In a scientific study published October 24, 2017, that validates what I and millions of others already experience, a team from Newcastle University in the UK followed up on recent research showing our cells are in a hypometabolic state. They looked at a portion of the white cells in the blood called peripheral mononuclear cells (PBMCs) from both people with ME/CFS (n=52) and healthy controls (n=35). PBMCs are lymphocytes and monocytes, the immune system cells at the forefront of fighting disease.
My disease still suffers from misogyny (75% of those affected are female) and is cursed with the trivial name given it in the 80’s–Chronic Fatigue Syndrome*. The disease was promptly dubbed “Yuppy Flu” since many of the people involved in one of the first outbreaks lived in a wealthy area near Reno, Nevada called Incline Village. I recall reading about it on a plane home to Milwaukee, WI from a client meeting on the East Coast and thinking, “Chronic fatigue syndrome. Yeah, I’m tired, too.”
Those of us diagnosed with ME/CFS are often thought to have a psychological illness wherein the unremitting fatigue, brain fog, and muscle/joint pain are all in our minds rather than something biologically wrong with our bodies. Studies with limited numbers of participants or poor parameters abound in the literature on this disease. This leaves us with the stigma of an imaginary illness and few options for treatment.**
In the Newcastle study, researchers looked at energy-dependent cellular actions (oxidative phosphorylation, OXPHOS, and glycolysis). These are two ways cells break apart chemical fuel molecules to transfer energy in cellular respiration. There were many differences between the two groups, but because of the mitochondrial impairment inherent in ME/CFS cells, maximal respiration was found to be the key parameter that differed most.
The finding suggests that when our cells experience physiological stress they find it difficult to increase their respiration rate to compensate and therefore are unable to meet cellular energy demands. The researchers found this to be true under both basal (resting) conditions and when mitochondria are stressed during high metabolic demand. Researchers determined that PBMCs from people with ME/CFS could only produce about another 50% more energy from their cells when stressed, unlike control PBMCs that nearly doubled their output under the same conditions.
While this research looked at just one type of blood cell, it is another step toward linking our symptoms of muscle pain, fatigue and hampered cognitive functions with a legitimate, reproducible biochemical and physiological process. With the publication in late 2016 of Dr. Naviaux’s research and studies by the Chronic Fatigue Syndrome Research Center at Stanford (CFSRC) headed by Dr. Ron Davis, we are entering a new era in ME/CFS research.
*There is an ongoing debate about whether CFS and ME are the same disease. The two conditions are similar, but people with ME suffer from post-exertional malaise (PEM) while people with CFS do not. PEM is a period (lasting days, weeks and even months) of intense exhaustion and an increase in other symptoms following emotional, mental or physical exertion.
**ME/CFS has historically poor funding at the federal level. In past years the National Institute of Health (NIH) allocated fewer research monies to my disease than they did for studies on male pattern baldness. We also suffer from having different clinical diagnostic criteria, some broad enough to include people with depression. Due in large part to neglect by the medical industry, there are no FDA-approved or evidence-based treatments for ME/CFS.
Other articles based on recent research: