June Research Round-up
June 27, 2016
Each month, Action for M.E. Volunteer Pharmacist Emily Beardall explains some of the recently published research studies on M.E.
Please note this is not an exhaustive list – we have selected to highlight the studies that we think are most likely to resonate with the daily lives of those affected by the condition. We will also report separately on further studies of significance, as and when they are published.
You can search online directory PubMed for most studies about M.E. published in peer-reviewed journals.
The following studies were published online between 22 May 2016 and 21 June 2016. In each case, we have used the same name for the illness as the researchers publishing the paper.
M.E. should now be a "solvable" problem
An editorial in the journal Fatigue: Biomedicine, Health and Behavior summarised the research into the biological mechanisms of M.E. and set out recommendations for the next steps in M.E. research. The editorial was written by an eminent researcher with a group of patients and carers, including Simon McGrath, who has M.E. and writes about research online and for publications including Action for M.E.’s InterAction magazine.
Three major categories of ongoing abnormalities which could be contributing to prolonging M.E./CFS were identified:
- the brain receiving chemical messengers from the immune system known as cytokines, or from energy metabolism
- a problem with house-keeping’ in the brain, such as an increase in activation of microglia, which are part of the brain’s immune defence
- abnormal messages from nerves concerned with body sensation.
The authors recommend seven ways of working towards effective treatments, which are:
- improving research infrastructure and collaboration of researchers, with a focus on using a common set of diagnostic criteria
- using new brain scan techniques
- further exploration of the immune system problems already found, such as abnormal natural killer cells, cytokines, autoimmunity, and responses to viruses
- examining nervous and hormone system regulation
- furthering research into post-exertional changes in physiology
- repeating key research findings to confirm them
- making data available for other researchers to use for tasks such as defining subgroups of M.E./CFS.
The authors conclude that the puzzle of M.E.CFS now appears to be “solvable” and they call on the wider biomedical research community to focus on the condition.
Potential biomarker for fatigue
A study published in the journal Biological Psychology looked at whether cell damage, called oxidative stress, which occurs during activity is worse in people with CFS than in healthy people. Anti-oxidants, which can be found in some fruits and vegetables are thought to prevent or delay some of this cell damage. The researchers found that levels of substances which are a result of oxidative stress were higher in the blood samples from CFS patients after exercise and at rest than in the healthy controls, whereas the levels of anti-oxidants was lower. The conclusion drawn was that these differences in blood results might be able to be used to confirm a diagnosis of CFS.
A review of studies on medication for M.E.
A study published in the journal Clinical Therapeutics looked back through all research on M.E. related to a treatment of the whole illness, as well as management of individual symptoms. The authors found that there have been studies of 20 classes of medication but that no universal treatment could be recommended from their review due to a variety of diagnostic criteria being used. Ten of the medication classes were slightly or moderately effective for individual symptoms and some patients may find these helpful. Recommendations for future research are that a universal set of diagnostic criteria are established, that studies need to be much larger, and that more research is needed into the underlying physiology of M.E. in order to find more effective treatments.
Immune system cells and their calcium channels in CFS
TRPM3 channels are one of the many types of switches on the surface of cells throughout the human body. When calcium moves through these channels into a cell this switches on and off various chemical reactions to maintain the correct balance of chemicals within it. A study published in the journal Biological Research compared blood samples from people with CFS and healthy controls and found that there were significantly fewer TRPM3 channels on the surface of the immune system cells of the people with CFS, and as a consequence there was also less calcium inside the cells. The researchers suggest further examination of these cell processes to find out whether TRPM3 and decreased calcium in cells has a role in CFS.