Iaroslav Youssim

Background: Cardiometabolic risk factors are major contributors to poor health outcomes and premature mortality. While the effect of prenatal exposure to stress on cardiometabolic outcomes has been examined, the findings remain inconsistent across studies, and even more so with regard to the timing of exposure. In the present study, we aimed to explore the association of short-term prenatal exposure to the acute stress of the 1967 Six-Day War with cardiovascular and anthropometric risk factors in adolescent offspring. Methods: Using a population-based birth cohort, we examined data from 61 237 offspring born in Jerusalem during 1964–76, linked to their military-draft records at age 17 years. These provided information on those exposed to acute prenatal stress and the timing of exposure within the pregnancy (N = 2471) as well as on height, weight, heart rate (HR), and blood pressure (BP) in adolescence. Linear regression models estimated the associations between prenatal stress and measurements at age 17 years, controlling for potential confounders. Results: Prenatal exposure to acute stress was associated with increased systolic blood pressure (SBP) and diastolic blood pressure (DBP) [SBP: B = 1.85, 95% confidence interval (CI): 1.15, 2.56; DBP: B = 1.89, 95% CI: 1.40, 2.38] and a decreased HR (B = –1.39, CI: –1.88, –0.91) but not with anthropometric outcomes. Furthermore, gestational age at exposure modified these associations: the associations with DBP and mean arterial pressure tended to increase and with HR to decrease the later the exposure occurred during the pregnancy. Conclusion: Findings suggest that acute maternal stress during pregnancy is associated with cardiovascular risk factors in offspring in adolescence and is modulated by the timing of the exposure.

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Background: While risks associated with congenital anomalies (CAs) in childhood are well documented, data on the long-term impact of CAs on adult mortality are lacking. We aimed to study mortality risks in adults born with CAs using the population-based Jerusalem Perinatal Study cohort. Methods: Individuals born in 1964–1976 who attained 18 years of age were followed up until 2016 or date of death (median 27.5 years). We categorized anomalies by presence/absence, severity, multiplicity, and body system affected. Cox regression models were constructed to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the association between CAs and all-cause mortality, adjusting for birth weight, delivery mode, maternal age, socioeconomic status at birth, maternal country of birth, and stratified by offspring sex and maternal education. Results: Of the 91 459 live-born offspring, 2429 (2.7%) died before attaining age 18 years and 1454 (1.6%) died thereafter. Of 87 621 who survived to age 18, 5621 (6.4%) had CAs. Mortality was increased in those bearing any (adjusted HR (HRadj) = 1.53, CI: 1.29–1.83), single (HRadj = 1.51, CI: 1.27–1.81), severe (HRadj = 2.21, CI: 1.75–2.77), and moderate and severe malformations combined (HRadj = 2.19, CI: 1.09–4.40), when compared to individuals without anomalies. Additionally, adult mortality was increased in individuals with cardiovascular (HRadj = 4.81, CI: 2.15–10.70), gastrointestinal (HRadj = 2.74, CI: 1.47–5.11), and genitourinary anomalies (HRadj = 1.51, CI: 1.07–2.14). Conclusion: Increased risks of premature mortality are observed in individuals with CA who reach adulthood and are modified by severity and the body system affected. Long-term and focused follow-up for adults with CAs is warranted.

Background: Accumulating evidence suggests links between ambient temperature and preterm birth. We aimed to explore susceptible exposure weeks and groups concerning temperature and preterm birth in an innovative methodological approach. Methods: We conducted a historical cohort study of 131 599 singleton live births in Southern Israel in 2005–19. Weekly mean temperatures were assessed based on residential address and a spatiotemporal model. We fitted Cox models with time-dependent covariates and distributed lag non-linear models, adapting them for the challenges of examining prenatal exposures. We further extended the models with time-dependent coefficients to assess variations by preterm birth categories. Finally, we estimated associations of cumulative exposures by using predicted survival curves contrasting realistic exposure trajectories by month of the last menstrual period (LMP). Results: Exposures to high temperatures in gestation Weeks 29–37 were associated with increased preterm birth risk. The highest hazard ratio was 1.04 [95% confidence interval (CI): 1.01–1.07] in Week 37 for the 99th percentile (31°C) compared with the minimum-risk temperature (16°C). There was a strong seasonal pattern in the estimated risk, with pregnancies with LMP in autumn having a higher risk. The average estimated risk by LMP month varied between 6.5% and 7.6% for pregnancies with LMP in March and October, respectively, corresponding to a relative risk of 1.17 (95% CI: 1.07–1.27). Conclusion: The final weeks of the third trimester are the key window for heat exposure in Southern Israel, creating a distinguished estimated risk by LMP month, with the highest risk for pregnancies conceived in the autumn.

Preeclampsia is a dangerous pregnancy disorder, with evidence suggesting that high ambient temperatures may increase its risk, making future incidence projections crucial for health planning. While temperature-related projections for all-cause mortality exist, disease-specific projections, especially for pregnancy complications, are limited due to data and methodological challenges. Vicedo-Cabrera et al. (2019) pioneered a time-series approach to project health impacts using the attributable fraction (AF) of cases due to climate change. We adjusted this method for preeclampsia, whose risk involves long-term exposures, with delivery as a competing event. We based our analysis on the exposure-response relationship estimated in our previous study in southern Israel using cause-specific hazard and distributed lag nonlinear models. In the current study, we modeled several demographic and climate scenarios in the region for 2020-2039 and 2040-2059. Scenario-specific AFs were calculated by comparing cumulative preeclampsia incidence with and without corresponding climate change. Finally, annual cases were estimated by applying climate scenario-specific AFs to cases projected under each demographic scenario. Our models show that climate change alone may increase preeclampsia by 3.2% to 4.3% in 2040-2059 relative to 2000-2019. Fertility trends are modeled to have a larger impact, with a 30% increase in cases by 2020-2039 under a low-fertility scenario. Extreme high-fertility and climate scenarios could result in a 2.3-fold rise in incidence, from 486 cases annually in 2000-2019 to 1,118 by 2040-2059.

Background: Childhood obesity is a major public health concern, and the global rate is rising. Rapid infant weight gain is a risk factor for later overweight. Studies have linked prenatal ambient temperature exposure to fetal growth, and preliminary evidence suggests postnatal exposure may be associated with infant weight gain. Methods: Using a population-based historical cohort study including 1 100 576 infants born 2011–2019, we assessed the relationship between prenatal and one-month postnatal ambient temperature exposure and rapid infant weight gain. We used a hybrid spatiotemporal model to assess temperatures at the family’s recorded residence at birth. Repeated weight measurements between birth and 15 months were used to model the outcome using the SuperImposition by Translation and Rotation (SITAR) method. We employed generalized linear models and distributed lag models to estimate the association between prenatal and postnatal exposure and rapid infant weight gain, defined as the upper tertile of the SITAR growth velocity. Results: Overall, higher ambient temperatures were associated with rapid infant weight gain. The cumulative adjusted relative risk for the highest exposure quintile during pregnancy compared with the lowest quintile was 1.33 [95% confidence interval (CI): 1.25, 1.40], and the corresponding association for the first postnatal month was 1.19 (95% CI: 1.15, 1.23). Exposure to high ambient temperature during early and mid-pregnancy, as well as the first postnatal month, was associated with rapid weight gain, while during late pregnancy, exposure to low temperatures was associated with this outcome. Conclusions: Prenatal and postnatal ambient temperatures are associated with rapid infant weight gain.

Biological age (BA), reflecting aging-related health decline beyond chronological age, varies among individuals. While previous research explored associations of maternal pregnancy-related body size with offspring health outcomes, its implications for BA in young adults remain unclear. Utilizing longitudinal data of 1,148 mother-offspring pairs from the Jerusalem Perinatal Study, we analyzed associations of maternal pre-pregnancy BMI and gestational weight gain (GWG) with offspring Klemera-Doubal method (KDM)-based BA at age 32, and potential familial life-course underlying mechanisms. Maternal pregnancy-related body size, adjusted for sociodemographic/lifestyle factors was associated with offspring BA (β_{maternal pre-pregnancy BMI}=0.183,95%CI:0.098,0.267;β_GWG=0.093,95%CI:0.021,0.165). Association of GWG with BA was largely direct (90%,95%CI,44%,100%), while association with maternal pre-pregnancy BMI was partially mediated through adolescent BMI (36%,95%CI=18%,75%), with both associations eliminated after adjustment for offspring adult BMI. Associations persisted after adjusting for offspring polygenic risk score for BMI (β_{maternal pre-pregnancy BMI}=0.128;95%CI=0.023,0.234; β_GWG=0.102;95%CI=0.006,0.198), and somewhat altered after adjustment for maternal cardiometabolic conditions (β_{maternal pre-pregnancy BMI}=0.144,95%CI=0.059, 0.230). Impact on GWG associations was negligible. Thus, perinatal obesogenic environment contributes to offspring BA beyond sociodemographic factors and maternal cardiometabolic history, yet intergenerational transmission of obesity seems to underlie these associations. Nonetheless, the period between adolescence and young adulthood could be targeted for weight-reducing interventions, ultimately promoting healthy aging.