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Although individuals born at extremely low birth weight (ELBW; ≤1000 g) are known to be at greater risk for mental health problems than individuals born at normal birth weight (NBW; ≥2500 g), contributions of postnatal growth to these relations have not been fully explored. We compared individual differences in the Ponderal Index [(PI; weight(kg)/height(m3)] and head circumference (HC) in predicting internalizing and externalizing behaviors in childhood and adolescence in a cohort of ELBW survivors (N = 137) prospectively followed since birth. Baseline models indicated that infants who were born thinner or with smaller HC showed greater PI or HC growth in the first 3 years. Latent difference score (LDS) models showed that compensatory HC growth in the first year (ΔHC = 20.72 cm), controlled for birth HC, predicted ADHD behaviors in adolescence in those born with smaller HC. LDS models also indicated that the PI increased within the first year (ΔPI = 1.568) but decreased overall between birth and age 3 years (net ΔPI = −4.597). Modeling further showed that larger increases in the PI in the first year and smaller net decreases over 3 years predicted more internalizing behaviors in adolescence. These findings suggest early growth patterns prioritizing weight over height may have negative effects on later mental health in ELBW survivors, consistent with developmental programming theories.
Effects of stresses associated with extremely preterm birth may be biologically “recorded” in the genomes of individuals born preterm via changes in DNA methylation (DNAm) patterns. Genome-wide DNAm profiles were examined in buccal epithelial cells from 45 adults born at extremely low birth weight (ELBW; ≤1000 g) in the oldest known cohort of prospectively followed ELBW survivors (Mage = 32.35 years, 17 male), and 47 normal birth weight (NBW; ≥2500 g) control adults (Mage = 32.43 years, 20 male). Sex differences in DNAm profiles were found in both birth weight groups, but they were greatly enhanced in the ELBW group (77,895 loci) versus the NBW group (3,424 loci), suggesting synergistic effects of extreme prenatal adversity and sex on adult DNAm profiles. In men, DNAm profiles differed by birth weight group at 1,354 loci on 694 unique genes. Only two loci on two genes distinguished between ELBW and NBW women. Gene ontology (GO) and network analyses indicated that loci differentiating between ELBW and NBW men were abundant in genes within biological pathways related to neuronal development, synaptic transportation, metabolic regulation, and cellular regulation. Findings suggest increased sensitivity of males to long-term epigenetic effects of extremely preterm birth. Group differences are discussed in relation to particular gene functions.
This study examined the link between two biological markers of stress vulnerability at 22–26 years of age and telomere length at 30–35 among extremely low birth weight (ELBW; <1000 g) survivors and normal birth weight (NBW; >2500 g) control participants. Sixteen ELBW and 22 NBW participants provided baseline afternoon salivary cortisol samples and resting frontal electroencephalogram (EEG) alpha asymmetry data at 22–26 years. Buccal cells were assayed for telomere length at 30–35 years. Analyses controlled for sex, postnatal steroid exposure, childhood socioeconomic status, time of cortisol sample collection, and body mass index at 22–26 years. Salivary cortisol and frontal asymmetry at age 22–26 independently predicted telomere length at age 30–35, such that relatively higher cortisol and greater relative right frontal asymmetry at rest predicted telomere shortening among NBW controls, but not among ELBW survivors. However, similar associations were not noted in ELBW survivors, suggesting that ELBW survivors may have different mechanisms of stress coping as a result of their early-life exposures. These findings offer preliminary evidence in support of the role of stress in the genesis of cellular senescence at least among those born at NBW, but that these links may differ in those born preterm.
The mental health of adult extremely low birth weight (ELBW) (<1000 g) survivors is poorer than their normal birth weight (NBW) peers. An understanding of the modifiable factors that affect this risk could provide targets for intervention. We set out to determine the extent to which a maternal history of mental health problems influenced mental health in ELBW and NBW offspring in adulthood. A total of 85 ELBW and 88 NBW individuals born between 1977 and 1982 in central west Ontario, Canada self-reported on internalizing (depression, anxiety) and externalizing (attention-deficit hyperactivity and antisocial) problems using the Diagnostic and Statistical Manual of Mental Disorders (DSM) scales of the Young Adult Self-Report at ages 22–26 and 30–35. They also reported on their mother’s maternal mental health using the Family History Screen. An interaction was found between birth weight status and maternal history of an anxiety disorder such that ELBW survivors showed a greater increase in internalizing scores than NBW participants at 22–26 (β = 10.27, p = 0.002) and at 30–35 years of age (β = 12.65, p = 0.002). An interaction was also observed between birth weight and maternal history of mood disorder, with higher externalizing scores in ELBW survivors than NBW adults at 22–26 (β = 7.21, p < 0.0001). ELBW adults appear to be more susceptible to the adverse mental health effects of exposure to maternal mood and anxiety disorders than those born at NBW. These links further highlight the importance of detecting and treating mental health problems in the parents of preterm survivors as a means of attempting to reduce the burden of psychopathology in this population.
Extremely low birth weight (ELBW) survivors have higher rates of shyness, a risk factor for poorer outcomes across the life span. Due to advances in fetal and neonatal medicine, the first generation of ELBW survivors have survived to adulthood and become parents. However, no studies have investigated the transmission of their stress vulnerability to their offspring. We explored this phenomenon using a population-based cohort of ELBW survivors and normal birth weight (NBW) controls. Using data from three generations, we examined whether the shyness and parenting stress of ELBW and NBW participants (Generation 2) mediated the relation between the parenting style of their parents (Generation 1) and shyness in their offspring (Generation 3), and the extent to which exposure to perinatal adversity (Generation 2) moderated this mediating effect. We found that among ELBW survivors, parenting stress (in Generation 2) mediated the relation between overprotective parenting style in Generation 1 (grandparents) and child shyness in Generation 3. These findings suggest that perinatal adversity and stress may be transmitted to the next generation in humans, as reflected in their perceptions of their children as shy and socially anxious, a personality phenotype that may subsequently place their children at risk of later mental and physical health problems.
Although shyness is a ubiquitous phenomenon with early developmental origins, little research has examined the influence of prenatal exposures on the developmental trajectory of shyness. Here, we examined trajectories of shyness from childhood to adulthood in three groups (N = 254), with varying degrees of prenatal adversity as indicated by the number of stressful exposures: extremely low birth weight (ELBW; <1000 g) survivors prenatally exposed to exogenous corticosteroids (ELBW+S, n = 56); ELBW survivors not prenatally exposed to exogenous corticosteroids (ELBW+NS, n = 56); and normal birth weight (NBW, n = 142) controls. Multilevel modeling revealed that the ELBW+S individuals exhibited the highest levels of childhood shyness, which remained stable into adulthood. The ELBW+NS and NBW controls had comparably low levels of childhood shyness; however, the ELBW+NS individuals experienced patterns of increasing shyness, while NBW controls displayed decreases in shyness into adulthood. We speculate that individuals exposed to multiple prenatal stressors (i.e., ELBW+S) may be developmentally programmed to be more sensitive to detecting social threat, with one manifestation being early developing, stable shyness, while increasing shyness among ELBW+NS individuals may reflect a later developing shyness influenced by postnatal context. We discuss the implications of these findings for understanding the developmental origins and developmental course of human shyness from childhood through adulthood.
Perinatal and later postnatal adversities have been shown to adversely affect socioeconomic trajectories, while enhanced early cognitive abilities improve them. However, little is known about the combined influence of these exposures on social mobility. In this study, we examined if childhood IQ moderated the association between four different types of postnatal adversity (childhood socioeconomic disadvantage, childhood sexual abuse, lifetime psychiatric disorder, and trait neuroticism) and annual earnings at 30–35 years of age in a sample of 88 extremely low birth weight survivors. Our results suggested that higher childhood IQ was associated with greater personal income at age 30–35. Extremely low birth weight survivors who did not face psychological adversities and who had higher childhood IQ reported higher income in adulthood. However, those who faced psychological adversity and had higher childhood IQ generally reported lower income in adulthood. Our findings suggest that cognitive reserve may not protect preterm survivors against the complex web of risk factors affecting their later socioeconomic attainment.
While the trajectory of self-esteem from adolescence to adulthood varies from person to person, little research has examined how differences in early developmental processes might affect these pathways. This study examined how early motor skill development interacted with preterm birth status to predict self-esteem from adolescence through the early 30s. We addressed this using the oldest known, prospectively followed cohort of extremely low birth weight (<1000 g) survivors (N = 179) and normal birth weight controls (N = 145) in the world, born between 1977 and 1982. Motor skills were measured using a performance-based assessment at age 8 and a retrospective self-report, and self-esteem was reported during three follow-up periods (age 12–16, age 22–26, and age 29–36). We found that birth weight status moderated the association between early motor skills and self-esteem. Stable over three decades, the self-esteem of normal birth weight participants was sensitive to early motor skills such that those with poorer motor functioning manifested lower self-esteem, while those with better motor skills manifested higher self-esteem. Conversely, differences in motor skill development did not affect the self-esteem from adolescence to adulthood in individuals born at extremely low birth weight. Early motor skill development may exert differential effects on self-esteem, depending on whether one is born at term or prematurely.
Extremely low birth weight (ELBW; <1000 g) infants have been exposed to stressful intrauterine and early postnatal environments. Even greater early adversity has been experienced by ELBW survivors who were also born small for gestational age (SGA; <10th percentile for GA) compared to those born appropriate for GA (AGA). ELBW survivors, particularly those born SGA, face increased risk for internalizing problems compared to normal BW (NBW; ≥2500 g) controls. Internalizing problems are related to allelic variations in the promoter region of the serotonin transporter linked polymorphic region gene (5-HTTLPR). We followed the oldest longitudinal cohort of ELBW survivors to adulthood. Participants provided buccal cells and reported on internalizing problems, using the Young Adult Self-Report when they were in their mid-20s (ELBW/SGA, N = 28; ELBW/AGA, N = 60; NBW, N = 81) and mid-30s (ELBW/SGA, N = 27; ELBW/AGA, N = 58; NBW, N = 76). The findings indicate that ELBW/SGAs carrying the 5-HTTLPR short allele reported increased internalizing problems, particularly depression, during the third and fourth decades of life. This is the first known report on gene–environment interactions predicting psychopathology among ELBW survivors. Our findings elucidate putative neurobiological pathways that underlie risk for psychopathology.
Although infants born at extremely low birth weight (ELBW; birth weight < 1000 g) are at increased risk for developing later psychopathology, the mechanisms contributing to this association are largely unknown. In the present study, we examined a putative cognitive link to psychopathology in a cohort of ELBW survivors. These individuals were followed up prospectively at age 8 and again at ages 22–26. At 8 years, participants completed measures of fluid and general intelligence. As young adults, a subset of ELBW survivors free of major neurosensory impairments provided self-reports of personality characteristics related to psychopathology. Data from 66 participants indicated that, as predicted, the association between ELBW and externalizing behaviors was moderated by fluid intelligence. Specifically, ELBW individuals with poor fluid intelligence who were born small for gestational age (birth weight < 10th percentile for gestational age) showed the highest level of externalizing behaviors. These findings provide support for a cumulative risk model and suggest that fluid intelligence might be a cognitive mechanism contributing to the development of psychopathology among nonimpaired individuals who were born at ELBW and small for gestational age.
The objective of this study was to explore the relationship among extremely low birthweight (ELBW), psychopathology, and impairments in adaptive functioning in a regional cohort of 7–8-year-old children with a birthweight of 501–1,000 g compared to a sample of full-term controls. One-hundred twenty-nine of 143 (90%) ELBW survivors and 145 controls, born between 1977 and 1981, agreed to participate in the study. The children were assessed at a mean, unadjusted age of 7.8 years. Results showed that parents of ELBW children were more likely than parents of controls to report specifically problems of attention-deficit hyperactivity disorder (ADHD). There were few differences between the groups in terms of impairments in adaptive functioning. Further analyses showed that the relationship between ELBW and ADHD could not be explained by confounding psychosocial risk factors, nor were ELBW children from disadvantaged environments more likely to have ADHD problems than ELBW children from nondisadvantaged environments. The relationships between ELBW and ADHD problems appeared to be associated with the lower IQ of the ELBW subjects.
The reliability of classification of cerebral palsy (CP) in low-birthweight children was assessed by using clinical and research study records sampled from population-based cohort studies in the USA, the Netherlands, Canada, and Germany. Records of neurological examination findings and functional motor assessments were submitted to up to five pediatricians with expertize in CP diagnosis, who grouped children into categories referred to as ‘disabling’ CP, ‘non-disabling’ CP, and no CP. Each study provided between 31 and 51 records of children assessed between 2 and 8 years of age, approximately equally divided among the three groupings. The discrimination between ‘any CP’ and ‘no CP’ was only fair (mean Kappa coefficients 0.37 to 0.69). However, when more detailed information describing motor function was used, children with ‘disabling’ CP could be distinguished, on the basis of records, from those without CP or with ‘non-disabling’ CP with good to excellent reliability (mean Kappa coefficients 0.69 to 0.88). Because of the substantially higher agreement observed when these functional distinctions are made, we recommend that reports or comparisons of rates of CP should include levels of motor function of children with CP, and not simply total CP, among the outcomes of interest.
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