to inconsistent conclusions. Future efforts should focus on developing muscle preservation strategies and multimodal diagnostic approaches that integrate both mass and functional parameters to improve diagnostic accuracy and clinical outcomes. Moreover, prospective studies are essential to establish causal relationships between sarcopenia and gastric cancer progression, thereby facilitating evidence-based clinical pathways.

Data availability statement

The original contributions presented in the study are included in the article/supplementary material. Further inquiries can be directed to the corresponding author.

Author contributions

XW: Investigation, Methodology, Writing – original draft. XS: Investigation, Methodology, Writing – original draft. YyW: Investigation, Methodology, Writing – original draft. YjW: Investigation, Methodology, Writing – original draft. JR: Supervision, Visualization, Writing – review & editing. XF: Supervision, Visualization, Writing – review & editing.

Funding

The author(s) declare that no financial support was received for the research and/or publication of this article.

Conflict of interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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The author(s) declare that no Generative AI was used in the creation of this manuscript.

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