• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

In the brain, energy and ATP produced by the MYELIN SHEATH mainly, and not the mitochondria, study suggests!


Senior Member
I was recently watching a video by Dr Karl Morten of the Morten Group in Oxford, a very interesting ME/CFS research group focused on the role of bacteria in ME/CFS, among other things.

At timecode 20:30 of the video, Dr Morten points out that the mitochondrial density in the brain is only 5%, whereas in other organs like the heart, kidney and liver, the mitochondria density is 20% to 40%.

This is perplexing, since the brain uses about 20% of the oxygen in the body, and is a major consumer of the body's energy. So Dr Morten asks: how can the brain, which is a such a great consumer of energy, have so few mitochondria?

Dr Morten then refers to a 2011 study which suggests that in the brain, it is the myelin sheath around the neurons which makes much of the brain's energy. The study hypothesizes that oxidative phosphorylation takes place in the myelin sheaf of neurons, and makes ATP.

Dr Morten thinks this could have significance for ME/CFS.

It's well worth watching the whole video by Dr Morten, as he runs through the various intriguing areas of ME/CFS research that the Morten Group in Oxford are focused on.

The Morten Group are interested in bacterial etiologies of ME/CFS, and interested in phenomena like: the mechanisms behind PEM, factors in the blood that influence mitochondrial function, the role of microbes in the gut in ME/CFS, the role of bacterial toxins in ME/CFS, intestinal hyperpermeability (leaky gut) in ME/CFS patients, the presence of L-form bacteria in the tissues of ME/CFS patients, and raman spectroscopy of the blood of ME/CFS patients.

The Morten Group Facebook page here. Like many ME/CFS research groups, the Morten Group is dependent on funding to continue the work. Their donation page is here.


Senior Member
If there was an issue with the myelin sheath, this would make the ME pathophysiology similar to the MS pathophysiology in that regard. The question, like always, in which brain areas it happens or if it affects the whole brain.

But air hunger doesn't necessarily mean that the brain doesn't get enough oxygen overall. It might just be a missense.

I have always assumed a lack of oxidative phosphorylation as part of my hypotheses, or rather a lack of oxidative capacity in general. This means that despite the oxygen concentration in the blood, only little of it is metabolized. How long can you hold your breath and how fast does your blood oxygen drop? I can surprisingly long for an unfit person, not that I recommend challenging it though. Oxidative phosphorylation is also required by mitochondrial ATP generation but I presume that much more ATP is produced per enzymatic iteration.

It might also be worth looking into specific lymphocyte subsets that are associated with ME and how their ATP/ADP status is and their mitochondrial status. It might explain their dysregulation as well, or not at all. The same counts for peripheral nerve cells.