Nutrition Interventions on Muscle-Related Components of Sarcopenia in Females: A Systematic Review of Randomized Controlled Trials.

Sarcopenia is a skeletal muscle disease categorized by low muscle strength, muscle quantity or quality, and physical performance. Sarcopenia etiology is multifaceted, and while resistance training is widely agreed upon for prevention and treatment, disease progression is also highly related to poor diet. The incidence of sarcopenia appears sex-specific and may be increased in females, which is problematic because dietary quality is often altered later in life, particularly after menopause. Identifying effective nutrition or supplementation interventions could be an important strategy to delay sarcopenia and related comorbidities in this vulnerable population. This systematic review examined randomized controlled trials (RCTs) of nutrition strategies on muscle-related components of sarcopenia in middle-aged and older females. A protocol was registered (PROSPERO CRD42022382943) and a systematic search of MEDLINE and CINAHL was undertaken. RCTs from 2013 to 2023 that assessed nutrition-only interventions on muscle mass, muscle strength, and physical function in female participants were included. Fourteen RCTs were included based on selection criteria. Study designs and interventions were heterogeneous in supplementation type and amount, age, and duration. Six RCTs reported beneficial effects of protein, Vitamin D, Vitamin D and Magnesium (Mg), and fish oil on muscle protein synthesis, muscle strength, and/or muscle function. Eight studies that examined various protein interventions, VitD alone, Mg alone, and dairy derivatives did not demonstrate any effect. Exercise appeared to modulate results in several studies. Nutrition interventions alone are likely to have a limited but positive effect on muscle-related components of sarcopenia in females. Current evidence suggests that a combination of dietary intervention and exercise is likely to be key to preventing and treating sarcopenia in middle aged and older females and there is a need for well-designed nutrition based studies in this population.

Performance Medicine: a novel and needed paradigm for proactive health care.

Performance Medicine is an emerging clinical practice that holds immense promise for advancing preventive health. To date, however, the concept remains imprecise, disorganized, and commercialized. The purpose of this perspective article is to define characteristics, core tenets, and practice standards to help build a common framework. We define performance broadly as "one's capacity to bring energy and attention to what matters most in a given moment". Performance Medicine, therefore, is predicated on the thesis that the critical practices that enhance one's daily wellbeing simultaneously increase both lifespan and healthspan. As a clinical practice, Performance Medicine is proactive and preventive. It focuses on the immediate and actionable strategies to address one's physical, mental, and emotional capabilities every day. The practice employs a values-centered approach that begins with a discovery process to elucidate the client's deeply held beliefs about their health status, life mission and goals, vision for optimal wellbeing, and motivations for change. Subsequent diagnostics and therapies combine evidence-based practices from multiple medical specialties including internal medicine, sports medicine, obesity medicine, integrative medicine, and others. This is complemented by the most recent scientific advancements in nutrition, exercise physiology, sleep, and recovery. The Performance Medicine prescription incorporates a personalized combination of lifestyle-based behavior change practices, evidence-based diagnostics and risk reduction therapies, ongoing monitoring, and community support. Finally, the iterative and incremental process towards enhanced and sustained health is guided and supported by a trusted partnership between the client and a team of expert practitioners and coaches.

Improved Access to and Impact of Registered Dietitian Nutritionist Services Associated with an Integrated Care Model in a High-Risk, Minority Population.

BACKGROUND: Integrated health care models create opportunities for registered dietitian nutritionists (RDNs) to provide nutrition-related care and engage in multidisciplinary teams to improve clinical outcomes. While benefits of integrated care (IC) have been reported, little is known about the impact of the RDN within an IC model. OBJECTIVE: Our primary objective was to identify whether IC vs traditional care (TC) increases the number of RDN patient visits. Our secondary objective was to evaluate clinical outcomes of patients seeing an RDN vs not, regardless of care model. DESIGN: This was a retrospective cohort study. PARTICIPANTS/SETTING: Patients were aged 3 to 94 years and from a patient-centered medical home in Boston, MA. MAIN OUTCOME MEASURES: We measured 3-month total and average number of patients seen by the RDN in TC vs IC. Changes in adult hemoglobin A1c, weight, and pediatric body mass index (measured as kg/m2) among high-risk patients seen by an RDN compared to patients not seen by an RDN. STATISTICAL ANALYSIS: Data were obtained from electronic medical records and analyzed utilizing Mann-Whitney U test, analysis of covariance, and paired sample t tests. RESULTS: The RDN saw 145 patients (137 adult, 8 pediatric) in the TC model compared to 185 patients (135 adult, 50 pediatric) in the IC model. Mean number of patients seen per session was 3.20 in the TC model vs 4.63 in the IC model (P=0.004). Adult hemoglobin A1c within-group differences decreased by 0.42%±1.49% (P=0.007) for patients seen by an RDN and decreased 0.15%±1.47% (P=0.012) for patients not seen by an RDN. Adult weight within-group differences decreased 1.0±7.2 kg (P=0.15) for patients seen by a RDN and increased 0.1±5.6 kg (P=0.70) for patients not seen by a RDN. Pediatric BMI showed no change between or within groups. CONCLUSIONS: The IC model increased 3-month total number of patients seen by an RDN. High-risk patients who saw an RDN had a significant decrease in hemoglobin A1c.

Vitamin D receptor protein is associated with interleukin-6 in human skeletal muscle.

Vitamin D is associated with skeletal muscle physiology and function and may play a role in intramuscular inflammation, possibly via the vitamin D receptor (VDR). We conducted two studies to examine (1) whether serum 25-hydroxyvitamin D (25OHD) and/or intramuscular VDR protein concentrations are associated with intramuscular interleukin-6 (IL-6) and/or tumor necrosis factor-α (TNFα); and (2) whether 16-week supplementation with vitamin D3 alters intramuscular IL-6 and/or TNFα. Potential-related signaling pathways were also examined. Muscle biopsies of 30 older, mobility-limited adults were obtained at baseline. A subset of 12 women were supplemented with either 4,000 IU/day of vitamin D3 (N = 5) or placebo (N = 7), and biopsies were repeated at 16 weeks. Serum 25OHD was measured, and intramuscular VDR, IL-6, and TNFα gene expressions and protein concentrations were analyzed. Baseline serum 25OHD was not associated with intramuscular IL-6 or TNFα gene expression or protein concentration. Baseline intramuscular VDR protein concentration, adjusted for baseline serum 25OHD, was positively associated with intramuscular IL-6 gene expression (n = 28; p = 0.04), but negatively associated with intramuscular IL-6 protein (n = 18; p = 0.03). Neither intramuscular IL-6 nor TNFα gene expression was different between placebo (n = 7) or vitamin D3 supplementation groups (n = 5) after 16 weeks (p = 0.57, p = 0.11, respectively). These data suggest that VDR is a better predictor than serum 25OHD concentration of intramuscular IL-6 gene and protein expressions. A similar relationship was not observed for TNFα expression. Further, supplementation with 4,000 IU vitamin D3 per day does not appear to affect intramuscular IL-6 or TNFα gene expression after 16 weeks.

Effects of 1,25-dihydroxyvitamin D3 and vitamin D3 on the expression of the vitamin d receptor in human skeletal muscle cells.

Vitamin D receptor (VDR) expression and action in non-human skeletal muscle have recently been reported in several studies, yet data on the activity and expression of VDR in human muscle cells are scarce. We conducted a series of studies to examine the (1) effect of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) on VDR gene expression in human primary myoblasts, (2) effect of 16-week supplementation with vitamin D3 on intramuscular VDR gene expression in older women, and (3) association between serum 25-hydroxyvitamin D (25OHD) and intramuscular VDR protein concentration in older adults. Human primary myoblasts were treated with increasing concentrations of 1,25(OH)2D3 for 18 h. A dose-dependent treatment effect was noted with 1 nmol/L of 1,25OH2D3 increasing intramuscular VDR mRNA expression (mean fold change±SD 1.36±0.33; P=0.05). Muscle biopsies were obtained at baseline and 16 weeks after vitamin D3 supplementation (4,000 IU/day) in older adults. Intramuscular VDR mRNA was significantly different from placebo after 16 weeks of vitamin D3 (1.2±0.99; -3.2±1.7, respectively; P=0.04). Serum 25OHD and intramuscular VDR protein expression were examined by immunoblot. 25OHD was associated with intramuscular VDR protein concentration (R=0.67; P=0.0028). In summary, our study found VDR gene expression increases following treatment with 1,25OH2D3 in human myoblasts. 25OHD is associated with VDR protein and 16 weeks of supplementation with vitamin D3 resulted in a persistent increase in VDR gene expression of vitamin D3 in muscle tissue biopsies. These findings suggest treatment with vitamin D compounds results in sustained increases in VDR in human skeletal muscle.

Effects of alkali supplementation and vitamin D insufficiency on rat skeletal muscle.

Data on the independent and potential combined effects of acid-base balance and vitamin D status on muscle mass and metabolism are lacking. We investigated whether alkali supplementation with potassium bicarbonate (KHCO3), with or without vitamin D3 (± VD3), alters urinary nitrogen (indicator of muscle proteolysis), muscle fiber cross-sectional area (FCSA), fiber number (FN), and anabolic (IGF-1, Akt, p70s6k) and catabolic (FOXO3a, MURF1, MAFbx) signaling pathways regulating muscle mass. Thirty-six, 20-month-old, Fischer 344/Brown-Norway rats were randomly assigned in a 2 × 2 factorial design to one of two KHCO3-supplemented diets (± VD3) or diets without KHCO3 (± VD3) for 12 weeks. Soleus, extensor digitorum longus (EDL), and plantaris muscles were harvested at 12 weeks. Independent of VD3 group, KHCO3 supplementation resulted in 35 % lower mean urinary nitrogen to creatinine ratio, 10 % higher mean type I FCSA (adjusted to muscle weight), but no statistically different mean type II FCSA (adjusted to muscle weight) or FN compared to no KHCO3. Among VD3-replete rats, phosphorylated-Akt protein expression was twofold higher in the KHCO3 compared to no KHCO3 groups, but this effect was blunted in rats on VD3-deficient diets. Neither intervention significantly affected serum or intramuscular IGF-1 expression, p70s6k or FOXO3a activation, or MURF1 and MAFbx gene expression. These findings provide support for alkali supplementation as a promising intervention to promote preservation of skeletal muscle mass, particularly in the setting of higher vitamin D status. Additional research is needed in defining the muscle biological pathways that are being targeted by alkali and vitamin D supplementation.