Complementing the United States Household Food Security Survey Module with Items Reflecting Social Unacceptability.

BACKGROUND: Social unacceptability of food access is part of the lived experience of food insecurity but is not assessed as part of the United States Household Food Security Survey Module (HFSSM). OBJECTIVES: The objectives were as follows: 1) to determine the psychometric properties of 2 additional items on social unacceptability in relation to the HFSSM items and 2) to test whether these 2 items provided added predictive accuracy to that of the HFSSM items for mental health outcomes. METHODS: Cross-sectional data used were from the Intersection of Material-Need Insecurities and HIV and Cardiovascular Health substudy of the Multicenter AIDS Cohort Study/Women's Interagency HIV Study Combined Cohort Study. Data on the 10-item HFSSM and 2 new items reflecting social unacceptability were collected between Fall 2020 and Fall 2021 from 1342 participants from 10 United States cities. The 2 social unacceptability items were examined psychometrically in relation to the HFSSM-10 items using models from item response theory. Linear and logistic regression was used to examine prediction of mental health measured by the 20-item Center for Epidemiologic Studies Depression scale and the 10-item Perceived Stress Scale. RESULTS: The social unacceptability items were affirmed throughout the range of severity of food insecurity but with increasing frequency at higher severity of food insecurity. From item response theory models, the subconstructs reflected in the HFSSM-10 and the subconstruct of social unacceptability were distinct, not falling into one dimension. Regression models confirmed that social unacceptability was distinct from the subconstructs reflected in the HFSSM-10. The social unacceptability items as a separate scale explained more (∼1%) variation in mental health than when combined with the HFSSM-10 items in a single scale, and the social unacceptability subconstruct explained more (∼1%) variation in mental health not explained by the HFSSM-10. CONCLUSIONS: Two social unacceptability items used as a separate scale along with the HFSSM-10 predicted mental health more accurately than did the HFSSM-10 alone.

Associations between the social environment and early childhood developmental outcomes of Puerto Rican children with prenatal Zika virus exposure: a cross-sectional study.

BACKGROUND: Prenatal exposure to the Zika virus can lead to microcephaly and adverse developmental outcomes, even in children without evident birth defects. The social environment plays a crucial role in infant health and developmental trajectories, especially during periods of heightened brain plasticity. The study aimed to assess socioenvironmental factors as predictors of developmental outcomes of 36-month-old children exposed to Zika virus prenatally. STUDY DESIGN: This cross-sectional study included 53 mothers and 55 children enrolled in the Pediatric Outcomes of Prenatal Zika Exposure cohort study in Puerto Rico. The study performs follow-up developmental assessments of children born to mothers with confirmed and probable Zika virus infection during pregnancy. Mothers completed socioenvironmental questionnaires (e.g., Perceived Neighborhood Scale and US Household Food Insecurity Survey). Children's developmental outcomes were assessed with the Bayley Scales of Infant and Toddler Development: Third Edition, the Ages and Stages Questionnaires: Third Edition, the Ages and Stages Questionnaire-Socioemotional: Second Edition, and the Child Adjustment and Parent Efficacy Scale. RESULTS: Linear regression models, adjusting for a child's sex and age and maternal education, revealed that early life exposure to food insecurity and maternal pregnancy stressors were significantly associated with poorer developmental outcomes in Zika virus-exposed children at 36 months of age. Maternal resilience representation of adaptive ability was associated with the preservation of adequate developmental outcomes in children. CONCLUSIONS: Pregnancy and early childhood are critical life periods for ensuring optimal brain development in children. While the mechanisms in the interaction of children with their environment are complex, the risk and protective factors identified in the study are modifiable through public policy and preventive initiatives. Implementation of comprehensive strategies that improve access to social support programs, educational and nutritional interventions, and mental health services during pregnancy and early childhood can enhance the developmental potential of vulnerable children.

Maternal-infant interaction quality is associated with child NR3C1 CpG site methylation at 7 years of age.

OBJECTIVE: Infancy is both a critical window for hypothalamic-pituitary-adrenal (HPA) axis development, and a sensitive period for social-emotional influences. We hypothesized that the social-emotional quality of maternal-infant interactions are associated with methylation of HPA-axis gene NR3C1 later in childhood. METHODS: Using a subsample of 114 mother-infant pairs from the Avon Longitudinal Study of Parents and Children (ALSPAC), linear regression models were created to predict variance in methylation of seven selected CpG sites from NR3C1 in whole blood at age 7 years, including the main predictor variable of the first principal component score of observed maternal-infant interaction quality (derived from the Thorpe Interaction Measure at 12 months of age) and covariates of cell-type proportion, maternal financial difficulties and marital status at 8 months postnatal, child birthweight, and sex. RESULTS: CpG site cg27122725 methylation was negatively associated with warmer, more positive maternal interaction with her infant (ß = 0.19, p = .02, q = 0.13). In sensitivity analyses, the second highest quartile of maternal behavior (neutral, hesitant behavior) was positively associated with cg12466613 methylation. The other five CpG sites were not significantly associated with maternal-infant interaction quality. CONCLUSIONS: Narrow individual variation of maternal interaction with her infant is associated with childhood methylation of two CpG sites on NR3C1 that may be particularly sensitive to environmental influences. Infancy may be a sensitive period for even small influences from the social-emotional environment on the epigenetic determinants of HPA-axis function.

Early Childhood Neurodevelopmental Outcomes in Children with Prenatal Zika Virus Exposure: A Cohort Study in Puerto Rico.

OBJECTIVE: To describe anthropometric, sensory, and neurodevelopmental outcomes of children who were Zika virus-exposed from birth to 36 months. STUDY DESIGN: The study cohort included 114 children born to mothers with confirmed and probable Zika virus pregnancy infection in 2016-2017. Children attending study visits from May 2017 through February 2020 underwent physical/neurologic, sensory examinations, and neurodevelopmental assessments with the Bayley Scales of Infant and Toddler Development, Third Edition (BSID-III) and Ages and Stages Questionnaires, Third Edition (ASQ-3). RESULTS: Three of the 114 children (2.6%) had microcephaly (z-score for head circumference ≤-2) at birth, 19 of 35 (54.3%) had posterior eye abnormalities in retinal images, and 11 of 109 (10.1%) had nonspecific findings on brain ultrasound. Three of 107 children (2.8%) failed hearing screening at birth. Of those children with follow-up data, 17 of 97 (17.5%) failed age-appropriate vision screening. The BSID-III identified developmental delay in at least 1 domain in at least one-third of children, with higher prevalence in the language domain. ASQ-3 screen positive delay peaked at around 24 or 36 months, with some domains showing a decrease at older ages. Correlations among BSID-III and ASQ-3 scores were observed, representing professional and parental perspectives at 24 and 36 months (r = 0.32-0.78; P < .05). CONCLUSIONS: The presence of neurodevelopmental sequelae in early childhood suggests that identification of long-term impairment remains critical to attaining optimal child development. Long-term follow-up highlights vulnerability in the language domain, which likely could be influenced by early intervention, promoting cognitive development and school readiness in exposed children.

Timing, duration, and differential susceptibility to early life adversities and cardiovascular disease risk across the lifespan: Implications for future research.

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.

Maternal depression, adverse childhood experiences, and social support in relation to gestational diabetes risk: results from the Albany Infant and Mother Study (AIMS).

BACKGROUND: Psychosocial factors are of increasing interest as potential influencers in disease development. This study explores associations between gestational diabetes mellitus (GDM) and maternal depression, adverse childhood experiences (ACEs), and social support, in response to emerging evidence in these areas. METHODS: An observational, prospective cohort study (AIMS) served as the source of secondary data for this study. Participants included 300 pregnant women aged 18-40 years at an upstate New York prenatal care clinic, who completed a set of self-report questionnaires assessing exposures and stressors both during and prior to their pregnancy. Data were also abstracted from infant and maternal medical records. RESULTS: Logistic regression modeling estimated the odds ratios (ORs) of developing GDM in relation to psychosocial factors. There was a significant association between depression and GDM (OR = 2.85, 95% CI: 1.15, 7.06), which persisted in the model adjusted for age and BMI (aOR = 3.19, 95% CI: 1.25, 8.10). No significant associations were found between ACEs or social support with GDM. CONCLUSIONS: Study findings support an association between maternal depression and GDM development. This study underscores the need for additional research on psychosocial factors and connections to health risks.

Response to "An Overlooked and more Complicated Association of Social Support with Infant Birth Size".

In this letter to the editor, we respond to our colleagues comments regarding the nature of our findings. We present a response that incorporates theory and data to bolster our claims. We conclude the letter with a statement to readers on what we believe to be an appropriate interpretation of our study findings given the theoretical framework from which the work was based, and our empirical findings.

Adverse childhood experiences and reproductive strategies in a contemporary U.S. population.

OBJECTIVES: Stressful experiences may initiate developmentally plastic responses toward a faster reproductive strategy. This study tests whether adverse childhood experiences (ACEs) are associated with characteristics of faster reproductive strategies: earlier menarche and reduced prenatal investment in offspring in a well-nourished, low-immune system burden population. MATERIALS AND METHODS: We analyzed the first 214 enrollees of the prenatal-birth Albany Infant and Mother Study. Mother's menarcheal age, offspring gestational age at birth, and cephalization index (head circumference/weight, cm/g) were derived from medical records. Linear regression models tested the contribution of self-reported ACEs from 0 to 18 years of age to menarcheal age and the contribution of menarcheal age to offspring gestational age and cephalization index. Birth outcome models included covariates self-reported maternal race, education, prenatal smoking, prenatal diet, newborn sex, parity, delivery method, and labor induction derived from medical records. RESULTS: More ACEs were associated with earlier age at menarche, controlling for covariates (ß = -.18, SE = 0.048, p < .001), though timing of ACEs relative to menarche is unknown. Earlier menarcheal age was associated with offspring higher cephalization index (ß = -.01, SE = 0.006, p < .05). Stratified models showed a significant relationship in high (≥2) ACEs group (ß = -.02, SE = 0.009, p < .05), not present among low ACEs. Menarcheal age predicted gestational age only among those with high ACEs (ß = .22, SE = 0.091, p < .05). DISCUSSION: In a well-nourished population, early life stress can result in faster reproductive strategies, initiating sexual maturation earlier, and reducing prenatal investment in individual offspring. Early age at menarche following childhood stress has a stronger relationship with adverse birth outcomes than early menarche without exposure to adverse childhood stress.

Optimism and Social Support Predict Healthier Adult Behaviors Despite Socially Disadvantaged Childhoods.

BACKGROUND: Studies have shown adverse effects of a disadvantaged childhood on adult health-promoting behaviors and related outcomes. Optimism and social support have been linked to greater likelihood of engaging in healthy behavior, but it is unclear whether these positive psychosocial factors may buffer harmful effects of early adversity. This study aims to determine if optimism and social support in adulthood can modify effects of childhood disadvantage on health behavior-related outcomes. METHODS: Longitudinal data were analyzed from a subset of participants in a US birth cohort established in 1959-1966 (ns of 681-840, per outcome). An index of childhood social disadvantage was derived from adverse socioeconomic and family stability factors reported by mothers at child's birth and age 7 years. Health behavior-related outcomes were self-reported when participants were of mean age 47 years. Multivariable adjusted robust Poisson regressions were performed. RESULTS: Regardless of level of childhood social disadvantage, we found higher levels of optimism and social support were both associated with higher probabilities of being a non-smoker (relative risk [RR]optimism = 1.17, 95% confidence interval [CI] = 1.09-1.26; RRsocial support = 1.24, 95%CI = 1.11-1.39), having a healthy diet (RRoptimism = 1.25, 95%CI = 1.10-1.43; RRsocial support = 1.27, 95%CI = 1.04-1.56), and a healthy body mass index (RRoptimism = 1.18, 95%CI = 1.00-1.40; RRsocial support = 1.29, 95%CI = 1.00-1.66). Interactions link higher optimism or social support with lower risk of smoking among those with moderate childhood disadvantage. CONCLUSIONS: Overall, these findings are consistent with the possibility that positive psychosocial resources contribute to maintaining a healthy lifestyle in mid-adulthood and may buffer effects of childhood social disadvantage.

Trajectories of childhood adversity and the risk of depression in young adulthood: Results from the Avon Longitudinal Study of Parents and Children.

BACKGROUND: The significance of the timing and chronicity of childhood adversity for depression outcomes later in life is unclear. Identifying trajectories of adversity throughout childhood would allow classification of children according to the accumulation, timing, and persistence of adversity, and may provide unique insights into the risk of subsequent depression. METHODS: Using data from the Avon Longitudinal Study of Parents and Children, we created a composite adversity score comprised of 10 prospectively assessed domains (e.g., violent victimization, inter-parental conflict, and financial hardship) for each of eight time points from birth through age 11.5 years. We used semiparametric group-based trajectory modeling to derive childhood adversity trajectories and examined the association between childhood adversity and depression outcomes at the age of 18 years. RESULTS: Among 9,665 participants, five adversity trajectories were identified, representing stable-low levels (46.3%), stable-mild levels (37.1%), decreasing levels (8.9%), increasing levels (5.3%), and stable-high levels of adversity (2.5%) from birth through late childhood. Approximately 8% of the sample met criteria for probable depression at 18 years and the mean depression severity score was 3.20 (standard deviation = 3.95, range 0-21). The risk of depression in young adulthood was elevated in the decreasing (odds ratio [OR] = 1.72, 95% confidence interval [CI] = 1.19-2.48), increasing (OR = 1.81, 95% CI = 1.15-2.86), and stable-high (OR = 1.80, 95% CI = 1.00-3.23) adversity groups, compared to those with stable-low adversity, when adjusting for potential confounders. CONCLUSIONS: Children in trajectory groups characterized by moderate or high levels of adversity at some point in childhood exhibited consistently greater depression risk and depression severity, regardless of the timing of adversity.

Social Support During Pregnancy Modifies the Association Between Maternal Adverse Childhood Experiences and Infant Birth Size.

Introduction Adverse childhood experiences (ACEs) can deleteriously affect health, including pregnancy and birth outcomes occurring later in life. Identification of modifiable factors during pregnancy that buffer the ill effects of adversity is warranted. Social support during pregnancy can promote better birth outcomes, yet it is unknown whether it could also mitigate perinatal risks stemming from ACEs. Thus, this study considers multiple forms of social support in pregnancy as modifiers of an ACEs and fetal growth association. Methods Data were collected from mother and infant pairs from an ongoing prospective birth cohort. Women enrolled around 27 weeks gestation and completed gold-standard assessments of ACEs and social support. Infant cephalization index scores [(head circumference /birthweight) × 100; a marker of asymmetric fetal growth] were derived. Multivariable regression models tested main effects and interaction between ACEs and social support in relation to infant cephalization. Results Higher levels of ACEs were associated with higher cephalization scores (ß = 0.01, SE = 0.01, p < 0.05) whereas higher social support was associated with lower cephalization scores (ß = - 0.03, SE = 0.01, p < 0.05). A significant interaction was observed showing a protective effect of social support among those with low (0 events) and moderate (1-3 events) ACEs but not among those with high ACEs (4 + events; p < 0.05). Tangible and emotional support, but not information support, contributed to the associations. Discussion Maternal ACEs can deleteriously affect birth size, yet social support during pregnancy provides some buffer from its enduring effects. Interventions designed to enhance pregnancy social support may not only improve maternal wellbeing, but may also safeguard infant health.

Measuring Childhood Adversity in Life Course Cardiovascular Research: A Systematic Review.

OBJECTIVE: Identifying the life course health effects of childhood adversity is a burgeoning area of research, particularly in relation to cardiovascular disease (CVD). However, adversity measurement varies widely across studies, which may hamper our ability to make comparisons across studies and identify mechanisms linking adversity to CVD. The purposes of this review are to summarize adversity measurement approaches in the context of CVD, identify gaps, and make recommendations for future research. METHODS: PubMed and PsycINFO searches were conducted through June 2016. Studies were selected if CVD end point or predisease risk markers were investigated in association with a measure of childhood adversity. Forty-three studies were reviewed. A meta-analysis was not conducted because of the variation in exposures and outcomes assessed. RESULTS: Adversity measurement was heterogeneous across studies. Metrics included different sets of adverse events, relational factors, and socioeconomic indicators. Thirty-seven percent measured childhood adversity prospectively, 23% examined a CVD end point, and 77% treated adversity as an unweighted summary score. Despite the heterogeneity in measurement, most studies found a positive association between childhood adversity and CVD risk, and the association seems to be dose-response. CONCLUSIONS: The literature on childhood adversity and CVD would benefit from improving consistency of measurement, using weighted adversity composites, modeling adversity trajectories over time, and considering socioeconomic status as an antecedent factor instead of a component part of an adversity score. We suggest conceptual and analytic strategies to enhance, refine, and replicate the observed association between childhood adversity and CVD risk.

Low-level arsenic exposure via drinking water consumption and female fecundity - A preliminary investigation.

High level arsenic exposure is associated with reproductive toxicity in experimental and observational studies; however, few data exist to assess risks at low levels. Even less data are available to evaluate the impact of low level arsenic exposure on human fecundity. Our aim in this pilot study was a preliminary evaluation of associations between low level drinking water arsenic contamination and female fecundity. This retrospective study was conducted among women previously recruited to a hospital-based case-control study of spontaneous pregnancy loss in Timis County, Romania. Women (n=94) with planned pregnancies of 5-20 weeks gestation completed a comprehensive physician-administered study questionnaire and reported the number of menstrual cycles attempting to conceive as the time to pregnancy (TTP). Drinking water samples were collected from residential drinking water sources and we determined arsenic levels using hydride generation-atomic absorption spectrometry (HG-AAS). Multivariable Cox-proportional hazards regression with Efron approximation was employed to evaluate TTP as a function of drinking water arsenic concentrations among planned pregnancies, adjusted for covariates. There was no main effect for drinking water arsenic exposure, yet the conditional probability for pregnancy was modestly lower among arsenic exposed women with longer TTPs, relative to women with shorter TTPs, and relative to unexposed women. For example, 1µg/L average drinking water arsenic conferred 5%, 8%, and 10% lower likelihoods for pregnancy in the 6th, 9th, and 12th cycles, respectively (P=0.01). While preliminary, our results suggest that low level arsenic contamination in residential drinking water sources may further impair fecundity among women with longer waiting times; however, this hypothesis requires confirmation by a future, more definitive study.

Prenatal Programming of Infant Neurobehaviour in a Healthy Population.

BACKGROUND: Identifying the prenatal origins of mental conditions is of increasing interest, yet most studies have focused on high-risk populations and cannot disentangle prenatal and postnatal programming effects. Thus, we examined whether profiles of neurobehaviour indicative of future risk could be identified in healthy 1-3-day-old infants, and examined associations with perinatal risk factors. METHODS: Participants included 627 healthy mothers and term infants from a population-based US cohort. Neurobehaviour was assessed within 24-72 h after delivery with the NICU Network Neurobehavioural Scales (NNNS). A model-based clustering algorithm was used to derive neurobehavioural profiles from NNNS scores. Maternal health histories, pregnancy conditions and behaviours, labour/delivery factors, and infant attributes were examined in relation to the neurobehavioural profiles. RESULTS: Seven discrete neurobehavioural profiles were identified, including one average functioning profile, and two inversely patterned below and above average profiles. Higher pregnancy weight gain (OR 1.44, 95% CI 1.10, 1.88) and birthweight percentiles (OR 1.46, 95% CI 1.10, 1.95) were associated with greater odds of below average newborn neurobehaviour. Above average neurobehaviour was associated with experiencing longer gestations (OR 1.29, 95% CI 1.02, 1.64) and higher 5-min APGAR scores (OR 2.43, 95% CI 1.07, 5.52). Maternal pregnancy alcohol use (OR 0.54, 95% CI 0.33, 0.89), and fetal distress (OR 0.10, 95% CI 0.01, 0.72) were associated with lower likelihood of having average neurobehaviour. CONCLUSION: Distinct profiles of neurobehaviour can be derived in a healthy population of newborns, with different sets of perinatal factors predicting different patterns of neurobehaviour. These findings suggest a potential in utero origin for mental health risk.

A prospective study of positive early-life psychosocial factors and favorable cardiovascular risk in adulthood.

BACKGROUND: The American Heart Association's national goals for cardiovascular health promotion emphasize that cardiovascular risk originates early in life, but little is known about childhood factors that may increase the likelihood of having a favorable cardiovascular risk (FCR) in adulthood. We examined the prospective association between positive childhood factors and the likelihood of midlife FCR. We also considered pathways through which childhood factors may influence FCR. METHODS AND RESULTS: We studied 415 adults (mean age=42.2 years) of the Collaborative Perinatal Project, a national cohort initiated in 1959 to 1966. We examined 3 positive childhood factors assessed at age 7 years: attention regulation (ability to stay focused), cognitive ability, and positive home environment. Of these adults, 10.6% had FCR in midlife. Adjusting for demographics and childhood cardiovascular health, a 1-unit increase in childhood attention regulation, cognitive ability, and positive home environment was associated with 2.4 (95% confidence interval, 1.1-4.7), 1.8 (95% confidence interval, 1.1-2.9), and 1.3 (95% confidence interval, 1.1-1.6) higher respective odds of having midlife FCR. The association with childhood attention regulation was maintained when accounting for adulthood factors; education and diet in part explained the associations with childhood cognitive ability and home environment. The effect of each attribute was additive as those with high levels of each childhood factor had 4.3 higher odds (95% confidence interval, 1.01-18.2) of midlife FCR in comparison with those low in all factors. CONCLUSIONS: Positive childhood psychosocial factors may promote healthy adult cardiovascular functioning. Primordial prevention efforts aimed at preventing the development of cardiovascular risk should consider building on childhood psychosocial resources.

Childhood social disadvantage, cardiometabolic risk, and chronic disease in adulthood.

Adverse social environments in early life are hypothesized to become biologically embedded during the first few years of life, with potentially far-reaching implications for health across the life course. Using prospective data from a subset of a US birth cohort, the Collaborative Perinatal Project, started in 1959-1966 (n = 566), we examined associations of social disadvantage assessed in childhood with cardiometabolic function and chronic disease status more than 40 years later (in 2005-2007). Social disadvantage was measured with an index that combined information on adverse socioeconomic and family stability factors experienced between birth and age 7 years. Cardiometabolic risk (CMR) was assessed by combining information from 8 CMR biomarkers; an index of chronic disease status was derived by assessing 8 chronic diseases. Poisson models were used to investigate associations between social disadvantage and CMR or chronic disease scores while adjusting for childhood covariates and potential pathway variables. A high level of social disadvantage was significantly associated with both higher CMR (incident rate ratio = 1.69, 95% confidence interval: 1.19, 2.39) and with a higher number of chronic diseases (incident rate ratio = 1.39, 95% confidence interval: 1.00, 1.92) in minimally adjusted models. Associations with CMR persisted even after accounting for childhood and adult covariates.

Divergent associations of antecedent- and response-focused emotion regulation strategies with midlife cardiovascular disease risk.

BACKGROUND: It is not known whether various forms of emotion regulation are differentially related to cardiovascular disease risk. PURPOSE: The purpose of this study is to assess whether antecedent and response-focused emotion regulation would have divergent associations with likelihood of developing cardiovascular disease. METHODS: Two emotion regulation strategies were examined: reappraisal (antecedent-focused) and suppression (response-focused). Cardiovascular disease risk was assessed with a validated Framingham algorithm that estimates the likelihood of developing CVD in 10 years. Associations were assessed among 373 adults via multiple linear regression. Pathways and gender-specific associations were also considered. RESULTS: One standard deviation increases in reappraisal and suppression were associated with 5.9 % lower and 10.0 % higher 10-year cardiovascular disease risk, respectively, in adjusted analyses. CONCLUSIONS: Divergent associations of antecedent and response-focused emotion regulation with cardiovascular disease risk were observed. Effective emotion regulation may promote cardiovascular health.

Remnant cholesterol, iron status and diabetes mellitus: a dose-response relationship and mediation analysis.

BACKGROUND: Remnant cholesterol (RC) is recognized as a risk factor for diabetes mellitus (DM). Although iron status has been shown to be associated with cholesterol metabolism and DM, the association between RC, iron status, and DM remains unclear. We examined the relationship between RC and iron status and investigated the role of iron status in the association between RC and DM. METHODS: A total of 7308 patients were enrolled from the China Health and Nutrition Survey. RC was calculated as total cholesterol minus low-density lipoprotein cholesterol and high-density lipoprotein cholesterol. Iron status was assessed as serum ferritin (SF) and total body iron (TBI). DM was ascertained by self-reported physician diagnosis and/or antidiabetic drug use and/or fasting plasma glucose ≥ 126 mg/dL and/or glycated haemoglobin ≥ 6.5%. General linear models were used to evaluate the relationships between RC and iron status. Restricted cubic splines were used to assess the association between RC and DM. Mediation analysis was used to clarified the mediating role of iron status in the association between the RC and DM. RESULTS: The average age of the participants was 50.6 (standard deviation = 15.1) years. Higher RC was significantly associated with increased SF (ß = 73.14, SE = 3.75, 95% confidence interval [CI] 65.79-80.49) and TBI (ß = 1.61, SE = 0.08, 95% CI 1.44-1.78). J-shape relationships were found in the association between RC levels with DM, as well as iron status with DM. Significant indirect effects of SF and TBI in the association between RC and DM were found, with the index mediated at 9.58% and 6.37%, respectively. CONCLUSIONS: RC has a dose-response relationship with iron status. The association between RC and DM was mediated in part by iron status. Future studies are needed to confirm these findings and further clarify the underlying mechanism.

Sex Hormones, the Stool Microbiome, and Subclinical Atherosclerosis in Women With and Without HIV.

CONTEXT: Cardioprotective roles of endogenous estrogens may be particularly important in women with HIV, who have reduced estrogen exposure and elevated cardiovascular disease risk. The gut microbiome metabolically interacts with sex hormones, but little is known regarding possible impact on cardiovascular risk. OBJECTIVE: To analyze potential interplay of sex hormones and gut microbiome in cardiovascular risk. METHODS: Among 197 postmenopausal women in the Women's Interagency HIV Study, we measured 15 sex hormones in serum and assessed the gut microbiome in stool. Presence of carotid artery plaque was determined (B-mode ultrasound) in a subset (n = 134). We examined associations of (i) sex hormones and stool microbiome, (ii) sex hormones and plaque, and (iii) sex hormone-related stool microbiota and plaque, adjusting for potential confounders. RESULTS: Participant median age was 58 years and the majority were living with HIV (81%). Sex hormones (estrogens, androgens, and adrenal precursors) were associated with stool microbiome diversity and specific species, similarly in women with and without HIV. Estrogens were associated with higher diversity, higher abundance of species from Alistipes, Collinsella, Erysipelotrichia, and Clostridia, and higher abundance of microbial ß-glucuronidase and aryl-sulfatase orthologs, which are involved in hormone metabolism. Several hormones were associated with lower odds of carotid artery plaque, including dihydrotestosterone, 3α-diol-17G, estradiol, and estrone. Exploratory mediation analysis suggested that estrone-related species, particularly from Collinsella, may mediate the protective association of estrone with plaque. CONCLUSION: Serum sex hormones are significant predictors of stool microbiome diversity and composition. The gut microbiome may play a role in estrogen-related cardiovascular protection.