The 17% of women who experienced severe physical or sexual abuse in childhood had 46% to 56% higher risks of cardiovascular events in early adulthood, after adjustment for childhood CVD risk factors. Adult risk factors known to be associated with early abuse, including adult experiences of intimate partner violence, smoking, BMI, hypertension, diabetes, and depression, accounted for as much as 60% to 80% of the associations of severe early abuse with CVD risk. This suggests that a large portion of the association of childhood abuse with adult CVD risk could be eliminated or reduced by targeted prevention efforts that have been successful in reducing CVD incidence among U.S. women.1
The structure of our dataset allowed us to examine several methodological questions. Similar results of prospectively and retrospectively reported cases () indicate that recall bias is unlikely to explain the associations. However, examination of all self-reported disease yielded considerably stronger associations than did examination of cases confirmed by additional data or medical record review. There could be several reasons for this gradient across case confirmation status. There was less statistical power to examine confirmed cases. Alternatively, the stronger estimates for the unconfirmed cases reported at baseline in 1989 could result from early, pre-baseline CVD events of women with a history of child abuse. However, such ‘attrition of susceptibles’ over time seems a less likely explanation than simple differences by case confirmation status, especially as we observed contrasts between ‘probable and definite’ versus ‘definite’ cases observed over the same follow-up period (1989–2007). Women with histories of childhood physical abuse tended to deny permission to review medical records (), precluding their classification as ‘definite’ cases. Unfortunately, it is unclear whether risk estimates based on ‘probable and definite cases’ or only ‘definite cases’ best reflect the association of abuse history with CVD risk: on the one hand, restriction to women willing to release records could induce a bias to the null if that restriction eliminates the very women whose abuse history is severe enough to affect CVD risk; on the other hand, the restriction to medically confirmed cases could be an appropriate way to eliminate any tendency of abused women to over-report disease outcomes. As analyses restricted to definite, record-confirmed CVD events exposed to severe physical abuse were null, the findings for physical abuse cannot be considered robust. However, the increased risk of CVD with forced sex was consistent and statistically significant, even with the most strict case confirmation status.
Our findings are generally consistent in direction, if not magnitude, with two large studies of child abuse.14–15
Differences between studies in assessment of abuse exposures and CVD outcomes make close comparisons problematic. The present study included 66,798 women age 43 to 60 years at the end of follow-up, of whom 0.8% experienced CVD events confirmed by corroborating medical information or records. The ACE study included 17,337 men and women of average age 56 years, of whom 10.6% reported a history of ischemic heart disease (IHD) in response to queries regarding history of heart attack, chest pain or heavy chest pressure with exertion, or use of nitroglycerine.14
Self-reports of IHD were not confirmed. The focus of the ACE study is a 10-item childhood trauma score that includes two items on physical abuse and two on sexual abuse. Results were not stratified by gender. Our finding of a 46% increased risk of CVD events with severe physical abuse appears to agree with the ACE report of 50% (40% to 90%) increased risk of IHD with physical abuse, although, in our data, the association of physical abuse with CVD was driven by a stronger association with stroke than with MI. The ACE study estimated a 40% (30% to 60%) increased IHD risk among individuals who experienced either sexual touching or intercourse; this appears to be intermediate between our null estimate for sexual touching and 56% increased risk of CVD with forced sex. Again, we observed stronger associations of sexual abuse with stroke than with MI.
The National Comorbidity Survey (NCS) questioned 5,877 men and women age 15–54; 0.4% of women endorsed an item regarding “heart attack or serious heart trouble” in the past 12 months.15
There was little evidence that women who indicated that they had been ‘physically abused as a child’ were more likely to report heart disease; on the other hand, women who reported a history of child or adolescent ‘rape or sexual molestation’ were 5 times more likely to report heart disease.15
Our estimates for sexual abuse are consistent in direction with those of the NCS, although much smaller in magnitude.
The only study to examine exclusively confirmed events in a prospective analysis, the Health and Social Support (HeSSup) study in Finland, was focused on child adversities as a whole rather than on child abuse in particular.10
Among the roughly 14,000 women studied, there were 91 CVD events. The risk of CVD events increased with the number of childhood adversities reported. When the adversity score was dissected into its components, ‘serious conflicts in the family’ was associated with an age-adjusted HR for CVD of 1.71 (1.07–2.73). However, ‘fear of a family member’ was associated with an HR of 1.33 (0.79–2.23). As in our study, adjustment for adult CVD risk factors attenuated these estimates. While these exposures do not correspond directly to physical and sexual child abuse, they do suggest that childhood social environment is associated with adult CVD risk, and that much of this association is mediated by preventable risk factors that are elevated in women with a history of childhood adversity.
Several strengths of the present study are notable. We were able to examine CVD events variously self-reported by nurses, corroborated by additional details, and/or confirmed by medical record review. The fact that some associations were weaker when restricted to ‘definite’ cases suggests that the use of unconfirmed self-reports may overestimate associations of abuse with CVD risk. Previous studies have been too small to permit more fine-grained examination of severity of abuse. In contrast, the NHS2 cohort is several times larger than the next largest study; distinguished between mild, moderate and severe abuse; examined CVD events that were confirmed by medical record or other evidence; and tested whether associations were similar among cases that occurred before and after the abuse assessment, permitting evaluation of the potential role of recall bias. Another strength that distinguishes the current study is the 18 years of prospectively collected data on risk factors such as family history, socioeconomic position, smoking, BMI, hypertension, and diabetes that enabled testing of confounders and intermediates.
Like most large abuse studies, our participants self-reported their abuse history. We used instruments employed by national surveys18–19
that reduce bias by querying specific acts of violence, rather than nominal questions regarding ‘abuse’ or ‘rape’.29
The alternative to self-report is police, court or other administrative records of abuse. However, only the minority of child abuse cases are reported to authorities; officially documented abuse cases are almost certainly a non-random sample of all cases; and it is impractical, if not impossible, to assemble a cohort of documented abuse cases large enough (and long ago enough) to study CVD endpoints. Given these issues, self-report is the gold standard abuse measurement for large cohort studies. The nurses in our cohort report somewhat more mild and moderate abuse than women in the NVAWS telephone survey.8
The NHS2 abuse prevalence is similar to that reported by ACE study, suggesting that survey methodology may explain some discrepancies.
We did not document other childhood neglect or traumas such as marital discord, mental illness or criminal activity in the home. Such factors are correlated with child abuse and are also associated with CVD risk.10, 14–15
In this analysis, we did not consider emotional abuse. The NHS2 participants are predominately white women with at least a college degree. Our findings need to be replicated in more diverse settings to determine their generalizability. Finally, as participants were age 43–60 at the end of follow-up, these findings pertain to early CVD; further follow-up will be necessary to determine whether early abuse also predicts CVD during the peak incidence period.
Several lines of evidence suggest that abuse in early life may increase cardiovascular risk. Preclinical and clinical studies demonstrate profound and lasting effects of early stress on the hypothalamic-pituitary-adrenal and noradrenergic stress systems, including heightened glucocorticoid, norepinephrine, and autonomic stress reactivity, as well as altered dopaminergic and serotonergic function.30–34
Survivors of childhood sexual abuse have increased heart rate and blood pressure response to cognitive and social challenges.35
Supporting, if indirect, evidence that abuse increases cardiovascular risk can be drawn from literature on post-traumatic stress disorder, which is prevalent among abused women36
and associated with increased risks of coronary heart disease,37
and possibly inflammation.46
This is consistent with literature that documents increased adiposity,6–7
with a history of child abuse.
Studies consistently document widespread physical and sexual abuse of children and adolescents. Early abuse is associated with behavioral and physiologic risk factors for CVD. The evidence is now growing that early abuse, especially sexual abuse, also predicts CVD events in adulthood. However, our findings suggest that this field may be vulnerable to differential reporting of disease endpoints by abuse status. We need to understand the complex physiological and behavioral pathways through which abuse leads to true CVD events, so that interventions that aim to alter CVD risk trajectories from childhood can be maximally effective.