Childhood Adversity, Chronic Pain, and Why I'm Telling You My ACE Score
I'm writing this the week of Mother's Day.
That's not incidental. For a lot of us, holidays organized around family feel less like celebration and more like a reminder of what was missing — or what was taken. For me, this week resurfaces something I've spent years integrating: the knowledge that some of my earliest experiences shaped not just who I became emotionally, but how my body functions today.
My ACE score is 4.
If you don't know what that means, I'll get to it. But first, I want to sit with why it matters that I'm saying it at all — because in clinical spaces, we don't talk about this enough.
What Are ACEs?
Adverse Childhood Experiences — ACEs — are a category of potentially traumatic events that occur before age 18. The original ACE Study, conducted by the CDC and Kaiser Permanente in the mid-1990s, surveyed more than 17,000 adults about their childhoods and then tracked their health outcomes over time. What researchers found was striking and has only been reinforced in the decades since: childhood adversity doesn't stay in childhood. It embeds itself in the body.
The ACE questionnaire covers 10 categories across three domains: abuse (physical, emotional, sexual), neglect (physical, emotional), and household dysfunction (witnessing domestic violence, substance use, mental illness, incarceration, or divorce). Each category you experienced counts as one point.
Take the ACE quiz here and read that article carefully, because it also explains what the score does and doesn't mean.
A score of 4 or more is where research consistently shows a significant shift in chronic disease risk.¹ About 13–24% of US adults fall into that range.² I am one of them. And if you're reading this on a blog about hypermobility and menopause, there's a real chance you are too.
What I See in My Patients
I won't pretend I came to this knowledge cleanly. I became a clinician before I fully understood my own history. But over time — as I started seeing the same patterns repeat in my hypermobile patients — something clicked into place.
The person who's had fibromyalgia since their twenties. Widespread, shifting pain that never quite resolves and never quite makes sense on imaging. A nervous system that seems turned all the way up, all the time. A history they mention almost in passing — an alcoholic parent, an absent one, years of walking on eggshells — and then quickly redirect back to their symptoms, because they've learned that providers don't connect those dots.
I connect those dots. Because the research is clear, and because I've lived in a version of that body.
Adults with ACEs are approximately twice as likely to develop chronic pain — a finding confirmed by a 2024 systematic review and meta-analysis of 52 studies (OR = 1.99).³ Trauma roughly triples the risk of fibromyalgia specifically (OR = 2.52 in meta-analytic data), and the association with physical abuse is particularly strong (OR = 3.23).⁴ A 2025 Swedish co-twin study — methodologically powerful because it controls for shared genetics — still found a meaningful association between childhood maltreatment and widespread chronic pain (aIRR 1.20), meaning this isn't just about biology we were born with.⁵ Something adversity does to the body persists independently of genetics.
That something has a name: central sensitization. It's a process by which the nervous system becomes durably recalibrated toward threat detection. Pain signals amplify. The threshold for triggering a stress response drops. Research confirms that ACE scores positively predict higher Central Sensitization Inventory scores, and that central sensitization mediates the link between childhood adversity and pain interference, depression, and anxiety.⁶ The body, in other words, learns to stay ready — because for a long time, it had to.
In hypermobile bodies, this matters even more. Our nervous systems are already structurally wired differently. Proprioception is altered. Autonomic regulation is often impaired. When you layer a history of early adversity on top of connective tissue that's inherently more reactive, you get a body that has been running in survival mode for a very long time.
The MCAS Layer
For those of us in the hEDS/HSD world, there's another piece worth naming: mast cell activation.
Mast cells are immune cells that release inflammatory chemicals — histamine, cytokines, prostaglandins — in response to perceived threats. They're supposed to do this. The problem in MCAS is that they do it too readily, too often, and in response to triggers that shouldn't register as threats at all: foods, smells, temperature changes, and — critically — emotional stress. Emotional stress is, in fact, the most commonly reported symptom trigger in systemic mastocytosis.⁷
Here's where the research gets both fascinating and sobering: the same stress hormone pathway that gets dysregulated by childhood adversity — the HPA axis, and specifically a hormone called corticotropin-releasing hormone (CRH) — directly activates mast cells via CRH receptor-1, triggering degranulation even more powerfully than antigen stimulation in some studies.⁷ ⁸ And mast cells themselves produce CRH, creating a self-amplifying loop.⁷
Animal studies add another layer: early-life adversity modeled through neonatal maternal separation increases mast cell numbers, increases histamine production, and produces visceral hypersensitivity in adulthood. When mast cells were pharmacologically blocked, that hypersensitivity disappeared — establishing that mast cells were necessary for the effect, not just bystanders.⁹
I want to be precise here, because honesty is a pillar of how I practice: no clinical study has yet directly measured ACE scores in patients with diagnosed MCAS. The connection is mechanistically plausible and supported by converging lines of evidence — but it has not been tested directly in a clinical population. This is an important gap, and one I hope researchers close. What I can say is that the biological story is coherent, and that in my clinical experience, the overlap is hard to ignore.
Your Body Is Not Broken. It Adapted.
This is the part I most want you to hold.
If you have a high ACE score and you also have fibromyalgia, or widespread pain that no one can explain, or a mast cell system that seems to fire at everything — your body is not broken. It is doing exactly what it learned to do to keep you safe.
The pain is real. The trauma is real. The nervous system dysregulation is measurable — including blunted cortisol stress reactivity, low-grade chronic inflammation (elevated CRP, IL-6, TNF-α), and altered immune function, all confirmed in large meta-analyses of ACE-exposed adults.¹⁰ None of this is psychosomatic in the dismissive sense that word is usually deployed. It is neuroimmune. It is biological. And it happened for a reason.
What I also want you to know is that this isn't a life sentence. The same neuroplasticity that allowed adversity to reshape your stress response is the mechanism through which healing is possible. That's not a promise of cure — it's an honest statement about biology.
Mother's Day asked me to think about abandonment this week. About what it costs a body to grow up in uncertainty. About how long I carried things I didn't have language for.
I also thought about my patients — the ones who come in with a stack of diagnoses and a lifetime of being told their symptoms don't add up. They add up. I just needed to learn the math.
If You Want to Go Deeper
If any of this resonated, you're welcome here.
The ACE quiz at NPR is a gentle starting place — and that article does a thoughtful job of contextualizing what the score means and what it doesn't predict about any individual person.
If you're navigating hypermobility, MCAS, or complex chronic illness in the context of midlife — and you're wondering whether trauma belongs in that conversation — it does. You can book a Clarity Consultation with our team, or follow along at @bendymenopause for more on exactly these intersections.
You don't have to figure this out alone. And you don't have to justify the complexity of your body to anyone.
— Vanessa
References
Alhowaymel FM, et al. Int J Environ Res Public Health. 2023;20(2):1651.
Guo N, et al. Child Abuse Negl. 2025;169(Pt 1):107628.
Senaratne DNS, et al. BMC Medicine. 2024;22(1):315. (52-study meta-analysis; OR = 1.99, 95% CI 1.53–2.60)
Dube SR, et al. Psychosom Med. 2009;71(2):243–50; fibromyalgia-specific OR from meta-analytic data cited in source document.
Swedish co-twin study, 2025. N = 25,418; aIRR 1.20 (95% CI 1.05–1.38) for chronic widespread pain.
Central Sensitization Inventory data; ACE–CSI association β = 0.434, P < 0.001, from chronic pain cohort study cited in source document.
Theoharides TC, et al. CRH–mast cell axis; mast cell CRH production and CRHR-1 activation. Referenced in source document.
Neuropeptide synergy (neurotensin, substance P) with CRH in mast cell activation. Referenced in source document.
Neonatal maternal separation model; mast cell necessity established via cromolyn blockade. Referenced in source document.
HPA dysregulation and inflammatory marker meta-analyses (CRP, IL-6, TNF-α); systematic review of 27 meta-analyses and 187-article meta-analysis cited in source document.
Vanessa Weiland, NP, HT, MSCP [she/her] is the founder of Phases Clinic and Bendy Menopause. She specializes in menopause, hypermobility, and complex midlife health — and has lived experience with both.
