Elevated Energy Production in Chronic Fatigue Syndrome Patients


Senior Member
This hyper/hypo energy production study on corts site deserves its own thread
Does it help explain PEM as well,if the energy production cycle is revved up just to put out minimal energy then when higher demand is placed on it,the demand cannot be met.
As a side note FOXO genes are considered tumour surpressors


Senior Member
In this article, Dr John McLaren-Howard very nicely explains the likely reason for this apparent contradiction in results from the Lawson et al study (which found higher than normal ATP levels the cells of ME/CFS patients), and the Myhill, Booth and McLaren-Howard study (which found lower than normal ATP levels the cells of ME/CFS patients).

The likely reason for this contradiction is this: the Lawson study used cultured cells (cells taken from ME/CFS patients and then grown in vitro), and McLaren-Howard says using cultured cells would likely fail to account for the effects of any mitochondrial blocking agent that was present in the blood and in the original cells taken from ME/CFS patients.

This is because as you grow new generations of cells in vitro, the blocking agent that was present in the original cells taken from the ME/CFS patient will get diluted down in the new cells, so that the agent will no longer block the mitochondria. Thus the previously blocked mitochondria in the ME/CFS patients' cultured cells are then able to start functioning normally again, and thereby increase their ATP production.

By contrast, the in the Myhill, Booth and McLaren-Howard study, they used cells taken directly from the ME/CFS patients' blood, so they tested the actual cells freshly extracted from the ME/CFS patient.

Dr John McLaren-Howard explains it thusly:

This also links up to the latest metabolic findings from Fluge and Mella, where they found that healthy muscle cells (myoblasts), when exposed in vitro to the blood serum of ME/CFS patients, developed energy metabolism alterations, including excessive lactate secretion. This finding suggests that there is a mitochondrial blocking agent in the blood serum of ME/CFS patients.

Thus if you grow new cells in vitro, outside of the blood of ME/CFS patients, as they did in the Lawson study, those cells will be healthy and function normally, as they will not be exposed to the blocking agent in the blood. It's the blocking agent in the blood that is the likely cause of the energy metabolism dysfunction in the cells of ME/CFS patients.
Great post Hip!!

You have summarised my first resonse to the article (that these cells were out of the normal serum environment).

I did not immediately consider metabolic blockings factors - though that is a good point well made.

I did however consider the general metabolic support available in serum. Things like fuel availability (Glucose or Fatty Acids) levels of Vitamins, Minerals, Amino Acids, Catechols, Cortisol and Thryoid hormones. All of these things will affect cellular performance. The chemical baths used to grow these cells will more than likely have optimsed all relevant items and will not have reflected the situation in the patients own serum.