Project description:PurposeThe single nutrient approach in nutrition research lacks the ability to account for synergistic relationships between dietary components. Current evidence suggests that diet quality, reflecting overall dietary intake, may influence muscle health. In a community-based observational study in Western Norway, we examined dietary patterns in relation to muscle mass and strength at age 67-70.MethodsThe current analysis was conducted in men and women of The Hordaland Health Study (HUSK), who participated in both the second (HUSK2) and third study wave (HUSK3). Dietary patterns were extracted by principal component analysis (PCA) on food frequency questionnaire (FFQ) data. Individual dietary pattern scores (DPS) for HUSK2 (age 46-49) and HUSK3 (age 67-70), and overall DPS (oDPS) were calculated. Outcome variables were appendicular skeletal muscle mass (ASMM) and handgrip strength (HGS) measured in HUSK3. The relationships of HUSK3 DPS and oDPS with ASMM and HGS were assessed by multivariate linear regression analysis adjusted for potential confounding factors.ResultsWe identified three distinct dietary patterns, labelled 'Western', 'Healthy', and 'Sweets-focused'. A significant positive association was observed between the oDPS for the 'Healthy' dietary pattern and ASMM in both men and women at age 67-70. No significant associations were found between HUSK3 DPS or oDPS for any of the identified dietary patterns and HGS in our population.ConclusionHigher oDPS on a dietary pattern predominantly rich in fish, vegetables, nuts and seeds, fruit and berries, and eggs was associated with better ASMM at age 67-70. To establish the influence of diet quality on muscle health, further long-term studies with repeated dietary assessments are warranted.
Project description:ObjectiveThe role of vitamin K in the regulation of vascular calcification is established. However, the association of dietary vitamins K1 and K2 with risk of coronary heart disease (CHD) is inconclusive.DesignProspective cohort study.SettingWe followed participants in the community-based Hordaland Health Study from 1997 - 1999 through 2009 to evaluate associations between intake of vitamin K and incident (new onset) CHD. Baseline diet was assessed by a past-year food frequency questionnaire. Energy-adjusted residuals of vitamin K1 and vitamin K2 intakes were categorised into quartiles.Participants2987 Norwegian men and women, age 46-49 years.MethodsInformation on incident CHD events was obtained from the nationwide Cardiovascular Disease in Norway (CVDNOR) Project. Multivariable Cox regression estimated HRs and 95% CIs with test for linear trends across quartiles. Analyses were adjusted for age, sex, total energy intake, physical activity, smoking and education. A third model further adjusted K1 intake for energy-adjusted fibre and folate, while K2 intake was adjusted for energy-adjusted saturated fatty acids and calcium.ResultsDuring a median follow-up time of 11 years, we documented 112 incident CHD cases. In the adjusted analyses, there was no association between intake of vitamin K1 and CHD (HRQ4vsQ1 = 0.92 (95% CI 0.54 to 1.57), p for trend 0.64), while there was a lower risk of CHD associated with higher intake of energy-adjusted vitamin K2 (HRQ4vsQ1 = 0.52 (0.29 to 0.94), p for trend 0.03). Further adjustment for potential dietary confounders did not materially change the association for K1, while the association for K2 was slightly attenuated (HRQ4vsQ1 = 0.58 (0.28 to 1.19)).ConclusionsA higher intake of vitamin K2 was associated with lower risk of CHD, while there was no association between intake of vitamin K1 and CHD.Trial registration numberNCT03013725.
Project description:BackgroundAs more people live more of their lives obese, it is unclear what impact this will have on muscle mass, strength, and quality. We aimed to examine the associations of body mass index (BMI) from age 15 years onwards with low muscle mass, strength, and quality in early old age.MethodsA total of 1,511 men and women from a British birth cohort study with BMI measured at 15, 20, 26, 36, 43, 53, and 60-64 years and dual-energy x-ray absorptiometry scans at 60-64 years were included. Four binary outcomes identified those in the bottom sex-specific 20% of (a) appendicular lean mass (ALM) index (kilogram per square meter), (b) ALM residuals (derived from sex-specific models in which ALM (kilogram) = β0 + β1 height [meter] + β2 fat mass [kilogram]), (c) grip strength (kilogram), (d) muscle quality (grip strength [kilogram]/arm lean mass [kilogram]). Associations of BMI with each outcome were tested.ResultsHigher BMI from age 15 years was associated with lower odds of low ALM but higher odds of low muscle quality (per 1 SD increase in BMI at 36 years, odds ratio of low ALM residuals = 0.50 [95% CI: 0.43, 0.59], and muscle quality = 1.50 [1.29, 1.75]). Greater gains in BMI were associated with lower odds of low ALM index but higher odds of low muscle quality. BMI was not associated with grip strength.ConclusionsGiven increases in the global prevalence of obesity, cross-cohort comparisons of sarcopenia need to consider our findings that greater gains in BMI are associated with higher muscle mass but not with grip strength and therefore with lower muscle quality.
Project description:IntroductionThe present study aimed to investigate the associations of depression with muscle mass and muscle strength, and whether these associations were modified or mediated by dietary energy intake and dietary quality.MethodsOur study included participants aged 40 and above from the 2011-2018 cycles of the National Health and Nutrition Examination Survey (NHANES). Depression was evaluated using the nine-item Patient Health Questionnaire. Skeletal muscle mass index (SMI) and handgrip strength (HGS) were used to evaluate muscle mass and muscle strength, respectively. Information on dietary intake were obtained via dietary recall. Dietary quality was assessed using healthy eating index-2015 (HEI-2015). We performed multivariable linear regression models to examine the associations of depression with SMI (N = 3,648) and HGS (N = 4,679). Interaction analyses and mediation analyses were conducted to test the effect of dietary energy intake and HEI-2015 on the associations of depression with SMI and HGS.ResultsDepression was associated with decreased SMI and HGS. Interactions between depression and HEI-2015 were observed for SMI, but not for HGS. The stratified analyses showed that depression was associated with decreased SMI in participants whose HEI-2015 were lower than the median. Mediation analyses revealed that dietary energy intake mediated the associations of depression with SMI and HGS.ConclusionHEI-2015 modified the associations between depression and muscle mass. The inverse associations of depression with muscle mass and muscle strength were partially mediated by dietary energy intake. These findings emphasized the importance of dietary energy intake and dietary quality in preventing muscle loss in middle-aged and older participants with depression.
Project description:Obesity is declared as a chronic multifaceted health problem, and young adults may be particularly vulnerable to weight gain. This study aims to identify the role of dietary calcium intake and the muscle strength index in handling excess of fat mass in young adults and to examine if the relationship between dietary calcium intake and fat mass percentage is mediated by muscle strength. A cross-sectional study including 355 Spanish college students (aged 21.05 ± 3.11) was performed during the 2017-2018 academic year. Pearson correlation coefficients were estimated to determine the relationship between dietary calcium intake, fat mass percentage, body mass index, muscle strength components, and total energy intake. ANCOVA models were used to analyze the differences in the muscle strength index by total dietary calcium intake categories, as well as the differences in % fat mass by total dietary calcium intake and muscle strength index categories, controlling for different sets of confounders. A mediator analysis was conducted to test if the relationship between dietary calcium intake and fat mass percentage was explained by muscle strength. Data on the fat mass percentage, dietary calcium intake, and muscle strength index as the sum of the standardized z-score of the standing long jump and z-score of handgrip/weight were collected. The muscle strength index was significantly better in young adults with higher dietary calcium intake. Moreover, the fat mass percentage was significantly lower in those with a higher dietary calcium intake and a better muscle strength index. Finally, the relationship between dietary calcium intake and fat mass percentage was fully mediated by muscle strength (z = -1.90; p < 0.05), explaining 33.33% of this relationship. This study suggests that both a major dietary calcium intake and muscle strength are associated with fat mass percentage. Moreover, muscle strength mediates the link between dietary calcium intake and fat mass percentage. Therefore, both high dietary calcium intake and exercise activities aimed at improving muscle strength levels may help to prevent the cardiometabolic risk associated with an excess of fat mass in young people.
Project description:Sarcopenia, or skeletal muscle atrophy, is a debilitating comorbidity of many physiological and pathophysiological processes, including normal aging. There are no approved therapies for sarcopenia, but the antihypertrophic myokine myostatin is a potential therapeutic target. Here, we show that treatment of young and old mice with an anti-myostatin antibody (ATA 842) for 4 wk increased muscle mass and muscle strength in both groups. Furthermore, ATA 842 treatment also increased insulin-stimulated whole body glucose metabolism in old mice, which could be attributed to increased insulin-stimulated skeletal muscle glucose uptake as measured by a hyperinsulinemic-euglycemic clamp. Taken together, these studies provide support for pharmacological inhibition of myostatin as a potential therapeutic approach for age-related sarcopenia and metabolic disease.
Project description:Pannexins (Panxs), glycoproteins that oligomerize to form hemichannels on the cell membrane, are topologically similar to connexins, but do not form cell-to-cell gap junction channels. There are 3 members of the family, 1-3, with Panx1 being the most abundant. All Panxs are expressed in bone, but their role in bone cell biology is not completely understood. We now report that osteocytic Panx1 deletion (Panx1Δot) alters bone mass and strength in female mice. Bone mineral density after reaching skeletal maturity is higher in female Panx1Δot mice than in control Panx1fl/fl mice. Further, osteocytic Panx1 deletion partially prevented aging effects on cortical bone structure and mechanical properties. Young 4-month-old female Panx1Δot mice exhibited increased lean body mass, even though pannexin levels in skeletal muscle were not affected; whereas no difference in lean body mass was detected in male mice. Furthermore, female Panx1-deficient mice exhibited increased muscle mass without changes in strength, whereas Panx1Δot males showed unchanged muscle mass and decreased in vivo maximum plantarflexion torque, indicating reduced muscle strength. Our results suggest that osteocytic Panx1 deletion increases bone mass in young and old female mice and muscle mass in young female mice, but has deleterious effects on muscle strength only in males.
Project description:ObjectiveLimiting SFA intake may minimise the risk of CHD. However, such reduction often leads to increased intake of carbohydrates. We aimed to evaluate associations and the interplay of carbohydrate and SFA intake on CHD risk.DesignProspective cohort study.SettingWe followed participants in the Hordaland Health Study, Norway from 1997-1999 through 2009. Information on carbohydrate and SFA intake was obtained from a FFQ and analysed as continuous and categorical (quartiles) variables. Multivariable Cox regression estimated hazard ratios (HR) and 95 % CI. Theoretical substitution analyses modelled the substitution of carbohydrates with other nutrients. CHD was defined as fatal or non-fatal CHD (ICD9 codes 410-414 and ICD10 codes I20-I25).Participants2995 men and women, aged 46-49 years.ResultsAdjusting for age, sex, energy intake, physical activity and smoking, SFA was associated with lower risk (HRQ4 v. Q1 0·44, 95 % CI 0·26, 0·76, Ptrend = 0·002). For carbohydrates, the opposite pattern was observed (HRQ4 v. Q1 2·10, 95 % CI 1·22, 3·63, Ptrend = 0·003). SFA from cheese was associated with lower CHD risk (HRQ4 v. Q1 0·44, 95 % CI 0·24, 0·83, Ptrend = 0·006), while there were no associations between SFA from other food items and CHD. A 5 E% substitution of carbohydrates with total fat, but not SFA, was associated with lower CHD risk (HR 0·75, 95 % CI 0·62, 0·90).ConclusionsHigher intake of predominantly high glycaemic carbohydrates and lower intake of SFA, specifically lower intake from cheese, were associated with higher CHD risk. Substituting carbohydrates with total fat, but not SFA, was associated with significantly lower risk of CHD.
Project description:BackgroundSarcopenia, a progressive loss of skeletal muscle mass and strength, can begin in the 4th decade of life. Protein intake predicts skeletal muscle mass and strength among older adults, but knowledge of similar associations among middle-aged adults is lacking.ObjectivesWe aimed to assess associations between protein intake and skeletal muscle mass, characterized by appendicular lean mass adjusted for BMI [in kg/m2 (ALMBMI)], and muscle strength, represented by handgrip strength adjusted for BMI (GSMAXBMI), among middle-aged adults.MethodsWe analyzed cross-sectional data from 1209 men and 1208 women aged 40-59 y in the 2011-2014 NHANES. Protein intake per kilogram actual body weight (BW), assessed by two 24-h recalls, was examined as continuous and categorical parameters [low (<RDA, 0.8 g/kg BW), moderate (≥RDA, <1.2 g/kg BW), and high (≥1.2 g/kg BW)]. ALM was measured using DXA, and GSMAX was measured using handgrip dynamometer. "Low lean mass" and "weakness" were defined using NIH criteria for ALMBMI and GSMAXBMI, respectively. Linear and logistic regression models were performed.ResultsAmong middle-aged adults, 15.6% of men and 13.4% of women had low lean mass and 3.5% of men and 2.3% of women exhibited weakness. Protein intakes per kilogram BW were positively associated with ALMBMI and GSMAXBMI among men and women after adjustment for age, race/Hispanic origin, physical activity, and self-rated health. Compared with the moderate protein group, the high protein group had a higher GSMAXBMI and the low protein group had a lower GSMAXBMI among men and women. The low protein group had a lower ALMBMI (women) and had a higher OR for low lean mass (men) compared with the moderate protein group.ConclusionsHigher protein intakes were associated with greater ALMBMI and GSMAXBMI in this representative sample of US middle-aged adults. Our findings highlight the need for further research on dietary protein as a potential modifying factor of sarcopenia risk in middle age.
Project description:In addition to driving contraction of skeletal muscles, acetylcholine (ACh) acts as an anti-synaptogenic agent at neuromuscular junctions (NMJs). Previous studies suggest that aging is accompanied by increases in cholinergic activity at the NMJ, which may play a role in neuromuscular degeneration. In this study, we hypothesized that moderately and chronically reducing ACh could attenuate the deleterious effects of aging on NMJs and skeletal muscles. To test this hypothesis, we analyzed NMJs and muscle fibers from heterozygous transgenic mice with reduced expression of the vesicular ACh transporter (VAChT; VKDHet), which present with approximately 30% less synaptic ACh compared to control mice. Because ACh is constitutively decreased in VKDHet, we first analyzed developing NMJs and muscle fibers. We found no obvious morphological or molecular differences between NMJs and muscle fibers of VKDHet and control mice during development. In contrast, we found that moderately reducing ACh has various effects on adult NMJs and muscle fibers. VKDHet mice have significantly larger NMJs and muscle fibers compared to age-matched control mice. They also present with reduced expression of the pro-atrophy gene, Foxo1, and have more satellite cells in skeletal muscles. These molecular and cellular features may partially explain the increased size of NMJs and muscle fibers. Thus, moderately reducing ACh may be a therapeutic strategy to prevent the loss of skeletal muscle mass that occurs with advancing age.