The impact of maternal physical activity on infant body composition remains understudied. This study aimed to investigate the association between maternal activity levels during pregnancy and infant body fat percentage, utilising data from the Western Australian ORIGINS birth cohort. A total of 323 pregnant women and their male (148) and female (175) infants born during 2016-2024 were included in the analysis. Maternal physical activity was measured with the International Physical Activity Questionnaire (IPAQ) and the Godin Leisure-Time Exercise (Godin) questionnaire during the second trimester. Infant body composition was measured within 7 d of birth using infant air displacement plethysmography (PEA POD). Associations were calculated using linear regression models adjusted for confounders. A significant difference in neonatal body fat percentage was observed between sexes, with males averaging 11.7% and females 13.0% (p = 0.005). Analyses of maternal physical activity during the second trimester demonstrated sex-specific effects on infant body fat percentage. High maternal activity levels were associated with lower body fat percentage for female infants (IPAQ: -3.23, 95% CI: -5.22, -1.23 and Godin: -1.73, 95% CI: -3.26, -0.22), while for males, no association was observed. These results suggest that tailored prenatal care strategies that promote exercise and a healthy diet would be beneficial to pregnant women. Further research is needed to explore additional factors that could influence infant body fat percentage, which in turn could enhance prenatal care recommendations.
Early tooth emergence may reflect developmental stress exposures and compose part of a broader set of growth measures that may be accelerated in response to early stress exposure. We test the hypothesis that timing of primary tooth emergence is associated with stress exposure and stress biology in young children. Tooth emergence was tracked prospectively in a diverse sample of initially caries-free 1-3 year-olds; socio-economic and psychosocial determinants of oral health, oral microbiology, and salivary stress markers were assessed at baseline and at 6-monthly intervals for 2 years. The number of tooth surfaces observed at the initial assessment in caries-free children was associated with a stress-related pattern of salivary cortisol reactivity: diminished cortisol response to a laboratory stressor was strongly associated with the number of surfaces (estimate -6.51 [SE 1.90], 95% CI -10.23--2.79, p < 0.001), after adjusting for covariates. This effect was also found in longitudinal analyses across the two-year study period. The findings provide novel evidence that a marker of stress biology is positively associated with tooth emergence in young children and may reflect additional developmental and biological influences that underlie oral health in children.
Embryonic exposures to perfluorobutanesulfonic acid (PFBS) in zebrafish have been shown to impair pancreas growth. This study investigated the persistence of the truncated pancreas phenotype, functional impacts on digestive enzyme production, and the hypothesis that redox stress contributes to these outcomes. Transgenic ptf1a:GFP zebrafish were exposed to 0 (0.01% dimethyl sulfoxide (DMSO)), 16, and 32 µM PFBS from 24 to 96 h post-fertilization (hpf) and raised in clean water to 15 days post-fertilization (dpf). Confocal microscopy revealed the pancreata regained normal size, suggesting "catch-up" growth. To evaluate the importance of redox stress in this recovery and acinar cell function, wild-type or mutant zebrafish embryos with a mutation in the DNA-binding domain of the Nrf2a transcription factor were exposed to PFBS from 3 to 96 hpf and raised to 9 dpf in clean water. At 9 dpf, Nrf2a mutants had shorter exocrine pancreases than wild-types with the same treatment, indicating this phenotype likely involves redox stress. Expression of pancreatic proteases and Trypsin were examined to assess functional changes. Although protease gene expression did not differ significantly at 4 or 9 dpf, Trypsin levels decreased with increasing PFBS concentrations in wild-type larvae at 6 and 9 dpf. Lipid analysis showed no change in cholesterol but lower triglycerides in Nrf2a mutants. Assessment of glutathione utilization using monochlorobimane fluorescence indicated more robust antioxidant responses in wild-type fish. This study increases understanding of how Nrf2a modulates the response to PFBS exposure, impacts on exocrine pancreas function, and has implications for understanding "catch-up" growth in response to embryonic toxicant exposures.
Abstract Adolescence is a peak period for myopia onset, which is closely related to environmental and lifestyle factors. Relative fat mass (RFM), a novel indicator of body fat, provides a more precise measure of adiposity. However, its relationship with myopia in adolescents remains poorly understood. To probe the connection between RFM and myopia in adolescents, this study included 8746 adolescents aged 12–19 years, utilizing data from the National Health and Nutrition Examination Survey (1999–2008). Myopia was defined as a spherical equivalent (SE) ≤ −1.0 D. The relationship between RFM and adolescent myopia was assessed using a weighted logistic regression model. Restricted cubic spline analysis was employed to examine the nonlinear relationship between RFM and the odds of myopia. Subgroup analysis and interaction tests were also conducted. Sensitivity analyses were performed using broader myopia diagnostic criteria (SE ≤ −0.75 D and SE ≤ −0.50 D). After adjusting for all confounding factors, the odds of myopia in the third and highest quartiles of RFM were 33% higher (odds ratio (OR) = 1.33, 95% CI: 1.07–1.64) and 35% higher (OR = 1.35, 95% CI: 1.01–1.80), respectively, compared to the lowest quartile. Each one-standard-deviation (9.06) increase in RFM was associated with a 12% higher odds of myopia in adolescents (OR = 1.12, 95% CI: 1.01–1.25). This association was more pronounced in males (OR = 1.25, 95% CI: 1.09–1.43). A significant positive association was also observed in the low-income population (OR = 1.27, 95% CI: 1.08–1.49). Sensitivity analysis showed that when using SE ≤ −0.75 D and SE ≤ −0.50 D as the diagnostic criteria for myopia, RFM remained significantly positively associated with the odds of adolescent myopia, indicating the robustness of the results. Increased RFM was significantly associated with higher odds of myopia in adolescents, with a stronger association observed among males, suggesting that body fat control and RFM reduction may represent a promising direction for comprehensive myopia prevention and management in adolescents. Targeted interventions integrating weight management, healthy diet, regular physical activity, and accessible eye health services could be developed, particularly for male and low-income adolescents. However, longitudinal studies are needed for further validation.
Maternal nutrition can influence offspring metabolism through metabolic programming, potentially leading to long-term disorders such as obesity and type 2 diabetes. However, the cellular- and tissue-level mechanisms involved in the metabolic programming, particularly regarding the endocrine pancreas, remain unclear. This study investigated the effects of maternal high-fat (HF) diet exposure on the biometric/metabolic profiles, β-cell morphometry, insulin secretion, and islet levels of the SNARE protein VAMP-2 and cytoskeletal F-actin, both critical to insulin granule exocytosis, in mouse offspring. Female C57BL6 mice were fed either a control (CON, 4.5% lipids) or a HF diet (35% lipids) during pregnancy and lactation. The offspring from both groups were evaluated at 3, 12, and 90 days of age. The offspring from HF diet-fed mothers exhibited significantly lower body weight from day 3 and increased visceral adiposity, hyperinsulinemia, glucose intolerance, and insulin resistance, associated with no significant changes in postprandial glycemia by adulthood. These alterations were accompanied by significant morphometric changes in the endocrine pancreas, including a reduction in total islet area, β-cell area, and β-cell number per islet, detectable from day 3 until adulthood. Additionally, adult islets from HF offspring showed elevated cellular F-actin labeling and reduced VAMP-2 protein levels, correlating with impaired glucose-stimulated insulin secretion in vitro. In conclusion, maternal HF diet exposure leads to metabolic disturbances and impaired β-cell function in offspring. These include reduced β-cell mass and secretory capacity, potentially due to an impaired cytoskeletal organization and insulin granule exocytosis, highlighting the long-term impact of maternal nutrition on offspring health.
Exposure to early life adversity (ELA) increases risk of poor mental health outcomes, including attention deficit/hyperactivity disorder (ADHD). In fact, ELA, especially in the form of "household ACEs" (e.g., socioeconomic disadvantage, incarceration of a caregiver), is among the most robust environmental predictors of a later ADHD diagnosis. Exposure to unpredictability is an understudied form of ELA that captures instability or inconsistency in routines, household experiences, and family relationships. The purpose of this study was to examine associations between unpredictability and ADHD symptoms in children and adolescents. Participants were drawn from two independent cohorts (Cohort 1: N = 99, Mage = 7.31 years [SD = 0.31]; Cohort 2: N = 217, Mage = 14.39 years [SD = 1.32]) participating in ongoing longitudinal studies of exposure to ELA. Unpredictability was measured by the Questionnaire of Unpredictability in Childhood, and ADHD symptoms were measured by the Child Behavior Checklist Attention Deficit/Hyperactivity Problems subscale, the Behavior Rating Inventory of Executive Function, and the Kiddie Schedules for Affective Disorders and Schizophrenia ADHD Screener. Childhood experiences of unpredictability were associated with ADHD symptoms in both cohorts and during childhood and adolescence. Further, associations were stronger in females than males. These findings show that unpredictability is a risk factor for ADHD which suggests that it should be explored as an early target for intervention to reduce the development of ADHD symptoms.
The developmental origins of health and disease (DOHaD) framework highlights the link between adverse early-life environments and later risk for non-communicable disease (NCDs). DOHaD research has primarily focused on maternal health and, more recently, paternal health. However, it is increasingly clear that investment in the adolescent window may afford the best opportunity to break the transgenerational cycle of NCDs. Data on DOHaD understanding in adolescents remains limited, and in the context of this article, there remains a paucity of research undertaken with adolescents in Oceania, particularly Pacific adolescents, who experience a disproportionately high NCD burden. NCDs represent a complex health issue and therefore multisectoral approaches and collaborative partnerships across different disciplines, health and social professions and communities is required. Due to the significance of DOHaD research and the importance of investing in our children and adolescents for the future, we developed a framework called Taumafa Kava to guide DOHaD-related research in Pacific communities across Oceania. This framework is based on a Tongan Taumafa Kava ceremony and it is an introduction to the cultural significance of the methysticum plant root (kava) and its relevance in highlighting a shared responsibility to serve Pacific Peoples well in DOHaD research. Furthermore, it is a call to action highlighting the importance of understanding the need to deliver DOHaD research that is inclusive of Pacific knowledges, cultures, languages, identities and contexts. This framework has been applied in a research project to showcase the potential for this approach to be utilised in DOHaD-related research in Pacific communities.
While maternal obesity is a well-established determinant of offspring cardiometabolic health, the contribution of paternal obesity to metabolic programming remains less well defined. This study investigated the impact of paternal obesity on obesity and metabolic health outcomes in male and female offspring using a Sprague Dawley rat model. Male rats were fed either a low-calorie control or high-calorie diet for a 6-week pre-conception period prior to mating with lean, control-fed females. Male and female offspring were assessed at weaning and in adulthood for growth parameters and cardiometabolic indices, including glycemic control, blood lipids and lipoprotein profiles, and liver fat. Paternal obesity was associated with adverse metabolic programming in offspring, characterized by dyslipidemia in both sexes, independent of early-life growth abnormalities or the development of obesity in adulthood. Newly-weaned offspring from obese fathers exhibited elevated total cholesterol in both sexes and increased serum triglycerides in females. In adulthood, offspring demonstrated increased LDL/VLDL-cholesterol, with male offspring displaying a specific increase in apolipoprotein B and a shift toward a more atherogenic lipoprotein subclass distribution, including higher concentrations of small LDL particles compared with male offspring from control fathers. These findings indicate that paternal obesity, even in the absence of postnatal overnutrition or offspring obesity, can program an advanced dyslipidemic phenotype in progeny. Paternal metabolic health may therefore represent an important and previously underappreciated early determinant of cardiometabolic disease risk in offspring.
This narrative review examines the development of the infant gut microbiota during the early months of life, highlighting the impact of delivery mode and feeding practices on microbial colonization and overall infant health. The search was conducted using the Virtual Health Library and PubMed databases, with the descriptors "gut microbiota" combined with "breastfeeding" (BF) and "infant formula." After screening, 18 articles were selected for final analysis. Findings indicate that cesarean section reduces initial gut microbial diversity by 30%-50% and decreases Bifidobacterium colonization, while increasing the abundance of Enterobacteriaceae and Clostridium. In contrast, exclusive BF supports a more favorable microbial profile, enriched in bifidobacteria, and contributes to immune system maturation. The literature also highlights the importance of other genera, including Lactobacillus, Veillonella, and Firmicutes, in regulating inflammation, producing short-chain fatty acids, and protecting against pathogens. Supporting vaginal birth and exclusive BF emerges as a key strategy to promote a more resilient and health-promoting gut microbiota during infancy.
Malathion is an insecticide widely used in agriculture and, in Brazil, was heavily applied in the 2010s to control Aedes mosquitoes. Its use exposes the general population, including children and adolescents, to this pesticide. As puberty reflects the maturing of the reproductive system, this study investigated whether preconception exposure to low doses of malathion during juvenile and pubertal stages affects fertility and pregnancy outcomes in Wistar rats. Female rats received daily gavage doses of 10 or 50 mg/kg from postnatal day (PND) 22 to 60. Puberty onset was monitored starting on PND 27. Following exposure, females were mated at the first proestrus and euthanized on gestational day (GD) 18. Malathion advanced puberty onset (M50) but did not impair fertility or serum hormonal levels. Females exposed to the higher dose showed increased urea levels. Additionally, placental integrity was compromised, with reduced placental glycogen (M10) and increased oxidative stress and reduced offspring CRL. These findings indicate that preconception exposure to low doses of malathion negatively impacted placentation and offspring's intrauterine development at GD 18.
Longitudinal, Indigenous-led research integrated with community-controlled continuity of care can improve and support perinatal outcomes for Aboriginal and Torres Strait Islander families in Australia. Across the past 35 years, seven cohorts have contributed complementary insights from pregnancy through early childhood with varying geographic reach and appropriate Indigenous governance. This paper discusses each of these cohorts and how these studies across pregnancy, birth and some continuing through early childhood, have substantially added to the body of knowledge related to perinatal health needs for women. Early cohorts (e.g., MUSP; Raine) advanced life‑course epidemiology but had low Indigenous representation, limiting perinatal inference for these communities. The Aboriginal Birth Cohort achieved exceptional long‑term retention and partnerships and from the late 2000s, Gomeroi gaaynggal enabled causation analyses using biomarkers. Finally, systems initiatives such as PANDORA and BiOC demonstrate successes with culturally safe pathways and Indigenous‑governed continuity models. Evidence suggests the approaches undertaken in the perinatal period must ensure the voices of Indigenous people are paramount particularly when care and research is being delivered to communities. Lessons learned from these cohorts highlight that Indigenous governance and workforce, co‑design and community‑embedded engagement enhance retention, relevance and translation; registries and continuity models deliver measurable outcome gains. The depth of knowledge identified in life-course research for Indigenous women can significantly add to the standard data collection tools used by state and national services.
Prenatal and early-life exposures may contribute to lifelong hypertension risk. We examined the relationships between an individual's birth weight or preterm birth status with their 1) risk for hypertension and 2) related quantitative blood pressure measures [mean systolic blood pressure (SBP), diastolic blood pressure (DBP), and 30-second pulse] among post-menopausal women from the Women's Health Initiative observational cohort. At study entry, birth weight and preterm birth status were self-reported by category (<6 lbs., 6-7 lbs. 15 oz., 8-9 lbs. 15 oz., or ≥10 lbs.; ≥4 weeks premature or full term). Prevalent and incident hypertension status were self-reported; baseline SBP, DBP, and 30-second pulse were measured by trained study staff. Linear, logistic, and Cox-proportional hazards regression models were used to estimate associations between birth weight and preterm birth and blood pressure outcomes. After adjustments, participants born weighing <6 lbs. had a higher mean SBP and were at increased risk for prevalent and incident hypertension compared to participants born at a normal birth weight (6-7 lbs. 15 oz.). Women born weighing ≥10 lbs. had a lower mean SBP and were at lower risk for prevalent and incident hypertension when compared to participants born at a normal birth weight. Compared to participants born full term, those born preterm were at increased risk for prevalent and incident hypertension; however, this relationship was weaker when stratifying by birth weight. Long-term follow-up or targeted counseling may be required for individuals born prematurely or at lower birth weights to prevent hypertension and associated cardiovascular outcomes.
The effects of maternal broccoli powder (BP) intake on inflammation and AMPK activation in weaning offspring programmed by maternal undernutrition remain poorly understood. This study aimed to investigate whether maternal BP intake during lactation ameliorates inflammation and affects AMPK phosphorylation in the hypothalamus and liver of weaning offspring subjected to maternal undernutrition. Pregnant rats received either a normal protein (NP, 20% casein) or a low protein (LP, 8% casein) diet. During lactation, dams were provided with either a normal protein diet without or with 0.74% BP (NP/NP or NP/NPBP) or a low protein diet without or with 0.74% BP (LP/LP or LP/LPBP). Blood, liver (left lateral lobular region), and hypothalamic samples (region estimated to include the arcuate nucleus and ventromedial hypothalamus) were collected on postnatal day 21. In the liver, macrophage count, NFκB p65 protein expression, and TNF-α mRNA expression were lower in LP/LPBP than in LP/LP. In the hypothalamus, Iba1 mRNA expression, NFκB p65 protein expression, and TNF-α mRNA expression were reduced in LP/LPBP compared to LP/LP. AMPK phosphorylation was upregulated in both the liver and hypothalamus of LP/LPBP offspring relative to LP/LP. In the liver, mTOR and Akt phosphorylation were downregulated in LP/LPBP compared to LP/LP. Additionally, Dnmt1 levels were lower in LP/LPBP than in LP/LP in the liver, whereas in the hypothalamus, Dnmt1 and Dnmt3a mRNA expression levels were higher in NP/NPBP than in NP/NP. In conclusion, maternal BP intake during lactation decreased inflammation and increased AMPK phosphorylation in the liver and hypothalamus of weaning rats programmed by maternal undernutrition.
The Developmental Origins of Health and Disease (DOHaD) hypothesis highlights the pivotal role of early-life nutrition in shaping lifelong health and disease risk. Low birth weight (LBW) remains a major public health issue associated with increased susceptibility to metabolic and cardiovascular disease, underscoring the need for early nutritional interventions. We investigated whether dietary supplementation with soy protein isolate (SPI) during lactation could mitigate adverse developmental programming in a rat model of LBW induced by maternal calorie restriction. Dams received an SPI-supplemented diet during lactation, and offspring were evaluated for postnatal growth, circulating IGF-1 and corticosterone concentrations, and pituitary expression of Gas5 lncRNA, miR-23b, and Pomc. Stress responsiveness and glucocorticoid receptor sensitivity were also assessed. SPI supplementation restored postnatal growth and IGF-1 concentrations in female offspring, and in males, it normalized pituitary Gas5 lncRNA and Pomc mRNA expressions, reduced stress-induced corticosterone hypersecretion, and improved pituitary glucocorticoid sensitivity. These findings indicate that SPI intervention during lactation can partially reverse epigenetic dysregulation of the stress and somatotropic axes caused by fetal undernutrition. Nutritional modulation during lactation thus represents a critical window for early intervention in LBW offspring. SPI supplementation may enhance endocrine and metabolic resilience, providing a practical nutritional programming approach to reduce future disease risk, consistent with the DOHaD paradigm.
Studies frequently view Black populations as homogenous, disregarding important diversity within this population. Furthermore, nativity can be key to distinguishing health risks among this population. Yet few researchers have examined these distinctions using body roundness index (BRI), a measure of central adiposity. We assessed the relationship between nativity and BRI among non-Hispanic Black people in the United States (US) using cross-sectional data from the 2011-2018 National Health and Nutrition Examination Survey (NHANES). BRI was calculated using height, weight, and waist circumference. Nativity was categorized as US-born and foreign-born. Multilinear regression analysis was used to evaluate the relationship between BRI and nativity, controlling for demographic characteristics and Healthy Eating Index scores. The average age and BRI score of participants were 44.74 ± 0.46 and 5.36 ± 0.04, respectively. Among eligible participants (3341), 9.6% were foreign-born (n = 322). In multivariate regression models adjusting for covariates, men had significantly lower BRI scores than women (4.67 ± 0.04 versus 5.96 ± 0.05; β = -1.25; t61 = 24.60; P < 0.0001), and BRI increased with age (β = 0.02; t61 = 9.17; P < 0.0001). US-born Black people had significantly higher BRI scores compared to their foreign-born counterparts (5.40 ± 0.04 versus 5.00 ± 0.09; β = -0.36; t61 = -3.99; P = 0.0002). Results suggest that nativity is associated with central adiposity, with potential implications for cardiometabolic disease risk.
The Developmental Origins of Health and Disease (DOHaD) paradigm posits that early environmental factors may influence a child’s development and long-term health outcomes. Developmental programming (DP) is central to this paradigm, whereby specific early life exposures during critical periods of development are associated with changes to physiological and metabolic pathways, potentially predisposing individuals to disease. However, no standard definition of DP exists, and various terms have been used to describe similar processes. This analysis aimed to develop a conceptual definition for DP to inform interdisciplinary research, education, and practice. Walker and Avant’s eight-step method was employed to analyze the literature, incorporating elements of Rogers’ evolutionary approach to present the temporal and contextual evolution of the concept. A systematic search of MEDLINE with the EBSCOhost database was performed using the search term “developmental programming,” resulting in 95 titles included in this review. Defining attributes associated with DP include epigenetics, ontogeny, critical periods, and plasticity. Antecedents for DP may include maternal and infant nutrition, maternal disease and medication, lifestyle choices, environmental exposures, and stress. The potential consequences include cardiovascular disease, metabolic disorders, diabetes, neurodevelopmental disorders, endocrine disruption, reproductive issues, and mental health conditions. Effective healthcare provider education, knowledge dissemination, and addressing the social determinants of health through a population health approach are essential to translate DP theory and empirical evidence into practice. A common language and understanding of DP can improve the interdisciplinary advancement of DOHaD research to inform practice and education.
This study examined the impact of maternal undernutrition during gestation and/or lactation on neonatal immune indices. From day 10 of gestation to term, pregnant rats received either ad libitum (AdLib) feeding or 50% food restriction (FR). After birth, pups were either nursed by their own dams or cross-fostered, resulting in three groups (n = 6 per group): a control group with AdLib feeding throughout (AdLib/AdLib), a group with FR only during gestation (FR/AdLib), and a group with FR during both gestation and lactation (FR/FR). At day of life 1 and at three weeks of age, spleen and thymus weights, as well as basal and lipopolysaccharide (LPS)-stimulated TNF levels and white blood cell indices, were measured in male offspring. At day of life 1, immunological indices were similar among groups. By three weeks, monocyte percentage was significantly decreased in FR/FR compared with AdLib/AdLib (1.6 ± 0.5% vs. 3.1 ± 0.4%). Relative spleen weight (adjusted for body weight) was also significantly lower in FR/FR compared with both AdLib/AdLib and FR/AdLib. Following LPS administration, TNF-α levels were reduced in FR/FR compared with FR/AdLib and AdLib/AdLib (206 ± 28 vs. 511 ± 91 and 484 ± 59 pg/ml, respectively; P < 0.05). Moreover, in FR/FR offspring, monocyte (5.4 ± 1.1% vs. 2.0 ± 0.6% and 2.0 ± 0.7%) and neutrophil (50.6 ± 5.5% vs. 17.2 ± 2.4% and 20.0 ± 4.2%) percentages were significantly increased, while lymphocyte percentage (43.2 ± 5.9% vs. 80.0 ± 2.4% and 77.2 ± 4.4%) was decreased compared with FR/AdLib and AdLib/AdLib. These findings suggest that undernutrition during both prenatal and postnatal periods can attenuate neonatal immunity by decreasing basal monocyte counts and impairing cytokine responses.
We aimed to determine the association between maternal bonding difficulty in the postpartum period and children's neurodevelopment, considering maternal psychological distress and child sex-specific differences. To evaluate the relationship, the dataset of the Japan Environment and Children's Study was used, as well as the Mother-to-Infant Bonding Scale (MIBS), the six-item version of the Kessler Psychological Distress Scale (K6) for mothers, and the Ages and Stages Questionnaires Third Edition for children aged 2 to 4 years. Maternal MIBS and K6 were administered at 1 year postpartum. Data from 24,798 boys and 24,025 girls were analyzed. Multivariate logistic regression analyses, with the reference groups being those with maternal MIBS scores ≤4 and K6 scores ≤4, were performed. The Benjamini-Hochberg procedure was employed to account for multiple testing. In boys, maternal bonding difficulty (MIBS score ≥5) without psychological distress (K6 score ≤4) was associated with a screen-positive result for neurodevelopmental delay in all five domains (communication, gross motor, fine motor, problem-solving, and personal-social) at ages 2 to 4 years. In girls, maternal bonding difficulty without psychological distress was associated with a screen-positive result for neurodevelopmental delay in all five domains at 2 years of age. However, at age 4 years, maternal bonding difficulty without psychological distress was no longer associated with a screen-positive result for problem-solving delay in girls. The association of maternal bonding difficulty without psychological distress at 1 year postpartum with screen-positive result for problem-solving delay persisted in boys, but at age 4 years in girls, the association no longer existed.
The influence of the maternal antenatal environment on infant growth and development beyond the neonatal period is not well understood. This study investigated associations between maternal cardiometabolic health and lifestyle on infant growth during the first year of life. This sub-study of the longitudinal Microbiome Understanding in Maternity Study included 87 mother-infant dyads. Maternal anthropometrics were collected at each trimester. Lifestyle was assessed through the Australian Eating Survey (Trimester T1 and T3) and International Physical Activity Questionnaire (T1, T2 and T3). Infant anthropometrics were measured at birth, 6 weeks, 6 months and 12 months. Changes in weight, weight-for-age z-score, length-for-age z-score, rapid weight gain and conditional weight gain (CWG) were determined. Multiple linear regression was used to assess associations between maternal parameters and infant growth, adjusting for common confounders. Maternal T1 weight (CWG: p = 0.03), T3 weight (CWG: p = 0.03) and GWG (weight z-score change: p = 0.031) were positively associated with increased infant growth from 0 to 6 months. Greater maternal fat mass was associated with increased CWG (p = 0.042) from 6 weeks to 6 months. Higher quality maternal T1 diet was associated with increased infant growth (weight z-score change: p = 0.022, CWG: p = 0.013) from 0 to 12 months. Increased maternal physical activity was associated with increased CWG (p = 0.022) and length z-score change (p = 0.024) from 0 to 12 months in T1, and increased CWG from 6 to 12 months in T2 (p = 0.014) and T3 (p = 0.047). Markers of maternal cardiometabolic health risk and healthier lifestyle were associated with increased infant growth. Further investigation is required to confirm findings and investigate links with future health sequelae.
