I began this project period with a clear goal in mind. I very much wanted to research a topic that I felt had real-world significance and was somewhat related with my activism/advocacy work.

At first, I was quite dubious that I would find research connected to the work that I do outside of school, but, researching on Science and Lancet proved more fruitful than I thought. I found a number of articles relating to childhood trauma, refugee trauma, gene expression, and telomeres, and the long-term effects of childhood adversity on one’s biology. I was particularly intrigued by this topic because I personally know a number of refugees, work with a class of refugees in Jordan via skype, and have followed the refugee crisis (especially that of Syrians) in horror for a decade now. I’d never considered the biological effects of trauma on one’s long-term physical health, although there is usually much talk on the psychological effects of that trauma.

The first article I dove into was titled childhood adversity reprograms gene expression and was written by Stanford professor Amit Etkin. This article provided me with a broad framework for my research DYO, in that it acted somewhat like a literature review, bringing together various articles regarding childhood trauma. An analysis of genome-wide gene expression in peripheral blood monocytes from control subjects and those who suffered from adversity in their early lives, using a cortisol-inducing public speaking challenge that helped reveal reactionary genes whose specific expression, was found to vary as a function of childhood trauma. This analysis also pointed to specific alterations in the transcription of protein-coding genes integral to immune system function. Interestingly enough, this article began exploring the role of cortisol in stress-induced biological responses, which very much aligned with the subsequent articles I read relating to the role of cortisol in destroying telomeres, and the effects of that destruction.

The next article I read, titled Stress and Telomere Biology: A Lifespan Perspective and written by seven professors from across the country, helped summarize the already established connection between telomere length and lifespan longevity, as well as introduced the evolutionary component behind my research question. Indeed, this article made crystal clear what studies conducted in the last decade have found: that shorter telomere length is associated with advancing chronological age and also increased disease morbidity and mortality, whereas longer telomere length is associated with decreased disease risk and increased life expectancy. This article’s survey of recent telomere research found that high stress and cortisol levels are thought to accelerate the erosion of telomeres from very early in life and possibly even influence one’s initial (newborn) setting of telomere length. This article also outlined how DNA and protein components of telomeres, like all other chromosome elements, evolve and co-evolve over time, responding to changes in the genome and to environmental stresses.

The third and final article I read, titled Exposure to violence during childhood is associated with telomere erosion from 5 to 10 years of age: a longitudinal study and written by eight professors from across the country, was the only article I read with primary research. This study explored the relationship between a child’s exposure to violence and their subsequent rate of telomere erosion between 5 and 10 years. The researchers of this study assessed violence as exposure to maternal domestic violence, frequent bullying victimization and physical maltreatment by an adult. Their findings are thought to extend more broadly, however, to children exposed to a wider range of violence, such as children living in war zones, children forced to seek refuge, and children who cross the US’s southern border. Participants were 236 children (49% females; 42% with one or more violence exposures). The researchers began by measuring the telomere length of each respondent as a baseline, using a quantitative PCR method. Compared with their counterparts, children who experienced two or more kinds of violence exposure showed significantly more telomere erosion between age-5 baseline and age-10 follow-up measurements, even after adjusting for sex, socioeconomic status and body mass index. Thus, this article supported a mechanism linking cumulative childhood stress to telomere maintenance, observed already at a young age, with potential impact for life-long health. Importantly, the violence-exposed children who experienced more rapid telomere erosion had not yet developed chronic disease, suggesting that telomere erosion may be a link in the causal chain connecting early-life stress exposure to later life disease.

Ultimately, these three articles, as well as my additional supplemental reading, very much helped shed light on the importance of this research in the long-term. It was fascinating and enlightening to learn about the effects of trauma on a biological, cellular, and molecular level. Understanding the evolution of telomeres was crucial to understanding the articles I read, and actually brought me to the research finding that telomere dysfunction, which often results in end-to-end chromosome fusions, can have a profound effect on chromosome evolution and maybe even speciation. Above all though, this research showed me how essential advocacy efforts for refugees are, as refugee crises around the world continue to devastate lives with little to no international action being taken to protect the lives of those most vulnerable, amongst them 31 million children. These children, likely to spend their entire childhoods away from home, sometimes separated from their families, and often at risk of abuse, neglect, violence, exploitation, trafficking or military recruitment even in exile, must take center stage in efforts to serve refugees in the coming years, mitigating their psychological and biological responses to trauma before it is too late.

The city begins to rattle,

Bombs bellow through the souk, the school, her home.

She awakens to fear.

It has crawled under her bedroom window,

climbed over her balcony,

seeped into her closet.

The roar of roofs collapsing lets her know

that it is time to leave,

to flee,

to seek refuge.

She collects her children,

dresses them in layers of clothes,

holds them by their hand.

They too are afraid,

of the planes and their shadows

of the soldiers and their weapons

of those who died and their ghosts.

As they run away from their house,

she grabs a picture.

In a few weeks time,

it will be pruned by water in their dinghy,

torn, by police officers at checkpoints,

stained by the tears of her hungry children.

But she will still carry it with her,

the photograph proof that she was once married, in love, alive.

Now, all she will do is flee, grieve, survive.

She’ll imagine the life waiting them in refuge.

But she does not know that her genes have begun to change,

that her cytokines and cell signaling regulators have been affected,

that her immune system will not properly function.

She does not know that she will see an increase in proinflammatory gene transcription,

or that her telomeres are being dismantled by cortisol,

cortisol induced by flashbacks she has of Aleppo at night, by violence she encounters at the Albanian border, by memories of her husband’s death.

Worse, she does not know that childhood adversity and stress combine to alter patterns of gene expression,

that her children’s biology is shifting more than her own,

that there is little she can do to stop the change.

She’ll have to watch,

and not know,

as cortisol depletes her children’s telomeres,

reducing their life-expectancy,

increasing their risk of disease.

But she is not alone.

She will hear about the Rohingyans on BBC,

learn about Hondurans at work,

meet Iraqis, Yemenis, Kurds in transit.

415 million children living in war zones,

she will see,

words written on a UNHCR flyer.

She will not have to wonder what trauma they have endured,

Because looking at her children,

She will know.

and,

as their own biology hurts them,

the world’s inhumanity kills them,

it is only evolution that may save them,

help them create molecular resilience,

not risk pathways,

produce telomeres,

not sabotage them.

If she ever understands all this,

she will think,

pray,

hope,

that evolution, biology, science,

can fix what they have destroyed.