“Millions of people continue to suffer from exhaustion, cognitive problems and other long-lasting symptoms after a coronavirus infection. The exact causes of the illness, known as long Covid, are not known. But new research offers clues, describing the toll the illness takes on the body and why it can be so debilitating.” Josh Keller
The New York Times recently published a superb and beautifully illustrated article, “How Long COVID Exhausts the Body“, by Josh Keller that it featured prominently on its website. Keller, who obviously did his homework, noted a possible chronic fatigue syndrome (ME/CFS) connection several times in the article. The full connection between the two was not explored.
Maybe it should be. Some groups, after all, don’t seem to believe these diseases have much in common. After the National Institutes of Health (NIH), for instance, received over a billion dollars to investigate and find treatments for long COVID, it has continued to dismiss and, in some cases, even cut ME/CFS funding. Its refusal to allow even a small number of people with ME/CFS to participate in its massive long-COVID studies, its decision to delay research center funding for 7 months, and then continue them at their paltry levels, it’s early termination of perhaps the most important study in the ME/CFS field’s history, and its removal of a mention of ME/CFS from its long-COVID website suggests that, if anything, the NIH may be moving backward on ME/CFS.
A major article by one of the biggest media outlets in the world on long COVID provides an opportunity to clarify where ME/CFS stands in relation to long COVID. (Thanks to Lisa White for the suggestion.)
How Long COVID and ME/CFS Exhaust the Body
“Researchers have also found evidence that Covid may trigger a lasting and damaging autoimmune response. Studies have found surprisingly high levels of autoantibodies, which mistakenly attack a patient’s own tissues, many months after an initial infection.” KellerStill, Autoimmunity provides a tantalizing way to explain the remarkable diversity of symptoms, the gender imbalance, and the infectious trigger found in ME/CFS.
The autoantibody explorations in long COVID already surpass those in ME/CFS in their size and complexity and suggest that a broad range of autoantibodies are unleashed by the coronavirus infection. Several ME/CFS studies have found evidence of increased levels of autoantibodies to receptors (beta-adrenergic (AdR), muscarinic acetylcholine receptors (M-AChR)) which, among other things, affect sympathetic nervous system functioning and the blood vessels. Small studies suggest that targeted therapies that remove those autoantibodies may be helpful as well and at least one is under investigation in long COVID.
Some researchers have proposed that the combination of autoimmune tendencies, dysautonomia, and small fiber neuropathy in ME/CFS, POTS, and some other diseases calls for a new disease designation called “autoimmune neurosensory dysautonomia“. (As we’ll see that combination is also found in long COVID). Several hypotheses as well as exercise studies suggest that autoimmunity plays a major role in ME/CFS
Exercise Tests Suggest Autoimmunity Causes the Exertion Problems in Chronic Fatigue Syndrome, Fibromyalgia and POTS
The Virus That Never Left?
“One possibility is that the body is still fighting remnants of the coronavirus. Researchers found that the virus spreads widely during an initial infection, and that viral genetic material can remain embedded in tissues — in the intestines, lymph nodes and elsewhere — for many months.” Keller
As ME/CFS, or a very similar state to it, has been shown to be triggered by many pathogens (Epstein-Barr virus, HHV-6, Coxsackie, Giardia, etc.) the idea that a virus, in some form, is still, even after it’s mostly been fought off, continuing to tweak the immune system has triggered some of the most creative explorations in ME/CFS.
Enterovirus – Several early studies found evidence of enteroviral RNA remaining in the muscles of some people with ME/CFS. Since 2005, Dr. John Chia has presented evidence of a “smoldering” enterovirus infection in ME/CFS including increased antibody levels, the presence of enteroviral RNA in the plasma and in stomach biopsies, usually following what Chia called “a severe flulike illness” of unknown origin. Chia believes that enteroviral RNA in the muscles may be responsible for the exertion problems in ME/CFS.
Epstein-Barr Virus – With studies now proclaiming that EBV is the cause of multiple sclerosis, EBV is getting more attention than ever. EBV was the first virus associated with ME/CFS and is still being studied almost 40 years later. In a long-running NIH grant, for instance, Ohio State researchers have found evidence that a strange, smoldering EBV infection that is unable to fully replicate itself, is nevertheless pumping proteins out that the immune system is reacting to in ME/CFS. A recent Norwegian study that found evidence of a continuing inflammatory response 6 months after an EBV infection suggested that the virus had triggered a long-running immune response in ME/CFS.
HHV-6 – In perhaps the most creative pathogenic hypothesis yet, Prusty and Naviaux propose that an HHV-6/7 reactivation may be triggering a cell danger response that ends up fragmenting the mitochondria and impairing energy production in ME/CFS.
“Many long Covid patients struggle with physical activity long after their initial infection, and experience a relapse of symptoms if they exercise. Initial studies suggest that dysfunction in the circulatory system might impair the flow of oxygen to muscles and other tissues, limiting aerobic capacity and causing severe fatigue.
In one study, patients with long-lasting Covid symptoms had unexpected responses to riding a bike. Despite having apparently normal hearts and lungs, their muscles were only able to extract a portion of the normal amount of oxygen from small blood vessels as they pedaled, markedly reducing their exercise capacity.
One possible culprit: Chronic inflammation may damage nerve fibers that help control circulation, a condition called small fiber neuropathy. The damaged fibers, seen in skin biopsies, are associated with dysautonomia, a malfunction of automatic functions like heart rate, breathing and digestion that is very common in long Covid patients.” Keller
While autoimmunity and viral persistence/reactivation are possibilities in ME/CFS, they remain just that – possibilities. The evidence that some sort of circulatory problem exists in ME/CFS, on the other hand, is quite strong. The first evidence showed up over 20 years ago when McCully/Natelson found reduced oxygen flows to the muscles. Problems with the microcirculation and endothelial cell functioning – two major concerns in both long COVID and ME/CFS/FM – subsequently appeared in three ME Research UK funding studies/papers in 2000, 2003, and 2005.
Blood flows to the muscles and the brain have seen the most study.
Blood Flows to the Brain
“Another research group found that long Covid may significantly reduce the amount of blood that reaches the brain, a finding that has was also seen in patients with a related chronic condition, ME/CFS, before the pandemic.” Keller
The evidence for reduced blood flows to the brain first surfaced in 1996 and has waxed and waned over the years. The brain blood flow question was largely resolved when Visser/Van Campen/Rowe, using a newer, more accurate technique, found reduced brain blood flows in virtually everyone with ME/CFS, including people who did not meet the criteria for orthostatic intolerance.
Further studies indicated that after tilt table testing, blood flows to the brain take much longer to return to normal in ME/CFS, that blood volume – a crucial aspect of circulatory function – is low, that in severe ME/CFS even sitting or mild “tilting” can result in significantly reduced brain blood flows, and that tilt-table testing produces similar effects in long-COVID patients.
Medow’s eye-opening 2014 study demonstrated the dramatic impact reduced oxygen flows to the brain may be having in ME/CFS. When Medow used phenylephrine in ME/CFS patients with orthostatic intolerance to increase blood flows to their brains, their cognitive issues and symptoms completely disappeared during the dreaded tilt table test.
“Many long Covid patients struggle with physical activity long after their initial infection, and experience a relapse of symptoms if they exercise. Initial studies suggest that dysfunction in the circulatory system might impair the flow of oxygen to muscles and other tissues, limiting aerobic capacity and causing severe fatigue.” Keller
Exercise studies have been amongst the most illuminating in what is probably the most exertion intolerant disease on the planet. (The symptom post-exertional malaise – which is now being used in long COVID studies – grew out of the ME/CFS field and experts proposed that ME/CFS be called Systemic Exertion Intolerant Disease (SEID).
Many studies have demonstrated problems with aerobic capacity in ME/CFS. Workwell’s novel 2-day exercise studies, which have become well-validated over time, demonstrate a feature that, until a recent long COVID study found it – had been documented only in ME/CFS: that exercise one day damages one’s ability to produce energy the next day.
David Systrom’s invasive exercise work suggests that two types of circulatory problems crop up in ME/CFS during exercise: a shunt appears to be preventing sufficient oxygen delivery to the muscles and leaky veins are preventing sufficient blood flows to the heart (and ultimately the heart). Vermeulen and others have also found evidence of reduced oxygen delivery to the muscles during exercise in ME/CFS.
Systrom’s and Mancini’s invasive and two-day exercise studies, respectively, may have – because they directly address the exertion issues in long COVID – produced the most significant findings to date. Both have found similar exercise issues in long-COVID patients and ME/CFS.
IACFS/ME Conference 2021 Pt. III – the Exercise Studies: Long COVID Moves Closer to ME/CFS, Metabolomic Weirdness, Two Symptoms to Rule Them All?
Finally, both ME/CFS and long-COVID studies suggest damaged or poorly functioning endothelial cells may be impairing blood flows as well.
“South African researchers found another circulation problem: Microscopic blood clots. Tiny clots that form during an initial Covid infection will typically break down naturally, but might persist in long Covid patients. These clots could block the tiny capillaries that carry oxygen to tissues throughout the body.” Keller
There’s no direct evidence that I know of, of microclots in FM or ME/CFS, but a few small studies found evidence of hypercoagulation in ME/CFS/FM and Gulf War Illness about 20 years ago.
Small Fiber Neuropathy (SFN) and Dysautonomia
“Chronic inflammation may damage nerve fibers that help control circulation, a condition called small fiber neuropathy. The damaged fibers, seen in skin biopsies, are associated with dysautonomia, a malfunction of automatic functions like heart rate, breathing, and digestion that is very common in long Covid patients.” Keller
Just one small study provides evidence of small fiber neuropathy in long COVID, but many studies indicate it’s present in ME/CFS/FM. Keller, interestingly, embraces Systrom’s and others’ hypothesis that the SFN found in the skin is the most obvious but least troubling manifestation of an issue that has body-wide consequences and which includes the diversion of blood away from the muscles.
Dysautonomia, of course, is a common theme in ME/CFS, fibromyalgia, and postural orthostatic tachycardia syndrome (POTS) and appears to be present in long COVID as well. Lower heart rate variability ratings that are indicative of sympathetic nervous system dominance, are found in ME/CFS, FM, POTS, and long COVID. A simple standing test that stresses the autonomic nervous system has been proposed as a diagnostic test by ME/CFS practitioners, and reduced heart rate variability measures were predictive of poor sleep.
An Inflamed Brain?
“Although it is unclear how often the virus directly penetrates the brain, even mild infections appear to cause significant brain inflammation, according to the researchers, who included Dr. Nath, Dr. Iwasaki and Dr. Michelle Monje, a neurologist at Stanford. Infections may trigger the over-activation of immune cells called microglia in a way that appears similar to the process that can contribute to cognitive problems in aging and some neurodegenerative diseases.” Keller
The degree to which neuroinflammation plays in ME/CFS is unclear, but several small studies have found evidence of widespread neuroinflammation. The high cost of brain imaging studies and the low support given ME/CFS means the neuroinflammation findings – suspected to be amongst the most potentially important in the field – have come slowly indeed with just three small studies published over the past 8 years. Studies that have displayed a similar brain signature in ME/CFS’s sister diseases – fibromyalgia and Gulf War Illness – cry out for more neuroinflammation studies . Those studies will, thankfully, surely come in long COVID.
Fibromyalgia, Chronic Fatigue Syndrome, Gulf War Illness – the Widespread Neuroinflammation Diseases
“Millions of people continue to suffer from exhaustion, cognitive problems, and other long-lasting symptoms after an infection. The exact causes of these illnesses, known as long COVID and chronic fatigue syndrome (ME/CFS), are not known. But new research offers clues, describing the toll the illness takes on the body and why it can be so debilitating.” Takeoff on Keller
The overlaps are remarkable but maybe even more remarkable is how quickly the same themes have emerged in long COVID and ME/CFS. That isn’t because long-COVID researchers are piggybacking on ME/CFS/FM research. Only a few have had anything to do with ME/CFS. Rather they’re assessing long-COVID patients based on what they see before them; i.e. Long COVID itself is pushing the research in the same direction it’s taken in ME/CFS. In almost every case, the findings Keller laid out in long COVID match up closely with those seen in ME/CFS.
We’re still very early in the game but the results are promising for both people with long COVID and people with ME/CFS. People with long COVID will benefit from the long years of study into ME/CFS, and people with ME/CFS will benefit from the enormous funding being poured into long COVID.
They also bring up an interesting question: if long COVID is worth $1.15 billion in research funding, how much is ME/CFS, which affects up to 2 million people in the U.S. and currently gets $15 million/year, worth?
Thank you, Cort!
Why does the NIH still hate us who have ME/CFS?
For me it seems like NIH does intentionally not want to find a cure. Maybe because it’s a man made disease.
Agreed. Avoiding lawsuits for miles.
I don’t know what’s going on with the NIH. I don’t think it hates us. I think it just doesn’t care enough to change its ways. I think it’s built (inadvertently) to deter new and different diseases from getting support. The big diseases hold sway and they’re not going to let us in. The NIH has been given the horrific statistics for decades and it’s meant nothing. Even their touted reinvigoration of ME/CFS simply returned funding levels to about where they were before – and they were bad before. It’s the most frustrating thing.
I would think that the NIH would have a commitment or a call to improve the health of all Americans no matter what their ailment but that’s clearly not true. I’m still, decades after recognizing that fact, still trying to come to terms with it.
Ultimately, we should be clear that NIH is devoid of morality or ethical underpinnings – there is simply nothing in it that assesses whether a disease is being neglected. The fact that human beings do have moral and ethical sensibilities suggests that the neglect of ME/CFS/FM must nag at some people who work there.
One would hope.
Well said, Cort.
The ME/CFS community needs to get real with government agencies. I’ve been sick for 15 years and it didn’t take long for me to realize that these agencies are not on our side. We are a cash cow to pharmaceutical companies. Our “health care” has nothing to do with health. It is only medical care, or in other words, drug care. No study will be funded until there is a drug that is discovered that could work for us. No org. is going to invest unless they’ll get a high rate of return on their money. It’s a trap because it would be a lot easier to find a drug if we had funding.
The ME/CFS community needs to try to push (or beg) for private donations from wealthy people. Many docs who specialize in this disease have been affected by it somehow. There must be a way to contact, educate, and explain our needs to people like Avril Lavigne who has struggled with Lyme. Also, Cher (not totally confident about this) struggled with Epstein Barr. There must be more people in the world of the “Elite” who would donate. I also think that if professional sports teams and athletes were educated about what happens to us – that the more we move, the sicker we get, and many of us were once athletic, that their ears might be wide open. This hits the hearts and souls of people who know how physical activity brings life and joy into our souls. They might have significant compassion. People out there must have a way to contact people like Mark Cuban (owner of Basketball team), or John Elway or Brett Favre. What about national athletic associations?
Physicians with impressive credentials WILL be able to get to athletes somehow. They DO have ways to present the disease, the devastation, the research, and the desperation for donations. Football players know about traumatic brain injury and how it leads to suicide and have lost friends. ME/CFS also leads to suicide, so again, a reason they might listen. Some of us go from being extremely physically conditioned to having to take breaks when we just blow dry our hair. This type of info will hit the hearts of athletes as they will be floored that this disease could happen to anyone. Anyone know Michael Phelps? He’ll have compassion for the severe depression. Mention that on top of the depression, we have no way to participate in the activities we loved
No way to release stress. No way to feed our spirits. He’s a great example of a possible donator.
The ME/CFS community is wasting precious time with these gov’t agencies. Every year, every month, I miss opportunities, I fall behind, I miss important parts of my son’s upbringing, I lost my job, lost my identity… Every day is another day too many. I believe that a Harvard Neurologist (or whatever) could use their “status” to gain access to wealthy people who have hearts and who are willing to give.
Let’s take a new path.
Most doctors don’t even believe that Dysautonomia, PEM, brain fog, small-fiber neuropathy, etc exist. They won’t say anything about my abnormal white-matter loss or cerebral atrophy; seizures, migraines etc. You all have probably found the same.
But it will be interesting to see what happens when that $1.1 billion in research really digs into all these issues. When (new and abundant) hard evidence is presented; causes are explored and hopefully found. Tests developed, eventually treatments.
Will the medical community accept those results? And then accept the existence of post-infectious syndromes other than long Covid?
I hope that we’ll at least have access to the tests that will be developed. We shall see.
Thank You Cort! I really hope they figure out the details of why we get such bad symptoms the next day after exercise, that don’t let up for a week. My exercise threshold dropped this year. I’m not bed bound but I only get to be upright doing things for 15 minutes, every 1 1/2 hours. I can’t go anywhere, trapped in my house. I had a bad enough relapse after doing too much in a day, that my upright time got cut by a third and hasn’t gotten better in four months. I’m getting more scared and depressed. If only they can find something to stop the reaction. Keeping my fingers crossed on the blood cleaning. I don’t have access to a doctor who knows ME/CFS either. Even if they find something with long covid, who would treat me? I tried to convince the major neurological practices in southern Michigan to treat me for ME, and they all refused, including University of Michigan and Michigan State. Maybe long Covid will change their minds, but they were so adamant. I brought them the science and it didn’t matter. Crying tonight.
I’m so sorry that your medical needs are being so shamefully neglected Christyne. 🙁
Thank you Tracey.
I am sorry, Christyne. The NIH should just read your post. It would take two seconds. Your experience is quite similar to so many others’.
(And, Cort, how many others is it? Has anyone undertaken an accurate study to designate not just how many people have CFS/ME, but how many are moderate or severe? My math says that there are maybe as many as half a million people in the U.S. who are suffering moderate or severe cases.) (Which is an astounding number, if true.)
(And how many of these cases get worse? How many get better? Why isn’t CFS/ME considered “progressive”?) (Is it even accepted to be a “disease”?)
(Also, does the NIH know that PEM isn’t just “fatigue,” but for many it is a kind of pain that is not just “extreme,” but “torturous”?)
Not sure if I am allowed to include a link, but I found this article in “Frontiers in Neurology” on PEM to be useful:
Links are great, Brian – thanks!
If I remember correctly a study did find that 25% figure was pretty accurate. I don’t know where the study is though. A few studies have assessed prognosis but I wouldn’t trust any of them. Solve ME’s Patient Registry could certainly help with that.
The only thing I know that the NIH knows is that this disease is not worth much funding.
Thank you Brian.
I feel for you. I’ve had ME/FM for 30 years. Occasionally I find a doctor who knows a bit about FM and rarely any who know what ME/CFS is. It took a decade to get properly diagnosed after I finally had to quit working as an RN. It truly is depressing but occasionally there is hope gained by the incredible researchers we have around the world. That keeps me going. Plus I just want to be childish and yell at these doctors etc “I told you so”!!!!
Just curious Christyne Bliton if this happen after you had an mRNA Covid “vaccine.” I had my first Pfizer (May 12, 2021) and had the worst of my reactions but had not recovered in 2 months and then had the second. These shots sent my symptoms back in time and I still live 3 decades back in the management of my illness in a similar fashion as you describe. The booster I had was Moderna (Jan. 13, 2022) and it didn’t seem to make things worse (some flares)
nor did it make anything better.
Many of us are crying along with you and for you. Please hang in there! There are good things coming. Even if the NIH is refusing to see reality, the researchers ARE connecting the dots. Sufferers of ME/CFS are the bravest, most resilient people any of us could know. –Caregiver to an amazing daughter with CFS
Thank you Rossy.
I’m currently living with moderate MECFS in Norway and am very interested in the obvious connection between long COVID and MECFS. I recently came across this interview on YouTube that shows the same reluctancy from the COVID-community to connect the dots, but also the work being done to do just so. If you haven’t yet, I would love for you to see this one: Fatigue, Pacing and PEM Management | Lessons from ME/CFS – With Dr Ben Marsh
Thanks Gertrud 🙂
Thanks Gertrud, I watched that again. The thorough discussion between Dr Ben Marsh and Dr Asad Kahn, is well worth watching. It’s about 45 mins long, so may need a few viewings to absorb it all.
Yes indeed …Mr. Keller did his research!
Josh Keller has Long Covid Carolyn, so he has insider experience.
gosh i really hope that the most severe form of Long Covid and ME/CFS are the same thing… if so, we have a realistic chance to find help… maybe even a cure… I have tears in my eyes while writing these lines…
on the other side… it would kill me emotionally if it wouldn’t be the same thing and if we’re again the odd (wo)man out… again nobody would care what happens to the ME/CFS community… That’s our big chance my friends… let’s pray that this virus will make our disease treatable eventually…
for me It’s like a thriller in the cinema of sadistic humor of planet earth and humankind lol. please excuse my theatrical language but that’s what i feel right now after reading this article.
Tks again for your work Cort. It’s so important to keep informed. You’re a hero!
Treatment of Long Covid Neurologic Syndromes
with Nasal Administered Mesenchymal Stem Cell Exosomes
Philip W. Askenase, MD, Professor of Medicine and Pathology, Section of Rheumatology, Allergy and Clinical Immunology, Department of Internal Medicine, Yale University School of Medicine, New Haven Connecticut, 06520, USA. 203-809-2031, firstname.lastname@example.org
Long Covid Syndromes are devastating debilitating chronic clinical conditions occurring in 10-30% of patients following recovery from acute COVID-19 SARS-CoV-2 virus infections after some gap in time. Thus, they are not a continuation, but have a delayed onset that dominantly involves central nervous system neurons and especially vasculature. These Long Covid Syndromes are proposed susceptible to the well known diverse healing effects of mesenchymal stromal cell-derived exosomes that are proposed to be given directly into the brain by nasal administration to achieve high therapeutic specific activity.
Long Covid Syndromes variably consist mainly of intractable profound fatigue, impaired concentration, headache, poor memory, sensory disturbances, dizziness and inability to accomplish everyday tasks, as well as depression, and in severe cases, delusions, paranoia and even psychosis, along with respiratory aspects consisting of dry cough, sore throat, palpitations, shortness of breath and chest tightness. The chronic fatigue is a distressing, persistent feeling of weariness or exhaustion not alleviated by rest nor proportional to activity. It interferes with usual function and negatively impacts on the quality of life.
Exosomes are nano sized sacs or vesicles released by all cells, but in the case of enriched mesenchymal stromal cell-derived exosomes they are trophic, healing, anti-inflammatory and anti-immunological in numerous diseases and injuries. Exosomes are part of group of extracellular vesicles that carry various proteins and most importantly genetic materials like RNAs and even DNAs to alter the behavior of targeted cells near and far away. Nasal therapy allows focus on nervous system aspects of Long Covid Syndromes for repair of altered micro vessel cells as a dominant aspect that is susceptible to nasal applied mesenchymal stromal cell-derived exosomes by targeting involved microglia and endothelium, as indicated by results of experiment in animal models and information from human autopsy studies of patients dying from acute COVID infections and studies of spinal fluid in patients with post-COVD Long Covid Syndromes.
Underlying this approach is discovery that mesenchymal stromal cell-derived exosome systemic treatment of neuro injury targets certain phagocytes like macrophages and likely microglia in the central nervous system that release secondary healing extracellular vesicles carrying and then transferring microRNAs that affect the gene expression of local capillary cells to restore vascular integrity. It is postulated that pathways of endothelial and neural pathology in acute SARS-CoV-2 virus infections may carry over to produce underlying vascular and neurological defects in Long Covid Syndromes that are susceptible to this proposed nasal Mesenchymal Stromal Cell exosome therapy.
Nasal administration of exosomes allows their passage into the brain via perforations in the skull for passage of cranial nerves. As natural and physiological, exosomes used for treatment then pass the otherwise impenetrable enclosing blood brain barrier to enter the central nervous system and then target the phagocytic cells that produce secondary vascular healing exosomes to reverse abnormal vessel permeability. There already is established efficacy of Mesenchymal Stromal Cell exosome therapy for targeting various central nervous system abnormalities and disease models, successful nasal administration of exosomes for some of these, use of Mesenchymal Stromal Cell-exosomes for treatment of acute COVID-19 infections and the beginning use of Mesenchymal Stromal Cell-exosomes administered systemically for Long Covid Syndromes.
I think this approach to long Covid and also ME/CFS is brilliant. For many years, I used a gel with mesenchymal stem cell factors prepared by Dr. Paul Cheney. This was so powerful that a tiny amount would knock you out for a day or so, but then you would feel better. Since my original diagnosis was chronic encephalopathy, I think that a nasal treatment would be ideal. Is this treatment being offered to patients or is it still in the testing phase?
I strongly suspect also an epigenetic component involved in PEM and possible incremental decline following crashes. (There was new study linked on @MECFSNews).
I like to make a point that not only the crashing part, but also the pushing part of push-crash-cycles should be researched, as in my personal experience crashes can often be triggered by “adrenaline” or positive/negative excitement, and stress I believe is known to be a strong epigenetic mediator. I always find it remarkable and research-worthy that people CAN still push themselves further when their body already tells them that they are going beyond the energy envelope and will crash. It’s not a like a broken leg! So how is the pushing beyond energy limits involved in causing PEM?
With longer-lasting illness, I suppose that other layers of exhaustive processes may add upon those specific to ME/CFS.
I suppose that the stressful situation of chronic illness might for example deplete resources needed for stress response such as I think magnesia, and maybe hormone precursors such as DHEA. (I also have BTW notoriously low testosterone which is not seen as pathological by doctors, as I’ve been told it happens in healthy individuals too; but I suspect it could also somehow be related to the continous stress-related depletion of resources that results from a chronically overactive sympathetic nervous system.)
However I suppose that fixing these additional issues isn’t always so easy on top of the underlying ME/CFS pathomechanism…In my personal experience, one needs to observe closely whether supplements such magnesia bring temporary better performance, only to enhance the risk of crashing afterwards. But I suppose everyone needs to try out for themselves what they may benefit from!
Also, nervous system related sensory hypersensitivity and filtering issues will cause additional exhaustion due to the continuous enhanced amount of information input and high stress reaction even to small stimuli (a bit similar to fatigue experienced by people with ADHD or SPS who can have similiar filtering issues).
I don’t know if I have long Covid or ME/CFS, but here in Nova Scotia we have a centre for complex chronic conditions and I asked my doctor for a referral there back in October 2020. My doctor didn’t believe I had Covid so I was tentatively diagnosed with CFS. Turns out there are two wait lists, one for Covid and one for everything else, so I ended up on the everything else wait list. For long Covid patients the wait time is a couple of months, for everyone else it’s two years; I’m still waiting. An indicator of the differences in funding I think. My two year experience with this disease is that it’s far worse in the winter than the summer. By end of summer I start thinking I’m in recovery, but October sets me straight ,I’m going nowhere. I suppose I should be grateful for a couple of months of enjoying summer, but at this time (early March) I’m out of bed maybe 4 hours a day and quite miserable.
So typical for the extended wait time…unless your the the ‘disease de jour’.
Perhaps you should check your Vit D level. SAD (seasonal affective disorder) is feelings of depression/lethargy/sadness in the winter months.
Did you have anything like that previously? It may be exacerbated if you have contracted something else as well.
Are your vaccinated? Sometimes the vaccine can induce symptoms akin to having experienced the actual virus!
Keep reading and look for the way out of this.
Why is MCAS (mast cell activation syndrome) never mentioned and included in these debilitating diseases?
I have been subscribed to and reading this site for years now. I also have been following the Long COVID syndrome. Both CFS/ME and Long COVID are quite similar to Gardasil (HPV Vaccine) Injury. I was hoping to gain some insight as to a healing process. My daughter was injured by Gardasil 8 years ago when she had her 2nd shot in the 3 shot series. She was sick within 5 days…headache, vertigo, and nausea which were the beginning of POTS…we never heard of POTS but her neurologist was well-versed in Autonomic Dysfunction. The list of medical issues evolved over the following months and years to include: sleep apnea, autoimmune encephalopathy, Mast Cell Activation Syndrome, seizures, Rayneud’s, brain fog and cognitive issues, psychiatric issues (PANS), AND she has lost her vision, both central and peripheral…she is legally blind now. This is the short list of comorbidities…the list goes on and on to include breathing issues, chest pain, tachycardia, hypoxia, and so much more. She has CRPS and gets very $$$$ Ketamine infusions for her relentless pain and neuropathic burning. The fatigue is awful, and if she overdoes one day, she pays for it the next and following days. She is loaded now with adrenergic and muscarinic autoantibodies. She is so sensitive with the Mast cell that she cannot tolerate IVIG…she tried for over a year. She cannot tolerate LDN (4 trials) or Mestonin (2 trials). I sympathize with all of you and the Long Covid people…I really think we walk in the same shoes. I appreciated your work, Cort, as I always find a valuable takeaway. We are not anti-vax, but Gardasil’s ingredients are troubling, both disclosed and undisclosed.