Abstract
Partner violence is associated with a wide range of negative outcomes, including poorer physical health in the form of increased risk for acute injuries, chronic disease onset, and premature mortality. Importantly, exposure to partner violence is not limited to adulthood and can be embedded within a larger context of interpersonal adversity extending from childhood into older age. In this review, we summarize recent research linking interpersonal adversity to poor health across the life course, focusing on psychosocial, behavioral, and physiological mechanisms relevant to health. We first highlight the importance of embedding the experience of partner violence and health into a broader context of interpersonal adversity spanning the life course. We then outline links from childhood interpersonal adversity to psychosocial and physiological dysfunction in adulthood, including a specific focus on recent studies examining emotion regulation, coping, attachment styles, and health behaviors. We next examine the current evidence linking interpersonal adversity to health-relevant psychosocial and physiological outcomes, including among older adults. In this section, we highlight recent findings linking interpersonal adversity to neural mechanisms, cognition, immune function, and accelerated biological aging. We end our review by identifying limitations of the current literature studying how interpersonal adversity could affect later health and present causal inference methodologies that could help address these challenges.
Keywords: Interpersonal violence, adversity, trauma, attachment, adverse childhood events, health
1. Introduction
People who experience partner violence in romantic relationships face a wide range of undesired outcomes, which include mental and physical health consequences [1–3]. Beyond injuries resulting from direct violence [4], partner violence is also associated with poor physical health broadly [1,5]. For example, individuals who experience partner violence are at increased risk for diabetes and cardiovascular disease [6,7]. Explanations for how partner violence influences health include changes in health-relevant behaviors and physiological dysfunction associated with the onset of chronic disease and premature mortality [6,7]. For example, people who experience partner violence are less likely to engage in healthy behaviors, such as preventative medical care [7], and show faster rates of biological aging [8] (i.e., physiological decline associated with chronological aging).
Experiences of partner violence are not isolated to romantic relationships, however, and are embedded within a broader context of interpersonal adversity extending from childhood into older age [9,10]. Interpersonal adversity encompasses harmful or stressful experiences that occur within any number of close relationships, which can include children and parents, friend groups, or romantic partners. Experiences of adversity in any close relationship can both influence, and be influenced by, partner violence. For example, adverse childhood experiences (ACEs) increase the likelihood that an individual experiences partner violence, as well as risk for poor health [11–13]. Partner violence can also affect future relationship functioning and health [14]. For example, older women with prior experiences of partner violence report increased vulnerability for elder abuse [15]. Understanding how partner violence is associated with poor health requires understanding how interpersonal adversity, biopsychosocial functioning, and health interact over the life course. In this review, we highlight the correlates of childhood adversity relevant to partner violence (Figure 1). We also examine how these mechanisms might interact with partner violence to increase risk for poor health. We end by highlighting challenges to studying interpersonal adversity, describing approaches that can support future research.
Figure 1.

This figure presents a conceptual illustration of how interpersonal adversity that can occur across the lifespan, as well as associated impacts on downstream biopsychosocial dysfunction and health. The top row presents types of interpersonal adversity from childhood into older age, including childhood adversity, partner violence, and elder abuse. The descending rows then present potential psychosocial and physiological mechanisms that might explain how these types of interpersonal adversity result in poor health over time. Although not exhaustive, these mechanisms present some of the constructs with the most current empirical evidence linking adversity to poor health outcomes.
2. Linking Childhood Adversity to Psychosocial and Physiological Dysfunction
Childhood adversity—particularly experiences of abuse or exposure to family violence—impacts psychosocial functioning in adulthood by shaping attachment styles that influence vulnerability to partner violence [16–18]. ACEs increase the risk for insecure parent-child attachment, as well as the risk for anxious and avoidant attachment styles in adulthood [18–20]. These insecure attachment styles reduce the quality and supportiveness of romantic and caregiving relationships [21,22]. Individuals with insecure attachment often struggle with conflict resolution, which increases susceptibility to relationships characterized by conflict, aggression, or partner violence [23,24]. In turn, the quality of relationships and conflict within relationships shape future health trajectories [1,25].
Childhood adversity can also affect emotional processes associated with partner violence and health [26,27]. Children exposed to threat, for example, may develop heightened emotional reactivity and difficulties modulating negative affect [28]. This dysregulation often manifests as hypervigilance or heightened sensitivity to negative interpersonal cues, increasing vulnerability to conflict in adult relationships [29]. The emotion regulation and coping strategies people use also likely influence interpersonal adversity. For example, aggression between parents predicts subsequent disengagement coping strategies [29]. Strategies that help children manage stress in threatening environments can become counterproductive in healthier relational contexts, perpetuating maladaptive emotional responses. Over time, these patterns create feedback loops in which difficulties in emotion regulation and coping amplify interpersonal adversity and stress, ultimately contributing to poor health.
Childhood adversity also contributes to poor health by shaping future health behaviors. For example, individuals with histories of childhood adversity are less likely to engage in healthy behaviors, such as physical activity, adequate sleep, and balanced nutrition [30–32]. Avoidance or numbing behaviors used to manage emotional pain (e.g., excess screen time, emotional eating) could contribute to obesity and health problems [33,34], in addition to established associations with unhealthy behaviors (e.g., substance use, smoking) [35,36]. However, some studies have suggested these associations may be attributable to social factors (e.g., socioeconomic disadvantage, discrimination [33]), at least in part.
Childhood adversity is also associated with physiological mechanisms relevant to future behavior and health, including neural processes, immune function, and biological aging. Research on the neural correlates of childhood adversity has largely focused on exposure to threat in the form of violence and abuse. For example, children exposed to threat have reduced amygdala, medial prefrontal cortex (mPFC), and hippocampal volume, as well as heightened amygdala activation to threat [37]. Similarly, a recent meta-analysis found that childhood adversity was associated with differences in two distinct networks, namely, an amygdala-centered network associated with emotion processing and an insula-centered network associated with somatosensory and motor processing [38]. Studies have also found that individuals with more ACEs generally have higher levels of inflammatory biomarkers in midlife and older age [39,40], and ACEs may sensitize individuals to greater inflammation in response to subsequent stressful events [41]. For example, childhood adversity is associated with higher levels of inflammation in adulthood, particularly among individuals with internalizing symptoms [42].
Accelerated biological aging has also been highlighted as a physiological mechanism linking childhood adversity to future health. Several recent studies have shown ACEs are associated with accelerated aging in midlife, as indexed by epigenetic measures of aging [43–45]. The relatively small number of recent studies investigating how ACEs might accelerate aging have found that ACEs are associated with poorer health behavior and more stressful life events in adulthood [46,47], each of which might contribute to faster aging and poor health.
3. Linking Interpersonal Adversity to Health-Relevant Psychosocial and Physiological Mechanisms
Interpersonal adversity predicts poorer psychosocial functioning and health across the life course, including in older age. Violence within intimate relationships is not limited to younger adulthood; abuse can begin or escalate in later life, sometimes triggered by increased dependency, retirement-related stress, or health declines [48]. People who experienced abuse and violence as a child or in early adulthood have higher odds of experiencing abuse in older adulthood [49,50]. Although most older adults face “passive” adversity, such as loss (e.g., death of relational partners), approximately one in 10 older adults experience violence in interpersonal relationships through elder abuse, which includes physical, emotional, sexual, or financial harm—or neglect—often by caregivers or family members [50]. Elder abuse has significant consequences for health [13], as caregiving and family dynamics that expose older adults to adversity (e.g., verbal or physical abuse, financial exploitation, physical or medical neglect) can have downstream effects on chronic disease, morbidity, and mortality.
Experiences of interpersonal adversity and partner violence also have lasting consequences on cognitive functioning. Cognition can be affected by adversity that occurs early in the life course or later in adulthood [51,52]. Intimate partner violence in adulthood is associated with worse cognition, including difficulties in attention, memory, and executive functioning [53,54], particularly in the context of traumatic brain injuries (TBI) resulting from partner violence [55]. Additionally, the emotional toll of partner violence (fear, hypervigilance, depressive symptoms) can impair cognitive processes, to the detriment of daily functioning and future health. Resulting cognitive impairments can derail the ability to navigate healthcare systems, adhere to treatment regimens, and maintain routines that protect physical health. In this way, cognitive impairments resulting from a history of interpersonal adversity can contribute to functional decline, dementia onset, disability, and premature mortality [56,57].
Interpersonal adversity and partner violence are also associated with neural, immune, and biological aging outcomes relevant to health. Partner violence has been broadly linked to changes in brain regions tied to emotion regulation and processing, memory, and cognition [58–60], as well as structural changes to regional volumes and cortical thickness [61,62]. The direct effects of physical partner violence, such as TBI, likely influence later health [63]. A recent study of 45 women with posttraumatic stress disorder found that the women with a history of TBI—the majority of injuries being the result of partner violence—showed lower mean cortical thickness, primarily in the left precentral gyrus [64]. In most cases, these neural correlates have not yet been tied directly to health outcomes, but likely impact health-relevant behavior. Chronic stress is also linked to higher systemic inflammation [65–67], which is predictive of poor clinical outcomes [68]. Interpersonal adversity likely contributes to higher levels of systemic inflammation as a highly salient chronic stressor. For example, a recent study of 214 people found that midlife and older adults who had more aggressive interactions with their romantic partners had higher levels of circulating inflammatory markers [69].
Partner violence is also associated withpredicts accelerated biological aging. For example, in a cohort of 974 New Zealanders, individuals with more partner violence had faster rates of aging over a 20-year period [8]. Accelerated aging is associated with increased risk for a wide range of chronic disease [70], highlighting how faster aging might help explain how partner violence could affect later health. There is also an opportunity to integrate neural and aging measures to link interpersonal adversity and health. Novel measures of aging that use brain imaging to characterize aging, such as DunedinPACNI [71], could help link partner violence to neural signatures of accelerated aging. Given the many physiological links from interpersonal adversity to health, mechanisms spanning multiple physiological systems and disease pathways, such as biological aging, are particularly useful in characterizing potentially causal pathways.
4. Current Challenges and New Opportunities in the Study of Interpersonal Adversity and Health
Although many high-quality studies examine interpersonal adversity and health, important challenges remain for future research. First, it is difficult to link interpersonal adversity and health longitudinally without relying on retrospective measurement. Although there are examples of interpersonal adversity, relationship functioning, and health investigated prospectively in the same cohort [8,47], these integrative studies require long periods of follow-up and are relatively rare as a result. Similarly, dyadic assessment of partner violence can be challenging for both ethical and logistical reasons. As a result, studies examining partner violence using dyadic data are (understandably) rare, despite partner violence occurring within the context of a romantic relationship by definition. Such dyadic data could help capture the experience of partner violence for both men and women, at least when studied in heterosexual relationships. Regardless of the challenges, studies that can leverage existing longitudinal cohorts or other innovative methods to produce additional longitudinal or dyadic evidence linking interpersonal adversity to health would benefit this area of study.
Relatedly, partner violence is a nonrandom exposure, which can result in selection bias and confounding, similar to other types of adversity like trauma and PTSD [72]. There are shared environmental and genetic risks that might explain, at least in part, the observational findings linking interpersonal adversity to poor health. These confounds are challenging to disentangle given the difficulty in applying experimental methods, such as random assignment, to study these exposures. However, there are methodological approaches that can support causal inference and could bolster the literature linking interpersonal adversity to health [72]. For example, propensity score matching can be used to account for differences in individual characteristics that might be relevant to both interpersonal adversity and health [73]. Similarly, polygenic risk scores can be used to account for genetic risk for exposures, such as partner violence or ACEs [74]. Finally, instrumental variable approaches [75,76] and twin studies [77,78] can leverage naturally existing random assignment and shared genetics among twins, respectively, to account for nonrandom selection, increasing confidence that associations are not better explained by genetic or shared environmental risks. When these approaches are embedded in larger longitudinal cohort studies, they produce useful opportunities to examine whether interpersonal adversity might be associated with health in a way that could be consistent with causation.
4.1. Conclusion
In short, partner violence is associated with poor health, likely through changes to psychosocial characteristics (e.g., emotion regulation, attachment styles), health-relevant behaviors (e.g., smoking), and physiological functioning (e.g., inflammation, biological aging). The experience of interpersonal adversity is not unique to adult romantic relationships; rather, it both shapes and is shaped by interpersonal adversity across the lifespan. Understanding the pathways from partner violence to poor health will require an accounting of how childhood adversity, partner violence, and biopsychosocial dysfunction interact and persist into older age to predict clinical outcomes.
Acknowledgements:
This work was supported by Award #IK2CX002694 to Dr. Bourassa from the Clinical Science Research and Development Service of VA ORD and Award #R00AG073617 to Dr. Brown from the National Institute on Aging. The views expressed in this article are those of the authors and do not necessarily reflect the position or policy of the VA, the U.S. government or any other affiliated institution. Neither author has conflicts of interest to report.
References and Recommended Reading
Papers of particular interest, published within the period of review, have been highlighted as:
* of special interest
** of outstanding interest
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