Case Study: Facebook-Instigated ‘Long COVID’ Research

These days, my primary goals for occasionally interacting with people on social media are to share information and compare notes. But usually, people don’t share any scientific studies with me at all, even when I specifically request it. I’ve stopped expecting constructive discourse, and try my best while it’s still allowed. I’ve documented this little interaction so avoid feeling like I’ve wasted my mind time and can share my bit of research.

This is in no way a systematic review of the available evidence. Instead, it highlights key thoughts from just my first four hours of really looking into this sub-topic of ‘long COVID’ — that I do not think is very relevant/important within the COVID-related debates. In an ideal world, I would have started with some actual debates among experts who express the dividing lines, and the strongest studies, and the strongest criticisms. Instead, the ‘skeptical’ experts I hear and read are ignored or censored by the mainstream Overton window.

And I assume that after I requested studies, this person just searched for something like “long haul covid studies” and shared a few of the links which appeared most authoritative. For the purposes of this post, I’ve changed the other private group user’s names to Group Members 1 through 3.

Group Member 1: yeah..the pandemic is so over..through I’ve just learned that a bunch of people in my town doing outdoor events like ‘normal’ just tested positive for I guess there’s that…Imagine that…

… half-dozen varied replies …

Group Member 1: Group Member 2 …99.7% Another point of misinformation since that rate varies depending on where you live, your age, your preconditions…not to mention try telling that to all the ‘long haulers’ damn dude that shit’s been a over a year out and you still have your facts all skewed…

Group Member 3: I’m having a hard time believing you’re serious about what you’re saying. It’s all a bunch of ignorance and childishness..and whining.

Me (Morgan Lesko): Have you seen any compelling studies regarding “long COVID,” Group Member 1?-) ❤

Group Member 1: Morgan Lesko ..uh yeah.. and you haven’t? I personally know people that are long haulers..’compelling studies’…L to the fucking O L.

Me: No, I haven’t. Personal anecdotes are a very different kind of evidence than peer-reviewed studies. Can you please share some sources with me?

Group Member 1: Morgan Lesko

Me (one hour later): Thanks so much for these, Group Member 1, I truly appreciate it!-) Here’s what I got out of them, in case it helps…

It appears the largest study based on 1,407 patients is still a pre-print posted March 5, 2021 (the MEDRXIV link about). Introduction: “… However, very little is known about the medium-and long-term consequences of COVID-19 among non-hospitalized individuals, although emerging data suggest a significant proportion of these subjects experience persistent symptoms associated with antecedent SARS-CoV-2 infection. Those with persistent symptoms have been labeled “long-haulers” or persons with long COVID-19. Recent estimates suggest that ∼10% of hospitalized patients go on to become long-haulers (3-5). However, the body of evidence regarding long-haulers, particularly among the 99% of non-hospitalized cases, is nascent. …”

The estimated ~10% of hospitalized patients becoming long-haulers cites a Medical News & Perspectives article, a Research Letter from July 2020 about Italy, and a BMJ Podcast — none of those appear to be peer-reviewed studies. If roughly 1-5% of infections are hospitalized (e.g. ), then 10% of that subset might not be enough to sell many of us on the new normal.

Patients were selected “with PCR-confirmed SARS-CoV-2 infection,” and “treated in the state of California.” I might have missed it, but there does not appear to be any control arm in this study, nor inclusion of others who did not experience novel lockdowns in addition to the novel virus. How many people in that state escaped the symptoms of anxiety and fatigue for much of the past year, and other health consequences caused indirectly by public health policies? (I’m not saying these things ‘invalidate’ the study, just that these are some of the reasons I don’t find it very actionable.)

The source next link within Davis article, “Sequelae in Adults at 6 Months After COVID-19 Infection” is a Research Letter from Feb 2021 discussing 177 participants. Its introduction cites a Viewpoint article, a Research Letter, a Letter To The Editor (analyzing 120 patients), and finally a peer-reviewed study from July 2020, “Characteristics of Adult Outpatients and Inpatients with COVID-19 — 11 Academic Medical Centers, United States, March–May 2020.” “During April 15–May 24, 2020, telephone interviews were conducted with a random sample of adults aged ≥18 years who had positive reverse transcription–polymerase chain reaction (RT-PCR) test results for SARS-CoV-2 in outpatient and inpatient settings at 11 U.S. academic medical centers in nine states.” This involved 350 interviewed patients — or an average of 39 per state.
The Davis article also includes Published Study, and a Mount Sinai pre-print involving 84 individuals. The published study involved 118 individuals enrolled in clinical trials at Stanford.
After reading these, this collection of articles helps confirm that there is not an overwhelming amount of peer-reviewed science on this sub-topic. If there were more data, for example, I would hope these scientists would have found and cited the stronger evidence on the latest pre-print. Surely there is not enough to dismiss or ridicule those who question these assumptions regarding a novel situation.

To help me understand your point of view… What did you find most compelling within these sources? ❤

Me (three more hour later): The Scientific American (SA) article has tons of citations, and it would have saved me a lot of time to focus in on the strongest studies cited, but I learned a lot!-p It cites an opinion blog on BMJ, a long video of a WHO forum quoting a “guesstimate,” a CDC guidance page, a BMJ Webinar, a JAMA Viewpoint, a Harvard Health blog post, a September review article generally on “Neurological Damage by Coronaviruses,” social media groups, and much more…

It cites a published paper from Jan 2021 titled “How and why patients made Long Covid,” discussing, “7. An unstable term — The aetiology of Long Covid is currently under scrutiny and may be multiple (Perego et al., 2020). Definitions of COVID-19 itself remain unstable: the pathology has been defined as a respiratory, cardiovascular, endothelial, or systemic condition (Lescure et al., 2020; Marini and Gattinoni, 2020). Whether COVID-19 will, for some, survive viral persistence and develop into a disease-specific, chronic or permanent condition, and/or whether SARS-COV-2 infection generates a new autoimmune disease remains unknown (Topol et al., 2020). Many patients, through use of Long Covid, wish to keep aetiological possibilities open while much remains unclear.”

The BMJ Webinar cites three references… BMJ News citing a Pre-Print from June 2020 with “2,700 selected subjects,” and a Cohort Study on cardiovascular consequences from July 2020 including 100 German patients, and a BMJ Podcast with countless footnotes — someone could try digging through for something strong that the March 2021 pre-print didn’t cite [if they’re really passionate about this sub-issue].

SA also cites a study accepted in 2016, “Methods: We conducted a mixed-methods pilot investigation of resilience among 43 survivors from two medical intensive care units (ICUs) within an academic health-care system. We interviewed survivors to identify barriers to and facilitators of recovery in the ICU, on the medical ward, and at home, using qualitative methods. … Measurements and Main Results: Resilience was low in 28% of survivors, normal in 63% of survivors, and high in 9% of survivors. Resilience was inversely correlated with self-reported executive dysfunction, symptoms of anxiety, depression, and post–traumatic stress disorder, difficulty with self-care, and pain (P < 0.05).” So as with many aspects of COVID, “Long Haulers” may not be as novel as advertised. This implies one of the control arms needed would be to track outpatients without COVID.

They cite an Oct 2020 study, “Follow-up of adults with noncritical COVID-19 two months after symptom onset,” which included “150 patients with noncritical COVID-19 confirmed by real-time reverse transcriptase PCR at Tours University Hospital from 17 March to 3 June 2020.” It cites the same Italian Research Letter from July mentioned in my previous reply.

It also cites a big King’s College review title “Long Covid: Reviewing the Science and Assessing the Risk” in October after “over 4 million people gave us their data.” This might be among the most compelling of the reviews I’ve read thus far on this sub-topic, though the most obvious problems with their data involve bias in voluntarily reporting. That would have similar data bias criticisms to those applied to VAERS reporting, though the COVID app is likely much more accessible and advertised. “While a range of studies have now been conducted on long Covid, many of these draw on only a small sample pool or rely on self-reporting. The King’s College London study appears to be the largest in scale and indicates around 10 per cent of those taking part in the survey had symptoms of long Covid for a month, with between 1.5 and 2 per cent still experiencing such symptoms after three months. These appear to be the most reliable statistics on which to base a rough estimate of the scale of long Covid on the population. While we do not have clear evidence about prevalence in asymptomatic cases, it is likely to be lower than these percentages.”

“… In order to gain a deeper understanding of the scale of long Covid, we recommend further studies are carried out. … Although the long-term impact of long Covid appears low (with 1.5 per cent suffering after three months), the shorter-term risks are higher. Given these symptoms have affected younger people and those otherwise fit, we recommend this issue be highlighted in government awareness campaigns. We believe doing so would help drive compliance with containment measures such as the use of masks.”

SA then cites a pre-print from October which also uses the King’s College data as a “prospective observational cohort study of COVID-19 symptoms in a subset of 4,182 users of the COVID Symptom Study app meeting inclusion criteria.”

It also cites an April 2020 review “focused on COVID‐19 cardiac manifestations not only by analyzing the preliminary available evidence about the virus, but also by making comparative considerations with SARS‐CoV, MERS‐CoV, and H1N1 influenza. It was observed, during these outbreaks, a significant association between underlying cardiovascular disease, myocardial injury, and worse outcomes. … Last but not least, influenza virus infection is well‐known to aggravate plenty of cardiovascular disorders, being associated with myocarditis, myocardial infarction, and HF exacerbation. … Multiple mechanisms have been proposed to explain influenza triggering arrhythmias, among them severe systemic, arterial, and myocardial inflammatory reaction seems to be one of the most plausible. Moreover, influenza is known to exacerbate congestive heart failure (CHF) and increase CHF‐related hospital admissions. … Conclusion: … Even though the prevalence of COVID‐19 arrhythmogenic effects has yet not been reported, close cardiovascular surveillance is advisable, particularly in patients with more severe presentation and in those with increased baseline risk due to previous cardiac co-morbidities. Since many medications are being used empirically to treat the infection and/or symptoms, there is a need to increase awareness to possible drug interactions and close monitoring in atrioventricular conduction and QT interval.”

The SA article cites a July 2020 pre-print study “involving 139 health care workers who developed coronavirus infection and recovered.” “Evidence before this study: Very little evidence exists describing long cardiac sequelae after SARS-CoV-2 infection. Although pericarditis and myocarditis are the two most frequent cardiac manifestations observed after a viral infection, as of May 13, 2020, the peer-reviewed literature was limited to isolated case reports of myocarditis and pericarditis during the COVID-19 hospitalization phase and to a retrospective observation in 26 recovered patients with COVID-19 pneumonia presenting cardiac complaints during hospitalization, revealing the presence of myocardial oedema in 14 (54%) patients and late gadolinium enhancement in 8 (31%) patients. These small size case series, limited to hospitalized RT-PCR patients with COVID-19 pneumonia, are insufficient to generalize conclusions about the true prevalence of pericardial and myocardial long involvement after SARS-CoV-2 infection. In addition, no study has investigated the immunological consequences of SARS-CoV-2 infection in the settings of pericarditis and myocarditis.”

It seems the most serious “long COVID” symptoms are not necessarily novel to our longstanding, seasonal experiences. I am not claiming that “long COVID” doesn’t exist, just that it is not novel enough — added on top of all of the other risk assessments of the virus — to justify this new normal. If anyone’s willing to build public policy based largely on scattered pre-print conclusions, then I can share plenty of studies that have evidence for many radically-non-‘consensus’ positions. As an engineer, I generally like to know how much uncertainty is in my data points. 😉

There appear to be zero published studies or pre-prints which use a control arm in their experiment — pretty important for science which I find most compelling. I would have been more optimistic about our knowledge base if I understood that some studies compared results against outpatients who did not test positive for COVID, or non-outpatients in a population who tested positive — or negative — for COVID.

So to me, claims that “The Science” is unquestionable on such points — or ridiculing and censoring ‘skeptics,’ or supporting novel laws to fine and imprison people for their public behavior, etc — sullies the good name and great value of the scientific method. It also contributes to the further destruction of the established institutions’ credibility.

Those studies would’ve been supported by far stronger evidence if this were not a fledgling area of scientific study. To me, it appears we’re just beginning to know how much we don’t know about “long COVID.” We seem early on in defining our questions, and countless years from actionable answers. Many of us require extraordinary evidence to relinquish extraordinary human rights — especially when it’s based on scientific rationale, where that should be possible. ❤

No reply yet a day later.

Sorry if I can be a pit bull on empirical evidence sometimes!-p Hopefully this little case study helps illuminate a few aspects of possible ways to explore the world. <3

Update: No reply yet 12 days later.