The term “double jointed” is a common way to describe a person who possesses unusual flexibility, but it is not an accurate medical or anatomical description. No one actually has two joints where there should only be one; the body’s joint count is standard for all humans. Instead, this flexibility is due to a condition called joint hypermobility, where joints can move beyond the typical range of motion. This article explores the anatomy, cause, and potential health implications of joint hypermobility.
The Anatomical Reality of Being Double Jointed
The phenomenon commonly called being “double jointed” is medically known as generalized joint hypermobility (GJH). This is not an extra joint but an increased looseness, or laxity, in the soft tissues that surround and stabilize the joints. A joint’s normal range of motion is limited by the shape of the bones, the joint capsule, and the tightness of the ligaments and tendons. People with hypermobility have ligaments and joint capsules that are stretchier than average, allowing the joint to move further before resistance is met.
This laxity allows individuals to perform movements that look impossible to others, such as bending fingers backward or hyperextending the knees and elbows past the straight 180-degree line. This flexibility is present without the need for extensive stretching, differentiating it from the flexibility acquired by dancers or gymnasts through training. Joint hypermobility is relatively common, affecting 10 to 25% of people. The condition is typically assessed using a simple nine-point scale that measures the range of motion in various joints, like the elbows, knees, and fingers.
What Causes Joint Hypermobility
The underlying reason for this joint looseness is biological and often inherited, relating to the structure of the body’s connective tissue. The primary component affected is collagen, the protein that provides strength and elasticity to tissues like ligaments, tendons, and skin. In individuals with hypermobility, a variation in the genes responsible for producing collagen often leads to a softer, more pliable form of the protein.
This genetically altered collagen results in ligaments and tendons that are less stiff and more elastic, offering less resistance to movement. Since ligaments connect bones to other bones, their increased stretchiness directly causes the joint’s expanded range of motion. The genetic component is strong, meaning hypermobility often runs in families. While collagen is the most studied factor, other fibrous proteins, such as elastin and fibrillin, can also play a role. The degree of joint laxity is generally highest in childhood, and while it tends to decrease with age, it can persist into adulthood.
Associated Health Considerations and Risks
Joint hypermobility exists on a spectrum, with many people experiencing no negative effects and enjoying above-average flexibility. For some, this flexibility can be an advantage in certain sports or activities that require extreme ranges of motion. However, when hypermobility leads to symptoms such as chronic pain or repeated injuries, it is classified as a hypermobility spectrum disorder (HSD).
The increased range of motion makes the joints less stable, raising the risk of joint sprains, partial dislocations (subluxations), and full dislocations. The muscles surrounding the loose joints must work harder to provide stability, which can lead to muscle strain, chronic fatigue, and joint pain.
In some cases, hypermobility is a symptom of a broader, systemic condition known as a heritable disorder of connective tissue (HDCT). The most common HDCT is hypermobile Ehlers-Danlos Syndrome (hEDS), characterized by joint hypermobility along with other systemic issues like easily bruised skin and chronic pain. Other conditions, like Marfan Syndrome, also feature hypermobility due to defects in connective tissue proteins. While flexible joints are common, persistent pain or instability should be evaluated by a medical professional.