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Early Career Awardee – Leda Kennedy

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Leda Kennedy

Hello, my name is Leda Kennedy and the focus of my research is to learn more about how
factors like cannabis use and early life adversity impact long-term outcomes for youth
identified as being at clinical high risk for psychosis.
So knowing more about these risk factors and how they relate to one another and how they
influence lifetime outcomes in this population will help us develop more precise early
interventions
for clinical high risk youth that are informed by lifetime evidence, meaning that these
interventions
may be more successful in the long term.
So a little background, youth at clinical high risk for psychosis are generally aged
between 12 and 30 and experience attenuated symptoms of psychosis, such as changes in
thinking, hallucinations, or difficulty completing daily tasks or being involved in their social
lives.
So these young people are considered at increased risk for developing chronic psychiatric
conditions,
with research showing that approximately 20 to 30% of CHR youth develop psychosis spectrum
conditions within the first two years following the onset of symptoms.
So despite significant attention placed towards studying these young people over time, we
actually
know very little about their clinical and functional outcomes beyond that typical two-year
window.
So essentially, what happens to these folks after this time period and what factors influence
whether symptoms continue to get worse, whether they remit, whether they improve, similarly
with functioning?
What factors impact whether someone's functioning, restores, comes back, how it was before
they
had symptoms?
What impacts whether functioning continues to decline?
So we also know that there are several important risk factors for CHR youth in the early course
of illness that do impact short-term outcomes.
So these could be factors like cannabis use, exposure to early life trauma, family history,
stress.
So we largely ask the question in our group, do these same risk factors influence outcomes
across the lifespan?
So why does this matter?
Why do we ask these questions?
So really we think identifying factors that do influence lifetime outcomes tells us about
interventions that might be important at the time of identification.
So when we deem that someone might be at clinical high risk for psychosis when symptoms first
start and interventions that might be important across the lifespan for CHR individuals, so
across different life stages.
So this information also gives us insight into naturalistic patterns of behavior over time
in this population.
So what are cannabis use patterns over the lifetime?
What are further exposure or compounded exposure to trauma over the lifetime in this
population?
And importantly, if we know what factors matter regarding long-term outcomes that are
detectable
at baseline, so immediately when we first identify someone as being a CHR for psychosis, we
can
intervene earlier and potentially with more success.
But importantly, it's been very difficult to study CHR youth for a long period of time
in our field.
So we're just starting now to have the opportunity and the availability to study these individuals
over the course of their life.
So, so far, and what's the focus of my poster presentation at this year's SIRS conference,
we found that cannabis use and exposure to early life adversity are associated with one
another in a large sample of CHR youth who are re-contacted and re-evaluated five to
20 years following initial identification as being a CHR.
Importantly, we also found that these factors like cannabis use and early life adversity
also appear to be associated with persistent symptoms across the lifetime compared to those
CHR youth without those risk factors.
So that signifies that cannabis use, early life adversity, and potentially the interaction
between the two are associated with poorer clinical outcomes across the lifespan in
the CHR sample.
So some important implications for the real world we think our questions might be able
to begin to address is that knowing more about the trajectory of CHR symptoms across
the lifetime helps us improve disease prediction and understanding of the overall course of
CHR.
It also highlights time periods in life beyond that traditional two-year window where interventions
may be important.
And most importantly, it allows us to improve the precision of those interventions.
So can we instead employ interventions that are targeted towards comorbid trauma and
substance
use or interventions that individually target some of these risk factors?
I want to thank you so much for your attention and I look forward to discussing my findings
in depth during poster session one.
I sincerely thank the SIRS Congress for this award and for the opportunity to share our
work with our SIRS colleagues.
I will see you all in Chicago.

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