Metabolic profiling of an ME cohort reveals disturbances in fatty acid and lipid metabolism, Hanson, Levine et al, 2018

Dr Carrot

Dr Carrot

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Have had limited success with the search function here, so if this has been posted already, please delete.

Abstract

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) remains a continuum spectrum disease without biomarkers or simple objective tests, and therefore relies on a diagnosis from a set of symptoms to link the assortment of brain and body disorders to ME/CFS.

Although recent studies show various affected pathways, the underlying basis of ME/CFS has yet to be established. In this pilot study, we compare plasma metabolic signatures in a discovery cohort, 17 patients and 15 matched controls, and explore potential metabolic perturbations as the aftermath of the complex interactions between genes, transcripts and proteins. This approach to examine the complex array of symptoms and underlying foundation of ME/CFS revealed 74 differentially accumulating metabolites, out of 361 (P<0.05), and 35 significantly altered after statistical correction (Q<0.15).

The latter list includes several essential energy-related compounds which could theoretically be linked to the general lack of energy observed in ME/CFS patients. Pathway analysis points to a few pathways with high impact and therefore potential disturbances in patients, mainly taurine metabolism and glycerophospholipid metabolism, combined with primary bile acid metabolism, as well as glyoxylate and dicarboxylate metabolism and a few other pathways, all involved broadly in fatty acid metabolism. Purines, including ADP and ATP, pyrimidines and several amino acid metabolic pathways were found to be significantly disturbed. Finally, glucose and oxaloacetate were two main metabolites affected that have a major effect on sugar and energy levels. Our work provides a prospective path for diagnosis and understanding of the underlying mechanisms of ME/CFS.
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Link to full study: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5365380/
 
Just read this. It's interesting but obviously a small pilot that needs reproducing with a larger and possibly more comprehensive cohort (only used 17 women aged 42-68). Clearly needs an overlay in terms of men vs women, and severity for future studies. These were the things I picked out:

  1. Interesting that it confirms some other work in terms of disrupted metabolic pathways.
  2. Adds weight to the argument that we could and should have a metabolic profile as a future biomarker (identifies 35-74 possible metabolic markers)
  3. Puts a focus on liver function as an area for further study and an explanation for some of the symptoms.
  4. Puts tenuous links to the neurological aspects in terms of phospholipid metabolism
  5. Highlights that perhaps taurine and lipid supplementation may be possible avenues for treatment?
  6. Falls short of coming up with a unifying theory for disease onset and progression.
 
arewenearlythereyet said:
Just read this. It's interesting but obviously a small pilot that needs reproducing with a larger and possibly more comprehensive cohort (only used 17 women aged 42-68). Clearly needs an overlay in terms of men vs women, and severity for future studies. These were the things I picked out:

  1. Interesting that it confirms some other work in terms of disrupted metabolic pathways.
  2. Adds weight to the argument that we could and should have a metabolic profile as a future biomarker (identifies 35-74 possible metabolic markers)
  3. Puts a focus on liver function as an area for further study and an explanation for some of the symptoms.
  4. Puts tenuous links to the neurological aspects in terms of phospholipid metabolism
  5. Highlights that perhaps taurine and lipid supplementation may be possible avenues for treatment?
  6. Falls short of coming up with a unifying theory for disease onset and progression.
Click to expand...
Very interesting.
I tried reading it but flamed out so thanks for the synopsis
 
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