Intimate partner violence is associated with increased maternal hair cortisol in mother–child dyads
Introduction
Violence against women inflicted by intimate partners is an important worldwide public health problem that significantly affects women's mental and physical health [1]. Globally, an estimated 30% of women are exposed to intimate partner violence during their lifetimes [2], [3]. In most cases, this chronic social traumatic stressor involves repeated episodes of physical, psychological, and sexual violence that dramatically disturb the victim's sense of security [4]. Specifically, sexual abuse occurs in approximately 40% of all cases of intimate partner violence. The mental health consequences are greater in women who are sexually abused than in those who are not [5], [6], [7]. Intimate partner violence (IPV) refers to physical violence, sexual violence, or psychological aggression (including coercive acts) perpetrated by a current or former intimate partner [8]. Despite the relevance of IPV, most research to date have focused on assessing the consequences of IPV on mental health [9], [10], [11], while its biological correlates have been relatively underexplored [5], [12], [13].
As in other stressful conditions, exposure to IPV might trigger a series of harmful biological consequences in victims [14], [15], [16], [17]. For example, chronic violence or sexual abuse is usually associated with short- and long-term alterations in the functioning of the hypothalamic-pituitary-adrenal (HPA) axis and with automatic nervous system dysregulation [18]. Although HPA axis activation acts primarily as a protective response against stress [19], chronic and recurrent exposure to stressful experiences increases metabolism. Resources are consumed without sufficient recovery, promoting long-term changes in the functioning of stress-related biological systems. Consequently, the risk for physical and mental health problems increases [14], [19]. This process, named “allostatic load”, can inhibit neurogenesis, block neuronal plasticity, and induce neurotoxicity [14]. Brain regions such as the hippocampus, amygdala, and prefrontal cortex undergo structural and functional remodeling in response to acute and chronic stress and chronic HPA axis activation [16].
Measurement of cortisol, a steroid hormone released from the adrenal gland, is often used to investigate the association between chronic stress exposure and HPA axis reactivity [20]. Previous investigations have yielded mixed results regarding cortisol levels in women exposed to IPV, with cortisol levels both higher and lower than those in control women [17], [21]. Psychiatric conditions such as the severity of depressive and posttraumatic stress disorder (PTSD) symptoms may be important mediators of the relationship between IPV and cortisol levels [4], [22]. For example, a systematic review [23] found that patients with major depression presented with increased cortisol levels, while patients with anxiety disorders (generalized anxiety, panic, and PTSD) presented with lower levels, suggesting that distinct pathways contribute to the dysregulation of the HPA axis in the development and/or maintenance of psychiatric conditions.
In addition, some studies have also shown higher cortisol levels and increased physiological arousal in children who witness marital violence [24]. Children and adolescents in families characterized by higher levels of marital functioning showed lower wake-up cortisol levels [25]. However, children whose parents recurrently engage in violent conflicts with intimate partners may often feel threatened and consequently stressed, leading to chronic elevation of cortisol levels. Furthermore, some authors highlight associations between hormone levels in parents and their children [25], [26]. In children with higher cortisol levels, one or both parents also exhibit elevated cortisol concentrations [25]. Specifically, for victims of intimate partner violence, maternal and infant salivary cortisol concentrations were positively correlated [26]. Therefore, the mother–child bond might deeply influence and regulate behavioral and physiological responses to stress [26], [27].
Although some studies have investigated the relationship between cortisol levels and intimate partner violence in women [23], [28], [29], [30], the majority have used plasma, serum, or saliva samples to assess cortisol. These measurement methods are subject to major physiological daily fluctuations, making the assessment of overall long-term systemic cortisol exposure difficult and leading to inconsistent results. On the other hand, in recent years, hair cortisol measurement has emerged as a promising way to measure chronic stress and capture systemic cortisol exposure over longer periods of time [28], [30], [31]. Hair grows at a median rate of 1 cm/month; therefore, the first centimeter of hair at the scalp follicle indicates the past month's cortisol production, while the second centimeter section indicates the cortisol production of the month before, and so on [30]. In addition, evidence has shown that hair cortisol concentrations are not affected by sex, hair treatments, or pharmacological interventions, indicating that hair cortisol could be a highly important biomarker in stress studies [30], [32]. On the other hand, a recent study found that hair cortisol was higher in boys than in girls [33].
Given that hair cortisol assessment is a promising approach with which to investigate chronic stress load in children and adults [34], [35], [36], [37], [38], the present study compared hair cortisol levels in women exposed to IPV and their children to hair cortisol levels in women without such exposure and their children. To our knowledge, this study is the first to test the hypothesis that both women exposed to IPV and their children will present with higher hair cortisol levels. We also hypothesized that PTSD or/and depressive symptoms would be associated with variations in cortisol levels.
Section snippets
Participants
A total of 118 participants were included in this study. Thirty-five women exposed to IPV and their biological children were recruited through the Center for Helping Women Victims of Intimate Partner Violence in Southern Brazil; three withdrew from the study (n = 32). This service is designed to protect women from contact with their partner in such a way that no participant had ongoing partner violence when assessed. For each woman, one child aged 6–12 years who had witnessed IPV in any form was
Results
The clinical and sociodemographic profiles of the groups are presented in Table 1. No differences were found regarding the age and sex of the child. We found that IPV mothers had a median of three children while control women had two. All women reported themselves as married or living in a stable relationship with their partner, with the exception of two divorced IPV participants. We identified lower education among IPV women. As expected, women exposed to IPV reported higher rates of physical
Discussion
The results of the current study highlight an association between IPV and higher levels of chronic cortisol in women exposed to such violence, but not in their children. An increase in cortisol related to intimate partner violence exposure was previously demonstrated [4], [17], [22]. However, to our knowledge, this is the first time that chronic HPA axis activity has been investigated in this specific population using hair cortisol assessment. This approach avoids the major limitations of
Conclusions
The results of the present study indicate a pattern of increased levels of hair cortisol among women exposed to IPV, when compared to levels in women without such exposure. Although we did not find any hair cortisol differences among children from IPV-exposed women and controls, the number of injury events was related to hair cortisol levels, and these children reported more PTSD symptoms than controls. Hence, given that experiencing and witnessing violence during childhood and adolescence are
Conflict of interest
The authors report no conflict of interest.
Acknowledgment
This study was supported by CNPq, FAPERGS and CAPES.
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