RESUMO
OBJECTIVES: This analysis examined if financial hardship was associated with age-related decrements in kidney function using a material-psychosocial-behavioral framework. We also tested if this association was mediated by comorbidity of cardiometabolic risk factors (obesity, elevated blood pressure, and insulin resistance). METHODS: Data from 1,361 Non-Hispanic (NH) Black and white adults (ages 26-94; NH Black = 258) were obtained from the Wave 3 and Refresher phases of the Midlife in the United States (MIDUS) project. Kidney function was based on serum creatinine-based estimated glomerular filtration rate (CKD-EPI formula without race adjustment). Financial hardship was evaluated in three domains: material (income to poverty line ratio, health insurance coverage, and public/government financial assistance), psychological (perceived financial status, control over financial status, and perceived financial strains), and behavioral responses (financial adjustment/coping such as sold possessions and cutting back on spending). RESULTS: More severe financial hardship (overall score and in each domain) was associated with age-related decrements in eGFR, even after adjusting for sociodemographic, education, and health-related covariates. The association between financial hardship and age-related decrements in eGFR was conditional on sex but not race. Finally, cardiometabolic risk factors mediated the association between financial hardship and age-related decrements in eGFR. CONCLUSIONS: These findings affirm the negative effects of financial hardship on age-related decrements in renal clearance. In addition to incorporating traditionally used indicators of SES, such as education and income, future research on social hallmarks of aging should also consider the role of financial hardship on the aging process and age-related diseases.
RESUMO
OBJECTIVE: This study replicates and expands Surachman et al.'s (2020) findings documenting socioeconomic status (SES) trajectories across the life course in an independent sample of Black (majority recruited from Milwaukee, WI) and white adults in the United States. We extend this work by examining whether SES trajectories and daily discrimination are independently associated with markers of inflammation. METHOD: Data were from 215 Black adults (188 recruited from Milwaukee, WI; 27 recruited from across the continental US) and 985 white adults (7 recruited from Milwaukee, WI; 978 recruited from across the continental US) who completed the baseline interview and biomarker assessment during the second wave of the Midlife in the United States (MIDUS) Study (ages = 34-84). SES life course trajectories were examined using latent class analysis based on objective (e.g., income and education) and subjective (e.g., social status and financial strain) indicators of SES. The association between life course SES trajectories and daily discrimination with markers of inflammation (IL-6, CRP, fibrinogen) were examined using multiple linear regression analyses, controlling for demographic, psychological, behavioral, and health-related covariates. RESULTS: Black and white participants showed different patterns of life course SES trajectories. Among Black participants, the trajectories were Objectively Stable Low (45.16%), Downwardly Mobile (18.05%), and Upwardly Mobile (36.79%). Compared to the Upwardly Mobile, the Objectively Stable Low class showed elevated IL-6 after controlling for all covariates. Further, daily discrimination, but not SES trajectories, was significantly associated with CRP and fibrinogen after controlling for demographic, psychological, and behavioral covariates. White participants' experiences of life course SES trajectories were characterized as Objectively Stable Low (7.02%), Subjectively Downward (12.48%), Upwardly Mobile (39.99%), and Stable High (40.51%). Among white participants, SES trajectories, but not daily discrimination, were associated with all markers of inflammation (controlling for age and sex). DISCUSSION: Consistent with the fundamental cause theory, multiple independent pathways link SES trajectories across the life course and daily discrimination to racial disparities in IL-6, CRP, and fibrinogen.
Assuntos
Negro ou Afro-Americano/estatística & dados numéricos , Inflamação/epidemiologia , Acontecimentos que Mudam a Vida , Racismo/estatística & dados numéricos , Status Social , População Branca/estatística & dados numéricos , Adulto , Idoso , Biomarcadores/análise , Proteína C-Reativa/análise , Feminino , Fibrinogênio/análise , Humanos , Interleucina-6/análise , Masculino , Pessoa de Meia-Idade , Classe Social , Estados UnidosRESUMO
OBJECTIVE: Using cross-sectional data on Black and white adults, this analysis examined whether age-related decrements in kidney function across adulthood were associated with parental education, and whether the association was differentially influenced by race. Further, this study assessed racial differences in life course pathways from parental education to age-related decrements in kidney function, through current SES and health-related risk factors. METHOD: Data from the main survey and the Biomarker Project of the Midlife in the United States (MIDUS) Wave 2 and Refresher samples were combined, resulting in 1861 adults (54.5% female; age 25-84, Mage = 53.37) who self-identified as non-Hispanic Black (n = 326) and non-Hispanic white (n = 1535). Estimated glomerular filtration rate (eGFR) was based on serum creatinine, calculated using the CKD-EPI formula. Adults SES was based on education, income, and financial strains. Health-related risk factors included obesity, elevated blood pressure (BP), and insulin resistance. Hypotheses were tested by utilizing multiple linear regression and regression-based moderated mediation analysis. RESULTS: Lower parental education was associated with steeper age-related decrements in eGFR (B = 0.38, SE = 0.15, p = .013, 95%CI = 0.08, 0.68), due to higher eGFR among younger participants and lower eGFR among older participants. In addition, age-related decrements in kidney function were steeper among Black relative to white adults (B = 0.41, SE = 0.13, p < .01, 95%CI = 0.16, 0.66), driven by higher proportion of younger Black adults that met criterion for renal hyperfiltration. Furthermore, parental education and race were associated with age-related decrements in kidney function in an additive rather than interactive way. There were some racial differences in the life course pathways from parental education to age-related differences in eGFR, glucoregulation, and hypertension. Among Black adults, lower parental education was associated with elevated eGFR among younger participants through insulin resistance. Among white adults, lower parental education was linked to higher eGFR among younger adults and lower eGFR among older adults, and the association was mediated by current SES, elevated BP, and insulin resistance. DISCUSSION: Early life SES can have a long-lasting influence on the preclinical renal senescence that is associated with the normal biology of aging for both Black and white adults.