Sarcopenia and the Common Mental Disorders: a Potential Regulatory Role of Skeletal Muscle on Brain Function?
TL;DR: An emerging body of evidence is presented to support the hypothesis that shared pathophysiological pathways for sarcopenia and the common mental disorders constitute links between skeletal muscle and brain function.
Abstract: While it is understood that body composition impacts on physical conditions, such as diabetes and cardiovascular disease, it is only now apparent that body composition might play a role in the genesis of common mental disorders, depression and anxiety. Sarcopenia occurs in ageing and comprises a progressive decline in muscle mass, strength and function, leading to frailty, decreased independence and poorer quality of life. This review presents an emerging body of evidence to support the hypothesis that shared pathophysiological pathways for sarcopenia and the common mental disorders constitute links between skeletal muscle and brain function. Contracting skeletal muscle secretes neurotrophic factors that are known to play a role in mood and anxiety, and have the dual role of nourishing neuronal growth and differentiation, while protecting the size and number of motor units in skeletal muscle. Furthermore, skeletal muscle activity has important immune and redox effects that impact behaviour and reduce muscle catabolism.
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TL;DR: Results revealed positive regulatory feedback between physical activity, apelin and muscle function and identified apelin both as a tool for diagnosis of early sarcopenia and as the target of an innovative pharmacological strategy to prevent age-associated muscle weakness and restore physical autonomy.
Abstract: Sarcopenia, the degenerative loss of skeletal muscle mass, quality and strength, lacks early diagnostic tools and new therapeutic strategies to prevent the frailty-to-disability transition often responsible for the medical institutionalization of elderly individuals. Herein we report that production of the endogenous peptide apelin, induced by muscle contraction, is reduced in an age-dependent manner in humans and rodents and is positively associated with the beneficial effects of exercise in older persons. Mice deficient in either apelin or its receptor (APLNR) presented dramatic alterations in muscle function with increasing age. Various strategies that restored apelin signaling during aging further demonstrated that this peptide considerably enhanced muscle function by triggering mitochondriogenesis, autophagy and anti-inflammatory pathways in myofibers as well as enhancing the regenerative capacity by targeting muscle stem cells. Taken together, these findings revealed positive regulatory feedback between physical activity, apelin and muscle function and identified apelin both as a tool for diagnosis of early sarcopenia and as the target of an innovative pharmacological strategy to prevent age-associated muscle weakness and restore physical autonomy.
190 citations
TL;DR: Sarcopenia was independently associated with depression, and the causal relationship between the two clinical conditions requires future validation with cohort studies.
Abstract: Objectives to explore whether sarcopenia is associated with depression. Design electronic literature databases from PubMed, Scopus, Embase and Google Scholar were searched. A systematic review and meta-analysis of observational studies was conducted. Setting community and outpatient clinic. Participants people with and without diagnoses of sarcopenia. Measurements outcome measures of depression. Results about 15 articles were included, 5 of which were retrieved for narrative review. The crude odds ratios (ORs) between sarcopenia and depression were extracted from the remaining 10 studies, 6 of which also included adjusted ORs. Sarcopenia was associated with depression without adjusting covariates (crude OR, 1.640; 95% confidence interval (CI), 1.247-2.155). After adjusting for potential confounders such as age, gender, cognitive performance and physical activity, sarcopenia still demonstrated a significant positive association with depression (adjusted OR, 1.821; 95% CI, 1.160-2.859). A stratified analysis showed that the studies that used bioelectrical impedance analysis for measurement of body composition tended to have an elevated association between sarcopenia and depression compared with those that used dual-energy X-ray absorptiometry or equation estimation. Conclusion sarcopenia was independently associated with depression. The causal relationship between the two clinical conditions requires future validation with cohort studies.
148 citations
Cites background from "Sarcopenia and the Common Mental Di..."
...Gender plays an important role in hormone regulation and muscle metabolism and influences the prevalence of depression in the general population [29, 30]....
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TL;DR: A review of the literature on the relationship between skeletal muscle health and cognition is presented in this paper, which suggests that sarcopenia and cognitive decline share pathophysiological pathways and lifestyle risk factors, such as physical inactivity, poor diet and smoking, are common risk factors for both disorders.
Abstract: Sarcopenia is the loss of skeletal muscle mass and function with advancing age. It involves both complex genetic and modifiable risk factors, such as lack of exercise, malnutrition and reduced neurological drive. Cognitive decline refers to diminished or impaired mental and/or intellectual functioning. Contracting skeletal muscle is a major source of neurotrophic factors, including brain-derived neurotrophic factor, which regulate synapses in the brain. Furthermore, skeletal muscle activity has important immune and redox effects that modify brain function and reduce muscle catabolism. The identification of common risk factors and underlying mechanisms for sarcopenia and cognition may allow the development of targeted interventions that slow or reverse sarcopenia and also certain forms of cognitive decline. However, the links between cognition and skeletal muscle have not been elucidated fully. This review provides a critical appraisal of the literature on the relationship between skeletal muscle health and cognition. The literature suggests that sarcopenia and cognitive decline share pathophysiological pathways. Ageing plays a role in both skeletal muscle deterioration and cognitive decline. Furthermore, lifestyle risk factors, such as physical inactivity, poor diet and smoking, are common to both disorders, so their potential role in the muscle–brain relationship warrants investigation.
59 citations
TL;DR: It is suggested that low grip strength is associated with age, female sex, height, depression and mobility problems in poor elderly and can be a simple, quick and inexpensive means of stratifying elders’ risk of sarcopenia in the primary care setting.
Abstract: Introduction
Sarcopenia is a condition diagnosed when the patient presents low muscle mass, plus low muscle strength or low physical performance. Muscle weakness in the oldest (dynapenia) is a major public health concern because it predicts future all-cause mortality and is associated with falls, disability, cardiovascular mortality and morbidity. Grip strength is a simple method for assessment of muscle function in clinical practice.
Objective
To estimate the grip strength and identify factors associated with handgrip strength variation in elderly people with low socioeconomic status.
Methods
Cross-sectional study based on a multidimensional assessment of primary care users that were 60 years or older. The sample size was calculated using an estimated prevalence of depression in older adults of 20%. A kappa coefficient of 0.6 with a 95% confidence interval was used to generate a conservative sample size of 180 individuals. Procedures: tests and scales to assess humor, cognition (MMSE), basic (ADL) and instrumental activities (IADL) of daily living, mobility (Timed Up and Go), strength, height, Body Mass Index (BMI) and social support were applied. Questions about falls, chronic diseases and self-rated health (SRH) were also included. Statistical Analysis: Mean, standard deviation and statistical tests were used to compare grip strength means by demographic and health factors. A multivariate linear model was used to explain the relationship of the predictors with grip strength.
Results
The group was composed predominantly by women (73%) with a very low level of education (mean 3 years of schooling), mean age of 73.09 (± 7.05) years old, good mobility and without IADL impairment. Mean grip strength of male and female were 31.86Kg (SD 5.55) and 21.69Kg (SD 4.48) [p- 0.0001], respectively. Low grip strength was present in 27.7% of women and 39.6% of men. As expected, men and younger participants had higher grip strength than women and older individuals. In the adjusted model, age (p- 0.03), female sex (p- 0.0001), mobility (p- 0.05), height (p- 0.03) and depression (p- 0.03) were independently associated with low grip strength. For every second more in the mobility test, there was a mean decrease of 0.08 Kg in the grip strength. Elders with depression had a mean reduction of 1.74Kg in the grip strength in relation to those in the comparison groups. There was an average reduction of 8.36Kg in the grip strength of elderly females relative to males. For each year of age after 60 years, it was expected an average reduction of 0.11 Kg in the grip strength.
Conclusion
our results suggest that low grip strength is associated with age, female sex, height, depression and mobility problems in poor elderly. Grip strength can be a simple, quick and inexpensive means of stratifying elders’ risk of sarcopenia in the primary care setting. Efforts should be made to recognize weaker persons and the conditions associated to low grip strength in order to target early interventions to prevent frailty and disability.
56 citations
TL;DR: Sarcopenia is highly prevalent in CKD/end stage renal disease patients and is associated with changes in early systemic indices of atherosclerosis and endothelial dysfunction, known as markers of worse prognosis.
55 citations
References
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TL;DR: This study provides a potential standardized definition for frailty in community-dwelling older adults and offers concurrent and predictive validity for the definition, and finds that there is an intermediate stage identifying those at high risk of frailty.
Abstract: Background: Frailty is considered highly prevalent in old age and to confer high risk for falls, disability, hospitalization, and mortality. Frailty has been considered synonymous with disability, comorbidity, and other characteristics, but it is recognized that it may have a biologic basis and be a distinct clinical syndrome. A standardized definition has not yet been established.
Methods: To develop and operationalize a phenotype of frailty in older adults and assess concurrent and predictive validity, the study used data from the Cardiovascular Health Study. Participants were 5,317 men and women 65 years and older (4,735 from an original cohort recruited in 1989-90 and 582 from an African American cohort recruited in 1992-93). Both cohorts received almost identical baseline evaluations and 7 and 4 years of follow-up, respectively, with annual examinations and surveillance for outcomes including incident disease, hospitalization, falls, disability, and mortality.
Results: Frailty was defined as a clinical syndrome in which three or more of the following criteria were present: unintentional weight loss (10 lbs in past year), self-reported exhaustion, weakness (grip strength), slow walking speed, and low physical activity. The overall prevalence of frailty in this community-dwelling population was 6.9%; it increased with age and was greater in women than men. Four-year incidence was 7.2%. Frailty was associated with being African American, having lower education and income, poorer health, and having higher rates of comorbid chronic diseases and disability. There was overlap, but not concordance, in the cooccurrence of frailty, comorbidity, and disability. This frailty phenotype was independently predictive (over 3 years) of incident falls, worsening mobility or ADL disability, hospitalization, and death, with hazard ratios ranging from 1.82 to 4.46, unadjusted, and 1.29-2.24, adjusted for a number of health, disease, and social characteristics predictive of 5-year mortality. Intermediate frailty status, as indicated by the presence of one or two criteria, showed intermediate risk of these outcomes as well as increased risk of becoming frail over 3-4 years of follow-up (odds ratios for incident frailty = 4.51 unadjusted and 2.63 adjusted for covariates, compared to those with no frailty criteria at baseline).
Conclusions: This study provides a potential standardized definition for frailty in community-dwelling older adults and offers concurrent and predictive validity for the definition. It also finds that there is an intermediate stage identifying those at high risk of frailty. Finally, it provides evidence that frailty is not synonymous with either comorbidity or disability, but comorbidity is an etiologic risk factor for, and disability is an outcome of, frailty. This provides a potential basis for clinical assessment for those who are frail or at risk, and for future research to develop interventions for frailty based on a standardized ascertainment of frailty.
16,255 citations
TL;DR: The evidence reviewed in this Position Stand is generally consistent with prior American College of Sports Medicine statements on the types and amounts of physical activity recommended for older adults as well as the recently published 2008 Physical Activity Guidelines for Americans.
Abstract: The purpose of this Position Stand is to provide an overview of issues critical to understanding the importance of exercise and physical activity in older adult populations. The Position Stand is divided into three sections: Section 1 briefly reviews the structural and functional changes that characterize normal human aging, Section 2 considers the extent to which exercise and physical activity can influence the aging process, and Section 3 summarizes the benefits of both long-term exercise and physical activity and shorter-duration exercise programs on health and functional capacity. Although no amount of physical activity can stop the biological aging process, there is evidence that regular exercise can minimize the physiological effects of an otherwise sedentary lifestyle and increase active life expectancy by limiting the development and progression of chronic disease and disabling conditions. There is also emerging evidence for significant psychological and cognitive benefits accruing from regular exercise participation by older adults. Ideally, exercise prescription for older adults should include aerobic exercise, muscle strengthening exercises, and flexibility exercises. The evidence reviewed in this Position Stand is generally consistent with prior American College of Sports Medicine statements on the types and amounts of physical activity recommended for older adults as well as the recently published 2008 Physical Activity Guidelines for Americans. All older adults should engage in regular physical activity and avoid an inactive lifestyle.
4,264 citations
TL;DR: A reciprocal link between depression and obesity was found to increase the risk of depression, most pronounced among Americans and for clinically diagnosed depression, in addition to depression being predictive of developing obesity.
Abstract: Context: Association between obesity and depression has repeatedly been established. For treatment and prevention purposes, it is important to acquire more insight into their longitudinal interaction. Objective: To conduct a systematic review and meta-analysis on the longitudinal relationship between depression, overweight, and obesity and to identify possible influencing factors. Data Sources: Studies were found using PubMed, PsycINFO, and EMBASE databases and selected on several criteria. Study Selection: Studies examining the longitudinal bidirectional relation between depression and overweight (body mass index 25-29.99) or obesity (body mass index >= 30) were selected. Data Extraction: Unadjusted and adjusted odds ratios (ORs) were extracted or provided by the authors. Data Synthesis: Overall, unadjusted ORs were calculated and subgroup analyses were performed for the 15 included studies (N = 58 745) to estimate the effect of possible moderators (sex, age, depression severity). Obesity at baseline increased the risk of onset of depression at follow-up (unadjusted OR, 1.55; 95% confidence interval [CI], 1.22-1.98; P = 60 years) but not among younger persons (aged < 20 years). Baseline depression (symptoms and disorder) was not predictive of overweight over time. However, depression increased the odds for developing obesity (OR, 1.58; 95% CI, 1.33-1.87; P < .001). Subgroup analyses did not reveal specific moderators of the association. Conclusions: This meta-analysis confirms a reciprocal link between depression and obesity. Obesity was found to increase the risk of depression, most pronounced among Americans and for clinically diagnosed depression. In addition, depression was found to be predictive of developing obesity.
3,499 citations
TL;DR: Investigation of the effect of antidepressants on hippocampal neurogenesis in the adult rat using the thymidine analog bromodeoxyuridine (BrdU) as a marker for dividing cells demonstrates that chronic antidepressant treatment significantly increases the number of BrdU-labeled cells in the dentate gyrus and hilus of the hippocampus.
Abstract: Recent studies suggest that stress-induced atrophy and loss of hippocampal neurons may contribute to the pathophysiology of depression. The aim of this study was to investigate the effect of antidepressants on hippocampal neurogenesis in the adult rat, using the thymidine analog bromodeoxyuridine (BrdU) as a marker for dividing cells. Our studies demonstrate that chronic antidepressant treatment significantly increases the number of BrdU-labeled cells in the dentate gyrus and hilus of the hippocampus. Administration of several different classes of antidepressant, but not non-antidepressant, agents was found to increase BrdU-labeled cell number, indicating that this is a common and selective action of antidepressants. In addition, upregulation of the number of BrdU-labeled cells is observed after chronic, but not acute, treatment, consistent with the time course for the therapeutic action of antidepressants. Additional studies demonstrated that antidepressant treatment increases the proliferation of hippocampal cells and that these new cells mature and become neurons, as determined by triple labeling for BrdU and neuronal- or glial-specific markers. These findings raise the possibility that increased cell proliferation and increased neuronal number may be a mechanism by which antidepressant treatment overcomes the stress-induced atrophy and loss of hippocampal neurons and may contribute to the therapeutic actions of antidepressant treatment.
3,053 citations
"Sarcopenia and the Common Mental Di..." refers background in this paper
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