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European Journal of Psychotraumatology logoLink to European Journal of Psychotraumatology
. 2026 Aug 13;17(1):2708407. doi: 10.1080/20008066.2026.2708407

Long-term impact of childhood exposure to interparental physical violence on cancer risk in adulthood: a prospective cohort study

Impacto a largo plazo de la exposición en la infancia a violencia Física entre los padres sobre el riesgo de cáncer en la edad adulta: un estudio de cohorte prospectivo

Lele Chang a,b,*, Yuting Shi a,b,*, Yaxin Kang a,b, Yuqin Wang a,b, Xinyu Zhang a,b, Jing Liu a,b, Na Lu c,†,CONTACT, Qin Xu a,b,✉
PMCID: PMC13474521  PMID: 42592666

ABSTRACT

Background: Adverse childhood experiences (ACEs) are known to contribute to increased long-term cancer risk. However, the specific association between childhood exposure to interparental physical violence and the incidence of cancer in adulthood remains poorly understood.

Methods: This prospective cohort study utilized data from the China Health and Retirement Longitudinal Study (CHARLS), which included 11,825 participants aged 45 years or older enrolled from 1 June 2011, and followed until 31 December 2020. Exposure to interparental physical violence during childhood was assessed via a life history questionnaire evaluating the frequency of witnessing physical violence between parents. Depressive symptoms were measured using the 10-item Center for Epidemiologic Studies Depression Scale. The primary outcome was physician-diagnosed cancer (excluding minor skin cancers), identified through follow-up self-reports. Multivariable Cox proportional hazards regression models with attained age as the time scale were employed for analysis.

Results: Among the 11,825 participants (mean age 58.4 ± 9.0 years; 52.2% female), childhood exposure to interparental violence was significantly associated with an elevated risk of cancer (HR = 2.97, 95% CI: 1.52–5.80). A significant dose–response relationship was observed (p for trend < 0.01). Depressive symptoms were more prevalent in the exposed group and mediated approximately 28.9% of the total association between violence exposure and cancer risk (HR = 2.40, 95% CI: 1.13–5.11).

Conclusions: In a national cohort, childhood exposure to interparental violence was associated with an elevated risk of adult cancer incidence, partly through depressive symptoms. Preventing domestic violence and early psychological intervention may reduce long-term cancer burden.

KEYWORDS: Adverse childhood experiences, interparental violence, cancer, depressive symptoms, cohort study

HIGHLIGHTS

  • Witnessing physical violence between parents during childhood was linked to a higher risk of developing cancer in adulthood.

  • The risk of cancer increased with more frequent exposure to parental violence, suggesting a dose–response relationship.

  • Depressive symptoms in adulthood partly explained this long-term connection, highlighting the importance of early family support and mental health care.

1. Introduction

Adverse childhood experiences (ACEs), encompassing physical, psychological, or sexual abuse, as well as household dysfunction such as parental divorce, incarceration of a family member, or mental illness within the household (Adams et al., 2005), have been extensively documented to exert profound and lasting effects on physical and mental health in adulthood (Bengtsson et al., 2023; Cheng et al., 2025). A dose–response relationship exists between cumulative childhood adversity and increased risk of adverse health behaviours and chronic diseases, including cancer (Felitti et al., 1998; Lin et al., 2021). Growing evidence indicates that ACEs disrupt optimal development and are associated with poorer outcomes across the life course (Anda et al., 2004; Finkelhor et al., 2013; Liu et al., 2013).

In recent years, there has been accumulating research on the mechanistic pathways linking childhood experiences to adult cancer. Karnes et al. (Karnes et al., 2025) highlighted a cross-culturally consistent association between social adversity (such as community or wartime violence) and chronic disease risk – including cancer – though specific risk patterns may vary across cultures and healthcare systems. Various forms of childhood adversity may contribute to increased cancer risk (Holman et al., 2016), and child abuse, in particular, is associated with elevated cancer incidence (Afifi et al., 2016; Hovdestad et al., 2020; Hu et al., 2021; Hyland et al., 2013). ACEs related to the family environment may operate through biological and behavioural pathways, warranting further investigation.

Although a limited number of studies have established an association between ACEs and adult cancer risk (Hughes et al., 2017), evidence specifically focusing on childhood exposure to interparental physical violence and its relationship with cancer incidence remains scarce. Furthermore, population-based studies quantifying the prevalence of childhood exposure to interparental violence and its association with cancer development in adulthood are still lacking. Therefore, this study aims to prospectively examine the association between childhood exposure to interparental violence and adult cancer risk, and to further investigate the potential mediating role of depressive symptoms in a nationally representative cohort.

2. Methods

2.1. Setting and data source

The China Health and Retirement Longitudinal Study (CHARLS) is an ongoing prospective cohort study established in 2011, which enrols adults aged 45 years or older. Participants are followed up every two years through face-to-face questionnaire surveys and in-person physical examinations. This analysis includes data from 1 June 2011, to 31 December 2020. The CHARLS protocol was approved by the Ethical Review Committee of Peking University, and all participants provided written informed consent. The study adheres to the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) reporting guidelines.

This study used publicly available data from the China Health and Retirement Longitudinal Study (CHARLS). The CHARLS study was approved by the Ethical Review Committee of Peking University, and all participants provided written informed consent prior to enrolment. Since this study involved only the analysis of de-identified, publicly accessible data, no additional ethical approval was required.

2.2. Definition of childhood interparental physical violence

Information on early life adversity, defined as adverse experiences occurring before the age of 17, was collected during the 2014 Life History Survey via face-to-face interviews (Lin et al., 2022). Specifically, participants were asked: ‘Has your father ever physically beaten your mother? Or has your mother ever physically beaten your father?’ Response options for each item included: never, not often, sometimes, and often. Those responding ‘sometimes’ or ‘often’ to either parent perpetrating violence were classified as exposed; others were non-exposed (Lin et al., 2022). The frequency of interparental physical violence was also analysed.

2.3. Definition of cancer

Based on previous studies, the primary outcome was defined as a cancer event identified through the following question: participants were asked whether they had ever been told by a physician that they had cancer or a malignant tumour (excluding minor skin cancers) (Gao et al., 2025; Yan et al., 2025). In the follow-up survey, those who responded ‘yes’ were considered cancer survivors (Gao et al., 2025; Yan et al., 2025). To further characterize the type of cancer, participants were also asked in which organ or part of the body the cancer was (or had been) located. Both primary and metastatic tumours were included.

2.4. Assessment of covariates

Information regarding sociodemographic characteristics, health-related behaviours, and history of chronic diseases was collected at baseline using a semi-structured questionnaire. Demographic information included age, gender (self-reported as male or female), marital status (married, single), and educational level (illiterate, primary school or below, secondary to vocational school, university or above). Health-related behaviours included smoking status, drinking status (yes, no). In this study, participants were asked: ‘Have you ever chewed tobacco, smoked a pipe, smoked self-rolled cigarettes, or smoked cigarettes/cigars?’ Those who responded ‘No’ were categorized as ‘Non-smokers.’ Participants who had smoked in the past but had quit were classified as former smokers, whereas those who reported current smoking were classified as current smokers. Drinking frequency included: (1) drinking more than once a month; (2) drinking but less than once a month; (3) none of these. In our analysis, participants who drink alcohol more than once a month and those who drink alcohol less than once a month are classified as drinkers. Body mass index (BMI) was calculated and categorized (<24 vs. ≥ 24 kg/m²) according to the body mass index criteria of the National Working Group for Obesity in China (WGOC-BMI criteria) (Zhou, 2002). Health status factors included self-reported physician-diagnosed comorbidities (hypertension, diabetes, dyslipidemia). Childhood physical abuse by parents was asked, ‘When you were growing up, did your female/male guardian ever hit you?’ (Lin et al., 2022). Participants were also be asked, ‘When you were a child, how often were you picked on or bullied by kids in your neighborhood? Is it often, sometimes, rarely or never?’ and ‘When you were a child, how often were you picked on or bullied by kids in your school? Is it often, sometimes, rarely or never?’ Depressive symptoms were measured via the short form of the 10-item CES-D. A total score of 12 or higher was used to indicate depressive symptoms (Chen & Mui, 2014; Cui et al., 2024; Lin et al., 2022). Details are shown in Supplement 1.

2.5. Statistical analysis

Baseline characteristics are presented as mean (standard deviation, SD) for continuous variables and as proportions (percentages) for categorical variables. Missing data were observed in 28% (3318/11825) of covariates, primarily involving drinking status, depressive symptoms, and BMI. To handle missing covariates, we employed complete-case analysis, which included only participants with complete data on all covariates (n = 8,507), and compared the baseline characteristics between the original and complete-case datasets.

We calculated the follow-up time for each participant from the baseline assessment until the date of cancer diagnosis, death, or the end of the follow-up period, whichever occurred first. Multivariable Cox proportional hazards regression models were employed to evaluate the associations between exposure to parental violence during childhood, the frequency of parental violence exposure, and cancer incidence, with results expressed as hazard ratios (HRs) accompanied by 95% confidence intervals (CIs) (Thiébaut & Bénichou, 2004). The analysis used age at baseline and age at the end of follow-up as the time scales in the Cox proportional hazards regression models (Cui et al., 2024). We employed two adjustment strategies: Model 1 adjusted for age and gender, while Model 2 additionally included educational level, smoking status, drinking status, and BMI. Considering their potential mediating role, hypertension, dyslipidemia, and diabetes were not adjusted for in the main analyses. Sensitivity analyses included: complete-case analysis (n = 8,507) to address missing data; applying the inverse probability of treatment weighting (IPTW) method to further control for confounding bias; and competing risk regression using Fine-Gray models to account for mortality. To evaluate potential effect modification, we assessed the relationship between childhood interparental violence exposure and cancer incidence stratified by drinking status, hypertension status, and BMI. Multiplicative interaction was tested by introducing product terms in Cox proportional hazards regression models.

We quantified the population-level impact of childhood interparental violence exposure on cancer risk by calculating the Population Attributable Fraction (PAF) (Liu et al., 2023; Xu et al., 2025). Using the ‘AF’ package in R, we estimated PAF and 95% CIs through Cox proportional hazards regression, with Model 1 adjusting for age and sex, and Model 2 further adjusting for education, smoking, drinking status, and BMI. To examine the potential mediating role of adult depressive symptoms in the association between childhood exposure to interparental violence and cancer, we conducted a mediation analysis by calculating the Percentage of Excess Risk Mediated (PERM) (Cui et al., 2024).

All statistical analyses were performed using R software, version 4.5.1 (R Project for Statistical Computing). A 2-sided p < 0.05 was considered statistically significant.

3. Results

3.1. Participant characteristics

Table 1 shows that the baseline characteristics according to the frequency of experiencing childhood interparental physical violence. Among the 11,825 participants included, the mean (SD) age was 58.4 (9.0) years, with 6,173 (52.2%) being female and 5,652 (47.8%) male. Gender distribution differed significantly across violence exposure groups, with a notably higher proportion of females in the ‘often’ exposed group (61.0%). A total of 173 participants (1.46%) reported experiencing interparental violence during childhood. Compared to those who were never exposed, participants who were often exposed to interparental violence in childhood tended to have lower educational attainment, higher rates of childhood physical abuse by parents, and a greater prevalence of depressive symptoms in adulthood (Table 1).

Table 1.

Baseline characteristics of participants by childhood exposure to interparental violence.

Frequency of interparental physical violenceb
  Overall No-exposure Exposure Never Rarely Sometimes Often
Characteristica (N=11825) (n=11652) (n=173) (n=11241) (n=411) (n=132) (n=41)
Age, mean (SD), y 58.4 (9.0) 58.4 (9.0) 57.7 (8.7) 58.4 (9.0) 58.4 (9.4) 57.6 (8.9) 57.8 (8.1)
Female, No. (%) 6173 (52.2) 6080 (52.2) 93 (53.8) 5903 (52.5) 177 (43.1) 68 (51.5) 25 (61.0)
Educational level, No. (%)              
 University or above 221 (1.9) 218 (1.9) 3 (1.7) 209 (1.9) 9 (2.2) 2 (1.5) 1 (2.4)
 Secondary to vocational school 3799 (32.1) 3749 (32.2) 50 (28.9) 3617 (32.2) 132 (32.1) 42 (31.8) 8 (19.5)
 Primary school or below 4768 (40.3) 4693 (40.3) 75 (43.4) 4513 (40.1) 180 (43.8) 58 (43.9) 17 (41.5)
 Illiterate 3037 (25.7) 2992 (25.7) 45 (26.0) 2902 (25.8) 90 (21.9) 30 (22.7) 15 (36.6)
Married, No. (%) 10581 (89.5) 10426 (89.5) 155 (89.6) 10057 (89.5) 369 (89.8) 120 (90.9) 35 (85.4)
Smoking status, No. (%)              
 Non-smoker 7140 (60.4) 7040 (60.4) 100 (57.8) 6814 (60.6) 226 (55.0) 70 (53.0) 30 (73.2)
 Former smoker 903 (7.6) 888 (7.6) 15 (8.7) 859 (7.6) 29 (7.1) 13 (9.8) 2 (4.9)
 Current smoker 3782 (32.0) 3724 (32.0) 58 (33.5) 3568 (31.7) 156 (38.0) 49 (37.1) 9 (22.0)
Drinking, No. (%) 4021 (34.0) 3953 (34.0) 68 (39.3) 3786 (33.7) 167 (40.7) 52 (39.4) 16 (39.0)
BMI≥24, No. (%) 3888 (40.4) 3828 (40.4) 60 (41.7) 3705 (40.5) 123 (36.7) 49 (43.0) 11 (36.7)
Depressive symptoms, No. (%)c 2910 (27.4) 2855 (27.2) 55 (35.3) 2744 (27.1) 111 (30.2) 40 (33.3) 15 (41.7)
Comorbidity, No. (%)              
 Hypertension 2841 (24.0) 2798 (24.0) 43 (24.9) 2714 (24.1) 84 (20.4) 35 (26.5) 8 (19.5)
 Diabetes 657 (5.6) 648 (5.6) 9 (5.2) 622 (5.5) 26 (6.3) 7 (5.3) 2 (4.9)
 Dyslipidemia 1061 (9.0) 1040 (8.9) 21 (12.1) 1015 (9.0) 25 (6.1) 18 (13.6) 3 (7.3)
Childhood physical abuse by parents, No. (%) 3996 (33.9) 3876 (33.4) 120 (69.8) 3600 (32.2) 276 (67.6) 93 (71.0) 27 (65.9)
Peer bullying, No. (%) 1755 (14.9) 1701 (14.6) 54 (31.8) 1582 (14.1) 119 (29.0) 40 (30.5) 14 (35.9)
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Abbreviation: BMI, body mass index (calculated using self-reported weight in kilograms divided by height in meters squared). a Covariate missingness: drinking (n = 41), BMI (n = 2658), and depressive symptoms (n = 1189). b Childhood exposure to interparental violence was defined as witnessing interparental violence before participants were 17 years of age. In the dichotomous analysis, responses of “sometimes” or “often” were classified as exposed, whereas “never” or “rarely” were classified as non-exposed. c Depressive symptoms were defined as a 10-item Center for Epidemiologic Studies Depression Scale score of 12 or more.

This study was conducted among participants common to both the 2011 Health Survey and the 2014 Early Life Experience Survey. The 2011 Health Survey included 17,705 subjects, and the 2014 Early Life Survey included 20,452 subjects, with 14,375 matched participants identified across both surveys. Subsequently, subjects with missing age or sex data and those lacking data on childhood exposure to interparental violence were excluded. Further exclusions were applied for age below 45 years and the presence of cancer at baseline. A total of 11,825 subjects were finally enrolled and followed until 2020. A detailed flowchart of the inclusion and exclusion procedures is presented in Figure A1.

3.2. Interparental physical violence and cancer

During a follow-up period of up to 9 years, 277 incident cases of physician-diagnosed cancer were documented. We observed that individuals who experienced interparental physical violence during childhood had a higher cumulative incidence of cancer compared to those without such exposure (2.8 vs. 6.2 per 1000 person-years) (Table 2), and the cumulative hazard is illustrated in Figure 1. After adjusting for age and gender in Model 1, a significantly increased hazard ratio was observed (HR = 2.33, 95% CI: 1.20–4.52). The association was further strengthened after additional adjustment for educational level, smoking status, drinking status, and BMI in Model 2 (HR = 2.97, 95% CI: 1.52–5.80) (Table 2). As shown in Table 3, a significant dose–response relationship was observed between the frequency of witnessing interparental violence and cancer risk. Compared with the ‘never’ group, participants who reported ‘often’ witnessing violence exhibited a substantially higher incidence rate (14.7 per 1000 person-years) and significantly increased hazards of cancer in both Model 1 (HR = 5.33, 95% CI: 2.20–12.93) and Model 2 (HR = 7.80, 95% CI: 3.20–19.04) (Table 3).

Table 2.

Association between childhood exposure to interparental physical violence and incident cancer, 2011–2020.

          Model 1a Model 2b
Outcome No. of participants Incident cases, No. Person-years Incidence rate (per 1000 person-years) HR (95% CI) HR (95% CI)
Dichotomous            
No interparental violence 11625 268 96816 2.8 1 [Reference] 1 [Reference]
Interparental violencec 173 9 1447 6.2 2.33（1.20-4.52） 2.97（1.52-5.80）
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Abbreviations: HR, hazard ratio; NA, not applicable.

a

Model 1: adjusted for age and gender.

b

Model 2: adjusted for age, gender, educational level, smoking status, drinking status and BMI.

c

Childhood exposure to interparental violence was defined as witnessing interparental violence sometimes or often when participants were younger than 17 years.

Figure 1.

Two line graphs showing age on the x axis and cancer cumulative hazard on the y axis by exposure level to interparental violence. The figure shows two line graphs of cancer cumulative hazard in relation to witnessing interparental physical violence during childhood. Both graphs have age in years on the horizontal axis ranging from 40 to 100 with tick marks every 10 years, and cumulative hazard on the vertical axis. The left graph is titled exposure to interparental physical violence for cancer sample size 277 and compares 2 step shaped curves: a lower curve labeled none and a higher curve labeled exposure. Both start near hazard 0.00 around age 45. The exposure curve rises more steeply, reaching about 0.25 by age 75, while the none curve increases gradually to about 0.18 by age 95. The right graph is titled frequency of exposure to interparental physical violence for cancer sample size 277 and displays 4 step shaped curves labeled never, rarely, sometimes, and often. All curves start near hazard 0.00 around age 45. The often curve stays at 0.00 until about age 52, then rises in large steps to about 0.60 by age 75. The rarely and sometimes curves increase more slowly, reaching around 0.20 to 0.30 by ages 80 to 90. The never curve remains the lowest, ending near 0.22 by age 100. All data are approximate.

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Cumulative hazard of cancer according to interparental physical violence experience. A: Exposure to interparental physical violence; B: Frequency of exposure to interparental physical violence.

Table 3.

Association between the frequency of witnessing interparental physical violence and incident cancer, 2011–2020.

Outcome No. of participants Incident cases, No. Person-years Incidence rate (per 1000 person-years) Model 1a HR (95% CI) Model 2b HR (95% CI)
Frequency            
Never 11241 258 93361 2.8 1 [Reference] 1 [Reference]
Rarely 411 10 3455 2.9 1.05（0.56-1.98） 0.97（0.45-2.06）
Sometimes 132 4 1107 3.6 1.37（0.51-3.67） 1.67（0.62-4.50）
Often 41 5 340 14.7 5.33（2.20-12.93） 7.80（3.20-19.04）
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Abbreviations: HR, hazard ratio; NA, not applicable.

a

Model 1: adjusted for age and gender.

b

Model 2: adjusted for age, gender, educational level, smoking status, drinking status and BMI.

c

P for trend was calculated using the frequency of witnessing interparental violence as a continuous variable. P for trend was 0.008 in Model 1 and 0.001 in Model 2.

3.3. Sensitivity analysis and competing risk analysis

The sensitivity analyses consistently demonstrated a robust association between childhood exposure to interparental physical violence and cancer risk across various model specifications. In the dichotomous exposure analysis, individuals exposed to interparental violence (having witnessed violence sometimes or often) showed significantly elevated cancer risks in the three sensitivity models. Table A1 summarizes the baseline characteristics between the whole dataset and complete dataset (n = 8507), showing generally similar distributions across most covariates. The results remained consistent after additional covariate adjustment, complete-case analysis, and applying the IPTW method, supporting a robust and dose-dependent association between childhood exposure to interparental violence and increased cancer risk in adulthood (Table A2). Considering the competing risk of death, the association between childhood exposure to interparental physical violence and cancer risk remained statistically significant. Results from both the Cox model (HR = 2.969, 95% CI: 1.521–5.795, p = 0.001) and the Fine-Gray subdistribution hazard model (HR = 2.922, 95% CI: 1.512–5.650, p = 0.001) were highly consistent after multivariable adjustment, supporting the robustness of this association (Table A3).

3.4. Subgroup analysis

Subgroup analyses revealed consistently elevated cancer risks associated with childhood exposure to interparental violence, with particularly strong effects observed among frequent-exposure subgroups. Notably, the highest risk was identified in participants with BMI ≥24 (HR = 11.13, 95% CI: 3.509–35.28 for often witnessing violence). No significant interaction effects were detected for drinking status, hypertension, or BMI (all p-interaction > 0.05) (Table A4).

3.5. PAF associated with childhood interparental physical violence

Table 4 presents the PAF of cancer associated with childhood exposure to interparental physical violence. In Model 1 (adjusted for age and gender), the PAF was 1.89% (95% CI: 0.28%–4.88%). After further adjustment for educational level, smoking status, drinking status, and BMI, the PAF increased to 2.75% (95% CI: 0.73%–6.47%). Moreover, the high-frequency exposure subgroup (‘often’ witnessing violence) exhibited a substantially higher attributable risk in Model 2, with a PAF of 29.79% (95% CI: 22.54%–33.41%).

Table 4.

Population Attributable Fraction (PAF) of childhood exposure to interparental physical violence (IPV) of cancer.

    Model 1a Model 2b
  No. of cancer cases / total exposed PAF (95% CI),% PAFd (95%CI),%
Interparental physical violence      
Dichotomous      
No-exposure 268/10071 NA NA
Exposure c 9/149 1.89(0.28-4.88) 2.75(0.73-6.47)
Frequency      
Never 258/9707 NA NA
Rarely 10/364 NA NA
Sometimes 4/113 NA NA
Often 5/36 21.36(12.67-26.80) 29.79(22.54-33.41)
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a

Model 1: adjusted for age and gender.

b

Model 2: adjusted for age, gender, educational level, smoking status, drinking status and BMI.

c

Childhood exposure to interparental violence was defined as witnessing interparental violence sometimes or often when participants were younger than 17 years.

d

PAF = [Exposure Prevalence * (HR - 1)] / [Exposure Prevalence * (HR - 1) + 1]. HR for the dichotomous (no exposure vs. exposure) and frequency-stratified (never, rarely, sometimes, and often) exposure groups are presented in Tables 2 and 3, respectively.

3.6. Mediation of adult depressive symptoms

At baseline, 2490 of the 9195 participants (27.1%) with available data on the 10-item Center for Epidemiologic Studies Depression Scale questionnaire exhibited depressive symptoms. We found that childhood exposure to interparental physical violence was significantly associated with depressive symptoms in adulthood. In the fully adjusted model (Model 2), the odds of depressive symptoms were significantly increased among exposed individuals compared with the unexposed group (OR = 1.519, 95% CI: 1.024–2.228) (Table A5). Mediation analysis indicated that adult depressive symptoms accounted for 28.9% (PERM = 28.9%) of the total association between childhood exposure to interparental violence and cancer risk. After further adjustment for depressive symptoms, HR for the association between violence exposure and cancer decreased from 2.969 (95% CI: 1.521–5.795) in the multivariate-adjusted model to 2.401 (95% CI: 1.128–5.111) (Table A6).

4. Discussion

4.1. Childhood exposure to interparental violence and adult cancer risk

In this large-scale prospective cohort study, childhood exposure to interparental physical violence was significantly associated with an elevated risk of adult cancer, with a clear dose–response relationship. The association remained robust across sensitivity analyses and competing risk models. Depressive symptoms mediated 28.9% of the effect, and the PAF was 2.75% overall, rising to 29.8% in the high-frequency exposure group.

4.2. Comparison with previous studies on adverse childhood experiences

Previous studies have reported a significant association between cumulative ACEs and an increased risk of cancer in adulthood (Bellis et al., 2015; Brown et al., 2013; Felitti et al., 1998; Hu et al., 2021; Kelly-Irving et al., 2013; Morton et al., 2012), with a well-established dose–response relationship between ACEs and cancer risk (Anda et al., 2010; Felitti et al., 1998; Lin et al., 2021). A meta-analysis by Hughes et al., focusing on the health impacts of multiple ACEs, found that individuals with at least four ACEs had a 2.31-fold higher risk of cancer compared to those with no ACEs (Hughes et al., 2017). Various forms of childhood adversity may contribute to an elevated risk of cancer (Holman et al., 2016). Hu et al. (2021) observed a significant dose–response relationship between ACEs and cancer risk in adulthood, with the magnitude of risk varying by ACE type and cancer site. Physical abuse, sexual abuse, exposure to intimate partner violence, and household economic hardship were positively associated with cancer incidence later in life. However, most studies have focused on the overall burden of ACEs or direct child maltreatment, while evidence specifically examining the association between exposure to interparental physical violence – a distinct form of household dysfunction – and cancer risk remains limited. Our study extends the current evidence by prospectively confirming the independent effect of this specific type of ACE.

4.3. Novelty and contribution of the present study

Although two cross-sectional studies have examined the association between childhood exposure to interparental violence and cancer prevalence (Amemiya et al., 2019; Langiano et al., 2026), both were limited by their cross-sectional design and neither examined the dose–response relationship between the frequency of witnessing interparental violence and cancer risk, nor quantified the mediating role of depressive symptoms in this association. Therefore, prospective evidence specifically focusing on childhood exposure to interparental physical violence as a distinct exposure type remains limited. By incorporating a nationally representative prospective cohort with detailed information on childhood exposure to interparental violence, we were able to investigate the relationship between the exposure and frequency of such experiences and adult cancer. Our findings indicate that childhood exposure to interparental physical violence is associated with an increased risk of cancer in later life, with a significant dose–response relationship – individuals frequently exposed to interparental violence exhibited the highest cancer risk compared to those unexposed. Consistent with our results, the landmark US Kaiser-CDC study also demonstrated that cumulative ACE exposure is associated with an elevated risk of cancer in adulthood.

4.4. Potential mechanisms and population context

In recent decades, the intergenerational impact of parental behaviour and family functioning on offspring has garnered increasing attention. Across different countries, the association between ACEs and cancer has been consistent; however, due to societal differences, the influence of certain ACEs (such as parental divorce, fear of a family member, or childhood poverty) may vary considerably between nations. A comparative cross-sectional study between Japan and Finland found that ‘fear of a family member’ (assessed directly in Finland and approximated by ‘witnessing domestic violence or physical abuse’ in Japan) was significantly associated with increased cancer incidence among Finnish adults, but not in the Japanese population, and vice versa (Amemiya et al., 2019). These cross-cultural differences may reflect variations in societal norms regarding family violence, differences in help-seeking behaviours and social support systems, as well as disparities in healthcare access and cancer screening practices between Asian and European populations. Our analysis revealed that 1.5% of participants reported exposure to interparental physical violence during childhood, and the PAF for cancer associated with such exposure was 2.75%. These findings enhance understanding of the intergenerational consequences of interparental violence and underscore the importance of reducing domestic violence.

The mechanisms linking childhood exposure to interparental violence and adult cancer risk are likely multifactorial, involving interconnected psychological, behavioural, and biological pathways (Karnes et al., 2025), as proposed in life-course epidemiology and stress-embedding theory (Shonkoff & Garner, 2012).

From a psychosocial perspective, exposure to interparental violence during childhood substantially increases the risk of long-term mental health problems, particularly depressive symptoms (Bellis et al., 2019; Hughes et al., 2017; Karnes et al., 2025; Özkan et al., 2023; Roland et al., 2021; Zhao et al., 2022). Consistent with this pathway, our mediation analysis demonstrated that depressive symptoms accounted for 28.9% of the association between childhood violence exposure and adult cancer risk, providing empirical support for depression as a key psychobiological mediator. Persistent depressive symptoms may translate early psychosocial stress into long-term physiological dysregulation.

Behavioural and metabolic pathways may further contribute to this association. Childhood adversity has been linked to established cancer risk behaviours, including smoking, alcohol consumption, physical inactivity, and unhealthy dietary patterns (Campbell et al., 2016; Duffy et al., 2018; Ford et al., 2011; Xu et al., 2023), as well as reduced adherence to cancer screening (Alcalá et al., 2017; Alcalá et al., 2018; Pohl et al., 2025). In addition, chronic stress related to early-life violence exposure may promote obesity (Kappes et al., 2023; Koball et al., 2024; Wiss & Brewerton, 2020; Zhou et al., 2024) and metabolic dysfunction (Pervanidou & Chrousos, 2012; Souama et al., 2024). In line with this pathway, our subgroup analysis revealed a markedly stronger association between interparental violence and cancer risk among participants with a BMI ≥24, suggesting a potential synergistic effect between metabolic dysregulation and early psychosocial adversity.

At the biological level, accumulating evidence indicates that early-life stress may induce long-lasting alterations in stress-regulatory systems, immune function, and inflammatory processes (Berens et al., 2017; Jiang et al., 2025; Reiche et al., 2004). Depression-related dysregulation of the hypothalamic–pituitary–adrenal axis (Dai et al., 2020; Iob et al., 2020; Reiche et al., 2004), chronic low-grade inflammation (Chen et al., 2025; Marinovic & Hunter, 2022), and impaired immune surveillance (Reiche et al., 2004; Spoletini et al., 2008) may jointly contribute to carcinogenesis. These biological processes provide plausible mechanisms through which childhood exposure to interparental violence may exert enduring effects on cancer risk across the life course.

Beyond individual-level psychological, behavioural, and biological mechanisms, socioeconomic and environmental factors may constitute additional pathways linking childhood adversity to cancer risk. Socioeconomic disadvantage, such as lower educational attainment and household income, may compound the effects of early-life stress by limiting access to health-promoting resources and increasing cumulative stress exposure (Nicolau et al., 2019; Shu et al., 2025; van der Linden et al., 2018). Furthermore, environmental factors, including geographical context and workplace conditions, may contribute to cancer risk through differential exposure to occupational carcinogens, ambient air pollution, and healthcare infrastructure (Carroll et al., 2023; Do & Zhang, 2025; Hurbain et al., 2024). These factors may interact with early-life adversity to shape long-term health trajectories.

4.5. Strengths and limitations

This large-scale, prospective, nationwide cohort study, with its long-term follow-up design, provides robust epidemiological evidence supporting the association between childhood exposure to interparental violence and increased cancer risk in adulthood, with a clear dose–response relationship that is consistent with a long-term adversity pathway. Notably, this study is the first to identify depressive symptoms as a partial mediator in this relationship among an Asian middle-aged and elderly population, accounting for 28.9% of the total effect, thereby offering valuable empirical insight into the psychobiological mechanisms linking early-life adversity to long-term health outcomes. Several limitations should be considered. First, assessment of childhood exposure to interparental violence was based on retrospective self-report, which may introduce recall bias. Second, although extensive adjustments were made for potential confounders, residual confounding – such as genetic predisposition or other unmeasured childhood adversities – cannot be fully excluded. Third, information on family history of cancer was not available in the CHARLS dataset, and detailed data on cancer subtypes were also lacking; moreover, the limited number of cancer cases (n = 277) precluded further stratification by specific cancer types. These limitations constrain our ability to adjust for genetic susceptibility and to explore potential heterogeneity across different cancer sites. Moreover, owing to the relatively small number of participants in the high-exposure group and the low incidence of cancer, future studies with larger sample sizes are warranted to more precisely estimate risk gradients by frequency of exposure. Finally, differences in familial and sociocultural contexts may affect the generalizability of our findings to other populations. Future research should involve multi-national cohorts to enhance statistical power and facilitate further investigation into: (1) the association between interparental violence and organ-specific cancer risks; (2) the biological, physiological, and behavioural pathways mediating the effect of adverse childhood experiences on cancer development; and (3) the efficacy of early psychological and behavioural interventions targeting children exposed to domestic violence.

4.6. Clinical implications

This study suggests that childhood exposure to interparental violence serves as an important warning sign for long-term cancer risk. In clinical practice, it should be systematically assessed to identify high-risk individuals and enhance early monitoring. At the public health level, it is essential to strengthen primary prevention of domestic violence and provide timely psychological support for exposed children, aiming to interrupt the depressive mediation pathway and reduce long-term disease risk. Furthermore, there is an urgent need to establish an interdisciplinary ‘pediatrics – psychology – adult medicine’ collaborative system to enable comprehensive intervention from childhood adversity to adult health, thereby alleviating the overall burden of disease.

5. Conclusions

Based on a nationally representative, large-scale prospective cohort, this study provides evidence for a significant association between childhood exposure to interparental physical violence and the risk of cancer in adulthood among middle-aged and older Chinese adults, with a clear dose–response relationship observed. Adult depressive symptoms partially mediated the association between childhood exposure to interparental violence and cancer incidence, suggesting that such early-life adversity may contribute to long-term cancer risk, in part through sustained psychological distress. These findings emphasize the need for early prevention of domestic violence and psychological support to reduce long-term cancer risk.

Supplementary Material

Table A3.doc
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Figure A1.tif
ZEPT_A_2708407_SM1969.tif (2.4MB, tif)
supplement 1.docx
ZEPT_A_2708407_SM1968.docx (13.8KB, docx)
Table A6.doc
ZEPT_A_2708407_SM1967.doc (29.5KB, doc)
Table A1.docx
ZEPT_A_2708407_SM1966.docx (16.6KB, docx)
Table A5.doc
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Table A4.doc
ZEPT_A_2708407_SM1964.doc (59.5KB, doc)
Table A2.docx
ZEPT_A_2708407_SM1963.docx (17.8KB, docx)

Acknowledgements

We sincerely extend our gratitude to all the members and every participant of the CHARLS for their time and effort dedicated to the project. Their contributions have been invaluable to our research, providing essential data resources and critical research opportunities.

Funding Statement

This work was supported by the Fujian Cancer Hospital High-Level Talent Training Program (2023YNG09), the Joint Funds for the Innovation of Science and Technology, Fujian Province (2023Y9449; 2023Y9451; 2024Y9593; 2024Y9600), and the National Clinical Key Specialty Construction Program (F2528Y-YZK09-03).

Disclosure statement

No potential conflict of interest was reported by the author(s).

Ethics approval and consent to participate

The research procedure of CHARLS strictly followed the Helsinki Declaration and was approved by the Ethics Committee of Peking University (Approval No.IRB00001052-11015). All respondents signed written informed consent before entering the group.

Data sharing

The data that support the findings of this study are available from the Institute of Social Science Survey, Peking University, Beijing, China (http://charls.pku.edu.cn). Data for 2020 will be available upon request to the corresponding author.

Data availability

The data reported in this manuscript were obtained from the publicly available CHARLS dataset (http://charls.pku.edu.cn). The variables and relationships examined in the present article have not been examined in any previous or current articles, or to the best of our knowledge in any papers that will be under review soon.

Supplemental Material

Supplemental data for this article can be accessed online at https://doi.org/10.1080/20008066.2026.2708407.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Table A3.doc
ZEPT_A_2708407_SM1970.doc (31KB, doc)
Figure A1.tif
ZEPT_A_2708407_SM1969.tif (2.4MB, tif)
supplement 1.docx
ZEPT_A_2708407_SM1968.docx (13.8KB, docx)
Table A6.doc
ZEPT_A_2708407_SM1967.doc (29.5KB, doc)
Table A1.docx
ZEPT_A_2708407_SM1966.docx (16.6KB, docx)
Table A5.doc
ZEPT_A_2708407_SM1965.doc (39KB, doc)
Table A4.doc
ZEPT_A_2708407_SM1964.doc (59.5KB, doc)
Table A2.docx
ZEPT_A_2708407_SM1963.docx (17.8KB, docx)

Data Availability Statement

The data reported in this manuscript were obtained from the publicly available CHARLS dataset (http://charls.pku.edu.cn). The variables and relationships examined in the present article have not been examined in any previous or current articles, or to the best of our knowledge in any papers that will be under review soon.

Articles from European Journal of Psychotraumatology are provided here courtesy of Taylor & Francis

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