Abstract
Background
Although increased attention has been placed on the potential deleterious consequences of paternal incarceration on maternal health, little empirical research has attempted to understand the physiological processes that might underlie this relationship. Moreover, exposure to incarceration and access to resources that shape family incarceration patterns are unequally distributed across racial and ethnic lines, yet few studies utilize analytic frameworks that account for this social reality. Using a within race/ethnicity analytic framework, the present study addresses these gaps by examining relationships between paternal incarceration and telomere length for Black, Latina/o, and White mothers.
Methods
Data were drawn from the Fragile Families and Child Wellbeing Study, a longitudinal, stratified multistage probability sample of couples and children in 20 large U.S. cities. The final analytic sample consisted of 2174 mothers that were followed from pregnancy to age 9 of the focal child.
Results
Findings revealed exposure to paternal incarceration was negatively associated with telomere length for Black mothers, but not for Latina/o and White mothers. Mediation analysis also showed paternal incarceration-telomere length relationships did not operate through secondary stressors, such as economic instability, poor mental health, and parenting stress.
Conclusion
Overall, results demonstrated that the detrimental physiological consequences of paternal incarceration for mothers depended on racial and ethnic background. Findings from this study can provide a foundation upon which health scholars and criminal justice stakeholders may better understand whether and how paternal incarceration shapes deleterious health patterns for the mothers who remain to care for the children of those incarcerated.
Introduction
The unprecedented growth of the U.S. criminal legal system over the last four decades has created an environment where incarceration has become a common occurrence for many U.S. families. According to recent estimates, nearly half of U.S. adults have an immediate family member with a history of incarceration [1]. Due to the long history of racialized social structures that have systematically targeted communities of color [2–4], incarceration’s direct and indirect effects on families remain unevenly distributed. Black men with low levels of education and who reside in disadvantaged neighborhoods have the greatest risk of incarceration [5–7], whereas Black women and children are more likely to experience family incarceration [1, 7].
A sizeable literature has, in turn, documented mass incarceration’s repercussions for families. Focusing largely on two groups—children of incarcerated parents and partners of incarcerated individuals—this body of research reveals widespread health consequences alongside other economic and social harms. For example, youth that have experienced parental incarceration are at a greater risk of hyperactivity disorder, speech or language problems, learning disabilities, developmental delays [8], accelerated cellular aging [9], and physiological dysregulation [10]. Because incarceration is disproportionately concentrated among men, an emerging body of literature also finds that male partner incarceration appears to simultaneously undermine the well-being of women whose partners are incarcerated, especially those with children. More specifically, male partner incarceration has been tied to increased work and financial strains [1, 11], harmful substance use [12, 13], and problematic parenting [14] among women. Due to the compounding social and economic harms associated with male partner incarceration, scholars have recently called for new research that focuses on understanding how male partner incarceration shapes health patterns among women [7]. The current study addresses this call.
In doing so, we draw on interdisciplinary research that consistently notes having to cope with a multitude of stressors exacts a heavy toll on the mind and body [15–18]. Not surprisingly, exposure to the U.S. criminal justice system can be a source of both acute and chronic stress [8, 14, 19–26], with the burden of familial incarceration contributing to a myriad of health inequities for women, in particular [7]. For instance, Wildeman and colleagues [24] observe that recent paternal incarceration increases a mother’s risk for a major depressive episode and diminishes overall life satisfaction. In the same manner, Lee and colleagues [27] demonstrate that, among a national sample of women, family member (not just partner) incarceration increases cardiovascular disease risk factors, including obesity, prior heart attack or stroke, and poor self-reported health.
Despite increased attention placed on the health and wellbeing of mothers who have experienced paternal incarceration, four critical gaps in the literature remain. First, scholarship has yet to unpack the potential physiological processes that might underlie relationships between paternal incarceration and maternal health. Scholars theorize and have empirically demonstrated that exposure to and coping with chronic stressors, such as family incarceration, can set into motion a series of physiological responses that accelerates the decline in physical functioning. Known as the weathering hypothesis, this framework posits vital regulatory systems respond to stressors by releasing hormones to upregulate functioning across systems. Empirical evidence demonstrates that with repeated overactivation of stress response systems, these mechanisms become inefficient and lead to an increased risk of disease susceptibility and early death [28–30]. Due to the range of social, economic, and psychological harms tied to family incarceration, it is plausible that the stress associated with male partner incarceration accelerates the normal aging process and leads to the onset of chronic health conditions via physiological processes. Due to data limitations and lack of focus on maternal health, however, few studies have tested this assertion on physiological outcomes like premature genetic aging (e.g., telomere length).
Second, more research is needed that explicitly examines the underlying processes linking incarceration and health, particularly paternal incarceration as it is related to the physiological health of mothers. Paternal incarceration as an initial stressor may lead to a myriad of associated economic and social “secondary stressors” across other life domains that reverberate throughout families—a process known as stress proliferation [14]. Stress proliferation can impact the health patterns of those with an incarcerated family member, including mothers caring for children, because they are more likely to struggle with diminished mental health, economic instability, and difficulties parenting. For example, Bruns and Lee [12] find elevated rates of substance abuse among mothers with incarcerated partners that, in turn, may exacerbate overall health issues. Others find male partner incarceration reduces financial resources, undermines mental health, increases the risk of material hardship, and forces women to rely on kin for financial support or to take on multiple jobs to supplement lost income [11, 31–33]. Scholars also find that paternal incarceration exacerbates depression and undermines life satisfaction for mothers [24], while simultaneously increasing caretaking responsibilities and heightening levels of parenting stress [34, 35]. Given that scholars continue to identify a myriad of potential secondary stressors tied to paternal incarceration, more empirical attention is needed on the mechanisms that might mediate the relationship between incarceration and physiological health among mothers.
Third, more empirical research is needed that specifically examines the association between paternal incarceration and maternal health uniquely for different racial and ethnic groups. While extant research continues to show that Black families are disproportionally exposed—both directly and indirectly—to the U.S. carceral system, few studies adopt research designs that fully address this inequality. Most scholarship examines whether general gaps in health exist but often fail to explore the multitude of racially stratified structural factors that may operate uniquely within each specific racial/ethnic group to drive health patterns [36]. Within the context of family incarceration, for example, underlying disparities in education, economic resources, and neighborhood composition might be differentially impacted by paternal incarceration for some racial groups and not others. More specifically, when compared to Whites, historically marginalized racial and ethnic groups are more likely to live in neighborhoods with fewer economic and social resources, resultant of racial residential segregation and undergirded by structural racism [37, 38]. Racial segregation creates and maintains concentrated poverty among historically marginalized racial and ethnic communities through constraining employment opportunities, quality of education, and disinvestment in critical infrastructure [38–40]. In essence, segregation impacts health indirectly through the neighborhood environment (as a stressor) and the clustering of stressors. Due to these structural factors, the prevalence of incarceration within some communities of color may adversely impact the health of minoritized mothers due to the inextricable relationship between segregation, neighborhoods, and race and ethnicity. For these reasons, there has been a recent shift among some scholars [41] to utilize a within-group analytic approach to demonstrate how racial stratification contributes to inequities between racial and ethnic groups. Unfortunately, a within-race analytic framework has yet to be applied to scholarship examining linkages between paternal incarceration and maternal health.
Finally, a growing body of research documents the health consequences of partner incarceration for women without separating or specifying the appropriate temporal order of incarceration and health outcomes. That is, few studies have attempted to understand potential linkages between prior paternal incarceration and subsequent women’s health. The use of such data provides scholars with the ability to address concerns of temporal ordering in a more robust analytic framework. Thus, greater attention is needed on how paternal incarceration impacts the health of mothers over time.
Using data from the Fragile Families Child Wellbeing Study and a within-race/ethnicity framework, the current study seeks to simultaneously fill these gaps using by examining whether and how paternal incarceration is associated with maternal health. We also test whether a series of secondary stressors mediate this key relationship. We begin by first examining the role of paternal incarceration on telomere length for Black, Latina/o, and White mothers. As an essential biomarker, telomeres are protective DNA–protein structures on the ends of eukaryotic chromosomes that bind to DNA clusters and consist of simple sequences of telomeric DNA (TTAGGG) tandemly repeated at the end of each chromosome. When cells divide, chromosome ends shorten with each chromosomal replication and cellular division. Once telomeres become critically shortened, active tumor suppressor genes are activated as a cellular defense mechanism and those cells enter into a state of senescence (arrest) and apoptosis (death). Telomere shortening generally occurs with advancing age in all somatic cells, including fibroblasts and leukocytes, and is, therefore, characterized as a broader sign of cellular aging.
Accumulating evidence suggests that exposure to stressors, such as exposure to the U.S. carceral system, can accelerate the shortening of telomeres [42–44]. Scholars theorize that frequent activation of the hypothalamus–pituitary–adrenal axis, sympathetic nervous system, and oxidative burden plays a role in premature cellular aging. In turn, shortened telomeres are associated with several deleterious biological and physical consequences such as chromosome and genomic instability, the onset of chronic health conditions, and premature death [45–51]. As such, evidence of accelerated cellular aging among mothers with a history of partner incarceration could potentially have wide-ranging implications for maternal health.
Following this initial analysis, we turn our attention to the role of secondary stressors and on whether economic hardship, neighborhood concentrated poverty, diminished mental health, and parenting stress mediate relationships between paternal incarceration and telomere length in unique ways for Black, Latina/o, and White mothers. Taken together, we address the following overarching research questions:
Are there divergent racial and ethnic patterns of cellular aging among mothers that have experienced paternal incarceration?
How do secondary stressors, such as economic hardship, neighborhood concentrated poverty, maternal mental health, and parenting stress shape paternal incarceration-cellular aging patterns for Black, Latina/o, and White mothers?
Data, Measures, and Method
Data
Data for this study were drawn from the Fragile Families Child Wellbeing Study (FFCWS), a longitudinal, stratified multistage probability sample of couples with children born between 1998 and 2000 in 20 large U.S. cities. The FFCWS systematically oversampled for unmarried parents, but when weighted, is representative of U.S. urban families and their children. Baseline interviews were conducted with mothers in the hospital within 24 h of their child’s birth. When possible, fathers were interviewed in the hospital. If the father was not present, interviews were conducted in other locations shortly after the child’s birth. Follow-up interviews were conducted with both parents when the child was 1, 3, 5, and 9 years old. At the ninth-year follow-up, a sub-sample of 2,421 mothers and 2482 children provided saliva samples to enable biological assays of telomere length. For inclusion in the final analytic sample, respondents had to have participated in the telomere sub-sample and had valid responses for all measures and valid sampling weights. The final analytic sample included 2174 mothers from 20 large U.S. cities. Neither telomere length nor paternal incarceration differed significantly between included and excluded cases.
Telomere Length
Telomere length, captured at year-9, was measured using a quantitative real-time polymerase chain reaction (PCR) that produced absolute measurements in kilobases (See S1 for a detailed description of the PCR-based measure included in this study). Given that extreme values could represent mismeasurement or oral pathology, 1% of both tails were trimmed from the sample, resulting in approximately a 2% reduction in the sample. It is important to note that respondents with extreme telomere length values do not appear to be more or less likely to share key characteristics across our control variables in ways that would indicate they would have undue influence on the results. Preliminary analyses also indicated that the telomere length measure was positively skewed in the overall sample and for each racial and ethnic group under examination. Therefore, to approximate normal distribution, the telomere length measure was log-transformed for all sample participants regardless of racial and ethnic background.
Paternal Incarceration
To ensure proper temporal ordering, paternal incarceration was measured using responses from year 1, year 3, and year 5 of the mother and father interviews. Maternal reports were used to supplement the operationalization of our paternal incarceration measure, given that some fathers either did not participate or refused to answer questions on incarceration history across FFCWS years. Fathers were considered recently incarcerated if either the maternal or paternal reports indicated they spent time in prison or jail at some point between the year 1 and year 5 surveys, including at the year 5 survey.
Maternal Race and Ethnicity
Maternal racial and ethnic background was assessed using two questions. First, mothers were asked to respond to the self-identification question: “which of these categories best describes your race?” Responses included White, Black/African American, Asian or Pacific Islander, American Indian/Eskimo/Aleut, and other/not specified. Mothers were then asked whether they were of Hispanic or Latino origin or descent. Due to small sizes across FFCWS years, we were unable to keep mothers who identified as Asian or Pacific Islander, American Indian/Eskimo/Aleut, and other/not specified in the final analytic sample. Moreover, FFCWS did not provide respondents with opportunities to select more than one racial category. Because of these limitations, our final race and ethnicity measure included categories for White, Black, and Latina/o mothers.
Secondary Stressors
Economic Hardship
Central to our second research question and the need to address the intervening processes shaping maternal health, we included two measures that capture economic hardship: material hardship and poverty status. The first measure, material hardship ranged from 0 to 11 and represents the sum of mother’s year-5 responses to a battery of questions regarding their experiences with 11 events in the last 12 months, including (a) received free food or meals, (b) child was hungry and could not afford food, (c) unable to pay rent or mortgage, (d) eviction, (e) unable to pay utility bills, (f) utilities were turned off due to failure to pay, (g) phone service disconnected, (h) borrowed money to help pay bills, (i) moved in with others due to financial problems, (j) stayed at a shelter, and (k) needed health services but could not afford it.
Second, poverty status, also measured at year 5, was assessed using household income-to-needs ratio based on U.S. poverty thresholds, adjusting for family composition and year. Respondents that scored a one or less were considered to be living in poverty.
Neighborhood Concentrated Poverty
Additionally, we include a measure of neighborhood concentrated poverty to capture the milieu effect of deleterious contexts above and beyond individual material hardship. Neighborhood concentrated poverty reflects the percentage of families living below the poverty line, percentage of families receiving public assistance, percentage of unemployed individuals, and percentage of female-headed families in a census tract at year 5. Scores for neighborhood concentrated poverty capture the mean of all four items, with higher values representing an increase in neighborhood concentrated poverty.
Mental Health‑Maternal Depression
Recent history of maternal depression was assessed using the Composite International Diagnostic Interview-Short Form, a standardized instrument commonly used in large-scale surveys to measure the prevalence of depression [52]. Mothers were asked if, at some time during the past year, they had feelings of depression or were unable to enjoy things that were normally pleasurable. Mothers that indicated they had experienced at least one of these symptoms most of the day, every day, or for a 2-week period, were then asked a battery of follow-up questions that addressed the domains of loss of interest in things, feeling tired, weight change of at least 10 pounds, sleep troubles, difficulty concentrating, feeling worthless, or thinking about death. If mothers indicated they had experienced one or more of these domains, they were considered to have major depressive disorder. Respondents were considered to have a recent history of depression if they were categorized as having major depressive disorder from year 1 to year 5 of the FFCWS.
Maternal Parenting Stress
Maternal parenting stress was assessed at year 5 using four items derived from the Parenting Stress Index [53, 54]. This index captures general perceptions of caring for children as a parent. The four items include (a) being a parent is harder than I thought it would be, (b) I feel trapped by my responsibilities, (c) I find that taking care of my children is much more work than pleasure, and (d) I often feel tired, worn out, or exhausted from raising a family. Original responses for each item ranged from 1 strongly agree to 4 strongly disagree. All of the items were reverse recoded and summed with higher scores representing higher levels of maternal parenting stress (Cronbach’s alpha 0.67).
Controls
We also control for a host of individual characteristics likely associated with either paternal incarceration and/or maternal health. These characteristics, which have been included in similar studies using FFCWS data [9, 12, 24, 55, 56], include maternal age, education level, family structure, and number of children. Maternal age was measured in years and ranged from ages 15 to 53. Maternal education, captured at baseline, was measured using four dummy variables: less than high school, high school or equivalent, some college, and college graduate (reference). Family structure assessed whether focal parents were cohabitating at year 5 of the FFCWS. The number of maternal biological children was derived from self-reports and ranged from 1 to 7.
Additional control variables include multi-partnered fertility, intimate partner violence, and heavy drinking. Multi-partnered fertility was assessed a year 5 and captured whether mothers reported having a child(ren) with another partner and was dummy coded (1 = multi-partnered fertility). Intimate partner violence was assessed using maternal reports of physical and sexual violence from the father of the focal child or a new partner from responses to the following items: (a) “he slapped or kicked you or he hit you with a dangerous object” (physical) and (b) “he tried to make you have sex or do sex or do sexual things you didn’t want to do” (sexual). A mother was dummy coded as having experienced either form of intimate partner violence from year-1 to year-5. Finally, mothers were asked about (a) the greatest number of drinks consumed in 1 day in the last 12 months. If respondents indicated they had consumed four or more drinks in one day during the last 12 months, they were then asked (b) how frequently they engaged in drinking four or more alcoholic drinks in 1 day. Original responses included “less than one month,” “about once a month,” “a few times a month,” “a few times a week,” and “every day or almost every day.” Mothers were considered to have engaged in heavy drinking if they consumed four or more drinks a few times a month or higher.
Analytic Strategy
Our analysis unfolds by, first, describing differences in telomere length, exposure to paternal incarceration histories, and other control variables. In doing so, we also note differences across mother’s racial and ethnic background. Second, we estimate a series of ordinary least squares regression models to assess the relationships between paternal incarceration and mother’s telomere length. The first model, or the “unadjusted model,” examines bivariate associations between paternal incarceration and telomere length. In the subsequent model, we adjust for all specified control variables to isolate the role of paternal incarceration on telomere length from other factors influencing telomere length. For both the unadjusted and adjusted models, equations were estimated separately for each racial and ethnic group.
As noted earlier, our race/ethnic-specific approach allows for the isolation of fundamental aspects of stratification for each racial and ethnic group under investigation, which can ultimately inform more targeted policy interventions designed to address observed inequities [36–38]. Moreover, preliminary analysis revealed no substantive differences in estimates using the within-race/ethnic approach when compared to a multiplicative approach. Finally, we also used a series of adjusted Wald tests to determine whether paternal incarceration-telomere length relationships were significantly different across race/ethnicity-disaggregated models (shown in Table 2). In the baseline models, results indicate relationships between paternal incarceration and telomere length did not vary significantly by racial and ethnic background. However, in the adjusted models, findings reveal significant differences in paternal incarceration and telomere length relationships between Black and White mothers, and between Black and Latina/o mothers.
Table 2.
Estimated associations between paternal incarceration and mother’s telomere length
| OLS regression estimates |
Wald tests |
|||||
|---|---|---|---|---|---|---|
| Black | Latina/o | White | Black/Latina/o | Black/White | Latina/o/White | |
| Β (S.E.) | Β (S.E.) | Β (S.E.) | p-value | p-value | p-value | |
| Unadjusted models | ||||||
| Paternal incarceration | − .05 (.04) | .00 (.05) | .12 (.09) | NS | NS | NS |
| Adjusted models | ||||||
| Paternal incarceration | − .09 (.04)* | .04 (.04) | .04 (.08) | < .05 | < .05 | NS |
| N = 473 | N = 1095 | N = 606 | ||||
Fragile Families and Child Wellbeing Study, baseline and years 1 3, 5, and 9
Survey-corrected ordinary least squares (OLS) coefficient estimates, and standard errors presented. The unadjusted models present results of OLS regressions where logged telomere length was regressed on paternal incarceration. The adjusted models present results of OLS regressions where logged telomere length was regressed on paternal incarceration with adjustment for the following maternal characteristics: age, education, family structure, number of children, multi-partnered fertility, intimate partner violence, and heavy drinking
NS, not significant (p-values ≥ .05)
p < .05,
p < .01,
p < .001
In the third stage of the analysis, we consider four mechanisms that may link paternal incarceration to telomere length: (1) economic hardship, (2) neighborhood concentrated poverty, (3) maternal mental health, and (4) parenting stress. We decompose the relationships between paternal incarceration and mother telomere length into the direct effect of paternal incarceration and indirect effect of paternal incarceration through these mechanisms using a series of regression-with-residuals (RWR) models for analyzing causal mediation [57]. RWR was developed to address a restrictive methodological assumption when decomposing a total effect of treatment on an outcome into natural direct and natural indirect effects (NDE and NIE). Prior to the development of this approach, the NDE and NIE could only be identified if there is no unobserved treatment-outcome confounding, no treatment mediator confounding, no unobserved mediator-outcome confounding, and no treatment-induced mediator-outcome confounding. The final assumption is highly restrictive since any variables that affect the mediator and outcome must not be affected by the treatment. RWR addresses these methodological challenges by utilizing an alternative set of estimates—known as the randomized intervention analogs to the natural direct effect (R-NDE) and randomized intervention analogs of the natural indirect effect (R-NIE)—which can be identified in the presence of treatment-induced confounding. Unlike other techniques designed to test for causal mediation, the RWR also allows scholars to include weights and account for clustering. As such, all analyses adjusted for the clustered nature of the FFCWS at the city level. To account for the unequal probability of selection due to oversampling of non-marital births, all analyses were also weighted using post-stratification weights [58].
Results
Descriptive Statistics
Table 1 presents means, proportions, and standard deviations for demographic characteristics for the overall sample and across history of paternal incarceration and racial and ethnic background. Results from the overall sample indicate approximately 18% of mothers experienced paternal incarceration. Moreover, the average telomere length was 1.84 kilobases, which is within the normal range for this age group. With respect to race and ethnicity, Black, Latina/o, and White mothers were roughly split into thirds, with Black mothers representing a plurality (37%) of the sample. The majority (56%) of mothers were cohabitating with the focal child’s father at year 5 and almost two-thirds of mothers had no education beyond a high school diploma or GED (64 percent). Approximately 40% of mothers were living in poverty.
Table 1.
Descriptive Statistics by Paternal Incarceration and Race and Ethnicity
| History of paternal incarceration |
Race and ethnicity |
|||||
|---|---|---|---|---|---|---|
| Overall | No incarceration | Incarceration | White | Black | Latina/o | |
| Mean/proportion | Mean/proportion | Mean/proportion | Mean/proportion | Mean/proportion | Mean/proportion | |
| Telomere length | ||||||
| Average telomere length (ln) | 1.84 (.02) | 1.84 (.02) | 1.83 (.02) | 1.80 (.04) | 1.83 (.02) | 1.88 (.02) |
| Incarceration exposure | ||||||
| Paternal incarceration | 0.18 (.02) | .09 (.03) | .27 (.03) | .17 (.04)** | ||
| Mother race/ethnicity | ||||||
| White | 0.29 (.03) | 0.33 (.04) | 0.15 (.05)** | |||
| Black | 0.37 (.03) | 0.33 (.03) | 0.54 (.06) | |||
| Latina/o | 0.34 (.03) | 0.35 (.03) | 0.31 (.05) | |||
| Secondary stressors | ||||||
| Economic hardship | ||||||
| Material hardship | 0.98 (.07) | 0.86 (.08) | 1.54 (.14)** | 0.79 (.17) | 1.17 (.08) | 0.95 (.11)** |
| Poverty status | 0.42 (.03) | 0.37 (.04) | 0.64 (.06)*** | 0.23 (.09) | 0.54 (.04) | 0.45 (.05)** |
| Neighborhood poverty | ||||||
| Concentrated poverty | 0.16 (.01) | 0.15 (.01) | 0.17 (.01) | 0.08 (.01) | 0.21 (.01) | 0.16 (.01)*** |
| Mental health | ||||||
| Maternal depression | 0.27 (.02) | 0.24 (.02) | 0.40 (.06)*** | 0.28 (.05) | 0.30 (.03) | 0.24 (.04) |
| Parenting stress | ||||||
| Parenting stress index | 4.69 (.12) | 4.66 (.10) | 4.85 (.05) | 4.92 (.26) | 4.66 (.17) | 4.53 (.22) |
| Controls | ||||||
| Maternal age | ||||||
| Age in years | 26.46 (.32) | 27.18 (.35) | 23.24 (.80)*** | 29.35 (.71) | 24.38 (.44) | 26.21 (.54)*** |
| Mother education | ||||||
| < high school | 0.37 (.03) | 0.33 (.03) | 0.55 (.06)*** | 0.14 (.03) | 0.40 (.04) | 0.52 (.04)*** |
| High school or equivalent | 0.27 (.030 | 0.25 (.04) | 0.37 (.06) | 0.25 (.08) | 0.32 (.04) | 0.24 (.04) |
| Some college | 0.22 (.02) | 0.25 (.02) | 0.08 (.02) | 0.20 (.04) | 0.24 (.04) | 0.21 (.03) |
| College graduate | 0.14 (.02) | 0.17 (.02) | 0.01 (.00) | 0.41 (.06) | 0.03 (.01) | 0.04 (.01) |
| Family structure | ||||||
| Mother/father cohabitating year 5 | 0.57 (.03) | 0.66 (.03) | 0.17 (.04)*** | 0.79 (.04) | 0.33 (.04) | 0.65 (.04)*** |
| Number of children | ||||||
| Number of children | 1.58 (.09) | 1.58 (.08) | 1.59 (.11) | 1.59 (.26) | 1.68 (.08) | 1.47 (.08) |
| Multi-partnered fertility | 0.29 (.02) | 0.56 (.06)*** | 0.10 (.02) | 0.56 (.04) | 0.29 (.04)*** | |
| Intimate partner violence | 0.06 (.01) | 0.19 (.05)** | 0.05 (.01) | 0.07 (.03) | 0.12 (.03) | |
| Heavy drinking | 0.02 (.00) | 0.11 (.04) | 0.05 (.03) | 0.03 (.01) | 0.02 (.01) | |
| N = 1634 | N = 540 | N = 473 | N = 1095 | N = 606 | ||
Fragile Families Child Wellbeing Study, baseline and years 1 3, 5, and 9
Asterisks indicate significant differences between mothers with and without a history of paternal incarceration and differences between racial and ethnic groups.
p < .05,
p < .01,
p < .001.
Descriptive statistics are weighted and adjust for the complex design of the FFCWS
The top of Table 1 reveals no notable differences in telomere length across incarceration categories and racial and ethnic background. We do, however, find significant differences in the remaining sample characteristics. Concerning history of paternal incarceration, mothers exposed to paternal incarceration from year 1 to year 5 were more likely to be Black, experience higher levels of material hardship, live in poverty, have children with multiple partners, and report evidence of depression and intimate partner violence. Comparisons across racial and ethnic groups (last three columns of Table 1) indicate that Black mothers were more likely to experience higher levels of material hardship, live in poverty, live in neighborhoods with greater concentrated poverty, and have children with multiple partners. Taken together, findings from Table 1 are consistent with broader patterns of racial stratification in incarceration and other life domains and point to the value of a within-race/ethnicity analytic framework.
Paternal Incarceration and Mother Telomere Length
Relevant to our first research question, Table 2 contains survey-corrected linear regression estimates that assess the relationships between a history of paternal incarceration and telomere length for Black, Latina/o, and White mothers. The “unadjusted model,” model 1, shows no evidence that paternal incarceration was significantly associated with mothers’ telomere length for any of the racial and ethnic groups included in the study. In turn, model 2, which adjusts for a host of additional control variables, demonstrates that paternal incarceration is not statistically significantly associated with accelerated cellular aging for White and Latina/o mothers. However, when accounting for demographic and social characteristics of mothers and their living situations, telomere length for Black mothers who experienced paternal incarceration was statistically significantly shorter. More specifically, paternal incarceration was associated with a − 0.09 smaller natural log telomere length, an approximately 8% reduction in telomere length (i.e., (1-exp(− 0.09))).
Central to our second research question, Table 3 displays the direct, indirect, and total effect estimates from the regression-with-residuals method for analyzing causal mediation. As a reminder, the focus here is on investigating whether three secondary stressors—economic hardship, maternal mental health, and parenting stress—mediate relationships between paternal incarceration and mothers’ telomere length. Within Table 3, each row represents an RWR model that adjusts for the full set of controls, one mediator, and the clustered nature of the Fragile Families (FFCWS) sample. The first column presents the direct effect estimates, which mirror the estimates presented in column 2 of Table 2. The second column provides estimates for the indirect effect of paternal incarceration through each secondary stressor. The final column represents the total effect of each secondary stressor on telomere length. Results demonstrate that the four mechanisms under investigation did not mediate paternal incarceration-telomere length relationships. More specifically, Values were mostly at zero and nonsignificant, particularly for the indirect effects of interest as mediators of the paternal incarceration-maternal health relationship.
Table 3.
Estimates of direct effects and indirect effects of paternal incarceration on mother’s telomere length mediated by economic disadvantage, maternal mental health, and parenting stress
| Direct b(SE) | Indirect effect b(SE) | Total effect b(SE) | Percentage of total effect mediated | |
|---|---|---|---|---|
| Black (N = 1,095) | ||||
| Economic hardship | ||||
| Material hardship | − .09 (.04)* | .00 (.00) | − .09 (.04)* | 0% |
| Poverty status | − .09 (.04)* | .00 (.00) | − .09 (.04)* | 0% |
| Neighborhood poverty | ||||
| Concentrated poverty | − .09 (.04)* | .00 (.00) | − .09 (.04)* | 0% |
| Maternal mental health | ||||
| Depression | − .09 (.04)* | .01 (.01) | − .10 (.04)* | − 10% |
| Parenting stress | ||||
| Parenting Stress Index | − .09 (.04)* | .00 (.01) | .09 (.04)* | 0% |
| Latina/o (N = 606) | ||||
| Economic hardship | ||||
| Material hardship | .04 (.04) | .00 (.00) | .04 (.04) | 0% |
| Poverty status | .04 (.04) | .00 (.00) | .04 (.04) | 0% |
| Neighborhood poverty | ||||
| Concentrated poverty | .04 (.04) | .00 (.00) | .04 (.04) | 0% |
| Maternal mental health | ||||
| Depression | .04 (.04) | .00 (.00) | .04 (.04) | 0% |
| Parenting stress | .04 (.04) | .00 (.00) | .04 (.04) | 0% |
| Parenting Stress Index | .04 (.04) | .00 (.00) | .04 (.04) | 0% |
| White (N = 473) | ||||
| Economic hardship | ||||
| Material hardship | .04 (.08) | .00(.00) | .04 (.08) | 0% |
| Poverty status | .04 (.08) | − .01 (.03) | .05 (.08) | − .20% |
| Neighborhood poverty | ||||
| Concentrated poverty | .04 (.08) | − .03 (.03) | .06 (.07) | − 50% |
| Maternal mental health | ||||
| Depression | .04 (.08) | − .01 (.02) | .05 (.08) | − .20% |
| Parenting stress | ||||
| Parenting Stress Index | .04 (.08) | .00 (.00) | .04 (.04) | 0% |
Fragile Families and Child Wellbeing Study, baseline and years 1 3, 5, and 9
Weighted regression-with-residuals estimates, and clustered robust standard errors are presented. Each model adjusts for following maternal characteristics: age, education, family structure, number of children, multi-partnered fertility, intimate partner violence, and heavy drinking
p < .05,
p < .01,
p < .001
Robustness Checks
To examine the robustness of our results, we constructed several additional models. Specifically, we (a) estimated models retaining all telomere values rather than eliminating the 1% on each tail; and (b) using multiple imputation rather than listwise deletion and re-estimating models for this larger sample. Results from both robustness checks are substantively identical to those displayed in Tables 1, 2, and 3 above. As such, we are confident that our results are sensitive to the specific methodological choices employed in our primary analysis.
Discussion
Despite early evidence documenting deleterious health consequences among women associated with the incarceration of a partner, little research has attempted to understand how paternal incarceration is linked to the physiological health of mothers, in particular. Moreover, although a broad interdisciplinary literature documents how Black families experience greater exposure to incarceration and how the mechanisms that shape these patterns are driven by deeply embedded racialized social structures, scholarship describing incarceration and women’s health has yet to utilize analytic frameworks that engage such racial and ethnic stratification directly. In this study, we drew from the stress process model and weathering hypothesis while utilizing a within-race/ethnicity framework to provide an accounting of the physiological consequences associated with paternal incarceration for Black, Latina/o, and White mothers. In doing so, we explored the linkage between paternal incarceration and maternal telomere length because of its broader implications for maternal health. Simultaneously, we explored the secondary stress processes that might mediate this critical relationship. Taken together, findings from this study offer three contributions to the literature on paternal incarceration and maternal health.
First, consistent with the stress process model and weathering hypothesis, we found that exposure to incarceration was unequally distributed, just as other mechanisms that increase the risk of incarceration were concentrated among historically marginalized groups. Our results indicated that Black mothers were more likely to report male partner incarceration and descriptive patterns across race and ethnicity revealed that Black mothers were more likely to be exposed to all three indicators of economic instability (material hardship, poverty, and neighborhood concentrated poverty) that are tied to risk of family incarceration. Taken as a whole, our descriptive findings align with our theoretical framework, while simultaneously providing further empirical support for the use of a within-race/ethnicity analytic framework.
Second, our multivariate analysis revealed that paternal incarceration as a stressor was not, in isolation, significantly associated with telomere length for Black, Latina/o, and White mothers. However, after accounting for a host of characteristics likely associated with paternal incarceration and maternal health, results indicated that exposure to paternal incarceration had statistically significant and negative associations with cellular aging, but only for Black mothers. Thus, exposure to paternal incarceration accelerated cellular aging among Black mothers in a manner not experienced by White or Latina/o mothers—a finding that would have been obscured without a race-disaggregated analysis.
This finding emerged as perhaps the most important in our analysis. On the one hand, we posit that observed heightened cellular aging linked to paternal incarceration may contribute to long-term population health discrepancies because of differential historical and contemporary exposure to racialized social structures that continue to systematically disadvantage historically marginalized groups, especially Black women. As demonstrated earlier, access to flexible resources and exposure to incarceration and other structural stressors are unequally distributed across racial lines and our results demonstrated that, after accounting for these mechanisms (e.g., maternal age and education, family structure, and heavy drinking), the physiological stress response tied to paternal incarceration disproportionately burdens Black mothers. That is, the relationship between paternal incarceration and telomere length among Black mothers was suppressed by these other critical factors that shape both the risk of exposure to the U.S. criminal legal system and racial disparities in health.
As our third key finding, we observed no evidence that stress proliferation via secondary stressors played a significant role in relationships between paternal incarceration and accelerated aging for Black, Latina/o, and White mothers. Guided by the stress process model, economic instability, maternal mental health, and parenting stress did not explain (mediate) the incarceration-telomere length relationships for Black, Latina/o, and White mothers as examined using regression-with-residual techniques. While the measures included in this study capture important aspects of stress proliferation, one explanation for this finding might be that paternal incarceration does not undermine such secondary stressors in the short-term but has longer-term cumulative effects that are more dependent on (a) the length of incarceration or (b) the number of spells of paternal absence due to incarceration. We were unable to assess such factors in the current study but see value in continuing this line of inquiry to unpack this key finding. Alternatively, additional forms of secondary stress exposures tied to family incarceration warrant future attention, including measures of psychosocial assets (e.g., mastery) and perceived racial discrimination as possible mechanisms linking paternal incarceration and maternal telomere length.
Our study is not without limitations and suggests several areas upon which future research might build. First, concerning our paternal incarceration measure, we were only able to capture whether the father of the focal child had a history of incarceration from year 1 to year 5 since the FFCWS survey design does not account for the duration of incarceration, specific criminal offenses, or delineate whether the father was incarcerated in jail, prison, or both. Future scholarship on paternal incarceration and maternal health would benefit from coupling survey reports with administrative, criminal reports that can account for the length of sentence, correctional facility, and offense type in ways that acknowledge the differential health consequences for families with qualitatively different paternal incarceration experiences. Such work could also be paired with other stress proliferation and pre-incarceration measures that are endogenous to family incarceration and health. For example, recent scholarship indicates that the use of composite measures may better capture the cumulative nature of secondary stressors and, therefore, provide a clearer assessment of the potential role of stress proliferation in population health disparities [59].
Second, while this is among one of the first studies to use longitudinal survey data to examine the physiological consequences of paternal incarceration among mothers, our study leverages those longitudinal measurements to examine cross-group differences in an essentially cross-sectional manner. Additionally, scholarship that employs fully longitudinal models that assess within-person change over time would be valuable when attempting to address causal inference. Moreover, the data used for this study are reflective of Black, Latina/o, and White mothers living in urban areas. Given that people living in rural areas are approximately 50% more likely to be incarcerated in U.S. prisons as compared to people living in urban areas [60], future survey designs would benefit from developing sampling strategies that capture exposure to family incarceration in rural areas. Though such data are scarce right now, scholars could better understand whether relationships between paternal incarceration and maternal health vary based on urban–rural contexts and whether and how stress proliferation processes might manifest uniquely in different community contexts.
Finally, due to sample size limitations, we were only able to include survey responses and telomere data from Black, Latina/o, and White mothers. Given that racialized social structures have also increased the risk of family incarceration for other historically marginalized women, more research is needed that captures paternal incarceration-maternal health relationships among women from other backgrounds. This might include additional scholarship focusing on Native [1] or Asian women.
Even in the context of these limitations, this study contributes to a nascent body of literature attempting to understand the health consequences of mass incarceration for mothers who experienced paternal incarceration. More specifically, our results provide a foundation upon which health scholars and criminal justice stakeholders may better understand whether and how paternal incarceration shapes deleterious health patterns for the mothers who remain to care for the children of those incarcerated. Utilizing a theoretical and analytic framework that acknowledges unequal access to exposure to incarceration and access to resources, findings reveal that the physiological consequences of paternal incarceration for mothers are dependent on racial and ethnic background. When accounting for resources and exposures that are unequally distributed and driven by racialized social structures, we find Black mothers exposed to paternal incarceration were more likely to experience accelerated cellular aging when compared to Black mothers with no history of paternal incarceration. Again, due to differences in exposure and resources, we find paternal incarceration did not play a role in accelerated cellular aging patterns for Latina/o and White mothers. These findings suggest that in order to address detrimental health outcomes associated with paternal incarceration for Black mothers, future policies must address underlying structural mechanisms that increase the risk of exposure and access to flexible resources. Future research should continue to interrogate relationships between paternal incarceration and maternal health and whether and how racialized social mechanisms shape these patterns.
Supplementary Material
Footnotes
Supplementary Information The online version contains supplementary material available at https://doi.org/10.1007/s40615-022-01388-2.
Declarations
Ethical Approval All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.
Informed Consent Informed consent was obtained from all individual participants included in the study.
Conflict of Interest The author declares no competing interests.
Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.
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