Fibromyalgia is known to run in families, suggesting that genetic factors contribute to the risk of developing this disease. However, little is known for certain about the genetic basis of fibromyalgia. It is likely that variations in many genes, each with a small effect, combine to increase the risk of developing this condition.
The signs and symptoms of fibromyalgia are related to the way the brain recognizes and interprets pain signals. People with fibromyalgia have an increased sensitivity to pain; they feel pain more acutely than others would in response to a given stimulus. Researchers describe this phenomenon as the “volume” of pain sensations being turned up too high (pain amplification). Studies of the genetics of fibromyalgia have focused on genes with roles in the way the brain processes pain. For example, several genes that may influence the condition are involved in the production and breakdown of certain chemical messengers called . These chemicals relay signals between nerve cells that can increase or decrease the sensation of pain, a process known as pain modulation.
Nongenetic (environmental) factors also play critical roles in a person’s risk of developing fibromyalgia. The disorder can be triggered by infection or illness that would not otherwise cause chronic pain, injury, and other physical stress. Psychological and social factors such as a history of childhood abuse or neglect, exposure to war or other catastrophic events, and low job or life satisfaction have also been associated with an increased risk of fibromyalgia. Additionally, physical inactivity, obesity, and sleep disturbances seem to increase risk. However, many people who develop this condition do not have any recognized triggers or risk factors. It is likely that environmental conditions interact with genetic factors to determine the overall risk of developing this disorder.