Research round-up: autoimmune disease and M.E./CFS
March 29, 2018
Supporting you to stay informed about M.E. research, we publish regular round-ups from Action for M.E. volunteer and pharmacist Emily Beardall, covering a selection of papers published in peer-reviewed journals.
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 17 January and 16 March 2018. In each case, we have used the same name for the illness as the researchers publishing the paper.
Autoimmunity and M.E./CFS
An article in the journal Clinical Rheumatology proposes a theory that CFS may be a condition that precedes a full-blown autoimmune disease, given that the early symptoms of some autoimmune diseases are very similar to CFS. Some patients also go on to develop autoimmune diseases such as lupus, multiple sclerosis, rheumatoid arthritis, or have family members with these conditions.
The journal Frontiers in Immunology also discusses this theory and goes further by piecing together recent autoimmunity, genetics and energy metabolism findings in M.E./CFS. The authors suggest their complex model of development of the illness is in line with current thought in immunology, which states that autoimmunity is a condition in its own right, with a genetic predisposition affecting how the body recognises itself, followed by an infection which triggers the specific condition to develop. The theory needs to be tested but the authors say it may help to provide a direction for future research.
Previous research has shown that in M.E./CFS there are is autoimmunity to receptors in the autonomic nervous system (which regulates the body’s basic functions such as blood circulation by heart rate, breathing and digestion) in a subset of patients. A pilot trial published in PLoS Oneremoved these antibodies, to see if there was an improvement in symptoms and functioning in ten patients with severe M.E./CFS. This procedure was carried out five times during the trial, although one of the patients suffered side effects and could not complete the course of treatment.
A rapid moderate improvement in overall symptoms was seen in seven of the patients, although none of the patients completely recovered and five had worsening of fatigue towards the end of treatment despite improvement of other symptoms, which may have been due to the physical exertion of travelling and hospital stays. Larger trials are needed to confirm whether this treatment would be helpful.
Blood volume: potential sub-group
A study published in the journal Open Heart found that levels of a chemical messenger called brain natriuretic peptide was significantly higher in the bloodstream of CFS participants than in the healthy controls. This chemical is released into the bloodstream when the heart muscles detect a higher volume of blood than usual, resulting in water being lost via urine to restore blood volume to a normal level. This study also confirms previous research which found blood volume to be lower in CFS patients, so the finding of high brain natriuretic peptide goes some way to explain why.
There were no relationships between fatigue severity or length of disease and so the authors state that these findings are unlikely to be related to deconditioning (ie. becoming unfit with inactivity over time). The authors also suggest that measuring brain natriuretic peptide could help to identify the subgroup of a third of people with CFS previously found to have impaired cardiac functioning so that a targeted treatment can be given.
Developing a diagnostic test
A study in the journal Scientific Reports looked at whether immune system and cardiology tests following exercise would be an effective way of diagnosing M.E./CFS. They noted several immune system components that set apart M.E./CFS patients from sedentary healthy controls, 18 hours after exercise, which could possibly be used as a diagnostic test. Limitations include that this test does not necessarily distinguish M.E./CFS from other fatiguing illnesses, and that it was a small study.
Accelerated cell ageing in women with CFS
A study published in the Journal of Translational Medicine examined the DNA of people with CFS, particularly the protective end caps of chromosomes, called telomeres. Each time cells divide to make more skin, hair and blood cells, for example, the telomeres get progressively shorter, and in women with CFS under 45 they were found to be much shorter, suggesting accelerated cell aging compared with healthy people of the same age. This phenomenon has also been found in diseases such as lupus and multiple sclerosis.
The authors suggest there are connections between this and other observations in CFS, such as the accelerated wearing out of the immune system, mitochondrial dysfunction, and early menopause in women with CFS, and that further research is needed to investigate these connections.
No link between childhood adversity and CFS
Previous studies have found a relationship between childhood adversity and CFS, assuming this contributes to development of the illness. A study in the journal Fatigue, however, used the Childhood Trauma Questionnaire to assess people with CFS and healthy controls for a history of emotional, physical, and sexual abuse, and emotional and physical neglect. Statistical analysis was then used to find the risk of developing CFS with and without depression.
The authors conclude that depression being common alongside CFS (for example as a result of the impact of the condition), has skewed results of psychological studies, leading to misdiagnoses and assumptions that CFS only develops in people with psychiatric disorders.
The cognitive behavioural model
A study in the Journal of Clinical Psychology re-examines this model of the illness which suggests that thought patterns and reduced activity perpetuate CFS. The authors examined nearly a thousand people with CFS and findings suggest that there is no significant relationship between beliefs about the cause of the illness and activity level. Although activity level and impairment were related, this may simply show illness severity rather than justifying the theory that activity reduction causes physical impairment.
The authors urge caution when prescribing CBT for illness beliefs and GET for deconditioning, whereas pacing may help improve functioning.