By Adrienne Dellwo, About.com Guide – Updated October 26, 2011
Several people in my family have had fibromyalgia and now I’m showing a lot of the symptoms. Is fibromyalgia hereditary?
What’s the Difference?
In a classical monogenic hereditary condition, the specific genes you get from your parents are the primary determining factor in whether you’ll get a disease. For example, in cystic fibrosis, the child of parents who are both disease carriers has a 25% chance of developing cystic fibrosis.
With polygenic predisposition, it’s not as simple or as certain because your genes only mean that a particular illness is possible under the right conditions. Typically, other factors come into play to actually trigger an illness.
In fibromyalgia, these other factors may include other sources of chronic pain, autoimmune disease, sleep disorders, chronic stress, infectious illness or abnormal brain chemistry. Some experts hypothesize that environmental things such as food sensitivities or exposure to toxins could also play a role.
Genetic Links in Fibromyalgia
Researchers began looking into a possible genetic component of fibromyalgia because it does tend to run in families. A 1989 study looked at siblings and parents of fibromyalgia patients and found that 52% of them had characteristic symptoms and other findings of fibromyalgia but had not been diagnosed with it. Another 22% didn’t have symptoms but did have evidence of abnormal muscle consistency. Later research confirmed the high rate of occurrence in families and showed that low pain threshold also appeared common in relatives of people with fibromyalgia.
We’re really just beginning to get a picture of the specific genetic factors associated with fibromyalgia. So far, we have multiple studies suggesting connections with numerous genes but many of these studies have not been replicated.
Genetic abnormalities that have been suggested by preliminary studies include genes that deal with neurotransmitters/hormones that have been implicated in fibromyalgia, including serotonin, norepinephrine, dopamine, GABA and glutamate. Others are involved in general brain function, inhibiting viral replication, and brain receptors for opioids and cannabinoids.
As we learn more about these genetic associations, researchers may identify which of them contributes to the risk of developing fibromyalgia as well as whether any can be used to diagnose or treat the condition.
Arnold LM, et. al. Arthritis and rheumatism. 2004 Mar;50(3):944-52. Family study of fibromyalgia.
Becker RM, et. al. Revista brasileira de reumatologia. 2010 Dec;50(6):617-24. Association between environmental quality, stress and APOE gene variation in fibromyalgia susceptibility determination.
Finan PH, et. al. Pain. 2011 Feb;152(2):300-7. Epub 2010 Dec 3. COMT moderates the relation of daily amadaptive coping and pain in fibromyalgia.
Matsuda JB, et. al. Revista brasileira de reumatologia. 2010 Apr;50(2):141-9. Serotonin receptor (5-HT 2A) and catechol-O-methyltransferase (COMT) gene polymorphisms: triggers of fibromyalgia?
Pellegrino MJ, Waylonis GW, Sommer A. Archives of physical medicine and rehabilitation. 1989 Jan;70(1):61-3. Familial occurrence of primary fibromyalgia.
Reeser JC, et. al. PM & R: the journal of injury, function, and rehabilitation. 2011 Mar;3(3):193-7. Apolipoprotein e4 genotype incrases the risk of being diabnosed with posttraumatic fibromyalgia.
Smith SB, et. al. Arthritis and rheumatism. 2011 Sep 8. doi: 10.1002/art.33338. Large candidate gene association study reveals genetic risk factors and therapeutic targets for fibromyalgia.
Xiao Y, He W, Russell IJ. Journal of rheumatology. 2011 Jun;38(6):1095-103. Genetic polymorphisms of the beta2-adrenergic receptor relate to guanosine protein-coupled stimulator receptor dysfunction in fibromyalgia syndrome.