Introducing Long COVID Essentials, a new resource series - The Sick Times

We are excited to announce Long COVID Essentials, a new collaboration between The Sick Times and Long COVID Justice. Over the next several months, we’ll be publishing over 30 resource sheets that provide foundational information about navigating Long COVID. Each sheet can be printed and/or shared as digital PDFs.

Long-Term Adverse Effects of Mild COVID-19 Disease on Arterial Stiffness, and Systemic and Central Hemodynamics: A Pre-Post Study

COVID-19-associated vascular disease complications are primarily associated with endothelial dysfunction; however, the consequences of disease on vascular structure and function, particularly in the long term (>7 weeks post-infection), remain unexplored. Individual pre- and post-infection changes in arterial stiffness as well as central and systemic hemodynamic parameters were measured in patients diagnosed with mild COVID-19. As part of in-laboratory observational studies, baseline measurements were taken up to two years before, whereas the post-infection measurements were made 2–3 months after the onset of COVID-19. We used the same measurement protocol throughout the study as well as linear and mixed-effects regression models to analyze the data. Patients (N = 32) were predominantly healthy and young (mean age ± SD: 36.6 ± 12.6). We found that various parameters of arterial stiffness and central hemodynamics—cfPWV, AIx@HR75, and cDBP as well as DBP and MAP—responded to a mild COVID-19 disease. The magnitude of these responses was dependent on the time since the onset of COVID-19 as well as age (pregression_models ≤ 0.013). In fact, mixed-effects models predicted a clinically significant progression of vascular impairment within the period of 2–3 months following infection (change in cfPWV by +1.4 m/s, +15% in AIx@HR75, approximately +8 mmHg in DBP, cDBP, and MAP). The results point toward the existence of a widespread and long-lasting pathological process in the vasculature following mild COVID-19 disease, with heterogeneous individual responses, some of which may be triggered by an autoimmune response to COVID-19.

Maintained imbalance of triglycerides, apolipoproteins, energy metabolites and cytokines in long-term COVID-19 syndrome patients

BackgroundDeep metabolomic, proteomic and immunologic phenotyping of patients suffering from an infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have matched a wide diversity of clinical symptoms with potential biomarkers for coronavirus disease 2019 (COVID-19). Several studies have described the role of small as well as complex molecules such as metabolites, cytokines, chemokines and lipoproteins during infection and in recovered patients. In fact, after an acute SARS-CoV-2 viral infection almost 10-20% of patients experience persistent symptoms post 12 weeks of recovery defined as long-term COVID-19 syndrome (LTCS) or long post-acute COVID-19 syndrome (PACS). Emerging evidence revealed that a dysregulated immune system and persisting inflammation could be one of the key drivers of LTCS. However, how these biomolecules altogether govern pathophysiology is largely underexplored. Thus, a clear understanding of how these parameters within an integrated fashion could predict the disease course would help to stratify LTCS patients from acute COVID-19 or recovered patients. This could even allow to elucidation of a potential mechanistic role of these biomolecules during the disease course.MethodsThis study comprised subjects with acute COVID-19 (n=7; longitudinal), LTCS (n=33), Recov (n=12), and no history of positive testing (n=73). 1H-NMR-based metabolomics with IVDr standard operating procedures verified and phenotyped all blood samples by quantify...

The biopsychosocial model: Its use and abuse - Medicine, Health Care and Philosophy

The biopsychosocial model (BPSM) is increasingly influential in medical research and practice. Several philosophers and scholars of health have criticized the BPSM for lacking meaningful scientific content. This article extends those critiques by showing how the BPSM’s epistemic weaknesses have led to certain problems in medical discourse. Despite its lack of content, many researchers have mistaken the BPSM for a scientific model with explanatory power. This misapprehension has placed researchers in an implicit bind. There is an expectation that applications of the BPSM will deliver insights about disease; yet the model offers no tools for producing valid (or probabilistically true) knowledge claims. I argue that many researchers have, unwittingly, responded to this predicament by developing certain patterns of specious argumentation I call “wayward BPSM discourse.” The arguments of wayward discourse share a common form: They appear to deliver insights about disease gleaned through applications of the BPSM; on closer inspection, however, we find that the putative conclusions presented are actually assertions resting on question-begging arguments, appeals to authority, and conceptual errors. Through several case studies of BPSM articles and literatures, this article describes wayward discourse and its effects. Wayward discourse has introduced into medicine forms of conceptual instability that threaten to undermine various lines of research. It has also created a potentially potent vector of medicalization. Fixing these problems will likely require reimposing conceptual rigor on BPSM discourse.

Trial By Error: Correctives from Putrino & Iwasaki (and Others) to the Long-Covid-Is-Psychosomatic Claims