Skip to main content
Download PDF

Association between oral intake magnesium and sarcopenia: a cross-sectional study

BMC Geriatrics volume 22, Article number: 816 (2022) Cite this article

Abstract

Background

Sarcopenia is a common skeletal muscle disorder in the elderly population. The patients with sarcopenia increased the cost of care and the risk for hospitalization. Magnesium deficiency might increase reactive oxygen species and protein damage. The purpose of our study was to demonstrate the relation between oral intake magnesium and sarcopenia by European Working Group on Sarcopenia in Older People (EWGSOP) 2 definition.

Methods

Our study included 2532 participants with 1310 males and 1222 females. The multiple logistic regression model was designed to test the cross-sectional protective outcome of oral intake magnesium for sarcopenia.

Results

Oral intake magnesium had a protective outcome with sarcopenia (odd ratio (OR) = 0.997, 95% CI = 0.996, 0.998, P < 0.001). After fully adjusted, the significance persisted with OR = 0.998 (95% CI = 0.996, 0.999, P < 0.001).

Conclusion

Results of the present study showed the dose dependent relationship between oral intake magnesium and sarcopenia. Sufficient oral intake magnesium might prevent patient from sarcopenia.

Peer Review reports

Introduction

Sarcopenia, one of the primary diseases of the elderly population, is a common skeletal muscle disorder that involves the progressive loss of skeletal muscle function and mass [1]. To date, the most widely cited diagnostic criteria is that proposed by the European Working Group on Sarcopenia in Older People (EWGSOP) and updated as EWGSOP2 in 2019 [2]. According to EWGSOP2, muscle strength, muscle quantity and physical performance were measured to evaluate sarcopenia [2]. Loss of skeletal muscle mass and function causes the risk of falls, fractures, physical disability, use of hospital services, poor quality of life, and death [3]. The patients with sarcopenia increase the risk for hospitalization and the cost of care during hospitalization [4]. In 2000, there was approximately $18.5 billion ($10.8 billion in men, $7.7 billion in women) health-care cost in the America due to sarcopenia [5]. Malnutrition plays a key role in the pathogenesis of sarcopenia [6] [7] [8]. There was a growing evidence base linking nutrition with greater muscle strength and better physical performance outcomes in patient with sarcopenia [9]. However, these articles paid more attention on protein [10], long-chain polyunsaturated fatty acids [11], vitamin D [12], and antioxidant nutrients [13]. Best to our knowledge, no previous data had discussed oral intake electrolyte and sarcopenia.

Magnesium is the second most intracellular cation after potassium in human. Several metabolic pathways and fundamental cellular activities including peptide and DNA synthesis, signal transduction, blood glucose control, stimulus-contraction coupling, stimulus-secretion coupling, and ion channel translocation related to magnesium [14]. Total body magnesium content is mainly located in bone and soft tissue [15]. The recommended daily intake of magnesium is 320 and 420 mg for adult women and men, respectively. Absorption mainly (80–90%) occurs in the jejunum and colon through passive and active transport [16]. Reabsorption of magnesium mainly occurred in the thin ascending limb of Henle (70%) and partially occurred in the proximal tubule and distal collecting tubule. Hypomagnesemia related to several clinical manifestations including neuromuscular and cardiovascular manifestations. Muscle spasms, muscle cramps, tremors, atrial fibrillation and ventricular arrhythmias were the specific symptoms of hypomagnesemia [17]. Further, electrolyte and hormone imbalanced including hypocalcemia, hypokalemia, and hypoparathyroidism were also associated with hypomagnesemia.

According to a previous study, magnesium deficiency might increase reactive oxygen species and lipid and protein damage and associate with damage of muscle [18]. The purpose of our study was to demonstrate the relation between oral intake magnesium and sarcopenia by EWGSOP2 definition.

Materials and methods

Study design and participants

We conducted a cross-sectional study using the National Health and Nutrition Examination Survey (NHANES) database in 1999-2002 period. The data included overall home interviews and laboratory assessments conducted by the National Center for Health Statistics (NCHS). Institutional Review Board (IRB) approval and documented consent was obtained from participants. The exclusion criteria were dysphagia; history of gastrointestinal tract disease; inflammatory bowel disease; history of cancer; participation in resistance training; participation regularly using steroids, diuretics, hormones, and growth factors; and subjects without complete clinical data, laboratory results, or medical history. (Fig. 1).

Fig. 1
figure 1

Flow chart representing the steps of analysis performed in the study

Full size image

EWGSOP2 guideline

The EWGSOP published a sarcopenia definition in 2010 [19]. In early 2018, the Working Group met again (EWGSOP2) to update the definition of sarcopenia. In the EWGSOP2, low muscle strength as the primary parameter of sarcopenia. A sarcopenia diagnosis is confirmed by low muscle strength with the presence of low muscle quantity or quality. Severe sarcopenia was considered with three components, including low muscle strength, low muscle quantity/quality and low physical performance.

Measurement: muscle quality index

The NHANES documentation provided measurement of the muscle quality index. We listed these methods and cut points to estimate components of muscle quality index in Table-S1.

Measurement of oral intake magnesium

Total magnesium intake in milligrams per day calculated from dietary information with 24 hours dietary recalls. Subjects were required to recall all intakes in one day period prior before the questionnaire. A measuring guides and a food model booklet was available for participants to help in reporting food amounts.

Assessment of Covariables

A computer-aided individual interviewing method was used for the collection of participants’ information. Demographic information, including sex, age, race was assembled. Smoking and drinking status were assessed by a detailed survey. We also recorded self-reported comorbidities, including cancer and cardiovascular disease. Based on the guidelines of Centers for Disease Control and Prevention, biochemical analyses in the database used standard methods.

Statistical analysis

SPSS (Version 18.0 for Windows, SPSS, Inc., Chicago, IL) was used for all the statistical analyses. Descriptive information of continuous and categorical covariates is presented as the mean (standard deviation) and several observations with percentage (%). Continuous variables were used Student’s t tests and categorical variables were used the χ 2 test for the comparison of characteristics and covariates across subgroups. The odds ratio (OR) with 95% confidence interval (CI) for sarcopenia was estimated by multivariate logistic regression analysis. We analyzed the association between oral intake magnesium and muscle quality index using a linear regression model. The beta coefficient is the degree of change in the muscle quality index for every 1-unit of change in the oral intake magnesium. The 2-sided P values less than 0.05 indicated significant differences. Four extended models were used for covariate adjustments. Model 1 examined unadjusted odd ratio (ORs). Model 2 presented ORs after adjusting sex, age, and race. Model 3 was adjusted for the variables included in Model 2 + the body mass index (BMI), Albumin, total calcium, creatinine, fasting glucose, C-reactive protein (CRP), daily carbohydrate intake, daily total fat intake, and daily protein intake. The variables in model 3 + the smoking history, comorbidities and education level were adjusted for model 4.

Result

Characteristics of the subjects

2532 subjects with 1310 males and 1222 females were included in our study. We separated subjects into two groups based on the EWGSOP definition of sarcopenia. (Table 1) The mean age were 73.14 ± 9.59 years in the sarcopenic group and 63.90 ± 9.32 years in the non-sarcopenic group, respectively. It was also observed that the mean oral intake magnesium amount was higher for non-sarcopenic group at 276.06 ± 142.04 compared to 235.97 ± 112.61 in the sarcopenic group (P < 0.001).

Table 1 Characteristics of study participants
Full size table

Association between oral intake magnesium and sarcopenia

In Table 2, we showed the association between different oral intake elements and sarcopenia. After adjusted all covariates, the association only showed in oral intake magnesium and potassium.

Table 2 The association between different oral intake elements and sarcopenia
Full size table

In Table 3, we performed logistic regression to exam the association between oral intake magnesium and sarcopenia. In Model 1, oral intake magnesium was significantly associated with sarcopenia (OR = 0.997, 95% confidence interval (CI) = 0.996, 0.998, P < 0.001) The significance persisted after adjusted all covariates in Model 4 (OR = 0.998, 95% CI = 0.996, 0.999, P = 0.007).

Table 3 Result of logistic regression predicting the presence of sarcopenia by oral intake magnesium
Full size table

Sensitivity analysis

Logistic regression was used for sensitivity analysis to compare the sarcopenic and non-sarcopenic groups and quartiles of oral intake magnesium. Similar outcomes were found for the relation between oral intake magnesium and sarcopenia in Table 4. In the unadjusted model, the highest quartile of oral intake magnesium had an odds ratio of 0.400 to be associated with sarcopenia (95% CI = 0.282, 0.568, P < 0.001). The odds ratio of subjects with the highest quartile of oral intake magnesium would have sarcopenia was 0.468 (0.274, 0.799) times fewer than subjects with the lowest quartile of oral intake magnesium after fully adjusted.

Table 4 Association between quartiles of oral intake magnesium and sarcopenia
Full size table

Correlation between oral intake magnesium and muscle quality index

In Table 5, the coefficients of oral intake magnesium and muscle strength, SMI, and gait speed were 0.207, 0.134, and − 0.137. The linear regression analysis of the relation of oral intake magnesium and muscle quality index was showed in Table 6. The association of oral intake magnesium and muscle strength (β = 0.145, 95% CI = 0.118, 0.172), SMI (β = 0.001, 95% CI = 0.001, 0.002), and gait speed (β = − 0.000365, 95% CI = − 0.000471, − 0.000258) had statistically significant result (P < 0.001). After fully adjusted, the association of oral intake magnesium and muscle strength (β = 0.048, 95% CI = 0.012, 0.083), SMI (β = − 0.000149, 95% CI = − 000434, 0.000136), and gait speed (β = − 0.000171, 95% CI = − 0.000338, − 0.000005).

Table 5 Pearson correlation coefficient between oral intake magnesium and muscle quality index
Full size table
Table 6 Association between oral intake magnesium and muscle quality index
Full size table

Discussion

In our presented study, the relationship between oral intake magnesium and the components of sarcopenia was closely inspected in 2532 adult population. Our results demonstrated strong relationships between oral intake magnesium and sarcopenia. Otherwise, based on the EWGSOP2, three components of sarcopenia all presented correlation with oral intake magnesium. To date, our study was the first article investigating the relation of oral intake magnesium and sarcopenia in a representative sample of the United States adult population.

Due to complicated pathogenesis, the development of sarcopenia remained controversial in the medical field. Previous study had mentioned different factors which associated with sarcopenia [20]. One of the main factors induced sarcopenia was the mitochondrial dysfunction [21]. Mitochondrial oxidative stress and dysfunction could be induced by intracellular magnesium deficiency [22]. Downregulating the electron transport chain increased the production of reactive oxygen species [23]. Low level of intracellular magnesium also suppressed the antioxidant defense system and reduced proteins such as superoxide dismutase, catalase, and glutathione [24]. Intracellular magnesium sufficient, in contrast, was found to suppress mitochondrial reactive oxygen species and improve mitochondrial function [25].

Intracellular and extracellular concentration of magnesium had thought to impact the synthesis of DNA and protein [26]. Magnesium regulated the onset of protein synthesis in activated frog oocytes and its rate in lymphocytes. Magnesium determines the onset of protein synthesis through the phosphatidylinositol-3-OH kinase (PI-3-K) pathway at mechanistic target of rapamycin (mTOR) phosphorylation of two translation-regulating proteins [27, 28]. One study measured intracellular concentration of magnesium and the rate of protein and DNA synthesis [29]. At the same magnesium concentration, the rate of DNA synthesis peaked as protein synthesis. This article provided strong evidence of magnesium as a regulator of DNA and protein synthesis.

Low magnesium status is also reported to associate with increasing reactive oxygen species and inflammation. Several articles had discussed that higher magnesium consumption was related to lower serum CRP [30]. People who takes magnesium at least 50 mg/day were 22% less likely to have higher level of plasma CRP compared with those dietary magnesium taking less than 50% of the recommended dietary allowance [31]. Magnesium supplement is associated with a lower serum CRP in these studies. One linear regression analysis of 3173 females aged 50–79 years found that magnesium supplement was associated with lower serum inflammatory biomarkers, such as CRP, interlukin-6 (IL-6), and tumor necrosis factor-α receptor 2 (TNF-α-R2, [32]].

Our study has several strengths. We screened the sarcopenia clearly by using EWGSOP2 guideline. We also screened other oral intake elements initially in our study. A large adult sample was included to discuss the protective outcome of oral intake magnesium for sarcopenia. In the current study, sufficient oral intake magnesium could reduce the incidence of sarcopenia. This result is not only effective, but also economical for preventing from sarcopenia in the public health system.

However, some limitations in our study should be identified. First, we used a cross-sectional database in which the oral intake magnesium was determined at single measure instead of a long observational period. Then, some information such as participants’ education levels and medical histories were based on questionnaires. The recall bias and other unknown bias might distort our results. Third, total magnesium intake was calculated from 24 hours dietary recalls and measured by guides and a food model booklet. This method caused inaccuracy of daily oral intake magnesium. Lastly, the factors of drug consumption, participants’ cognitive and nutritional status were not included our results. Thus, the confounding bias could not be estimated.

Conclusion

In our presented study, we identified the protective outcome of oral intake magnesium with sarcopenia. The significance especially showed in muscle strength and gait speed. Otherwise, dose dependent relationship was observed between oral intake magnesium and sarcopenia. Our findings suggested that sufficient oral intake magnesium might prevent patient from sarcopenia. Further prospective studies may be warranted to find the curative effect of oral intake magnesium in the patient with sarcopenia.

Availability of data and materials

The datasets used and/or analyzed during the current study are available from the NHANES database, https://www.cdc.gov/nchs/nhanes/index.htm.

Abbreviations

EWGSOP:

European Working Group on Sarcopenia in Older People

NHANES:

National Health and Nutritional Examination Survey

NCHS:

National Center for Health Statistics

DXA:

Dual-energy X-ray absorptiometry

SMI:

Skeletal muscle index

BMI:

Body mass index

CRP:

C-Reactive protein

OR:

Odds ratio

CI:

Confidence interval

ROC:

Receiver operating characteristic curve

AUROC:

Area under receiver operating characteristic curve

IL-6:

Interlukin-6

TNF-α-R2:

Tumor necrosis factor-α receptor 2

References

  1. Bauer J, Morley JE, Schols A, Ferrucci L, Cruz-Jentoft AJ, Dent E, et al. Sarcopenia: a time for action. An SCWD Position Paper J Cachexia Sarcopenia Muscle. 2019;10(5):956–61.

    Article  Google Scholar 

  2. Cruz-Jentoft AJ, Bahat G, Bauer J, Boirie Y, Bruyère O, Cederholm T, et al. Sarcopenia: revised European consensus on definition and diagnosis. Age Ageing. 2019;48(1):16–31.

    Article  Google Scholar 

  3. Santilli V, Bernetti A, Mangone M, Paoloni M. Clinical definition of sarcopenia. Clin Cases Miner Bone Metab. 2014;11(3):177–80.

    PubMed  PubMed Central  Google Scholar 

  4. Sousa AS, Guerra RS, Fonseca I, Pichel F, Ferreira S, Amaral TF. Financial impact of sarcopenia on hospitalization costs. Eur J Clin Nutr. 2016;70(9):1046–51.

    Article  CAS  Google Scholar 

  5. Dodds RM, Roberts HC, Cooper C, Sayer AA. The epidemiology of sarcopenia. J Clin Densitom. 2015;18(4):461–6.

    Article  Google Scholar 

  6. Bloom I, Shand C, Cooper C, Robinson S, Baird J. Diet quality and sarcopenia in older adults: a systematic review. Nutrients. 2018;10(3).

  7. de Sire A, Ferrillo M, Lippi L, Agostini F, de Sire R, Ferrara PE, et al. Sarcopenic dysphagia, malnutrition, and Oral frailty in elderly: a comprehensive review. Nutrients. 2022;14(5).

  8. Avola M, Mangano GRA, Testa G, Mangano S, Vescio A, Pavone V, et al. Rehabilitation strategies for patients with femoral neck fractures in sarcopenia: a narrative review. J Clin Med. 2020;9(10).

  9. Robinson S, Cooper C, Aihie SA. Nutrition and sarcopenia: a review of the evidence and implications for preventive strategies. J Aging Res. 2012;2012:510801.

    Article  Google Scholar 

  10. Wolfe RR, Miller SL, Miller KB. Optimal protein intake in the elderly. Clin Nutr. 2008;27(5):675–84.

    Article  CAS  Google Scholar 

  11. Calder PC. N-3 polyunsaturated fatty acids, inflammation, and inflammatory diseases. Am J Clin Nutr. 2006;83(6 Suppl):1505s–19s.

    Article  CAS  Google Scholar 

  12. Hamilton B. Vitamin D and human skeletal muscle. Scand J Med Sci Sports. 2010;20(2):182–90.

    CAS  PubMed  PubMed Central  Google Scholar 

  13. Semba RD, Ferrucci L, Sun K, Walston J, Varadhan R, Guralnik JM, et al. Oxidative stress and severe walking disability among older women. Am J Med. 2007;120(12):1084–9.

    Article  CAS  Google Scholar 

  14. Gröber U, Schmidt J, Kisters K. Magnesium in prevention and therapy. Nutrients. 2015;7(9):8199–226.

    Article  Google Scholar 

  15. Van Laecke S. Hypomagnesemia and hypermagnesemia. Acta Clin Belg. 2019;74(1):41–7.

    Article  Google Scholar 

  16. de Baaij JH, Hoenderop JG, Bindels RJ. Magnesium in man: implications for health and disease. Physiol Rev. 2015;95(1):1–46.

    Article  Google Scholar 

  17. Gragossian A, Bashir K, Friede R. Hypomagnesemia. In: StatPearls. Treasure Island. FL: StatPearls Publishing; 2022.

    Google Scholar 

  18. Rock E, Astier C, Lab C, Vignon X, Gueux E, Motta C, et al. Dietary magnesium deficiency in rats enhances free radical production in skeletal muscle. J Nutr. 1995;125(5):1205–10.

    CAS  PubMed  Google Scholar 

  19. Cruz-Jentoft AJ, Baeyens JP, Bauer JM, Boirie Y, Cederholm T, Landi F, et al. Sarcopenia: European consensus on definition and diagnosis: report of the European working group on sarcopenia in older people. Age Ageing. 2010;39(4):412–23.

    Article  Google Scholar 

  20. Dhillon RJ, Hasni S. Pathogenesis and Management of Sarcopenia. Clin Geriatr Med. 2017;33(1):17–26.

    Article  Google Scholar 

  21. Marzetti E, Calvani R, Cesari M, Buford TW, Lorenzi M, Behnke BJ, et al. Mitochondrial dysfunction and sarcopenia of aging: from signaling pathways to clinical trials. Int J Biochem Cell Biol. 2013;45(10):2288–301.

    Article  CAS  Google Scholar 

  22. Rodríguez-Zavala JS, Moreno-Sánchez R. Modulation of oxidative phosphorylation by Mg2+ in rat heart mitochondria. J Biol Chem. 1998;273(14):7850–5.

    Article  Google Scholar 

  23. Kramer JH, Misík V, Weglicki WB. Magnesium-deficiency potentiates free radical production associated with postischemic injury to rat hearts: vitamin E affords protection. Free Radic Biol Med. 1994;16(6):713–23.

    Article  CAS  Google Scholar 

  24. Shah NC, Liu JP, Iqbal J, Hussain M, Jiang XC, Li Z, et al. Mg deficiency results in modulation of serum lipids, glutathione, and NO synthase isozyme activation in cardiovascular tissues: relevance to de novo synthesis of ceramide, serum mg and atherogenesis. Int J Clin Exp Med. 2011;4(2):103–18.

    CAS  PubMed  PubMed Central  Google Scholar 

  25. Liu M, Jeong EM, Liu H, Xie A, So EY, Shi G, et al. Magnesium supplementation improves diabetic mitochondrial and cardiac diastolic function. JCI insight. 2019;4(1).

  26. Rubin H. Intracellular free mg (2+) and MgATP (2-) in coordinate control of protein synthesis and cell proliferation. In: Vink R, Adelaide NM, editors. Magnesium in the central nervous system. AU: University of Adelaide Press; 2011.

    Google Scholar 

  27. Richardson CJ, Schalm SS, Blenis J. PI3-kinase and TOR: PIKTORing cell growth. Semin Cell Dev Biol. 2004;15(2):147–59.

    Article  CAS  Google Scholar 

  28. Schmelzle T, Hall MN. TOR, a central controller of cell growth. Cell. 2000;103(2):253–62.

    Article  CAS  Google Scholar 

  29. Rubin H. Central roles of Mg2+ and MgATP2- in the regulation of protein synthesis and cell proliferation: significance for neoplastic transformation. Adv Cancer Res. 2005;93:1–58.

    Article  CAS  Google Scholar 

  30. King DE, Mainous AG 3rd, Geesey ME, Ellis T. Magnesium intake and serum C-reactive protein levels in children. Magnes Res. 2007;20(1):32–6.

    CAS  PubMed  Google Scholar 

  31. King D, Mainous A, Geesey M, Egan B, Rehman S. Magnesium supplement intake and C-reactive protein levels in adults. Nutr Res. 2006;26.

  32. Chacko SA, Song Y, Nathan L, Tinker L, de Boer IH, Tylavsky F, et al. Relations of dietary magnesium intake to biomarkers of inflammation and endothelial dysfunction in an ethnically diverse cohort of postmenopausal women. Diabetes Care. 2010;33(2):304–10.

    Article  CAS  Google Scholar 

Download references

Acknowledgements

Not applicable.

Funding

All authors did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Author information

Authors and Affiliations

  1. Division of Plastic and Reconstruction Surgery, Department of Surgery, Tri-service General Hospital, National Defense Medical Center, Taipei, Taiwan, Republic of China

    Shih-Wei Yang

  2. Division of Family Medicine, Department of Family and Community Medicine, Tri-Service General Hospital; and School of Medicine, National Defense Medical Center, Taipei, Taiwan, Republic of China

    Shih-Wei Yang, Yuan-Yuei Chen & Wei-Liang Chen

  3. Department of General Medicine, Tri-Service General Hospital; and School of Medicine, National Defense Medical Center, Taipei, Taiwan, Republic of China

    Shih-Wei Yang

  4. Division of Geriatric Medicine, Department of Family and Community Medicine, Tri-Service General Hospital; and School of Medicine, National Defense Medical Center, Number 325, Section 2, Chang-gong Rd, Nei-Hu District, 114, Taipei, Taiwan

    Wei-Liang Chen

  5. Department of Pathology, Tri-Service General Hospital Songshan Branch; and School of Medicine, National Defense Medical Center, Taipei, Taiwan, Republic of China

    Yuan-Yuei Chen

Authors
  1. Shih-Wei Yang
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Yuan-Yuei Chen
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Wei-Liang Chen
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

Shih-Wei Yang and Wei-Liang Chen designed the initial study. Shih-Wei Yang also managed and retrieved the data, contributed to primary data analysis and explanation, and drafted the initial script. Shih-Wei Yang, Yuan-Yuei Chen, and Wei-Liang Chen decided on the methods of data collection. Shih-Wei Yang and Wei-Liang Chen were both responsible for the decisions of data analysis. Wei-Liang Chen conceptualized the study, inspected all sides of the study, critically reviewed, and revised the initial script, and approved the final manuscript as submitted. All authors meet the ICMJE criteria for authorship.

Corresponding author

Correspondence to Wei-Liang Chen.

Ethics declarations

Ethics approval and consent to participate

The health data collection protocols were performed by the CDC’s NCHS and approved by the NCHS IRB (Protocol Number: Protocol #98-12). All informed consents had been obtained from the eligible subjects before initiating data collection and NHANES health examinations. All methods were performed in accordance with the relevant guidelines and regulations.

Consent for publication

Not applicable.

Competing interests

There is no support, financial or otherwise received from any organization that may have an interest in the submitted work, and there are no other relationships or activities that could appear to have influenced the submitted work.

Additional information

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Supplementary Information

Additional file 1 Supplement

Table 1. Standard measurement protocol of muscle quality index in NHANES.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Yang, SW., Chen, YY. & Chen, WL. Association between oral intake magnesium and sarcopenia: a cross-sectional study. BMC Geriatr 22, 816 (2022). https://doi.org/10.1186/s12877-022-03522-5

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/s12877-022-03522-5

Keywords

BMC Geriatrics

ISSN: 1471-2318

Contact us