TY - JOUR
T1 - Prospective network analysis of proinflammatory proteins, lipid markers, and depression components in midlife community women
AU - Zainal, Nur Hani
AU - Newman, Michelle G.
N1 - Publisher Copyright:
Copyright © The Author(s), 2022. Published by Cambridge University Press.
PY - 2023/8/4
Y1 - 2023/8/4
N2 - Background Vulnerability theories propose that suboptimal levels of lipid markers and proinflammatory proteins predict future heightened depression. Scar models posit the reverse association. However, most studies that tested relationships between non-specific immune/endocrine markers and depression did not separate temporal inferences between people and within-person and how different immunometabolism markers related to unique depression symptoms. We thus used cross-lagged prospective network analyses (CLPN) to investigate this topic. Methods Community midlife women (n = 2224) completed the Center for Epidemiologic Studies-Depression scale and provided biomarker samples across five time-points spanning 9 years. CLPN identified significant relations (edges) among components (nodes) of depression (depressed mood, somatic symptoms, interpersonal issues), lipid markers [insulin, fasting glucose, triglycerides, low-density lipoprotein-cholesterol (LDL), high-density lipoprotein-cholesterol (HDL)], and proinflammatory proteins [C-reactive protein (CRP), fibrinogen], within and across time-points. All models adjusted for age, estradiol, follicle-stimulating hormone, and menopausal status. Results In within-person temporal networks, higher CRP and HDL predicted all three depression components (d = 0.131-2.112). Increased LDL preceded higher depressed mood and interpersonal issues (v. somatic symptoms) (d = 0.251-0.327). Elevated triglycerides predicted more somatic symptoms (v. depressed mood and interpersonal problems) (d = 0.131). More interpersonal problems forecasted elevated fibrinogen and LDL levels (d = 0.129-0.331), and stronger somatic symptoms preceded higher fibrinogen levels (d = 0.188). Conclusions Results supported both vulnerability and scar models. Long-term dysregulated immunometabolism systems, social disengagement, and related patterns are possible mechanistic accounts. Cognitive-behavioral therapies that optimize nutrition and physical activity may effectively target depression.
AB - Background Vulnerability theories propose that suboptimal levels of lipid markers and proinflammatory proteins predict future heightened depression. Scar models posit the reverse association. However, most studies that tested relationships between non-specific immune/endocrine markers and depression did not separate temporal inferences between people and within-person and how different immunometabolism markers related to unique depression symptoms. We thus used cross-lagged prospective network analyses (CLPN) to investigate this topic. Methods Community midlife women (n = 2224) completed the Center for Epidemiologic Studies-Depression scale and provided biomarker samples across five time-points spanning 9 years. CLPN identified significant relations (edges) among components (nodes) of depression (depressed mood, somatic symptoms, interpersonal issues), lipid markers [insulin, fasting glucose, triglycerides, low-density lipoprotein-cholesterol (LDL), high-density lipoprotein-cholesterol (HDL)], and proinflammatory proteins [C-reactive protein (CRP), fibrinogen], within and across time-points. All models adjusted for age, estradiol, follicle-stimulating hormone, and menopausal status. Results In within-person temporal networks, higher CRP and HDL predicted all three depression components (d = 0.131-2.112). Increased LDL preceded higher depressed mood and interpersonal issues (v. somatic symptoms) (d = 0.251-0.327). Elevated triglycerides predicted more somatic symptoms (v. depressed mood and interpersonal problems) (d = 0.131). More interpersonal problems forecasted elevated fibrinogen and LDL levels (d = 0.129-0.331), and stronger somatic symptoms preceded higher fibrinogen levels (d = 0.188). Conclusions Results supported both vulnerability and scar models. Long-term dysregulated immunometabolism systems, social disengagement, and related patterns are possible mechanistic accounts. Cognitive-behavioral therapies that optimize nutrition and physical activity may effectively target depression.
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U2 - 10.1017/S003329172200232X
DO - 10.1017/S003329172200232X
M3 - Article
C2 - 35924730
AN - SCOPUS:85170666680
SN - 0033-2917
VL - 53
SP - 5267
EP - 5278
JO - Psychological medicine
JF - Psychological medicine
IS - 11
ER -