I interviewed Dr. ALan Light, Ph. D by Skype in a three part video series. His research is among the very most innovative and important in the fields of chronic fatigue syndrome and Fibromyalgia. He, along with Lucinda Bateman, M.D. and colleagues from the University of Utah School of Medicine, has successfully conducted one study out of a very few that identify an objective laboratory marker which closely correlates with the patients’ “subjective” complaint of prolonged fatigue after modest exertion. This proves that the patients’ subjective reports of post-exertional malaise (PEM) are honest, real and based on physical events. More details on this study and its significance can be found on the following three 10-minute videos and text below.
Segment 1: Provides background on why and how this research was developed
Segment 2: Provides details about this critical study
Segment 3: Reactions from the scientific study and next steps
Details of Study
Dr. Light, Lucinda Bateman, M.D. and colleagues from the University of Utah School of Medicine measured output of messenger RNA output from 13 selected genes. They did this just before, shortly after, and for 48 hours following very modest exercise on a stationary bicycle. The subjects included 48 patients with CFS with or without co-occurring FM, 18 patients who had FM but not CFS, and 49 healthy controls. The 13 genes monitored related to sensory nerve signaling, cytokine and immune function and the sympathetic nervous system.
Results
All CFS and FM patients reported increased symptoms of pain or fatigue for a full 48 hours following the exercise. In controls, there was no reported fatigue and no significant change in gene expression. All subjects showed objective changes in the RNA output from key genes which also lasted a full 48 hours.
There were two distinct patterns of response: In 71% of patients with CFS moderate exercise increased messenger RNA output from 12 of the 13 genes. This was true whether or not they also had FM. Most of these genes related to inflammation or nerve signaling. In the other 29% of CFS patients, exercise caused a decrease in output of messenger RNA from an adrenalin related gene. Many of these patients also had a clinical history of orthostatic intolerance (low blood pressure with prolonged standing). In contrast, the FM-only patients showed no post exercise changes in gene expression. Text on the full study and results can be found at http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2011.02405.x/full
Significance
By showing changes in gene output this objectively proves that the fatigue and pain are real and are mainly physical., Dr. Light’s work appears to identify two different subgroups of CFS patients—one where pro-inflammatory genes turn on, and a second type where blood pressure tends to fall and an adrenalin related gene turns down its activity. Dr. Light’s work also suggests that Fibromyalgia can occur in two different forms—one that is closely associated with CFS and one which is not.