TY - JOUR
T1 - Timing, duration, and differential susceptibility to early life adversities and cardiovascular disease risk across the lifespan
T2 - Implications for future research
AU - Suglia, Shakira F.
AU - Appleton, Allison A.
AU - Bleil, Maria E.
AU - Campo, Rebecca A.
AU - Dube, Shanta R.
AU - Fagundes, Christopher P.
AU - Heard-Garris, Nia J.
AU - Johnson, Sara B.
AU - Slopen, Natalie
AU - Stoney, Catherine M.
AU - Watamura, Sarah E.
N1 - Publisher Copyright:
© 2021 Elsevier Inc.
PY - 2021/12
Y1 - 2021/12
N2 - Early life adversities (ELA), include experiences such as child maltreatment, household dysfunction, bullying, exposure to crime, discrimination, bias, and victimization, and are recognized as social determinants of cardiovascular disease (CVD). Strong evidence shows exposure to ELA directly impacts cardiometabolic risk in adulthood and emerging evidence suggests there may be continuity in ELA's prediction of cardiometabolic risk over the life course. Extant research has primarily relied on a cumulative risk framework to evaluate the relationship between ELA and CVD. In this framework, risk is considered a function of the number of risk factors or adversities that an individual was exposed to across developmental periods. The cumulative risk exposure approach treats developmental periods and types of risk as equivalent and interchangeable. Moreover, cumulative risk models do not lend themselves to investigating the chronicity of adverse exposures or consider individual variation in susceptibility, differential contexts, or adaptive resilience processes, which may modify the impact of ELA on CVD risk. To date, however, alternative models have received comparatively little consideration. Overall, this paper will highlight existing gaps and offer recommendations to address these gaps that would extend our knowledge of the relationship between ELA and CVD development. We focus specifically on the roles of: 1) susceptibility and resilience, 2) timing and developmental context; and 3) variation in risk exposure. We propose to expand current conceptual models to incorporate these factors to better guide research that examines ELA and CVD risk across the life course.
AB - Early life adversities (ELA), include experiences such as child maltreatment, household dysfunction, bullying, exposure to crime, discrimination, bias, and victimization, and are recognized as social determinants of cardiovascular disease (CVD). Strong evidence shows exposure to ELA directly impacts cardiometabolic risk in adulthood and emerging evidence suggests there may be continuity in ELA's prediction of cardiometabolic risk over the life course. Extant research has primarily relied on a cumulative risk framework to evaluate the relationship between ELA and CVD. In this framework, risk is considered a function of the number of risk factors or adversities that an individual was exposed to across developmental periods. The cumulative risk exposure approach treats developmental periods and types of risk as equivalent and interchangeable. Moreover, cumulative risk models do not lend themselves to investigating the chronicity of adverse exposures or consider individual variation in susceptibility, differential contexts, or adaptive resilience processes, which may modify the impact of ELA on CVD risk. To date, however, alternative models have received comparatively little consideration. Overall, this paper will highlight existing gaps and offer recommendations to address these gaps that would extend our knowledge of the relationship between ELA and CVD development. We focus specifically on the roles of: 1) susceptibility and resilience, 2) timing and developmental context; and 3) variation in risk exposure. We propose to expand current conceptual models to incorporate these factors to better guide research that examines ELA and CVD risk across the life course.
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U2 - 10.1016/j.ypmed.2021.106736
DO - 10.1016/j.ypmed.2021.106736
M3 - Review article
C2 - 34293381
AN - SCOPUS:85111304174
SN - 0091-7435
VL - 153
JO - Preventive Medicine
JF - Preventive Medicine
M1 - 106736
ER -