Autism Spectrum Disorder (ASD) is a neurodevelopmental condition characterized by differences in social communication and interaction, alongside restricted interests and repetitive behaviors. Joint hypermobility, also known as generalized joint laxity, refers to joints that can move beyond the typical range of motion due to inherent differences in connective tissue.
For a long time, these two conditions were considered separate medical concerns. However, a growing body of scientific evidence suggests a biological connection between ASD and hypermobility. Research proposes that the conditions frequently co-occur because they may share underlying biological pathways. Understanding these mechanisms is key to improving support.
Documenting the Co-occurrence
Research has established that hypermobility is overrepresented in the autistic population compared to the general public. Studies consistently find that individuals diagnosed with ASD exhibit significantly higher rates of generalized joint hypermobility (GJH) and related connective tissue conditions.
Specific data indicates that adults with ASD are over three times more likely to have GJH than their non-autistic peers. The odds increase to nearly five times higher when symptomatic hypermobility is present. Furthermore, the prevalence of Hypermobility Spectrum Disorders (HSD) or hypermobile Ehlers-Danlos Syndrome (hEDS)—conditions characterized by symptomatic joint laxity—is notably elevated in autistic individuals. Nearly 28% of autistic people meet the criteria for these connective tissue disorders, a figure substantially higher than in the general population.
This co-occurrence is not limited by age or gender, though some research highlights a particularly high prevalence in autistic females. The stark difference in occurrence rates supports the necessity of considering joint flexibility as a physical characteristic that often accompanies neurodevelopmental differences.
Shared Biological and Genetic Basis
The frequent co-occurrence points toward a shared biological basis centered on the body’s connective tissue. Connective tissue provides structure and support to nearly all parts of the body and relies heavily on the protein collagen. Differences in the genes governing collagen production lead to the laxity seen in hypermobility, and these differences may also influence the central nervous system (CNS).
The same genetic factors that result in flexible joints can affect the architecture and function of the brain. Collagen and related proteins support neural development and signaling pathways, not just ligaments and skin. Variations in these foundational proteins could contribute to both physical joint instability and the neurological differences observed in ASD, such as altered sensory processing.
A related mechanism involves the autonomic nervous system (ANS), which regulates involuntary body functions like heart rate and digestion. Individuals with hypermobility disorders often experience ANS dysfunction, known as dysautonomia, which can manifest as conditions like Postural Orthostatic Tachycardia Syndrome (POTS). Dysautonomia symptoms, such as dizziness, fatigue, and gastrointestinal issues, can overlap with or exacerbate sensory and internal regulation challenges common in ASD.
Clinical Implications for Diagnosis and Support
Recognizing the link between hypermobility and ASD carries immediate practical implications for clinical care and support. The physical symptoms associated with hypermobility, such as chronic pain, frequent joint subluxations, and persistent fatigue, are often overlooked when a clinician’s focus is primarily on neurodevelopmental traits. Routine screening for hypermobility in autistic individuals is relevant to ensure these physical issues are identified early.
Hypermobility can also contribute to motor difficulties, including poor proprioception—the sense of body position—and motor planning difficulties (dyspraxia). These challenges significantly impact daily functioning and movement. A formal diagnosis of hypermobility helps explain these motor differences, addressing an underlying physical cause rather than simply labeling a person as “clumsy.”
Support plans for individuals with both conditions require a multidisciplinary approach, integrating neurology, rheumatology, and physical therapy. Physical interventions should focus on increasing joint stability and muscle strengthening rather than traditional stretching, which can be detrimental to lax joints. Addressing the physical discomfort and instability caused by hypermobility can reduce secondary issues like anxiety, fatigue, and sensory overload, leading to a more comprehensive support strategy.