EDS is due to a mutation in one of more than a dozen different genes. There are identified genes for all subtypes except hEDS (hypermobility type), but that gene may have been found recently and is still awaiting peer review.

The subtypes are:

• Arthrochalasia EDS (aEDS)
• Brittle Cornea Syndrome (BCS)
• Cardiac-valvular EDS (cvEDS)
• Classical EDS (cEDS)
• Classical-like EDS (clEDS)
• Classical-like EDS (clEDS2) – formerly unnamed variant involving the AEPB1 gene
• Dermatosparaxis EDS (dEDS)
• Hypermobile EDS (hEDS)
• Kyphoscoliotic EDS (kEDS)
• Musculocontractuaral EDS (mcEDS)
• Myopathic EDS (mEDS)
• Periodontal EDS (pEDS)
• Spondylodysplastic EDS (spEDS)
• Vascular EDS (vEDS)

While there are unique signs & symptoms associated with each subtype, EDS symptoms are known to crossover from one subtype to another. Because of these crossover symptoms, it is not uncommon for geneticists to only genetically test for the more serious types suspected (such as vEDS) and simply diagnose hEDS (which has no known genetic testing and therefore is diagnosed by clinical observation) if the more serious subtype is ruled out. This method may have significantly skewed the data on how common each subtype is believed to be.

We will be referencing the Ehlers-Danlos Society quite a bit this year because their research and organization of information are exceptional.

• https://www.ehlers-danlos.com/eds-types/ https://www.ehlers-danlos.com/a-new-type-of-ehlers-danlos-syndrome-discovered/
• https://www.frontiersin.org/journals/genetics/articles/10.3389/fgene.2023.1102101/full