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HOME > Endocrinol Metab > Volume 40(3); 2025 > Article
Editorial
Mineral, bone & muscle Calorie Restriction and Bone Health: Lessons from Bariatric Metabolic Surgery
Bukyung Kimorcid
Endocrinology and Metabolism 2025;40(3):388-390.
DOI: https://doi.org/10.3803/EnM.2025.2452
Published online: June 11, 2025

Division of Endocrinology and Metabolism, Department of Internal Medicine, Kosin University Gospel Hospital, Busan, Korea

Corresponding author: Bukyung Kim. Division of Endocrinology and Metabolism, Department of Internal Medicine, Kosin University Gospel Hospital, 262 Gamcheon-ro, Seo-gu, Busan 49267, Korea Tel: +82-51-990-6243, Fax: +82-51-248-5686, E-mail: 79kyung@daum.net
• Received: May 15, 2025   • Revised: May 16, 2025   • Accepted: May 20, 2025

Copyright © 2025 Korean Endocrine Society

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Calorie restriction (CR) has long been advocated for its potential benefits in improving metabolic health and promoting longevity. However, recent insights suggest that prolonged CR may have negative effects, particularly on bone health. Liu and Rosen [1] provide an insightful review summarizing the paradoxical impact of CR on the skeleton. Specifically, they focus on bone marrow adipose tissue (BMAT) as a central mechanism through which caloric restriction impairs bone health. Although their discussion emphasizes findings from animal models and mechanistic studies, these concepts are highly relevant in clinical settings, particularly among patients undergoing intentional weight loss through bariatric metabolic surgery (BMS). This relevance arises from the fact that CR is the primary mechanism responsible for weight loss following BMS.
Traditionally, obesity was considered beneficial in preventing osteoporosis due to increased mechanical load and higher bone mineral density (BMD). This perspective has recently been challenged, as accumulating evidence indicates that the effects of obesity on bone health vary by skeletal site and structural characteristics; thus, assessing bone solely by areal BMD can be misleading [2]. For instance, although obese adults typically exhibit higher BMD at the hip and spine, high-resolution peripheral quantitative computed tomography analysis reveals increased cortical porosity and trabecular bone deterioration, suggesting poor bone quality despite elevated BMD [2]. Additionally, recent large-scale Korean cohort data demonstrated that individuals with normal body mass index (BMI) but elevated body fat percentage had an increased risk of annual BMD loss. This finding underscores the importance of evaluating body composition rather than relying solely on BMI when assessing bone risk [3].
The skeletal effects of CR are not only theoretical but also clinically evident among patients undergoing metabolic BMS. In a recent study published in Endocrinology and Metabolism, visceral fat—but not subcutaneous fat—was significantly associated with bone loss following gastrectomy, highlighting the differential impacts of fat depots on skeletal metabolism [4]. Moreover, unpublished data from Korean patients with severe obesity revealed that despite comparable BMD between obese and non-obese individuals, the trabecular bone score (TBS)—a surrogate measure of bone microarchitecture—was significantly lower in obese subjects [5]. This dissociation between bone density and microarchitecture highlights the metabolic imprint on skeletal health and supports integrating TBS and metabolic markers into comprehensive bone risk assessments. These observations align closely with the mechanistic model proposed by Liu and Rosen [1]: CR can suppress anabolic signals, shifting mesenchymal stem cell differentiation from osteogenic toward adipogenic pathways. Concurrently, the expansion of BMAT promotes the secretion of factors such as receptor activator of nuclear factor kappa-B (RANK), enhancing bone resorption and inhibiting bone formation [1].
How, then, can clinicians effectively support patients undergoing CR for weight loss? Clinical guidelines for post-bariatric management recommend regular monitoring of BMD, supplementation with vitamin D and calcium, and implementation of strength training [6]. Consistent with these guidelines, clinicians should emphasize patient education as a critical element of care. By clearly communicating the potential skeletal risks associated with caloric restriction, clinicians empower patients to actively participate in preventive strategies. These include adequate calcium and vitamin D intake as well as adherence to regular physical activity, particularly resistance exercises. Such proactive engagement can help mitigate bone loss and optimize long-term musculoskeletal health during weight loss efforts (Fig. 1).
The relationship between obesity and bone health extends beyond assessment by BMD alone. The metabolic benefits of weight loss through caloric restriction must be balanced against associated skeletal risks. Therefore, it is essential to adopt a multidimensional approach to bone health that integrates body composition, metabolic profile, and microarchitectural assessments within the context of caloric restriction. This paradigm will enable clinicians to identify patients who have apparently ‘normal’ BMD but remain at high risk of fracture. Furthermore, clinicians should recognize that bone strength can improve despite decreased BMD following weight loss, provided bone quality is adequately addressed. From the standpoint of obesity management and bariatric surgery, adopting this perspective is increasingly critical. Bone must no longer be viewed as merely a passive victim of metabolic interventions. Instead, bone should be recognized as an active endocrine and structural organ requiring dedicated monitoring and proactive care, especially in the context of significant weight loss.

CONFLICTS OF INTEREST

No potential conflict of interest relevant to this article was reported.

Fig. 1.
Conceptual model of the relationship between calorie restriction (CR) and skeletal effects. While CR induces metabolic improvements that may indirectly benefit bone health—such as reductions in inflammatory cytokines and insulin resistance—it simultaneously increases skeletal vulnerability due to mechanical unloading and altered mesenchymal stem cell (MSC) differentiation. Specifically, CR promotes the expansion of bone marrow adipose tissue (BMAT), suppresses anabolic signaling pathways, and enhances bone resorption by increasing receptor activator of nuclear factor κB ligand (RANKL) and decreasing insulin-like growth factor-1 (IGF-1) and estrogen levels. Collectively, these effects result in decreased bone density. Consequently, CR may lead to discordant changes in fracture risk depending on the relative balance between improved metabolic status and compromised bone quality. Clinical strategies—including supplementation with calcium and vitamin D, resistance exercise training, patient education regarding CR-induced skeletal vulnerability, and individualized fracture risk assessment—are essential for optimizing skeletal outcomes. AGE, advanced glycation end-product; PPARγ, peroxisome proliferator- activated receptor gamma.
enm-2025-2452f1.jpg
  • 1. Liu L, Rosen CJ. New insights into calorie restriction induced bone loss. Endocrinol Metab (Seoul) 2023;38:203–13.ArticlePubMedPMCPDF
  • 2. Evans AL, Paggiosi MA, Eastell R, Walsh JS. Bone density, microstructure and strength in obese and normal weight men and women in younger and older adulthood. J Bone Miner Res 2015;30:920–8.ArticlePubMedPDF
  • 3. Yoon H, Sung E, Kang JH, Kim CH, Shin H, Yoo E, et al. Association between body fat and bone mineral density in Korean adults: a cohort study. Sci Rep 2023;13:17462.ArticlePubMedPMCPDF
  • 4. Cho S, Shin S, Lee S, Rhee Y, Kim HI, Hong N. Differential impact of subcutaneous and visceral fat on bone changes after gastrectomy. Endocrinol Metab (Seoul) 2024;39:632–40.ArticlePubMedPMCPDF
  • 5. Kim BK. Skeletal vulnerability after bariatric surgery: mechanisms and preventive approaches. Presented at: 2025 Seoul International Congress of Endocrinology and Metabolism; 2025 May 1-3; Seoul, Korea.
  • 6. Sayadi Shahraki M, Mahmoudieh M, Kalidari B, Melali H, Mousavi M, Ghourban Abadi MR, et al. Bone health after bariatric surgery: consequences, prevention, and treatment. Adv Biomed Res 2022;11:92.PubMedPMC

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        Calorie Restriction and Bone Health: Lessons from Bariatric Metabolic Surgery
        Endocrinol Metab. 2025;40(3):388-390.   Published online June 11, 2025
        DOI: https://doi.org/10.3803/EnM.2025.2452
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      Calorie Restriction and Bone Health: Lessons from Bariatric Metabolic Surgery
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      Fig. 1. Conceptual model of the relationship between calorie restriction (CR) and skeletal effects. While CR induces metabolic improvements that may indirectly benefit bone health—such as reductions in inflammatory cytokines and insulin resistance—it simultaneously increases skeletal vulnerability due to mechanical unloading and altered mesenchymal stem cell (MSC) differentiation. Specifically, CR promotes the expansion of bone marrow adipose tissue (BMAT), suppresses anabolic signaling pathways, and enhances bone resorption by increasing receptor activator of nuclear factor κB ligand (RANKL) and decreasing insulin-like growth factor-1 (IGF-1) and estrogen levels. Collectively, these effects result in decreased bone density. Consequently, CR may lead to discordant changes in fracture risk depending on the relative balance between improved metabolic status and compromised bone quality. Clinical strategies—including supplementation with calcium and vitamin D, resistance exercise training, patient education regarding CR-induced skeletal vulnerability, and individualized fracture risk assessment—are essential for optimizing skeletal outcomes. AGE, advanced glycation end-product; PPARγ, peroxisome proliferator- activated receptor gamma.

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      Calorie Restriction and Bone Health: Lessons from Bariatric Metabolic Surgery
      Endocrinol Metab : Endocrinology and Metabolism
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