Precision nutrition最新文献

Background: While consuming a Mediterranean-style diet (MSD) among pregnant women is expected to affect offspring neurodevelopment, the current evidence is limited. This prospective birth cohort study aimed to explore the association of maternal MSD with neurodevelopmental disabilities (NDD) in offspring, especially among children born to mothers with overweight or obesity (OWO) and/or diabetes mellitus (DM) since they have a higher risk for oxidative stress and immune/metabolic disturbances.

Methods: We analyzed data from a subgroup of mother-child dyads enrolled in the Boston Birth Cohort. Maternal dietary information (via food frequency questionnaires, Food frequency questionnaires [FFQ]) and sociodemographic information were obtained via in-person interviews within 24 to 72 hours postpartum. Maternal clinical information and child diagnosis of NDD including autism, attention-deficit/hyperactivity disorder (ADHD), and other developmental disabilities (DD) were extracted from medical records. A Mediterranean-style diet score (MSDS) was calculated using the FFQ. The association of maternal MSDS with NDD, autism, ADHD, and other DD was evaluated using multivariable logistic regression models adjusted for pertinent covariates.

Results: This study included 3153 mother-child pairs, from which we identified diagnoses of 1362 (43.2%) NDD, including 123 (3.9%) case of autism, 445 (14.1%) ADHD, and 794 (25.2%) other DD. In the overall sample, women with a higher maternal MSDS (per standard deviation increase) were less likely to have offspring with NDD (adjusted odds ratio [OR]: 0.904, 95% confidence interval [CI]: 0.817-1.000; P value: 0.049). Using MSDS quintile 1 as the reference, being in the combined group of quintiles 3-5 was associated with a 26% lower likelihood of NDD (adjusted OR: 0.738, 95% CI: 0.572-0.951; P value: 0.019). When stratified by mothers with OWO/DM vs. without OWO/DM, the association between maternal MSDS and offspring NDD was greater in children born to mothers with OWO/DM.

Conclusions: In this prospective birth cohort, a higher maternal MSDS was associated with a lower likelihood of NDD in the offspring. Furthermore, this association of maternal MSDS with offspring NDD was greater in children born to women with OWO/DM. More studies are needed to replicate the findings and further analyze NDD subgroups and explore underlying molecular pathways.

Background: Smoking during pregnancy has been associated with reduced risk of a spectrum of hypertensive (HTN) disorders, known as the "smoking-hypertension paradox."

Objective: We sought to test potential epidemiologic explanations for the smoking-hypertension paradox.

Methods: We analyzed 8,510 pregnant people in the Boston Birth Cohort, including 4,027 non-Hispanic Black and 2,428 Hispanic pregnancies. Study participants self-reported tobacco, alcohol, cannabis, opioids, or cocaine use during pregnancy. We used logistic regression to assess effect modification by race/ethnicity, and confounding of concurrent substances on hypertensive disorders or prior pregnancy. We also investigated early gestational age as a collider or competing risk for pre-eclampsia, using cause-specific Cox models and Fine-Gray models, respectively.

Results: We replicated the paradox showing smoking to be protective against hypertensive disorders among Black participants who used other substances as well (aOR: 0.61, 95% CI: 0.41, 0.93), but observed null effects for Hispanic participants (aOR: 1.14, 95% CI: 0.55, 2.36). In our cause-specific Cox regression, the effects of tobacco use were reduced to null effects with pre-eclampsia (aOR: 0.81, 95% CI: 0.63, 1.04) after stratifying for preterm birth. For the Fine-Gray competing risk analysis, the paradoxical associations remained. The smoking paradox was either not observed or reversed after accounting for race/ethnicity, other substance use, and collider-stratification due to preterm birth.

Conclusions: These findings offer new insights into this paradox and underscore the importance of considering multiple sources of bias in assessing the smoking-hypertension association in pregnancy.

Background: Smoking during pregnancy has been associated with reduced risk of a spectrum of hypertensive (HTN) disorders, known as the "smoking-hypertension paradox."

Objective: We sought to test potential epidemiologic explanations for the smoking-hypertension paradox.

Methods: We analyzed 8510 pregnant people in the Boston Birth Cohort, including 4027 non-Hispanic Black and 2428 Hispanic pregnancies. Study participants self-reported tobacco, alcohol, cannabis, opioids, or cocaine use during pregnancy. We used logistic regression to assess effect modification by race/ethnicity, and confounding of concurrent substances on hypertensive disorders or prior pregnancy. We also investigated early gestational age as a collider or competing risk for pre-eclampsia, using cause-specific Cox models and Fine-Gray models, respectively.

Results: We replicated the paradox showing smoking to be protective against hypertensive disorders among Black participants who used other substances as well (aOR: 0.61, 95% CI: 0.41, 0.93), but observed null effects for Hispanic participants (aOR: 1.14, 95% CI: 0.55, 2.36). In our cause-specific Cox regression, the effects of tobacco use were reduced to null effects with pre-eclampsia (aOR: 0.81, 95% CI: 0.63, 1.04) after stratifying for preterm birth. For the Fine-Gray competing risk analysis, the paradoxical associations remained. The smoking paradox was either not observed or reversed after accounting for race/ethnicity, other substance use, and collider-stratification due to preterm birth.

Conclusions: These findings offer new insights into this paradox and underscore the importance of considering multiple sources of bias in assessing the smoking-hypertension association in pregnancy.

Background: Pantothenate (vitamin B5) is a precursor for coenzyme A (CoA) synthesis, which serves as a cofactor for hundreds of metabolic reactions. Cysteine is an amino acid in the CoA synthesis pathway. To date, research on the combined role of early life pantothenate and cysteine levels in childhood neurodevelopmental disabilities is scarce.

Objective: To study the association between cord pantothenate and cysteine levels and risk of autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD) and other developmental disabilities (DD) in children born term and preterm.

Methods: The study sample (n = 996, 177 born preterm) derived from the Boston Birth Cohort included 416 neurotypical children, 87 ASD, 269 ADHD, and 224 other DD children, who were mutually exclusive. Participants were enrolled at birth and were followed up prospectively (from October 1, 1998, to June 30, 2018) at the Boston Medical Center. Cord blood sample was collected at birth. Plasma pantothenate and cysteine levels were measured using liquid chromatography-tandem mass spectrometry.

Results: Higher cord pantothenate (≥50th percentile vs. <50th percentile) was associated with a greater risk of ASD (adjusted odds ratio [aOR]: 1.94, 95% confidence interval [CI]: 1.06, 3.55) and ADHD (aOR: 1.66, 95% CI: 1.14, 2.40), after adjusting for potential confounders. However, cord cysteine alone was not associated with risk of ASD, ADHD, or other DD. When considering the joint association, greater ASD risk was noted when both cord pantothenate and cysteine levels were elevated (≥50th percentile) (aOR: 3.11, 95% CI: 1.24, 7.79), when compared to children with low cord pantothenate (<50th percentile) and high cysteine. Even though preterm and higher pantothenate independently increased the ASD risk, the greatest risk was found in preterm children who also had elevated pantothenate (≥50th percentile), which was true for all three outcomes: ASD (aOR: 5.36, 95% CI: 2.09, 13.75), ADHD (aOR: 3.31, 95% CI: 1.78, 6.16), and other DD (aOR: 3.39, 95% CI: 1.85, 6.24).

Conclusions: In this prospective birth cohort, we showed that higher cord pantothenate individually and in combination with higher cysteine or preterm birth were associated with increased risk of ASD and ADHD. More study is needed to explore this biologically plausible pathway.

Background: Overweight or obesity (OWO) in school-age childhood tends to persist into adulthood. This study aims to address a critical need for early identification of children at high risk of developing OWO by defining and analyzing longitudinal trajectories of body mass index percentile (BMIPCT) during early developmental windows.

Methods: We included 3029 children from the Boston Birth Cohort (BBC) with repeated BMI measurements from birth to age 18 years. We applied locally weighted scatterplot smoothing with a time-limit scheme and predefined rules for imputation of missing data. We then used time-series K-means cluster analysis and latent class growth analysis to define longitudinal trajectories of BMIPCT from infancy up to age 18 years. Then, we investigated early life determinants of the BMI trajectories. Finally, we compared whether using early BMIPCT trajectories performs better than BMIPCT at a given age for predicting future risk of OWO.

Results: After imputation, the percentage of missing data ratio decreased from 36.0% to 10.1%. We identified four BMIPCT longitudinal trajectories: early onset OWO; late onset OWO; normal stable; and low stable. Maternal OWO, smoking, and preterm birth were identified as important determinants of the two OWO trajectories. Our predictive models showed that BMIPCT trajectories in early childhood (birth to age 1 or 2 years) were more predictive of childhood OWO (age 5-10 years) than a single BMIPCT at age 1 or 2 years.

Conclusions: Using longitudinal BMIPCT data from birth to age 18 years, this study identified distinct BMIPCT trajectories, examined early life determinants of these trajectories, and demonstrated their advantages in predicting childhood risk of OWO over BMIPCT at a single time point.