Sarcopenic obesity in older adults: a clinical overview

Abstract

Sarcopenic obesity is characterized by a concurrent decline in muscle mass and function, along with increased adipose tissue. Sarcopenic obesity is a growing concern in older adults owing to significant health consequences, including implications for mortality, comorbidities and risk of developing geriatric syndromes. A 2022 consensus statement established a new definition and diagnostic criteria for sarcopenic obesity. The pathophysiology of this condition involves a complex interplay between muscle, adipose tissue, hormonal changes, inflammation, oxidative stress and lifestyle factors, among others. Sarcopenic obesity is treated with a range of management approaches, such as lifestyle interventions, exercise, nutrition and medical therapies. Emerging therapies that were developed for treating other conditions may be relevant to sarcopenic obesity, including novel pharmacological agents and personalized approaches such as precision medicine. In this Review, we synthesize the current knowledge of the clinical importance of sarcopenic obesity, its assessment and diagnosis, along with current and emerging management strategies.

Introduction

Our understanding of the prevalence and clinical relevance of abnormal body composition phenotypes in clinical settings is evolving rapidly. Previously overlooked abnormalities are now recognized and are at the forefront of clinical research, given the prevalence and importance of these disorders among older adults. Among these phenotypes, sarcopenic obesity has emerged as a major health challenge. Sarcopenic obesity was first defined in 1996 (ref. 1) as a syndrome characterized by the simultaneous presence of excess adipose tissue and reduced muscle mass. However, the definition has evolved to also incorporate reduced muscle function in the diagnosis of sarcopenia in older adults^2,3, with muscle strength being the predominant measure of function.

Sarcopenic obesity exemplifies the intersection of two prevalent health crises: ageing populations and the obesity epidemic⁴. Predominantly observed in older adults, this syndrome is increasingly being studied in relation to various clinical conditions. The prevalence of sarcopenic obesity in older adults varies substantially, depending on which diagnostic criteria are applied⁵. A number of commonly used body compartments and physical function tests are used for the diagnosis of sarcopenia, obesity and sarcopenic obesity (Table 1). Previously used definitions and cut-off points for sarcopenic obesity are comprehensively reviewed elsewhere⁶.

Table 1 |.

Selected common body compartments and physical function tests used in the definition of sarcopenia and sarcopenic obesity

Condition	Tests and compartments
	Muscle mass	Muscle function	Fat mass
Sarcopenia	Skeletal muscle mass Appendicular skeletal musclea Appendicular skeletal muscle index Mid-thigh skeletal muscle area Lumbar skeletal muscle area	Handgrip strength Chair stand Gait speed Short physical performance battery test Timed up and go 400 m walk	NA
Sarcopenic obesity	Skeletal muscle mass/weight Appendicular lean mass/weight	Handgrip strength Knee extension strength Five times sit-to-stand 30 s chair stand	Fat mass percentage

NA, not applicable.

^aMore correctly termed appendicular lean soft tissue.

Population-representative data for the USA demonstrated a prevalence of sarcopenic obesity of 28.3% in people >60 years of age, with a higher prevalence of 66.6% in Mexican Americans⁷. Indeed, certain populations, such as hospitalized or institutionalized older adults, might be at higher risk of having sarcopenic obesity. Given the concomitant rising rates of obesity and sedentary lifestyles in ageing populations, we can expect a substantial surge in the prevalence of this syndrome in the next decade. These projections are especially relevant in the context of the COVID-19 pandemic and its aftermath, which is marked by quarantine, isolation, reduced physical activity, unfavourable dietary modifications⁸ and/or the effects of COVID-19 infection^9,10.

Of note, not all older adults with obesity will exhibit sarcopenia, as excess body weight usually stimulates muscle (and bone) mechanoreceptors, triggering growth factor synthesis that leads to muscle formation¹¹. However, in individuals with sarcopenic obesity, this adaptive physiological process can falter, leading to excessive adipose tissue accumulation (‘load’) without a corresponding increase in muscle mass and functionality (‘capacity’)^12,13. Although this description is an over-simplification, the complex pathophysiology of sarcopenic obesity is described in greater detail below. Various metabolic scenarios, such as weight gain or loss, can contribute to the development of sarcopenic obesity. In the context of weight gain, individuals can evolve in two ways. They might accrue an average amount of muscle alongside the additional body weight, resulting in a condition of general obesity. Alternatively, if their rate of muscle accretion is low while they gain weight, they might develop sarcopenic obesity. Conversely, a similar transformation can occur in individuals experiencing considerable weight loss, such as those with class III obesity (BMI ≥40 kg/m²) who reduce their weight but not by enough to be classified with overweight (BMI <30 kg/m²). The weight loss in these individuals can induce varying degrees of muscle loss, potentially leading to the development of sarcopenic obesity, especially if the loss in muscle mass is substantial¹⁴.

In addition, changes in body composition may result from precipitating events, such as falls, hip fractures, stroke or other illnesses, all of which temporarily or permanently impair mobility, and are accompanied by acute-phase responses¹⁵. Long-term accumulation of adipose tissue, when paired with the secondary consequences of triggers such as ageing, including oxidative stress and chronic inflammation, among others, may progressively induce muscle loss and gain in adipose tissue, leading to sarcopenic obesity¹⁵. Both acute and chronic scenarios lead to progressive loss of muscle that could eventually lead to physical impairment and disability, perpetuating the aforementioned factors. Ultimately, a vicious cycle of muscle loss and adipose tissue gain can cause sarcopenic obesity¹⁵. Consequently, early detection and ongoing interventional strategies are crucial to mitigate the development of this syndrome.

In this Review, we explore the multiple factors that lead to the development of sarcopenic obesity, highlight the latest consensus on a definition and diagnostic criteria for this syndrome, discuss a range of both established and emerging management strategies, and address challenges and opportunities for future research. We provide illustrative examples that should facilitate the translation of research into clinical practice.

Clinical importance

The clinical importance of sarcopenic obesity in older adults arises from the cumulative impact of excess adiposity and the functional and systemic roles of skeletal muscle¹⁶. Pioneering research^17,18 has laid the foundation for our understanding of the health consequences of sarcopenic obesity.

For this narrative Review, we sourced information from our previous review⁶ and expanded on it using similar search terms, incorporating the terms ‘consequences’ and ‘outcomes’. We searched PubMed to identify relevant publications up to May 2023, selecting studies based on a non-systematic approach, with a focus on systematic reviews, meta-analyses, and cross-sectional and longitudinal studies that involved older adults, primarily those more than 65 years of age. Interventional studies were not included. For this assessment, we were interested solely in studies reporting adverse clinical outcomes of sarcopenic obesity; thus, two studies^19,20 that did not show an association between sarcopenic obesity and clinical outcomes were not included. For instances in which a clinical outcome was evident in both an individual study and a meta-analysis, we prioritized the meta-analysis data.

A summary of the clinical consequences^21–46 of sarcopenic obesity is shown in Fig. 1 and the risk of specific clinical consequences, as determined from meta-analysis studies^26,35,39, are shown in Fig. 2. These data demonstrate that sarcopenic obesity has a considerable clinical impact, as it is linked to a high risk of death, comorbidities, metabolic disorders and geriatric syndromes, including frailty.

Fig. 1 |. Clinical consequences of sarcopenic obesity.

The schematic summarizes the consequences of sarcopenic obesity, including metabolic dysfunction (dyslipidaemia³⁵, diabetes mellitus³⁵, metabolic syndrome³⁵, insulin resistance³⁵ and decreased vitamin D levels³¹), geriatric syndromes (cognitive impairment^35,43, functional limitation³⁵, risk of falls^25,35, depressive symptoms^28,39, dementia⁴³, prefrailty and frailty^29,45, osteoporosis²³, short sleep duration²⁴, low physical activity level²⁴, fatigue²⁴ and disability⁴⁰), effects on cancer outcomes and treatment (decreased overall^26,32,36, recurrence-free^26,32 and disease-free survival²⁶, surgical complications^26,27,30,38, prolonged hospital length of stay (LOS)²⁶, decreased tolerance to therapy (dose-limiting toxicity risk)²⁷), increased risk of various mortality outcomes (all-cause³⁵, cardiovascular disease (CVD)³⁵, post-hospitalization (2-years)²¹, heart failure⁴¹ and cardiovascular (CV) surgery⁴⁴) and morbidity outcomes (CVD³⁵, hypertension³⁵, lung diseases^33,35, stroke³⁵ and arthritis³⁵), and development of various other clinical conditions (hospitalization⁴⁰, poor nutritional status³⁷, poor improvement in activity of daily living (ADL) and dysphagia after stroke⁴⁶, low quality of life⁴², inflammation²², poor recovery in knee flexion range of motion after total knee replacement³⁴).

Fig. 2 |. Risk of various clinical consequences of sarcopenic obesity.

Odds ratios for risk of comorbidities (part a) and of metabolic disorders (part b) and hazard ratios for mortality (part c) in people with sarcopenic obesity³⁵. Odds ratios for risk of comorbidities (part d) and hazard ratios for survival (part e) in older patients with cancer and sarcopenic obesity⁵. Odds ratios for risk of geriatric syndromes in people with sarcopenic obesity^35,39 (part f). CVD, cardiovascular disease.

Pathophysiology

The pathophysiology of sarcopenic obesity involves complex interactions between multiple factors, including genetic factors, dietary and other lifestyle factors (that is, physical activity, environmental and social factors, and mental stress), age-related changes in body composition⁴⁷, hormonal imbalances⁴⁸, declining neuromuscular function⁴⁹, increased inflammation and oxidative stress⁵⁰, reduced activity of muscle satellite cells⁵¹, altered energy metabolism, and impaired metabolic–vascular coupling⁵² (Fig. 3). These factors become even more important when older adults are affected by acute or chronic conditions, which can magnify the impact of these factors by further increasing inflammation, limiting mobility or leading to prolonged bed rest, altering medication pharmacokinetics and pharmacodynamics, and inducing nutrition impact symptoms.

Fig. 3 |. Factors contributing to the development of sarcopenic obesity.

Sarcopenic obesity occurs due to a myriad of pathophysiological factors associated with healthy ageing, which combine to result in loss of muscle and gain of adipose tissue. The presence of chronic or acute conditions in older adults further increases the risk of sarcopenic obesity, intensifying both the number and severity of contributing factors.

Changes in muscle health

The progressive loss of muscle mass and function in sarcopenic obesity can also occur alongside changes in muscle composition⁵³. The loss of muscle mass is closely associated with ageing and typically begins in middle age and accelerates in later years. Muscle mass is estimated to decrease by about 3–8% per decade after the age of 30 years, primarily due to a decrease in the size and number of muscle fibres⁵⁴. With ageing, there is an increase in infiltration of skeletal muscle by adipose tissue (termed myosteatosis) within multiple different adipose depots, including intermuscular adipose tissue and intramyocellular lipids⁵⁵.

This shift in composition contributes to decreased muscle ‘quality’ (that is, composition) and impaired muscle function. Along with loss of muscle mass, sarcopenia is characterized by a decline in muscle strength and function. The ageing process leads to a gradual decline in the proportion of fast-twitch (type II) muscle fibres, which may contribute to decreased muscle strength and power⁵⁶. Neuromuscular function impairment could also contribute to the development of sarcopenia via reduction in the number of active motor units, altered neuromuscular junction activity, reduced activation and innervation of muscle fibres, and impaired excitation–contraction coupling⁴⁹.

Changes in adipose tissue

Ageing is associated with an increase in adipose tissue mass and distribution (that is, an increase in visceral adipose tissue), which can be attributed to various factors such as hormonal changes, low muscle mass, low physical activity, unfavourable changes in metabolism and lifestyle factors⁴⁷. Weight gain can result in an increase in adipose cell size, which may promote the recruitment of immune cells and secretion of inflammatory factors within adipose tissue, such as IL-6, C-reactive protein and tumour necrosis factor, creating a state of low-grade chronic inflammation that can impair insulin sensitivity⁵⁷. Insulin resistance impairs protein anabolism, directly affecting muscle fibre atrophy and promoting muscle catabolism. Mitochondrial dysfunction and myosteatosis may further contribute to insulin resistance, which in turn, impacts glucose metabolism and muscle protein synthesis. Insulin stimulates the uptake of glucose and amino acids into muscle cells, promoting protein synthesis and muscle growth. Reduced insulin signalling or insulin resistance can impair muscle protein metabolism, leading to muscle wasting and sarcopenia⁵⁸.

Oxidative stress and hormonal shifts

Ageing is associated with an increase in oxidative damage to muscle cells, with oxidative stress identified as a key factor in the development and progression of sarcopenia⁵⁹. Oxidative stress adversely impacts muscle health through muscle protein breakdown⁶⁰, muscle inflammation⁶¹, impaired muscle regeneration⁶², mitochondrial dysfunction⁶³ and insulin resistance⁵⁰. Hormonal shifts associated with ageing and obesity strongly influence the pathophysiology of sarcopenic obesity⁴⁸. Decreased levels of anabolic hormones, such as growth hormone, insulin-like growth factor 1 (IGF1) and testosterone, contribute to muscle loss and hindered protein synthesis⁴⁸. Production of myostatin, a growth-inhibiting myokine, is upregulated in sarcopenia⁶⁴, whereas that of muscle-mass-stimulating irisin seems to be downregulated⁶⁵. Ageing-associated decline in testosterone and oestrogen levels weakens muscle, reducing both muscle mass and strength⁶⁶. Concurrently, increased levels of catabolic hormones, such as cortisol, promote protein breakdown and inhibit protein synthesis, exacerbating muscle wasting and sarcopenia⁶⁷. These hormonal alterations further contribute to reduced muscle mass and adipose tissue deposition. Chronic stress and consistently high cortisol levels can negatively impact muscle tissue and increase sarcopenia risk⁶⁸. Mechanisms that might link high cortisol levels to the loss of muscle mass include inhibition of the mammalian target of rapamycin (mTOR) pathway⁶⁹, suppression of the anabolic effects of IGF1 (ref. 69) and testosterone⁷⁰, and activation of the ubiquitin–proteasome system in skeletal muscle⁷¹. Chronic stress can lead to overeating and/or a sedentary lifestyle^67,72, factors that may increase the risk of sarcopenia. Furthermore, cortisol can negatively affect bone health⁷³ and exacerbate age-related bone density decline, possibly contributing to the development of osteosarcopenic obesity⁷⁴. The pathophysiology of osteosarcopenic obesity is reviewed elsewhere^74,75.

Nitric oxide production

Ageing has also been related to a decline in nitric oxide (NO) production⁷⁶ and skeletal muscle blood flow⁷⁷. NO and insulin are crucial for muscle metabolism and are implicated in the development and progression of sarcopenia^78,79. NO modulates insulin signalling pathways in muscle cells⁸⁰, while obesity and metabolic syndrome are associated with decreased whole-body NO synthesis⁸¹. NO can enhance insulin sensitivity by activating insulin receptor substrates and downstream signalling molecules, such as Akt and mTOR, which are involved in protein synthesis in muscle⁸². Increased insulin signalling in response to NO might help maintain muscle mass and function. NO is also a potent vasodilator that regulates blood flow. Sufficient blood flow is crucial for the delivery of nutrients, including glucose and amino acids, to muscle tissues⁸³. NO-mediated vasodilation can enhance blood flow and nutrient delivery to muscles, supporting muscle metabolism and potentially mitigating sarcopenia⁸⁴. Both NO and insulin have crucial roles in regulating mitochondrial function by enhancing mitochondrial respiration and promoting mitochondrial biogenesis, whereas insulin stimulates cellular glucose uptake and its subsequent utilization within the mitochondria⁸⁵. The interplay between NO and insulin in maintaining mitochondrial health may contribute to muscle preservation.

Energy metabolism and dietary factors

Energy metabolism is also disrupted in sarcopenia and sarcopenic obesity⁸⁶. Decreased muscle mass leads to a lowered basal metabolic rate and consequently, reduced total energy expenditure, creating an energy surplus that promotes adipose tissue accumulation. Physical inactivity and a sedentary lifestyle are common risk factors for developing sarcopenic obesity⁸⁷. Reduced muscle mass and function make physical activity more challenging, leading to a vicious cycle of decreased activity, muscle loss and adipose tissue accumulation. Physical inactivity further impairs insulin sensitivity, exacerbating obesity-related muscle loss⁸⁸. Poor quantity and quality of nutrients might also influence the pathophysiology of sarcopenic obesity. For example, older adults might be at high risk of a low protein intake and inadequate consumption of essential amino acids⁸⁹. Insufficient intake of some micronutrients, such as vitamin D, calcium, ω−3 fatty acids and antioxidant nutrients, which are vital for muscle health, can also contribute to sarcopenia⁹⁰. Furthermore, lifetime over-consumption of high-calorie, low-nutrient quality foods can contribute to the sarcopenic obesity phenotype. Food insecurity has also been proposed as a risk factor in developing sarcopenic obesity⁹¹, as it may be associated with poor diet quality, nutritional deficiencies, physical inactivity and unfavourable metabolic changes. Figure 4 presents a proposed model for the pathogenesis of sarcopenic obesity.

Fig. 4 |. Factors that contribute to weight gain and resulting changes in body composition, including sarcopenic obesity.

This integrated pathogenic model explains how weight gain can result in different body composition phenotypes based on changes in fat mass (FM) and fat-free mass (FFM) and the resultant effects on metabolic health. For example, the sarcopenic obesity phenotype is identified when the increase in FM outweighs the increase in FFM. The health implications of each body composition phenotype may be associated with the adaptive allostatic responses²²⁸ that follow weight gain, reflecting respective alterations in FM and FFM. A normal allostatic response involves an initial disruption of homeostatic control, triggering adaptive compensatory physiological responses that restore normal physiological conditions, resulting in a low health risk. This situation may be associated with a metabolically healthy obesity phenotype. A weaker (that is, moderate) allostatic response could be linked to more balanced changes in FM and FFM after weight gain, leading to moderate health risks (that is, an obesity phenotype). The sarcopenic obesity phenotype might be more susceptible to exhibiting an abnormal allostatic response (that is, prolonged or inadequate response), resulting in a higher likelihood of developing health complications.

Genetic and epigenetic factors

Our current understanding of genetic and epigenetic factors in sarcopenic obesity is limited. Muscle phenotypes show strong heritability, but the specific genetic factors underlying these phenotypes remain unclear. Genetic variants of α-actinin 3 (ACTN3), caveolin 1, vitamin D receptor, methylenetetrahydrofolate reductase (MTHFR) and nuclear respiratory factor 2 might contribute to the development of sarcopenia^92–95. A combined genetic risk score including ACTN3, MTHFR and nuclear respiratory factor 2 genotypes could explain 39% of sarcopenia risk variability⁹⁵. A limited number of the studies on DNA methylation patterns have found age-related changes in muscle tissue^96–100. In individuals with sarcopenia, specific regions of DNA methylation are enriched in genes associated with myotube fusion, oxidative phosphorylation and voltage-gated calcium channel activity¹⁰¹. Numerous studies have identified several genes associated with obesity risk, including α-ketoglutarate-dependent dioxygenase FTO (FTO), melanocortin 4 receptor (MC4R), proprotein convertase subtilisin/kexin type 1 (PCSK1) and leptin receptor (LEPR)¹⁰². These genes have been linked to various aspects of metabolism, appetite regulation, lipid storage and energy expenditure¹⁰². While genetic factors alone do not solely determine obesity risk, they interact with environmental factors, such as diet and physical activity, to influence individual risk¹⁰³. Understanding the potential links between sarcopenia and obesity-related genes could provide a better understanding of the pathogenesis of sarcopenic obesity.

Screening, assessment and diagnosis

A lack of standardized definitions and the use of various indexes pose considerable challenges in characterizing the prevalence and clinical importance of sarcopenic obesity in older adults. Defining sarcopenic obesity is as complex as defining sarcopenia or obesity individually, with ongoing debates about absolute versus relative measurements, regional versus total body composition values, and the balance between muscle mass and function needed for sarcopenia diagnosis. The establishment of an expert international panel, the Sarcopenic Obesity Global Leadership Initiative (SOGLI), by the European Society for Clinical Nutrition and Metabolism (ESPEN) and the European Association for the Study of Obesity (EASO) marked an important step towards standardizing the assessment and diagnosis of sarcopenic obesity^2,3,6,104, culminating in the release of a consensus statement in 2022 (refs. 2,3).

Screening

Screening methods should be quick, practical and cost-effective, and not require specialized expertise. Accordingly, the suggested screening process incorporates BMI or high waist circumference identified using ethnicity-specific thresholds (specified in the consensus statement^2,3) and surrogate markers of sarcopenia, including, but not limited to, clinical signs, risk factors and validated questionnaires (Fig. 5). Additionally, clinical symptoms or risk factors can be used for the screening of sarcopenic obesity, including older age (>70 years), presence of chronic disease, recent acute disease, history complaint of fatigue, and functional limitations^2,3.

Fig. 5 |. Proposed algorithm for screening and diagnosis of sarcopenic obesity.

This algorithm is published by the Sarcopenic Obesity Global Leadership Initiative (SOGLI) group^2,3. Sarcopenic obesity is defined by the co-existence of excess adiposity and diminished muscle mass and function. The diagnostic process begins with screening, utilizing tools such as BMI, waist circumference (WC) and surrogate markers. Following a positive screening result, a comprehensive diagnosis is undertaken, emphasizing the assessment of both muscle functionality and body composition. Finally, patients are categorized based on the presence or absence of complications resulting from high fat mass and reduced muscle mass and/or function: those without are classified as stage 1, whereas those with complications are classified as stage 2. Staging guides the choice of treatment approaches. ALM/W, appendicular lean mass/weight; BIA, bioelectrical impedance analysis; DXA, dual-energy X-ray absorptiometry; FM, fat mass; SARC-F, Strength, Assistance in walking, Rise from a chair, Climbing stairs, and Falls (questionnaire); SMM/W, skeletal muscle mass/weight. Adapted from refs. 2,3, CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/).

An awareness of potential limitations of screening approaches is crucial, as screening informs clinical judgement. For example, an individual can have a normal BMI and/or waist circumference but high adipose tissue. Individuals with excess adiposity located primarily in the lower body may not be identified as being at risk of developing sarcopenic obesity. Both BMI and waist circumference lack precision and may not accurately represent body composition¹⁰⁵. Regarding surrogate methods for sarcopenia screening, questionnaires such as the Strength, Assistance in Walking, Rise from a Chair, Climb Stairs, and Falls (SARC-F) questionnaire have low sensitivity but high specificity and may therefore fail to identify patients with sarcopenia. Incorporating calf circumference into the SARC-F questionnaire (SARC-Calf)¹⁰⁶ enhances its sensitivity, although the utility of SARC-Calf in diagnosing sarcopenic obesity remains to be explored^2,3. Similarly, clinical signs and symptoms can be misleading because they are generally quite non-specific and overlap with those of related conditions. Despite limitations, these indicators offer valuable diagnostic insights and should be utilized in clinical practice, where pragmatic and flexible use of screening procedures is needed¹⁰⁷. Moving forward, the development and validation of new tools and approaches is crucial.

Diagnosis

A positive screening result prompts initiation of the diagnostic process, which encompasses two sequential stages: assessing muscle function and assessing body composition (Fig. 5). The consensus statement includes a comprehensive list of criteria based on the selected technique, unit of measurement and target population^2,3. Muscle function is an umbrella term that includes an evaluation of muscle strength or physical performance. Although only six of 75 studies assessed by the SOGLI defined sarcopenic obesity by the presence of both low muscle function and low muscle mass⁶ (that is, most studies focused mainly on muscle mass), the consensus group recommended including muscle function parameters as an essential component in the diagnostic process. This recommendation aligns with current practices for diagnosing sarcopenia in older adults and underscores the importance of functional consequences in the context of quality of life and treatment protocols. Given the practicality of assessing muscle strength, this aspect should be prioritized. The debate between the muscle mass and function aspect of sarcopenia — as a geriatric versus a clinical syndrome — is discussed elsewhere¹⁶ and further investigation is warranted.

Assessment of body composition in individuals with obesity is especially challenging. For example, bioelectrical impedance analysis may underestimate fat mass owing to inaccurate body shape assumptions and increased fat-free mass hydration, whereas dual energy X-ray absorptiometry may overestimate fat mass^108,109. Although awareness of these limitations is needed, the implications for sarcopenic obesity diagnosis remain to be investigated. More sophisticated techniques, such as CT, MRI), ultrasonography and D-3 creatinine dilution, are available for body composition assessment^110–113. However, these techniques are still rarely available in clinical, especially geriatric, settings. In the absence of body composition measurements, anthropometry can be used. Technical difficulties in assessing skinfolds present a considerable limitation when accessing mid–upper arm circumference and derivatives, potentially leading to intraindividual and interindividual error. Calf circumference is a reasonable alternative as an indicator of low muscle mass. Furthermore, the utility of calf circumference in patients with obesity has recently surged, thanks to simple adjustment factors¹¹⁴. Importantly, sex-specific cut-off points (for example, <33 cm for women and <34 cm for men¹¹⁴) should be applied, as opposed to the proposed <31 cm for both sexes recommended previously^53,115, as this cut-off point was established in women only¹¹⁶. After measuring calf circumference of a person with overweight or obesity, this value should be decreased by 3 cm (BMI in the overweight category), 7 cm (BMI within obesity class I or II categories) or 12 cm (BMI in the obesity class III category), owing to the confounding effects of adiposity¹¹⁴. Of note, anthropometric techniques are less accurate for tracking changes in body composition over time.

Considerations for adjustments to body mass are crucial. Body composition and corresponding thresholds for defining abnormalities (such as low muscle mass and high adipose tissue) are typically presented as measurements adjusted for height (specifically, height in metres squared due to allometric scaling)¹¹⁷. However, this type of adjustment may not be appropriate in individuals with obesity, owing to the potential masking effect of high adiposity. Despite an apparent reduction in muscle mass relative to total body weight, these individuals may have an absolute muscle mass similar to or even greater than individuals without obesity; however, their muscle function may remain compromised. Consequently, the concept of ‘relative adequate muscle’ has been proposed for the clinical identification of sarcopenic obesity^2,3, but additional research is needed. Therefore, body weight should be considered alongside muscle mass when diagnosing sarcopenic obesity^2,3. An alternative approach is to use BMI as a denominator, but the evidence to date is insufficient to support this approach^118,119 and further research should provide more clarity.

A related discussion concerns adjustments for muscle strength. These adjustments were not fully endorsed by the SOGLI working group^2,3 owing to the absence of well-stablished cut-off points for relative muscle handgrip strength, although they were noted as a crucial area for research¹⁰⁴.

Staging

Sarcopenic obesity is staged based on the presence or absence of complications, which include functional disabilities (such as difficulty or a need for assistance with activities of daily living or instrumental activities of daily living essential for independent living), falls, low gait speed, and metabolic, cardiovascular and respiratory diseases^120,121. Individuals without complications are classified as stage 1, whereas individuals with at least one complication attributable to altered body composition and skeletal muscle functional parameters are classified as stage 2.

Given the recent publication of the consensus statement, the included diagnostic framework has only been utilized in a handful of studies to date^122,123. The SOGLI group provide an in-depth rationale for the consensus definition of sarcopenic obesity in the consensus statement⁶. Although this definition has provided a new perspective, it still requires validation.

Management strategies

The key objectives in treating sarcopenic obesity are to combine exercise and nutritional interventions with the aim of creating a negative energy balance to reduce adipose tissue (improving adipose markers and reducing inflammatory parameters) while preserving and ideally increasing muscle mass and function^124–128. Management strategies are summarized in Fig. 6.

Fig. 6 |. Current, emerging and potential management strategies for sarcopenic obesity.

The schematic depicts an overview of management strategies for sarcopenic obesity, ranging from strategies with more robust evidence, to approaches with strong evidence but which were developed for other conditions, and to emergent therapies that require further research and clinical trials to confirm their efficacy. Collectively, the strategies aim to achieve specific outcomes, which include a reduction in adiposity, increase in muscle mass and strength, mitigation or halting of myosteatosis, and a subdued inflammatory response. With adequate postoperative care, bariatric surgery is expected to result in a proportional increase in muscle. ↔, maintain; GIP, gastric inhibitory polypeptide; GLP1, glucagon-like peptide 1; SARM, selective androgen receptor modulator.

While calorie-restricted, multicomponent interventions may lead to a loss of lean mass, which includes muscle mass (the ‘quarter fat-free mass’ rule)¹²⁹, the proportionally greater reduction in adipose tissue may promote substantial and synergistic improvements in physical function¹³⁰. Despite the lack of specifically defined intervention protocols, the expert consensus is that the most effective interventions include both diet-induced weight loss and consistent aerobic and resistance-based exercise strategies. In particular, a 2023 systematic review¹³¹ found that resistance training may be effective in modifying body composition by reducing adipose tissue and improving muscle mass, functional parameters of muscle strength and gait speed in older adults. The benefits of non-calorie-restricted, multicomponent interventions on physical disability and sarcopenia in older adults have been demonstrated by the LIFE¹³² and SPRINTT¹³³ trials. Both studies randomly assigned older subjects (age range 70–90 years) who were at risk of disability and frailty to a healthy ageing education programme or a multicomponent intervention involving an intensive, age-tailored physical activity programme and nutritional counselling (average duration was 2.6 years for the LIFE trial and 3 years for the SPRINTT trial). Both trials showed a reduction in incident disability events and, in the SPRINTT trial, women assigned to the multicomponent intervention experienced a smaller decline in handgrip strength and lost less appendicular lean mass at 24 months than women receiving the control intervention^132,133. A considerable proportion of participants in both trials probably had sarcopenic obesity, given that the average BMI was 28.7 ± 5.7 kg/m² in the SPRINTT trial and 30.2 ± 5.9 kg/m² in the LIFE trial. This finding suggests that even in the absence of diet-induced weight loss, multimodal interventions could positively impact age-related decline in muscle mass and function, and reduce the risk of sarcopenia and frailty in individuals with sarcopenic obesity.

Effective management of sarcopenic obesity calls for a patient-centric approach that highlights the importance of personalized care strategies and patient education. This approach can also include mindfulness methods, underscoring the importance of psychology in managing sarcopenic obesity. Specifically, digital technology has a crucial role in facilitating the delivery of nutritional and exercise interventions that are well accepted among older adults^134,135. Despite prevalent misconceptions about older adults being able or willing to use these tools¹³⁶, studies have shown that that they are both feasible and well accepted among older adults. Such technology holds considerable potential for mitigating the effects of sarcopenic obesity in older adults, particularly considering the rapidly evolving digital health landscape.

Exercise and physical activity

Exercise is a well-established intervention for preventing and managing sarcopenia^137,138. Exercise-induced muscle contractions stimulate NO production^139,140 and enhance insulin sensitivity^141,142, potentially improving muscle protein synthesis and adaptation^143,144. The interaction between NO and insulin during exercise may have synergistic effects on muscle metabolism, promoting muscle maintenance and potentially attenuating sarcopenia¹⁴⁴.

Exercise has also been shown to be beneficial in addressing sarcopenic obesity. Exercise regulates energy balance¹⁴⁵, increases muscle protein synthesis¹⁴³, reduces myostatin expression¹⁴⁶, increases intramuscular IGF1 levels¹⁴⁷, improves skeletal muscle sensitivity to the anabolic effects of insulin¹⁴⁸, improves nutrient-stimulated vasodilation and nutrient delivery to muscle¹⁴⁹, enhances mitochondrial function¹⁵⁰, activates skeletal muscle satellite cells¹⁵¹, and decreases pro-inflammatory gene expression in skeletal muscle¹⁵². Exercise may enhance both breakdown and synthesis of muscle protein¹⁴³; however, the net effect is increased muscle protein and improved physical function in individuals with sarcopenia, obesity or sarcopenic obesity^137,138.

The ability of resistance exercise to improve skeletal muscle function in sarcopenic obesity is well established. The American College of Sports Medicine¹⁵³ recommends that a strength training programme be performed on a minimum of two non-consecutive days each week, with one set of 8–12 repetitions in healthy adults or 10–15 repetitions in older and frail individuals. Resistance training incorporating both slow-velocity and fast-velocity exercises should predominantly consist of one or two sets, with 8–12 repetitions at ~65% of one repetition maximum (maximal force in a single repetition)^154,155. The goal is to gradually progress to a goal of two or three sets at 75% of one repetition maximum over time. This approach increases the cross-sectional area of both type I and type II muscle fibres, improves muscle quality, function, strength and flexibility, and concurrently promotes adipose tissue loss in older adults¹⁵⁶. These effects may be attributed to increased anabolic hormone production, decreased pro-inflammatory cytokine-induced catabolic activity, enhanced muscle protein synthesis, activation of satellite cells, reductions in oxidative stress and increases in mitochondrial function (including biogenesis and adaptation related to DNA content, protein synthesis, volume and cristae density)¹⁵⁶.

Aerobic activity is a potentially important strategy to improve muscle function, as it improves muscle aerobic capacity, insulin sensitivity and cardiovascular function, promotes mitochondrial adaptation, increases capillary density of muscle tissue, reduces oxidative stress and induces adipose tissue loss (both total and visceral)^157,158. Aerobic exercise generally consists of activities that focus on large-muscle groups, such as walking, stair climbing, running, rowing, swimming and cycling. A target of ~65% of the peak heart rate is recommended, aiming to reach 70–85% of peak heart rate over the duration of the exercise regimen.

Combining both resistance and aerobic exercise is more effective in improving skeletal muscle mass and function, and concurrently promoting adipose tissue loss (total, relative and trunk) in individuals with sarcopenic obesity, than either form of exercise alone^{154,159–162}. Specifically, high-intensity interval training (repeated short bursts of intense exercise that last from seconds to minutes interspersed with breaks or recovery periods) has the potential to improve muscle protein synthesis and muscle function by upregulating PGC1α and mitochondrial biogenesis, while improving insulin sensitivity¹⁶³. Protocols for exercise intervention have not yet been well defined, and not all experts agree on the recommendations related to including resistance and/or aerobic training and the frequency and intensity of the activities performed. Importantly, all exercise programmes start at fairly low-to-moderate intensity, duration and frequency to minimize risk of injury, induce exercise adaptation and maximize adherence. Lastly, electromyostimulation shows promising yet inconsistent results in less severe sarcopenic obesity¹⁶⁴, and therefore requires more research.

Nutritional interventions

Nutritional interventions are an important strategy to prevent and treat sarcopenic obesity¹⁶⁵. Hypocaloric diets can effectively reduce adipose tissue but may promote muscle loss by downregulating muscle protein synthesis and increasing proteolysis. Potential negative effects on micronutrient status and on bone mineral density may also occur¹⁶⁶. Of note, muscle loss following diet-induced intentional weight loss may be more frequently observed in older adults with pre-existing sarcopenia^159,165,167.

Frequent monitoring of nutritional status is of paramount importance. To date, evidence is lacking about the effects of macronutrient manipulation¹⁶⁸ (that is, fat versus carbohydrate restriction) compared with conventional calorie restriction (that is, total calorie intake) in terms of weight loss and effects on body composition, particularly on the sarcopenic obesity phenotype. A modest reduction in energy intake (a deficit of ~200–700 kcal per day) aiming for moderate weight loss (0.5–1 kg per week or 8–10% of initial body weight after 6 months) is recommended, in line with the most recent obesity management guidelines¹⁶⁹. Of note, adherence to a moderate energy-restricted diet¹⁷⁰ (for example, a reduction of ~500 kcal per day) may be further enhanced by a potential satiating effect attributed to protein intake.

Very-low-calorie diets (VLCDs) have been used for rapid weight loss in older adults. Considering the often-reduced energy expenditure in these individuals, a conventional hypocaloric diet would lead to a gradual, long-term approach to weight loss¹⁷¹. However, the long-term feasibility of VLCDs is debated because of concerns about nutrient deficiencies, the emergence of disordered eating behaviours, and the risk of muscle loss despite sufficient protein consumption. Moreover, the sustainability of VLCDs is questionable, with many individuals regaining weight after transitioning off the diet. Based on the available evidence, VLCDs are not recommended in older adults¹⁷².

Protein intake of 1.0–1.2 g/kg body weight, and a proposed higher intake (1.2–1.5 g/kg body weight)^126,173 in individuals with multimorbidity, is strongly recommended to maintain and recover muscle mass and function over the long term. Interestingly, recommendations based on current body weight may not be feasible in individuals with obesity, especially in the context of a low-calorie diet. More research is needed to establish optimal and feasible recommendations. Importantly, a higher protein intake is particularly important in older adults who are at higher risk of anabolic resistance^174,175. This increased intake amounts to an intake of approximately 25–30 g of protein per meal (80% of the total dietary intake consumed during three main meals, referred to as the ‘pulse diet’). Below this amount, muscle protein synthesis may be suboptimal, while no substantial advantages in the anabolic response have been found with an intake above 30 g^176,177.

Providing (a high proportion of) essential amino acids may counteract the first-pass extraction effect by splanchnic tissues¹⁷⁸ (mainly gut and liver) that reduces amino acid availability (particularly in older subjects with high BMI) for muscle protein synthesis. As such, not only the amount of protein but also the source of protein might be crucial for preserving muscle mass. Amino acids derived from animal-based sources have a more pronounced anabolic effect than those derived from plant-based sources¹⁷⁹. Whey proteins are effective in stimulating postprandial muscle protein accretion, owing to their fast digestion and absorption kinetics and high leucine content¹⁸⁰. Supplementation with leucine (2.0–2.5 g per day) is associated with increased muscle protein synthesis in older adults, independently of ingestion of other amino acids¹⁸¹.

Robust evidence on the benefits of combined nutrition and exercise interventions is limited, particularly in relation to protein supplementation^182,183. Nevertheless, based on the available evidence, physiologically the combination of nutrition and exercise may substantially reduce adiposity with concomitant increase in muscle mass (in some cases without any BMI variation) and physical function (for example, handgrip strength and gait speed).

Some nutrients and ingredients have been proposed to enhance muscle health owing to their anabolic, anti-inflammatory, anticatabolic and/or antioxidant capacities. These nutrients and ingredients include ω−3 fatty acids, β-hydroxy β-methylbutyrate, carotenoids, selenium, vitamins D, E and C, and isoflavones^{113,170,184–187}. However, the current evidence for these treatments is inconclusive and sometimes conflicting owing to the limited number of studies and small sample sizes. Although existing evidence hints at an important role of specific nutrients and ingredients in muscle health and treatment of sarcopenic obesity, comprehensive studies are needed.

Time-restrictive eating may be an attractive, safe and feasible dietary approach to be explored in future studies. This dietary approach can lead to weight loss without substantial loss of muscle mass and is associated with improvements in cardiovascular function and other physiological markers^188–190.

Bariatric surgery

Bariatric surgery is an underutilized weight treatment strategy, and decision-making to identify appropriate candidates for this surgery is even more challenging in older than in younger adults. The number of studies of this treatment that focused specifically on individuals with sarcopenic obesity is low. Although bariatric surgery leads to marked adipose tissue loss with relative improvements in physical function, it also leads to profound muscle mass losses. Although all types of surgery lead to reduced muscle mass, sleeve gastrectomy demonstrated greater preservation of bone and muscle than Roux-en-Y bypass in a study in 71 patients¹⁹¹. Few studies have evaluated the impact of bariatric surgery on sarcopenic obesity, as most studies focused solely on postsurgical evaluation of musculoskeletal health. In one study assessing the influence of sarcopenia on outcomes in 69 individuals with obesity, the observed remission rates for comorbidities were similar, with no difference at 1 year¹⁹². A separate study in 80 women with obesity assigned to Roux-en-Y bypass with or without exercise found no differences in the phenotypic and genotypic characteristics between groups¹⁹³. A score for predicting the risk of sarcopenia 1 year after bariatric surgery in patients with a BMI of ≥40 kg/m² had an area under the receiver operating characteristic curve approaching 0.95 when skeletal muscle cross-sectional area at the L3 vertebra was used, and 0.92 in those with sarcopenia defined by skeletal muscle index¹⁹⁴. Thus, as with marked calorie deficits discussed above, we strongly recommend that individuals should be treated at highly specialized multidisciplinary centres of excellence for bariatric surgery that focus on quantity and quality of food intake, combined with aerobic and resistance-based exercise interventions, and additional medical support.

Existing studies have focused on younger populations that differ in the type of surgery, in age groups and in comorbidities. Mixed findings have been observed in strength measures, while more consistent improvements have been found in physical function measures, including walking speed and sit-to-stand tests^193,195,196. Importantly, all such measures of strength and physical function consistently demonstrate improvements when bariatric surgery is coupled with a resistance exercise programme^197–199.

Medical therapies

A number of emerging and experimental therapies hold promise for the management of sarcopenic obesity^127,128, although further testing and large-scale clinical trials are necessary to confirm their efficacy.

Obesity medications.

Emerging anti-obesity medications (AOMs) are currently being prescribed for adults across the lifespan. In particular, the newer glucagon-like peptide 1 (GLP1) receptor agonists semaglutide and tirzepatide have received considerable attention among both the scientific and lay communities. A weight loss of >20% with marked improvements in both subjective and objective physical function measures has been reported with these newer medications^200–203. These AOMs have not been specifically tested in populations with sarcopenic obesity and, furthermore, clinical trials have both restricted the number of older adults enrolled in their studies and limited the number of individuals with chronic diseases. Existing data suggest that marked adipose tissue loss with semaglutide and tirzepatide occurs with concomitant muscle loss^202,204,205. However, the proportion of muscle mass loss (relative to adipose tissue) and the degree of resolution of myosteatosis and ectopic adipose tissue deposition (that is, improvement in muscle composition) remain unclear. Myosteatosis and ectopic adipose tissue deposition are extremely important as they are at the heart of a vicious, pro-inflammatory cycle observed in the pathophysiology of sarcopenic obesity. For example, in the STEP 1 study, semaglutide treatment resulted in a total lean mass loss of 5.26 kg²⁰⁴, representing a proportion of ~38% lean mass loss, which exceeds the 25% quarter fat-free mass rule¹²⁹ discussed above, a deviation that is likely to be attributable to the substantial weight changes observed.

The effect of GLP1 receptor agonists on muscle metabolism is the subject of debate. The important loss of weight seems to elicit a substantial loss of muscle mass²⁰⁶. On the other hand, studies in rodents showed that GLP1 receptor agonists may increase microvascular blood volume and glucose transport in skeletal muscle cells, leading to increased delivery of oxygen, nutrients and hormones, such as insulin, to myocytes^207,208. Another study in rodents showed that GLP1 directly induces myogenesis via a complex cAMP-dependent signalling network in skeletal muscle²⁰⁹.

Trials of tirzepatide, including the SURMOUNT trial, demonstrated dose-dependent changes in lean mass, using various modalities for assessing body composition. To our knowledge, subanalyses of only two studies have evaluated outcomes in older adults. The SURPASS-1 trial demonstrated improvements in HbA_1c that were lower in older adults than in younger individuals and not dose-dependent²¹⁰, and a 2023 subanalysis of East Asian participants in the SURPASS trials²¹¹ demonstrated similar outcomes in younger adults (<65 years of age) and older adults (≥65 years of age). Crucially, body composition was not assessed, and in all such trials there have been no objective measurements of physical function. Last, adverse effects may be more pronounced in older than in younger adults, again in a dose-dependent fashion, as demonstrated in the 2023 subanalysis²¹¹. There is an urgent need to further evaluate these medications in populations with sarcopenic obesity across the life course, using sophisticated imaging techniques such as MRI.

While the use of newer medications may lead to substantial weight loss, with resultant improvements in comorbidities and reductions in risk of heart failure²¹², obtaining a solid understanding of the long-term consequences of these interventions is of the utmost importance, particularly in older adults. In addition, multicomponent interventions that include resistance exercise training, as performed with dietary interventions¹⁵⁹, require additional evaluation.

Testosterone.

Ageing leads to testosterone deficiency that may impair muscle adaptation to exercise, as reduced muscle mass and IGF1 expression can increase pro-inflammatory cytokines²¹³. When combined with growth hormone, testosterone supplementation can mitigate the negative effects of obesity (increasing diet-induced adipose tissue loss) and of the ageing process, by promoting IGF1 mRNA and protein expression, and increasing muscle protein synthesis, and muscle mass and function, particularly when combined with exercise intervention. Nonetheless, the data are conflicting: some trials found no significant effects of testosterone supplementation on muscle health, while others found there was no impact on physical function. Of note, potential improvements in muscle (and lean) mass may not directly result in improved muscle function^214,215. This lack of association can be related to how muscle mass was assessed (that is, quantity only versus quantity and composition), or to other factors associated with muscle function besides muscle mass. Future studies should evaluate whether testosterone replacement helps preserve muscle mass and bone mass during weight loss in patients with sarcopenic obesity.

Selective androgen receptor modulators.

Selective androgen receptor modulators (SARMs) selectively target androgen receptors on muscle and bone tissues. SARMs indirectly affect non-muscle androgen receptor pathways mediated by muscle fibroblasts and, in some but not all studies have been shown to increase muscle mass and physical function²¹⁶. SARMs may be of benefit in patients with sarcopenic obesity who require muscle mass increases rather than strength improvements. However, conclusive evidence is still needed.

Anamorelin.

This oral ghrelin analogue has mostly been studied in cancer^217–219 and has anti-inflammatory and anabolic properties. Studies investigating anamorelin are characterized by high heterogeneity; however, treatment with this hormone analogue improved lean mass but failed to improve muscle function in different trials. Studies in patients with sarcopenic obesity have not been conducted, and it is unclear whether the improvements in lean mass observed have differential effects in different patient populations.

Myostatin inhibitors.

Emerging trials of myostatin inhibitors have been the subject of keen interest to the sarcopenic obesity community, as myostatin is a contributor to muscle–adipose tissue crosstalk. Myostatin is a member of the TGFβ superfamily and inhibits skeletal muscle growth and development. While inhibition of myostatin leads to muscle cell hyperplasia and hypertrophy, suppresses irisin and downregulates pro-inflammatory cytokines, it may also have beneficial effects on metabolism, adiposity and insulin sensitivity²²⁰. Individuals with sarcopenia have elevated levels of myostatin, which is also expressed in adipose tissue. These aspects of myostatin are all inherent targets in the pathophysiology of sarcopenic obesity and therefore their inhibition has potential therapeutic consequences. Interestingly, myostatin can be modulated by diet²²¹. In a trial of the activin receptor type 2B inhibitor bimagrumab (700 mg vs placebo monthly for 6 months) in combination with a healthy diet and a home-based exercise programme among 180 community-dwelling individuals >70 years of age with sarcopenia, bimagrumab improved functional parameters and lean mass²²². While the study population included participants with BMI up to 32 kg/m², there was no specific subanalysis for those with obesity. In another trial in adults with type 2 diabetes mellitus, a BMI between 28 and 40 kg/m², and an average age of 60.4 ± 7.7 years, a combination intervention of a diet and exercise advice with either bimagrumab infusion or placebo (every 4 weeks for 48 weeks), bimagrumab treatment resulted in notable adipose tissue loss, increased lean mass and metabolic improvements; however, there was no distinct analysis for those with sarcopenic obesity.

Cell and gene therapies.

Mesenchymal stem cells (MSCs) hold considerable promise as a key precursor in the development of muscle, bone and cartilage, and the pluripotent potential of MSCs may help in muscle regeneration²²³. To date, studies have demonstrated promising results in mice, suggesting that MSC transplantation may bolster improvements observed with exercise without worsening inflammation²²⁴. In mice fed a high-fat diet, injection of umbilical cord MSCs led to improvements in physical function and mitigated obesity-related muscle atrophy²²⁵. To our knowledge, there are no equivalent studies in humans. In addition to ethical barriers, the implementation of these techniques in clinical practice is probably premature, and further evaluation is required.

Personalized approaches

Precision medicine is currently a major focus in clinical medicine and is also a major research initiative, particularly at the National Institutes of Health, which has funded large-scale projects including the All of Us Research Program and, in the nutritional realm, the Nutrition for Precision Health study. Large-scale studies such as LOOK-AHEAD²²⁶ and PREDIMED²²⁷ established that individuals have different responses and outcomes to dietary interventions based on individual and genetic characteristics. Emerging laboratory technologies to identify these characteristics include genomics, epigenetics, metabolomics and proteomics, and further studies of senescence-associated secretory phenotype proteins, will enable an improved understanding of not only the heterogeneity of the sarcopenic obesity phenotype but also of the ageing process. Understanding which individuals respond to which interventions — to deliver the right intervention to the right person at the right time — aligns with the premise of precision medicine. This approach allows the effective use of resources and a more personalized strategy in patient care. While the application of novel machine learning analytics to identify specific subgroups that respond to specific interventions is still in its infancy, the future is promising.

Conclusions

In the clinical landscape, sarcopenic obesity is increasingly recognized as a considerable challenge to healthy ageing in older adults. The development and progression of this complex syndrome is influenced by an interplay of multiple factors including ageing, inflammation, lifestyle, among others. The clinical implications of sarcopenic obesity span from physical impairments to elevated morbidity and mortality rates.

Despite the strides made in the understanding of sarcopenic obesity, considerable obstacles remain, including the validation (and development) of diagnostic tools and effective prevention and management strategies. Addressing this syndrome requires an integrative, multidisciplinary approach focusing on reducing adipose tissue and improving muscle mass and function, while optimizing metabolic regulation, diet and physical activity.

Further clinical research is essential to increase our understanding of the underlying pathophysiology of sarcopenic obesity, improve diagnosis, identify at-risk groups, and assess the effectiveness of interventions. Given the global rise in obesity and ageing populations, sarcopenic obesity is likely to become an even more important health issue. As such, it presents both a challenge to health-care systems and researchers, and an opportunity for innovative solutions that can improve the health and quality of life of older adults. We direct readers to the areas recommended by the SOGLI group for prioritized research directions concerning the pathophysiology, screening, diagnosis, staging, and prevention and treatment strategies of sarcopenic obesity¹⁰⁴.

Finally, a patient-centric approach is needed for managing sarcopenic obesity, accentuating the value of personalized care strategies and patient education. Enhancing awareness of this syndrome among patients, health-care providers and the wider public is a pivotal step in devising more effective solutions to this growing clinical concern.

Key points.

• Sarcopenic obesity involves an ageing-associated increase in adiposity and reduction in muscle mass and function, poses a major health risk to older adults, and presents diagnostic and management challenges in clinical settings.

• The multifaceted pathophysiology of sarcopenic obesity requires a comprehensive understanding of hormonal shifts, inflammation, muscle and adipose tissue changes, and lifestyle factors for effective patient care.

• Recently proposed consensus criteria developed by international experts are enhancing the clinical diagnosis and assessment of sarcopenic obesity and aid in achieving more precise and consistent patient evaluations.

• Management strategies vary from lifestyle modifications, including exercise and targeted nutritional plans, to emerging drug therapies, broadening the treatment options for sarcopenic obesity.

• As sarcopenic obesity research progresses, the need for clinician involvement in collaborative research efforts and the implementation of new findings into clinical practice is paramount.

• The increasing use of digital technology in delivering diet and exercise interventions offers a promising avenue for modernized, patient-centred care, countering outdated perceptions about engagement with e-health by older adults.