This episode reviews recent reporting on chronic pain and ADHD/autism, a webinar on ADHD, inflammation, and dysautonomia, and a feature on nonhuman primate autism research. Across the discussion, the hosts emphasize the difference between association and causation, screening and diagnosis, and where the evidence remains preliminary or uncertain.
Severe Chronic Pain Overlaps with ADHD Traits in One-Quarter of Patients
ADDitude reported on a University of Tokyo study published in Scientific Reports. It was a cross-sectional screening study of 958 adults being treated for chronic pain at 13 pain centers in Japan. The average age was 58, and about 41 percent were male. Overall, 17.1 percent screened positive for ADHD symptoms and 4.4 percent for autism-related symptoms.
ADHD symptoms were linked to higher pain intensity. About 27 percent of people in the severe-pain group screened positive, and almost one-third of those rating pain at 9 or 10 out of 10 did. No relationship was found between autistic traits and chronic pain in this adult sample. Adults with chronic pain were reported as 2.4 times more likely to have ADHD traits than the general population.
Because the data were cross-sectional, the study cannot show which comes first or establish causation. Anxiety, depression, and pain catastrophizing appeared to mediate part of the link; when researchers adjusted for those factors, the association got weaker. Separate from what the study tested, the conversation noted that pain can disrupt attention and sleep, and ADHD can affect coping and emotional regulation.
The screening measure matters: participants self-reported symptoms rather than receiving formal diagnoses. The ADHD screening questionnaire used, the ASRS, had a false-negative rate of 31.3 percent in the article. Researchers speculated the true proportion could be higher—around 24.9 percent overall and 39.9 percent among those with extremely severe pain—but those were estimates, not measured diagnosis rates. The study did not test whether treating ADHD reduces pain; the article notes prior research on ADHD medication and argues for prioritizing screening and management in chronic pain care.
When Everything Hurts: Chronic Pain in Neurodivergent Youth
Pediatric pain psychologists Gloria Han and Anna Wilson write that chronic pain is about twice as common in neurodivergent youth. They cite about 16 percent of autistic children experiencing frequent or chronic pain—nearly twice the rate in neurotypical peers—rising to about 20 percent among children with developmental conditions. In their own study, about 30 percent of pediatric pain clinic patients were autistic. These populations differ from the adult pain-center study.
The article gives two ADHD figures that should not be merged: about one-quarter of youth with chronic pain have ADHD, while 65 percent of children with ADHD report chronic pain. These reflect different directions and denominators.
The article lists signs families might notice: guarding a body part, avoiding movement, new irritability or meltdowns, sudden anxiety or clinginess, needing help with things a child used to do independently, more nurse visits or school refusal, sleep changes, and pulling back from special interests. These are not a diagnostic checklist.
The article distinguishes acute pain from nociplastic pain, which is common in chronic pain and can occur without ongoing tissue or nerve damage. The nervous system’s alarm system becomes overprotective; this does not make the pain less real. The authors explain this through the fear-avoidance model: biological, psychological, and social factors interact, and neurodivergence can make a child more susceptible to sympathetic fight-or-flight activation through sensory sensitivity, interoception differences, emotional dysregulation, hyperfocus, uncertainty intolerance, and social stress.
The article says caregivers did not cause the child’s pain, and that a calm presence can influence how the child responds over time. It also says chronic pain is highly treatable, though it does not give a quantified treatment-response rate. Coordinated pain programs focus on function, not just pain reduction—getting back to daily activities. For neurodivergent children, plans can address sensory regulation, executive function, daily living tasks, and school supports. School accommodations might include a quiet space for short breaks, noise-reducing headphones or sunglasses, reminders to use pain-management strategies, alternative seating, excused absences or extra transition time, access to notes or speech-to-text, and adapted physical education. These are options to discuss with a team, not one-size-fits-all rules.
At home, the article suggests validating the pain first and warns against framing a child as noncompliant or attention-seeking, because power struggles can increase stress and dysregulation. It suggests starting low and going slow—if walking to the driveway is hard, start with a few steps—and using a comfort toolbox: breathing exercises, music, coloring, puzzles, guided imagery, meditation, and special interests. Visual cues and routines can help. Sleep support matters too: screening for sleep disorders, dimming lights and turning off screens an hour before bed, a short visual bedtime routine, comfortable bedding, a dark cool quiet room, and consistent sleep-wake times. These are tools the article offers, not requirements.
ADHD’s Curious Connections to Chronic Inflammation and Dysautonomia
This ADDitude piece came from a webinar by Dr. James Kustow and discusses POTS, MCAS, hypermobility, and inflammation. It stresses that much of this is preliminary.
The article says about half of people with ADHD are hypermobile, but many have no problems. Some develop hypermobile Ehlers-Danlos syndrome or hypermobility spectrum disorder—conditions where lax connective tissue can cause symptoms across the body—and those are linked with mast cell activation syndrome, or MCAS, and with dysautonomia. In MCAS, immune cells called mast cells overreact to triggers and release too many inflammatory chemicals. Dysautonomia is an umbrella term for disorders of the autonomic nervous system, which controls heart rate, blood pressure, digestion, and body temperature. POTS is a common form of dysautonomia where standing causes a heart-rate spike, dizziness, or fatigue.
The article cites a 2008 study showing more inattention symptoms in POTS patients, but calls the ADHD-POTS link preliminary and says more research is needed. The MCAS-as-common-thread idea is attributed to some clinicians, not established. The conversation described it as interesting but not a reason to jump to conclusions.
Autism research involving monkeys contends with uphill battle
The Transmitter published a news feature by Diana Kwon on November 2, 2026, about autism research involving genetically modified macaques and marmosets, including a macaque with a CHD8 variant and SHANK3 models in macaques and marmosets. Researchers argue these models can answer questions that mice cannot—for example, mice lack some autism-linked brain regions such as the dorsolateral prefrontal cortex and do not reliably model social deficits. The promise is better understanding of neurobiology and testing therapies. The article is also about uncertainty: funding pressure, limited facilities and expertise, and policy shifts, especially in the United States.
David Amaral’s team at UC Davis, working with the Oregon National Primate Research Center, celebrated the birth of its first macaque with a CHD8 variant in September 2025. CHD8 is linked to autism and co-occurring intellectual disability and macrocephaly. Amaral estimates they need 10 genetically modified monkeys to adequately study megalencephaly, the brain overgrowth condition. They are genotyping and phenotyping the first animal, keeping behavioral records and longitudinal MRI scans, and creating a second. The Oregon center, after negotiations about possibly becoming an animal sanctuary, plans to downsize and pivot toward nonanimal models, with uncertainty about which monkey research continues. Amaral says its artificial reproductive technology core is essential to his project and losing access could end it prematurely.
The feature also describes SHANK3 macaques created in China through a collaboration involving MIT’s Guoping Feng and Robert Desimone and the Shenzhen Institutes of Advanced Technology. SHANK3 monkeys carrying one altered copy of the gene showed sleep disturbances, abnormal social interactions, cognitive impairment, repetitive behaviors, and altered functional connectivity—features that parallel people carrying SHANK3 variants. The macaques remain in China because most U.S. institutions—other than the seven federally supported primate research centers—lack the space and facilities to house the large number needed, according to Desimone. Desimone later established a SHANK3 marmoset model in the U.S. and says macaque transgenic work is very difficult there, while marmoset work is expensive but more feasible because the animals are smaller and easier to handle and breed.
Feng developed a SHANK3 “minigene” therapy tested in monkey models and licensed to Jaguar Gene Therapy, which is investigating it in a clinical trial. The article is careful: Feng says a monkey model is not required for clinical trials; the monkey studies gave confidence about safety and efficacy, not proof of clinical benefit.
Policy context in the article includes the China Brain Project, a 5 billion yuan initiative—about 750 million dollars—launched in 2022 with nonhuman primate studies at its core, and Japan’s national brain project, which focused on mapping the marmoset brain, though the latest iteration emphasizes human research more. Feng warned that if monkey models turn out to be critical for developing medicines for brain disorders, other countries will be way ahead of the U.S. Alternatives like organoids and human recordings are advancing, though some gene-therapy studies still require living animals for now. Feng’s line: each model is good for certain questions, and “No model is perfect. Not even a human is a perfect model for another human.”
The conversation framed this as mostly preclinical science—not something that changes diagnosis or care today—while policy decisions affect the research pipeline.
Podcast Transcript
Aaron: Welcome to Living on the Spectrum. I’m Aaron, and I’m here with Jamie. Today we’re starting with a number that caught my eye: in a study of 958 adults being treated for chronic pain at 13 pain centers in Japan, about 17 percent screened positive for ADHD symptoms. That’s from an ADDitude report on a University of Tokyo study published in Scientific Reports. Jamie, what exactly did they find?
Jamie: It was a cross-sectional screening study, so it’s a snapshot rather than a long-term follow-up. The average age was 58, and about 41 percent were male. Overall, 17.1 percent screened positive for ADHD symptoms and 4.4 percent for autism-related symptoms. ADHD symptoms were linked to higher pain intensity. About 27 percent of people in the severe-pain group screened positive, and almost one-third of those rating pain at 9 or 10 out of 10 did. There was no relationship found between autistic traits and chronic pain in this adult sample.
Aaron: So does that mean people with ADHD are more likely to have chronic pain, or people with chronic pain are more likely to have ADHD? It sounds like the study can’t really settle direction.
Jamie: Exactly. It’s an association, and cross-sectional data can’t tell us which comes first. The article notes adults with chronic pain were 2.4 times more likely to have ADHD traits than the general population, but that doesn’t establish causation. And just as general reasoning, separate from what this study tested, pain can disrupt attention and sleep, and ADHD can affect coping and emotional regulation. Anxiety, depression, and pain catastrophizing seemed to mediate part of the link—when researchers adjusted for those, the association got weaker. That suggests emotional and cognitive factors may be part of the pathway, not that ADHD causes pain.
Aaron: And the screening part matters, right? A positive screen isn’t a diagnosis.
Jamie: Right. They used self-reported symptoms, not formal diagnoses. The ADHD screening questionnaire they used—the ASRS—has a fairly high false-negative rate, 31.3 percent in the article, so the researchers speculated the true proportion could be higher, around 24.9 percent overall and 39.9 percent among those with extremely severe pain. But that’s their estimate, not a measured diagnosis rate. It’s also worth saying this study didn’t test whether treating ADHD reduces pain; the article notes prior research on ADHD medication and argues for prioritizing screening and management in chronic pain care.
Aaron: That makes sense. And this really connects to something I was reading in another ADDitude piece, this one by pediatric pain psychologists Gloria Han and Anna Wilson. They’re writing about chronic pain in neurodivergent youth. They say chronic pain is about twice as common in neurodivergent youth. They cite about 16 percent of autistic children experiencing frequent or chronic pain—nearly twice the rate in neurotypical peers—and that rises to about 20 percent among children with developmental conditions. In their own study, about 30 percent of pediatric pain clinic patients were autistic.
Jamie: Yes, and the populations are different from the adult study. The pediatric article is looking at prevalence and pain clinic samples, while the adult study was screening adults at pain centers. The pediatric article also gives two different ADHD figures that shouldn’t be merged: about one-quarter of youth with chronic pain have ADHD, while 65 percent of children with ADHD report chronic pain. Those are different directions and different denominators.
Aaron: I appreciate that. For me, the part that stuck was how easy it is to miss pain in kids. They listed signs like guarding a body part, avoiding movement, new irritability or meltdowns, sudden anxiety or clinginess, needing help with things they used to do independently, more nurse visits or school refusal, sleep changes, and pulling back from special interests. That’s not a checklist for diagnosis—just things families might notice.
Jamie: And the article is careful about the biology. It distinguishes acute pain from nociplastic pain, which is common in chronic pain and can occur without ongoing tissue or nerve damage. The nervous system’s alarm system becomes overprotective. That doesn’t make the pain less real. The authors explain it through the fear-avoidance model: biological, psychological, and social factors interact, and neurodivergence can make a child more susceptible to that sympathetic fight-or-flight activation—through sensory sensitivity, interoception differences, emotional dysregulation, hyperfocus, uncertainty intolerance, and social stress.
Aaron: I think that’s the reassuring part for parents: the article says caregivers didn’t cause the child’s pain, and a calm presence can influence how the child responds over time. It also says chronic pain is highly treatable, though it doesn’t give a quantified treatment-response rate. What kinds of support did they describe?
Jamie: They describe coordinated pain programs that focus on function, not just pain reduction—getting back to daily activities. For neurodivergent children, plans can address sensory regulation, executive function, daily living tasks, and school supports. School accommodations might include a quiet space for short breaks, noise-reducing headphones or sunglasses, reminders to use pain-management strategies, alternative seating, excused absences or extra transition time, access to notes or speech-to-text, and adapted physical education. Those are options to discuss with a team, not one-size-fits-all rules.
Aaron: And at home?
Jamie: The article suggests validating the pain first. It warns against framing a child as noncompliant or attention-seeking, because power struggles can increase stress and dysregulation. It suggests starting low and going slow—if walking to the driveway is hard, start with a few steps—and using a comfort toolbox: breathing exercises, music, coloring, puzzles, guided imagery, meditation, special interests. Visual cues and routines can help. Sleep support matters too: screening for sleep disorders, dimming lights and turning off screens an hour before bed, a short visual bedtime routine, comfortable bedding, a dark cool quiet room, consistent sleep-wake times. Again, these are tools the article offers, not requirements.
Aaron: There was also a third ADDitude piece about ADHD and chronic inflammation or dysautonomia. I want to mention it briefly because it’s a possible mechanism people may hear about. It came from a webinar by Dr. James Kustow and discusses POTS, MCAS, hypermobility, and inflammation. But it stresses that a lot of this is preliminary, right?
Jamie: Yes. It says about half of people with ADHD are hypermobile, but many have no problems. Some develop hypermobile Ehlers-Danlos syndrome or hypermobility spectrum disorder—conditions where lax connective tissue can cause symptoms across the body—and those are linked with mast cell activation syndrome, or MCAS, and with dysautonomia. In MCAS, immune cells called mast cells overreact to triggers and release too many inflammatory chemicals. Dysautonomia is an umbrella term for disorders of the autonomic nervous system, which controls heart rate, blood pressure, digestion, and body temperature. POTS is a common form of dysautonomia where standing causes a heart-rate spike, dizziness or fatigue. The article cites a 2008 study showing more inattention symptoms in POTS patients, but it calls the ADHD-POTS link preliminary and says more research is needed. The MCAS-as-common-thread idea is attributed to some clinicians, not established. So it’s interesting, but not a reason to jump to conclusions.
Aaron: Let’s shift to a very different research story. The Transmitter published a news feature by Diana Kwon on November 2, 2026, about autism research involving monkeys—specifically genetically modified macaques and marmosets, including a macaque with a CHD8 variant and SHANK3 models in macaques and marmosets. This feels like a big science-policy story. What’s happening?
Jamie: The feature describes efforts to develop nonhuman primate models of autism-related biology. Researchers argue these models can answer questions that mice can’t—for example, mice lack some autism-linked brain regions such as the dorsolateral prefrontal cortex and don’t reliably model social deficits. The promise is better understanding of neurobiology and testing therapies. But the article is also about uncertainty: funding pressure, limited facilities and expertise, and policy shifts, especially in the United States.
Aaron: What are the concrete developments?
Jamie: David Amaral’s team at UC Davis, working with the Oregon National Primate Research Center, celebrated the birth of its first macaque with a CHD8 variant in September 2025. CHD8 is linked to autism and co-occurring intellectual disability and macrocephaly. Amaral estimates they need 10 genetically modified monkeys to adequately study megalencephaly, the brain overgrowth condition. They’re genotyping and phenotyping the first animal, keeping behavioral records and longitudinal MRI scans, and creating a second. The Oregon center, after negotiations about possibly becoming an animal sanctuary, plans to downsize and pivot toward nonanimal models, with uncertainty about which monkey research continues. Amaral says its artificial reproductive technology core is essential to his project and losing access could end it prematurely.
Aaron: So this isn’t just a distant animal-research debate. It affects whether a specific long-term project can continue.
Jamie: Right. The feature also describes SHANK3 macaques created in China through a collaboration involving MIT’s Guoping Feng and Robert Desimone and the Shenzhen Institutes of Advanced Technology. SHANK3 monkeys carrying one altered copy of the gene showed sleep disturbances, abnormal social interactions, cognitive impairment, repetitive behaviors, and altered functional connectivity—features that parallel people carrying SHANK3 variants. The macaques remain in China because most U.S. institutions—other than the seven federally supported primate research centers—lack the space and facilities to house the large number needed, according to Desimone. Desimone later established a SHANK3 marmoset model in the U.S. and says macaque transgenic work is very difficult here, while marmoset work is expensive but more feasible because the animals are smaller and easier to handle and breed.
Aaron: And there’s a therapy angle?
Jamie: Feng developed a SHANK3 “minigene” therapy tested in monkey models and licensed to Jaguar Gene Therapy, which is investigating it in a clinical trial. But the article is careful: Feng says a monkey model is not required for clinical trials; the monkey studies gave confidence about safety and efficacy, not proof of clinical benefit. That distinction matters.
Aaron: What does this mean for families in everyday life?
Jamie: Mostly it’s preclinical science, not something that changes diagnosis or care today. But policy decisions affect the research pipeline. The article mentions the China Brain Project, a 5 billion yuan initiative—about 750 million dollars—launched in 2022 with nonhuman primate studies at its core, and Japan’s national brain project, which focused on mapping the marmoset brain, though the latest iteration emphasizes human research more. Feng warned that if monkey models turn out to be critical for developing medicines for brain disorders, other countries will be way ahead of the U.S. At the same time, alternatives like organoids and human recordings are advancing, though some gene-therapy studies still require living animals for now. Feng’s line is useful: each model is good for certain questions, and “No model is perfect. Not even a human is a perfect model for another human.”
Aaron: I think that’s the right note. For parents, it’s hope for better understanding, but not a promise around the corner. And for the chronic pain stories, the takeaway I’m sitting with is that pain and neurodivergence can overlap in ways that deserve attention, without blaming the person or jumping to causation.
Jamie: Agreed. Screening, validation, and coordinated support are the themes—along with a lot of uncertainty that researchers are still working through.
Aaron: Thanks for listening to Living on the Spectrum. Take care.