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The longitudinal effects of fathers’ incarceration on families’ well-being
Abstract
Background: Despite their positive intention to increase school safety, zero-tolerance policies may perpetuate racial disparities in health. Zero tolerance refers to school policies and practices that mandate predetermined punishment in response to student misbehavior regardless of the context or rationale for the behavior. Black children are subjected to more discipline and are more likely to attend schools that frequently use discipline than their White peers. Given the racial nature of school discipline, experiencing frequent, vicarious school discipline may come at a cost to the overall wellbeing of Black children. Thus, we examined whether schools’ discipline practices predicted Black and White children's telomere length, a biomarker for chronic stress, and whether children's genetic sensitivity moderated the observed effects.
Method: We used nationally representative data from 1058 Black and White children (75.5% Black; 50% boys; Mage = 9.24) from 20 urban cities as part of the Fragile Families and Child Wellbeing Study. School discipline was measured using school record data, and telomere lengths were assessed via salivary DNA samples.
Results: After accounting for covariates, results showed that Black (but not White) children who attended schools that frequently employed multiple out-of-school suspensions exhibited shorter telomere lengths. This effect was stronger for Black children with the most reactive alleles of the serotonin transporter genes when compared to those with the least reactive alleles.
Conclusion: Exclusionary school disciplinary practices may contribute to health disparities between Black and White children in the United States. Suggestions for interventions and policy will be discussed.
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Use of telomere length (TL) as a biomarker for various environmental exposures and diseases has increased in recent years. Various methods have been developed to measure telomere length. Polymerase chain reaction (PCR)-based methods remain wide-spread for population-based studies due to the high-throughput capability. While several studies have evaluated the repeatability and reproducibility of different TL measurement methods, the results have been variable. We conducted a literature review of TL measurement cross-method comparison studies that included a PCR-based method published between January 1, 2002 and May 25, 2020. A total of 25 articles were found that matched the inclusion criteria. Papers were reviewed for quality of methodologic reporting of sample and DNA quality, PCR assay characteristics, sample blinding, and analytic approaches to determine final TL. Overall, methodologic reporting was low as assessed by two different reporting guidelines for qPCR-based TL measurement. There was a wide range in the reported correlation between methods (as assessed by Pearson’s r) and few studies utilized the recommended intra-class correlation coefficient (ICC) for assessment of assay repeatability and methodologic comparisons. The sample size for nearly all studies was less than 100, raising concerns about statistical power. Overall, this review found that the current literature on the relation between TL measurement methods is lacking in validity and scientific rigor. In light of these findings, we present reporting guidelines for PCR-based TL measurement methods and results of analyses of the effect of assay repeatability (ICC) on statistical power of cross-sectional and longitudinal studies. Additional cross-laboratory studies with rigorous methodologic and statistical reporting, adequate sample size, and blinding are essential to accurately determine assay repeatability and replicability as well as the relation between TL measurement methods.
Importance
In 2016, an estimated 8% of US children younger than 18 years had experienced the incarceration of a parent, and rates were substantially higher among children from racial and ethnic minority backgrounds and disadvantaged groups. Little is known about whether parental incarceration during childhood is associated with adult psychiatric problems and functional outcomes.
Objective
To examine whether parental incarceration is associated with increased levels of psychiatric diagnosis and poor outcomes in health, legal, financial, and social domains in adulthood.
Design, Setting, and Participants
This cohort study used data from the community-representative, prospective, longitudinal Great Smoky Mountains Study. Children and their parents were interviewed up to 8 times from January 1993 to December 2000 (ages 9-16 years; 6674 observations of 1420 participants) using the Child and Adolescent Psychiatric Assessment, which assessed parental incarceration, childhood psychiatric diagnoses, and other adversities. Young adults were followed up at ages 19, 21, 25, and 30 years from January 1999 to December 2015 (4556 observations of 1334 participants) to assess psychiatric diagnoses and functional outcomes indicative of a disrupted transition to adulthood. Data analysis was conducted from June 2018 to June 2019.
Results
By age 16 years, 475 participants (weighted percentage, 23.9%) had a parental figure who had been incarcerated, including 259 young men (22.2%) and 216 young women (25.5%). Parental incarceration was associated with higher prevalence of childhood psychiatric diagnoses (eg, any depressive diagnosis: adjusted odds ratio [aOR], 2.5; 95% CI, 1.3-4.6; P = .006; attention-deficit/hyperactivity disorder: aOR, 2.3; 95% CI, 1.0-5.5; P = .06; and conduct disorder: aOR, 2.5; 95% CI, 1.4-4.3; P = .001). After accounting for childhood psychiatric diagnoses and adversity exposure, parental incarceration remained associated with increased odds of having an adult anxiety disorder (aOR, 1.7; 95% CI, 1.0-3.0; P = .04), having an illicit drug use disorder (aOR, 6.6; 95% CI, 2.6-17.0; P < .001), having a felony charge (aOR, 3.4; 95% CI, 1.8-6.5; P < .001), incarceration (aOR, 2.8; 95% CI, 1.4-5.4; P = .003), not completing high school (aOR, 4.4; 95% CI, 2.2-8.8; P < .001), early parenthood (aOR, 1.7; 95% CI, 1.0-3.0; P = .04), and being socially isolated (aOR, 2.2; 95% CI, 1.2-4.0; P = .009).
Conclusions and Relevance
This study suggests that parental incarceration is associated with a broad range of psychiatric, legal, financial, and social outcomes during young adulthood. Parental incarceration is a common experience that may perpetuate disadvantage from generation to generation.
The human telomerase reverse transcriptase (hTERT) gene is repressed in most somatic cells, whereas the expression of the mouse mTert gene is widely detected. To understand the mechanisms of this human-specific repression, we constructed bacterial artificial chromosome (BAC) reporters using human and mouse genomic DNAs encompassing the TERT genes and neighboring loci. Upon chromosomal integration, the hTERT, but not the mTert, reporter was stringently repressed in telomerase-negative human cells in a histone deacetylase (HDAC)-dependent manner, replicating the expression of their respective endogenous genes. In chimeric BACs, the mTert promoter became strongly repressed in the human genomic context, but the hTERT promoter was highly active in the mouse genomic context. Furthermore, an unrelated herpes simplex virus-thymidine kinase promoter was strongly repressed in the human, but not in the mouse, genomic context. These results demonstrated that the repression of hTERT gene was dictated by distal elements and its chromatin environment. This repression depended on class I HDACs and involved multiple corepressor complexes, including HDAC1/2-containing Sin3B, nucleosome remodeling and histone deacetylase, and corepressor of RE1 silencing transcription factor complexes. Together, our data indicate that the lack of telomerase expression in most human somatic cells results from its repressive genomic environment, providing new insight into the mechanism of long-recognized differential telomerase regulation in mammalian species.-Cheng, D., Zhao, Y., Wang, S., Zhang, F., Russo, M., McMahon, S. B., Zhu, J. Repression of telomerase gene promoter requires human-specific genomic context and is mediated by multiple HDAC1-containing corepressor complexes.
Background: No research has estimated the cumulative risk of paternal or maternal incarceration in any country other than the U.S., so it remains unclear how much more likely U.S. children are to be exposed to parental incarceration than children living in other countries.
Objective: To estimate the cumulative risks of paternal and maternal incarceration (including even very short jail stays of less than 24 hours) by age 14 for the 1990 Danish birth cohort. We then compare these estimates to equivalent estimates for the 1990 U.S. birth cohort.
Methods: We use birth cohort life tables and Danish registry data, which provide administrative records on all incarcerations in Denmark, to estimate the cumulative risks of paternal and maternal incarceration. We follow the full 1990 Danish birth cohort (N = 62,982) up to age 14 to see whether each child has ever experienced different lengths of paternal and maternal incarceration.
Results: We estimate that 1.54% of Danish children experienced paternal imprisonment and that 8.78% of Danish children experienced any paternal incarceration (including jail stays less than 24 hours), indicating that U.S. children are almost as likely to have their fathers sent to prison (which usually results from a sentence of at least one year in the U.S.) as Danish children are to have their fathers spend less than one day in jail. Results for maternal imprisonment are similar.
Conclusions: U.S. children are far more likely to be exposed to parental incarceration than Danish children, suggesting that imprisonment contributes not only to inequality among children within the U.S., but also to inequality between children in the U.S. and children in other developed democracies.
Telomeres shorten with each cell division and are essential for chromosomal stability. Short telomeres in surrogate tissues (e.g., blood cells) are associated with increased cancer risk in several case-control studies, but findings are inconsistent in prospective studies.
We systematically reviewed studies published prior to August 30, 2010, on the association between telomere length (TL) in surrogate tissues and cancer. There were 27 reports on 13 cancers and/or incident cancer investigating this association. The majority, 16, were retrospective case--control studies, 11 were prospective studies. Meta-analyses were conducted to determine ORs and 95% CIs for these studies.
Studies on bladder, esophageal, gastric, head and neck, ovarian, renal, and overall incident cancer found associations between short telomeres and these cancers. Non-Hodgkin lymphoma, breast, lung, and colorectal cancer reports were inconsistent. Single studies on endometrial, prostate, and skin cancers were null. In a random-effects meta-analysis, short TL was significantly associated with cancer in retrospective studies (pooled OR for the shortest TL quartile compared with the longest: 2.9, 95% CI: 1.75-4.8, P < 0.0001). The pooled OR for prospective studies was 1.16 (95% CI: 0.87-1.54, P = 0.32). All studies combined yielded a pooled OR of 1.96 (95% CI: 1.37-2.81, P = 0.0001) for the association of short TL and cancer. CONCLUSION AND IMPACT: There is suggestive evidence that short surrogate tissue TL is associated with cancer; the strongest evidence exists for bladder, esophageal, gastric, and renal cancers. Additional prospective studies with consistent methodology are needed to confirm this hypothesis.
We describe a simple and reproducible method to measure absolute telomere length (aTL) using quantitative real-time polymerase chain reaction (qPCR). This method is based on the Cawthon method for relative measurement of telomere length (TL) but modified by introducing an oligomer standard to measure aTL. The method describes the oligomer standards, the generation of the standard curve and the calculations required to calculate aTL from the qPCR data. The necessary controls and performance characteristics of the assay are described in detail and compared relative to other methods for measuring TL. Typical results for this assay for a variety of human tissue samples are provided as well as a troubleshooting schedule. This method allows high throughput measurement of aTL using small amounts of DNA making it amenable for molecular epidemiological studies. Compared to the traditional relative TL qPCR assays, the aTL method described in this protocol enables a more direct comparison of results between experiments within and between laboratories.
High U.S. incarceration rates have motivated recent research on the negative effects of imprisonment on later employment, earnings, and family relationships. Because most men in jail and prison are fathers, a large number of children may be placed at considerable risk by policies of incarceration. This article examines one dimension of the economic risk faced by children of incarcerated fathers: the reduction in the financial support that they receive. We use a population-based sample of urban children to examine the effects of incarceration on this support. Both cross-sectional and longitudinal regressions indicate that formerly incarcerated men are less likely to contribute to their families, and those who do contribute provide significantly less. The negative effects of incarceration on fathers' financial support are due not only to the low earnings of formerly incarcerated men but also to their increased likelihood to live apart from their children. Men contribute far less through child support (formal or informal) than they do when they share their earnings within their household, suggesting that the destabilizing effects of incarceration on family relationships place children at significant economic disadvantage.
The transcriptional activation of human telomerase reverse transcriptase (hTERT) is an important step during cellular immortalization and tumorigenesis. To study how this activation occurs during immortalization, we have established a set of genetically related pre-crisis cells and their immortal progeny. As expected, hTERT mRNA was detected in our telomerase-positive immortal cells but not in pre-crisis cells or telomerase-negative immortal cells. However, transiently transfected luciferase reporters controlled by hTERT promoter sequences exhibited similar levels of luciferase activity in both telomerase-positive and -negative cells, suggesting that the endogenous chromatin context is likely required for hTERT regulation. Analysis of chromatin susceptibility to DNase I digestion consistently identified a DNase I hypersensitivity site (DHS) near the hTERT transcription initiation site in telomerase-positive cells. In addition, the histone deacetylase inhibitor trichostatin A (TSA) induced hTERT transcription and also a general increase in chromatin sensitivity to DNase treatment in telomerase-negative cells. The TSA-induced hTERT transcription in pre-crisis cells was accompanied by the formation of a DHS at the hTERT promoter. Furthermore, the TSA-induced hTERT transcription and chromatin alterations were not blocked by cycloheximide, suggesting that this induction does not require de novo protein synthesis and that TSA induces hTERT expression through the inhibition of histone deacetylation at the hTERT promoter. Taken together, our results suggest that the endogenous chromatin environment plays a critical role in the regulation of hTERT expression during cellular immortalization.
Background:
Adverse childhood experiences (ACEs) are an identified risk factor for the social and emotional development of children. What is less known is the long-term effects of ACEs when poverty and ACEs coincide.
Objective:
Using longitudinal cohort-panel data, we examined whether exposure to ACEs by the age of three among poor children would longitudinally result in behavioral problems at ages three, five, nine, and 15, after controlling for mothers' socioeconomic status and their children's characteristics.
Participants and setting:
We used a subsample of 2750 children and their parents living in urban poverty from the Fragile Families and Child Wellbeing study.
Methods:
Logistic regression modeling was used to obtain adjusted odds ratios of ACE categories predicting behavioral problems after accounting for family socioeconomic position.
Results:
Our findings indicate that experiencing ACEs in early childhood was significantly associated with later behavioral outcomes from childhood to adolescence. Exposure to multiple ACEs before the age of three was significantly associated with the top-risk behavior group at age five; the odd ratios were 2.0 (CI = 1.3-3.1) and 2.9 (CI = 1.8-4.6) for two ACEs and three or more ACEs, respectively. At both ages nine and 15, children experiencing two or more ACEs had 1.9 to 3.2 times higher odds to demonstrate more the top 10th percentile of behavioral problems. Among covariates, mothers' race and education, and children's gender and temperament were identified as significant factors to determine behavior problems.
Conclusions:
The findings support policies and programs for families with children who have experienced economic disadvantages and early childhood adversity.
Objectives
I extend the life-course theory of cumulative disadvantage to focus on continuity in punishment across generations. Specifically, I examine (1) the association between paternal incarceration and elementary school suspension or expulsion and (2) the extent to which behavior problems and weakened social bonds explain this association.
Method
Analyses rely on logistic regression, propensity score matching, and mediation methods with data from the Fragile Families and Child Wellbeing Study ( N = 3,201), a birth cohort of children born in large U.S. cities between 1998 and 2000.
Results
The odds of school punishment among children who had a residential father incarcerated by age 5 are 75 percent greater than the odds for children in a matched control group. About one third of this association is accounted for by behavior problems and weakened social bonds. Even after accounting for behavior problems and social bonds, children whose fathers were incarcerated are at greater risk of school punishment.
Conclusions
I find evidence of an intergenerational stability of punishment and mixed support for an intergenerational extension to cumulative disadvantage theory. Paternal incarceration is associated with children’s likelihood of experiencing formal punishment in elementary school, and behavior problems and weakened social bonds explain part of this association.
Background and objectives:
Father loss during childhood has negative health and behavioral consequences, but the biological consequences are unknown. Our goal was to examine how father loss (because of separation and/or divorce, death, or incarceration) is associated with cellular function as estimated by telomere length.
Methods:
Data come from the 9-year follow-up of the Fragile Families and Child Wellbeing Study, a birth cohort study of children in 20 large American cities (N = 2420). Principal measures are as follows: salivary telomere length (sTL), mother reports of father loss, and polymorphisms in genes related to serotonergic and dopaminergic signaling.
Results:
At 9 years of age, children with father loss have significantly shorter telomeres (14% reduction). Paternal death has the largest association (16%), followed by incarceration (10%), and separation and/or divorce (6%). Changes in income partially mediate these associations (95% mediation for separation and/or divorce, 30% for incarceration, and 25% for death). Effects are 40% greater for boys and 90% greater for children with the most reactive alleles of the serotonin transporter genes when compared with those with the least reactive alleles. No differences were found by age at father loss or a child's race/ethnicity.
Conclusions:
Father loss has a significant association with children's sTL, with the death of a father showing the largest effect. Income loss explains most of the association between child sTL and separation and/or divorce but much less of the association with incarceration or death. This underscores the important role of fathers in the care and development of children and supplements evidence of the strong negative effects of parental incarceration.
A growing literature documents the myriad penalties for children of incarcerated fathers, but relatively little is known about how paternal incarceration contributes to educational outcomes in early and middle childhood. In this article, we use data from the Fragile Families and Child Wellbeing Study to provide the first estimates of the relationship between paternal incarceration and children’s grade retention in elementary school. Propensity score matching models indicate that children of incarcerated fathers are more likely to experience early grade retention than their counterparts. This relationship is not driven by test scores or behavior problems; preliminary evidence suggests this relationship may be driven by teachers’ perceptions of children’s academic proficiency. These findings suggest that elementary school teachers may play an important role in the lives of children experiencing paternal incarceration and, more generally, highlight yet another way in which the large-scale incarceration of men limits their children’s potential.
In response to dramatic increases in imprisonment, a burgeoning literature considers the consequences of incarceration for family life, almost always documenting negative outcomes. But effects of incarceration may be more complicated and nuanced. In this article, we consider the countervailing consequences of paternal incarceration for a host of family relationships, including fathers' parenting, mothers' parenting, and the relationship between parents. Using longitudinal data from the Fragile Families and Child Wellbeing Study, we find recent paternal incarceration sharply diminishes parenting behaviors among residential but not nonresidential fathers. Virtually all of the association between incarceration and parenting among residential fathers is explained by changes in fathers' relationships with their children's mothers. Consequences for mothers' parenting, however, are weak and inconsistent. Furthermore, our findings show recent paternal incarceration sharply increases the probability a mother repartners, potentially offsetting some losses from the biological father's lesser involvement while simultaneously leading to greater family complexity. Taken together, the collateral consequences of paternal incarceration for family life are complex and countervailing.
Significance
This paper makes two contributions to research on the link between the social environment and health. Using data from a birth cohort study, we show that, among African American boys, those who grow up in highly disadvantaged environments have shorter telomeres (at age 9) than boys who grow up in highly advantaged environments. We also find that the association between the social environment and telomere length (TL) is moderated by genetic variation within the serotonin and dopamine pathways. Boys with the highest genetic sensitivity scores had the shortest TL when exposed to disadvantaged environments and the longest TL when exposed to advantaged environments. To our knowledge, this report is the first to document a gene–social environment interaction for TL, a biomarker of stress exposure.
High rates of incarceration in the United States have motivated a broad examination of the effects of parental incarceration on child well-being. Although a growing literature documents challenges facing the children of incarcerated men, most incarcerated fathers lived apart from their children before their arrest, raising questions of whether they were sufficiently involved with their families for their incarceration to affect their children. The author used the Fragile Families and Child Wellbeing Study (N = 4,071) to examine father–child contact among incarcerated fathers and found that most incarcerated fathers maintained a degree of contact with their children through either coresidence or visitation. Moreover, the results revealed robust reductions in both father–child coresidence and visitation when fathers are incarcerated—between 18% and 20% for coresidence and 30% to 50% for the probability of visitation. The findings suggest that these reductions are driven by both incapacitation while incarcerated and union dissolution upon release.
Reports 3 errors in the original article by K. O. McGraw and S. P. Wong (Psychological Methods, 1996, 1[1], 30–46). On page 39, the intraclass correlation coefficient (ICC) and r values given in Table 6 should be changed to r = .714 for each data set, ICC(C,1) = .714 for each data set, and ICC(A,1) = .720, .620, and .485 for the data in Columns 1, 2, and 3 of the table, respectively. In Table 7 (p. 41), which is used to determine confidence intervals on population values of the ICC, the procedures for obtaining the confidence intervals on ICC(A,k) need to be amended slightly. Corrected formulas are given. On pages 44–46, references to Equations A3, A,4, and so forth in the Appendix should be to Sections A3, A4, and so forth. (The following abstract of this article originally appeared in record 1996-03170-003.). Although intraclass correlation coefficients (ICCs) are commonly used in behavioral measurement, psychometrics, and behavioral genetics, procedures available for forming inferences about ICC are not widely known. Following a review of the distinction between various forms of the ICC, this article presents procedures available for calculating confidence intervals and conducting tests on ICCs developed using data from one-way and two-way random and mixed-effect analysis of variance models. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
The long-term sequelae of adverse early-life experiences have long been a focus in psychiatry, with a historic neurobiological emphasis on physiological systems that are demonstrably stress-responsive, such as the hypothalamic-pituitary-adrenal axis and neuroimmune function. However, there has been increasing recognition in the general medical literature that such sequelae might encompass more pervasive alterations in health status and physiology. Recent findings in telomere biology have suggested a new avenue for exploring the adverse health effects of childhood maltreatment. Telomere length in proliferative tissues declines with cell replication and the effect can be accelerated by such factors as inflammation, oxidative stress, radiation, and toxins. Reduced telomere length, as a proxy for cellular aging, has been associated with numerous chronic somatic diseases that are generally considered to be diseases of aging, such as diabetes, cancer, and heart disease. More recently, shorter telomeres have been demonstrated in several psychiatric conditions, particularly depression. Sustained psychosocial stress of a variety of types in adulthood appears to be associated with shorter telomeres. Now, emerging work suggests a robust, and perhaps dose-dependent, relationship with early-life stress. These findings present new opportunities to reconceptualize the complex relationships between experience, physical and psychiatric disease, and aging.
Advances in fields of inquiry as diverse as neuroscience, molecular biology, genomics, developmental psychology, epidemiology, sociology, and economics are catalyzing an important paradigm shift in our understanding of health and disease across the lifespan. This converging, multidisciplinary science of human development has profound implications for our ability to enhance the life prospects of children and to strengthen the social and economic fabric of society. Drawing on these multiple streams of investigation, this report presents an ecobiodevelopmental framework that illustrates how early experiences and environmental influences can leave a lasting signature on the genetic predispositions that affect emerging brain architecture and long-term health. The report also examines extensive evidence of the disruptive impacts of toxic stress, offering intriguing insights into causal mechanisms that link early adversity to later impairments in learning, behavior, and both physical and mental well-being. The implications of this framework for the practice of medicine, in general, and pediatrics, specifically, are potentially transformational. They suggest that many adult diseases should be viewed as developmental disorders that begin early in life and that persistent health disparities associated with poverty, discrimination, or maltreatment could be reduced by the alleviation of toxic stress in childhood. An ecobiodevelopmental framework also underscores the need for new thinking about the focus and boundaries of pediatric practice. It calls for pediatricians to serve as both front-line guardians of healthy child development and strategically positioned, community leaders to inform new science-based strategies that build strong foundations for educational achievement, economic productivity, responsible citizenship, and lifelong health.
Although much research has focused on how imprisonment transforms the life course of disadvantaged black men, researchers have paid little attention to how parental imprisonment alters the social experience of childhood. This article estimates the risk of parental imprisonment by age 14 for black and white children born in 1978 and 1990. This article also estimates the risk of parental imprisonment for children whose parents did not finish high school, finished high school only, or attended college. Results show the following: (1) 1 in 40 white children born in 1978 and 1 in 25 white children born in 1990 had a parent imprisoned; (2) 1 in 7 black children born in 1978 and 1 in 4 black children born in 1990 had a parent imprisoned; (3) inequality in the risk of parental imprisonment between white children of college-educated parents and all other children is growing; and (4) by age 14, 50.5% of black children born in 1990 to high school dropouts had a father imprisoned. These estimates, robustness checks, and extensions to longitudinal data indicate that parental imprisonment has emerged as a novel-and distinctively American-childhood risk that is concentrated among black children and children of low-education parents.
The relationship of health risk behavior and disease in adulthood to the breadth of exposure to childhood emotional, physical, or sexual abuse, and household dysfunction during childhood has not previously been described.
A questionnaire about adverse childhood experiences was mailed to 13,494 adults who had completed a standardized medical evaluation at a large HMO; 9,508 (70.5%) responded. Seven categories of adverse childhood experiences were studied: psychological, physical, or sexual abuse; violence against mother; or living with household members who were substance abusers, mentally ill or suicidal, or ever imprisoned. The number of categories of these adverse childhood experiences was then compared to measures of adult risk behavior, health status, and disease. Logistic regression was used to adjust for effects of demographic factors on the association between the cumulative number of categories of childhood exposures (range: 0-7) and risk factors for the leading causes of death in adult life.
More than half of respondents reported at least one, and one-fourth reported > or = 2 categories of childhood exposures. We found a graded relationship between the number of categories of childhood exposure and each of the adult health risk behaviors and diseases that were studied (P < .001). Persons who had experienced four or more categories of childhood exposure, compared to those who had experienced none, had 4- to 12-fold increased health risks for alcoholism, drug abuse, depression, and suicide attempt; a 2- to 4-fold increase in smoking, poor self-rated health, > or = 50 sexual intercourse partners, and sexually transmitted disease; and 1.4- to 1.6-fold increase in physical inactivity and severe obesity. The number of categories of adverse childhood exposures showed a graded relationship to the presence of adult diseases including ischemic heart disease, cancer, chronic lung disease, skeletal fractures, and liver disease. The seven categories of adverse childhood experiences were strongly interrelated and persons with multiple categories of childhood exposure were likely to have multiple health risk factors later in life.
We found a strong graded relationship between the breadth of exposure to abuse or household dysfunction during childhood and multiple risk factors for several of the leading causes of death in adults.
When parents are incarcerated: Interdisciplinary research and interventions to support children
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Washington, DC, US: American Psychological Association; 2018:53-81.