Joint hypermobility describes an increased range of motion in the joints, meaning they can move beyond typical limits of flexibility. This condition is often systemic, affecting connective tissues throughout the body, and may be a feature of Hypermobility Spectrum Disorder (HSD) or Ehlers-Danlos Syndrome (EDS). Autism Spectrum Disorder (ASD) is a neurodevelopmental condition characterized by differences in social interaction, communication, and restricted or repetitive patterns of behavior. A growing body of research recognizes a frequent co-occurrence between the two conditions, suggesting a deeper biological connection.
The Research Evidence Connecting Hypermobility and Autism
Epidemiological studies consistently show that joint hypermobility is significantly more common in individuals diagnosed with ASD than in the general population. Some research indicates that up to 39% of autistic individuals may meet the criteria for HSD or EDS when clinically evaluated. This prevalence is notably higher than the estimated 10-20% of the general population who experience generalized joint hypermobility.
Conversely, individuals diagnosed with conditions like EDS are substantially more likely to have an autism diagnosis compared to those without the connective tissue disorder. A large-scale study found that people with EDS were approximately 7.4 times more likely to have an ASD diagnosis than matched controls. This strong statistical association suggests the overlap is not coincidental and points toward shared underlying factors.
Autistic individuals often experience motor challenges, sensory processing differences, and difficulties with coordination. Hypermobility can amplify these issues, as joint laxity contributes to poor body awareness, also known as proprioception. This physical instability may underlie some motor difficulties frequently observed in the autistic population, which were previously attributed solely to neurological differences.
Underlying Biological Mechanisms of the Link
The shared biology between hypermobility and autism is thought to involve the body’s connective tissue, primarily composed of the protein collagen. Collagen provides structure and strength to joints, skin, and blood vessels. Genetic variations that affect collagen integrity can lead to joint hypermobility, and these same variations may influence structures beyond the joints, including the central nervous system.
Collagen is abundant in the membranes that surround and protect the brain and spinal cord, and it is hypothesized to play a role in early neurodevelopment. If collagen structure is compromised systemically, it could disrupt the optimal development of the brain’s structural scaffold, contributing to the distinct neurological features seen in ASD. Research suggests that certain genes involved in connective tissue formation may also influence neurodevelopmental pathways.
Another frequently observed connection is the co-occurrence of autonomic nervous system dysfunction, or dysautonomia, in both hypermobility and autism. Dysautonomia involves automatic bodily functions, leading to issues like Postural Orthostatic Tachycardia Syndrome (POTS). POTS causes symptoms such as dizziness, rapid heart rate, and fatigue upon standing. This autonomic dysregulation is often more prevalent in individuals who have both hypermobility and a neurodevelopmental condition.
The systemic nature of connective tissue disorders also frequently involves gastrointestinal problems and immune system differences. Maternal immune-related issues, which are sometimes more frequent in mothers with EDS or HSD, have been suggested as a potential factor influencing the neurodevelopment of their children. This overlap suggests a complex interplay where a shared systemic vulnerability manifests as both physical laxity and neurological differences.
Implications for Diagnosis and Therapeutic Care
Recognizing the strong link between hypermobility and autism has significant implications for how clinicians approach diagnosis and care. Motor difficulties, chronic pain, and fatigue in an autistic individual should prompt a screening for joint hypermobility, HSD, or EDS. Without this awareness, musculoskeletal symptoms stemming from unstable joints may be mistakenly attributed solely to autism-related motor differences, leading to ineffective interventions.
For individuals with co-occurring conditions, therapeutic approaches, such as physical and occupational therapy, must be carefully adjusted. Traditional strengthening exercises may unintentionally cause strain or injury to hypermobile joints, which are already compensating for lax ligaments. Instead, therapy should focus on building muscle stability, endurance, and improving proprioception.
A holistic management plan should also address the associated systemic symptoms that commonly accompany hypermobility. This includes managing chronic joint and muscle pain, and addressing the fatigue and orthostatic intolerance associated with dysautonomia. Understanding the physical burden of hypermobility allows for targeted support and accommodations. This support can dramatically improve an individual’s overall quality of life and engagement in other therapies.