Along with debilitating fatigue, Myalgic Encephalomyelitis (ME) and Chronic Fatigue Syndrome (CFS) patients suffer from neurocognitive issues such as difficulty processing information, impaired memory, poor concentration and challenges with locating words and speaking. Abnormal sleep patterns are present, causing interrupted and ineffective sleep. Gastrointestinal problems, such as irritable bowel syndrome, bacterial infections and candida are also common.
Additionally, cardiovascular symptoms such as palpitations and arrhythmias are noted, along with hypotension – low blood pressure – and postural orthostatic tachycardia syndrome (POTS). Problems with temperature regulation, swollen lymph glands, impaired vision, light sensitivity, sensitivities to certain foods and chemicals, muscle weakness and poor coordination are all hallmark symptoms of the illness. Tremors, seizures and paralysis have also been documented in ME/CFS patients.
Studies have consistently shown compromised mitochondria function in ME/CFS, which is why avoiding overexertion is so crucially important for patients. Dr. Alan Light has reported acquired – meaning they weren’t present at birth – mutations in both the autoimmune and mitochondria genes of patients, indicating problems with energy production and blood flow. This gene expression increases in white blood cells during and after exercise, compared to healthy controls. This suggests an unusual immune response is occurring as a result of exertion, causing a low energy state, that inhibits immune cells from filtering out autoantibodies. They then attack receptors involved in blood flow and other processes, resulting in extreme fatigue.
It has even been theorized that the mitochondria, in an attempt to protect themselves from an initial pathogen, create a protective coating that is not removed after the instigating infection is controlled. Instead, this reaction by mitochondria seems to mimic a state similar to hibernation. A chemical signature found in the blood plasma of ME/CFS patients, tested by researchers at the University of California San Diego School of Medicine, indicated reduced metabolites consistent with hypometabolic syndrome, causing long-term pain and disability.
Loss of activity in AMPK, the enzyme master regulator of energy levels in cells, and RNase L dysfunction, designed to stop viruses from reproducing in the body, may be contributing to this hibernation-like state in Myalgic Encephalomyelitis. When these controls are not working properly, liver function declines, allowing the body to become even more susceptible to toxins, most common in the gut. This can result in increased levels of hydrogen sulfite, which has been shown to create a hibernation state in clinical studies, caused by mitochondria poisoning.
All of these studies show promise in understanding the causes for Myalgic Encephalomyelitis. The next important step is in developing a diagnostic test that can be used commercially to distinguish ME/CFS from other diseases. Griffith University in Australia recently received a grant for $4 Million to develop a test, based on their findings of a biomarker in the ion channel of natural killer cells.
For suffers of this debilitating illness, renewed hope now exists. The discovery of a biomarker, along with the creation of a diagnostic test, will go a long way toward bringing increased awareness, research, and funding toward a cure. And, perhaps, even more importantly for many patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, this breakthrough validates the real physiological causes of a greatly misunderstood condition.