There are a subset of patients with increased B cell activity and autoantibodies, possibly as a result of decreased NK cell regulation or viral mimicry. In 2015, a large German study found 29% of ME/CFS patients had elevated autoantibodies to M3 and M4 muscarinic acetylcholine receptors as well as to ß2 adrenergic receptors. A 2016 Australian study found that ME/CFS patients had significantly greater numbers of single nucleotide polymorphisms associated with the gene encoding for M3 muscarinic acetylcholine receptors. Energy metabolism
Studies have observed mitochondrial abnormalities in cellular energy production, but recent focus has concentrated on secondary effects that may result in aberrant mitochondrial function because inherent problems with the mitochondria structure or genetics have not been replicated. Diagnosis
No characteristic laboratory abnormalities are approved to diagnose CFS; while physical abnormalities can be found, no single finding is considered sufficient for diagnosis. Blood, urine, and other tests are used to rule out other conditions that could be responsible for the symptoms. The CDC states that a medical history should be taken and a mental and physical examination should be done to aid diagnosis. Diagnostic tools
The CDC recommends considering the questionnaires and tools described in the 2015 Institute of Medicine report, which include:
The Chalder Fatigue Scale
Multidimensional Fatigue Inventory
Fisk Fatigue Impact Scale
The Krupp Fatigue Severity Scale
DePaul Symptom Questionnaire
CDC Symptom Inventory for CFS
Work and Social Adjustment Scale (WSAS)
SF-36 / RAND-36: 270 A two-day cardiopulmonary exercise test (CPET) is not necessary for diagnosis, although lower readings on the second day may be helpful in supporting a claim for social security disability.
Differences of research participants cognitive abilities pre- and post-illness onset are naturally variable and are difficult to measure because of a lack of specialized analytical tools that can consistently quantify the specific cognitive difficulties in CFS.The frequency of neuropsychiatric and neuropsychological symptoms is increased in the population of persons with CFS; the understanding of why this occurs is unresolved. Various hypotheses have been advanced to try to explain the relationship between the cognitive symptoms and the illness. Some researchers believe psychiatric causes underlie or contribute to the illness, while other researchers believe the illness causes biochemical and sociological changes in people that produce the symptoms. Cause
The cause of CFS is unknown. Genetic and physiological factors are thought to work together to precipitate and perpetuate the condition. A 2016 report by the Institute of Medicine states that CFS is a biologically based illness, but that the biologic abnormalities are not sensitive or specific enough to be useful as a diagnosis.Because it may begin as an influenza-like illness with a sudden onset, various infectious causes have been proposed, but evidence is insufficient to support such causation. Infections proposed include mononucleosis, Chlamydophila pneumoniae, human herpesvirus 6, and Lyme disease. Inflammation may be involved. Often, the illness will follow a viral illness such as mononucleosis or gastroenteritis. Risk factors
All ages, ethnic groups, and income levels are susceptible to the illness. The CDC states that Caucasians may be diagnosed more frequently than other races in America, but the illness is at least as prevalent among African Americans and Hispanics.