Parental imprisonment (PI) is linked to a range of adverse behavioral and health outcomes in the life course. Studies have shown that PI is associated with childhood aggression and internalizing behaviors, along with increased risk for mental health and antisocial and delinquent behaviors in adolescence and adulthood [1–6]. Physical health outcomes, including asthma, childhood sleep problems, increased BMI and blood pressure, sexually transmitted infections, physical disability, and premature mortality, are also linked with having a parent imprisoned [7–14]. PI is also associated with a complex array of adversities and outcomes, such as poorer academic performance, social exclusion, and criminal justice involvement that compound over the life course, leading to cumulative disadvantages that may impact health and well-being [15–17]. Depending on the level of adversity, PI may either directly lead to poorer health outcomes, or act as an indicator for poorer health [18].
The prevalence of imprisonment in the U.S., the U.K. and Australia indicate that PI has the potential to significantly impact population health, particularly among minority populations. In Australia, an estimated 4% of all children and up to one-fifth of Indigenous children may experience PI by age 16 [19]. In the U.S., one-third of young adults ages 18–29 report a parent who has undergone detention, with 4% of white and one-fourth of African American children having experienced a parent spend one year or more in prison [20, 21]. In England and Wales., an estimated 310,000 children per year experience PI [22]. The large number of children impacted by parental imprisonment has increasingly led for calls to focus on PI as a cause of health disparities and a public health issue [23, 24].
When thinking about risks of PI on physical health outcomes, it is critical to consider the interrelationship of imprisonment with a range of overlapping adverse childhood experiences (ACEs), known by Giordano & Copp as “packages of risk,” which include parental absence, residential instability, parental mental health and substance abuse, and childhood poverty [16, 25–28]. These “packages of risk” may also include broader psycho-social factors, such as neighborhood and school effects like living in a food desert or lacking educational support services, which may contribute to broader inequalities in health [29]. A recent national study of American adolescents found that 51% of adolescents who experienced a PI reported having four or more ACEs in childhood, compared with 12% of adolescents in the general population [30]; a recent literature review found that adults reporting four or more ACEs were at twice the risk for experiencing cardiovascular disease and premature death [31]. Recent studies have found that depression and anxiety mediate the association between ACEs (including PI) and cardiovascular disease [32, 33]. The associations between increased adversity and mental health issues may help to explain a growing body of research linking parental or familial imprisonment and subsequent cardiovascular and metabolic disease risk in later life [9, 10, 34–36].
One research question which has not been addressed are whether early childhood emotional problems and PI may be linked with cardiometabolic risk in later life. Longitudinal studies suggest that delinquency and depression differentiate risk for increased BMI among females who experience PI in adulthood [9, 37]; however, potential interrelationships between PI and early childhood mental health and behavioral issues has, to our knowledge, not been explored. Research suggests a potential association between early childhood behaviors and psychiatric illness with adult obesity and BMI gain [38–40], while other research suggests that ACEs are associated with a range of childhood emotional and behavioral problems [41, 42]. A recent literature review examining the associations between parental separation and cardiometabolic disease, noted that childhood psychosocial problems may act as a mediating or moderating mechanism [43]. This body of research is suggestive, in the light of the association between ACEs and cardiometabolic disease discussed above, that behavioral problems associated with parental imprisonment may moderate cardiometabolic disease risk in later life.
The link between PI and cardiometabolic risk may also vary by sex or gender. Research on parental and familial incarceration also suggests that cardiometabolic risk markers and diseases are concentrated in females and women [9, 10, 34, 36, 37, 44], with only one study linking familial incarceration with ischemic heart disease in men at mid-life [35]. Using a stress paradigm may be helpful for understanding potential variations, given PI is recognized as a stressor which has been found to vary in magnitude by biological sex for a a range of adverse behaviors and outcomes, including internalizing behaviors and delinquency, substance use, poor social outcomes, and health [15, 45–48]. General research has linked incarceration of a parent with measures of biological stress and premature aging in adolescence and young adulthood, including early menarche, reduced telomere length, and higher allostatic load [45, 49, 50]. However, results from studies examining sex and gender variations for PI find that stress-related cardiometabolic risk factors, including BMI, waist circumference, blood pressure, and C-Reactive Protein are concentrated in adolescent and young adult females, potentially indicating that biological stress-markers associated with PI manifest as increased risk for early cardiovascular and metabolic diseases in females [6, 9, 10, 50].
Given research linking childhood internalizing and externalizing behaviors with the emergence of cardiometabolic risk in adolescent girls, PI and cardiometabolic risk for females in adolescence and adulthood may be mediated by high levels of emotional and behavioral problems childhood [51, 52]. Thus, while PI may lead to stress processes associated with increased risk, the association between PI and cardiovascular risk may manifest in adolescence and adulthood among women who experience mental health issues in childhood. The current will investigate if mediating/moderating effects between PI and cardiovascular risk vary by respondent’s biological sex.
Another major limitation of previous research on PI is the lack of longitudinal and prospective cohort studies in general population studies, both generally and with measures of physical health [13, 53]. One recent prospective cohort study found that PI in early childhood (≥ 5 age) was associated with a range of cardiovascular risks, but did not find an association for a larger group of children reporting PI through age 14 [10]. The present study builds on these findings by examining if PI through age 14 and cardiometabolic risk is mediated by early childhood problems.
A final limitation in existing literature is potential bias arising from attrition. Using multiple imputation, we assess the bias of missing data present in longitudinal analysis, an issue with the prior MUSP study by Roettger et al [10]. Missing data may bias existing results and this paper will examine whether the overall consistency of findings remains after accounting for missing observations. Addressing missing data issues can help to ameliorate concerns about the validity of complete case analysis in the MUSP data.