Periodic Reporting for period 1 - RefugeeBioEmbed (Individual Differences in the Biological Embedding of Developmental Origins of Health and Illness in Syrian Refugee Children)
Periodo di rendicontazione: 2021-05-31 al 2023-05-30
More than 15 million Syrians have been forcibly displaced as a result of the Syrian Civil War, leading to an unprecedented humanitarian crisis which is still ongoing today. Of the roughly 5.6 million registered Syrian refugees, nearly half are children. These youth, after facing a bloody and brutal conflict and flight from Syria, have then had to contend with poor living conditions, often in temporary settlements, and the losses of family, friends, and stabilizing institutions. Given these conditions, it is no surprise that refugee children are at significantly higher risk of developing poor mental health than the general population.
This project aimed to shed light on how exposure to war and displacement impact child development and health by focusing on how these experiences ‘get under the skin’. With greater insight into these processes, we are better prepared to meet the needs of displaced children as well as other children who experience similar challenges. Furthermore, by learning more about how certain risk and protective factors influence the biological embedding of traumatic experiences, we can identify potential targets for intervention research.
The Research Fellow (RF) investigated whether war and displacement experiences influenced refugee children’s pubertal timing. Previous research on pubertal timing–largely based on Western populations living in high-income countries–has demonstrated that certain kinds of adversity (e.g. threats, violence, abuse) are linked to accelerated pubertal timing while others (e.g. neglect, malnutrition) are linked to delayed pubertal timing. Abnormal pubertal timing, in turn, forecasts a number of mental and physical health problems later in life.
In recent years, evidence has pointed to the idea that accelerated pubertal timing is one part of a broader process of accelerated biological aging. Briefly, biological aging refers to systemic deterioration which accompanies aging. Importantly, biological aging is modifiable; that is, it can be shifted faster or slower following certain exposures. This makes biological aging processes particularly attractive targets for potential interventions.
Thus, the overall aims of this project were to: 1) investigate how war and displacement experiences impact children’s developmental trajectories, and 2) investigate whether modifiable risk and protective factors moderate the impact of adverse exposures on both pubertal timing and mental health outcomes. These aims were accomplished with three specific research objectives:
1) Investigate whether childhood adversity and protective factors impact pubertal timing of Syrian refugee children, accounting for ‘subtypes’ of environmental conditions and integrating physiological measures of stress response systems and pubertal onset. [RO1]
2) Investigate the relations among developmental trajectories (pubertal timing) and mental health outcomes, including both adverse and positive outcomes as well as modifiable risk/protective factors that influence those outcomes. [RO2]
3) Investigate whether self-report and genetic measures of Environmental Sensitivity moderate the effects of adversity and protective effects on pubertal timing, as well as the effects of pubertal timing on positive and negative mental health outcomes—also accounting for genetic correlates of mental health conditions. [RO3]
This project aimed to shed light on how exposure to war and displacement impact child development and health by focusing on how these experiences ‘get under the skin’. With greater insight into these processes, we are better prepared to meet the needs of displaced children as well as other children who experience similar challenges. Furthermore, by learning more about how certain risk and protective factors influence the biological embedding of traumatic experiences, we can identify potential targets for intervention research.
The Research Fellow (RF) investigated whether war and displacement experiences influenced refugee children’s pubertal timing. Previous research on pubertal timing–largely based on Western populations living in high-income countries–has demonstrated that certain kinds of adversity (e.g. threats, violence, abuse) are linked to accelerated pubertal timing while others (e.g. neglect, malnutrition) are linked to delayed pubertal timing. Abnormal pubertal timing, in turn, forecasts a number of mental and physical health problems later in life.
In recent years, evidence has pointed to the idea that accelerated pubertal timing is one part of a broader process of accelerated biological aging. Briefly, biological aging refers to systemic deterioration which accompanies aging. Importantly, biological aging is modifiable; that is, it can be shifted faster or slower following certain exposures. This makes biological aging processes particularly attractive targets for potential interventions.
Thus, the overall aims of this project were to: 1) investigate how war and displacement experiences impact children’s developmental trajectories, and 2) investigate whether modifiable risk and protective factors moderate the impact of adverse exposures on both pubertal timing and mental health outcomes. These aims were accomplished with three specific research objectives:
1) Investigate whether childhood adversity and protective factors impact pubertal timing of Syrian refugee children, accounting for ‘subtypes’ of environmental conditions and integrating physiological measures of stress response systems and pubertal onset. [RO1]
2) Investigate the relations among developmental trajectories (pubertal timing) and mental health outcomes, including both adverse and positive outcomes as well as modifiable risk/protective factors that influence those outcomes. [RO2]
3) Investigate whether self-report and genetic measures of Environmental Sensitivity moderate the effects of adversity and protective effects on pubertal timing, as well as the effects of pubertal timing on positive and negative mental health outcomes—also accounting for genetic correlates of mental health conditions. [RO3]
The goal of RO1 was to understand how different environmental exposures ‘get under the skin’ using a model guided by life history theory that suggests certain types of exposures may alter developmental trajectories in children. The analysis revealed that Syrian refugee boys accelerated pubertal timing following exposure to mortality threats specifically, as predicted. In addition, boys exposed to mortality threats as well as elevated energetic stress (lower BMI-for-age), the accelerating effect was attenuated, also as expected. Surprisingly, we did not find this pattern in Syrian refugee girls. Rather, energetic stress significantly decreased girls’ odds of achieving menarche (this was predicted), but there was no corresponding effect of war exposure at all.
The goal of RO2 was to test whether accelerated pubertal timing should be labeled a “transdiagnostic mechanism”—in other words, that accelerated pubertal timing is a risk factor for a number of disorders. This claim usually accompanies calls to screen for pubertal timing in medical and mental health settings to identify trauma-affected children. Yet, as shown by our RO1 research, exposure to trauma may not always translate into accelerated pubertal timing, especially when children face resource scarcity (which may be the case more often that not for the >90% of the world’s children who live in LMICs). To investigate whether pubertal timing was a transdiagnostic mechanism in our sample, the RF tested whether pubertal timing mediates relations between war/displacement experiences and mental health outcomes, and whether Environmental Sensitivity moderates effects of war/displacement on pubertal timing and mental health.
We found that accelerated pubertal timing predicts elevated PTSD symptoms in boys and anxiety symptoms in girls. Among boys, mortality exposure and better access to facilities (i.e. clean water, washing facilities, cooking facilities) accelerate pubertal timing. In contrast better quality of accommodation (i.e. adequate space and heat) and more supportive household relationships slowed pubertal timing. Only the effect of accommodation was statistically significant, while the other effects were marginally significant. Among girls, we found no effects of war exposure, nor of refugee environment, on pubertal timing. We did not find any evidence in boys nor girls that pubertal timing mediates relations between adverse exposures (war, refugee camps) and poor mental health. Nor did we find any evidence of moderated mediation. Environmental Sensitivity did not moderate effects of any war or displacement exposures on pubertal timing in either boys nor girls.
The goal of RO3 is to investigate biological embedding processes themselves. Whereas previous ROs focused primarily on external factors (e.g. war exposure, refugee camp characteristics), RO3 was designed to examine how person-specific characteristics interact with situation-specific exposures. We will investigate whether certain exposures predict children’s physiological profiles (e.g. chronic stress as measured by hair cortisol, biological aging as measured by qPCR- and DNAm- telomere length, associations of TL with pubertal timing) and whether these physiological profiles are linked to physical health, coping skills, and socioemotional adjustment.
The goal of RO2 was to test whether accelerated pubertal timing should be labeled a “transdiagnostic mechanism”—in other words, that accelerated pubertal timing is a risk factor for a number of disorders. This claim usually accompanies calls to screen for pubertal timing in medical and mental health settings to identify trauma-affected children. Yet, as shown by our RO1 research, exposure to trauma may not always translate into accelerated pubertal timing, especially when children face resource scarcity (which may be the case more often that not for the >90% of the world’s children who live in LMICs). To investigate whether pubertal timing was a transdiagnostic mechanism in our sample, the RF tested whether pubertal timing mediates relations between war/displacement experiences and mental health outcomes, and whether Environmental Sensitivity moderates effects of war/displacement on pubertal timing and mental health.
We found that accelerated pubertal timing predicts elevated PTSD symptoms in boys and anxiety symptoms in girls. Among boys, mortality exposure and better access to facilities (i.e. clean water, washing facilities, cooking facilities) accelerate pubertal timing. In contrast better quality of accommodation (i.e. adequate space and heat) and more supportive household relationships slowed pubertal timing. Only the effect of accommodation was statistically significant, while the other effects were marginally significant. Among girls, we found no effects of war exposure, nor of refugee environment, on pubertal timing. We did not find any evidence in boys nor girls that pubertal timing mediates relations between adverse exposures (war, refugee camps) and poor mental health. Nor did we find any evidence of moderated mediation. Environmental Sensitivity did not moderate effects of any war or displacement exposures on pubertal timing in either boys nor girls.
The goal of RO3 is to investigate biological embedding processes themselves. Whereas previous ROs focused primarily on external factors (e.g. war exposure, refugee camp characteristics), RO3 was designed to examine how person-specific characteristics interact with situation-specific exposures. We will investigate whether certain exposures predict children’s physiological profiles (e.g. chronic stress as measured by hair cortisol, biological aging as measured by qPCR- and DNAm- telomere length, associations of TL with pubertal timing) and whether these physiological profiles are linked to physical health, coping skills, and socioemotional adjustment.
The research conducted as part of this Fellowship pushed the boundaries of our knowledge about biological embedding of stressful experiences in war-affected children. The Research Fellow has been able to elucidate biological aging processes in war-affected youth using several, unique measures including pubertal timing, qPCR telomere length, and DNAm telomere length. Many biological aging studies use just one measure; furthermore, very few studies investigate biological aging in children. In documenting these mechanistic processes and their links to health outcomes in children and adolescents, we lay the groundwork for further research to identify targets for intervention research that benefits a number of underserved communities facing concentrated adversity.