The research nobody’s talking about
In early March 2026, I sat in a consulting room at FV Hospital in Ho Chi Minh City and watched a doctor flip through test results that said, essentially, nothing to see here.
I’d travelled six hours from Đà Lạt to get those results. I’d spent months preparing the case. I’d written to the hospital citing van der Kolk, McEwen, and Raymaker in my referral letter, because I know from decades of clinical practice that if you don’t frame the question precisely, the system will answer a different one.
Here is what my body was doing while my quarterly blood panels kept returning normal.
A chronic daily headache, present almost every morning for ten months, with characteristics resembling a hangover despite no alcohol consumption. Standard analgesics, ibuprofen, paracetamol, couldn’t touch it. Previous CT and MRI scans at the same hospital had found no structural cause.
Severe, persistent fatigue characterised by approximately one hour of normal energy followed by prolonged exhaustion lasting several hours. Sleep provided no restoration. Constant yawning throughout the day.
Widespread body pain with myofascial trigger points so severe that even light pressure caused extreme pain; my massage therapist, who has worked on hundreds of bodies, described mine as the worst case he had encountered.
Brain fog.
Reduced concentration.
Balance difficulties.
Previously documented episodes of unexplained bruising.
Blood pressure recorded at 170/89 during an emergency visit to my local hospital in Đà Lạt, where the doctor glanced at my Vietnamese-language medical summary, laughed, and walked away.
I want you to sit with that inventory for a moment. Because it is not unusual. If you’re reading this and you have AuDHD, I suspect at least three of those symptoms are familiar. The headache that doesn’t respond. The fatigue that sleep doesn’t fix. The pain nobody can explain. The blood tests that keep telling you you’re fine.
You’re not imagining it. Your tests are answering the wrong question.
In my referral letter to FV, I framed the clinical reasoning around allostatic load. I explained that sixty-six years of undiagnosed neurodivergence had required chronic masking and autonomic hypervigilance, resulting in sustained HPA axis activation and cumulative physiological damage. I requested cortisol rhythm testing, extended thyroid panels, inflammatory markers, iron studies, coagulation profiles, and autonomic assessment. I also flagged a drug interaction between my clopidogrel and escitalopram that increases bleeding risk and may have been contributing to the unexplained bruising nobody had connected to the medication combination. I’d been on both for months. Nobody had flagged it.
The comprehensive results confirmed no acute pathology. A medication review and adjustment resolved the headache that had tormented me for ten months. The new regime is working. I feel healthier than I have in decades.
But something about that outcome kept me thinking. The headache wasn’t structural. It wasn’t a tumour. It wasn’t vascular. It was, as best anyone can determine, my nervous system’s response to cumulative, unrelieved strain. The body pain wasn’t orthopaedic. It was fascial: the physical residue of decades of bracing, hypervigilance, and chronic stress held in tissue that nobody had thought to examine through a neurodivergent lens. The fatigue wasn’t laziness. It was a system running vastly above normal energy expenditure without anyone accounting for the metabolic cost of performing neurotypicality for six decades.
My quarterly blood panels were normal because quarterly blood panels don’t ask the right questions about a neurodivergent body.
I went looking for the right questions. What I found kept me awake at 4am.
The chapter this is building toward
I’m currently writing the fourth edition of Understanding AuDHD. Chapter 3 is called ‘The invisible toll: AuDHD, allostatic load, and what it costs the body.’ Its argument is this: decades of sensory overload, masking exhaustion, executive function taxation, chronic social stress, and financial precarity produce measurable biological damage that accelerates aging at the cellular level. AuDHD is not just a neurodevelopmental profile. It may be an unrecognised risk factor for premature physical decline and, emerging evidence suggests, for neurodegeneration.
I want to share the research backbone of this chapter with you, because I think you deserve to see it. Not filtered through a clinician’s reassuring summary. Not softened for comfort. Just the studies, what they found, and the picture they form when placed side by side.
The life expectancy evidence
A 2025 UK study used mortality data from 30,000 adults with diagnosed ADHD and found life expectancy reductions of 4.5 to 9 years for men and 6.5 to 11 years for women (O’Nions et al., 2025). A landmark Swedish study of 27,000 autistic individuals found premature mortality was markedly increased across a multitude of medical conditions, with the strongest effects among women and those with intellectual disabilities (Hirvikoski et al., 2016). The AuDHD-specific life expectancy gap, the one that would tell me what having both conditions together actually costs, has never been studied.
Nobody has done that research.
I wonder why.
The allostatic load evidence
This is where my own experience starts to make biological sense.
A 2023 Columbia University study found that chronic stress hormone exposure increases cellular energy expenditure by approximately 60% and accelerates biological aging as measured by DNA methylation clocks and telomere shortening (Bobba-Alves et al., 2023). Sixty percent. That’s the metabolic surcharge of a body running on chronic stress. Nobody gets a bill for it. The body pays anyway.
A 2026 study confirmed that financial strain and everyday discrimination are associated with accelerated epigenetic aging across the lifespan (Ciciurkaite et al., 2026). A 2025 neuroimaging study found that allostatic load is linked to structural brain changes in regions sensitive to aging (Palix et al., 2025).
Now map those findings onto a life spent navigating neurotypical systems with an AuDHD brain. The masking. The sensory management. The executive function taxation. The social performance. The financial instability that follows executive function differences through every career decision. Every one of those experiences generates exactly the kind of chronic, unrelieved stress that the allostatic load research identifies as biologically damaging. It is the mechanism behind symptoms like mine: the headache that imaging can’t find, the pain that blood tests can’t explain, the fatigue that sleep can’t repair.
A real-world study of 2.3 million insurance members found that co-occurring autism and ADHD synergistically increases the odds of additional comorbid conditions beyond what either condition produces alone (Thomas Craig et al., 2025). Not additively. Synergistically. The combination is worse than the sum of its parts.
And Raymaker’s foundational 2020 study defined what the autistic community had been describing for years: autistic burnout as a distinct syndrome resulting from chronic mismatch between expectations and capacity, characterised by pervasive exhaustion, loss of previously reliable skills, and reduced sensory tolerance (Raymaker et al., 2020). That’s not a metaphor. That’s a clinical description of what happens when a system exceeds its load-bearing capacity.
The dementia evidence
The allostatic load research was sobering. What follows is worse.
A 2023 Israeli cohort study following 109,218 people over 17 years found that adults with ADHD had nearly three times the risk of developing dementia, with a hazard ratio of 2.77. Notably, psychostimulant medication appeared to reduce the association (Levine et al., 2023). A Swedish registry study of 3.59 million individuals found an ADHD dementia hazard ratio of 2.92, attenuating to 1.62 after adjusting for psychiatric comorbidities but remaining significant (Dobrosavljevic et al., 2022).
A 2024 Argentine study, small but mechanistically striking, found a hazard ratio of 54.54 for Lewy body dementia specifically in the ADHD cohort, with 95% of ADHD participants who developed dementia developing the Lewy body variant (Golimstok et al., 2024). That confidence interval is wide enough to drive a truck through, but the dopaminergic pathway makes biological sense.
The autism evidence is equally sobering. A 2021 Medicaid study found autistic adults were approximately 2.6 times more likely to be diagnosed with early-onset dementia than the general population (Vivanti et al., 2021). A 2025 follow-up using linked Medicare and Medicaid data from over 114,000 autistic adults found that among those over 64, 35.1% carried a dementia diagnosis, versus approximately 10 to 11% in the general population (Vivanti et al., 2025). A Swedish family study found elevated dementia risk not only in autistic people but in their biological relatives, suggesting shared genetic pathways (Zhang et al., 2025).
A 2025 Geneva University study identified the first plausible neurobiological mechanism: altered iron distribution in the brains of adults with ADHD, correlated with elevated neurofilament light chain protein, a marker of neuronal damage seen in early-stage dementias (Berberat et al., 2025).
And the 2023 International Summit on Intellectual Disability and Dementia produced a consensus document identifying overlapping symptoms of autism and dementia as a critical barrier to accurate diagnosis (Janicki et al., 2025). Executive function decline, increased rigidity, memory difficulties, anxiety. These are features of both conditions. Clinicians may interpret early dementia in an autistic person as ‘just their autism.’
I wonder how many people that’s already happened to.
What connects my body to these numbers
I want to be careful here. I’m not arguing that AuDHD causes dementia. The research doesn’t support that claim and neither do I.
What I’m arguing is that the conditions of life, the decades of environmental mismatch, the masking, the chronic stress, the inadequate healthcare, the financial precarity, produce allostatic load that may accelerate biological aging and elevate neurodegenerative risk. And that this load produces real physical symptoms along the way. Symptoms like mine. Symptoms that routine blood panels don’t capture because they were designed to measure acute pathology, not the slow accumulation of physiological debt from sixty-six years of running the wrong operating system in the wrong environment.
The good news, and there is good news, is that allostatic load is modifiable.
Environmental change reduces allostatic load. I moved to Vietnam and my depression vanished within months. Same brain. Different environment. Same pension. Different cost of living.
Appropriate medical investigation reduces allostatic load. Once the right questions were asked at FV Hospital, the right medications were found, and a headache that had tortured me for ten months resolved.
Accurate diagnosis reduces allostatic load. Understanding at sixty-six that I was neurodivergent, not broken, reframed decades of suffering from personal failure to systemic mismatch.
Stopping the performance of neurotypicality reduces allostatic load. Learning to unmask, imperfectly, gradually, is the most important thing I’ve done for my body since arriving in this country.
The research suggests that the dementia risk associated with AuDHD may be driven substantially by these modifiable factors. That is not a reason for complacency. It is a reason for urgency. Because the generation of late-diagnosed AuDHD adults, the ones who spent their entire working lives undiagnosed and unsupported, are entering the age range where the consequences become visible. Their bodies have been paying the allostatic surcharge for decades. The question is not whether damage has occurred. The question is how much can be recovered, and how quickly the systems that produced the damage can be changed.
I wonder what it costs a body to spend fifty years pretending to be someone else.
I wonder whether the medical establishment will take this seriously before the answers are written in dementia statistics.
I wonder whether destigmatising neurodivergence and taking its physical health consequences seriously might turn out to be the same project, not competing ones.
Why I’m showing you this
Chapter 3 of Understanding AuDHD, fourth edition, will explore all of this with the appropriate caveats, the honest uncertainties, and the gentle contrarian position that asking these questions is itself an act of care, not an act of alarm.
But I wanted you to see the studies now. Because you deserve to make your own assessment of what the evidence is saying, without anyone, including me, telling you what to conclude.
The references are below. Every one has been independently verified against the original publication.
Lee
Đà Lạt, Vietnam, 17 March 2026
References
Berberat, J., Kagerer, S. M., Späni, C., Hua, J., Bavato, F., Gruber, P., van Zijl, P. C., Perroud, N., Li, X., Stämpfli, P., Seifritz, E., Lövblad, K.-O., Quednow, B. B., & Unschuld, P. G. (2025). Brain iron load and neuroaxonal vulnerability in adult attention-deficit hyperactivity disorder. Psychiatry and Clinical Neurosciences, 79(5), 282–289. https://doi.org/10.1111/pcn.13806
Bobba-Alves, N., Sturm, G., Lin, J., Ware, S. A., Karan, K. R., Monzel, A. S., Bris, C., Procaccio, V., Lenaers, G., Higgins-Chen, A., Levine, M., Horvath, S., Santhanam, B. S., Kaufman, B. A., Hirano, M., Epel, E., & Picard, M. (2023). Cellular allostatic load is linked to increased energy expenditure and accelerated biological aging. Psychoneuroendocrinology, 155, 106322. https://doi.org/10.1016/j.psyneuen.2023.106322
Ciciurkaite, G., Peng, S., Mitchell, C., Perry, B. L., & Lee, B. (2026). Psychosocial stressors, accelerated biological aging, and multiple morbidities: Evidence from an age-diverse sample. PLOS ONE. https://doi.org/10.1371/journal.pone.0343987
Dobrosavljevic, M., Solares, C., Cortese, S., Andershed, H., & Larsson, H. (2022). Attention-deficit/hyperactivity disorder as a risk factor for dementia and mild cognitive impairment: A population-based register study. European Psychiatry, 65(1), e2. https://doi.org/10.1192/j.eurpsy.2021.2261
Golimstok, Á., García Basalo, M. J., Majul, M., Buonanotte, W., Rojas, M., Campos Fein, M., & Eichel, R. (2024). Adult attention deficit-hyperactivity disorder is associated with Lewy body disease and cognitive impairment: A prospective cohort study with 15-year follow-up. The American Journal of Geriatric Psychiatry, 32(10), 1220–1230. https://doi.org/10.1016/j.jagp.2024.04.016
Hirvikoski, T., Mittendorfer-Rutz, E., Boman, M., Larsson, H., Lichtenstein, P., & Bölte, S. (2016). Premature mortality in autism spectrum disorder. The British Journal of Psychiatry, 208(3), 232–238. https://doi.org/10.1192/bjp.bp.114.160192
Janicki, M. P., McCallion, P., Jokinen, N., Service, K. P., Mughal, D. T., Watchman, K., Gomiero, T., Larsen, F. K., & Keller, S. M. (2025). Autism, diagnostics, and dementia: A consensus report from the 2nd International Summit on Intellectual Disabilities and Dementia. International Journal of Geriatric Psychiatry, 40(6), e70110. https://doi.org/10.1002/gps.70110
Levine, S. Z., Rotstein, A., Kodesh, A., Sandin, S., Lee, B. K., Weinstein, G., Schnaider Beeri, M., & Reichenberg, A. (2023). Adult attention-deficit/hyperactivity disorder and the risk of dementia. JAMA Network Open, 6(10), e2338088. https://doi.org/10.1001/jamanetworkopen.2023.38088
O’Nions, E., El Baou, C., John, A., Lewer, D., Mandy, W., McKechnie, D. G. J., Petersen, I., & Stott, J. (2025). Life expectancy and years of life lost for adults with diagnosed ADHD in the UK: Matched cohort study. The British Journal of Psychiatry, 226(5), 261–268. https://doi.org/10.1192/bjp.2024.199
Palix, C., Chauveau, L., Felisatti, F., Chocat, A., Coulbault, L., Hébert, O., Mézenge, F., Landeau, B., Haudry, S., Fauvel, S., Collette, F., Klimecki, O., Marchant, N. L., De La Sayette, V., Vivien, D., Chételat, G., Poisnel, G., & the Medit-Ageing Research Group. (2025). Allostatic load, a measure of cumulative physiological stress, impairs brain structure but not β-accumulation in older adults: An exploratory study. Frontiers in Aging Neuroscience, 17, 1508677. https://doi.org/10.3389/fnagi.2025.1508677
Raymaker, D. M., Teo, A. R., Steckler, N. A., Lentz, B., Scharer, M., Delos Santos, A., Kapp, S. K., Hunter, M., Joyce, A., & Nicolaidis, C. (2020). “Having all of your internal resources exhausted beyond measure and being left with no clean-up crew”: Defining autistic burnout. Autism in Adulthood, 2(2), 132–143. https://doi.org/10.1089/aut.2019.0079
Thomas Craig, K. J., Khan, R., Hariharaputran, S., Gao, J., & Haber, M. (2025). Real-world evaluation of prevalence, cohort characteristics, and healthcare utilization and expenditures among adults and children with autism spectrum disorder, attention-deficit hyperactivity disorder, or both. BMC Health Services Research, 25, 1048. https://doi.org/10.1186/s12913-025-13296-2
Vivanti, G., Tao, S., Lyall, K., Robins, D. L., & Shea, L. L. (2021). The prevalence and incidence of early-onset dementia among adults with autism spectrum disorder. Autism Research, 14(10), 2189–2199. https://doi.org/10.1002/aur.2590
Vivanti, G., Lee, W. L., Ventimiglia, J., Tao, S., Lyall, K., & Shea, L. L. (2025). Prevalence of dementia among US adults with autism spectrum disorder. JAMA Network Open, 8(1), e2453691. https://doi.org/10.1001/jamanetworkopen.2024.53691
Zhang, L., et al. (2025). Association between autism and dementia across generations: Evidence from a family study of the Swedish population. Molecular Psychiatry. https://doi.org/10.1038/s41380-025-03045-6