The Impact of Childhood Trauma on Chronic Pain

By Grant Frost · Physiotherapist • Last clinically reviewed: 14 May 2026

Chronic low back pain (cLBP) is a leading cause of disability worldwide. While the biopsychosocial model has long recognised that pain is influenced by biological, psychological, and social factors, research on the social dimensions remains surprisingly limited.

A 2025 study published in The Journal of Pain (Thomas et al.) addresses this gap by examining two specific social factors: adverse childhood experiences (ACEs) and neighborhood deprivation. The researchers measured conditioned pain modulation (CPM) - the body's ability to inhibit one pain in the presence of another - in 183 adults with chronic low back pain.

The findings reveal a nuanced relationship: early life adversity impairs pain inhibition, but this effect depends significantly on where a person lives. The study has important implications for how we assess and treat chronic pain, particularly in diverse populations.

What is conditioned pain modulation (CPM)?

Conditioned pain modulation (CPM) is a laboratory measure of the body's endogenous pain inhibition system - essentially, your brain's ability to turn down the volume on pain. The phenomenon is often described as "pain inhibits pain."

In CPM testing, researchers apply a painful stimulus (the test stimulus) before and during the application of a second, conditioning painful stimulus elsewhere on the body. A healthy, efficient CPM response is characterised by reduced pain ratings during the conditioning stimulus - meaning your brain is successfully inhibiting the test pain.

Importantly, a less efficient CPM response (i.e., less pain inhibition) has been associated with the development and maintenance of chronic pain conditions, including chronic low back pain. Understanding what impairs CPM may help identify targets for treatment.

Study design and participants

This study analysed baseline data from a larger parent trial (ERASED - Examining Racial and SocioEconomic Disparities in Chronic Low Back Pain). The sample included 183 community-dwelling adults with chronic low back pain.

Participants completed:

• Adverse Childhood Experiences (ACEs) questionnaire - a standardised measure of early life trauma and adversity
• Area Deprivation Index (ADI) - a validated measure of neighborhood-level disadvantage based on factors like income, education, employment, and housing quality
• Conditioned pain modulation (CPM) testing - laboratory measure of pain inhibition capacity
• Sociodemographic data - including age, sex, race/ethnicity

Key findings: ACEs and pain inhibition

The study tested whether greater exposure to adverse childhood experiences was associated with less efficient conditioned pain modulation (i.e., poorer natural pain inhibition). The answer was not straightforward - it depended on neighborhood deprivation.

For individuals living in less deprived neighborhoods: Higher ACE scores were significantly associated with poorer CPM (less pain inhibition). This suggests that early life adversity has a detectable negative impact on the pain modulation system when current socioeconomic conditions are relatively favourable.

For individuals living in average or highly deprived neighborhoods: There was no significant association between ACEs and CPM. This does not mean that ACEs are not harmful - rather, it suggests that the ongoing stressors of living in a disadvantaged neighborhood may independently impair pain inhibition, making it difficult to isolate the specific contribution of childhood adversity.

The neighbourhood effect: a critical moderator

The most important finding of this study is that the relationship between early life adversity and pain inhibition depends significantly on current socioeconomic context. Why might this be?

High deprivation neighborhoods: People living in disadvantaged areas face numerous ongoing psychosocial stressors - financial strain, food insecurity, exposure to violence, limited healthcare access, and chronic stress. These factors independently impair conditioned pain modulation, creating a "floor effect" where pain inhibition is already compromised regardless of childhood history.

Low deprivation neighborhoods: In more advantaged areas, where current stressors are lower, the specific impact of early life adversity on pain modulation becomes detectable. Without the overwhelming burden of ongoing socioeconomic stress, the long-term consequences of childhood adversity on the pain system become apparent.

As the authors state: "People from disadvantaged backgrounds may experience numerous psychosocial stressors that hinder CPM, making it difficult to assess the specific impact of ACEs on CPM."

From my clinical experience: the sensitised nervous system

This research aligns closely with what I see clinically, day in and day out. The patients who struggle the most with persistent pain are often the ones whose nervous systems have been placed on high alert - not just by the physical insult of an injury, but by the accumulated weight of adverse experiences, chronic stress, trauma, and ongoing life pressures.

Here is what I have learned over 20 years of clinical practice. Your central nervous system does not distinguish between different types of threats. A physically demanding job, financial stress, poor sleep, a difficult childhood, relationship strain, social isolation - your brain processes all of these as signals that the environment is not safe. And when your brain perceives threat, it turns up the volume on pain. It is a protective mechanism. But when the threat signals keep coming - day after day, year after year - that volume knob gets stuck in the up position. The nervous system becomes chronically heightened, sensitised, and hypervigilant.

This is why two people can have identical MRI findings - the same disc bulge, the same arthritic changes - yet one is completely pain-free while the other is debilitated. It is not about the tissue. It is about how the brain is interpreting signals from that tissue. And that interpretation is profoundly shaped by life experience, stress, and perceived safety.

The study's finding that ongoing socioeconomic stressors impair pain inhibition regardless of childhood history makes complete clinical sense. If you are currently living in a high-stress environment - whether that is financial strain, housing instability, job insecurity, or neighbourhood violence - your nervous system is already on high alert. It does not matter whether your childhood was idyllic or traumatic; the current threat signals are dominating the system.

Conversely, in patients who live in relative safety and stability, we can more clearly see the lingering effects of early life adversity. When the current environment is not screaming "threat," the older, quieter programming from childhood becomes audible.

So, what does this mean for treatment? It means we cannot just chase the tissue. We cannot just prescribe stretches and strengthening exercises and wonder why they are not working. We have to ask different questions. We have to understand the person - their history, their current circumstances, their stress load. And we have to help them find ways to signal safety to their nervous system. That might mean addressing sleep, breathing, stress management, social connection, or connecting them with resources to reduce financial or housing stress. It might mean simply helping them understand that their pain is not a sign of damage, but a sign of a sensitised system that needs to learn safety again.

This is not soft science. This is the neuroscience of persistent pain. And studies like this one are finally giving us the language and the evidence to have these conversations.

Clinical implications for physiotherapists and clinicians

This study has several important implications for clinical practice:

1. Assess social context, not just symptoms. A patient's current living situation - neighborhood quality, financial stress, housing stability - may be as important as their clinical presentation in understanding their pain. A thorough biopsychosocial assessment should include questions about socioeconomic context.

2. Childhood adversity matters, but not in isolation. Asking about adverse childhood experiences can provide valuable information, but the interpretation of that history depends on current circumstances. A patient with high ACE scores living in relative advantage may need different support than a patient with similar ACE scores living in poverty.

3. Pain processing can be impaired by multiple pathways. The study demonstrates that both early life adversity AND current socioeconomic stress can impair endogenous pain inhibition. Treatment approaches that only address the peripheral injury or movement mechanics may miss these central pain processing factors.

4. Help patients understand the "why" behind their pain. Explaining that a sensitised nervous system - not just a damaged tissue - is driving their pain can be profoundly reassuring. Many patients have been told their scans look "terrible" and believe they are broken. Reframing chronic pain as a nervous system that has learned to be overprotective (rather than a body that is damaged) opens the door to recovery.

5. Consider referrals to supportive services. For patients living in high-deprivation neighborhoods, addressing pain may require more than physiotherapy alone. Connections to social work, financial counselling, food assistance, or mental health services may be essential components of care.

Study limitations

Several limitations should be considered when interpreting these findings:

• Cross-sectional design - The study cannot establish causation. The observed associations may be bidirectional or influenced by unmeasured factors.
• Self-reported ACEs - Adverse childhood experiences were measured by retrospective self-report, which may be subject to recall bias.
• Area Deprivation Index is a proxy - ADI measures neighborhood-level factors, not individual socioeconomic status. Individual-level factors may differ within neighborhoods.
• Single CPM measurement - Conditioned pain modulation was measured once; test-retest reliability of CPM can be variable.
• Specific sample - Findings may not generalise to other chronic pain conditions or populations outside the geographic region studied.
• No direct measure of current stress - The study did not measure current psychosocial stress directly, which may be the mechanism linking neighborhood deprivation to impaired CPM.

Conclusions

This study demonstrates that early life adversity is associated with abnormal endogenous pain modulation, but only for individuals living in less deprived neighbourhoods. For those in highly deprived areas, the ongoing stressors of disadvantaged living may independently impair pain inhibition, making it difficult to detect the specific contribution of childhood adversity.

The findings highlight the importance of assessing both historical and current social factors when evaluating and treating chronic low back pain. A purely biomedical or even psychological approach that ignores socioeconomic context is incomplete.

As the authors conclude: "People from disadvantaged backgrounds may experience numerous psychosocial stressors that hinder CPM, making it difficult to assess the specific impact of ACEs on CPM." Clinically, this means that patients living in disadvantage may need support addressing current stressors before the long-term consequences of childhood adversity can be effectively addressed.

Frequently asked questions

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