A question about mitochondria

[Arnie Pye]

I'm not a scientist, so bear that in mind if you read this and think I'm asking a stupid question.

I've been thinking about mitochondria. Various quotes from the wikipedia article about them :

Mitochondria have a double membrane structure and use aerobic respiration to generate adenosine triphosphate (ATP), which is used throughout the cell as a source of chemical energy.[

The mitochondrion is popularly nicknamed the "powerhouse of the cell"

n addition to supplying cellular energy, mitochondria are involved in other tasks, such as signaling, cellular differentiation, and cell death, as well as maintaining control of the cell cycle and cell growth.

The number of mitochondria in a cell can vary widely by organism, tissue, and cell type. A mature red blood cell has no mitochondria,[19] whereas a liver cell can have more than 2000.

There are many mitochondrial diseases known and some are listed in this link :

https://en.wikipedia.org/wiki/Mitochondrial_disease

I gather that mitochondrial diseases occur due to problems with the DNA in the mitochondrion of a cell.

Getting to my actual question...

Is it possible for a healthy cell to have, say, 2000 mitochondria, then when the "owner" of that cell catches an infection, either viral or bacterial, the number diminishes to, say, 1000 but leaves the cell able to continue to live and function but when it divides it creates "offspring" with just a 1000 mitochondria?

I was wondering whether there could be no obvious disease in a cell, but instead just too few mitochondria to produce the required amount of energy for the cell to do its job.

 

[Creekside]

Also no expert, but I get the impression that number of mitochondria in a cell is relatively easy to measure, and a distinct difference between cells in PWME vs people without ME would have been noticed already.

 

[Adrian]

I thought the idea that some were talking about was that its not the mitrocondria that are bad but the signalling to them so they are not functioning as required. But I've not been following closely.

 

[Arnie Pye]

I thought the idea that some were talking about was that its not the mitrocondria that are bad but the signalling to them so they are not functioning as required. But I've not been following closely.

I haven't come across that idea about signalling. Do you have a link?

 

[Adrian]

I haven't come across that idea about signalling. Do you have a link?

No and perhaps that means I'm talking rubbish - I thought I had heard people talking about the mitrocondria not performing correctly but not due to structural issues (which could be what happens in typical mitrocondrial disease). Hence the issue of signalling (i.e. not producing energy when needed as something is going wrong in the produce more energy signal).

 

[Jonathan Edwards]

o and perhaps that means I'm talking rubbish

Not a bit of it. That is exactly what we have been discussing on threads here for years!!

 

[poetinsf]

I was wondering whether there could be no obvious disease in a cell, but instead just too few mitochondria to produce the required amount of energy for the cell to do its job.

I reject mitochondrial theory on the account that it doesn't explain PEM. If the problem is energy production, the result should be similar to that of COPD or obesity. Some people say that people with mitochondrial disease also suffer from PEM, but it's more like vague post-exercise fatigue, not PEM. PEM is a whole bunch of symptoms getting worse after a precise delay. Mine used to roll in like a truck almost exactly 24 hours when I was in severe/moderate end.

 

[Creekside]

poetinsf makes a good point: where's the weight gain expected from mitochondrial dysfunction? Some PWME gain weight, while others lose weight.

 

[Yann04]

Don’t know if anyone has experienced this, but after meticulously tracking weight, I realise that I gain weight when pacing well and loose weight in PEM episodes

 

[Arnie Pye]

I reject mitochondrial theory

I have done some reading (but not a lot) on the subject of mitochondrial health, and I thought that mitochondrial disease was caused by a fault in the mitochondrial DNA. I assumed that if no fault was found in the DNA then the patient was assumed to not have a mitochondrial fault. That's why I wondered about the numbers of mitochondria in a cell.

 

[SNT Gatchaman]

I don't think mitochondrial function in cells is dependent on numbers, so much as quality. And mtDNA is not the only determinant. There's a whole field of mitochondrial quality control research, looking at eg mitophagy (mitochondrial autophagy), fission/fusion kinetics etc. The NIH WASF3 and DMissa's studies showed problems in the electron transport chains that may not relate to their DNA.

I haven't read it but here's a very recent and quite long review article which is open access Mitochondrial quality control in human health and disease (2024, Military Medical Research)

 

[Creekside]

I realise that I gain weight when pacing well and loose weight in PEM episodes

I never noticed any weight changed due to PEM, but all my PEM episodes only lasted <24 hrs. It would be interesting to see whether there are any interesting correlations among people who regularly suffer much longer PEM episodes. Of course you'd have to correct for diet changes and physical activity changes.

 

[Lindberg]

Don’t know if anyone has experienced this, but after meticulously tracking weight, I realise that I gain weight when pacing well and loose weight in PEM episodes

The same for me. I had to eat day and night during my worst PEM crash. The body burned energy like never before while being bedridden. I lost a lot of weight until the body stabilized.

 

[Frith]

Last week I had an online “Initial Appointment Group Session” with my local ME clinic, slightly behind schedule as I ‘celebrate’ 37 years at the end of this month. I’ve no idea what they thought I’d gain from it but I went along with it just to keep on their books.

It started fairly uncontentiously with a PowerPoint presentation mostly cribbed from a BACME document on dysregulation in ME, and then hit us with this explanation for PEM (copied and pasted from the slides):

“One of the main chemicals producing energy for everything we do and feel comes from Adenosine Triphosphate (ATP) which is produced in our energy factories commonly called the mitochondria

In ME/CFS the energy factories struggle to reproduce and store energy efficiently. When you complete activities you get to the stage where you run out of energy leading to no available ATP causing a ‘crash’

After a crash it can take the body up to 3 days to begin making ATP again.

When your body does not have enough energy to run it triggers the stress response commonly known as the ‘fight or flight system’”

My understanding of ATP is that of the most forgetful layman but making no ATP for three days sounds very much like being dead for three days to me.

I did ask them where they got this interesting fact from but was pretty much shut down, both by other participants (apparently it was ‘quite nasty’ of me to ask) and by the people running it, who said that the explanation is in the BACME document. To be fair to BACME, they make no such claim.

 

[Creekside]

They found an easy (for them) explanation, and of course don't want challenges to that. If they're crediting a source falsely, you might consider reporting that to their superiors.