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In this double-blind trial, patients with chronic kidney disease and type 2 diabetes were randomly assigned to receive the nonsteroidal, selective mineralocorticoid receptor antagonist finerenone or placebo. Treatment with finerenone resulted in lower risks of chronic kidney disease outcomes and cardiovascular outcomes than placebo.

The Journal of Cachexia, Sarcopenia and Muscle (JCSM) aims to publish articles with relevance to wasting disorders and illnesses of the muscle in the broadest sense. In order to avoid publication of inappropriate articles and to avoid protracted disputes, the Editors have established ethical guidelines that detail a number of regulations to be fulfilled prior to submission to the journal. This article updates the principles of ethical authorship and publishing in JCSM and its two daughter journals JCSM Rapid Communication and JCSM Clinical Reports. We require the corresponding author, on behalf of all co‐authors, to certify adherence to the following principles: All authors listed on a manuscript considered for publication have approved its submission and (if accepted) approve publication in the journal; Each named author has made a material and independent contribution to the work submitted for publication; No person who has a right to be recognized as author has been omitted from the list of authors on the submitted manuscript; The submitted work is original and is neither under consideration elsewhere nor that it has been published previously in whole or in part other than in form; All authors certify that the submitted work is original and does not contain excessive overlap with prior or contemporaneous publication elsewhere, and where the publication reports on cohorts, trials, or data that have been reported on before the facts need to be acknowledged and these other publications must be referenced; All original research work has been approved by the relevant bodies such as institutional review boards or ethics committees; All relevant conflicts of interest, financial or otherwise, that may affect the authors' ability to present data objectively, and relevant sources of funding of the research in question have been duly declared in the manuscript; All authors certify that they will submit the original source data to the editorial office upon request; The manuscript in its published form will be maintained on the servers of the journal as a valid publication only as long as all statements in these guidelines remain true; If any of the aforementioned statements ceases to be true, the authors have a duty to notify as soon as possible the Editor‐in‐Chief of the journal, so that the available information regarding the published article can be updated and/or the manuscript can be withdrawn.

The new ICD‐10‐CM (M62.84) code for sarcopenia represents a major step forward in recognizing sarcopenia as a disease. This should lead to an increase in availability of diagnostic tools and the enthusiasm for pharmacological companies to develop drugs for sarcopenia.

Key Points Cardiac cachexia is defined as an advanced stage of heart failure associated with involuntary loss of at least 5% of non-oedematous body weight Muscle wasting, also known as sarcopenia, can occur earlier than cachexia in the course of the body-wasting process and might not be associated with weight loss Therapeutic approaches remain poorly defined, but can involve a combined approach of exercise, nutritional counselling, and pharmacotherapy Nutritional advice includes avoiding excessive salt and fluid intake, replenishment of deficiencies in trace elements, administration of omega-3 polyunsaturated fatty acids, and high-calorific nutrition Several drugs have been tested in small studies for the treatment of body wasting, with testosterone having the strongest evidence base, although the number of patients studied is small Muscle wasting (sarcopenia) and loss of weight (cachexia) can occur in patients with heart failure. In this Review, von Haehling and colleagues provide an overview of the prevalence and pathophysiological mechanisms of these processes in heart failure, and discuss potential therapeutic strategies, including exercise training, nutritional supplements, and drug treatments. Body wasting is a serious complication that affects a large proportion of patients with heart failure. Muscle wasting, also known as sarcopenia, is the loss of muscle mass and strength, whereas cachexia describes loss of weight. After reaching guideline-recommended doses of heart failure therapies, the most promising approach to treating body wasting seems to be combined therapy that includes exercise, nutritional counselling, and drug treatment. Nutritional considerations include avoiding excessive salt and fluid intake, and replenishment of deficiencies in trace elements. Administration of omega-3 polyunsaturated fatty acids is beneficial in selected patients. High-calorific nutritional supplements can also be useful. The prescription of aerobic exercise training that provokes mild or moderate breathlessness has good scientific support. Drugs with potential benefit in the treatment of body wasting that have been tested in clinical studies in patients with heart failure include testosterone, ghrelin, recombinant human growth hormone, essential amino acids, and β 2 -adrenergic receptor agonists. In this Review, we summarize the pathophysiological mechanisms of muscle wasting and cachexia in heart failure, and highlight the potential treatment strategies. We aim to provide clinicians with the relevant information on body wasting to understand and treat these conditions in patients with heart failure.

Cachexia is a serious clinical consequence of almost all chronic diseases when reaching advanced stages. Its prevalence ranges from 5–15% in end‐stage chronic heart failure to 50–80% in advanced malignant cancer. Cachexia is also frequently occurring in patients with chronic kidney disease, chronic obstructive pulmonary disease (COPD) or neurological diseases, and rheumatoid arthritis. Mortality rates of patients with cachexia range from 15–25% per year in severe COPD through 20–40% per year in patients with chronic heart failure or chronic kidney disease to 20–80% in cancer cachexia. In the industrialized world (North America, Europe, and Japan) where epidemiological data are to some degree available, the overall prevalence of cachexia (due to any disease and not necessarily associated with hospital admission) is growing with the growth of the chronic illness prevalence, and it currently affects around 0.5–1.0% of the population, i.e. around 6–12 million people. From this, one can estimate that 1.5–2 million deaths are occurring in patients with cachexia per year. It is also a very significant health problem in other parts of the globe, but epidemiological data are scarce. The multifactorial nature of cachexia is now much better understood, and particularly, the role of inflammatory mediators and the imbalance of anabolism and catabolism are considered important therapeutic targets. Several approaches to develop cachexia and muscle wasting treatments have failed to be successful in phase III clinical trials, but new approaches are in development. Given the high prevalence and very high mortality associated with cachexia, advances are urgently needed for patients worldwide.

The coronavirus‐2 spikes protein, uses the angiotensin converter enzyme 2 (ACE2) receptor to bind to a cell resulting in fusion of the viral envelope to fuse with cell membrane and allows the viral genetic material to enter the cell. 2 ACE2 receptors are present ubiquitously throughout the body resulting in a variety of tissue damages. 4 Its clinical features are weight loss, low albumin, anorexia, increased muscle protein breakdown and inflammation. Mice infected with coronavirus‐2 had had significant weight loss which was reversed by a ribonucleoside analog. 12 Sarcopenia is defined as the decreased muscular function in the presence of muscle loss. 13 Primary sarcopenia is age related while secondary sarcopenia is when the sarcopenia is related to a chronic disease such as diabetes mellitus or chronic obstructive pulmonary disease. 14 In older persons, the need for social isolation during the COVID‐19 pandemic has led to a decrease in daily physical activity which accelerates the loss of muscle strength and function.

At least half of all patients with heart failure (HF) are affected by frailty, a syndrome that limits an individual ability to recover from acute stressors. While frailty affects up to 90% of patients with HF with preserved ejection fraction, it is also seen in ~30–60% of patients with HF with reduced ejection fraction, with ~26% higher prevalence in women compared with men. The relationship between frailty and HF is bidirectional, with both conditions exacerbating the other. Frailty is further complicated by a higher prevalence of sarcopenia (by ~20%) in HF patients compared with patients without HF, which negatively affects outcomes. Several frailty assessment methods have been employed historically including the Fried frailty phenotype and Rockwood Clinical Frailty Scale to classify HF patients based on the severity of frailty; however, a validated HF‐specific frailty assessment tool does not currently exist. Frailty in HF is associated with a poor prognosis with a 1.5‐fold to 2‐fold higher risk of all‐cause death and hospitalizations compared to non‐frail patients. Frailty is also highly prevalent in patients with worsening HF, affecting >50% of patients hospitalized for HF. Such patients with multiple readmissions for decompensated HF have markedly poor outcomes compared to younger, non‐frail cohorts, and it is hypothesized that it may be due to major physical and functional limitations that limit recovery from an acute episode of worsening HF, a care aspect that has not been addressed in HF guidelines. Frail patients are thought to confer less benefit from therapeutic interventions due to an increased risk of perceived harm, resulting in lower adherence to HF interventions, which may worsen outcomes. Multiple studies report that <40% of frail patients are on guideline‐directed medical therapy for HF, of which most are on suboptimal doses of these medications. There is a lack of evidence generated from randomized trials in this incredibly vulnerable population, and most current practice is governed by post hoc analyses of trials, observational registry‐based data and providers' clinical judgement. The current body of evidence suggests that the treatment effect of most guideline‐based interventions, including medications, cardiac rehabilitation and device therapy, is consistent across all age groups and frailty subgroups and, in some cases, may be amplified in the older, more frail population. In this review, we discuss the characteristics, assessment tools, impact on prognosis and impact on therapeutic interventions of frailty in patients with HF.

Cachexia is a serious but underrecognised consequence of many chronic diseases. Its prevalence ranges from 5–15 % in end-stage chronic heart failure to 50–80 % in advanced cancer. Cachexia is also part of the terminal course of many patients with chronic kidney disease, chronic obstructive pulmonary disease (COPD) and rheumatoid arthritis. Mortality rates of patients with cachexia range from 10–15 % per year in COPD through 20–30 % per year in chronic heart failure and chronic kidney disease to 80 % in cancer. The condition is also associated with poor quality of life. In the industrialised world, the overall prevalence of cachexia (due to any disease and not necessarily associated with hospital admission) is growing and it currently affects around 1 % of the patient population, i.e. around 9 million people. It is also a significant health problem in other parts of the globe. Recently there have been advances in our understanding of the multifactorial nature of the condition, and particularly of the role of inflammatory mediators and the imbalance of anabolism and catabolism. Several promising approaches to treatment have failed to live up to the challenge of phase III clinical trials, but the ghrelin receptor agonist anamorelin seems to have fulfilled at least some early promise. Further advances are urgently needed.

To develop a framework for the definition and classification of cancer cachexia a panel of experts participated in a formal consensus process, including focus groups and two Delphi rounds. Cancer cachexia was defined as a multifactorial syndrome defined by an ongoing loss of skeletal muscle mass (with or without loss of fat mass) that cannot be fully reversed by conventional nutritional support and leads to progressive functional impairment. Its pathophysiology is characterised by a negative protein and energy balance driven by a variable combination of reduced food intake and abnormal metabolism. The agreed diagnostic criterion for cachexia was weight loss greater than 5%, or weight loss greater than 2% in individuals already showing depletion according to current bodyweight and height (body-mass index [BMI] <20 kg/m 2) or skeletal muscle mass (sarcopenia). An agreement was made that the cachexia syndrome can develop progressively through various stages—precachexia to cachexia to refractory cachexia. Severity can be classified according to degree of depletion of energy stores and body protein (BMI) in combination with degree of ongoing weight loss. Assessment for classification and clinical management should include the following domains: anorexia or reduced food intake, catabolic drive, muscle mass and strength, functional and psychosocial impairment. Consensus exists on a framework for the definition and classification of cancer cachexia. After validation, this should aid clinical trial design, development of practice guidelines, and, eventually, routine clinical management.

Sarcopenia is now defined as a decline in walking speed or grip strength associated with low muscle mass. Sarcopenia leads to loss of mobility and function, falls, and mortality. Sarcopenia is a major cause of frailty, but either condition can occur without the other being present. Sarcopenia is present in about 5 to 10 % of persons over 65 years of age. It has multiple causes including disease, decreased caloric intake, poor blood flow to muscle, mitochondrial dysfunction, a decline in anabolic hormones, and an increase in proinflammatory cytokines. Basic therapy includes resistance exercise and protein and vitamin D supplementation. There is now a simple screening test available for sarcopenia—SARC-F. All persons 60 years and older should be screened for sarcopenia and treated when appropriate.