Precision nutrition最新文献

Background: Understanding of maternal and fetal factors affecting leptin, adiponectin and adiponectin: leptin ratio at birth, may provide valuable insights into potential future risk of metabolic alterations and inform primordial prevention and precision nutrition strategies.

Objective: To identify maternal and fetal risk factors that affect leptin and adiponectin levels (markers of adiposity) and adiponectin/leptin ratio (a marker of dysfunctional adipose tissue) at birth.

Methods: We studied mother-infant pairs in the Boston Birth Cohort. Cord blood was collected at birth. We used student t-tests to compare log normalized cord leptin and adiponectin levels. Regression analysis were performed to examine the association of maternal and fetal factors with leptin and adiponectin levels and adiponectin: leptin ratio at birth in both term and preterm infants.

Results: We analyzed 1012 infants (245 preterm). Both cord leptin and adiponectin were higher in term infants than preterm infants (10.2 ± 0.9 vs. 9.2 ± 1.3, p < 0.0001 and 9.5 ± 0.7 vs. 8.9 ± 0.8, p < 0.0001 respectively). Cord leptin was higher for Black infants (10.1 ± 1.1 vs. 9.9 ± 1.2; p < 0.001) although Black (ref: non Black) infants had lower cord adiponectin levels (9.3 ± 0.8 vs. 9.5 ± 0.7; p = 0.01). Ratio of adiponectin to leptin (log normalized) was higher in preterm infants (-0.24) vs. term infants (-0.69). On regression analysis cord leptin was positively associated with longer gestational age, birth weight z score, Black race, maternal overweight and obesity, gestational diabetes and pregestational diabetes mellitus and negatively associated with male sex. Cord adiponectin was positively associated with gestational age, birth weight z score and negatively with Black race and male sex. Adiponectin: leptin ratio was positively with male sex and negatively with GA, birth wt. z score, Black race, gestational DM, pregestational DM and maternal overweight and obesity.

Conclusion: We identified several factors that affect leptin and adiponectin levels along with adiponectin-leptin ratio at birth beyond GA and birth weight which could also play an important role in influencing the trajectory of these hormones and future cardio metabolic outcomes. This knowledge can help tailor precision nutrition interventions.

In 1998, the Boston Birth Cohort (BBC) was initiated at Boston Medical Center (BMC) in response to persistently high rates of preterm birth (PTB, defined as birth before 37 weeks of gestation) in the US population and the longstanding profound PTB disparity among Black, Indigenous, and people of color (BIPOC). The BBC encompasses two linked study protocols: The Preterm Birth Study serves as the baseline recruitment in the BBC. It aims to address fundamental questions about the causes and consequences of PTB. The study oversamples preterm babies using a case/control study design, in which cases are defined as mothers who deliver a preterm and/or low birthweight baby (<2500 grams regardless of gestational age). Controls are enrolled at a 2:1 control/case ratio and matched by maternal age (±5 years), self-reported race and ethnicity, and date of delivery (± 7 days for case delivery). From inception, it was designed as a comprehensive gene-environmental study of PTB. As a natural extension, the Children's Health Study, under a separate but linked IRB protocol, is a longitudinal follow-up study of the participants who were recruited at birth in the Preterm Birth Study and who continue pediatric care at BMC. This linked model allows for investigation of early life origins of pediatric and chronic disease in a prospective cohort design. The BBC is one of the largest and longest NIH-funded prospective birth cohort studies in the US, consisting of 8733 mother-child dyads enrolled in the Preterm Birth Study at birth, and of those, 3,592 children have been enrolled in the Children's Health Study, with a median follow-up of 14.5 years. The BBC mirrors the urban, under-resourced and underrepresented BIPOC population served by BMC. A high proportion of BBC children were born prematurely and had chronic health conditions (e.g., asthma, obesity and elevated blood pressure) in childhood. The BBC's long-term goal has been to build a large, comprehensive database (epidemiological, clinical, multi-omics) and biospecimen repository to elucidate early life origins of pediatric and chronic diseases and identify modifiable upstream factors (e.g., psychosocial, environmental, nutritional) to improve health across the life course for BIPOC mothers and children.

In1998, the Boston Birth Cohort (BBC) was initiated at Boston Medical Center (BMC) in response to persistently high rates of preterm birth (PTB, defined as birth before 37 weeks of gestation) in the US population and the longstanding profound PTB disparity among Black, Indigenous, and people of color (BIPOC). The BBC encompasses two linked study protocols: The PTB Study serves as the baseline recruitment in the BBC. It aims to address fundamental questions about the causes and consequences of PTB. The study oversamples preterm babies using a case/control study design, in which cases are defined as mothers who deliver a preterm and/or low birthweight baby (<2500 grams regardless of gestational age). Controls are enrolled at a 2:1 control/case ratio and matched by maternal age (±5 years), self-reported race and ethnicity, and date of delivery (± 7 days for case delivery). From inception, it was designed as a comprehensive gene-environmental study of PTB. As a natural extension, the Children's Health Study, under a separate but linked Institutional Review Board protocol, is a longitudinal follow-up study of the participants who were recruited at birth in the PTB Study and who continue pediatric care at BMC. This linked model allows for investigation of early life origins of pediatric and chronic disease in a prospective cohort design. The BBC is one of the largest and longest National Institutes of Health-funded prospective birth cohort studies in the United States, consisting of 8733 mother-child dyads enrolled in the PTB Study at birth, and of those, 3592 children have been enrolled in the Children's Health Study, with a median follow-up of 14.5 years. The BBC mirrors the urban, underresourced, and underrepresented BIPOC population served by BMC. A high proportion of BBC children were born prematurely and had chronic health conditions (e.g., asthma, obesity, and elevated blood pressure) in childhood. The BBC's long-term goal has been to build a large, comprehensive database (epidemiological, clinical, and multiomics) and biospecimen repository to elucidate early life origins of pediatric and chronic diseases and identify modifiable upstream factors (e.g., psychosocial, environmental, and nutritional) to improve health across the life course for BIPOC mothers and children.

Background: Understanding of maternal and fetal factors affecting leptin, adiponectin, and adiponectin:leptin ratio at birth may provide valuable insights into potential future risk of metabolic alterations and inform primordial prevention and precision nutrition strategies. The objective of this study is to identify maternal and fetal risk factors that affect leptin and adiponectin levels (markers of adiposity) and adiponectin/leptin ratio (a marker of dysfunctional adipose tissue) at birth.

Methods: We studied mother-infant pairs in the Boston Birth Cohort. Cord blood was collected at birth. We used student t- tests to compare log normalized cord leptin and adiponectin levels. Regression analysis was performed to examine the association of maternal and fetal factors with leptin and adiponectin levels and adiponectin:leptin ratio at birth in both term and preterm infants.

Results: We analyzed 1012 infants (245 preterm). Both cord leptin and adiponectin were higher in term infants than preterm infants (10.2 ± 0.9 vs. 9.2 ± 1.3, P < 0.0001 and 9.5 ± 0.7 vs. 8.9 ± 0.8, P < 0.0001, respectively). Cord leptin was higher for Black infants (10.1 ± 1.1 vs. 9.9 ± 1.2; P < 0.001) although Black (ref: non-Black) infants had lower cord adiponectin levels (9.3 ± 0.8 vs. 9.5 ± 0.7; P = 0.01). Ratio of adiponectin to leptin (log normalized) was higher in preterm infants (-0.24) vs. term infants (-0.69). On regression analysis, cord leptin was positively associated with longer gestational age (GA), birth weight z score, Black race, maternal overweight and obesity, gestational diabetes and pregestational diabetes mellitus and negatively associated with male sex. Cord adiponectin was positively associated with GA, birth weight z score and negatively with Black race and male sex. Adiponectin:leptin ratio was positively with male sex and negatively with GA, birth weight z score, Black race, gestational DM, pregestational DM and maternal overweight and obesity.

Conclusions: We identified several factors that affect leptin and adiponectin levels along with adiponectin-leptin ratio at birth beyond GA and birth weight which could also play an important role in influencing the trajectory of these hormones and future cardiometabolic outcomes. This knowledge can help tailor precision nutrition interventions.

Background: Per- and polyfluoroalkyl substances (PFAS) are a major public health concern worldwide due to their ubiquitous exposures, environmental persistence, maternal-to-fetal transfer, and multi-organ toxicity. This pilot study aimed to generate preliminary data to inform future studies to address data gaps in the field, including early life PFAS exposure levels, longitudinal changes, determinants, and associated metabolomic alterations in understudied Black and Hispanic children in the United States (U.S.).

Methods: This study leveraged existing biosamples and data in the Boston Birth Cohort and measured 12 legacy and emerging PFAS, including Me-PFOSA-AcOH, PFDA, PFDoA, PFHxS, PFNA, PFOA, PFOS, PFUnA, GenX, ADONA, 9Cl-PF3ONS, and PFHpS, in paired cord and early childhood plasma samples. Summary statistics and graphic plots were used to depict PFAS levels at the two time points and their longitudinal changes. Linear regression models were used to identify the early-life factors associated with cord and early childhood PFAS levels. Associations of cord PFAS with cord metabolites were explored using a metabolome-wide association approach and a targeted approach.

Results: This study included 39 children, of whom 25 (64%) were Black, 14 (36%) were Hispanic, and 15 (38%) were female. PFOA, PFOS, PFNA, and PFHpS were detectable in all cord and early childhood plasma samples, while GenX and ADONA were not detectable in any sample. Cord PFAS levels were weakly-to-moderately correlated with early childhood PFAS levels (r = -0.03 to 0.40). Several maternal and child factors, including gestational age, year at blood collection, and race/ethnicity, were associated with cord and early childhood PFAS levels. The metabolome-wide association study and the targeted study identified several cord metabolites that may have been affected by in utero PFAS exposure.

Conclusions: This pilot study found ubiquitous exposure to multiple PFAS in cord plasma (reflects in utero exposure) and in early childhood plasma (reflects both prenatal and postnatal exposure) among U.S. Black and Hispanic children. Metabolomic analysis suggests that in utero PFAS exposures may alter fetal metabolism. Future large-scale studies are needed to replicate the findings and further examine the associations of fetal PFAS exposure with long-term health outcomes and underlying metabolic pathways.