TY - JOUR
T1 - Modeling the association between lifecourse socioeconomic disadvantage and systemic inflammation in healthy adults
T2 - The role of self-control
AU - Hostinar, Camelia E.
AU - Ross, Kharah M.
AU - Chen, Edith
AU - Miller, Gregory E.
N1 - Publisher Copyright:
© 2014 American Psychological Association.
PY - 2015/6/1
Y1 - 2015/6/1
N2 - Objective: We sought to identify pathways connecting lifecourse socioeconomic status (SES) with chronic, low-grade inflammation, focusing on the explanatory roles of self-control, abdominal adiposity, and health practices. Methods: Participants were 360 adults aged 15-55 who were free of chronic medical conditions. They were roughly equally divided between low and high current SES, with each group further divided between low and high early-life SES. Structural equation modeling (SEM) was used to identify direct and indirect pathways linking early-life and current SES with low-grade, chronic inflammation in adulthood, as manifest by serum interleukin-6 and C-reactive protein. Low SES was hypothesized to relate to inflammation by reducing self-control, which in turn was hypothesized to facilitate lifestyle factors that potentiate inflammation (smoking, alcohol use, sedentary behavior, and weight gain). Results: Analyses revealed that self-control was pivotal in linking both early-life and current SES to inflammation. Low early-life SES was related to a harsher family climate, and in turn lower adult self-control, over and above the effects of current SES. Controlling for early-life SES, low current SES was associated with perceived stress and, in turn, diminished self-control. Results showed that lower self-control primarily operated through higher abdominal adiposity to associate with greater inflammation. Conclusions: The findings suggest a mechanistic scenario wherein low SES in early life or adulthood depletes self-control and, in turn, fosters adiposity and inflammation. These pathways should be studied longitudinally to elucidate and potentially ameliorate socioeconomic disparities in health.
AB - Objective: We sought to identify pathways connecting lifecourse socioeconomic status (SES) with chronic, low-grade inflammation, focusing on the explanatory roles of self-control, abdominal adiposity, and health practices. Methods: Participants were 360 adults aged 15-55 who were free of chronic medical conditions. They were roughly equally divided between low and high current SES, with each group further divided between low and high early-life SES. Structural equation modeling (SEM) was used to identify direct and indirect pathways linking early-life and current SES with low-grade, chronic inflammation in adulthood, as manifest by serum interleukin-6 and C-reactive protein. Low SES was hypothesized to relate to inflammation by reducing self-control, which in turn was hypothesized to facilitate lifestyle factors that potentiate inflammation (smoking, alcohol use, sedentary behavior, and weight gain). Results: Analyses revealed that self-control was pivotal in linking both early-life and current SES to inflammation. Low early-life SES was related to a harsher family climate, and in turn lower adult self-control, over and above the effects of current SES. Controlling for early-life SES, low current SES was associated with perceived stress and, in turn, diminished self-control. Results showed that lower self-control primarily operated through higher abdominal adiposity to associate with greater inflammation. Conclusions: The findings suggest a mechanistic scenario wherein low SES in early life or adulthood depletes self-control and, in turn, fosters adiposity and inflammation. These pathways should be studied longitudinally to elucidate and potentially ameliorate socioeconomic disparities in health.
KW - Adiposity
KW - Childhood family
KW - Inflammation
KW - Self-control
KW - Socioeconomic status
KW - Stress
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U2 - 10.1037/hea0000130
DO - 10.1037/hea0000130
M3 - Article
C2 - 25110854
AN - SCOPUS:84930753680
SN - 0278-6133
VL - 34
SP - 580
EP - 590
JO - Health Psychology
JF - Health Psychology
IS - 6
ER -