Dataset Information

Paternal factors to the offspring birth weight: the 829 birth cohort study.

ABSTRACT:

Objective

To investigate the contributions of parental, especially paternal factors to the offspring birth weight.

Methods

Eligible 829 live-born, singleton children living in Hubei, China were recruited. Birth weight were measured immediately after birth and information about the parents were collected by face-to-face interview using questionnaire. Association between parental factors and birth weight was evaluated using univariate linear regression and multinomial logistic regression models.

Results

Fathers living in the rural area had offspring with higher risk of low birth weight when compared with fathers who live in the capital city. Maternal lower education, lower gestational weight gain, being primipara and shorter gestational age were risk factors for low birth weight. In addition, Mothers with the history of chronic disease had higher risk to deliver a low birth weight baby. On the contrary, women who increased non-staple food consumption during pregnancy had higher risk to have a macrosomic pregnancy. However, lifestyle factors including diet, exercise, screen time, drinking and smoking from both maternal and paternal exhibited little influence on fetal birth weight.

Conclusion

Paternal as well as maternal factors exert influence on the fetal birth weight, although maternal factors make bigger contributions. Compared with socioeconomic and obstetric factors, lifestyle before and during pregnancy has less influence on fetal birth weight, suggested that special attention should be paid to antenatal care for the pregnant women with lower socioeconomic status in rural area.

SUBMITTER: Fan C

PROVIDER: S-EPMC4565335 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature

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Publications

Paternal factors to the offspring birth weight: the 829 birth cohort study.

Fan Cuifang C Huang Tingting T Cui Fangfang F Gao Mengting M Song Lifang L Wang Suqing S

International journal of clinical and experimental medicine 20150715 7

<h4>Objective</h4>To investigate the contributions of parental, especially paternal factors to the offspring birth weight.<h4>Methods</h4>Eligible 829 live-born, singleton children living in Hubei, China were recruited. Birth weight were measured immediately after birth and information about the parents were collected by face-to-face interview using questionnaire. Association between parental factors and birth weight was evaluated using univariate linear regression and multinomial logistic regre ...[more]

PMID: 26379952

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Project description:PurposeWhile it is well documented that maternal adverse exposures contribute to a series defects on offspring health according to the Developmental Origins of Health and Disease (DOHaD) theory, paternal evidence is still insufficient. Advanced paternal age is associated with multiple metabolism and psychiatric disorders. Birth weight is the most direct marker to evaluate fetal growth. Therefore, we designed this study to explore the association between paternal age and birth weight among infants born at term and preterm (<37 weeks gestation).MethodsA large retrospective study was conducted using population-based hospital data from January 2015 to December 2019 that included 69,964 cases of singleton infant births with complete paternal age data. The primary outcome was infant birth weight stratified by sex and gestational age including small for gestational age (SGA, 10th percentile) and large for gestational age (LGA, 90th percentile). Birth weight percentiles by gestational age were based on those published in the INTERGROWTH-21st neonatal weight-for gestational-age standard. Logistic regression analysis and linear regression model were used to estimate the association between paternal age and infant birth weight.ResultsAdvanced paternal age was associated with a higher risk for a preterm birth [35-44 years: adjusted odds ratio (OR) = 1.13, 95%CI (1.03 to 1.24); >44 years: OR = 1.36, 95%CI (1.09 to 1.70)]. Paternal age exerted an opposite effect on birth weight with an increased risk of SGA among preterm infants (35-44years: OR = 1.85, 95%CI (1.18 to 2.89) and a decreased risk among term infant (35-44years: OR = 0.81, 95%CI (0.68 to 0.98); >44 years: OR = 0.50, 95%CI (0.26 to 0.94). U-shaped associations were found in that LGA risk among term infants was higher in both younger (<25 years) (OR = 1.32; 95%CI, 1.07 to 1.62) and older (35-44 years) (OR = 1.07; 95% CI, 1.01 to 1.14) fathers in comparison to those who were 25 to 34 years old at the time of delivery.ConclusionsOur study found advanced paternal age increased the risk of SGA among preterm infants and for LGA among term infants. These findings likely reflect a pathophysiology etiology and have important preconception care implications and suggest the need for antenatal monitoring.

Project description:ObjectiveTo examine the association between paternal antidepressant use at conception and offspring preterm birth, malformations, autism spectrum disorder, and intellectual disability.DesignObservational prospective cohort study with regression methods, and negative control comparison.SettingSweden nationwide.Participants170?508 children conceived from 29 July 2005 and born in 2006-07, followed up to 2014 at age 8-9 years. This cohort included 3983 children born to fathers receiving antidepressant treatment during the conception period (that is, from four weeks before conception to four weeks after), a control group of 164?492 children not exposed to paternal antidepressant use, and a negative control comparison group of 2033 children born to fathers who did not use antidepressants during the conception period but began antidepressant treatment later during the pregnancy period (that is, from four weeks after conception to childbirth).Main outcome measureOffspring preterm birth, malformation diagnosed at birth, diagnosis of autism spectrum disorder, and diagnosis of intellectual disability.ResultsPaternal antidepressant use during conception was not associated with preterm birth (adjusted odds ratio 0.91 (95% confidence interval 0.79 to 1.04)) or malformations (1.06 (0.90 to 1.26)) using logistic regression, compared with offspring born to unexposed fathers. No association was seen between antidepressant use during conception and autism (adjusted hazard ratio 1.13 (0.84 to 1.53)) or intellectual disability (0.82 (0.51 to 1.31)) using Cox regression. In children whose fathers initiated antidepressant treatment during pregnancy, results were similar for all outcomes apart from intellectual disability, which had an increased adjusted hazard ratio (1.66 (1.06 to 2.59)). Compared with the 2033 children whose fathers initiated antidepressant treatment during pregnancy, the 3983 children exposed to paternal use of antidepressants at conception had no differences in preterm birth, malformation, and autism, but a reduced risk of intellectual disability (adjusted hazard ratio 0.49 (0.26 to 0.93)).ConclusionPaternal intake of antidepressants during the period around conception is safe with respect to the risk of the four major adverse outcomes in offspring-preterm birth, malformation, autism, or intellectual disability.

Project description:Background Low birth weight (LBW) and fetal growth restriction are associated with the development of cardio-metabolic diseases later in life. A recent Mendelian randomization study concluded that the susceptibility of LBW infants to develop hypertension during adulthood is due to the inheritance of hypertension genes from the mother and not to an unfavorable intrauterine environment. Therein, a negative linear association has been assumed between genetically estimated maternal blood pressure (BP) and birth weight, while the observed relationship between maternal BP and birth weight is substantially different from that assumption. As many hypertension genes are likely involved in vasculature development and function, we hypothesized that BP-increasing genetic variants could affect birth weight by reducing the growth of the placenta, a highly vascular organ, without overtly elevating the maternal BP. Methods Using a birth cohort in the Japanese population possessing time-series fetal growth velocity data as a target and a GWAS summary statistics of BioBank Japan as a base data, we performed polygenic score (PGS) analyses for systolic BP (SBP), diastolic BP, mean arterial pressure, and pulse pressure. A causal mediation analysis was performed to assess the meditation effect of placental weight on birth weight reduced by maternal BP-increasing PGS. Maternal genetic risk score constituted of only “vasculature-related” BP single nucleotide polymorphisms (SNPs) was constructed to examine the involvement of vascular genes in the mediation effect of placental weight. We identified gestational week in which maternal SBP-increasing PGS significantly decreased fetal growth velocity. Results We observed that maternal SBP-increasing PGS was negatively associated with offspring birth weight. A causal mediation analysis revealed that a large proportion of the total maternal PGS effect on birth weight was mediated by placental weight. The placental mediation effect was remarkable when genetic risk score was constituted of “vasculature-related” BP SNPs. The inverse association between maternal SBP PGS and fetal growth velocity only became apparent in late gestation. Conclusions Our study suggests that maternal hypertension genes are strongly associated with placental growth and that fetal growth inhibition is induced through the intrauterine environment established by the placenta. Supplementary Information The online version contains supplementary material available at 10.1186/s12916-021-02131-0.

Dataset Information

Paternal factors to the offspring birth weight: the 829 birth cohort study.

Objective

Methods

Results

Conclusion

Publications

Paternal factors to the offspring birth weight: the 829 birth cohort study.

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