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Sarcopenia and malnutrition are increasingly recognized as major determinants of morbidity and functional decline in aging and chronically ill populations. Thyroid hormones (THs), particularly triiodothyronine (T3), play a critical role in regulating skeletal muscle homeostasis, influencing myogenesis, mitochondrial function, metabolic rate, and fibre-type specification. Alterations in thyroid function, both hypo- and hyperthyroidism, negatively impact muscle protein turnover, leading to impaired strength and muscle wasting. Notably, nutritional status modulates TH metabolism at multiple levels: malnutrition impairs deiodinase activity, alters TH transport, and reduces peripheral T3 availability, thereby contributing to the low T3 syndrome frequently observed in frail or undernourished individuals. Conversely, excessive T3 levels, as seen in hyperthyroid states or during inappropriate replacement therapy, exacerbate catabolism and accelerate muscle loss. This review synthesizes current evidence on the bidirectional interactions among thyroid dysfunction, nutritional deficiencies, and sarcopenia, proposing an integrative pathophysiological model. We discuss the clinical implications of TH replacement in sarcopenic and malnourished patients, highlighting the need for personalised, multimodal interventions that include hormonal, nutritional, and physical strategies to prevent or mitigate muscle deterioration in endocrine and geriatric contexts.
Nappi et al. (Sat,) studied this question.