New research: distinct biological differences in M.E.
September 02, 2016
Findings of research facilitated by the Open Medicine Foundation could be set to rock the world of medicine, writes Action for M.E. Volunteer Pharmacist Emily Beardall.
Published online in Proceedings of the National Academy of Sciences of the United States of America, and reported in UK press including the Telegraph and the Economist, the study looked closely at the blood chemistry in people with M.E. with a research technique called “metabolomics.” This involves measuring the chemicals in our blood created by the different steps and by-products of metabolising, or breaking down, the energy and nutrients from our food into the chemicals that can be used for energy, hormones and building blocks of new cells.
The research found 20 abnormal metabolic processes in people with M.E.; nine in both men and women with the illness, and a further eleven which varied between gender. This means normal metabolites found in healthy people were found to be low in M.E., so the illness could be described as a “hypometabolic” disease and the body is effectively in hibernation.
The researchers suggest that many of these abnormalities might be part of the body’s own response to try to limit the spread and effect of viral or bacterial infection because cells are using alternative pathways to create the substances it needs. This is normally only seen in acute infection but this state is ongoing in M.E. patients.
What abnormalities did the researchers find?
The disrupted processes that the researchers have found affect:
- cell building blocks sphingolipids and glycosphingolipids which are used by the body to form cell membranes in brain and nerve tissue
- cholesterol, which is needed for the production of cell membranes and steroid hormones such as cortisol and aldosterone
- bile acid, which is important for normal fat digestion; not enough bile acid secreted into the bowel can lead to a “leaky gut” where nutrients aren’t absorbed as efficiently
- mitochondria, the powerhouses of cells, leading to a lower reserve of energy and an inability to replenish high-energy stores after exertion
- the body’s ability to convert vitamins from food into the form needed by cells; those affected are vitamin A and the B vitamins riboflavin (B2), niacin (B3), pyridoxine (B6), folic acid (B9), and cobalamin (B12). These vitamins are essential for energy production, new cell development such as red blood cells, and for normal nervous system function.
- a substance normally produced by the body as an antifungal and antibacterial, called HICA
A quarter of the abnormalities found were common to all the M.E. patients but the rest varied between individuals, giving each person their own characteristic pattern of abnormalities. The authors suggest that instead of focusing on the common disrupted processes in M.E. for developing a treatment, a personalised medicine approach, ie. giving each person a treatment for their own specific metabolic abnormalities, would be more successful.
The study also uncovered five different types of triggers for the illness:
- biological infections (viral, bacterial, fungal, and parasitic infections)
- exposure to toxic chemicals
- physical trauma
- psychological trauma
- and a category of unknown triggers.
Regardless of what triggered someone’s M.E., the underlying disease process was found to be exactly the same, contributing to the distinct chemical signature found for the condition.
Such a huge amount of biological processes in people with M.E. being affected could be the game-changer so desperately needed to move research forward to find treatments and change attitudes towards M.E.
If you would like to know more about this research study, visit the Open Medicine Foundation for commentary from Prof Ron Davies and a Q&A with the principal researcher, Dr Robert Naviaux.
To learn more about related “-omics” research, read the summary of Prof George Davey Smith’s presentation at the 2015 UK CFS/M.E. Research Collaborative conference, and the planned big data study by the M.E./CFS Epidemiology and Genomics Alliance.