Dr. Alan R. Light, PhD.A new study has found that genes involved in muscle pain sensation, fatigue, the function of adrenaline, and immune activity, are all expressed more so in chronic fatigue syndrome patients than healthy individuals following exercise.

The research could be a milestone in our understanding of chronic fatigue syndrome (ME/CFS) and its diagnosis and treatment as the scientists feel the biomarkers they have identified could be used to develop a diagnostic test and open up new avenues for therapeutic interventions.

The research could be a milestone in our understanding of chronic fatigue syndrome (ME/CFS) and its diagnosis and treatment as the scientists feel the biomarkers they have identified could be used to develop a diagnostic test and open up new avenues for therapeutic interventions.

This positive news for ME/CFS patients everywhere comes hot on the heels of research presented by Belgian researcher Dr. Kenny De Meirleir and colleagues at a press conference and at Invest in ME’s International ME/CFS Conference in London at the end of May. Dr. De Meirleir and his team believe that hydrogen sulfide (H2S) produced by certain gut bacteria found at abnormally high levels in ME/CFS patients could be a cause for the disease and have developed a simple urine test to detect excess H2S.

The latest potentially groundbreaking study was conducted by Alan R. Light, PhD, and his research team at the University of Utah Health Sciences Center, USA, and the results were published online on July 30th before appearing in print in an upcoming issue in the Journal of Pain.

What Light and colleagues have done is show that the activity of specific genes increased after exercise in ME/CFS patients significantly more than in healthy people. Furthermore, the type of exercise used in the study was the type of moderate, full-body, aerobic exercise that is known to cause post-exertional fatigue in ME/CFS but is well-tolerated by individuals who are healthy.

Recent advances in molecular analysis means the activity of thousands of genes can now be examined at one time and quantified by measuring the amount of messenger RNA (mRNA). The researchers used these techniques to look at gene activity in ME/CFS patients and healthy controls, targeting genes they had indentified as being important in mouse models of the disease. The studies of mice had shown that there are sensory receptors that act together to detect the metabolites produced by muscle use during exercise.

The study included a total of 19 ME/CFS patients (15 women and 4 men) and 16 healthy controls matched for variables such as gender and age (11 women and 5 men). Of the ME/CFS patients 68 per cent also met the criteria for a diagnosis of fibromyalgia.

Each subject was asked to exercise on an Airdyne exercise bicycle which requires the use of both arms and legs to turn the wheel for 25 minutes. Blood samples were collected before exercise started and again at 30 minutes, 8 hours, 24 hours and 48 hours after exercise. Heart rate and perceived level of effort were monitored throughout the exercise challenge. The mRNA was then extracted from each of the blood samples and gene activity was analyzed.

The researchers analzyed muscle activity metabolite-detecting genes (ASIC3, P2X4, P2X5), adrenergic genes involved in adrenal gland and sympathetic nervous system (SNS) function (A2A, B-1, B-2, COMT), and immune system genes (IL6, IL10, TNF alpha, TLR4 and CD14). When the activity of these genes in ME/CFS and the healthy controls was compared before exercise was compared, there was little difference between the two groups, aside from the ME/CFS having lower expression of beta-2 adrenergic receptors (whose functions include promoting smooth muscle relaxation, blood sugar control, and inhibiting histamine release).

However, as early as 30 minutes after exercise, the team detected significant increases in gene activity for the ASIC3, P2X4, P2X5 metabolite-detecting genes, the B-1, B-2 and COMT adrenergic genes, and the IL10, TLR4 and CD14 immune system genes. Moreover, this increased gene persisted for up to 48 hours after exercise had ended in the ME/CFS patients which certainly corresponds with most patients' subjective exeperiences of post-exertional malaise. As would be expected with moderate exercise, there was no gene activity increase in the healthy control subjects.

Light and colleagues report that in this study the activity of these nine genes could be used to distinguish most of the ME/CFS patients from the control subjects.

For the first time these findings show, based on the expression of genes, that ME/CFS patients have problems with sensory signaling that could certainly help to explain the symptoms of muscle pain and fatigue following even moderate exercise. Essentially their nervous systems become hypersensitive to the metabolic by-products produced by muscles during activity. The fact the increased sensitivity persists for up to 48 hours is important given that patients are often bedridden with pain and fatigue for days following exercise.

The other genes whose activity was increased are also important and confirm long-standing assumptions about the etiology of ME/CFS which research has pointed to for a long time. The increased adrenergic genes confirm findings that dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis is important in ME/CFS, along with the increased activity of the sympathetic nervous system that results. SNS activation is associated with arousal and the stress response as opposed to the parasympathetic nervous system (PNS) which predominates during times of relaxation in healthy individuals.

The immune system genes seen to be increased also confirm previous research and point to a shift towards Th2 biased immunity which predisposes an individual to allergic diseases. Allergies are more common in ME/CFS patients than in the general population.

Light and colleagues believe that the techniques they used and the increased gene expression found in ME/CFS patients could be used to develop blood tests for use in diagnosing ME/CFS, something which would be a first and a major breakthrough in a condition that is still diagnosed based on symptoms and the ruling out of other diagnoses. However, for this to become reality further study is needed, repeating this experiment with much larger numbers of ME/CFS patients, and also comparing the gene expression in these patients with subjects with other fatiguing diseases and pain disorders. The Light team has been awarded a grant by the CFIDS Association of America for just this purpose, so the results will be awaited with baited breath.


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