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.
