Most of us take recovery for granted. If you’re healthy, you trust that if you get a cold or the flu, you’ll get better. But sometimes that doesn’t happen.
WINSTON: It’s difficult to imagine what it would be like if that level of illness just persisted and lasted for weeks and then months and then years.
You’ve probably heard of Long Covid. According to a recent government survey, about one in five adults who’ve had Covid-19 in the U.S. have experienced lingering symptoms from the illness. Now, long Covid is new — an outcome of the recent pandemic. But the experience of symptoms lasting after an illness isn’t new to some people, like Winston.
WINSTON: A number of people would tell me that I was the most athletic person they’d ever met. My regular day-to-day life was pretty rigorous at the time.
Years ago, Winston was an ambitious twenty-something living in San Francisco. He went camping on the weekends, snowboarding in the winter, and cycled year-round. He even spent 24 days biking across Europe during the summer of 2015.
WINSTON: It was actually a race called the Transcontinental, and it started in Brussels and ended in Istanbul. You just have to go as far as you can every day, unsupported.
The Transcontinental is one of the toughest ultra-endurance bike races in the world. Now obviously, Winston wasn’t participating in a 2,700-mile bike race every day, but by any measure, he was athletic. Today?
WINSTON: My lifestyle is decidedly more geriatric these days.
Six years ago, Winston was diagnosed with an illness called myalgic encephalomyelitis, also known as chronic fatigue syndrome. It’s called “ME/CFS,” that’s M-E-slash-C-F-S. Not much is known or understood about the disease, but most people get it after an infectious illness. Winston got it after a bad case of mononucleosis. Three months after he recovered, though, a new set of symptoms set in.
WINSTON: I woke up one day and I felt like my legs were lead. I remember getting into the shower and just feeling slightly off balance. And I had this strange sense of fatigue come over me.
He thought he might have the flu.
WINSTON: That’s your only reference point when you’ve been a healthy person to date, and you haven’t had to deal with chronic illness. You never assume, “Oh, this must be some kind of serious condition.”
But it was a serious condition.
WINSTON: The early weeks of my illness, I made the connection that the more I was cycling, the worse I felt. At a certain point, I recall being in my garage and setting my bike up against the side of the wall and just thinking like, “All right, old pal, it’s going to be a couple of weeks before I get to ride you again.” And that was six years ago.
On Winston’s best days he takes a slow, meditative walk around his neighborhood. On a bad day —
WINSTON: I don’t do anything. So, those are bed days. I’m one of the lucky ones. I’m not permanently bed bound.
Winston rests on these days. Because when it comes to ME/CFS, sometimes rest is all there is.
KOMAROFF: There are no F.D.A.-approved treatments.
From the Freakonomics Radio Network, this is Freakonomics, M.D. I’m Bapu Jena. I’m an economist and I’m also a medical doctor. Each episode, I dissect an interesting question at the sweet spot between health and economics. Today — why has a debilitating illness received so little attention from the medical community? And might that be changing, thanks to Long Covid?
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Let’s start by diving into what ME/CFS looks like for patients. It’s not something I’ve seen a lot of so to help me understand more about the disease, I spoke to Dr. Tony Komaroff, a senior physician at Brigham and Women’s Hospital in Boston and a professor at Harvard Medical School. He’s treated ME/CFS patients for over 30 years.
KOMAROFF: The main symptoms are fatigue, feeling wiped out following even modest physical or mental exertion, unrefreshing sleep, awakening multiple times at night, brain fog or difficulty concentrating, difficulty remaining upright for very long.
JENA: And so, this fatigue is — This is not normal fatigue. I mean, you would describe it as pathologic, right?
KOMAROFF: Yes. That’s a very important point. Every human being gets tired. This is qualitatively different. It’s severe enough that it interferes with your life at home and at work, if you can work. And it is not relieved by rest.
Up to 75 percent of ME/CFS patients can’t work, but Winston still can.
WINSTON: Most of my energy goes toward retaining my job. And it means that I need to forgo things like watching T.V. that could kind of tax my energy envelope too much. So, yeah. Um — I’m just kind of recollecting myself for a second.
To get through the interview, Winston had to take breaks. He explained how even the act of talking to us was exhausting.
WINSTON: I feel a profound sensation of fatigue. But I also feel kind of an adrenaline buzzing. A lot of people call it “tired but wired.” And it’s this funny kind of paradox of this condition that you feel this extraordinarily deep fatigue at all times, but you also can’t sleep. Another thing that I’m feeling right now is a lot of pressure in my head. So, it feels like my brain is being squeezed. And the more energy I expend, the tighter and tighter it squeezes. And it’s just more difficult to think clearly. And at a certain point it just becomes totally incapacitating.
JENA: What’s the progression of the disease?
KOMAROFF: It begins in most people pretty suddenly. And it begins with what seems to be an infectious-like illness. Most of the people I’ve seen — close to 500 — say that they were perfectly fine, perfectly healthy. And then one day they came down with a virus, like the flu, or a virus they’d had many times in the past, but this time they never got better.
ME/CFS affects up to two and a half million people in the U.S., and millions more globally. From an epidemiologic standpoint, there actually aren’t many clues as to who’s at risk. A report from the National Academy of Medicine said that patients with the illness are more functionally impaired than those with other disabling illnesses like congestive heart failure, hypertension, depression, and multiple sclerosis. What’s most scary about all of this is that only 5 percent of people with ME/CFS recover. And, while there are no F.D.A. approved treatments, as Tony told us earlier, some options exist.
KOMAROFF: There are a whole bunch of different already approved drugs — approved for other purposes — that appear to give some people relief from some of the symptoms. There’s certainly nothing that would approach a cure, but there are medicines that help some people.
JENA: Do you think that they’re treating the symptoms or they’re treating the underlying cause of the symptoms?
KOMAROFF: I think it’s largely treating the symptoms.
Fatigue is a symptom of so many illnesses — anemia, cancer, heart disease. So, I wondered how patients are even diagnosed — is it based on symptoms or are there specific diagnostic tests that can confirm if someone has ME/CFS?
KOMAROFF: The case definition still relies entirely on symptoms. No objective marker of any kind — blood test, urine test, imaging study — has been found to have high enough sensitivity and specificity to constitute a diagnostic test. But that is very different than asking the question: Are there any biomarkers that significantly distinguish patients with this illness from healthy people of the same age and gender?
ME/CFS has been around for a while, but it captured national attention in the mid-1980s when outbreaks occurred in Nevada and New York. Tony started seeing patients around this time with an unusual group of symptoms and realized it was something new. But the diagnostic tests available to him back then made it hard to identify anything abnormal in patients. Medical testing today is a lot more advanced, though, and able to pick up on abnormalities in patients with ME/CFS. It’s still a very complex disease to diagnose, because doctors have to rely only on symptoms. This has led to a lot of stigma. ME/CFS has been called derogatory names like “yuppie flu” or “shirker syndrome.”
WHITTEMORE: It was really referred to as being a psychiatric, psychological hysteria.
That’s Vicky Whittemore. She’s a program director at the National Institutes of Health. To this day, there’s the perception that ME/CFS is psychosomatic, or that people with the disease are just depressed.
WHITTEMORE: We’re really working against that stigma, but it still does exist out there. I heard someone this morning say that she had just heard from a retired chair of neurology that “It’s really hysteria — there’s no such thing as ME/CFS as a disease,” which is pretty frightening.
Even the name, “Chronic Fatigue Syndrome,” shortchanges the disease. Fatigue gives the impression that people are just tired, but the level of fatigue they experience isn’t normal. It’s pathologic. Some people with ME/CFS describe it like their body is a battery that’s run out of charge.
JENA: Talk to me a little bit about the sort of uncertainty in the diagnostic process and what that means for how physicians perceive the illness — stigmatization of the illness.
KOMAROFF: When a patient walks through the door with symptoms that lead you to say, “Oh my goodness, they have something for which there is no approved diagnostic test. And there is no F.D.A.-approved treatment.” That’s frustrating. And people, including doctors, like to avoid frustrating situations.
Doctors’ unfamiliarity with the disease or discomfort in diagnosing it could stem from the fact that, at least until recently, less than one-third of medical schools cover ME/CFS in their curriculum. A 2015 report found that it takes most patients more than a year to be diagnosed, and many of them much longer than that. In fact, it’s believed that up to 91 percent of patients are undiagnosed.
Over the past two years, doctors have started seeing patients with a range of symptoms that remain after a Covid-19 infection — what’s been termed Long Covid. But to doctors who treat ME/CFS, the symptoms are extremely familiar. And biologically, the illnesses look alike in many ways. They can affect the autonomic nervous system, energy metabolism, and autoimmunity. There’s also more and more evidence that patients of Long Covid and ME/CFS have abnormal gut bacteria, which causes inflammation. But beyond the biological similarities among patients, the two illnesses can also cause similar reactions from doctors: frustration and skepticism.
KOMAROFF: It’s an example of blaming the victim. To imply to the patient that the patient doesn’t really have a problem. Or that if they have a problem, it’s a problem of their imagination or a mental problem. That does happen. And it’s inexcusable, I think, on the part of doctors, with both Long Covid and ME/CFS.
JENA: I’m thinking as an economist now — Long Covid, I suspect, is much more prevalent than ME/CFS and will continue to be. Do you think that the presence of Long Covid will advance potential therapeutics and diagnostic understanding that will then spill over positively into ME/CFS?
KOMAROFF: I absolutely do. The federal government has dedicated over a billion dollars to study the chronic health consequences of acute Covid-19, one part of which is the development of Long Covid. If I’m right, that the similarities between ME/CFS and Long Covid are much greater than the differences, then whatever is going to be learned about Long Covid is probably going to be applicable to ME/CFS
Another thing ME/CFS and Long Covid have in common is that we still don’t know why some people develop the conditions and others don’t. When most of us have an infection, the body deals with it. You get better. But with ME/CFS and Long Covid, the body’s response persists. According to Tony, this could be caused by a number of things. If the initial insult to the body is an infection, say by a virus, it could be that there are reservoirs of the infection that remain in the body. Viral persistence has been documented in Long Covid patients. That’s one thought.
KOMAROFF: Another is that many of the ongoing symptoms may reflect a reactivation of viruses that are already in the body. Practically all of us have certain viruses that live within us for most of our lives. They’re usually asleep, but they can reawaken or reactivate and then multiply. And then that can potentially cause symptoms. So, there are some people in which Covid infection seems to have reawakened viruses that were in the body for many decades and that maybe the symptoms that are chronic are being caused by those reactivated viruses, not by the Covid virus.
Essentially, Tony is saying that the symptoms of ME/CFS or Long Covid might be caused by a virus that’s been lying dormant in someone’s system, possibly for years, until something reawakens it.
KOMAROFF: I think the most important unanswered question about ME/CFS and Long Covid and all of these other chronic fatiguing illnesses is: what causes the symptoms? The theory, with some scientific support, that I think is the most interesting was first suggested to me by the first patient I ever saw with this illness, who said, “It’s like the flu, but the flu that never goes away.” And that led me to think, “Well, actually, why do we feel the way we do when we get the flu?”
Why do we? When humans get sick — let’s say with the flu — there’s a reliable set of symptoms that we have. We feel fatigued, lethargic, we lose our appetite, maybe we find it difficult to think straight. Sick behaviors are present in most animals — even worms. These adaptive changes in physiology have been evolutionarily preserved as a way to protect ourselves and increase our chance at survival when we get sick. How do these symptoms do that? Well, they cause you to reduce energy-consuming activities. You move less, you think less, you eat less. That leaves more energy to fight the infection or heal the injury. Tony thinks there could be one pathway in the brain that, when it’s triggered by infection, causes these symptoms.
KOMAROFF: My thought was there’s probably a group of neurons in the brain, a nucleus of neurons that’s dedicated just to generating sickness symptoms. So, that behavior will change so that energy consuming activities will be reduced so that more energy will be available to fight the infection. And that was a beautiful theory without a shred of evidence until about a week ago.
JENA: Okay, now I’m on the edge of my seat.
KOMAROFF: A paper was published in Nature that finds exactly this kind of a nucleus of neurons in the brains of mice, in the hypothalamus. When it’s stimulated, the mice don’t move around much. They don’t want to eat much. Their behaviors suggest they are having the same group of symptoms. With ME/CFS and Long Covid and similar illnesses, could it be that nucleus — either the switch to turn it off after the acute infection got stuck and it can’t turn off? More attractive to me is there is a chronic process in the body, that is acting on this nucleus in the brain to produce persistent sickness symptoms. And if I wanted to put my money on a bet, that’s where I’d put my money.
JENA: So, to borrow your language, there’s an on and off switch. The switch goes on when the nucleus detects something that’s wrong. And sometimes pathologically that switch could just stay on, even if there’s nothing else in the body that’s happening.
JENA: And when that switch turns on, it creates from this evolutionary perspective, the symptoms that we’ve been talking about. And so, if we’re in this world where the switch is inappropriately on, then figuring out how to turn off that switch would perhaps solve the problem of the symptoms. But if we’re in a world where the switch is appropriately on, turning off that switch — could that cause more problems?
KOMAROFF: It could. You’ve got it exactly right. And since I think it’s more likely that the switch is appropriately turned on chronically, then trying to turn the switch off probably isn’t a good idea, even if it were possible.
Long Covid has been around just over two years, but it’s already received over a billion dollars in funding from the federal government. Meanwhile, ME/CFS has been studied since the 1980s — nearly 40 years — but there’s still a lot that’s unknown and funding has been sparse. So, why is that?
WHITTEMORE: There was really an outcry from the community that N.I.H. was not doing enough.
Coming up… when an illness is stigmatized and hard to diagnose, do patients pay the price? I’m Bapu Jena, and this is Freakonomics, M.D.
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Over a billion dollars has been allocated to studying Long Covid. That’s way more money than has ever been spent on ME/CFS research.
DAVIS: Needs to be 10 times that amount, minimally, and then increase over time.
That’s Ronald Davis. He’s an ME/CFS researcher and a professor of biochemistry and genetics at Stanford University.
DAVIS: A geneticist studies your inherited material, which is largely D.N.A.
He’s well known for his pioneering work on the Human Genome Project and has enjoyed a long history of successful funding by the N.I.H.
Ronald has a son named Whitney Dafoe. Whitney has a very severe form of ME/CFS. He can’t leave his bed and at times has been unable to communicate or feed himself.
DAVIS: In the past, he could not look at a letter or a number in his room because he said, “When I see a letter, my brain interprets that’s an ‘A’. Well, that’s almost beyond my capacity. It’ll cause me to crash. So, I cannot see letters or numbers because I know that they mean something.” And so, I had to go into his room with my Dremel tool and grind off anything that had a letter or number on it.
When he was healthy, Whitney was a photographer and avid traveler. But in his early 20s he began to feel sick with a strange constellation of symptoms. He noticed that travel and photography shoots would make his symptoms feel worse, but doctors couldn’t figure out what was wrong. Eventually, he had to move home.
DAVIS: When it became clear he couldn’t take care of himself. That was the turning point for me.
Around 2012, Whitney was finally diagnosed with ME/CFS. Ronald did what any scientist would do — he looked for answers.
DAVIS: The field of ME/CFS was bit of a desert. And it was clear to me that he was not going to get a cure to this unless some good scientists got involved in it. So, I started working on it and reading, and the biggest problem is, of course, there’s not very much money. And so, a lot of researchers will work a little bit on it, but they can’t really fund their entire lab because of the lack of funding.
To make inroads into the illness, in 2014 Ronald shifted his lab’s focus to ME/CFS.
DAVIS: Our program is No. 1, trying to figure out how to cure this disease. That’s, of course, very hard. You got to understand a lot about it. The other one is can we come up with something that would help the patients? Make them feel better? That is not quite as hard as curing. The other one is to develop a diagnostic test because the diagnosis of this disease is just from symptoms. The fourth thing is can we figure out how to prevent the disease from happening in the first place? We have to understand what is the fundamental problem? And we don’t know that yet.
To fund his ME/CFS research center, Ronald applied for funding from the National Institutes of Health, the largest funding organization for all medical research.
DAVIS: I wrote grant after grant, after grant. All of which were turned down for various reasons.
Only one of his 24 grants on ME/CFS has been successfully funded.
The N.I.H. spends $17 million a year on ME/CFS research. For comparison, in 2021 the institute provided $126 million for multiple sclerosis research, $129 million for lupus, and over $3 billion for H.I.V./AIDS. Each of these illnesses affects fewer Americans than ME/CFS. Here’s Vicky Whittemore from the N.I.H., again. She manages the grant portfolio for ME/CFS.
WHITTEMORE: The barriers to increasing the amount of money is really the many demands that each institute at N.I.H. has. So, if you think about the hundreds of neurological diseases ME/CFS is just one of those diseases. It’s a very complex disease, and so it’s really been a challenge to encourage and identify researchers to come into the field. It’s also really challenging, at times, to work with the patient community who, rightly so, wants more funding, more research, things to move faster.
But there has been an effort to increase research into the disease. Until 2015, the funding level for ME/CFS at the N.I.H. was only $6-8 million per year.
WHITTEMORE: There was really an outcry from the community that N.I.H. was not doing enough. Dr. Collins, who was the N.I.H. director, asked the Institute directors, “What are we doing for research on ME/CFS?” And that led to conversations that indicated that we really needed to up our game, both for funding of research outside of N.I.H. and initiating a study.
Out of that effort came an in-house study of ME/CFS that did extensive testing of 20 individuals with the disease to look at their metabolism, genetics, and cardiovascular function, with the hope of finding an underlying cause. A sample size of 20 is small, but the N.I.H. had very strict criteria for enrollment. Winston, who we spoke to earlier, took part in that study.
WINSTON: I remember for some of these procedures being so depleted that I couldn’t even respond to the attendant who was helping me. There were just hours and hours of tests. They want to see what happens as you become more fatigued — how this impacts your performance. Nut it definitely took it out of me as a patient.
Then, starting in 2017, the N.I.H. began funding three research centers dedicated to studying ME/CFS. The hope is that these centers will bring in researchers from different disciplines to tackle the underlying mechanisms of the disease.
However, there’s still a feeling that ME/CFS is underfunded. A group of outside researchers found that ME/CFS has the lowest amount of funding relative to disease burden of any disease funded by the N.I.H. When their work was published, ME/CFS received $15 million annually from the N.I.H.— but based on their calculations it should have been receiving over $200 million in annual funding.
WHITTEMORE: You may have a disease that there is a huge disease burden, but if there’s not a research community out there, N.I.H. doesn’t designate a certain dollar amount that they’re going to put towards that disease. We don’t pit one disease against another because they’re all devastating and all need support.
Ronald Davis’s issue with N.I.H. funding stems from a specific requirement that the N.I.H. has for large grant proposals: preliminary data.
DAVIS: You won’t ever get a grant if you don’t have a lot of preliminary data. It’s almost like you have to have it 95 percent done, and then you write the grant. And then they’re pretty sure it will work. That’s a little bit of an exaggeration, but it’s not far off.
It’s a chicken and egg problem, really — to get funding, researchers need preliminary data. But they need preliminary data to get funding.
Ronald thinks that’s difficult in a field where so little is understood. Smaller grants that support exploratory research do exist, but they’re much less money than the grants Ronald typically applies for.
While ME/CFS researchers are scrambling for money, Congress provided $1.15 billion in N.I.H. funding for research into Long Covid. In theory, this could be a huge boon for ME/CFS since the two illnesses look so much alike in symptoms and biological underpinnings, but Ronald has some doubts.
DAVIS: Well, I am actually concerned that the people studying Long Covid are focusing on it as this new disease and aren’t paying attention to ME/CFS work at all. Because you see people reinventing the wheel and also making the same mistakes.
Dr. Tony Komaroff.
KOMAROFF: I do have some concern that the early research on Long Covid may not be as directed by the lessons learned from ME/CFS as it should be. I hope I’m wrong.
Tony is referring to a recently published N.I.H. study on Long Covid. In the study, researchers did extensive lab testing on people who had Covid in 2020. Some of those people went on to develop Long Covid and others didn’t. They compared the results between these two groups and found no significant differences. While those results were disappointing in terms of offering insights into Long Covid, Tony was further disappointed that the tests in the study were not ones that are known to detect abnormalities in people with ME/CFS.
KOMAROFF: It was as if they had started in 2020 and said, “Well, let’s just think on our own of what tests might be informative.” And as it turned out, those tests weren’t.
Newer studies of Long Covid have used the tests that can uncover abnormal biomarkers in ME/CFS patients. And unsurprisingly, they’re abnormal for Long Covid patients too.
All that said, there is hope that Long Covid will bring attention and understanding to a group of people that have felt ignored by the medical community for a long time. Here’s Winston again.
WINSTON: I do have hope. I don’t know how logical it is. But the global pandemic and the occurrence of Long Covid and the heightened awareness of post-viral conditions brings us all hope that this disease that has been so stigmatized in the past will continue to move more and more toward the mainstream.
And some answers may be on the horizon. In a few months, researchers at the N.I.H. should be publishing the results from their in-house study on ME/CFS, which Winston participated in. And on that note, a truly special thanks to Winston for sharing his story. And thanks to Dr. Tony Komaroff, Dr. Vicky Whittemore, and Dr. Ronald Davis.
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Next week on Freakonomics, M.D., we’re going to revisit the question of if and when my dad — or any of us — should retire.
COE: Our identities are very much wrapped up in our careers
Our identities and our brains. So, what happens to our brains, to our cognitive health, when we decide to stop working?
PERELMEN: There is a risk associated with this special moment in life when we turn to retirement.
We’ll talk about this risk — whether it outweighs other benefits of retiring, and how we might keep our minds stimulated as we get older.
COE: It really matters what you’re doing in your job, but also it matters what you’re doing once you retire.
We’ll try to answer these questions, along with one more: Did my dad finally retire? That’s all coming up next week, on Freakonomics, M.D.
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Freakonomics, M.D. is part of the Freakonomics Radio Network, which also includes Freakonomics Radio, No Stupid Questions, and People I (Mostly) Admire. All our shows are produced by Stitcher and Renbud Radio. You can find us on Twitter and Instagram at @drbapupod. This episode was produced by Morgan Levey and mixed by Eleanor Osborne. Our senior producer is Julie Kanfer. Our staff also includes Neal Carruth, Gabriel Roth, Greg Rippin, Rebecca Lee Douglas, Zack Lapinski, Ryan Kelley, Jasmin Klinger, Emma Tyrrell, Lyric Bowditch, Jacob Clemente, Alina Kulman, and Stephen Dubner. Original music composed by Luis Guerra. If you like this show, or any other show in the Freakonomics Radio Network, please recommend it to your family and friends. That’s the best way to support the podcasts you love. As always, thanks for listening.
JENA: I have to tell you, I think I need to switch careers. This is absolutely fascinating.
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- “Neuropathology of Patients With COVID-19 in Germany: A Post-Mortem Case Series,” by Jakob Matschke, Marc Lütgehetmann, Christian Hagel, Jan P. Sperhake, Ann Sophie Schröder, Carolin Edler, Herbert Mushumba, Antonia Fitzek, Lena Allweiss, et al. Glatzel (The Lancet: Neurology, 2020).
- “Highlight Preliminary Data in Your Application,” by the National Institutes of Health (NIAID Funding News, 2020).
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