New research seems to offer some long-sought insights into the perplexing and devastating condition known as myalgic encephalomyelitis, also called chronic fatigue syndrome. The National Institutes of Health-led study found several potentially key differences in the brains and immune systems of people with ME/CFS compared to healthy controls. The findings could help point to possible future treatments, the researchers say.
ME/CFS is a debilitating ailment. It’s characterized by three core symptoms, according to the Centers for Disease Control and Prevention: a greatly reduced ability to perform daily functions and long-term fatigue (lasting at least six months)—fatigue that isn’t driven by strenuous exertion or relieved by rest; a worsening of symptoms after bouts of activity that previously didn’t tire someone out, also known as post-exertional malaise; and sleep problems. Sufferers will also often experience a variety of other health issues, such as brain fog, blood pressure spikes upon standing up, chronic pain, and digestive problems.
The term chronic fatigue syndrome was first coined in the 1980s, though reports of a similar illness date back to the early 20th century. For much of its history, the public and some doctors have viewed ME/CFS as a purely psychological disorder, and patients have struggled to receive recognition and care as a result (this is one reason why advocates prefer the term myalgic encephalomyelitis over chronic fatigue). More recently, the medical establishment has come to a consensus view of ME/CFS as a physiological disease, though not one with easy answers.
ME/CFS is thought to predominantly be a post-infectious condition, triggered by the body’s dysfunctional reaction to a germ. There appear to be several pathogens that are more likely to cause ME/CFS than others, such as the Epstein-Barr virus. And some experts argue that at least a subset of long covid cases are effectively ME/CFS cases caused by the coronavirus. But only a small percentage of people seem to ever develop ME/CFS (according to one estimate from the National Academy of Medicine, up to 2.5 million Americans may be living with it). And scientists haven’t yet figured out how the condition emerges following an infection, nor established biomarkers that would allow us to diagnose it easily. There are no approved treatments for it, either.
This new research, published Wednesday in Nature Communications, may be one of the most comprehensive analyses of ME/CFS patients to date. It was led by scientists from the National Institutes of Health, as part of an initiative begun in 2016 to study the condition. The researchers recruited volunteers suspected to have ME/CFS and ultimately selected 17 patients to undergo an array of medical exams, such as spinal fluid collection, brain scans, skin biopsies, and blood tests. These patients were then matched against healthy controls.
Compared to the baseline of controls, ME/CFS patients had clear biological differences, the researchers found. Patients were more likely to have lower brain activity in the temporal-parietal junction region of the brain, for instance. They also tended to have lower levels of neurotransmitters called catecholamines as well as altered levels of certain immune cells and possible signs of immune exhaustion.
“People with ME/CFS have very real and disabling symptoms, but uncovering their biological basis has been extremely difficult,” said Walter Koroshetz, director of NIH’s National Institute of Neurological Disorders and Stroke (NINDS), in a statement. “This in-depth study of a small group of people found a number of factors that likely contribute to their ME/CFS.”
While the team did conduct a deep dive into the physiology of these patients, the findings are still based on a small sample size (one unexpected factor in this was the covid-19 pandemic in 2020, which stopped further recruitment). So it’s possible these results may not be generalizable to the wider population of ME/CFS patients. But the researchers say their work is already providing some important clues to how the condition actually causes people’s symptoms.
They found no clear differences in how the muscles of those with CFS/ME worked that would explain people’s unusual fatigue in performing physical tasks, for instance. But they did find strange patterns of brain activity in people’s motor cortex during these tasks. It’s possible, the authors argue, that the immune and other disruptions seen in ME/CFS cause dysfunction in the brain regions that unconsciously affect our perception of the body’s ability to exert itself. This dysfunction could then lead to a long-term reduction in people’s physical activity, causing other bodily changes that only make it harder for them to perform once-normal tasks.
“We may have identified a physiological focal point for fatigue in this population,” said lead Brian Walitt, an associate research physician at NINDS, in a statement. “Rather than physical exhaustion or a lack of motivation, fatigue may arise from a mismatch between what someone thinks they can achieve and what their bodies perform.”
If Walitt and his team’s hypothesis is correct, then it might be possible to reverse these changes by attacking the root causes of ME/CFS, such as drugs that can clear the foreign antigens that are sending the immune system into overdrive. They also found differences between men and women with ME/CFS, however. So it’s possible that a combination of treatments, geared to a person’s personal biology, will be needed to truly treat the condition. For now, though, these findings should lead to new avenues of research and possibly hope for ME/CFS patients in the near future.
“Now researchers can test whether these findings apply to a larger patient group and move towards identifying treatments that target core drivers of the disease,” said Koroshetz.
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