Nutrient Intake and Its Association with Appendicular Total Lean Mass and Muscle Function and Strength in Older Adults: A Population-Based Study

Nutrients. 2024 Feb 19;16(4):568. doi: 10.3390/nu16040568.

Abstract

Treatment options for sarcopenia are currently limited, and primarily rely on two main therapeutic approaches: resistance-based physical activity and dietary interventions. However, details about specific nutrients in the diet or supplementation are unclear. We aim to investigate the relationship between nutrient intake and lean mass, function, and strength. Data were derived from the Gothenburg H70 birth cohort study in Sweden, including 719,70-year-olds born in 1944 (54.1% females). For independent variables, the diet history method (face-to-face interviews) was used to estimate habitual food intake during the preceding three months. Dependent variables were gait speed (muscle performance), hand grip strength (muscle strength), and the appendicular lean soft tissue index (ALSTI). Linear regression analyses were performed to analyze the relationship between the dependent variables and each of the covariates. Several nutrients were positively associated with ALSTI, such as polyunsaturated fatty acids (DHA, EPA), selenium, zinc, riboflavin, niacin equivalent, vitamin B12, vitamin D, iron, and protein. After correction for multiple comparisons, there were no remaining correlations with handgrip and gait speed. Findings of positive correlations for some nutrients with lean mass suggest a role for these nutrients in maintaining muscle volume. These results can be used to inform clinical trials to expand the preventive strategies and treatment options for individuals at risk of muscle loss and sarcopenia.

Keywords: aging; body composition; diet; muscle strength; sarcopenia; walking speed.

MeSH terms

  • Aged
  • Aged, 80 and over
  • Body Composition / physiology
  • Cohort Studies
  • Eating
  • Female
  • Hand Strength / physiology
  • Humans
  • Male
  • Muscle Strength / physiology
  • Muscles
  • Sarcopenia*

Grants and funding

This research was funded by: The Alzheimerfonden (AF-842471, AF-737641, AF-929959, AF-939825); the Swedish Research Council (2019-02075), Stiftelsen Psykiatriska Forskningsfonden, Stiftelsen Demensfonden, Stiftelsen Hjalmar Svenssons Forskningsfond, Stiftelsen Wilhelm och Martina Lundgrens vetenskapsfond. SK was financed by grants from the Swedish state under the agreement between the Swedish government and the county councils, the ALF-agreement (ALFGBG-965923, ALFGBG-81392, ALFGBG-771071). In addition, this paper represents independent research supported by the Norwegian government through the hospital owner Helse Vest (Western Norway Regional Health Authority) (F-12511). It was also funded by the National Institute for Health Research (NIHR) Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King’s College London. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, or the Department of Health and Social Care. LW is supported by a Canadian Institutes of Health Research Banting Postdoctoral Fellowship award.