Polli, Andrea, Godderis, Lode, Martens, Dries S et al. · BMC medicine · 2025 · DOI
This study followed 358 people who had COVID-19 to understand why some develop Long-COVID with symptoms like extreme fatigue, sleep problems, and post-exertional malaise (feeling much worse after activity). Researchers measured biological markers in blood and found that two factors—elevated troponin T (a heart protein) and shortened telomeres (the protective caps on DNA)—were most strongly linked to Long-COVID, particularly the fatigue cluster. The study shows that Long-COVID is not a single illness but has different symptom patterns, suggesting different underlying causes may be at play.
This study is important because it identifies potential biological mechanisms underlying Long-COVID and PEM, two conditions closely related to ME/CFS. By linking cardiac markers and cellular aging (telomere shortening) to persistent symptom clusters, it provides biological support for why some patients develop debilitating fatigue and post-exertional symptoms, potentially guiding future diagnostic and therapeutic approaches.
This study cannot prove that troponin T elevation or telomere shortening *cause* Long-COVID or PEM; they are merely associated markers. The predominantly hospitalized sample limits generalizability to mild Long-COVID cases, and the cross-sectional molecular measurements prevent determining whether these biological changes precede, accompany, or result from Long-COVID symptoms. Association does not establish causation or identify the underlying disease mechanisms.
About the PEM badge: “PEM required” means post-exertional malaise was an explicit required diagnostic criterion for participant inclusion in this study — not that PEM was studied, observed, or discussed. Studies using criteria that do not require PEM (e.g. Fukuda, Oxford) are tagged “PEM not required”. How the atlas works →
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