Genetic counseling and genetic testing is recommended for families who may be carriers of familial dysautonomia.Worldwide, there have been approximately 600 diagnoses recorded since discovery of the disease, with approximately 350 of them still living. Research
In January 2001, researchers at Fordham University and Massachusetts General Hospital simultaneously reported finding the genetic mutation that causes FD, a discovery that opens the door to many diagnostic and treatment possibilities. Genetic screening subsequently became available in 2001, enabling Ashkenazi Jews to find out if they are carriers.Stem-cell therapy has been proposed as a potential future treatment. Eventually, treatment could be given in utero. Research into treatments is being funded by foundations organized and run by parents of those with FD. There is no governmental support beyond recognizing those diagnosed with FD as eligible for certain programs. See also
Dysautonomia
Medical genetics of Ashkenazi Jews

References
Further reading
Axelrod FB, Hilz MJ (2003). "Inherited autonomic neuropathies". Semin Neurol. 23 (4): 381–90. doi:10.1055/s-2004-817722. PMID 15088259. Axelrod FB (2004). "Familial dysautonomia". Muscle Nerve. 29 (3): 352–63. doi:10.1002/mus.10499. PMID 14981733. S2CID 222032372. Slaugenhaupt SA, Gusella JF (2002). "Familial dysautonomia". Curr Opin Genet Dev. 12 (3): 307–11. doi:10.1016/S0959-437X(02)00303-9. PMID 12076674. Felicia B Axelrod; Gabrielle Gold-von Simson (October 3, 2007). "Hereditary sensory and autonomic neuropathies: types II, III, and IV". Orphanet Journal of Rare Diseases. 2 (39): 39. doi:10.1186/1750-1172-2-39. PMC 2098750. PMID 17915006.
Impaired fasting glucose is a type of prediabetes, in which a persons blood sugar levels during fasting are consistently above the normal range, but below the diagnostic cut-off for a formal diagnosis of diabetes mellitus. Together with impaired glucose tolerance, it is a sign of insulin resistance. In this manner, it is also one of the conditions associated with metabolic syndrome. Those with impaired fasting glucose are at an increased risk of vascular complications of diabetes, though to a lesser extent. The risks are cumulative, with both higher blood glucose levels, and the total amount of time it spends elevated, increasing the overall complication rate. IFG can eventually progress to type 2 diabetes mellitus without intervention, which typically involves lifestyle modification. Those with impaired fasting glucose have a 1.5 fold increased risk of developing clinical diabetes within 10 years, when compared to the general population. Some studies suggest that without lifestyle changes, IFG will progress to clinically diagnosable diabetes in just under 3 years, on average.Impaired fasting glucose is often, though not always, associated with impaired glucose tolerance, though it may occur in isolation, with such persons having a normal response to a glucose tolerance test. Signs and symptoms
Impaired fasting glucose is often without any signs or symptoms, other than higher than normal glucose levels being detected in an individuals fasting blood sample. There may be signs and symptoms associated with elevated blood glucose, though these are likely to be minor, with significant symptoms suggestive of complete progression to type 2 diabetes.