Childhood Adversities and Chronic Pain

A young blonde girl with her hands over her ears, as her parents shout in the background
Adam Foster

This article is part of our comprehensive guide to living with fibromyalgia.

Childhood adversity does raise the odds of having chronic pain as an adult, and the effect is real, repeatedly replicated and not especially small. Pooled across the largest bodies of work we have, people who report adverse childhood experiences carry somewhere around one and a half to two times the odds of chronic pain later on, and the more adversity there was, the higher those odds climb [1][2][3]. That’s the headline finding really, and it’s been sat there stable for about twenty years now.

What it isn’t, is an explanation for any one person’s pain. A risk factor spread across a population, and a cause sitting inside a single body, are genuinely different objects, and the gap between them is where most of the bad advice on this subject actually lives. Plenty of people with fibromyalgia, chronic widespread pain or hypermobility had perfectly unremarkable childhoods, and plenty of people who had a genuinely awful one are absolutely fine. Both of those groups turn up in the numbers rather than as exceptions to them.

So this isn’t about blame, and it definitely isn’t a polite route to telling you the pain is psychological. Adversity loads the same system that a hypermobile ankle loads and that a bad night’s sleep loads, and none of those things makes pain any less real or any less physical.

Start with the size of it: reporting any adverse childhood experience, with or without the household sort that usually gets counted separately, comes with raised odds of a painful long term condition in adulthood, and that pooled figure sits in the region of one and a half to two times [1].

The same rough magnitude turns up when anxiety is brought into the modelling [2], and when the question is asked about depression alongside pain [4], and it turned up in the earliest work on abuse and adult pain as well, which is a fairly good sign that we’re not actually looking at a recent fashion in how the question gets asked [3].

Now, it’s a dose response, so one adverse experience nudges the odds, four or more pushes them considerably higher, and that pattern has replicated in pooled analyses, in general populations and in people already sitting in pain services [1][5][6]. Cumulative burden is the variable that behaves consistently, which matters practically, as it means the question isn’t really “was there one big thing” so much as “how much was there, and for how long”.

Adversity also seems to be linked to more than whether pain shows up at all, as it tracks with greater severity, with pain in more places, with worse disability and worse quality of life, and with a lower chance of the pain improving over time [5][7]. That last one barely gets mentioned, and it’s the difference between a risk factor for getting pain and a risk factor for keeping it.

And it isn’t an artefact of pain services either, as the association turns up in ordinary working populations in their middle years, in people who were never recruited because of their pain in the first place [8].

One thing worth understanding before you go any further though, is how crude the measurement is at this end of the research. Adversity, in most of this work, means a tick list: physical abuse, emotional abuse, sexual abuse, neglect, someone in the house with an alcohol problem, violence between parents, a parent lost or in prison, poverty, bullying [5][9]. You answer yes or no to each one, and the answers get added up. Which means a single dreadful year and a decade of low grade fear can produce the exact same score, and two people with a four can have had almost nothing in common. That blunt instrument is what all of the numbers above are built on, and it’s part of why the association is moderate rather than enormous.

What Happens When You Ask Children Rather Than Adults

If adversity only mattered through decades of accumulated illness, stress and disadvantage, you’d expect the pain to arrive much later on. It doesn’t, as it’s already there in children.

In a nationally representative group of children and adolescents in the United States, exposure to one or more adverse experiences came with a clearly higher likelihood of chronic pain, with the upper estimates approaching three times, and getting on for one in five of the children with four or more had chronic pain [10]. In Portuguese children, the same dose response was visible at age ten across any pain, pain in several places, and high intensity pain, with the children who’d been through six or more sitting markedly higher on all three [11], and the pattern held as those children moved on into early adolescence [12].

It follows them forwards as well, as early adversity predicted pain that persisted or kept coming back across early adolescence, with part of that route running through anxiety and depression symptoms [13], and by twelve and thirteen, three or more adverse experiences came with higher odds of pain in multiple sites [14].

None of which proves causation, but it does considerably weaken the tidiest sceptical explanation, which is that adults in pain simply remember their childhoods a lot more darkly. A ten year old reporting pain in four places isn’t doing that.

Which Adversities, and Does the Type Matter

Almost everything that gets counted as adversity has been linked to pain somewhere or other: physical abuse, emotional abuse, sexual abuse, neglect, bullying, economic hardship, parental alcohol problems, family violence and losing a parent early have all shown up against pain outcomes in at least some populations [5][9][8].

Model both the type and the total together though, and the total tends to win. Cumulative adversity is the more reliable predictor of common chronic pain conditions in young adults, more so than any individual subtype [15], and there’s some evidence that when it happened matters as well, with particular developmental windows carrying more weight than others [6].

Where it lands is patchier, as adversity has been associated with chronic pelvic pain, period pain and pain with sex [16], with urogenital pain, where negative affect and pain catastrophising carried part of the association [17], with fibromyalgia and chronic widespread pain [5], and with pain in cancer survivors [18]. The strength and consistency vary a great deal by condition though, so this is a family of related findings rather than one clean effect that expresses itself identically everywhere.

Some groups appear to be carrying considerably more of this than others: among people with chronic pain who are lesbian, gay, bisexual, transgender or queer, high adverse experience scores came with higher pain ratings, and sexual trauma specifically was linked to pelvic pain and to fibromyalgia [19].

How Much of This Is Cause, and How Much Is Memory

Most of this evidence is people reporting, as adults, both what happened to them and how much pain they’re in, at the same moment, on the same afternoon [5][20]. Which has an obvious hole in it, as being in long term pain plausibly changes how you remember your childhood, and it certainly changes what you think is worth mentioning.

So the useful question is whether anything at all gets around that, and a bit of it does. Children born in Britain in 1958 who went into institutional care, lost their mother, went through financial hardship, or were in hospital after a road traffic accident by the age of seven, were more likely to have chronic widespread pain at forty five, and that held up after their adult distress and social class were accounted for [21]. Nobody was remembering anything in that one, as the adversity was recorded while they were children.

Adults reporting childhood maltreatment also carried around one and a half times the risk of chronic pain all over the body, and where adult stressful life events were in the picture as well, the combined risk was higher than simply adding the two together would predict [22]. That’s a causal inference method rather than proof, but it does point the same way as the prospective work, which makes pure recall bias an incomplete explanation rather than a dismissal.

There’s a third possibility that deserves a great deal more airtime than it gets, which is that adversity rarely travels alone. It comes with poverty, with disrupted schooling, with housing that moves, with worse access to healthcare and with a family too stretched to chase a diagnosis, and every one of those independently makes long term pain more likely and harder to treat. Some of the work has tried to account for that, and the childhood associations survived adjustment for adult social class in the group followed from 1958 [21], which is reassuring rather than conclusive. Circumstance is part of the biopsychosocial picture, and it’s the part that consistently gets dropped, usually because it’s the part nobody can prescribe for.

Now, the nulls, which are both real and informative, as the association isn’t uniform across every population or design. In adults in their mid eighties it didn’t show up [23], in some clinical samples it’s been absent or much weaker than expected [24], and the prospective work specifically on documented maltreatment is genuinely mixed rather than confirmatory [20].

Read together, the honest position is this: adversity is a real and clinically important contributor, the direction of the effect is consistent, and nobody has demonstrated that it causes chronic pain in the way a fracture causes a limp.

Where Mental Health Fits In

Depression, anxiety and post traumatic stress symptoms explain part of the link, reliably, across adult and adolescent populations [25][26][13]. Part is the operative word though, as the dose response often survives being adjusted for mental health, which means there’s something else going on underneath it [5][25][27].

Post traumatic stress and dissociation look particularly important in people who’ve been through the worst of it, and in high risk groups trauma related symptoms carry a meaningful share of the association [28][29]. The dedicated work on that is thinner than you’d expect for something so clinically obvious, so treat it as a well supported suspicion rather than a settled mechanism.

Beyond the diagnoses, a whole cluster of things have each explained a slice of it in some group or other. Pain catastrophising is raised in those with childhood trauma, though anxiety sensitivity isn’t [30]. Difficulty with emotion regulation accounts for part of the association with chronic low back pain [31], and sleep quality, catastrophising and emotional dysregulation together mediate between post traumatic stress disorder and pain in central sensitisation conditions [32]. How stressful you judge your own life events to be, and how much resilience you’ve got, both change the long term pain picture as well [33].

That list is genuinely the state of knowledge, and it’s a great deal messier than any diagram would have you believe. None of them explains it universally, and every one of them explains a bit of it somewhere.

One thing to keep in mind though, as this is exactly where the biopsychosocial model gets misused. Partial mediation through depression or anxiety doesn’t mean the pain is depression wearing a coat, it means two systems that share a lot of wiring and a lot of history are both being affected by the same early load.

What Might Be Happening in the Body

The epidemiology is in better shape than the mechanisms, by a large margin, and anybody selling you a clean biological story here is ahead of the evidence. What we’ve actually got is four families of candidate explanation, at four quite different levels of confidence.

– Stress system regulation: Probably the strongest of the biological candidates, and it’s still only moderate. Cortisol patterns carried part of the relationship between childhood neglect and both pain and emotional symptoms in people with fibromyalgia [34], and stress system and inflammatory alterations have been looked at together as a route from adversity and anxiety through to adult pain [35]. It fits mechanistically, and it’s still nowhere near nailed down.

– Sensitisation of the nervous system: In adults with chronic back pain and a history of childhood maltreatment, pressure pain thresholds were altered and wind up was increased [36]. Wind up is worth explaining properly, as it’s one of the few things in this whole area you can actually measure in a room. Poke somebody at the same intensity, at the same spot, repeatedly, and the nociceptive input arriving at the spinal cord starts to summate, so the tenth poke is reported as considerably worse than the first, even though nothing about the poke has changed at all. That’s the system turning its own gain up, and it’s a perfectly normal mechanism that can end up set too high. Childhood adversity has also been associated with pain sensitisation more generally [37]. Moderate confidence, on a much smaller evidence base than the epidemiology.

– Brain network differences: Salience, default mode and reward systems all show trauma related differences in people with chronic pain [38], with more recent work pointing at insulo cingulo thalamic dynamics in emotional abuse and neglect (try saying that out loud) [39] and at the reward system where adverse experiences, depression and chronic pain overlap [40]. Weak to moderate, and early, as two of those three are very new, the imaging methods vary enormously between groups, and nobody should be building a treatment on this yet.

– Inflammation: The weakest of the four, and the one most often oversold. C reactive protein and cytokines are plausible candidates, and some of the biomarker work does support a role for them [35][41]. But when inflammatory reactivity was measured directly against both childhood adversity and provoked changes in nociception, it was unrelated to either [42]. Mixed at best, and a pretty poor foundation for anything.

There’s also a strand of animal work in here, and it needs labelling as such. Early life stress alters nociception and neurobiological function in animals, and that work is where a lot of the mechanistic thinking originally came from [43][44]. Early life adversity increasing the risk of chronic pain after trauma has been examined in both people and rodents [45]. Animal findings tell you a mechanism is possible, not that it’s what’s actually happening in a thirty five year old with widespread pain, and nobody has tested most of these pathways directly in people.

Where the Pain Sensitivity Research Disagrees With Itself

One set of findings says adversity leaves the system more sensitive, so lower pressure pain thresholds, more wind up, more generalised hyperalgesia, all in the direction you’d expect [36][37].

The other set says the opposite: in some trauma exposed adolescents, and in young people with depressive disorders, sensitivity was lower and tolerance to experimental heat and cold was greater [46][47].

Both sets of findings are in decent journals, measured with similar equipment, and they point in opposite directions (which is genuinely unhelpful). The best current guess is that trauma shifts how pain is processed differently depending on the population, the age and the task being used to measure it, but that’s an explanation of the inconsistency rather than a resolution of it. If anyone tells you childhood adversity makes you more pain sensitive, full stop, they haven’t read the awkward half.

What Nobody Knows Yet

Quite a lot, actually, and the gaps are specific rather than vague. The research is heavily skewed towards high income countries, and adversity is too often narrowed down to abuse, which leaves neglect, household dysfunction, medical adversity and cultural context badly undermeasured [5][4][42]. If your own history is mostly neglect or chaos rather than anything that would appear in a case file, you are in the least well studied part of this literature.

There are also very few studies that follow pain, adversity and psychiatric symptoms together, repeatedly, over the years that actually matter [5], which is the design that would settle the mediation question, and it mostly hasn’t been done.

And the treatment question is wide open. Adverse childhood experiences have been linked to worse analgesia related outcomes, which is a genuine clinical signal worth knowing about [48], and screening for adversity gets recommended fairly often. Direct evidence that tailoring pain treatment to somebody’s adversity history improves their pain, their function or whether they stick with the programme is limited to the point of absence [48][28]. That’s a gap in the evidence rather than a reason to avoid the subject, and in our opinion it’s the single thing most worth funding.

What This Means If It’s Your History

Right, the practical part! What usually happens first is worth naming, as most people reading this will have already lived through it. A history gets taken, the childhood comes up, and the referral quietly changes direction. Suddenly it’s counselling rather than rehab, and the physical work that was on the table twenty minutes ago is off it, on the unstated assumption that one explanation crowds out the other. The community has been complaining about that for years now and it’s a perfectly reasonable complaint, as psychological support is genuinely useful for a lot of people and it doesn’t replace teaching a nervous system to trust a joint again.

– Treat it as context: Knowing that adversity raises population level odds tells you something true about why your system might be running hot. It doesn’t tell you which tissue hurts, why it hurts today, or what to do in the gym on Tuesday. A conceptual framework for how early adversity feeds into paediatric pain has been sketched out for years now, and it’s still a framework rather than a protocol [49].

– The treatable parts are the ones still happening: You can’t change what happened, obviously. Sleep, emotion regulation and catastrophising are all part of the route, they’re all measurable, and they all respond to work [31][32]. None of that means thinking your way out of pain, it’s the same logic as going after blood volume in POTS, you work on the parts of the system that will actually move.

– Where post traumatic stress is in the picture, treat the post traumatic stress: It carries a real share of the association with pain [28][29], and it’s treatable in its own right. Whether treating it improves the pain specifically hasn’t been shown, so go into that with your eyes open.

– Being asked about it is reasonable: If a clinician asks about your childhood in a pain consultation, that’s defensible, as the association is real and it affects things like how you respond to pain relief [48]. If your history then becomes the whole explanation, and the hypermobility, the sleep, the deconditioning and the dysautonomia all get filed under trauma, that’s a misuse of a population statistic, and you’re allowed to say so out loud.

– Nobody has earned the right to tell you it’s the cause: The evidence supports adversity as one contributor among several. It doesn’t support anybody diagnosing your pain from your childhood, and it certainly doesn’t support the version where a bad childhood means the pain is imaginary.

Adversity is one of the more consistently replicated risk factors we’ve got for chronic pain, and the size of it is moderate rather than overwhelming. What nobody can do though, is take your history and tell you how much of your pain it accounts for.

The Fibro Guy


References

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