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details. Hi,

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this is Your Health Quickly, a Scientific

0:33

American podcast series. We bring you

0:36

the latest vital health news, discoveries that

0:38

affect your body and your mind. And

0:40

we break down the medical research to help you stay

0:42

healthy. I'm Tanya Lewis. I'm

0:44

Josh Fishman. We're

0:47

Scientific American senior health editors. Today,

0:51

we are delving into the disease

0:53

originally known as Chronic Fatigue Syndrome.

0:55

Now it's called ME CFS. Recently,

0:58

a big study looked at people who

1:00

got the illness after an infection, and

1:03

it turned up a few clues

1:05

about what might be causing their

1:07

debilitating and often lifelong symptoms. The

1:13

disease once called Chronic Fatigue Syndrome

1:15

has historically been dismissed by doctors

1:18

and other healthcare professionals as a

1:20

psychosomatic illness without any real physiological

1:22

causes. In recent years,

1:24

researchers have begun to take the

1:26

disease, whose official name is now

1:28

Myalgic Encephalomyelitis slash Chronic Fatigue Syndrome,

1:31

or ME CFS for short. More

1:33

seriously. That really is a mouthful,

1:35

and I'm not even going to try it, but

1:37

Tanya, what does it mean? Well, it

1:40

comes from myalgia, which means muscle

1:42

pain, and encephalomyelitis, which is inflammation

1:44

of the brain and spinal cord

1:46

due to an infection. And

1:48

while it's sometimes referred to as just Chronic

1:50

Fatigue Syndrome, people with ME CFS prefer to

1:52

call it ME because it's really more than

1:55

just fatigue. And during the

1:57

COVID pandemic, millions of people developed

1:59

something that was very,

2:01

very similar to ME CFS

2:03

symptoms. And that's a long COVID. So

2:06

scientists started taking that a lot more

2:08

seriously. Even before the pandemic, I know

2:11

the National Institutes of Health was

2:13

starting to study ME CFS. Yeah,

2:15

that's right. So Francis Collins, who

2:18

was the director of NIH at the time,

2:20

approached a scientist named Avindra Nast and asked

2:22

him to launch a comprehensive study of people

2:24

with ME CFS to really try and find

2:27

some clues as to what was causing

2:29

their exhausting symptoms. Yeah, like you said,

2:31

in addition to fatigue, there's a whole

2:33

bunch of other very serious problems.

2:36

People with ME CFS often

2:38

experience brain fog, hypersensitivity to

2:40

light, and short-term memory problems.

2:43

And another really common issue is

2:45

something called post-exertional malaise. It's

2:47

basically a worsening of your symptoms after

2:49

any kind of physical activity. And

2:52

there really aren't any good treatments for it.

2:54

I've known some people with ME CFS, and

2:58

it can be really devastating. Yeah, it

3:00

really can. So starting in

3:03

2016, Avi and his colleagues set out to study

3:05

this, but since ME CFS is sort of an

3:07

umbrella term for a wide array of disease forms,

3:10

they wanted to find a group of

3:12

people who fit a very specific patient

3:14

profile. They specifically recruited people who had

3:16

developed the disease after an infection, and

3:19

they also had to be well enough to travel to

3:21

NIH for the experiments. They ended up with a total

3:23

of 17 participants with ME

3:25

CFS and 21 healthy volunteers.

3:28

Next, they set about putting the participants through

3:30

a whole series of tests of

3:32

pretty much every organ system. I'm

3:35

Avi Nath. I'm the Clinical Director of

3:37

the National Institute of Neurological

3:39

Disorders and Stroke, and also the Chief

3:41

of the Section of Infections of the

3:43

Nervous System. We did a very thorough

3:46

investigation, looking at MRI

3:48

scans, cognitive function. We did spinal

3:50

taps, lots of blood draws. At

3:53

various time points, we looked

3:55

at the immune function metabolomics.

3:57

We looked at the gut microbiome. We looked at...

4:00

their heart rates and blood

4:02

pressures and autonomic function. I

4:05

know that it was a really complete workup.

4:08

What did they find? A lot of this

4:10

is described in an online news story written by

4:12

Kamal Nahas, which we'll link to in the transcript.

4:15

Here's Avi. We found that

4:17

there were multiple systems that were

4:19

involved. It wasn't a single abnormal

4:22

observation. We found that there were

4:24

a number of abnormalities. Then

4:26

we found that there was activation of the

4:28

immune system in the ME CFS patients. It

4:31

was almost like the immune system was

4:33

exhausted from being chronically activated. And

4:36

interestingly, we found that there were differences

4:38

between men and women, such that

4:40

women had predominantly B cell pathways that were

4:42

activated, and in men it was predominantly T

4:45

cell. And so

4:47

that in itself is a very important

4:49

observation because it tells us that what

4:51

may work for women may not work for men. ME

4:54

CFS occurs predominantly in women, but men can

4:56

obviously get it too. So treatment

4:58

could look different for men versus women. The

5:01

researchers also found differences in the brains and

5:03

nervous systems of people with ME CFS. We

5:06

found a lot of abnormalities in

5:08

the metabolites and the neurotransmitters. We

5:11

tested the brain in many different ways

5:14

by stimulating the brain with transcranial magnetic

5:16

stimulation and a functional

5:18

MRI scan. And whereby

5:20

you can look at the metabolism of

5:22

the brain in a resting

5:24

state when you exercise the brain.

5:27

In order to exercise the brain, we did

5:29

a simple motor task. We

5:31

found that the motor cortex itself was

5:33

fine, but there's an area

5:36

of the brain that integrates

5:39

all the information together, and

5:41

it's at the junction of the temporal and the parietal

5:43

lobe. And we found that

5:45

that was inactive. It's not a

5:47

structural abnormality, it's a functional abnormality.

5:50

Avi says this functional brain abnormality

5:52

might explain the post-exertional malaise that

5:54

many people with ME CFS experience.

5:58

But it's a pretty preliminary finding. Right,

6:00

that doesn't really seem like it

6:02

would explain the whole story. Right,

6:05

probably not. I actually talked to

6:07

one of the study participants, a journalist named

6:09

Brian Fosthogg. Oh, Brian is

6:11

actually a friend of mine. He's

6:14

the reason that NIH started doing

6:16

this study because he wrote

6:18

a op-ed in The Washington Post

6:21

complaining that scientists weren't studying ME-CFS

6:23

enough. That's really interesting. I know

6:25

he's been a big activist for

6:28

people with ME-CFS. I've

6:30

known Brian for a long time.

6:32

I've known him before he got

6:34

sick and after

6:36

he got sick. And I can tell you

6:38

it's made a huge

6:41

difference in his life. He was

6:43

a great journalist and

6:47

then he couldn't do that

6:49

anymore. He's a really bright,

6:51

very curious, and

6:53

very intelligent person.

6:57

And all of a sudden,

6:59

he just didn't have this body

7:01

that would let him follow through with

7:04

the things that he wanted to find out

7:07

about. Because he just

7:10

didn't have the physical ability. It was

7:12

kind of like having

7:14

this really bright mind locked in

7:16

this body that wouldn't

7:19

work anymore. Again, he doesn't

7:21

really know what caused it. I

7:23

had a sudden fever. It basically went

7:25

from being well to being sick in like

7:27

five minutes. It went very stark. He

7:30

actually had a false positive test for

7:32

West Nile virus, but they never actually

7:34

found the true pathogen. And I

7:37

asked him what he thought about the

7:39

study. I don't think he was too

7:41

thrilled about the results that Nath

7:43

was talking about before. The findings

7:45

were pretty meager. He

7:48

was so conflicted about how the study turned out. Yeah,

7:50

I mean he's glad they did the study, but he

7:52

didn't really think it found a whole lot that was

7:54

new. He also took issue

7:56

with the fMRI findings, which he thought was

7:58

not an appropriate test. and was only based

8:01

on a handful of participants. Overall

8:03

though, the study just may have been too small to

8:05

draw out strong conclusions. That

8:08

said, he did think the study helps

8:10

validate that ME CFS is a real

8:12

illness with real biological causes. And

8:14

that's important given that many doctors still dismiss

8:17

people with the disease, and we don't really

8:19

have that many treatments. Okay, that's

8:21

Brian. What about Avi? Does Avi think

8:23

the study will help lead to potential

8:26

treatments? Avi really hopes that this will

8:28

lead to treatments. Even though the

8:30

study didn't find so-called autoantibodies, which are a

8:32

sign that the body is attacking itself, like

8:34

some studies have found, it did

8:36

find signs of B and T cell wonkiness,

8:39

if you will. And the treatments

8:41

could depend on your sex. So in

8:43

women, you could try things like checkpoint

8:45

inhibitors, which are used as a type of

8:47

immunotherapy for cancer. And for

8:49

men, you might be able to try various T

8:51

cell therapies. I feel like they

8:54

need to do treatment trials, like that needs

8:56

to be the next step. Patients need

8:58

to do treatment. We can't just wait

9:00

to figure out the entire path of

9:02

physiology that we need to start. So

9:05

researchers are already testing some of these

9:07

therapies. Well, I'm glad to hear

9:10

that they're starting. But what about

9:12

long COVID? Could this research

9:14

benefit people with that? Yeah,

9:16

it might. There's certainly a lot

9:18

more interest in these conditions now, given how many

9:20

people have long COVID. That's really

9:23

important because ME, CFS, and long

9:25

COVID both take a real toll.

9:27

They ruin lives. I want people

9:29

to know that this is a

9:31

matter of life success.

9:34

You know, you try 100 different medicines, and

9:36

nothing ever helps you. It's really hard to

9:38

keep going. Your

9:42

Health Quickly is produced by Timmy Broderick,

9:45

Talika Bose, Jeff Delvicio, and by us.

9:48

It's edited by Ella Federer and Alexa Limb.

9:51

Our music is composed by Dominic Smith. Our

9:54

show is part of Scientific American's podcast, Science

9:56

Quickly. Subscribe wherever you get

9:58

your podcasts. If you like the show,

10:00

give us a rating or a review. And

10:03

if you have a topic you want us to cover,

10:05

you can email us at yourhealthquickly at sciam.com. That's

10:08

yourhealthquickly at sciam.com.

10:11

Just a quick request. My colleague, Lauren Young,

10:14

and I are working on a podcast series

10:16

on caregiving for older family members and

10:19

the challenges of navigating care at home

10:21

versus institutional care. We're

10:23

hoping to speak with people who have experience caring

10:25

for their own family members. Please

10:28

email yourhealthquickly at sciam.com with the

10:30

subject caregiving if you're interested. For

10:35

Your Health Quickly, I'm Tanya Lewis. And

10:38

I'm Josh Gifton. See you next time.