what we do
stress is an inevitable experience- we have all experienced stress. but when stress becomes too severe (e.g., exposure to violence) or chronic (e.g., poverty), it can increase risk for a number of diseases, including cardiovascular, respiratory, and autoimmune diseases.
our goal is to answer two questions:
1 _ how does stress get under the skin to impact biology?
2 _ what factors may break the stress-disease association?
how we see it
rome wasn’t built in a day. many chronic diseases have long latency periods with pathogenic processes unfolding and becoming established over decades. nonetheless, many traditional health psychology models neglect how psychosocial processes vary by developmental stages as well as the implications of such temporal variations for health.
therefore, we take a lifecourse approach in examining the mechanistic and moderating factors of the stress-disease link, thereby paying attention to the roles of time and timing. for example, our work has begun to address questions like “does it matter to the body when or at which developmental stage stress is exposed?” and “is time a necessary ingredient for stress to brew pathogenic processes, like unresolved inflammation, into a disease?”
answering these questions will help us map out — developmental stage by developmental stage — the mechanisms underlying the stress-disease link as well as the most effective protective factors that curb this link. ultimately, our hope is that these answers can inform intervention efforts, so we know when to intervene what.
how we do it
answering lifecourse questions is not easy. it requires having a large sample of data with a wide age span, which can be very resource intensive to collect. however, there are publicly available datasets as well as existing research of different age groups, so by utilizing integrative data analytical (“mega-analytical”) and meta-analytical approaches, we can string together these datasets and their findings to “build our own” lifecourse samples of individuals, from infants to older adults.
we balance these cumulative data approaches with more precise investigations using primary data collected with a variety of methods, including cell culture experiments to measure how immune cells respond to threat and regulation, daily diaries and actigraphy devices to capture social interactions, feelings, and sleep as they unfold in real time, as well as extensive interviews to assess socioeconomic backgrounds and life exposures.
building lifecourse samples using meta- and mega-analytical approaches.
-
we synthesized the literature on childhood stress and inflammation, identifying 922 associations, which emanated from 168 unique samples reported in 187 papers, involving 173,089 unique participants. in this meta-analytical context, we examined three questions:
(1) does the strength of this association change over the lifecourse?
(2) do different types of childhood stressors have differential associations with inflammation?
(3) which components of the inflammatory response are involved?
-
we integrated data from five independent studies to create a diverse sample of 1,607 individuals (960 with longitudinal data; 8 to 64 years old; 359 asian, 205 black, and 151 latino/a). leveraging the resulting lifecourse data, rich interview assessments of disadvantage and stress, and ex vivo assessments of inflammation, we examined two questions:
(1) does chronic stress account for the link between disadvantage and proinflammatory phenotype?
(2) is there a developmental period during which inflammatory responses are more sensitive to disadvantage and chronic stress?
how the scribbles, slings and arrows, that make up our every day lives become biologically embedded.
-
On days when you feel more stressed (e.g., when the demands seem to exceed your capacity), do you tend to sleep worse, better, or about the same? This pattern—referred to as sleep reactivity to daily stress—varies from person to person and may carry health implications. We found that Black youth who tended to sleep worse on more stressful days also showed greater subclinical risk for cardiovascular disease. Importantly, this link held even after accounting for how well they typically slept (their average sleep quality) and how stressed they generally felt (their average stress level).
artwork by the 25-month-old theo.
look “under the hood” at immune processes to gain deeper mechanistic understanding of the stress-disease link.
-
the biological embedding model (miller, chen, parker 2011) posits that early life stress, having experienced when the immune system is still developing and highly malleable, can calibrate immune cells to exhibit a “pro-inflammatory phenotype.”
this phenotype is characterized by immune cells mounting more exaggerated inflammatory responses to threats that are not as sensitive to stop signals.
-
when considering a single threat challenge, the more exaggerated and prolonged inflammatory response may be advantageous. but if each time, immune cells mount such strong defenses, leaving behind unresolved inflammation, then gradually across the lifecourse, you may have a problem of the body is sustaining chronic inflammation.
that is, time is a necessary ingredient that gradually brews early life stress into adulthood chronic inflammation.