I had a patient who had been misdiagnosed and placed in a psychiatric unit. Eventually that patient was diagnosed with ME/CFS, which stands for myalgic encephalomyelitis/chronic fatigue syndrome. They were also diagnosed with mast cell activation syndrome and postural orthostatic tachycardic syndrome (POTS), which tend to occur along with ME/CFS.

ME/CFS has been poorly recognized and was first included as an actual illness by the Institutes of Medicine in 2015. Because of this, it has not been included in medical training. “Myalgic” means muscle. “Encephalo” means brain. And myelitis is inflammation of the coating of the nerves. So we know that the nervous system is involved. But what we also know now is that it affects multiple systems, including the endocrine and gastrointestinal systems. Patients also experience changes in cognition.

Diagnosis of ME/CFS is clinical at this point, meaning that it is based on symptoms, and that has been one of the major hurdles for patients who suffer from it. Symptoms are unrelenting fatigue, brain fog, difficulty standing up, nausea, numbness and tingling, flulike symptoms, severe muscle aches, nonrestorative sleep, difficulty coordinating movements, and cognitive disturbances, such as word-finding difficulties and slowed speech.

The symptoms that make up the diagnostic criteria are quite simple. However, from a research perspective, we’re able to take those patients and run a variety of different laboratory tests that are not available to your general provider. This is why providers have a very difficult time validating the patients’ experiences. The regular tests that doctors run just don’t show anything.

With the robust laboratory resources that researchers have, we have found objective evidence of pathology. Two examples that have been documented are inflammation in the brain and dysfunctional natural killer cells, a kind of white blood cell.

It’s been estimated that at least 50 percent of those with ME/CFS had a viral or other infection prior to developing long-standing chronic disease. We look for a multitude of viruses by using PCR to detect viral RNA or DNA. What we found is that there are specific types of viruses that like to set up shop in the body and cause long-term problems that don’t seem to go away. This is a twofold problem: It’s not only the virus but it’s also how our immune system responds to it. What we’re finding is that in many patients, even if the virus has left, the immune response has become altered. Epstein-Barr virus, human herpesvirus 6, and cytomegalovirus are viral infections that we have seen ultimately lead to ME/CFS.

About 12 percent of young adults who get infectious mononucleosis—caused by Epstein-Barr virus—never recover from it and develop symptoms of ME/CFS. So this is not something that we have never heard of before. We know that viruses can cause long-standing problems.

The reason that we began to study this at Stanford is because Ron Davis, PhD, the cochair of the Stanford Genome Technology Center, who is one of the prior leaders of the Human Genome Project, became a champion for this condition. Ron’s son, Whitney Dafoe, has been severely affected by ME/CFS and is virtually unable to leave his room. Ron has written a book with Tracy White called The Puzzle Solver, about Ron’s quest to determine the biological basis of ME/CFS and to help his son. That name was given because Ron was at the forefront of being able to solve something as complex as deciphering the human genome. He tends to take on very difficult and challenging problems that others fear taking on. And this has now become his life’s work, and mine as well.

With other coronaviruses such as SARS and MERS, 10 percent of patients never fully recover, and we’re seeing the same pattern in COVID-19 patients.

The set of symptoms that we see in ME/CFS is identical to those that the COVID-19 long-haulers are experiencing. A long-hauler is someone who’s been affected by COVID and never seems to recover completely. Many of the documented cases of long-haulers suggest that patients are unable to go back to work, take care of their families, or perform day-to-day activities that were previously very simple for them.

Certainly, there’s other pathology that can be going on in the COVID long-haulers, such as lung scarring and damage to heart tissue. But the other systems that are broken down—the autonomic nervous system, for example—are heavily hit in both ME/CFS and in COVID-19 long-haulers.

Prior to COVID, there were already up to 2.5 million people in the country who were affected by ME/CFS. Many of the people are disabled, and 75 percent of patients are, at some point, bedbound or homebound. And they don’t have the clinical diagnostic workup that is required for them to get services like Social Security Disability. Insurance companies don’t have a code for ME/CFS. There are codes, diagnostic tests, and treatments for overlapping conditions, such as POTS, small fiber neuropathy, subclinical hypothyroidism, etc., if clinicians are trained to look for them.

Our concern is that with all the people who have now been infected with COVID, if 10 percent of them develop ME/CFS-type symptoms, then we have an enormous amount of disability to contend with in the future.

We need to define clearly what a COVID long-hauler is and compare that to ME/CFS. In my opinion as a physician, a percentage of people who are COVID-positive are ME/CFS patients. Unfortunately, we’ve had a very difficult time historically obtaining funds from the NIH to truly dive into this. We’ll be able to start this study after we obtain funding.

At Stanford, we are developing a study where we collect samples of blood and sputum from COVID patients in order to look at genetics, epigenetics, and multiomics to see what is occurring on a molecular level within the body as the patients develop symptoms over time. And we are looking at changes in the immune system that occur as a response to COVID.

What we need for ME/CFS research now is funding and for the NIH to start looking at this as a serious condition. We’re hoping that providing this information to the community will help stimulate an infusion of private philanthropy and funding to accelerate this research. COVID is upon us now. We have to take action while it’s happening because if we don’t figure this out, millions more are going to end up suffering and becoming disabled.

The Stanford Genome Technology Center has a website where people can donate so that we can get our research started.

The other action item is to connect with us at [email protected] if you’ve been diagnosed with COVID, especially if you’re local in the San Francisco Bay area. We’d like to follow people over time, beginning when someone is diagnosed with COVID, so that we can understand what is happening as patients are converting to long-haulers.

People with chronic fatigue syndrome have extreme exhaustion after exercise. They are unable to produce enough adenosine triphosphate (ATP) so that they can sustain their daily activities. Blood flow to tissue doesn’t meet the needs of the body. This is called postexertional malaise, a hallmark of the disease.

Physicians are recommending that patients perform what’s called graded exercise therapy. The recommendation that patients should push themselves to perform graded exercise therapy is harmful. Patients who have undergone forty-eight-hour cardiopulmonary exercise testing just to prove to insurance companies that something is wrong have ended up harming themselves for long periods of time. So I would say get your rest.

It is important for physicians to rule out other conditions but not to forget that ME/CFS could also be the problem. I think that physicians need to know that they’re harming their patients if they’re telling their patients to continue to push themselves, especially if they haven’t evaluated them for potentially having ME/CFS.