Fibromyalgia is **not considered an autoimmune disease**, although it shares some overlapping features with autoimmune conditions and involves complex interactions within the body’s systems. It is primarily recognized as a chronic disorder characterized by widespread musculoskeletal pain, fatigue, sleep disturbances, and cognitive difficulties, but it does not involve the immune system attacking the body’s own tissues, which is the hallmark of autoimmune diseases.
To understand why fibromyalgia is not classified as autoimmune, it helps to first clarify what autoimmune diseases are. Autoimmune diseases occur when the immune system mistakenly identifies parts of the body as foreign and mounts an immune response against them, leading to inflammation and tissue damage. Common examples include rheumatoid arthritis, lupus, and multiple sclerosis. These diseases often show specific markers such as autoantibodies or inflammatory changes in tissues.
Fibromyalgia, by contrast, is considered a **functional somatic syndrome** or a disorder of pain regulation rather than a disease caused by immune system dysfunction. The pain in fibromyalgia is thought to arise from abnormal processing of pain signals in the central nervous system, a phenomenon known as **central sensitization** or **nociplastic pain**. This means the nervous system becomes hypersensitive and amplifies pain signals even in the absence of tissue damage or inflammation.
While fibromyalgia patients often experience symptoms that overlap with autoimmune diseases—such as fatigue, joint pain, and cognitive issues—there is no evidence of the immune system attacking the body’s own tissues. Laboratory tests for autoimmune markers typically come back normal in fibromyalgia patients. Moreover, fibromyalgia does not cause the kind of inflammation or organ damage seen in autoimmune diseases.
That said, fibromyalgia can coexist with autoimmune diseases. For example, people with lupus or rheumatoid arthritis may also develop fibromyalgia, which can complicate diagnosis and treatment. In these cases, fibromyalgia contributes to the overall symptom burden but remains a distinct condition from the underlying autoimmune disease.
Some research suggests that the immune system might play a role in fibromyalgia symptoms indirectly. For instance, low-level immune activation or dysregulation could influence how pain is processed or contribute to fatigue and other symptoms. However, this immune involvement is not the same as the autoimmune process where the immune system targets the body’s own cells.
Fibromyalgia is also linked to other factors such as stress, sleep disturbances, hormonal imbalances, and metabolic changes. These factors can affect the nervous system and pain perception, further differentiating fibromyalgia from autoimmune diseases.
In summary, fibromyalgia is a complex chronic pain condition rooted in nervous system dysfunction rather than immune system attack. It is not classified as an autoimmune disease because it lacks the defining immune-mediated tissue damage and autoantibodies characteristic of autoimmune disorders. Instead, it is best understood as a disorder of pain regulation with multifactorial causes, sometimes occurring alongside autoimmune diseases but fundamentally different in its underlying mechanisms.
