Parental pre-pregnancy BMI is a dominant early-life risk factor influencing BMI of offspring in adulthood.
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ABSTRACT: Objective
We examined parental and early-life variables in order to identify risk factors for adulthood overweight and obesity in offspring. We report here on the longitudinal prevalence of overweight and obesity in Australian children born between 1989 and 1991 and followed from birth to age 22.Methods
Data were analysed on 1355 participants from the Western Australian Pregnancy Cohort (Raine) Study, with anthropometry collected during pregnancy, at birth, one year and at three yearly intervals thereafter. Multivariate analyses and cross-sectional logistic regression quantified the timing and contribution of early-life risk factors for overweight and obesity in young-adulthood.Results
At five years of age 12.6% of children were overweight and 5.2% were obese. By early adulthood, the prevalence of obesity had increased to 12.8%, whilst overweight remained relatively stable at 14.2% (range from early childhood to adulthood 11-16%). Parental pre-pregnancy body mass index (BMI) was the strongest determinant of adult offspring BMI. Although rapid first year weight gain was associated with increased offspring BMI, the impact of first year weight-gain diminished over childhood, whilst the impact of parental BMI increased over time.Conclusions
Parental pre-pregnancy BMI and rapid early-life weight gain predispose offspring to obesity in adulthood.
SUBMITTER: Rath SR
PROVIDER: S-EPMC5067549 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:AimsA growing body of evidence suggests that a higher maternal pre-pregnancy body mass index results in higher offspring's blood pressure, but there is inconsistency about the impact of father's body mass index. Furthermore, evidence is limited with regard to low and middle income countries. We aimed to determine the association between parental pre-pregnancy body mass index and offspring's blood pressure during the first year of life.MethodsIn 587 infants of the BReastfeeding Attitude and Volume Optimization (BRAVO) trial systolic and diastolic blood pressure were measured twice at the right leg in a supine position, using an automatic oscillometric device at day 7, month 1, 2, 4, 6, 9 and 12. Parental pre-pregnancy body mass index was based on self-reported weight and height. Linear mixed models were performed to investigate the associations between parental pre-pregnancy body mass index and offspring blood pressure patterns.ResultsEach unit increase in maternal body mass index was associated with 0.24 mmHg (95% confidence interval 0.05; 0.44) and 0.13 mmHg (0.01; 0.25) higher offspring's mean systolic and diastolic blood pressure, respectively, during the first year of life. A higher offspring blood pressure with increased maternal pre-pregnancy body mass index was seen at birth and remained higher during the first year of life. The association with systolic blood pressure remained similar after including birth size and offspring's weight and height over time. The association with diastolic blood pressure attenuated slightly to a non-significant result after including these variables. Paternal body mass index was not associated with offspring's blood pressure.ConclusionHigher maternal pre-pregnancy body mass index, but not paternal pre-pregnancy body mass index, is associated with higher offspring blood pressure already from birth onwards.
| S-EPMC6753651 | biostudies-literature
Project description:ObjectiveTo investigate the association between maternal pre-pregnancy BMI and offspring body composition in adulthood.DesignRetrospective cohort. Undergraduates of nutrition or nutritionists were recruited at the baseline of the Nutritionists' Health Study between 2014 and 2017. Maternal pre-pregnancy BMI and current life aspects were self-reported through online questionnaires. Three body compartments were dual-energy x-ray absorptiometry-determined. The following variables were obtained: body fat (%), fat mass index (FMI) (kg/m2), android-to-gynoid fat ratio, visceral adipose tissue (VAT) (cm3), appendicular skeletal muscle mass index (ASMI) (kg/m2), total bone and femur mineral content (g) and density (g/cm2). Linear regression adjusted according to directed acyclic graphs recommendation was performed.SettingSão Paulo, Brazil.ParticipantsHealthy non-pregnant women (aged 20-45 years) (n 150).ResultsMedian age and BMI were 22 years (IQR = 20, 29) and 22·3 kg/m2 (IQR = 20·4, 25·3), respectively. Pre-pregnancy BMI ≥ 25 kg/m2 was reported by 14·7 % of mothers. In fully adjusted models, maternal pre-pregnancy BMI was associated with their daughters' body fat % (β = 0·31; 95 % CI 0·0004, 0·63), FMI (β = 0·17; 95 % CI 0·03, 0·30), android-to-gynoid ratio (β = 0·01; 95 % CI 0·004, 0·02) and VAT (β = 0·09; 95 % CI 0·02, 0·16), but not with total bone density (β = 0·001; 95 % CI -0·003, 0·006) and content (β = 7·13; 95 % CI -4·19, 18·46). Direct association with ASMI was also detected, but lost statistical significance when participants whose mothers were underweight were excluded.ConclusionsMaternal pre-pregnancy BMI was directly associated with offspring general and visceral adiposity but seems not to be associated with bone mass. Results reinforce importance of avoiding excess of maternal adiposity, as an attempt to break the vicious cycle of obesity transmission.
| S-EPMC10195459 | biostudies-literature
Project description:Congenital heart diseases (CHDs) are the most common congenital anomaly. The causes of CHDs are largely unknown. Higher prenatal body mass index (BMI), smoking and alcohol consumption are associated with increased risk of CHDs. Whether these are causal is unclear. Seven European birth cohorts including 232,390 offspring (2,469 CHD cases [1.1%]) were included. We applied negative exposure paternal control analyses to explore the intrauterine effects of maternal BMI, smoking and alcohol consumption during pregnancy, on offspring CHDs and CHD severity. We used logistic regression and combined estimates using a fixed-effects meta-analysis. Analyses of BMI categories resulted in similar increased odds of CHD in overweight (mothers OR: 1.15 (1.01, 1.31) and fathers 1.10 (0.96, 1.27)) and obesity (mothers OR: 1.12 (0.93, 1.36) and fathers 1.16 (0.90, 1.50)). The association of mean BMI with CHD was null. Maternal smoking was associated with increased odds of CHD (OR: 1.11 (0.97, 1.25)) but paternal smoking was not (OR: 0.96 (0.85, 1.07)). The difference increased when removing offspring with genetic/chromosomal defects (mothers OR: 1.15 (1.01, 1.32) and fathers 0.93 (0.83, 1.05)). The positive association with maternal pregnancy smoking appeared to be driven by non-severe CHD cases (OR: 1.22 (1.04, 1.44)). Associations with maternal (OR: 1.16 (0.52, 2.58)) and paternal (OR: 1.23 (0.74, 2.06)) moderate/heavy pregnancy alcohol consumption were similar. We found evidence of an intrauterine effect for maternal smoking on offspring CHDs, but no evidence for higher maternal BMI or alcohol consumption. Our findings provide further support for why smoking cessation is important during pregnancy.
| S-EPMC7654878 | biostudies-literature
Project description:Intrauterine modifiable maternal metabolic factors are essential to the early growth of offspring. The study sought to evaluate the associations of pre-pregnancy BMI and third-trimester fasting plasma glucose (FPG) with offspring growth outcomes within 24 months among GDM-negative pregnant women. Four hundred eighty-three mother -offspring dyads were included from the Shanghai Maternal-Child Pairs Cohort. The pregnant women were categorized into four mutually exclusive groups according to pre-pregnancy BMI as normal or overweight/obesity and third-trimester FPG as controlled or not controlled. Offspring growth in early life was indicated by the BAZ (BMI Z-score), catch-up growth, and overweight/obesity. Among those with controlled third-trimester FPG, pre-pregnancy overweight/obesity significantly increased offspring birth weight, BAZ, and risks of overweight/obesity (RR 1.83, 95% CI 1.23 to 2.73) within 24 months. Those who had uncontrolled third-trimester FPG had a reduced risk of offspring overweight/obesity within 24 months by 47%. The combination of pre-pregnancy overweight/obesity and maternal uncontrolled third-trimester FPG increased 5.24-fold risk of offspring catch-up growth within 24 months (p < 0.05). Maternal pre-pregnancy overweight/obesity and uncontrolled third-trimester glycemia among GDM-negative women both have adverse effects on offspring growth within 24 months. With the combination of increasing pre-pregnancy BMI and maternal third-trimester FPG, the possibility of offspring catch-up growth increases.
| S-EPMC8619788 | biostudies-literature
Project description:We examine the influences of a set of early life conditions (ELCs) on all-cause and cause-specific mortality among elderly individuals, with special attention to one of the most dramatic early events in a child's, adolescent's, or even young adult's life, the death of a parent. The foremost question is, once controlling for prevailing (and potentially confounding) conditions early in life (family history of longevity, paternal characteristics (SES, age at time of birth, sibship size, and religious affiliation)), is a parental death associated with enduring mortality risks after age 65? The years following parental death may initiate new circumstances through which the adverse effects of paternal death operate. Here we consider the offspring's marital status (whether married; whether and when widowed), adult socioeconomic status, fertility, and later life health status. Adult health status is based on the Charlson Co-Morbidity Index, a construct that summarizes nearly all serious illnesses afflicting older individuals that relies on Medicare data. The data are based on linkages between the Utah Population Database and Medicare claims that hold medical diagnoses data. We show that offspring whose parents died when they were children, but especially when they were adolescents/young adults, have modest but significant mortality risks after age 65. What are striking are the weak mediating influences of later-life comorbidities, marital status, fertility and adult socioeconomic status since controls for these do little to alter the overall association. No beneficial effects of the surviving parent's remarriage were detected. Overall, we show the persistence of the effects of early life loss on later-life mortality and indicate the difficulties in addressing challenges at young ages.
| S-EPMC4087105 | biostudies-literature
Project description:AIM:The objective of this study was to identify potential epigenetic mediating pathways linking early life social disadvantage (ELSD) to adulthood BMI. METHODS:Sex-specific epigenome-wide two-stage mediation analyses were conducted in blood and adipose tissue, and mediation estimates were obtained using cross-product mediation analysis. Pathway analyses were conducted using GREAT software (Bejerano Lab, CA, USA). RESULTS:Candidate mediation CpG sites were identified in adipose tissue, but not blood, and were sex-specific. Significant mediation sites in females included CpG loci in genes: PKHG1, BCAR3, ADAM5P, PIEZO1, FGFRL1, FASN and DPP9, among others. Pathway analyses revealed evidence of enrichment for processes associated with TFG-? signaling and immunologic signatures. In males, significant mediation loci included sites in MAP3K5 and RPTOR, which have previously been associated with adipogenesis, inflammation and insulin resistance. CONCLUSION:Our findings provide supportive evidence for the mediating role of epigenetic mechanisms in the effect of early life social disadvantage on adulthood BMI.
| S-EPMC6367732 | biostudies-literature
Project description:Infant feeding practices have been hypothesized to influence offspring's body mass index (BMI) later in life, and women with overweight or obesity tend to wean their infants earlier than women with healthy BMI. We, therefore, aimed to investigate how much early age of weaning mediated the maternal-offspring adiposity relationship. The study included 4920 mother-child pairs from the Avon Longitudinal Study of Parents and Children birth cohort. G-computation was applied to estimate the natural direct (NDE) and indirect (NIE) effects, via the age of weaning (<3 months, 3 months, >3 months), of maternal pre-pregnancy overweight or obesity on offspring's BMI and fat mass index. The NDE of maternal overweight or obesity on offspring BMI at 17 years old was 2.63 kg/m2 (95% CI: 2.27 to 2.99). The NIE via the age of weaning was 0.02 kg/m2 (95% CI: 0.00 to 0.04), corresponding to 0.8% of the total effect. Similar results were observed for the offspring's fat mass index. The NDE and NIE were similar to the main analyses when we looked at the relationship stratified by breastfeeding status. Our study found a minimal influence of age of weaning on the pathway between maternal and offspring adiposity, indicating the age of weaning may not be a key mediator.
| S-EPMC10343873 | biostudies-literature
Project description:BackgroundThe importance of the maternal-infant dyad in the genesis of nonalcoholic fatty liver disease (NAFLD) is of increasing interest. The Avon Longitudinal Study of Parents and Children (ALSPAC) showed that at age 24, 1 in 5 had NAFLD measured by transient elastography and controlled attenuation parameter (CAP). Our aim was to investigate the association between breastfeeding duration and maternal pre-pregnancy BMI on offspring NAFLD in young adulthood.Methods4021 participants attended clinic for FibroScan and CAP measurement using Echosens 502 Touch®. 440 participants with Alcohol Use Disorders were excluded. Offspring of 100 non-singleton pregnancies were excluded. 2961 valid CAP measurements for NAFLD were analysed. Exposures of interest were breastfeeding of any duration, ≥6months exclusive breastfeeding, and maternal pre-pregnancy BMI. Multivariable regression models estimated the odds of NAFLD at 24 years. We performed a paternal negative control test to explore residual confounding in the analyses of pre-pregnancy BMI.FindingsThere was a modest inverse association of exclusive and non-exclusive breastfeeding ≥6 months having a protective effect on NAFLD in offspring (OR 0·92 [95%CI 0·66-1·27] and OR 0·90 [0·67-1·21] respectively).The odds of offspring NAFLD in overweight pre-pregnancy maternal BMI and paternal BMI was OR 2·09 [1·62-2·68] and OR 1·33 [95%CI 1·07-1·65] respectively, with the ratio of effect sizes OR 1·57 [1·11-2·22]. Similarly, odds of offspring NAFLD with obese pre-pregnancy maternal BMI and paternal BMI was OR 2·66 [1·71-4·14] and OR 1·35 [0·91-2·00] respectively, with the ratio of effect sizes OR 1·98 [1·05-3·74].InterpretationHigher maternal pre-pregnancy BMI was associated with offspring NAFLD, having accounted for shared parental confounding. We did not replicate previous work that found a strong association between breastfeeding and NAFLD.FundingMedical Research Council UK, Alcohol Research UK, David Telling Charitable Trust.
| S-EPMC8589711 | biostudies-literature
Project description:BackgroundMaternal pre-pregnancy obesity is an established risk factor for childhood obesity. Investigating epigenetic alterations induced by maternal obesity during fetal development could gain mechanistic insight into the developmental origins of childhood obesity. While obesity disproportionately affects underrepresented racial and ethnic mothers and children in the USA, few studies investigated the role of prenatal epigenetic programming in intergenerational obesity of these high-risk populations.MethodsThis study included 903 mother-child pairs from the Boston Birth Cohort, a predominantly urban, low-income minority birth cohort. Mother-infant dyads were enrolled at birth and the children were followed prospectively to age 18 years. Infinium Methylation EPIC BeadChip was used to measure epigenome-wide methylation level of cord blood. We performed an epigenome-wide association study of maternal pre-pregnancy body mass index (BMI) and cord blood DNA methylation (DNAm). To quantify the degree to which cord blood DNAm mediates the maternal BMI-childhood obesity, we further investigated whether maternal BMI-associated DNAm sites impact birthweight or childhood overweight or obesity (OWO) from age 1 to age 18 and performed corresponding mediation analyses.ResultsThe study sample contained 52.8% maternal pre-pregnancy OWO and 63.2% offspring OWO at age 1-18 years. Maternal BMI was associated with cord blood DNAm at 8 CpG sites (genome-wide false discovery rate [FDR] < 0.05). After accounting for the possible interplay of maternal BMI and smoking, 481 CpG sites were discovered for association with maternal BMI. Among them 123 CpGs were associated with childhood OWO, ranging from 42% decrease to 87% increase in OWO risk for each SD increase in DNAm. A total of 14 identified CpG sites showed a significant mediation effect on the maternal BMI-child OWO association (FDR < 0.05), with mediating proportion ranging from 3.99% to 25.21%. Several of these 14 CpGs were mapped to genes in association with energy balance and metabolism (AKAP7) and adulthood metabolic syndrome (CAMK2B).ConclusionsThis prospective birth cohort study in a high-risk yet understudied US population found that maternal pre-pregnancy OWO significantly altered DNAm in newborn cord blood and provided suggestive evidence of epigenetic involvement in the intergenerational risk of obesity.
| S-EPMC10463574 | biostudies-literature
Project description:The article aims to describe the association between midlife body mass index (BMI) and cardiovascular disease (CVD)- and all-cause mortality, and to use early adulthood BMI as an instrumental variable for midlife BMI, in order to obtain an estimate less distorted by midlife confounders and reverse causality. Data from Norwegian health surveys (1974-2003) (midlife BMI, smoking, blood pressure, total cholesterol, heart rate), Military Conscription Records, National Tuberculosis Screenings (early adulthood BMI), National Educational Registry and Cause of Death Registry were linked. Participants with data on BMI in early adulthood and midlife were included (n?=?148.886). Hazard Ratio (HR) for CVD mortality was higher in men with midlife obesity relative to normal weight (HR?=?1.46(95% CI 1.25, 1.70). For all-cause mortality, HR was higher in those with obesity or underweight in midlife relative to normal weight (Men:HR?=?1.19(95% CI 1.09, 1.29), HR?=?2.49(95% CI 1.81, 3.43) Women:HR?=?1.33(95% CI 1.13, 1.56), HR?=?1.61(95% CI 1.22, 2.13)). In instrumental variable analyses, increased BMI became more strongly associated with CVD and all-cause mortality, and the increased risk of all-cause mortality among the underweight attenuated.
| S-EPMC6068135 | biostudies-other