Associations between Paternal Anxiety and Infant Weight Gain.
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ABSTRACT:
SUBMITTER: Nawa N
PROVIDER: S-EPMC8618665 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:PurposeSome mental illnesses have been suggested to be associated with obesity, although results are somewhat inconsistent and research has focused mainly on depression.MethodsAssociations between anxiety, depression, medications for these illnesses, and obesity were investigated cross-sectionally among women aged 25-74 (n = 3004) who participated as population controls in a cancer case-control study. Participants self-reported information on anxiety, depression, height, current weight and weight at age 25.ResultsNo association was observed between either anxiety or depression and either current overweight or obesity status. However, depressed women taking antidepressants were more likely to be obese [OR = 1.71 (95%CI ?=? 1.16-2.52) daily antidepressant use; OR = 1.89 (95% CI = 1.21-2.96) ever tricyclic antidepressant use]. In the full study sample consistent positive associations between anxiety, depression and obesity among women with a history of antidepressant use, and generally negative associations among women without, were suggested. Finally, weight gain was associated with history of anxiety [5-19 kg OR = 1.29 (95% CI = 1.06-1.57); ? 20 kg OR = 1.43 (95% CI = 1.08-1.88)] and depression [? 20 kg OR = 1.28 (95% CI = 0.99-1.65)].ConclusionsThese results suggest depression and anxiety may be associated with weight gain and antidepressant use may be associated with obesity.
| S-EPMC4059657 | biostudies-literature
Project description:ObjectiveInfant growth trajectories, in terms of size, tempo and velocity, may programme lifelong obesity risk. Timing of breastfeeding cessation and weaning are both implicated in rapid infant growth; we examined the association of both simultaneously with a range of growth parameters.DesignLongitudinal population-based twin birth cohort.SubjectsThe Gemini cohort provided data on 4680 UK infants with a median of 10 (interquartile range=8-15) weight measurements between birth and a median of 6.5 months. Age at breastfeeding cessation and weaning were reported by parents at mean age 8.2 months (s.d.=2.2, range=4-20). Growth trajectories were modelled using SuperImposition by Translation And Rotation (SITAR) to generate three descriptors of individual growth relative to the average trajectory: size (grams), tempo (weeks, indicating the timing of the peak growth rate) and velocity (% difference from average, reflecting mean growth rate). Complex-samples general linear models adjusting for family clustering and confounders examined associations between infant feeding and SITAR parameters.ResultsLonger breastfeeding (>4 months vs never) was independently associated with lower growth velocity by 6.8% (s.e.=1.3%) and delayed growth tempo by 1.0 (s.e.=0.2 weeks), but not with smaller size. Later weaning (⩾6 months vs <4 months) was independently associated with lower growth velocity by 4.9% (s.e.=1.1%) and smaller size by 102 g (s.e.=25 g).ConclusionsInfants breastfed for longer grew slower for longer after birth (later peak growth rate) but were no different in size, while infants weaned later grew slower overall and were smaller but the timing of peak growth did not differ. Slower trajectories with a delayed peak in growth may have beneficial implications for programming later obesity risk. Replication in cohorts with longer follow-up, alternative confounding structures or randomised controlled trials are required to confirm the long-term effects and directionality, and to rule out residual confounding.
| S-EPMC4088337 | biostudies-literature
Project description:Background:Excessive gestational weight gain and rapid infancy weight gain (RIWG) are associated with increased susceptibility to childhood obesity. Since low-income and minority children are particularly at risk, investigation of the associations between gestational weight gain and rate of infancy weight gain may inform childhood obesity prevention. This study investigated the associations between gestational weight gain and rate of infancy weight gain during the first four to six months postpartum in participants from the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) in Hawai'i and Puerto Rico. Methods:This was a cross-sectional secondary data analysis from a text message-based intervention in WIC participants in Hawai'i and Puerto Rico. The analysis included 80 mother/infant pairs from the control group who completed the follow-up visit when infants were four to six months old. Maternal weight, height, and gestational weight gain were self-reported. Infant weight was measured at baseline and follow-up. A proportional odds model was used to investigate the association between gestational weight gain and infancy weight gain rate (rapid or extremely rapid, on-track, or slow), adjusting for maternal age, pregravid body mass index (BMI) status, parity, and being up-to-date with infant vaccinations. Results:In comparison to recommended gestational weight gain, excessive and inadequate (under the recommended amount) gestational weight gain was associated with 77% decreased (adjusted odds ratio [AOR]?=?0.23; 95% confidence interval [CI]?=?0.08, 0.70; p?=?0.01) and 71% decreased (AOR?=?0.29; 95% CI?=?0.09, 0.94; p?=?0.04) odds of RIWG versus on-track or slow infant weight gain, respectively. In comparison to women with one child, women with two children (AOR?=?0.31; 95% CI?=?0.11, 0.87; p?=?0.03) or three or four children (AOR?=?0.24; 95% CI?=?0.07, 0.88; p?=?0.03) had significantly lower odds of RIWG versus on-track or slow infancy weight gain. Conclusions:Women with excessive or inadequate gestational weight gain had lower proportional odds of RIWG and were more likely to have slower infant weight gain than women who gained the recommended amount of weight. Trial registration:ClinicalTrials.gov Identifier; NCT02903186; September 16, 2016.
| S-EPMC6276143 | biostudies-literature
Project description:Prenatal air pollution exposure inhibits fetal growth, but implications for postnatal growth are unknown.We assessed weights and lengths of US infants in the Project Viva cohort at birth and 6 months. We estimated 3rd-trimester residential air pollution exposures using spatiotemporal models. We estimated neighborhood traffic density and roadway proximity at birth address using geographic information systems. We performed linear and logistic regression adjusted for sociodemographic variables, fetal growth, and gestational age at birth.Mean birth weight-for-gestational age z-score (fetal growth) was 0.17 (standard deviation [SD] = 0.97; n = 2,114), 0- to 6-month weight-for-length gain was 0.23 z-units (SD = 1.11; n = 689), and 17% had weight-for-length ?95th percentile at 6 months of age. Infants exposed to the highest (vs. lowest) quartile of neighborhood traffic density had lower fetal growth (-0.13 units [95% confidence interval (CI) = -0.25 to -0.01]), more rapid 0- to 6-month weight-for-length gain (0.25 units [95% CI = 0.01 to 0.49]), and higher odds of weight-for-length ?95th percentile at 6 months (1.84 [95% CI = 1.11 to 3.05]). Neighborhood traffic density was additionally associated with an infant being in both the lowest quartile of fetal growth and the highest quartile of 0- to 6-month weight-for-length gain (Q4 vs. Q1, odds ratio = 3.01 [95% CI = 1.08 to 8.44]). Roadway proximity and 3rd-trimester black carbon exposure were similarly associated with growth outcomes. For 3rd-trimester particulate matter (PM2.5), effect estimates were in the same direction, but smaller and imprecise.Infants exposed to higher traffic-related pollution in early life may exhibit more rapid postnatal weight gain in addition to reduced fetal growth.
| S-EPMC4285344 | biostudies-literature
Project description:Given the unpredictable rapid onset and ubiquitous consequences of weight gain induced by antipsychotics, there is a pressing need to get insights into the underlying processes at the brain system level that will allow stratification of "at risk" patients. The pathophysiological hypothesis at hand is focused on brain networks governing impulsivity that are modulated by neuro-inflammatory processes. To this aim, we investigated brain anatomy and functional connectivity in patients with early psychosis (median age: 23 years, IQR = 21-27) using anthropometric data and magnetic resonance imaging acquired one month to one year after initiation of AP medication. Our analyses included 19 patients with high and rapid weight gain (i.e., ≥5% from baseline weight after one month) and 23 patients with low weight gain (i.e., <5% from baseline weight after one month). We replicated our analyses in young (26 years, IQR = 22-33, N = 102) and middle-aged (56 years, IQR = 51-62, N = 875) healthy individuals from the general population. In early psychosis patients, higher weight gain was associated with poor impulse control score (β = 1.35; P = 0.03). Here, the observed brain differences comprised nodes of impulsivity networks - reduced frontal lobe grey matter volume (Pcorrected = 0.007) and higher striatal volume (Pcorrected = 0.048) paralleled by disruption of fronto-striatal functional connectivity (R = -0.32; P = 0.04). Weight gain was associated with the inflammatory biomarker plasminogen activator inhibitor-1 (β = 4.9, P = 0.002). There was no significant association between increased BMI or weight gain and brain anatomy characteristics in both cohorts of young and middle-aged healthy individuals. Our findings support the notion of weight gain in treated psychotic patients associated with poor impulse control, impulsivity-related brain networks and chronic inflammation.
| S-EPMC10965915 | biostudies-literature
Project description:BackgroundMaternal obesity is a risk factor for childhood obesity; this is a major public health concern given that ∼40% of pregnant women are either overweight or obese. Whether differences in milk composition in lean compared with obese women contribute to childhood obesity is unclear.ObjectivesWe aimed to analyze relationships between maternal obesity and human milk metabolites, infant body composition, and postnatal weight gain.MethodsThis was a prospective study in which mothers intending to breastfeed exclusively, and their newborn infants, were enrolled at delivery (n = 35 mother-infant pairs). We excluded mothers with diabetes, other medical conditions, or pregnancy complications. Participants were grouped by maternal prepregnancy BMI <25 (lean) or ≥25 kg/m2 (overweight/obese). We analyzed infant body composition by dual-energy X-ray absorptiometry and used untargeted liquid chromatography-gas chromatography-mass spectrometry to measure the milk content of 275 metabolites at 1 and 6 mo postpartum.ResultsAt 1 mo postpartum, 10 metabolites differed between overweight/obese and lean groups with nominal P < 0.05, but none was altered with a false discovery rate <0.25. Many differentially abundant metabolites belonged to the same chemical class; e.g., 4/10 metabolites were nucleotide derivatives, and 3/10 were human milk oligosaccharides. Milk adenine correlated positively with both continuously distributed maternal BMI and with infant adiposity and fat accrual. Analysis of milk composition at 6 mo postpartum revealed 20 differentially abundant metabolites (P < 0.05) in overweight/obese compared with lean women, including 6 metabolites with a false discovery rate of <0.25. At both 1 and 6 mo, human milk abundance of 1,5-anhydroglucitol, which has not previously been described in milk, was positively associated with maternal BMI.ConclusionsMaternal obesity is associated with changes in the human milk metabolome. While only a subset of metabolites correlated with both maternal and infant weight, these point to potential milk-dependent mechanisms for mother-child transmission of obesity. This trial was registered at www.clinicaltrials.gov as NCT02535637.
| S-EPMC6599743 | biostudies-literature
Project description:ObjectiveTo systematically examine the relationship between sleep duration and subsequent weight gain in observational longitudinal human studies.MethodsSystematic review of twenty longitudinal studies published from 2004-October 31, 2010.ResultsWhile adult studies (n = 13) reported inconsistent results on the relationship between sleep duration and subsequent weight gain, studies with children (n = 7) more consistently reported a positive relationship between short sleep duration and weight gain.ConclusionWhile shorter sleep duration consistently predicts subsequent weight gain in children, the relationship is not clear in adults. We discuss possible limitations of the current studies: 1) the diminishing association between short sleep duration on weight gain over time after transition to short sleep, 2) lack of inclusion of appropriate confounding, mediating, and moderating variables (i.e., sleep complaints and sedentary behavior), and 3) measurement issues.
| S-EPMC3202683 | biostudies-literature
Project description:Obesity and asthma have increased in westernised countries. Maternal obesity may increase childhood asthma risk. If this relation is causal, it may be mediated through factors associated with maternal adiposity, such as fetal development, pregnancy complications or infant adiposity. We investigated the relationships of maternal body mass index (BMI) and fat mass with childhood wheeze, and examined the influences of infant weight gain and childhood obesity.Maternal prepregnancy BMI and estimated fat mass (from skinfold thicknesses) were related to asthma, wheeze and atopy in 940 children. Transient or persistent/late wheeze was classified using questionnaire data collected at ages 6, 12, 24 and 36 months and 6 years. At 6 years, skin-prick testing was conducted and exhaled nitric oxide and spirometry measured. Infant adiposity gain was calculated from skinfold thickness at birth and 6 months.Greater maternal BMI and fat mass were associated with increased childhood wheeze (relative risk (RR) 1.08 per 5 kg/m(2), p=0.006; RR 1.09 per 10 kg, p=0.003); these reflected associations with transient wheeze (RR 1.11, p=0.003; RR 1.13, p=0.002, respectively), but not with persistent wheeze or asthma. Infant adiposity gain was associated with persistent wheeze, but not significantly. Adjusting for infant adiposity gain or BMI at 3 or 6 years did not reduce the association between maternal adiposity and transient wheeze. Maternal adiposity was not associated with offspring atopy, exhaled nitric oxide, or spirometry.Greater maternal adiposity is associated with transient wheeze but not asthma or atopy, suggesting effects upon airway structure/function but not allergic predisposition.
| S-EPMC3661999 | biostudies-literature
Project description:ObjectiveTo quantify the combined effect of maternal prepregnancy obesity and maternal gestational weight gain (GWG) on the shape of infant growth throughout the first year of life.MethodsA retrospective cohort of mother-child dyads with children born between January 2007 and May 2012 was identified in a linked electronic medical record. Data were abstracted to define the primary exposures of maternal prepregnancy body mass index (BMI) and GWG, and the primary outcome of infant growth trajectory.ResultsWe included 499 mother-child dyads. The average maternal age was 28.2 years; 55% of mothers were overweight or obese before pregnancy, and 42% of mothers had excess GWG, as defined by the Institute of Medicine. Maternal prepregnancy BMI (P < .001) and the interaction between prepregnancy BMI and maternal GWG (P = .02) showed significant association with infant growth trajectory through the first year of life after controlling for breast-feeding and other covariates, while GWG alone did not reach statistical significance (P = .38). Among infants of mothers with excess GWG, a prepregnancy BMI of 40 kg/m(2) versus 25 kg/m(2) resulted in a 13.6% (95% confidence interval 5.8, 21.5; P < .001) increase in 3-month infant weight/length percentile that persisted at 12 months (8.4%, 95% confidence interval 0.2, 16.5; P = .04).ConclusionsThe combined effect of excess maternal GWG and prepregnancy obesity resulted in higher infant birth weight, rapid weight gain in the first 3 months of life, with a sustained weight elevation throughout the first year of life. These findings highlight the importance of the preconception and prenatal periods for pediatric obesity prevention.
| S-EPMC4151184 | biostudies-literature
Project description:Existing research on neighborhood environment and gestational weight gain (GWG) focuses on point-in-time measures of neighborhood context. This precludes understanding how long-term exposure to adverse neighborhood environments influences GWG. We estimated associations between average exposure to and trajectories of long-term neighborhood socioeconomic deprivation and risk of inadequate or excessive GWG. Using data from 5690 full-term, singleton pregnancies in the 1979 National Longitudinal Survey of Youth, we estimated associations between cumulative deprivation and GWG, overall and by race/ethnicity, controlling for individual and residential covariates. A one standard deviation unit (8-point) increase in neighborhood deprivation increased risk of inadequate GWG (Relative Risk (RR): 1.08; 95% Confidence Interval (CI): 1.00-1.16) for all women and excessive GWG (RR: 1.11; 95% CI 1.02-1.21) for white women. Persistent low deprivation (RR: 0.78; 95% CI: 0.64-0.94) and upward mobility (RR: 0.76; 95% CI: 0.61-0.96), compared to persistent high deprivation, reduced risk of inadequate GWG. Persistent low deprivation also reduced risk of excessive GWG (RR: 0.84; 95% CI: 0.71-0.98). Long-term neighborhood deprivation contributes to patterns of GWG over women's life course.
| S-EPMC6960020 | biostudies-literature