Increased Resting Energy Expenditure in the Chronic Fatigue Syndrome, 2011, Watson et al

[forestglip]

Increased Resting Energy Expenditure in the Chronic Fatigue Syndrome
Walter S. Watson, Donald C. McMillan, Abhijit Chaudhuri, Peter O. Behan

Abstract
It has been suggested that resting energy expenditure may be raised in chronic fatigue syndrome due to an upregulation of transmembrane ion transport. We measured resting energy expenditure by indirect calorimetry in 11 women with chronic fatigue and in 11 healthy women. Total body potassium, by whole body counting, and total body water, extracellular water and intracellular water, by a bioelectrical impedance method, were also measured.

When individual resting energy expenditure was predicted on the basis of total body potassium values for the chronic fatigue group, 5 out of 11 of these subjects had resting energy expenditure above the upper limit of normal as defined by the control group data. This is consistent with the hypothesis that there is upregulation of the sodium-potassium pump in chronic fatigue syndrome.

Link (Journal of Chronic Fatigue Syndrome) [Paywall]

 

[SNT Gatchaman]

Sci-Hub: https://sci.bban.top/pdf/10.1300/J092v04n04_02.pdf

 

[forestglip]

It has been proposed recently that cardiac thallium-201 uptake abnormalities seen in a group of patients with chronic fatigue could be secondary to a cell membrane abnormality resulting in an abnormal efflux of intracellular ions such as potassium (3). This hypothesis was first suggested to explain the similar cardiac abnormacties seen in Syndrome X (4). If the hypothesis applies in chronic fatigue, then it would be expected that the sodium-potassium pump would be upregulated in an effort to maintain intracellular integrity. Approximately 30% of resting energy expenditure is associated with the maintenance of transmembrane ion gradients ( S ) , therefore, upregulation of this process could well bring about a measurable increase in resting energy expenditure.

It's a bit hard for me to follow, but I think in essence, they found that there was a strong correlation between potassium and resting energy expenditure in healthy controls. (black dots, n = 11, r = 0.89, p = 0.0003). They also found that CFS group seemed to be significantly higher than the predicted regression line, with five participants out of eleven higher than 2 standard deviations above the mean of the controls in terms of distance from that line.




They also did not find a significant difference in the raw energy expenditure values between the groups.

So energy expenditure in CFS is higher than one would expect based on a person's total body potassium, which is a good predictor of EE in healthy people.

I checked the data from the deep phenotyping study to see if it matches, and it doesn't seem to replicate this, though I'd welcome someone to make sure I didn't interpret this incorrectly.

There does not appear to be a strong correlation of energy expenditure to potassium in controls:


And energy expenditure normalized to potassium doesn't seem to be higher in ME/CFS:

Mann-Whitney test p-value = 0.58

Edit: See next post.

 

[forestglip]

Okay, this study is using total body potassium, which I don't think would actually correlate well with the plasma potassium measured in the NIH study (I assume that's what the potassium test was, found in the "clinical master labs" dataset. Only 2% of TBK is plasma potassium. So ignore my analysis of the NIH study above. I don't think it has the data to test this.

 

[forestglip]

Another study did report that in paraplegia, energy expenditure has an even stronger correlation with total body potassium than it does with fat free mass (0.86 vs 0.80):

Body composition changes occur with spinal cord injury (SCI): fat-free mass (FFM) decreases and fat mass (FM) increases. FFM has been reported to correlate with resting energy expenditure (REE) in non-SCI individuals. This report addresses the question as to whether REE correlates with measures of FFM in individuals with paraplegia. Twelve males with chronic paraplegia had measurements of total body potassium (TBK), an indicator of lean tissue, by whole body 40K counting, and FFM by dual photon x-ray absorptiometry (FFMdpx). REE was measured using a metabolic cart for exhaled gas analysis. Correlations between REE and TBK, and REE and FFMdpx were determined. The mean TBK for the group was 2,850 ± 190mEq. In all subjects, TBK was below that of expected (predicted from age, height, and weight). For the group this was 34 ± 0.04% below predicted. The mean FFMdpx was 58.3 ± 3.3kg. Following an overnight fast, REE was measured for each subject while in a seated position. The mean REE was 1,855 ± 70kcal/day. REE correlates well with both TBK (r = 0.86, p < 0.0005) and FFMdpx (r = 0.80, p < 0.005). In summary, despite losses in metabolically active tissue in individuals with chronic paraplegia, TBK and FFMdpx continue to have a strong relationship with REE. REE (kcal/d) may be used as an indicator of TBK or FFMdpx using the following linear regression equations: TBK (mEq) = 2.28 · REE (kcal/d) − 1,377 (SEE = ±347) or FFMdpx (kg) = 0.038 · REE (kcal/d) − 11.5 (SEE = ±7). In conclusion, a reduction in FFM is associated with a reduction in REE in chronic paraplegia.