A new preprint confirms that generalized joint #hypermobility is a risk factor for #LongCOVID, while breaking new ground by examining risks of extreme hypermobility and whether hypermobility risk varies based on severity of initial COVID infection. 1/12 medrxiv.org/content/10.110…
Echoing prior research, this study found that, in a sample of 1,816, people w/ generalized joint hypermobility (GJH) were at higher risk of Long COVID. This comes from a regression that controlled for age, sex at birth, number of infections and number of vaccine doses. 2/12
One of the innovations of this research was to examine whether the severity of symptoms during the initial COVID infection affects the relationship between hypermobility and #LongCOVID. Answer: It does, at least in the sample studied. 3/12
Among those with mild or no symptoms during initial infection, GJH was a strong risk factor for #LongCOVID, but among those with severe initial symptoms, GJH was not a significant predictor of Long COVID. 4/12
At the same time, the study found that individuals with GJH were more likely to develop severe symptoms during the initial infection. This is one reason GJH leads to higher risk of #LongCOVID. The other is that GJH increases risk among those with mild/no initial symptoms. 5/12
The study also examines the extent to which people who were particularly hypermobility are as risk of #LongCOVID. Using 9 questions, the study identified as extremely hypermobile individuals in the top 10th percentile of hypermobility within their age and gender group. 6/12
While necessarily exploratory, this chart illustrates how the extent of hypermobility affects #LongCOVID risk. Regardless of whether they had no/mild or severe symptoms from initial infection, Long COVID spikes for people in the top 10th percentile of hypermobility. 7/12
In a discussion on pages 18-19, the article outlines several hypotheses that could help explain why hypermobility increases the risk of #LongCOVID. I will summarize these hypotheses in a subsequent thread. 8/12
The study is based on data collected in early 2024 from a sample of 1,816 respondents drawn from representative online panels in the US and UK, 352 (19.4%) who reported Long COVID and 1,464 (80.6%) who did not. 9/12
The study benefitted from a similar pilot study recruited from social media. Much thanks to everyone who completed that survey! While there were not enough non-Long-COVID respondents to analyze it separately, the pilot dataset will be included in a future metaanalysis. 10/12
Authors include @regina_anita_ @Rena_Rudy @LisaQuadt @BendyBrain and me. Deeply appreciate the ongoing collaboration! 11/12
Among other caveats: this is a preprint and has not yet been peer-reviewed; the study it limited in that it relies on a retrospective survey rather than prospective direct observation and measurement. 12/12
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Calling on #LongCOVID patients, advocates, and allies. Can you help us get the word out about this survey? The goal of the survey, which was developed in collaboration with individuals with LC, is to clarify the risk factors for LC in order to identify new treatment avenues.
We've made substantial progress in initial enrollment, but still need additional respondents, including both people with #LongCOVID and people who had #COVID >3 months ago but haven't developed Long COVID. No geographical limitations. Must be fluent in English and 18 or older.
If you have ideas for other dissemination vehicles, please let us know. Similarly, happy to answer any questions. My DM is open.
@fereshtehjahan1 Thx! It's interesting that the build-up of fluid seems to be causing brain fog. I wonder why. Is it because of toxins not being removed or more just related to the fluid build-up itself, either flooding cells and creating hypoxic conditions or maybe irritating glial cells or
@fereshtehjahan1 Putting pressure on the brain? I also wonder why fluid is building up now. She has been bed-bound for last 2+ years, and her brain fog has gotten a lot better and been mostly under control over last few months so it doesn't seem likely it's immobility.
@fereshtehjahan1 My daughter's hypothesis is that something went out in her back causing a localized increase in interstitial fluid, which then blocks the normal flow of the lymph. Seems plausible to me. We definitely see increased fluid whenever a joint goes out of place.
It's still early, but I wanted to share some initial indications of a significant breakthrough in the treatment of my daughter's #hEDS & #MECFS. I attribute progress to Calcium D-Glucarate, a supplement known for improving phase 2 detox of estrogen & other steroid hormones. 1/
The usual caveats: I am a patient caregiver, and not an MD or a medical researcher. It is early. This is just one patient. This is a very complicated area. I am sharing not so much to encourage people to try the supplement but rather to encourage more research in this area. 2/
By far, the most important events in the lifecourse of my daughter's #MECFS were two massive relapse events that severely degraded her baseline level of functioning. Hoping to crowdsource ideas from #Medtwitter and #NEISVoid on this phenomenon and how to study it effectively. 1/
A better understanding of exactly what happens during these events would help us make faster progress in understanding #MECFS and perhaps #LongCOVID. Yet this phenomenon remains dramatically understudied. We need to change this! 2/
The field lacks clear and uniform terminology for describing these events, which is one of many obstacles to studying them. For now I have settled on the term "massive relapse event" for these reasons: 3/
Assume for a moment that an impaired lymphatic system contributes to #MECFS and #LongCOVID, what would we expect to see? And how could we evaluate the merits of this hypothesis? Hoping to refine these ideas through the wisdom of #MedTwitter and #NEISvoid 1/
To be clear, I am not proposing that an impaired lymphatic system is the single or ultimate cause of ME/CFS and LongCOVID. Rather, my hypothesis is that it contributes to the overall syndromes along with endothelial dysfunction, inflammation and other well-recognized factors 2/
Let's start with the brain. Research shows that an impaired glymphatic system can contribute to intracranial hypertension, so that is one possible sign along with its consequences. 3/ academic.oup.com/braincomms/art…
A question for people with #MECFS or #LongCOVID: in your experience, is post-exertional malaise a single phenomenon? Or is it possible there are distinct phenomena that are not being adequately distinguished, impeding understanding? #NEISvoid
With my daughter -- who has #hEDS, #MECFS, #POTS, etc. -- we have observed at least 2 and possibly 3 separate phenomena that all seem to fit the description of #PEM. Let's call them (a) "major crash," (b) "day to day PEM" and (3) "cumulative exertion PEM"
She has had 2 major crashes. These were biphasic events that appear to have caused severe damage lasting years. First major crash (2017) was what made us aware of her illness. She felt very hot in the morning. Then, some time after a long hike, she had whole-body chills/shaking.