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Ta k e 5 a n d t r y A B M P F i v e - M i n u t e M u s c l e s a t w w w. a b m p . c o m / f i v e - m i n u t e - m u s c l e s . 39 molecules to take a triple helix shape. Then, they may align and make chemical bonds to form fibrils in tight formation (the building blocks of many tough connective tissues, including tendons and ligaments). Alternatively, fibrils may become arranged in a three-dimensional packet that allows a structure to bear compressive and shearing force—this is articular cartilage. Collagen also provides the scaffolding for our bones and organs, providing stretch, strength, and resilience throughout the body. It takes a lot of steps going exactly right for collagen to be produced in precise amounts and locations, forming the correct triple helices, joining to make fibrils, and then linking up to compose our many connective tissue structures. Because this is such a complex sequence of events, collagen is especially susceptible to malformations. In the absence of adequate ascorbic acid, for instance, the correct bonds cannot form between fibrils, and certain types of collagen fail—we call this scurvy. A whole collection of genetic mutations affecting a variety of mature collagen molecules, along with procollagen precursors, lead to the conditions grouped under the umbrella name of EDS. WHAT IS EHLERS-DANLOS SYNDROME? Medical records of patients with easily injured skin and unusually lax joints date back to 400 BCE. Although descriptions had appeared in the medical literature before, in the early 20th century two doctors, Edvard Ehlers and Henri-Alexandre Danlos, combined their findings to identify and label this group of inherited connective tissue problems. The name Ehlers-Danlos syndrome was adopted in 1936. The common factor in EDS is that some kind of genetic disruption occurs during collagen production. EDS encompasses many different genetic anomalies. Some are extremely unusual—only a few cases have been documented. Others appear to be more common, but it is hard to gather exact statistics because affected people may not be identified. One thing that is clear, however, is that each subtype of EDS is inherited separately. In other words, if a person has a certain type of EDS, then that person's child might inherit the same genetic mutation—and won't develop a different subtype of EDS. EDS is considered to be a rare disease, which has a couple of important implications. One is that many general practitioners are not well informed about it, and may miss the combinations of seemingly disconnected physical problems it can cause. Being a so-called rare disease also means that EDS is not the subject of a lot of research, so our understanding of these conditions remains limited. HOW DOES EDS AFFECT FUNCTION? The main ways EDS affects physical function depend on what kind of collagen is affected, and how severe the problem is. Some specialists categorize the consequences of EDS into how these disorders affect joints, the skin, and other miscellaneous tissues. Joint Problems The main joint problem seen with most types of EDS is hypermobility, which is not to be confused with healthy flexibility. Hypermobility is the result of pathologically lax ligaments and joint capsules—not healthy, stretchy muscles. Hypermobility of the joints leads to frequent Watch "Connective Issues" EDS is a genetic disease, and as such, no "cure" currently exists, but massage therapy can be a part of an overall strategy to help cope with the challenges of this condition, which is probably more common than we know.

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