Sarcopenia, a prevalent degenerative muscle condition predominantly affecting older individuals, has emerged as a critical global public health concern. It is characterized by a marked reduction in skeletal muscle mass and strength, leading to diminished mobility, increased risk of falls, and reduced quality of life (1). Currently, approximately 50 million people worldwide are estimated to have sarcopenia, with this number projected to rise to 200 million by 2050 (2). The global prevalence ranges between 10 and 30%, with an anticipated increase as populations continue to age (3). Although prevalence rates vary by region, they are notably higher in developed countries and areas experiencing rapid demographic changes (4). Sarcopenia significantly contributes to disability, functional decline, and rising healthcare costs among the elderly (5). Its impact not only reduces the quality of life for affected individuals but also places a considerable strain on global healthcare systems, exacerbating the burden of non-communicable diseases (6).

Unhealthy eating habits are major contributors to chronic conditions such as obesity, cardiovascular diseases, diabetes, and premature mortality. These habits also adversely affect the environment, contributing to greenhouse gas emissions, resource depletion, and biodiversity loss (7, 8). The EAT-Lancet Commission introduced the Planetary Health Diet Index (PHDI) in 2019 to address these interlinked challenges (9). PHDI emphasizes plant-based dietary patterns, encouraging the consumption of whole grains, vegetables, fruits, legumes, and nuts while limiting red meat, sugar, and processed foods. This diet aims to enhance public health by reducing chronic disease risks and simultaneously promoting environmental sustainability. However, evidence regarding the relationship between PHDI and sarcopenia remains an unexplored area.

Growing evidence underscores a complex link between obesity and sarcopenia, with obesity contributing to insulin resistance, chronic inflammation, disrupted glucose metabolism, and dyslipidemia (10, 11). Non-high-density lipoprotein to high-density lipoprotein cholesterol ratio (NHHR), reflecting the balance between pro-and anti-atherogenic lipids, has emerged as a promising marker for assessing lipid imbalances in conditions like atherosclerosis and insulin resistance (12). Recent studies suggest NHHR is associated with sarcopenia (13, 14). However, its potential role as a mediator in the relationship between PHDI adherence and sarcopenia remains underexplored.

This study aims to address this gap by investigating the association between adherence to the PHDI and sarcopenia using a comprehensive cross-sectional analysis of National Health and Nutrition Examination Survey (NHANES) data. We hypothesize that higher adherence to a healthy dietary pattern, as reflected by a higher PHDI, is inversely associated with sarcopenia. Furthermore, we propose that the NHHR mediates this relationship. Specifically, we posit that healthier dietary patterns improve lipid metabolism by lowering NHHR, thereby reducing pro-inflammatory processes that contribute to muscle degradation. By exploring these mechanisms, our study seeks to offer novel insights into the interplay between diet, lipid metabolism, and sarcopenia, with significant implications for targeted prevention and management strategies.

This study highlights a significant association between adherence to the PHDI and sarcopenia, with higher PHDI scores associated with a reduced likelihood of sarcopenia. Additionally, our findings suggest that the NHHR may act as a partial mediator in this association. RCS and subgroup analyses further support these findings, demonstrating that increased PHDI adherence is associated with a lower prevalence of sarcopenia.

There is an increasing amount of evidence linking PHDI to the likelihood of several chronic diseases (22, 23). Although there are limited studies directly examining the relationship between PHDI and sarcopenia, current research suggests an association between healthy eating patterns and the maintenance of muscle mass (24). A systematic review of prospective cohort studies indicates that adhering to a diet rich in plant-based foods may reduce the likelihood of developing sarcopenia (25). Additionally, a cross-sectional study involving 12,000 individuals reported that greater intake of whole grains, nuts, and vegetables was associated with a decreased likelihood of sarcopenia (OR: 0.64, 95% CI: 0.49–0.84) (26). Together, these findings support the understanding of the negative association between PHDI and sarcopenia, emphasizing the potential importance of diet quality for maintaining muscle health.

Additionally, emerging studies emphasize the significance of NHHR in relation to sarcopenia. Various cross-sectional investigations have reported a negative correlation between the ratio of triglycerides to HDL cholesterol and relative grip strength, suggesting that markers of lipid metabolism may serve as predictors of muscle degeneration (27). Furthermore, there is evidence indicating that fatty acids and muscle metabolism are interconnected processes contributing to muscle loss (28). For example, research involving 9,012 participants identified an association between NHHR and an increased likelihood of reduced muscle mass in middle-aged Americans (13). Consistent with these findings, our study shows a positive association between NHHR and sarcopenia, highlighting NHHR’s potential as an indicator of muscle deterioration. This underscores the importance of NHHR for understanding the fundamental mechanisms underlying sarcopenia.

This study examines the association between the PHDI and sarcopenia, identifying the NHHR as a potential mediator. Both inflammation and lipid metabolism are known to contribute to the likelihood of sarcopenia (29, 30), with elevated pro-inflammatory markers, such as Tumor Necrosis Factor-alpha (TNF-α), Interleukin-6(IL-6), and C-Reactive Protein (CRP), being observed in both sarcopenia and dyslipidemia, suggesting shared pathogenic mechanisms (31–33). Inflammatory mediators may influence lipid metabolism by stimulating lipolysis in adipocytes, increasing free fatty acid (FFA) levels, and promoting insulin resistance (34, 35). Such metabolic disturbances are linked to systemic inflammation, which can exacerbate muscle loss. Elevated FFAs and Low-Density Lipoprotein (LDL) may further trigger oxidative stress and inflammation, impairing muscle function and regeneration (36, 37). Lipid peroxidation leads to oxidative damage, contributing to muscle fiber deterioration and accelerating sarcopenia (38). Additionally, recent studies have highlighted the broader implications of lipid metabolism in related health outcomes. For example, dysregulated lipid metabolism has been linked to the progression of liver steatosis, where malnutrition and impaired hepatic metabolism can negatively impact overall health (39). Moreover, emerging evidence suggests that HDL-bound non-coding RNAs play a regulatory role in cardiovascular risk, offering insights into the molecular interactions between lipid metabolism and systemic inflammation (40). Given the shared inflammatory and metabolic pathways between cardiovascular disease and sarcopenia, these novel biomarkers may also have relevance in predicting muscle health and function. Dietary patterns play a crucial role in modulating inflammation and lipid metabolism, thereby affecting the likelihood of sarcopenia (41). The PHDI, which emphasizes plant-based food intake, aligns with these protective effects. For example, polyphenols found in fruits and vegetables possess anti-inflammatory properties, contributing to lower systemic inflammation (42). Additionally, a diet rich in fiber and antioxidants from whole grains can improve lipid metabolism by reducing LDL and FFA levels (43). Previous research supports that plant-based diets can modulate lipid profiles and inflammation, which are essential for muscle preservation (44–46). In our study, NHHR acted as a mediator in the PHDI-sarcopenia relationship, reinforcing the importance of diet quality for maintaining muscle health. Higher PHDI scores are associated with better lipid profiles and lower inflammation, both of which are protective against sarcopenia.

The ROC curve analysis indicated that NHHR outperformed protein intake in predicting sarcopenia, with a significantly higher AUC. These results indicate the potential utility of NHHR may as a more reliable biomarker for mediating sarcopenia assessment.

Even after excluding participants on lipid-lowering medications, the associations of both PHDI and NHHR with sarcopenia remained significant. These findings highlight the robustness of the relationships and suggest that both dietary patterns and lipid metabolism play critical roles in the pathogenesis of sarcopenia.

Our study highlights the potential clinical use of PHDI and NHHR scores in identifying and managing patients at sarcopenia. Both scores correlate with sarcopenia likelihood, making them useful tools for clinicians. Integrating these scores into clinical practice can help identify patients who may benefit from preventive interventions, such as personalized dietary advice and tailored exercise programs to address lipid imbalance and muscle loss. Regular monitoring of these scores could also track sarcopenia progression and guide treatment adjustments. Although further validation is needed, incorporating PHDI and NHHR scores into routine assessments could improve sarcopenia prevention and management in at-risk populations.

This study has several strengths. First, the PHDI serves as a comprehensive metric of both healthy eating and environmental sustainability, demonstrating its potential to predict sarcopenia. By promoting plant-based food intake while limiting red meat and processed foods, PHDI is closely associated with improvements in muscle health. Second, our analysis utilized a large, nationally representative dataset, enhancing the generalizability of our findings. Finally, to the best of our knowledge, this study is the first to explore NHHR as a mediator between PHDI and sarcopenia, addressing a significant research gap.

However, this study has several limitations. First, the cross-sectional design precludes establishing causality between PHDI, NHHR, and sarcopenia. While the mediation analysis suggests a potential pathway involving NHHR, prospective cohort studies, randomized controlled trials, or experimental research are necessary to confirm these findings and elucidate the causal mechanisms. Second, NHANES relies on self-reported data, including dietary intake via food frequency questionnaires and clinical conditions, which may introduce recall bias or misclassification. Self-reported data inherently carry the risk of bias and should be interpreted with caution. Using more objective measures, such as physician-confirmed diagnoses or dietary biomarkers, could improve result reliability. Third, despite adjusting for numerous potential confounders, residual confounding cannot be entirely ruled out due to the inherent limitations of the NHANES dataset. Factors like genetic predispositions, environmental exposures, or unmeasured lifestyle variables may influence the observed associations. Lastly, while NHANES data are nationally representative of the U. S. population, the generalizability of these findings to other populations with differing dietary habits, demographics, or health profiles may be limited. Future longitudinal and experimental studies are warranted to validate these results and explore the mechanisms in greater depth.

In conclusion, elevated PHDI levels are associated with a lower likelihood of sarcopenia, whereas diminished NHHR levels might enhance this connection. Therefore, following a PHDI-oriented dietary plan and managing NHHR levels may hold substantial clinical importance in reducing the likelihood of sarcopenia.