Victimization refers to harms that occur to individuals because other human beings are behaving in ways that violate social standards (Finkelhor and Kendall-Tackett, 1997), which is conceptualized herein as physical or sexual abuse, neglect, or psychological victimization. Numerous studies have examined mental and physical health outcomes of victimization, including the risk of psychopathology (Moffitt, 2013; Russell et al., 2019) and cardiometabolic diseases (Baldwin and Danese, 2019). Given emerging evidence showing that elevated inflammation is related to adverse health outcomes (Osimo et al., 2021), increased inflammation may play a role in accounting for the relationship between victimization and adverse health consequences (Baumeister et al., 2016; Coelho et al., 2014). Inflammation refers to an innate immune response that fights against infection or injury, in the body's attempt to heal (Nasef et al., 2017). Understanding biological mechanisms such as the inflammatory process are necessary to mitigate the risk of psychopathology (Russell et al., 2019). Therefore, targeted intervention programs are needed to reduce the risk of inflammation-related diseases in people with experiences of victimization.

Three inflammatory markers commonly examined in the literature of victimization are acute-phase protein C-reactive protein (CRP)/high-sensitivity CRP, cytokine Interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) (Baumeister et al., 2016; Kerr et al., 2021). Specifically, CRP, a comparatively stable indicator of chronic inflammation, is an acute protein produced by the liver in response to elevations in IL-6 (Ridker and Cook, 2004). IL-6 is a cytokine mainly produced by visceral adipose tissue and could be induced by other cytokines, including TNF (Maggio et al., 2006). TNF-a is a pro-inflammatory cytokine that is primarily produced by macrophages and T cells, but can also be released by other cells, such as B cells, neutrophils, and endothelial cells (Zelová and Hošek, 2013).

Previous meta-analyses and systematic reviews have reached incongruent results regarding the associations between victimization/adversity and increased inflammation. Baumeister et al. (2016) included 25 articles showing that childhood trauma was significantly related to adulthood inflammation (overall effect size: z = 0.10 for CRP, z = 0.08 for IL-6, and z = 0.23 for TNF-α). However, another meta-analysis of 27 articles investigating the association between early life adversity and markers of inflammation in children and adolescents found the effect sizes for IL-6 and CRP were both 0.06, and non-significant (Kuhlman et al., 2020). It is possible that their work included various types of adversities, which cannot tease out the impact of victimization and thus affect the effect sizes of the relationship. Moreover, systematic reviews have found strong evidence supporting the relationship between childhood victimization and CRP (Coelho et al., 2014; Kerr et al., 2021), but not with IL-6 (Coelho et al., 2014). The main limitation of these previous studies is that they typically spanned infancy through adolescence; few investigated the relationship between adulthood victimization and dysregulation of inflammation. The major differences in inflammatory processes among children and adults open up the possibility that the age stages in which victimization occurs may cause the victimization to exert different effects on inflammation (Kuhlman et al., 2017).

The inconsistent timings of victimization and inflammation assessments across studies may explain the current mixed findings of previous reviews (Russell et al., 2019). The association between victimization and inflammation may be strong when victimization occurred in childhood and inflammation measurements were relatively proximate to the time that the childhood victimization took place (Slopen et al., 2013). A study examining whether victimization that occurred in different age periods differentially impacts inflammation is needed. In a prospective observational cohort study from the prenatal period through to 23 years, the researchers differentiated periods of victimization (i.e., prenatal, 0–3, 3–7, 7–12, and 12–18 years) and identified different CRP trajectories (9, 15 and 18 years of age). They found that adverse childhood experiences, particularly bullying victimization and sexual abuse in late childhood/adolescence were associated with elevated CRP trajectories (Iob et al., 2022). Our current study extends previous work by examining the different timings of victimization and their associations with inflammation. Specifically, victimization and inflammation were both measured in childhood (childhood victimization – childhood inflammation), victimization occurred during childhood when inflammation was measured in adulthood (childhood victimization – adulthood inflammation), and victimization and inflammation were both measured in adulthood (adulthood victimization– adulthood inflammation). By exploring this important issue, the present study emphasizes the need to prioritize more precise policies and determine the optimal times to intervene in particularly salient periods in which inflammation affected by victimization may be most profound. Moreover, there are limited reviews exploring the different effect sizes of the relationships between victimization and different inflammatory markers within a single study. Knowledge about different effect sizes could provide more accurate and effective support to the most affected forms of inflammation caused by victimization.

Potential moderators may also explain the inconsistent findings of previous work on the relationship between victimization and inflammation. Some studies included both male and female samples (Bücker et al., 2014; Carpenter et al., 2010), while some involved only female samples (Boeck et al., 2016). Some studies employed clinical samples (Walsh et al., 2016), while some selected community (Schreier et al., 2020) or mixed samples (both clinical and community samples) (Quidé et al., 2019). With regard to victimization measure types, some used a self-reported method (Mitchell et al., 2018), while interviews were employed in other work (McCormack et al., 2021). Sample sizes varied among different studies (Archer et al., 2012; Kuzminskaite et al., 2020). Previous meta-analyses have only reviewed some potential moderators. For example, Baumeister et al. (2016) explored age, BMI, sex, and sample populations, showing no significant moderating results for age, BMI, or sex. Kuhlman et al. (2020) further found some factors, such as tissue type, were non-significant moderators. Comprehensive knowledge of moderating variables within a single study could help to provide more accurate and effective support to those whose inflammation is affected by victimization.

The primary aim of this meta-analysis was to synthesize and quantify existing studies and examine the association of childhood and adulthood victimization with inflammation. We further explored whether or not the association was influenced by the aforementioned moderators (i.e., sex, sample populations, victimization measure type, time of victimization and inflammation measures, whether adjusted for covariates, and sample sizes of study).