Reply to Lawson Paper on "Elevated Energy Production" in CFS patients

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In 2016, Nick Lawson, Chung-Han Hsieh, Dana March, Xinnan Wang published a paper with the title "Elevated Energy Production in Chronic Fatigue Syndrome Patients" in the Journal of Nature and Science (J Nat Sci 2016; 2(10):e221. The full paper can be viewed here:

"Elevated Energy Production in Chronic Fatigue Syndrome Patients" Nick Lawson, Chung-Han Hsieh, Dana March, and Xinnan Wang

At first sight, the conclusions of this paper may seem to be at odds with the three papers that I have co-authored on mitochondrial dysfunction.

Lawson et al conclude that:

"To thoroughly reveal mitochondrial deficiencies in CFS patients, here we examine the key aspects of mitochondrial function in blood cells from a paired CFS patient-control series. Surprisingly, we discover that in patients the ATP levels are higher......"

This compares with the conclusion that Professor Norman E. Booth, Dr John McLaren-Howard and I came to in our first published paper, "Chronic fatigue syndrome and mitochondrial dysfunction":

"Our observations strongly implicate mitochondrial dysfunction as the immediate cause of CFS symptoms."

Our first published paper can be found here - "Chronic fatigue syndrome and mitochondrial dysfunction"

This conclusion of impaired energy production in CFS patients was supported by our two subsequent papers which can be found as below:

I explain these ideas in more detail on my webpage - CFS - The Central Cause: Mitochondrial Failure

Explanation of this apparent conflict

Dr John McLaren-Howard has produced the note below to explain this apparent conflict. The note is reproduced in full with John's permission.

Full text of John McLaren-Howard note

On initial perusal of the title, the following paper may initially seem to be a contradiction of our test findings in CFS/ME patients. However, closer examination of the contents of this publication leads to some very important possibilities.

Ref: Nick Lawson, Chung-Han Hsieh, Dana March, Xinnan Wang. Elevated Energy Production in Chronic Fatigue Syndrome Patients. J Nat Sci 2016; 2(10):e221

The authors conclude that CFS/ME patients have higher ATP levels that controls. Their work was done on cultured cells while all of our test data is on the patients’ cells as separated from a whole-blood sample. So why the difference?

About 35% of our abnormal ATP-profiles show chemical blocking of ADP to ATP re-conversion at the translocator (TL) sites of the inner mitochondrial membranes and over 90% show poor ADP to ATP re-conversion even if TL-sites are not apparently blocked. This presumably reflects other problems with the electron-transport chain (oxidative phosphorylation). That could include chemical or metabolic blocking of one-or-more of the enzyme complexes.

If the ATP levels are measured on cultured cells the effect of any blocking agent may be negated. For argument’s sake, let’s take a situation where 20% of the TL sites are blocked by a chemical we will call X. If the cells are cultured the ‘new’ cells will be unaffected by the blocking agent X which is not itself cultured: X probably being an environmental chemical, drug or metabolic biochemical. In our hypothetical example, when in the culture 10 times the original cell number is reached only 2% would be affected by X. When a very moderate amplification of 100 times the cell numbers is reached only 0.2% of the cells would be affected by X etc etc…………

The changes we see in terms of the blocking of TL sites and other chemical interferences are negated when cultured cells are used to assess ATP metabolism in CFS/ME patients. That being the reason why I rejected the use of cultured cells during the development of the ATP-profile performed here.

BUT, this paper does reflect exciting work. It demonstrates the ability of the ‘new’ cells to produce increased levels of ATP. This supports what many doctors have reported to me and what has been my own experience. When steps are taken to eliminate blocking chemicals, whether affecting TL sites or interfering with steps in the electron-transport chain, and/or substrate deficiencies are addressed, there are almost always clinical improvements. These can be dramatic, moderate, but very welcome by the patients, and sometimes only mild. In the latter cases there is clearly more to learn although it often pivots on renewed individual assessment rather than some as yet unknown scientific area.

I am very grateful to the authors of the above paper for their work and contribution although I could wish they had chosen a different title in order to avoid confusion.

If I can find the time I will carry out some comparisons between the ATP in cells directly from CFS patients and in the cultured cells. It would be of even greater value if this was assessed by a third party laboratory.''

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