Reducing health disparities requires an understanding of the mechanisms that generate disparities. Life course approaches to health disparities leverage theories that explain how socially patterned ...physical, environmental, and socioeconomic exposures at different stages of human development shape health within and across generations and can therefore offer substantial insight into the etiology of health disparities. Life course approaches are informed by developmental and structural perspectives. Developmental perspectives emphasize how socially patterned exposures to risk factors during sensitive life stages shift health trajectories, whereas structural perspectives emphasize how social identity and position within socially patterned environments disproportionately allocate risk factors and resources, resulting in altered health trajectories. We conclude that the science of health disparities will be advanced by integrating life course approaches into etiologic and intervention research on health disparities. The following 4 strategies are offered to guide in this process: (1) advance the understanding of multiple exposures and their interactions, (2) integrate life course approaches into the understanding of biological mechanisms, (3) explore transgenerational transmission of health disparities, and (4) integrate life course approaches into health disparities interventions.
The authors examined the impact of cumulative neighborhood risk of psychosocial stress on allostatic load (AL) among adolescents as a mechanism through which life stress, including neighborhood ...conditions, may affect health and health inequities. They conducted multilevel analyses, weighted for sampling and propensity score-matched, among adolescents aged 12-20 years in the National Health and Nutrition Examination Survey (1999-2006). Individuals (first level, n = 11,886) were nested within families/households (second level, n = 6,696) and then census tracts (third level, n = 2,191) for examination of the contextual effect of cumulative neighborhood risk environment on AL. Approximately 35% of adolescents had 2 or more biomarkers of AL. A significant amount of variance in AL was explained at the neighborhood level. The likelihood of having a high AL was approximately 10% higher for adolescents living in medium-cumulative-risk neighborhoods (adjusted odds ratio (OR) = 1.09, 95% confidence interval (CI): 1.08, 1.09), 28% higher for those living in high-risk neighborhoods (adjusted OR = 1.28, 95% CI: 1.27, 1.30), and 69% higher for those living in very-high-risk neighborhoods (adjusted OR = 1.69, 95% CI: 1.68, 1.70) as compared with adolescents living in low-risk areas. Effect modification was observed by both individual- and neighborhood-level sociodemographic factors. These findings offer support for the hypothesis that neighborhood risks may culminate in a range of biologically mediated negative health outcomes detectable in adolescents.
Exposure to violence continues to be a growing epidemic, particularly among children. An enhanced understanding of the biological effect of exposure to violence is critical.
To examine the ...association between neighborhood violence and cellular and biological stress in children.
A matched, cross-sectional study of 85 black children aged 5 to 16 years from 52 neighborhoods took place in the greater New Orleans, Louisiana, area between January 1, 2012, and July 31, 2013.
Density of businesses where individuals can purchase alcohol as measured by rates per capita of liquor or convenience stores, and violence as measured by reports of violent crime and reports of domestic violence, operationalized as reports per capita of crime and domestic violence. Rates of exposure within a 500-, 1000-, and 2000-m radius from the child's home were calculated.
Primary biological outcomes were telomere length and cortisol functioning.
Among the 85 children in the study, (mean SD age, 9.8 3.1 years; 50 girls and 35 boys) significant variation in telomere length and cortisol functioning was observed at the neighborhood level, with intraclass correlation coefficients of 6% for telomere length, 3.4% for waking cortisol levels, and 5.5% for peak cortisol levels following a stressor. Density of liquor or convenience stores within a 500-m radius of a child's home was associated with a decrease in mean telomere length by 0.004 for each additional liquor store or convenience store (β SE, -0.004 0.002; P = .02). The rate of domestic violence was significantly and inversely associated with a decrease in mean telomere length by 0.007 for each additional report of domestic violence in a 500-m radius of a child's home (β SE, -0.007 0.001; P < .001). The rate of violent crime was significantly associated with a decrease in mean telomere length by 0.006 for each additional report of violent crime in a 500-m radius of a child's home (β SE, -0.006 0.002; P < .001). Children exposed to more liquor and convenience stores within 500 m of their home were significantly less likely to reduce cortisol levels after a reactivity test (β, 0.029; P = .047), as were children exposed to high rates of domestic violence (β, 0.088; P = .12) and violent crime (β, 0.029; P = .006). Children exposed to more liquor and convenience stores within 500 m of their home had a steeper diurnal decline in cortisol levels during the day (β SE, -0.002 0.001; P = .04), as did children exposed to more violent crime within 500 m of their home (β SE -0.032 0.014; P = .02).
Neighborhoods are important targets for interventions to reduce the effect of exposure to violence in the lives of children. These findings provide the first evidence that objective exposures to neighborhood-level violence influence both physiological and cellular markers of stress, even in children.
Adverse childhood experiences (ACEs) are associated with mental and physical health risks that, through biological and psychosocial pathways, likely span generations. Within an individual, telomere ...length (TL), an established marker of cellular stress and aging, is associated with both ACE exposure and psychopathology, providing the basis for an emerging literature suggesting that TL is a biomarker of the health risks linked to early-life adversity both within and across generations. The authors tested the effect of maternal ACEs on both the trajectory of infant TL and infant social-emotional problems at 18 months of age.
Pregnant women were recruited, and maternal scores on the Adverse Childhood Experience questionnaire were obtained, along with demographic and prenatal stress measures. Postnatal visits with 155 mother-infant dyads occurred when infants were 4, 12, and 18 months of age. At each visit, infant buccal swabs were collected for TL measurement, and mothers completed measures of maternal depression. Mothers also completed the Child Behavior Checklist at the 18-month visit. Mixed-effects modeling was used to test how maternal ACEs influenced infant TL trajectory. Linear regression was used to test the association between maternal ACEs and infant internalizing and externalizing behaviors. Finally, the interaction between telomere attrition from 4 to 18 months and maternal ACEs was examined as a predictor of infant scores on the Child Behavior Checklist.
Higher maternal ACEs were associated with shorter infant TL across infancy and higher infant externalizing behavioral problems at 18 months. No associations were found with internalizing behavioral problems. Telomere attrition from 4 to 18 months interacted with maternal ACEs to predict externalizing behaviors. In infants whose mothers reported higher scores on the Adverse Childhood Experience questionnaire, greater telomere attrition predicted higher externalizing problems, even when accounting for maternal postnatal depression and prenatal stress.
These data demonstrate an interactive pathway between maternal early-life adversity and infant TL that predicts emerging behavioral problems in the next generations.
Pregnancy can exacerbate or prompt the onset of stress-related disorders, such as post-traumatic stress disorder (PTSD). PTSD is associated with heightened stress responsivity and emotional ...dysregulation, as well as increased risk of chronic disorders and mortality. Further, maternal PTSD is associated with gestational epigenetic age acceleration in newborns, implicating the prenatal period as a developmental time period for the transmission of effects across generations. Here, we evaluated the associations between PTSD symptoms, maternal epigenetic age acceleration, and infant gestational epigenetic age acceleration in 89 maternal-neonatal dyads. Trauma-related experiences and PTSD symptoms in mothers were assessed during the third trimester of pregnancy. The MethylationEPIC array was used to generate DNA methylation data from maternal and neonatal saliva samples collected within 24 h of infant birth. Maternal epigenetic age acceleration was calculated using Horvath's multi-tissue clock, PhenoAge and GrimAge. Gestational epigenetic age was estimated using the Haftorn clock. Maternal cumulative past-year stress (GrimAge: p = 3.23e-04, PhenoAge: p = 9.92e-03), PTSD symptoms (GrimAge: p = 0.019), and difficulties in emotion regulation (GrimAge: p = 0.028) were associated with accelerated epigenetic age in mothers. Maternal PTSD symptoms were associated with lower gestational epigenetic age acceleration in neonates (p = 0.032). Overall, our results suggest that maternal cumulative past-year stress exposure and trauma-related symptoms may increase the risk for age-related problems in mothers and developmental problems in their newborns.
Our objective was to explore the utility of salivary telomere length (sTL) as an early indicator of neighborhood-level social environmental risk during child development. We therefore tested the ...hypothesis that sTL would be associated with markers of social stress exposure in children. Children age 4–14 from 87 neighborhoods were recruited through five urban schools in New Orleans, Louisiana, U.S. Data were collected at the level of the child, family/household, and neighborhood. DNA was obtained from saliva using commercially available kits and sTL was determined for 104 children using quantitative PCR. Analysis was performed on 99 children who had complete data including sTL, social environmental stress, and additional covariates. The mean sTL value was 7.4 T/S (telomere signal/single-copy signal) ratio units (±2.4, range = 2.5–18.0), and 4.7% of the variance in sTL was attributed to differences across neighborhoods. Children living in neighborhoods characterized by high disorder had an sTL value 3.2 units lower than children not living in high disordered environments (p < 0.05) and their odds of having low relative sTL (defined as <1 standard deviation below standardized Z-score mean) values was 3.43 times that of children not living in high disorder environments (adjusted OR = 3.43, 95% CI = 1.22, 9.62). Our findings are consistent with previous studies in adults demonstrating a strong link between psychosocial stress and sTL obtained from peripheral blood, consistent with previous studies in youth demonstrating an association between early life stress and sTL obtained from buccal cell DNA and offer increased support for the hypothesis that sTL represents a non-invasive biological indicator of psychosocial stress exposure (i.e., neighborhood disorder) able to reflect differences in stress exposure levels even in young children.
► Telomere length has been associated with health outcomes and socioeconomic status. ► In children, telomeres also associated with social deprivation and violence. ► We provide support for telomere length as an early indicator of health inequities. ► Children in high disordered neighborhoods had significantly shorter telomeres. ► Salivary telomere length may represent a biological marker of psychosocial stress.
Legacy effects from one disturbance may influence successional pathways by amplifying or buffering forest regeneration after the next disturbance. We assessed vegetation and tree regeneration in ...non-serotinous Sierra lodgepole pine (
Pinus contorta
var.
murrayana
) stands after a 1984 wildfire which burned with variable severity and again after a high-severity subsequent fire in 2012. The legacy effects of the 1984 fire were amplified; seedlings and saplings were abundant in areas initially burned at low severity (1267 stems ha
−1
) despite high reburn severity, but regeneration was low in areas twice burned at high severity (31 stems ha
−1
). Our results suggest that the severity of the 1984 fire may have influenced post-2012 tree regeneration by creating variable fuel loading, which may have affected soils, litter cover and shade after the 2012 fire and therefore affected seedling establishment and survival. A canopy seed bank of unburnt cones from trees killed by the 2012 fire potentially contributed to a strong effect of prior burn severity on regeneration after the 2012 fire despite a lack of serotinous or resprouting tree species, although the influence of this canopy seedbank was likely limited to the year following the fire. Our results suggest that a low- to moderate-severity fire increases forest resilience relative to a high-severity fire even when the next fire burns at high severity.
Fire severity patterns are driven by interactions between fire, vegetation, and terrain, and they generate legacy effects that influence future fire severity. A century of fire exclusion and fuel ...buildup has eroded legacy effects, and contemporary fire severity patterns may diverge from historical patterns. In recent decades, area burned and area burned at high severity have increased and landscapes are transitioning back to an active fire regime where disturbance legacies will again play a strong role in determining fire severity. Understanding the drivers of fire severity is crucial for anticipating future fire severity patterns as active fire regimes are reestablished. We identified drivers of fire severity in the Klamath Mountains, a landscape with an active fire regime, using two machine learning statistical models: one model for non‐reburns (n = 92) and one model for reburns (n = 61). Both models predicted low better than moderate or high‐severity fire. Fire severity drivers contrasted sharply between non‐reburns and reburns. Fire weather and fuels were dominant controls in non‐reburns, while previous burn severity, fuel characteristics, and time since last fire were drivers for reburns. In reburns, areas initially burned at low (high) severity burned the same way again. This tendency was sufficiently strong that reburn fire severity could be predicted equally well with only severity of the previous fire in the model. Thus, reburn fire severity is more predictable than severity in non‐reburns that are driven by the stochastic influences of fire weather. Reburn severity in aggregate was also higher than non‐reburn severity suggesting a positive feedback effect that could contribute to an upward drift in fire severity as area burned increases. Terrain had low importance in both models. This indicates strong terrain controls in the past may not carry into the future. Low‐ and moderate‐severity fire effects were prevalent in non‐reburns under moderate fire weather and self‐reinforcing behavior maintained these effects in reburns even under more extreme weather, particularly in reburns within 10 yr. Our findings suggest deliberate use of wildfire and prescribed fire under moderate conditions would increase fire resilience in landscapes transitioning to an active fire regime.
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