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Demographic correlates of inflammatory and antiviral gene expression in the study of Midlife in the United States (MIDUS).

ABSTRACT: The present study examined the demographic correlates of gene expression in a sample of adults (n = 543) from the Study of Midlife in the United States (MIDUS). Inflammatory and antiviral gene sets were operationalized using a priori composite scores and empirically derived co-regulatory gene sets. For both composite scores and co-regulatory gene sets, White/European Americans showed lower while Black/African Americans showed higher expression of genes involved in interferon responses and antibody synthesis. The effects of chronological age on gene expression varied by sex, such that pro-inflammatory gene expression increased with age more rapidly for females than males. The difference between the average expression of inflammatory and antiviral genes also increased with age for females but not males. Results shed light on differential gene expression as a potential physiological correlate for race/ethnicity, age, and sex-related health disparities in adulthood.

SUBMITTER: Mann FD

PROVIDER: S-EPMC8702472 | biostudies-literature | 2020 Jul-Sep

REPOSITORIES: biostudies-literature

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Demographic correlates of inflammatory and antiviral gene expression in the study of Midlife in the United States (MIDUS).

Mann Frank D FD Krueger Robert F RF Clouston Sean S Cole Steven S

Biodemography and social biology 20200701 3-4

The present study examined the demographic correlates of gene expression in a sample of adults (<i>n</i> = 543) from the Study of Midlife in the United States (MIDUS). Inflammatory and antiviral gene sets were operationalized using <i>a priori</i> composite scores and empirically derived co-regulatory gene sets. For both composite scores and co-regulatory gene sets, White/European Americans showed lower while Black/African Americans showed higher expression of genes involved in interferon respon ...[more]

PMID: 34622724

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Project description:BackgroundCryptosporidium are parasitic protozoa that infect humans, domestic animals, and wildlife globally. In the United States, cryptosporidiosis occurs in an estimated 750,000 persons annually, and is primarily caused by either of the Cryptosporidium parvum genotypes 1 and 2, exposure to which occurs through ingestion of food or water contaminated with oocytes shed from infected hosts. Although most cryptosporidiosis cases are caused by genotype 1 and are of human origin, the zoonotic sources of genotype 2, such as livestock, are increasingly recognized as important for understanding human disease patterns. Social inequality could mediate patterns of human exposure and infection by placing individuals in environments where food or water contamination and livestock contact is high or through reducing the availability of educational and sanitary resources required to avoid exposure.Methodology/principal findingsWe here analyzed data from the National Health and Nutritional Examination Survey (NHANES) between 1999 and 2000, and related seropositivity to Cryptosporidium parvum to correlates of social inequality at the household and individual scale. After accounting for the complex sampling design of NHANES and confounding by individual demographics and household conditions, we found impaired household food adequacy was associated with greater odds of Cryptosporidium seropositivity. Additionally, we identified individuals of non-white race and ethnicity and those born outside the United States as having significantly greater risk than white, domestic-born counterparts. Furthermore, we provide suggestive evidence for direct effects of family wealth on Cryptosporidium seropositivity, in that persons from low-income households and from families close to the poverty threshold had elevated odds of seropositivity relative to those in high-income families and in households far above the poverty line.Conclusions/significanceThese results refute assertions that cryptosporidiosis in the United States is independent of social marginalization and poverty, and carry implications for targeted public health interventions for Cryptosporidium infection in resource-poor groups. Future longitudinal and multilevel studies are necessary to elucidate the complex interactions between ecological factors, social inequality, and Cryptosporidium dynamics.

Project description:BackgroundThere is a lack of empirical effort that systematically investigates the clustering of comorbidity among known risk factors (obesity, hypertension, diabetes, hypercholesterolemia, and elevated inflammation) of chronic kidney disease (CKD) and how different types of comorbidity may link differently to kidney function among healthy adult samples. This study modeled the clustering of comorbidity among risk factors, examined the association between the clustering of risk factors and kidney function, and tested whether the clustering of risk factors was associated with childhood SES.MethodsThe data were from 2118 participants (ages 25-84) in the Midlife in the United States (MIDUS) Study. Risk factors included obesity, elevated blood pressure (BP), high total cholesterol levels, poor glucose control, and increased inflammatory activity. Glomerular filtration rate (eGFR) was estimated from serum creatinine, calculated with the CKD-EPI formula. The clustering of comorbidity among risk factors and its association with kidney function and childhood SES were examined using latent class analysis (LCA).ResultsA five-class model was optimal: (1) Low Risk (class size = 36.40%; low probability of all risk factors), (2) Obese (16.42%; high probability of large BMI and abdominally obese), (3) Obese and Elevated BP (13.37%; high probability of being obese and having elevated BP), (4) Non-Obese but Elevated BP (14.95%; high probability of having elevated BP, hypercholesterolemia, and elevated inflammation), and (5) High Risk (18.86%; high probability for all risk factors). Obesity was associated with kidney hyperfiltration, while comorbidity between obesity and hypertension was linked to compromised kidney filtration. As expected, the High Risk class showed the highest probability of having eGFR < 60 ml/min/1.73 m2 (P = .12; 95%CI = .09-.17). Finally, higher childhood SES was associated with reduced probability of being in the High Risk rather than Low Risk class (β = - 0.20, SE = 0.07, OR [95%CI] = 0.82 [0.71-0.95]).ConclusionThese results highlight the importance of considering the impact of childhood SES on risk factors known to be associated with CKD.

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Demographic correlates of inflammatory and antiviral gene expression in the study of Midlife in the United States (MIDUS).

Publications

Demographic correlates of inflammatory and antiviral gene expression in the study of Midlife in the United States (MIDUS).

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