The commonality of autoimmune conditions within patients and among their family members is compatible with some researchers’ theories (157, 158) that ME/CFS might have an autoimmune basis. It is well-known that individuals with one autoimmune disease are more likely to be affected by another autoimmune disease (159). The same but also diverse autoimmune diseases might affect families; the former phenomenon is labeled as a “familial autoimmune disease” while the latter is known as “familial autoimmunity” (160). Furthermore, many of the traits displayed by ME/CFS fit Rose and Witebsky’s circumstantial criteria (161, 162) for determining when a condition qualifies as an autoimmune condition. For example, ME/CFS is more common in women, runs in families, can be triggered by infections, can be alleviated by immunosuppressants and is associated with autoantibodies [e.g., to adrenergic and cholinergic receptors (97, 98)]. Fluge et al. (163) also demonstrated in vitro that serum transferred from patients’ bodies adversely affected the function of healthy, cultured muscle cells. This serves as a more direct piece of evidence for autoimmunity. Rose and Witebsky’s criteria could operate as a guideline for future studies to prove or disprove the role of autoimmunity in ME/CFS. For example, to test maternal transfer of autoantibodies, infants of ME/CFS patients could have their blood tested for ME/CFS-specific autoantibodies and be followed serologically and clinically for ME/CFS symptoms. Four percent of our subjects and 6% of Jason’s (164) admit to being sick as long as they can remember. Another project might devise animal models capable of developing ME/CFS: if exposure to patient serum or a putative antigen replicates the illness in these animals, that would corroborate the autoimmune foundations of ME/CFS.
