The most comprehensive metabolomics study to date came up with a plus – a new kind of “comic: analysis – lipidomics – the study of fats
Widespread changes in amino acid and lipid metabolites pointed to a possible dysfunction in energy production.
This study suggested as past studies have, that the cells of people with ME/FS are trying to get a hold of energy in any way they can. Instead of relying on carbohydrate metabolism for a clean source of energy, they’re turning, for some reason, to “dirty fuels” such as fatty acids and amino acids.
Despite the fact that people with ME/CFS are neither starving nor are engaging in intensive exercise, their metabolic and lipid results are similar to those found in starvation and after intensive exercise. The authors proposed that the metabolic systems in ME/CFS are stressed even while they are at rest.
While a core metabolic issue seemed to be present in all the ME/CFS patients, three subsets of patients could also be identified. The authors proposed that the three subsets represented different ways the cells of people with ME/FS are attempting to compensate for their metabolic deficiencies.
One group – the M1 group (about 40%) was characterized by high degrees of fatty acid and amino acid breakdown. High levels of ketone derivatives also suggested this group had a ketogenic slant. Little evidence of mitochondrial problems was found, and the authors characterized this as the “lipolytic” group. Their metabolic profile was similar to that seen in starvation and after high-intensity exercise.
The M2 group (about 45%) displayed increased fatty acid breakdown but was characterized more by increased amino acid breakdown. Evidence of mitochondrial dysfunction (high pyruvate levels) was also found. This group, which had the most severe symptoms, had similar metabolomic/lipidomic profiles to diseases characterized by inflammation.
The M3 group (@15% of the study) appeared to be intermediate between the healthy controls and other ME/CFS groups but was too small to be assessed statistically.
Calling ME/CFS an “immunometabolic” disease, the authors posited that an autoimmune reaction is impairing blood flows to the tissues and pointed to a finding suggesting that the oxygen in the blood is not getting to the mitochondria.
The idea that blood flow problems are playing a key, even central role in ME/CFS has gained traction lately with these authors, Wirth and Scheibenbogen, Systrom, Shungu, and others proposing it.