Guided by insights from the life course perspective and concepts from models of stress and coping, this study examined linkages between profiles of violence in childhood from parents and odds of obesity in adulthood. Findings indicated that adults who reported the most severe profiles of childhood violence from parents (i.e., experiencing both physical and psychological violence from one or both parents with at least one type reportedly having occurred sometimes or often) were at greater risk for adult obesity than respondents who reported never having experienced either type of violence from parents. These findings are consistent with previous scholarship on the problematic neurophysiological effects of stress that is particularly severe and long lasting (Adam & Epel, 2007
). Results from this study are also consistent with findings from Williamson et al.’s (2002)
study, which similarly found that adults who reported having experienced multiple types of abuse, especially at high levels of frequency, were most at risk for adult obesity.
To help elucidate processes through which violence in childhood from parents contributes to greater risk of obesity in adulthood, this study examined adults’ greater use of food in response to stress as an explanatory factor for linkages between problematic profiles of childhood family violence and greater odds of adult obesity. Results from models testing mediation provided support for this causal hypothesis, suggesting the importance of the quality of life course social relationships—particularly with respect to their implications for individuals’ psycho-behavioral uses of food—as part of dynamic processes that contribute to adult obesity. Additional studies are necessary to test the extent to which other types of stress within children’s relationships—such as parental death or parental substance abuse—are similarly associated with greater use of food in response to stress, as well as greater risk of adult obesity. Also, as the association between the problematic profiles of violence and odds of adult obesity were reduced by about one-quarter in size within mediation models, additional studies are also necessary to examine other factors that contribute to processes from severe experiences of childhood family violence to greater risk of adult obesity, such as those comprising more direct neurophysiological processes (Adam & Epel, 2007
The results of this study suggest the importance of advising social services and health care professionals to assess patterns of eating among children facing family violence, as well as among adults with histories of violence. Nonetheless, better understanding the mechanisms from violence to problematic eating is critical for developing effective interventions to reduce rates of obesity due to childhood family violence. Scholars have suggested a variety of mechanisms through which childhood family violence might be linked to adult obesity, including more negative mood and emotions, behavioral impulsivity, body image disturbance, substance abuse, poor self-esteem, and psychobiological dysregulation (Gustafson & Sarwer, 2004
). Identifying for whom which mechanisms most strongly contribute to causal processes from violence to greater use of food in response to stress holds the promise of ascertaining more targeted interventions. For example, psychosocial mechanisms suggest the importance of more psychosocial-oriented interventions, such as mental health counseling, whereas more psychobiologically rooted mechanisms suggest the potential additional utility of biomedically focused interventions, such as pharmacological agents.
An additional critical direction for future research is the timing of obesity among individuals with histories of violence. For decades, scholars have noted childhood obesity as a powerful risk factor for adult obesity (National Institutes of Health Consensus Statement Online, 1985
), and scholarship on obesity increasingly emphasizes that individuals who are obese at a particular point in their adulthood differ as to how long they have been obese (e.g.,Ferraro, Thorpe, & Wilkinson, 2003
; Schafer & Ferraro, 2007
). These conceptualizations of obesity as a life course phenomenon suggest the importance of considering the time sequences over which childhood family violence contributes to adult obesity, particularly through using food to cope with stress. For some individuals, severe experiences of violence in childhood might lead to (or reinforce) emotion-based eating and subsequent obesity in childhood that directly persist into adulthood; whereas for others, early experiences of violence might lead to weight gain that takes place more gradually over time, resulting in obesity only in adulthood. Moreover, associations between using food to cope with stress and obesity might be reciprocal over time. A more refined understanding of the timing of processes linking interpersonal relationships, behavioral uses of food, and obesity can help guide programs to reduce rates of obesity, especially with respect to programs focused on prevention.
Despite this study’s contributions to advancing the understanding of early life course risk factors for adult obesity, several methodological features limit the full extent to which conclusions can be made. First, processes of selective memory make possible incongruencies between individuals’ reported experiences of childhood family violence and their actual experiences—particularly with respect to the frequency by which they actually experienced particular types of violence. (For a discussion of the use of retrospective reports in studies of childhood family violence, refer to Kendall-Tackett & Becker-Blease, 2004
; Widom, Raphael, & DuMont, 2004
.) Another limitation of this study’s measure of childhood family violence is the remaining variability in experiences of violence even among specific profile groups of violence. Sources of variability include specificity regarding the particular parent or parents who engaged in violence, as well as differences in the motivation and contexts surrounding the use of violence (e.g., reasoned discipline versus acts of unprovoked rage). Furthermore, despite this study’s inclusion of many statistical controls, there are other factors that this study did not control for, which might account for both respondents’ reported experiences of violence in childhood from parents, as well as greater risk of adult obesity—including obesity in childhood; psychological distress that follows from obesity in adulthood (that also might, in part, lead to individuals reporting more negative experiences in childhood); and genetic characteristics. Taking into account these other factors could render a more complex causal story than we have suggested here. Furthermore, this study’s assessments of obesity and use of food in response to stress were conducted at the same point in time, limiting the strength of conclusions regarding use of food in response to stress as a unidirectional cause of greater risk of obesity.
Other limitations of this study relate to its measure of obesity. This study classified respondents’ problematic weight status by using a dichotomous measure of obesity. This study did not classify respondents along other important weight-related characteristics, which also have been linked to health outcomes, such as severity levels of obesity, distributions of adiposity across the body, and weight cycling (e.g., Diaz, Mainous, & Everett, 2005
). Also, this study relied on respondents’ self-reported weight and height, which previous studies have found to lead to an underestimation of body mass index, particularly among certain subgroups of adults (e.g., Spencer, Appleby, Davey, & Key, 2001
Another potential measurement limitation involves this study’s two-item index that gathered respondents’ self-reports of consuming more food in response to stress; this measure does not correspond exactly with diagnostic definitions of disordered eating. For example, this index did not ask respondents to report on their potential feelings of loss of control when eating in response to stress, which is a criterion for a diagnosis of binge eating (American Psychiatric Association, 2000
). Additionally, both items comprising this index asked respondents about eating more
in response to stress. Previous studies have documented that some individuals eat less when faced with stress (Torres & Nowson, 2007
)—a pattern of using food in response to stress that this study did not address. Furthermore, linkages among childhood family violence, obesity, and use of food in response to stress are likely to differ in other national contexts where food is not as readily available for individuals to consume when confronted with stress.
Finally, although we used a national probability sample for these analyses, because individuals who experience childhood family violence are more likely to experience incarceration (e.g., Browne, Miller, & Maguin, 1999
) and homelessness (e.g., Sullivan, Burnam, & Koegel, 2000
), some adults with histories of violence are less likely to be included in this study’s noninstitutionalized sample.
Despite these limitations, this study’s findings regarding linkages between profiles of severe violence in childhood from parents and greater risk of obesity in adulthood—as well as evidence for greater use of food in response to stress as a mechanism of risk—help to advance understanding of interpersonal, life course contributors to adult obesity. Results also indicate away in which individuals’ experiences of violence in childhood can have long-lasting and interconnected mental and physical health effects. Continuing to develop a better understanding of the complex biopsychosocial processes that comprise pathways from childhood stressors, such as childhood family violence, to poorer physical health in adulthood is critical for informing programs and policies aimed at reducing disparities in health across the life course.