The DOI matches its Crossref record; 233 of the 234 references it cites were found in a registry or an index; 19 of the 132 sources its claims cite were checked for support.
Sarcopenic obesity in older adults: a clinical overview
Open accessAbstract
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.
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Claims the paper makes
76 Not checked yet · 13 No basis given · 8 Own interpretation · 5 Partly supported · 3 Supported so far · 1 Supported · 1 Not supported · accuracy not yet measured
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Nitric oxide production
What the sources say
- Disputedcites [82] Muniyappa, R. & Sowers, J. R. Role of insulin resistance in endothelial dysfunction. Rev. Endocr. Metab. Disord. 14, 5–12 (2013). sourceExperimental — accuracy not yet measured
In “Selective Resistance to Insulin Actions in the Endothelium” (page unavailable), the paper gives the opposite signalling direction: insulin activates IRS-1 and Akt, which lead to NO production. The Introduction says NO can increase skeletal-muscle glucose uptake through increased blood flow, but the paper does not describe NO activating IRS-1, Akt, or mTOR to promote muscle protein synthesis. (LLM, conf=0.85)
Checked by a reasoning model — may be wrong.
plaindirect- Asserted: passes — The authors put it forward as true.
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- Disputed
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“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 in older adults: a clinical overview > Abstract
What the sources say
- Partly supportedcites [47] JafariNasabian, P., Inglis, J. E., Reilly, W., Kelly, O. J. & Ilich, J. Z. Aging human body: changes in bone, muscle and body fat with consequent changes in nutrient intake. J. Endocrinol. 234, R37–R51 (2017). sourceExperimental — accuracy not yet measured
The hormonal-changes section describes muscle and fat as interconnected endocrine tissues, and the discussion at 234:1 links inflammation and fat accumulation to sarcopenic obesity. The discussion at 234:1 also links diet and reactive oxygen species to adipogenesis and bone changes, but it does not establish oxidative stress as part of the pathophysiology of sarcopenic obesity specifically; that part of the claim is more specific than the source. (LLM, conf=0.82)
- Supportedcites [48] Sakuma, K. & Yamaguchi, A. Sarcopenic obesity and endocrinal adaptation with age. Int. J. Endocrinol. 2013, 204164 (2013). source
The Conclusions describe sarcopenic obesity as having a complex, multifactorial pathogenesis involving lifestyle, endocrine and immunological factors. Section 2 links adipose tissue, inflammation and changes in muscle; the Introduction also identifies oxidative stress among factors involved in age-related muscle loss. Page numbers are not provided in our copy. (LLM, conf=0.88)
- Not checked yetcites [49] Moreira-Pais, A., Ferreira, R., Oliveira, P. A. & Duarte, J. A. A neuromuscular perspective of sarcopenia pathogenesis: deciphering the signaling pathways involved. Geroscience 44, 1199–1213 (2022). source
- Supportedcites [50] Gonzalez, A. et al. The critical role of oxidative stress in sarcopenic obesity. Oxid. Med. Cell Longev. 2021, 4493817 (2021). source
Section 3 identifies adipose and skeletal muscle dysfunction, age-associated hormonal changes, proinflammatory cytokines, oxidative stress, and decreased physical activity as factors in sarcopenic obesity. Section 3.4 further describes how physical inactivity and increased adipose tissue reinforce one another. (LLM, conf=0.93)
- Partly supportedcites [51] Huo, F., Liu, Q. & Liu, H. Contribution of muscle satellite cells to sarcopenia. Front. Physiol. 13, 892749 (2022). sourceExperimental — accuracy not yet measured
The Introduction and §2.2 (page unavailable) describe sarcopenia as involving hormonal changes, inflammation, reactive oxygen species, inactivity, and nutrition. Section 2.2 also discusses fat gain and fat infiltration into muscle, but it does not establish the claimed interplay with adipose tissue as the pathophysiology of sarcopenic obesity specifically. (LLM, conf=0.85)
- Partly supportedcites [52] Jeon, Y. K. et al. Vascular dysfunction as a potential culprit of sarcopenia. Exp. Gerontol. 145, 111220 (2021). sourceExperimental — accuracy not yet measured
The Introduction lists hormonal changes, inflammation, oxidative stress, reduced physical activity, and malnutrition as factors present in older adults with sarcopenia. The cited passages do not establish the claimed interplay with adipose tissue or address the pathophysiology of sarcopenic obesity specifically. (LLM, conf=0.87)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Introduction
What the sources say
- Partly supportedcites [12] Siervo, M. et al. Body composition indices of a load-capacity model: gender- and BMI-specific reference curves. Public. Health Nutr. 18, 1245–1254 (2015). sourceExperimental — accuracy not yet measured
The paper’s discussion of sarcopenic obesity describes high adiposity alongside low muscle mass, and its load–capacity discussion treats adiposity as ‘load’ and skeletal muscle as ‘capacity’ (page numbers unavailable). It also notes that fat-free mass normally increases with body mass. However, it does not establish that an adaptive process fails or that muscle functionality fails to increase as adipose tissue accumulates. (LLM, conf=0.83)
- Partly supportedcites [13] Wells, J. C. Historical cohort studies and the early origins of disease hypothesis: making sense of the evidence. Proc. Nutr. Soc. 68, 179–188 (2009). sourceExperimental — accuracy not yet measured
In “Interpreting birth weight” (page unavailable), Wells describes homeostatic adaptation to metabolic load and a disease model based on disparity between load and capacity. The paper treats adiposity and lean mass as contributors to load, but does not address sarcopenic obesity or say that adipose tissue accumulates without a corresponding increase in muscle mass or function. (LLM, conf=0.84)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“muscle loss following diet-induced intentional weight loss may be more frequently observed in older adults with pre-existing sarcopenia159,165,167.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Nutritional interventions
What the sources say
- Partly supportedcites [159] Villareal, D. T. et al. Aerobic or resistance exercise, or both, in dieting obese older adults. N. Engl. J. Med. 376, 1943–1955 (2017). This study involving 160 older adults with obesity finds that weight loss combined with aerobic and resistance exercise is most effective in enhancing functional status and mitigating the muscle and bone mass loss typically seen with weight reduction, compared with other exercise modalities or no exercise at all. sourceExperimental — accuracy not yet measured
The Abstract and Discussion report muscle or lean-mass loss during weight loss in obese older adults. They do not say that loss occurs more frequently in those with pre-existing sarcopenia; the Abstract instead describes sarcopenia as a possible result of accelerated muscle loss. (LLM, conf=0.85)
- Partly supportedcites [165] Batsis, J. A. et al. Weight loss interventions in older adults with obesity: a systematic review of randomized controlled trials since 2005. J. Am. Geriatr. Soc. 65, 257–268 (2017). This systematic review of clinical trials between 2005 and 2015 finds that combined dietary and exercise interventions are more effective for improving physical performance and quality of life in older adults with obesity than either intervention alone. sourceExperimental — accuracy not yet measured
The Results (Other Findings; page not provided) report greater loss of fat-free mass with diet alone, and the Discussion warns of sarcopenia with dietary weight loss without resistance exercise. Neither passage says muscle loss is more frequent in older adults with pre-existing sarcopenia than in those without it. (LLM, conf=0.86)
- Partly supportedcites [167] Villareal, D. T. et al. Weight loss, exercise, or both and physical function in obese older adults. N. Engl. J. Med. 364, 1218–1229 (2011). In a 1-year study of 107 older adults with obesity, combining weight loss and exercise led to greater enhancements in physical function and performance than either strategy alone, with participants also experiencing less decrease in lean body mass and bone density. sourceExperimental — accuracy not yet measured
The Results (Body Weight and Composition; page unavailable) report a 5% decline in lean body mass in the diet-only group, and the Discussion describes the participants as having sarcopenic obesity. The paper does not compare participants with and without pre-existing sarcopenia, so it does not establish that muscle loss is more frequent in those with sarcopenia. (LLM, conf=0.86)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Importantly, all such measures of strength and physical function consistently demonstrate improvements when bariatric surgery is coupled with a resistance exercise programme197–199.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Bariatric surgery
What the sources say
- Not checked yetcites [197] Hassannejad, A., Khalaj, A., Mansournia, M. A., Rajabian Tabesh, M. & Alizadeh, Z. The effect of aerobic or aerobic-strength exercise on body composition and functional capacity in patients with BMI ≥35 after bariatric surgery: a randomized control trial. Obes. Surg. 27, 2792–2801 (2017). source
- Not checked yetcites [198] Huck, C. J. Effects of supervised resistance training on fitness and functional strength in patients succeeding bariatric surgery. J. Strength. Cond. Res. 29, 589–595 (2015). source
- Supportedcites [199] Oliveira, G. S. et al. Resistance training improves muscle strength and function, regardless of protein supplementation, in the mid- to long-term period after gastric bypass. Nutrients 14, 14 (2021). source
The Results (section 3; page unavailable) report significant improvements across the measured strength and physical-function outcomes in the resistance-training groups, with no significant changes in the non-exercise groups. The study concerns people 2–7 years after Roux-en-Y gastric bypass, a form of bariatric surgery. (LLM, conf=0.92)
boosteddirect- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Abstract
What the sources say
- Not checked yetcites 21–46
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Hormonal shifts associated with ageing and obesity strongly influence the pathophysiology of sarcopenic obesity48.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Oxidative stress and hormonal shifts
What the sources say
- Not checked yetcites [48] Sakuma, K. & Yamaguchi, A. Sarcopenic obesity and endocrinal adaptation with age. Int. J. Endocrinol. 2013, 204164 (2013). source
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Changes in muscle health
What the sources say
- Not checked yetcites [55] Correa-de-Araujo, R. et al. Myosteatosis in the context of skeletal muscle function deficit: an Interdisciplinary Workshop at the National Institute on Aging. Front. Physiol. 11, 963 (2020). This workshop discusses the impact of myosteatosis on skeletal muscle function during aging, detailing its connection to metabolic disease, evaluation techniques and prospective interventions, and emphasizing the importance of innovative research domains and interdisciplinary synergy. source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Changes in muscle health
What the sources say
- Not checked yetcites [56] Larsson, L. et al. Sarcopenia: aging-related loss of muscle mass and function. Physiol. Rev. 99, 427–511 (2019). source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Introduction
What the sources say
- Not checked yetcites [15] Baumgartner, R. N. & Waters, D. L. in Principles and Practice of Geriatric Medicine (eds Pathy, M. S. J., Sinclair, A. J. & Morley, J. E.) 909–933 (Wiley, 2005). source
hedgeddirect- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 45
- Probably not a substantial claim. 8
Every source the paper cites for this claim was checked and supports it.
In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Introduction
What the sources say
- Supportedcites [11] Stenholm, S. et al. Sarcopenic obesity: definition, cause and consequences. Curr. Opin. Clin. Nutr. Metab. Care 11, 693–700 (2008). source
The Introduction says bone and muscle normally grow with changes in weight, through gravity stimulating mechanoreceptors that modulate growth-factor production. It also says this adaptation may be impaired in some older people who become obese without corresponding muscle growth, supporting the distinction between obesity with and without sarcopenia. (LLM, conf=0.91)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“NO and insulin are crucial for muscle metabolism and are implicated in the development and progression of sarcopenia78,79.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Nitric oxide production
What the sources say
- Not checked yetcites [78] Cleasby, M. E., Jamieson, P. M. & Atherton, P. J. Insulin resistance and sarcopenia: mechanistic links between common co-morbidities. J. Endocrinol. 229, R67–R81 (2016). source
- Supportedcites [79] Timmerman, K. L. & Volpi, E. Endothelial function and the regulation of muscle protein anabolism in older adults. Nutr. Metab. Cardiovasc. Dis. 23, S44–S50 (2013). source
The section on age-related insulin resistance reports that inhibiting nitric oxide synthesis attenuated insulin’s effects on muscle protein synthesis. The Conclusions link impaired endothelial dilation and anabolic response to insulin to the possible development and progression of sarcopenia. (LLM, conf=0.90)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Medical therapies
What the sources say
- Partly supportedcites [216] Bhasin, S., Krishnan, V., Storer, T. W., Steiner, M. & Dobs, A. S. Androgens and selective androgen receptor modulators to treat functional limitations associated with aging and chronic disease. J. Gerontol. A Biol. Sci. Med. Sci. 78, 25–31 (2023). sourceExperimental — accuracy not yet measured
The Selective Androgen Receptor Modulators section reports increases in lean body mass or muscle size in trials, while physical-function improvements were inconsistent. It describes tissue-specific androgen-receptor activity but does not support the claimed indirect pathway mediated by muscle fibroblasts; the mechanisms section instead discusses receptor binding and tissue-dependent signaling. Page numbers are unavailable in our copy. (LLM, conf=0.87)
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“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 markers188–190.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Nutritional interventions
What the sources say
- Partly supportedcites [188] Kirkham, A. A. et al. Implementation of weekday time-restricted eating to improve metabolic health in breast cancer survivors with overweight/obesity. Obesity 31, 150–160 (2023). sourceExperimental — accuracy not yet measured
In Preliminary efficacy for metabolic outcomes (page unavailable), the paper reports a median 1.0 kg decrease in body mass; Steatosis reports a 1.5% decrease in thigh muscle, consistent with a small rather than substantial muscle loss. The Metabolism section does not support the claimed cardiovascular improvement: blood pressure and cardiorespiratory fitness did not change significantly, and fasting insulin increased. The claim also generalizes beyond the breast cancer survivors with overweight or obesity studied here. (LLM, conf=0.88)
- Partly supportedcites [189] Kirkham, A. A., Parr, E. B. & Kleckner, A. S. Cardiometabolic health impacts of time-restricted eating: implications for type 2 diabetes, cancer and cardiovascular diseases. Curr. Opin. Clin. Nutr. Metab. Care 25, 378–387 (2022). sourceExperimental — accuracy not yet measured
The review’s Summary of Recent Evidence reports weight and fat loss and improvements in some cardiometabolic markers, while noting that other studies found no effect. Its Safety of TRE section says more data on lean-mass changes are needed, so it does not establish weight loss without substantial muscle loss. The CVD Measures section discusses cardiovascular risk factors and risk scores, not a demonstrated improvement in cardiovascular function. (LLM, conf=0.87)
- Partly supportedcites [190] Martens, C. R. et al. Short-term time-restricted feeding is safe and feasible in non-obese healthy midlife and older adults. Geroscience 42, 667–686 (2020). sourceExperimental — accuracy not yet measured
In the Results sections on body composition and cardiovascular function (page unavailable), six weeks of time-restricted feeding preserved leg fat-free mass but did not reduce body mass or improve measured cardiovascular function. The Oral glucose tolerance results report a modest improvement in glucose tolerance. Thus, the paper supports muscle preservation and some physiological benefit, but not the claimed weight loss or cardiovascular improvement in its study. (LLM, conf=0.89)
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“This oral ghrelin analogue has mostly been studied in cancer217–219 and has anti-inflammatory and anabolic properties.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Medical therapies
What the sources say
- Supportedcites [217] Currow, D. C., Maddocks, M., Cella, D. & Muscaritoli, M. Efficacy of anamorelin, a novel non-peptide ghrelin analogue, in patients with advanced non-small cell lung cancer (NSCLC) and cachexia – review and expert opinion. Int. J. Mol. Sci. 19, 3471 (2018). source
The citation is attached to the statement that anamorelin has mostly been studied in cancer. In §1, “Appetite-Improving Drugs: Ghrelin and Ghrelin Agonists” (page unavailable), the review identifies anamorelin as an oral ghrelin analogue and describes its phase 3 trials in patients with advanced non-small cell lung cancer and cachexia. The same section reports effects on inflammation and lean body mass, although those properties appear after the citation in the citing sentence. (LLM, conf=0.88)
- Not checked yetcites [218] Fonseca, G. W. P. D. & von Haehling, S. An overview of anamorelin as a treatment option for cancer-associated anorexia and cachexia. Expert. Opin. Pharmacother. 22, 889–895 (2021). source
- Not checked yetcites [219] Wakabayashi, H., Arai, H. & Inui, A. Anamorelin in Japanese patients with cancer cachexia: an update. Curr. Opin. Support. Palliat. Care 17, 162–167 (2023). source
plain- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Supported
In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Clinical importance
What the sources say
- Not checked yetcites 21–46
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“A 2022 consensus statement established a new definition and diagnostic criteria for sarcopenic obesity.”
§ Sarcopenic obesity in older adults: a clinical overview > Abstract
What the sources say
- Not checked yetcites [2] Donini, L. M. et al. Definition and diagnostic criteria for sarcopenic obesity: ESPEN and EASO consensus statement. Clin. Nutr. 41, 990–1000 (2022). Collaboration between ESPEN and EASO has established a unified definition and diagnostic criteria for sarcopenic obesity, aiming to streamline research and treatment approaches for this prevalent condition. source
- Not checked yetcites [3] Donini, L. M. et al. Definition and diagnostic criteria for sarcopenic obesity: ESPEN and EASO consensus statement. Obes. Facts 15, 321–335 (2022). source
plaindirect- Asserted: passes — The authors put it forward as true.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Changes in adipose tissue
What the sources say
- Not checked yetcites [47] JafariNasabian, P., Inglis, J. E., Reilly, W., Kelly, O. J. & Ilich, J. Z. Aging human body: changes in bone, muscle and body fat with consequent changes in nutrient intake. J. Endocrinol. 234, R37–R51 (2017). source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Introduction
What the sources say
- Not checked yetcites [15] Baumgartner, R. N. & Waters, D. L. in Principles and Practice of Geriatric Medicine (eds Pathy, M. S. J., Sinclair, A. J. & Morley, J. E.) 909–933 (Wiley, 2005). source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Introduction
What the sources say
- Not checked yetcites [1] Heber, D. et al. Clinical detection of sarcopenic obesity by bioelectrical impedance analysis. Am. J. Clin. Nutr. 64, 472s–477s (1996). source
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
None of the sources cited for this claim have been checked yet.
In the paper
“Oxidative stress adversely impacts muscle health through muscle protein breakdown60, muscle inflammation61, impaired muscle regeneration62, mitochondrial dysfunction63 and insulin resistance50.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Oxidative stress and hormonal shifts
What the sources say
- Not checked yetcites [50] Gonzalez, A. et al. The critical role of oxidative stress in sarcopenic obesity. Oxid. Med. Cell Longev. 2021, 4493817 (2021). source
- Not checked yetcites [60] Powers, S. K., Smuder, A. J. & Criswell, D. S. Mechanistic links between oxidative stress and disuse muscle atrophy. Antioxid. Redox Signal. 15, 2519–2528 (2011). source
- Not checked yetcites [61] Chen, M., Wang, Y., Deng, S., Lian, Z. & Yu, K. Skeletal muscle oxidative stress and inflammation in aging: focus on antioxidant and anti-inflammatory therapy. Front. Cell Dev. Biol. 10, 964130 (2022). source
- Not checked yetcites [62] Lian, D., Chen, M. M., Wu, H., Deng, S. & Hu, X. The role of oxidative stress in skeletal muscle myogenesis and muscle disease. Antioxidants 11, 755 (2022). source
- Not checked yetcites [63] Ferri, E. et al. Role of age-related mitochondrial dysfunction in sarcopenia. Int. J. Mol. Sci. 21, 5236 (2020). source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Various metabolic scenarios, such as weight gain or loss, can contribute to the development of sarcopenic obesity.”
§ Sarcopenic obesity in older adults: a clinical overview > Introduction
What the sources say
- Not checked yetcites [14] Prado, C. M. M., Wells, J. C. K., Smith, S. R., Stephan, B. C. M. & Siervo, M. Sarcopenic obesity: a critical appraisal of the current evidence. Clin. Nutr. 31, 583–601 (2012). This review highlights the significance of sarcopenic obesity due to its dual metabolic burden, and underscores the inconsistency in study methodologies. source
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In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Introduction
What the sources say
- Not checked yetcites [7] Murdock, D. J. et al. The prevalence of low muscle mass associated with obesity in the USA. Skelet. Muscle 12, 26 (2022). source
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“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Oxidative stress and hormonal shifts
What the sources say
- Not checked yetcites [59] Meng, S. J. & Yu, L. J. Oxidative stress, molecular inflammation and sarcopenia. Int. J. Mol. Sci. 11, 1509–1526 (2010). source
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In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Changes in adipose tissue
What the sources say
- Not checked yetcites [57] Kawai, T., Autieri, M. V. & Scalia, R. Adipose tissue inflammation and metabolic dysfunction in obesity. Am. J. Physiol. Cell Physiol. 320, C375–C391 (2021). source
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In the paper
“Production of myostatin, a growth-inhibiting myokine, is upregulated in sarcopenia64, whereas that of muscle-mass-stimulating irisin seems to be downregulated65.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Oxidative stress and hormonal shifts
What the sources say
- Not checked yetcites [64] White, T. A. & LeBrasseur, N. K. Myostatin and sarcopenia: opportunities and challenges – a mini-review. Gerontology 60, 289–293 (2014). source
- Not checked yetcites [65] Chang, J. S. et al. Circulating irisin levels as a predictive biomarker for sarcopenia: a cross-sectional community-based study. Geriatr. Gerontol. Int. 17, 2266–2273 (2017). source
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In the paper
“However, the definition has evolved to also incorporate reduced muscle function in the diagnosis of sarcopenia in older adults2,3, with muscle strength being the predominant measure of function.”
§ Sarcopenic obesity in older adults: a clinical overview > Introduction
What the sources say
- Not checked yetcites [2] Donini, L. M. et al. Definition and diagnostic criteria for sarcopenic obesity: ESPEN and EASO consensus statement. Clin. Nutr. 41, 990–1000 (2022). Collaboration between ESPEN and EASO has established a unified definition and diagnostic criteria for sarcopenic obesity, aiming to streamline research and treatment approaches for this prevalent condition. source
- Not checked yetcites [3] Donini, L. M. et al. Definition and diagnostic criteria for sarcopenic obesity: ESPEN and EASO consensus statement. Obes. Facts 15, 321–335 (2022). source
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In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Abstract
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In the paper
“Ageing-associated decline in testosterone and oestrogen levels weakens muscle, reducing both muscle mass and strength66.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Oxidative stress and hormonal shifts
What the sources say
- Not checked yetcites [66] Gupta, P. & Kumar, S. Sarcopenia and endocrine ageing: are they related? Cureus 14, e28787 (2022).
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In the paper
“Sarcopenic obesity exemplifies the intersection of two prevalent health crises: ageing populations and the obesity epidemic4.”
§ Sarcopenic obesity in older adults: a clinical overview > Introduction
What the sources say
- Not checked yetcites [4] Roubenoff, R. Sarcopenic obesity: the confluence of two epidemics. Obes. Res. 12, 887–888 (2004). This commentary discusses how the convergence of the obesity epidemic with an ageing population magnifies the risk of sarcopenic obesity, posing unprecedented health challenges and underscoring the urgent need for interdisciplinary collaboration. source
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In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Oxidative stress and hormonal shifts
What the sources say
- Not checked yetcites [48] Sakuma, K. & Yamaguchi, A. Sarcopenic obesity and endocrinal adaptation with age. Int. J. Endocrinol. 2013, 204164 (2013). source
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In the paper
“NO modulates insulin signalling pathways in muscle cells80, while obesity and metabolic syndrome are associated with decreased whole-body NO synthesis81.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Nitric oxide production
What the sources say
- Not checked yetcites [80] Bergandi, L. et al. Insulin stimulates glucose transport via nitric oxide/cyclic GMP pathway in human vascular smooth muscle cells. Arterioscler. Thromb. Vasc. Biol. 23, 2215–2221 (2003). source
- Not checked yetcites [81] Siervo, M., Jackson, S. J. & Bluck, L. J. In-vivo nitric oxide synthesis is reduced in obese patients with metabolic syndrome: application of a novel stable isotopic method. J. Hypertens. 29, 1515–1527 (2011). source
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In the paper
“Ageing has also been related to a decline in nitric oxide (NO) production76 and skeletal muscle blood flow77.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Nitric oxide production
What the sources say
- Not checked yetcites [76] Sverdlov, A. L., Ngo, D. T. M., Chan, W. P. A., Chirkov, Y. Y. & Horowitz, J. D. Aging of the nitric oxide system: are we as old as our NO? J. Am. Heart Assoc. 3, e000973 (2014). source
- Not checked yetcites [77] Hearon, C. M. Jr & Dinenno, F. A. Regulation of skeletal muscle blood flow during exercise in ageing humans. J. Physiol. 594, 2261–2273 (2016). source
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In the paper
“For example, older adults might be at high risk of a low protein intake and inadequate consumption of essential amino acids89.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Energy metabolism and dietary factors
What the sources say
- Not checked yetcites [89] Deutz, N. E. et al. Protein intake and exercise for optimal muscle function with aging: recommendations from the ESPEN Expert Group. Clin. Nutr. 33, 929–936 (2014). This expert opinion highlights the importance of maintaining muscle function during ageing through adequate protein intake (1.0–1.2 g/kg body weight daily for healthy older adults and 1.2–1.5 g/kg daily for malnourished adults or those facing illness) and daily physical activity or exercise for sustained muscle health. source
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In the paper
“As such, not only the amount of protein but also the source of protein might be crucial for preserving muscle mass.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Nutritional interventions
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Concurrently, increased levels of catabolic hormones, such as cortisol, promote protein breakdown and inhibit protein synthesis, exacerbating muscle wasting and sarcopenia67.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Oxidative stress and hormonal shifts
What the sources say
- Not checked yetcites [67] Braun, T. P. & Marks, D. L. The regulation of muscle mass by endogenous glucocorticoids. Front. Physiol. 6, 12 (2015). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Chronic stress can lead to overeating and/or a sedentary lifestyle67,72, factors that may increase the risk of sarcopenia.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Oxidative stress and hormonal shifts
What the sources say
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Chronic stress and consistently high cortisol levels can negatively impact muscle tissue and increase sarcopenia risk68.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Oxidative stress and hormonal shifts
What the sources say
- Not checked yetcites [68] Yanagita, I. et al. A high serum cortisol/DHEA-S ratio is a risk factor for sarcopenia in elderly diabetic patients. J. Endocr. Soc. 3, 801–813 (2019). source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Furthermore, cortisol can negatively affect bone health73 and exacerbate age-related bone density decline, possibly contributing to the development of osteosarcopenic obesity74.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Oxidative stress and hormonal shifts
What the sources say
- Not checked yetcites [73] Chiodini, I., Torlontano, M., Carnevale, V., Trischitta, V. & Scillitani, A. Skeletal involvement in adult patients with endogenous hypercortisolism. J. Endocrinol. Invest. 31, 267–276 (2008). source
- Not checked yetcites [74] Ormsbee, M. J. et al. Osteosarcopenic obesity: the role of bone, muscle, and fat on health. J. Cachexia Sarcopenia Muscle 5, 183–192 (2014). source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Nitric oxide production
What the sources say
- Not checked yetcites [85] Tengan, C. H., Rodrigues, G. S. & Godinho, R. O. Nitric oxide in skeletal muscle: role on mitochondrial biogenesis and function. Int. J. Mol. Sci. 13, 17160–17184 (2012). The review discusses the physiological roles of nitric oxide in mitochondrial energetics and skeletal muscle function. source
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In the paper
“Importantly, a higher protein intake is particularly important in older adults who are at higher risk of anabolic resistance174,175.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Nutritional interventions
What the sources say
- Not checked yetcites [174] Burd, N. A., Gorissen, S. H. & van Loon, L. J. C. Anabolic resistance of muscle protein synthesis with aging. Exerc. Sport. Sci. Rev. 41, 169–173 (2013). source
- Not checked yetcites [175] Boirie, Y., Morio, B., Caumon, E. & Cano, N. J. Nutrition and protein energy homeostasis in elderly. Mech. Ageing Dev. 136–137, 76–84 (2014). source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Energy metabolism and dietary factors
What the sources say
- Not checked yetcites [91] Fonseca-Pérez, D., Arteaga-Pazmiño, C., Maza-Moscoso, C. P., Flores-Madrid, S. & Álvarez-Córdova, L. Food insecurity as a risk factor of sarcopenic obesity in older adults. Front. Nutr. 9, 1040089 (2022). source
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In the paper
“NO-mediated vasodilation can enhance blood flow and nutrient delivery to muscles, supporting muscle metabolism and potentially mitigating sarcopenia84.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Nitric oxide production
What the sources say
- Not checked yetcites [84] Wagenmakers, A. J., Strauss, J. A., Shepherd, S. O., Keske, M. A. & Cocks, M. Increased muscle blood supply and transendothelial nutrient and insulin transport induced by food intake and exercise: effect of obesity and ageing. J. Physiol. 594, 2207–2222 (2016). source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Pathophysiology > Oxidative stress and hormonal shifts
What the sources say
- Not checked yetcites [69] Shimizu, N. et al. Crosstalk between glucocorticoid receptor and nutritional sensor mTOR in skeletal muscle. Cell Metab. 13, 170–182 (2011). source
- Not checked yetcites [70] Brownlee, K. K., Moore, A. W. & Hackney, A. C. Relationship between circulating cortisol and testosterone: influence of physical exercise. J. Sports Sci. Med. 4, 76–83 (2005).
- Not checked yetcites [71] Sun, L., Trausch-Azar, J. S., Muglia, L. J. & Schwartz, A. L. Glucocorticoids differentially regulate degradation of MyoD and Id1 by N-terminal ubiquitination to promote muscle protein catabolism. Proc. Natl Acad. Sci. USA 105, 3339–3344 (2008). source
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In the paper
“The SURPASS-1 trial demonstrated improvements in HbA1c that were lower in older adults than in younger individuals and not dose-dependent210”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Medical therapies
What the sources say
- Not checked yetcites [210] Rosenstock, J. et al. Efficacy and safety of a novel dual GIP and GLP-1 receptor agonist tirzepatide in patients with type 2 diabetes (SURPASS-1): a double-blind, randomised, phase 3 trial. Lancet 398, 143–155 (2021). source
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In the paper
“Few studies have evaluated the impact of bariatric surgery on sarcopenic obesity, as most studies focused solely on postsurgical evaluation of musculoskeletal health.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Bariatric surgery
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In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Bariatric surgery
What the sources say
- Not checked yetcites [193] Gil, S. et al. A randomized clinical trial on the effects of exercise on muscle remodelling following bariatric surgery. J. Cachexia Sarcopenia Muscle 12, 1440–1455 (2021). source
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In the paper
“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).”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Nutritional interventions
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In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Medical therapies
What the sources say
- Not checked yetcites [212] Harris, E. Semaglutide improves heart failure and cardiovascular disease. JAMA 330, 1127–1127 (2023).
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In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Medical therapies
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In the paper
“Crucially, body composition was not assessed, and in all such trials there have been no objective measurements of physical function.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Medical therapies
plain- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Medical therapies
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Medical therapies
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Medical therapies
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Medical therapies
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“Ageing leads to testosterone deficiency that may impair muscle adaptation to exercise, as reduced muscle mass and IGF1 expression can increase pro-inflammatory cytokines213.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Medical therapies
What the sources say
- Not checked yetcites [213] Pataky, M. W., Young, W. F. & Nair, K. S. Hormonal and metabolic changes of aging and the influence of lifestyle modifications. Mayo Clin. Proc. 96, 788–814 (2021). source
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In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Medical therapies
plain- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Medical therapies
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“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 tests193,195,196.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Bariatric surgery
What the sources say
- Not checked yetcites [193] Gil, S. et al. A randomized clinical trial on the effects of exercise on muscle remodelling following bariatric surgery. J. Cachexia Sarcopenia Muscle 12, 1440–1455 (2021). source
- Not checked yetcites [195] Alba, D. L. et al. Changes in lean mass, absolute and relative muscle strength, and physical performance after gastric bypass surgery. J. Clin. Endocrinol. Metab. 104, 711–720 (2019). source
- Not checked yetcites [196] Reinmann, A. et al. Bariatric surgery: consequences on functional capacities in patients with obesity. Front. Endocrinol. 12, 646283 (2021). source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Interestingly, myostatin can be modulated by diet221.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Medical therapies
What the sources say
- Not checked yetcites [221] Perry, C. A., Van Guilder, G. P. & Butterick, T. A. Decreased myostatin in response to a controlled DASH diet is associated with improved body composition and cardiometabolic biomarkers in older adults: results from a controlled-feeding diet intervention study. BMC Nutr. 8, 24 (2022). source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“In mice fed a high-fat diet, injection of umbilical cord MSCs led to improvements in physical function and mitigated obesity-related muscle atrophy225.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Medical therapies
What the sources say
- Not checked yetcites [225] Song, J. et al. Mesenchymal stromal cells ameliorate diabetes-induced muscle atrophy through exosomes by enhancing AMPK/ULK1-mediated autophagy. J. Cachexia Sarcopenia Muscle 14, 915–929 (2023). source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“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.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Medical therapies
What the sources say
- Not checked yetcites [220] Consitt, L. A. & Clark, B. C. The vicious cycle of myostatin signaling in sarcopenic obesity: myostatin role in skeletal muscle growth, insulin signaling and implications for clinical trials. J. Frailty Aging 7, 21–27 (2018).
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“While the study population included participants with BMI up to 32 kg/m2, there was no specific subanalysis for those with obesity.”
§ Sarcopenic obesity in older adults: a clinical overview > Management strategies > Medical therapies
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
Acute or chronic conditions magnify the impact of pathophysiological factors in older adults by increasing inflammation, limiting mobility, causing prolonged bed rest, altering medication pharmacokinetics and pharmacodynamics, and inducing nutrition impact symptoms.
“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.”
The paper relies on this without support.
Loss of muscle mass is closely associated with ageing and typically begins in middle age and accelerates in later years.
“The loss of muscle mass is closely associated with ageing and typically begins in middle age and accelerates in later years.”
The paper relies on this without support.
The shift in muscle composition toward adipose infiltration contributes to decreased muscle quality and impaired muscle function.
“This shift in composition contributes to decreased muscle ‘quality’ (that is, composition) and impaired muscle function.”
The paper relies on this without support.
Insulin resistance impairs protein anabolism, directly affecting muscle fibre atrophy and promoting muscle catabolism.
“Insulin resistance impairs protein anabolism, directly affecting muscle fibre atrophy and promoting muscle catabolism.”
The paper relies on this without support.
Mitochondrial dysfunction and myosteatosis may further contribute to insulin resistance, which in turn impacts glucose metabolism and muscle protein synthesis.
“Mitochondrial dysfunction and myosteatosis may further contribute to insulin resistance, which in turn, impacts glucose metabolism and muscle protein synthesis.”
The paper relies on this without support.
Insulin stimulates uptake of glucose and amino acids into muscle cells, promoting protein synthesis and muscle growth.
“Insulin stimulates the uptake of glucose and amino acids into muscle cells, promoting protein synthesis and muscle growth.”
The paper relies on this without support.
Hormonal alterations further contribute to reduced muscle mass and adipose tissue deposition.
“These hormonal alterations further contribute to reduced muscle mass and adipose tissue deposition.”
The paper relies on this without support.
Increased insulin signalling in response to NO might help maintain muscle mass and function.
“Increased insulin signalling in response to NO might help maintain muscle mass and function.”
The paper relies on this without support.
NO is a potent vasodilator that regulates blood flow.
“NO is also a potent vasodilator that regulates blood flow.”
The paper relies on this without support.
The interplay between NO and insulin in maintaining mitochondrial health may contribute to muscle preservation.
“The interplay between NO and insulin in maintaining mitochondrial health may contribute to muscle preservation.”
The paper relies on this without support.
Hypocaloric diets can promote muscle loss by downregulating muscle protein synthesis and increasing proteolysis.
“Hypocaloric diets can effectively reduce adipose tissue but may promote muscle loss by downregulating muscle protein synthesis and increasing proteolysis.”
The paper relies on this without support.
The long-term sustainability of very-low-calorie diets is questionable because many individuals regain weight after stopping the diet.
“Moreover, the sustainability of VLCDs is questionable, with many individuals regaining weight after transitioning off the diet.”
The paper relies on this without support.
Recommendations based on current body weight may not be feasible in individuals with obesity, especially during a low-calorie diet.
“Interestingly, recommendations based on current body weight may not be feasible in individuals with obesity, especially in the context of a low-calorie diet.”
The paper relies on this without support.
Bariatric surgery leads to marked adipose tissue loss and relative improvements in physical function but also profound muscle mass losses.
“Although bariatric surgery leads to marked adipose tissue loss with relative improvements in physical function, it also leads to profound muscle mass losses.”
The paper relies on this without support.
Myosteatosis and ectopic adipose tissue deposition are at the heart of a vicious pro-inflammatory cycle in the pathophysiology of sarcopenic obesity.
“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.”
The paper relies on this without support.
SARMs selectively target androgen receptors on muscle and bone tissues.
“Selective androgen receptor modulators (SARMs) selectively target androgen receptors on muscle and bone tissues.”
The paper relies on this without support.
Myostatin is a contributor to muscle–adipose tissue crosstalk.
“myostatin is a contributor to muscle–adipose tissue crosstalk.”
The paper relies on this without support.
Myostatin is a member of the TGFβ superfamily and inhibits skeletal muscle growth and development.
“Myostatin is a member of the TGFβ superfamily and inhibits skeletal muscle growth and development.”
The paper relies on this without support.
Individuals with sarcopenia have elevated levels of myostatin, which is also expressed in adipose tissue.
“Individuals with sarcopenia have elevated levels of myostatin, which is also expressed in adipose tissue.”
The paper relies on this without support.
The development and progression of sarcopenic obesity is influenced by an interplay of multiple factors including ageing, inflammation, and lifestyle.
“The development and progression of this complex syndrome is influenced by an interplay of multiple factors including ageing, inflammation, lifestyle, among others.”
The paper relies on this without support.
The clinical implications of sarcopenic obesity span from physical impairments to elevated morbidity and mortality rates.
“The clinical implications of sarcopenic obesity span from physical impairments to elevated morbidity and mortality rates.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Specifically, the current definition of SO may not include adults exhibiting early signs of risk factors for SO, potentially delaying therapeutic or preventive interventions [19, 20, 21, 22].”
From Sarcopenic Obesity Phenotype Index (SOP i ): A Population‐Based Study (2025) · cites this paper as [22]
Experimental — accuracy not yet measuredIn the citing paper
“Protein plays a central role in the preservation of LBM and a high protein diet that exceeds the recommended 0.8 g protein/kg bodyweight/day is the best option to mitigate the reduction in LBM, with patients encouraged to increase their protein intake to maintain and recover muscle mass and function over the long term [51,59,73,74].”
From Application of nutrition interventions with GLP-1 based therapies: A narrative review of the challenges and solutions (2025) · cites this paper as [59]
In the citing paper
“In addition to higher protein intake, addressing physical inactivity through regular exercise can further help to preserve muscle mass and functionality [49,54,59,74,78].”
From Application of nutrition interventions with GLP-1 based therapies: A narrative review of the challenges and solutions (2025) · cites this paper as [59]
Citations
Cites
Sarcopenia: revised European consensus on definition and diagnosis
Cruz-Jentoft, A. J., Bahat, G., Bauer, J., Boirie, Y., Bruyère, O., Cederholm, T., Cooper, C., Landi, F., Rolland, Y., Sayer, A. A., et al. (2019) · Age and Ageing · doi:10.1093/ageing/afy169 · Cited by 13,818 · cited 2×
“The progressive loss of muscle mass and function in sarcopenic obesity can also occur alongside changes in muscle composition 53 .”
The metabolic phenotype in obesity: Fat mass, body fat distribution, and adipose tissue function
Goossens, G. H. (2017) · Obesity Facts · doi:10.1159/000471488 · Cited by 8,481
Protective and Damaging Effects of Stress Mediators
McEwen, B. S. (1998) · New England Journal of Medicine · doi:10.1056/nejm199801153380307 · Cited by 6,733
Once-Weekly Semaglutide in Adults with Overweight or Obesity
Wilding, J. P. H., Batterham, R. L., Calanna, S., Davies, M., Van Gaal, L. F., Lingvay, I., McGowan, B. M., Rosenstock, J., Tran, M. T. D., Wadden, T. A., et al. (2021) · New England Journal of Medicine · doi:10.1056/nejmoa2032183 · Cited by 5,205
Gait speed and survival in older adults.
Studenski, S. (2011) · JAMA · doi:10.1001/jama.2010.1923 · Cited by 4,558 · cited 1×
“…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 .”
2013 AHA/ACC/TOS Guideline for the Management of Overweight and Obesity in Adults
Jensen, M. D., Ryan, D. H., Apovian, C. M., Ard, J. D., Comuzzie, A. G., Donato, K. A., Hu, F. B., Hubbard, V. S., Jakicic, J. M., Kushner, R. F., et al. (2014) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2013.11.004 · Cited by 4,058
Tirzepatide Once Weekly for the Treatment of Obesity
Jastreboff, A. M., Aronne, L. J., Ahmad, N. N., Wharton, S., Connery, L., Alves, B., Kiyosue, A., Zhang, S., Liu, B., Bunck, M. C., et al. (2022) · New England Journal of Medicine · doi:10.1056/nejmoa2206038 · Cited by 3,838 · cited 1×
“Existing data suggest that marked adipose tissue loss with semaglutide and tirzepatide occurs with concomitant muscle loss 202,204,205 .”
Physical Activity and Public Health in Older Adults
Nelson, M. E., Rejeski, W. J., Blair, S. N., Duncan, P. W., Judge, J. O., King, A. C., Macera, C. A., & Castaneda‐Sceppa, C. (2007) · Circulation · doi:10.1161/circulationaha.107.185650 · Cited by 3,057
Jensen, M. D., Ryan, D. H., Apovian, C. M., Ard, J. D., Comuzzie, A. G., Donato, K. A., Hu, F. B., Hubbard, V. S., Jakicic, J. M., Kushner, R. F., et al. (2014) · Circulation · doi:10.1161/01.cir.0000437739.71477.ee · Cited by 2,735
Kaiser, M., Bauer, J. M., Rämsch, C., Uter, W. J. C., Guigoz, Y., Cederholm, T., Thomas, D. R., Anthony, P. S., Charlton, K. E., Maggio, M. G., et al. (2009) · The journal of nutrition health & aging · doi:10.1007/s12603-009-0214-7 · Cited by 2,083
Cited by
Sorted by citations
Sayer, A. A., Cooper, R., Arai, H., Cawthon, P. M., Essomba, M.-J. N., Fielding, R. A., Grounds, M. D., Witham, M. D., & Cruz-Jentoft, A. J. (2024) · Nature Reviews Disease Primers · doi:10.1038/s41572-024-00550-w · Cited by 441
Look, M., Dunn, J. P., Kushner, R. F., Cao, D., Harris, C., Gibble, T. H., Stefanski, A., & Griffin, R. (2025) · Diabetes, Obesity and Metabolism · doi:10.1111/dom.16275 · Cited by 181
Sattar, N., Neeland, I. J., Dahlqvist Leinhard, O., Fernández Landó, L., Bray, R., Linge, J., & Rodriguez, A. (2025) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(25)00027-0 · Cited by 131
2025 ACC Scientific Statement on the Management of Obesity in Adults With Heart Failure
Kittleson, M. M., Benjamin, E. J., Blumer, V., Harrington, J., Januzzi, J. L., McMurray, J. J. V., & Vest, A. R. (2025) · JACC · doi:10.1016/j.jacc.2025.05.008 · Cited by 79
Updates in Cancer Cachexia: Clinical Management and Pharmacologic Interventions
Pandey, S., Bradley, L., & Fabbro, E. D. (2024) · Cancers · doi:10.3390/cancers16091696 · Cited by 42
Metadata
- Authors
- Prado, C. M., Batsis, J. A., Donini, L. M., Gonzalez, M. C., & Siervo, M.
- Affiliations
- University of Alberta (CA)
- University of North Carolina at Chapel Hill (US)
- Sapienza University of Rome (IT)
- Curtin University (AU)
- Corresponding author
- Prado, Carla M.
- Venue
- Nature Reviews Endocrinology
- Published
- 2024-02-06
- Volume
- 20
- Issue
- 5
- Pages
- 261-277
- ISSN
- 1759-5029 (ISSN-L)
- 1759-5037
- PMC
- PMC12854800
- OpenAlex
- W4391577587
- Cited by
- 355
- References
- 234
- Citations by year
- 2026: 178 · 2025: 146 · 2024: 31
- FWCI
- 20.17
- Type
- journal article
- Language
- en
- Open access
- Licence
- Locations
- Nature Reviews Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (acceptedVersion)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
- Funders
- National Institute on Aging (R01AG077163)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK056350)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nutrition and Health in Aging
- Health Sciences › Medicine › Physiology (medical) › Body Composition Measurement Techniques
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Keywords
- sarcopenic obesity, older adults, adipose tissue, geriatric syndromes, pathogenesis, inflammation, oxidative stress, hormonal changes, exercise therapy, nutritional therapy, pharmacotherapy, precision medicine, mortality, comorbidities
- MeSH terms
- Aged, Body Composition, Humans, Nutritional Status, Obesity, Exercise, Comorbidity, Sarcopenia
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