Written By Alana Karran
A biomarker has been found in Myalgic Encephalomyelitis (ME), also known as Chronic Fatigue Syndrome (CFS). Griffith University in Australia discovered the biomarker – a measurable substance that helps identify the pathology of an illness – while studying natural killer cells in ME/CFS patients and healthy controls.
Myalgic Encephalomyelitis (ME), also known as Chronic Fatigue Syndrome (CFS), is considered a rare disorder, even though more people suffer from it worldwide than commonly recognized diseases such as Multiple Sclerosis (MS). Similar to MS, ME is a neurological condition that impacts the central nervous system.
First documented in 1934, ME has been attributed to illnesses much earlier, including in famous individuals such as Charles Darwin, Madame Curie and Florence Nightingale. Famous current day sufferers include Laura Hillenbrand, Cher and Stevie Nicks.
Myalgic Encephalomyelitis is best known for its trademark symptom of debilitating fatigue, which is exacerbated by exertion. Recent studies, including one conducted by Dr. Joe Montoya at Stanford University, suggest increased inflammation caused by exercise may contribute to the increased fatigue. Montoya asserts ME/CFS has strong similarities with Systemic Inflammatory Response Syndrome (SIRS).
The generally agreed to working hypothesis is that ME begins with an assault to the immune system, most frequently by a virus, although instances of bacterial infections and physical traumas have also been noted. Instead of fighting off the assault and then returning to normal function, the immune system becomes overactive, increasing inflammation, similar to other autoimmune diseases.
In the Australian study, researchers sought to identify why cytotoxicity in natural killer cells –the agent that is released by the killer cell into an infected cell to eradicate it – is reduced and consistently identified as an immune abnormality in ME/CFS. The researchers first found mutations in the ion channels of natural killer cells in patients.
Ion channels allow calcium and magnesium into cells. These mutations were found to impact calcium flow – an important mineral that is responsible for cellular signaling in muscle contraction during exercise, neurotransmitter release to the nerves, enzyme activity including to the mitochondria which produce energy for the body and overall stability of cells in the body.
It was discovered that cytoplasmic calcium was low in the natural killer cells of ME/CFS patients as a result of the mutations in the ion channels. Further, these dysfunctional ion channels were identified throughout the entire body, potentially causing issues in every area. In attempts to increase the calcium levels in cells during the study, it was also discovered that one of the enzymes needed for this process to occur in T-cells – extracellular-regulated kinase – was also depleted.
So how does this deficiency impact the body at large? These ion channels may be effecting sensory neurons, which are found in the brain and spinal cord, along with many other organs of the body, as well as blood vessels and fatty tissue. Essentially, no area is safe, which explains why ME/CFS patients suffer so many symptoms.