The ICanCME Collaborative Conference on Myalgic Encephalomyelitis (ME) is a virtual conference driven by people with ME and their loved ones held between November 4th and November 6th. The conference is fully virtual and free to make it more accessible to people with ME. I’ll also be posting live updates on X.

Day 1: ME Foundations and Current Research Landscape

Maya Dusenbery | Women's Health and "Unexplained" Chronic Illness: How Gender Bias Leads to Medical Neglect

Maya Dusenbery is a journalist and author of Doing Harm: The Truth About How Bad Medicine and Lazy Science Leave Women Dismissed, Misdiagnosed, and Sick. 

After being diagnosed with rheumatoid arthritis, Dusenbery started getting a deeper interest in women’s healthcare and disparities. She found that the medical care system was not well-equipped to diagnose and care for women.

Women have more vulnerability to autoimmune diseases but they also experience long diagnostic delays and dismissal for malingering, or having to navigate doctors that don’t have the relevant training. After interviewing almost 200 woman, she identified two big problems that are affecting women’s healthcare that are also relevant to ME, a knowledge gap and a trust gap.

The Knowledge Gap

Women have been historically underrepresented in clinical research. Policies originally excluded women in favor of studying men, who were simpler to study (no hormones) making trials more cost effective.

She highlighted one pilot study looking at obesity in breast and uterine cancer that didn’t enroll a single woman. Though the NIH Revitalization Act in 1993, researchers had to start including women. But clinical researchers sometimes still fail to take into account sex and gender differences. Still, many animal studies even in the 2000s were only conducted using male animals, even for diseases predominantly affecting women.

​The other factor contributing to the knowledge gap is that these findings are still slow to trickle into medical practice. Doctors are less equipped to diagnose and treat women’s conditions.

The Trust Gap

Dusenbery looks at the history of hysteria, evolving from descriptions of a wandering womb in ancient times to psychosomatic explanations for medically unexplained symptoms. These symptoms in women are frequently minimized, normalized, or blamed on emotions, stress, or malingering.​

Class and race also plays a role, with marginalized women less likely to get timely care. “You’re either stoic and nothing is wrong, or you’re crying and being hysterical,” she explained. Doctors also aren’t getting feedback that they’re making diagnostic errors.

A History of ME and Gender Bias

While the earliest outbreak of ME in 1955 that struck 300 doctors and nurses was taken seriously and investigated as an infection, influential psychiatrists argued that it was hysteria since most of the people affected in the outbreaks were young women. Part of it relates to stereotypes of women, like being overextended or trying to combine family and career, as legitimizing the “fatigue.”

In terms of research funding, ME like other diseases predominantly affecting women is also underfunded. That’s the “catch-22” in women’s health: unexplained illnesses are presumed psychosomatic until proven otherwise, but little effort or funding is devoted to studying these conditions, so proof never materializes.

“I think that the history of me is a really good, tragic illustration of how the trust gap has directly contributed to the knowledge gap,” said Dusenbery. “It's really hindered our understanding of a very serious women's health condition.”

Todd Davenport, Professor at University of the Pacific | Exertion and PEM

Davenport focused on post-exertional malaise (PEM) and how you can measure it to differentiate people with ME from sedentary and otherwise healthy people. His work involves using two-day cardiopulmonary tests (CPET) to understand the underlying pathophysiology of PEM.

I was surprised to learn that PEM was only defined in the scientific literature in 1991, about 36 years since ME was first coined. He also introduced another piece of lingo, post-exertional neuroimmune exhaustion which is functionally equivalent to PEM but might better represent all the changes that occur after exertion.

The two-day CPET makes it remarkably clear who has ME: “As time goes on during recovery, fewer symptoms are necessary to differentiate between normal and impaired exercise recovery response.”

This model of physical exertion is standardized and also accepted by many insurers for disability claims. However, cognitive and other forms of exertion can also lead to PEM. Importantly, PEM is very personalized: Some people recover faster than others, some people might take a week or longer to recover while others might bounce back sooner.

Rob Wüst, Assistant Professor at Amsterdam UMC | Skeletal muscle alterations and post-exertional malaise in Long COVID and ME

Wüst discussed his work looking at skeletal muscle alterations in PEM and also presented new, unpublished data. This summary will only focus on the work that has already been published.

His team takes biopsies before and one day after CPET to see how PEM affects the muscle tissue. In his Nature Communications study published last year found changes in the mitochondria and muscle tissue that differentiated Long COVID rom the healthy controls who recovered from an infection. After exercise, people with PEM showed more muscle damage. To address some of the criticism of the study, the team also found similar differences when comparing Long COVID and ME patients to people who are deconditioned.

He also talked about the growing number of people with ME using wearables to track heart rate variability to stay below their PEM threshold.

Is the mitochondria the key to PEM? His team is involved in an upcoming Phase 2 study of a drug called sonlicromanol to see if it could improve mitochondrial function, up exercise capacity, and increase the PEM threshold while lowering its duration.

The take home: PEM is not fatigue or deconditioning. There’s something going on in the muscles and mitochondria that they hope they can disentangle and treat.

Danielle Beckman, Neuroscientist at UC Davis| Cognitive Dysfunction - Lessons We Can Learn from Long COVID

Beckman provides a broad overview of the evidence showing that SARS-CoV-2 can infect brain cells and the blood vessels that feed them. In her own research, Beckman uses microscopy to understand the physiological and cellular alterations associated with infection that may lead to cognitive dysfunction.

Neuroscientists used to believe that the brain was immune-privileged. Now, there’s more evidence that viruses, bacteria, and microplastics do get to the brain. They get there through olfactory or trigeminal nerves, or through the blood stream. SARS-CoV-2 enters through the olfactory system or the blood stream.

What are we seeing in the real world? In studies that track people’s electronic health records, we see that older adults who are infected are more likely to develop dementia within the next few years. (Simon note: From what I’ve covered in other outlets, it seems like SARS-CoV-2 might speed up processes that might already be occurring in the brain, building up for decades, sparking the decline. Also emerging studies suggest that vaccines could reduce dementia risk.)

Beckman connects these cellular changes to brain imaging studies showing changes in brain volume after SARS-CoV-2 infection. She’s also very hopeful about the research that’s comparing the brain of healthy controls to people with Long COVID and ME. One study she presented found changes in lactate levels that were specific to people with ME.

“It’s not your fault, it’s not your imagination. It’s physical,” said Beckman.

Akiko Iwasaki, Professor at Yale School of Medicine | Deep Immune Profiling

Iwasaki focused on auto-immunity, discussing her research looking at the IgG class of antibodies. Most of the research she presents comes from a pre-print, meaning the research is published but not yet peer-reviewed.

They took IgG antibodies from healthy controls, people who were infected with SARS-CoV-2 but recovered, and those with Long COVID. They put these antibodies on slices of nerves and brains from mice and humans, and saw that the Long COVID antibodies seemed to bind the most. This suggested that their antibodies might be attacking healthy tissue.

They injected the IgG into mice to see if that would change their behaviors or make them more sensitive to pain. IgG from people with Long COVID who had headaches made mice more sensitive to pain caused by a hotplate. Their neurons and nerve fibers also appeared to be damaged after receiving the IgG.

If these findings are replicated by other researchers, and shown in Long COVID and ME, it may imply that a subset of these symptoms might be explained by antibodies attacking healthy tissue.

Amy Proal, PolyBio Research Foundation | Infections and the Damage They Cause

Persistent viral infection might play a role in ME, argues Proal. She started off her talk discussing the research conducted by John Chia that looked at enterovirus infection in ME, which provided some of the earliest evidence for this idea.

The challenge with finding these viruses is that they might stick around in different tissues. In the context of ME, the brainstem might be an important place to look because of its connections to the vagus nerve and other key clusters of neurons. This might explain some of the symptoms including PEM, cognitive dysfunction, autonomic problems, and sleep problems.

Different infections caused by tick-borne diseases and viruses might affect similar pathways leading to similar symptoms. Until recently, we didn’t the molecular and diagnostic tools to detect this persistence. To accelerate our capacity, the PolyBio Research Foundation has donated to UCSF for the LIINC project that will look for evidence of persistent viral infection across many different tissues in people with ME.

Dr. Daisy Fung | A Canadian Family Medicine Perspective

Despite being a doctor, Fung who lives with ME, still faced skepticism and disbelief from her colleagues. They attributed her medical symptoms to depression, conversion disorder or other neurological issues.

People with ME face barriers to care from insufficient medical education, rushed clinical appointments, doctor’s discomfort with uncertainty, and the general dismissal of symptoms.

Although there is no cure for ME, there are still plenty of things that primary care doctors can do: Advise PEM, aggressive rest, compression socks, hydration and increased salt intake, and treating some symptoms before even seeing a specialist. Low risk, low cost interventions like antihistamines might be worth trying out.

Fung advocates to a team approach for care that involves social work, ME-informed physiotherapy (not graded-exercise therapy), and home care. She highlighted the needs of caregivers as well.

Fung argues that family doctors should the first-line of care, not a barrier for getting help.

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I'm a science and health journalist who is disappointed and fed up with the lack of news coverage surrounding Long COVID, ME/CFS, chronic illness, and disability issues in Canada. I decided to start this newsletter to provide a home for the news stories that don’t get coverage in Canada’s news ecosystem, which lacks outlets for good, science-based reporting.