An October 18th post from Putrino Lab on “X” (Twitter) caught my eye. I am sure not all of my readers will see it, so I wanted to share what was said.
While this mainly discusses Long COVID, the premise behind the information will very likely apply to people with myalgic encephalomyelitis. I base that on having followed the researchers involved and their previous recognition of the ME International Consensus Criteria (ME-ICC) and recognition of the importance of stratifying patients.
Because I have recently seen a lot of attention being paid to the news about serotonin findings in Long COVID and how that may or may not apply to people with ME, I want to highlight the comment made about serotonin. From the thread:
“I DID mention that the serotonin findings were interesting because it explains why *some* folks with #LongCOVID experience benefit from low dose SSRIs. I know that not ALL people experience benefit, and in fact some people experience worsening symptoms, but we must not ignore those who experience benefit just because it doesn't fit everyone's narrative. “
There is a long history of medications causing terrible reactions in people with ME. I appreciate the words of caution while also recognizing the importance of seeking help for subsets who may respond.
I am grateful for the permission to repost this information here.
Note: This is copy and pasted directly from the multiple posts on X. Due to the restrictions on X, some words and sentences are abbreviated to save space.
“As we continue to learn more each day about #LongCOVID and other infection-associated complex chronic illnesses like chronic #Lyme and #MECFS, I want to once again transparently share our team's approach, thought process and philosophy for interpreting science and translating it into common clinical practice.
We are approaching our new center through the lens of establishing novel ways of treating chronic, persisting pathogens and the damage that they cause. This is why our scientific strategy is being led by the incredible @microbeminded2 [Amy Proal], because IMO there is no one better in the world who has been consistently and relentlessly leading and facilitating great research in this space.
Part of understanding how to detect AND treat persistent pathogens in the body is to understand how they affect physiology.
Why is this important?
Because often we cannot reliably test for evidence of the persisting pathogen itself. Not everyone with #LongCOVID has easily measurable evidence of persistent virus in their gut, only around 30% have circulating spike proteins in their blood, many tissues that may harbor persistent SARS-CoV-2 can only reasonably be accessed post-mortem, so what I'm saying is that at this time testing for persistent virus, though we still try, is shaky.
There is technology on the horizon being developed for radioligands that bind to spike and can be used in conjunction with PET scanning to search the whole body for viral persistence. I think that this is a very promising direction, but I'm also mindful of the fact that PET scans carry with them a non-zero chance of causing malignancy (~0.16%) - which sounds small until 60M ppl get tested...either way, we are all in when it comes to new techniques for identifying persistent pathogens, but also IN PARALLEL (not in isolation) we see the value in understanding the effect on physiology of these pathogens.
Hence our excitement about our own recent study in people with #LongCOVID that we completed with the wonderful @VirusesImmunity [Prof. Akiko Iwasaki] and other work like that completed by @MaayanLevy_Lab [Maayan Levy] and co-authors this week.
These studies highlight biological differences between people with LC and health controls. We strongly acknowledge that due to the complexity of infection-associated chronic illness not all people with #LongCOVID will show these differences.
When media reports on work like this they often want to overstate the importance of the work so that it fits into a nice press-release, but the source materials will ALWAYS present a more nuanced interpretation.
You will not see serious authors of this sort of work saying "we've done it: this is THE biomarker", because that it NOT what our research shows. We also won't say that cortisol is a TREATMENT for #LongCOVID or even an appropriate treatment for the low cortisol that we saw in the MY-LC cohort we published in @Nature earlier this month.
Similarly, my team IS NOT is saying that based on the results of this weeks @CellCellPress paper that all folks with #LongCOVID should take prozac.
I DID mention that the serotonin findings were interesting because it explains why *some* folks with #LongCOVID experience benefit from low dose SSRIs. I know that not ALL people experience benefit, and in fact some people experience worsening symptoms, but we must not ignore those who experience benefit just because it doesn't fit everyone's narrative.
Similarly it is important to highlight physiological reasons WHY these people may be experiencing benefit because for too long this benefit has been framed as treating depression and contributes to ongoing gaslighting. The same can be said of folks with #LongCOVID, #MECFS and #Lyme who respond to low-dose ativan because it is a mast cell stabilizer NOT because it is treating anxiety.
Mechanisms matter, and fitting these pieces of the puzzle are crucial for making sure less people are being minimized and gaslit as they attempt different treatments. Our team is highly focused on understanding the underlying pathophysiology of #LongCOVID and other infection-associated complex chronic illness.
We have multiple clinical trials in the works that focus on symptom management (such as use of enzymes, antihistamines and nerve stimulation) and addressing persistent pathogens (various antiviral therapies). We believe both to be important because while cures are the goal, people need treatments that can move the needle NOW, and we also must acknowledge that persistent pathogens cause damage that may need to be fixed even if the persistent pathogen is eventually eliminated.
That is why understanding how people with #LongCOVID, #Lyme and #MECFS biologically differ from healthy controls is a research priority for us.
Once again - this is *our* approach and thought process as we tackle these challenging issues. We are aware that there are other approaches exist and have validity, so we are respectful of differing opinions (and ask for the same grace!).
One thing you can count on is that we won't stop looking for new, better and actionable solutions for people living with infection-associated complex chronic illnesses.”
Here is the link to the Nature article dated Sept 25, 2023: Distinguishing features of long COVID identified through immune profiling
I wrote about the new Long COVID center in a previous article: Putrino Lab to Open a Center in 2024.
Closing thoughts
I know we are going to have answers about myalgic encephalomyelitis someday… how fast we get there depends on how effectively the researchers use the tools at their disposal… and, of course, funding.
My post response to that thread:
“For decades it felt like Myalgic Encephalomyelitis researchers were searching for answers in the front yard because it was easier than going into the basement where the chaos is happening. This feels like researchers are finally shining a light into the basement.”
Colleen
See Putrino Lab HERE.
See Amy Proal (Polybio) HERE (donate to Polybio HERE)
See Prof. Akiko Iwasaki HERE
See Levy Lab HERE
FYI - The label ME/CFS has varied meanings including:
ME and CFS - two separate conditions
ME/CFS as defined by the Canadian Consensus Criteria (precursor to the International Consensus Criteria (ICC)
ME/CFS as defined by the IOM report (what is on CDC website)
ME/CFS as per the NICE guidelines (UK)
While ME/CFS as used here is not clarified, I am hopeful the approach being taken by Putrino Lab and colleagues recognizes the importance of stratifying the different patient groups.
Information provided here or in comments is not to be considered medical advice