Several studies have been published studying association between parental low birth weight (BW) and neonatal outcomes of their children. To date no systematic review and meta-analysis (SRM) has been published to quantify the impact of maternal and paternal BW on outcomes in the next generation. The aim of this SRM was to analyse the association between parental BW and anthropometric and metabolic outcomes in their children.

Electronic databases were searched for studies documenting BW of parents and children with neonatal outcomes. Primary outcome was to evaluate impact of parental BW on occurrence of LBW in children. Secondary outcomes were to assess impact of parental BW on occurrence of macrosomia, small for gestational age (SGA), preterm labour/delivery, and burden of non-communicable disease in later life.

We screened 54,961 articles, data from 14 studies (320,515 parent–child pairs), which fulfilled all criteria, were analysed. Maternal LBW was associated with higher chances of neonatal LBW [odds ratio (OR)1.95 (95% CI:1.56–2.46); P < 0.01; I2 = 91%], neonatal SGA [OR 2.29(95% CI:1.72–3.05); P < 0.01; I2 = 37%], lower chances of neonatal macrosomia [OR 0.50 (95% CI:0.39–0.65); P < 0.01; I2 = 35%] and had no impact on preterm labour/delivery [OR1.20(95% CI:0.67–2.16); P = 0.53; I2 = 88%]. Maternal macrosomia was associated with higher neonatal macrosomia [OR 2.66 (95% CI:2.44–3.16); P < 0.01; I2 = 48%], lower SGA [OR 0.40(95% CI:0.29–0.53); P < 0.01; I2 = 0%] and preterm labour/delivery [OR 0.77 (95% CI:0.63–0.94); P < 0.01; I2 = 4%]. Paternal but not maternal LBW was predictor of metabolic syndrome and diabetes in adulthood.

Maternal LBW is an important predictor of LBW and SGA in neonates. Maternal macrosomia is an important predictor of neonatal macrosomia; is protective against SGA and preterm labour/childbirth. Neonatal size of parents is reflected in neonatal size of their children.

Research into the Developmental Origins of Health and Disease (DOHaD) has established links between environmental exposures in early life and later-life health outcomes. Emerging interventions typically focus on improving maternal nutrition and neonatal healthcare practices yet often neglect to assess or enhance subject understanding of potential long-term impacts or to communicate the benefits of maximising parental health prior to conception. This study critically evaluates a survey tool developed to measure knowledge of non-communicable diseases (NCDs) and early-life contributors to lifelong health. The rationale behind the wording and format of the questions is examined alongside options for coding and statistical interpretation of the data. Considerations for implementation are discussed, illustrated by key findings arising from tracking of the tool’s application in Aotearoa New Zealand over ten years. We demonstrate that the survey tool can be adapted for use in a variety of contexts, producing both quantitative and qualitative baseline data suitable for informing health promotion interventions and monitoring changes in population knowledge. This research also highlights a key difference between awareness of and understanding of scientific concepts and the importance of distinguishing between these when considering public engagement with science.

Maternal hyperglycemia is associated with higher risk of metabolic diseases in offspring. Despite various hypotheses, the exact mechanisms remain unclear and the neural implication is yet to be fully investigated. The hypothalamus plays a critical role in energy regulation. In utero exposure to maternal hyperglycemia might selectively affect the developing hypothalamus. To test this hypothesis, we investigated associations between in utero exposure to maternal hyperglycemia and hypothalamic volume at 10–12 years of age. We included 82 mother–child pairs from the Gen3G prospective birth cohort, followed up 10–12 years after birth. Women underwent a 75g Oral Glucose Tolerance Test (OGTT) at 24–30 weeks of gestation, and we calculated the area-under-the-curve of glucose (AUCgluc) from maternal glucose measurements at fasting, 1h and 2h during OGTT to reflect prenatal hyperglycemia exposure. During the follow-up visit at 10–12 years of age, a subsample of children (n = 82) completed 3 T brain magnetic resonance imaging (MRI) to quantify brain volumes with FreeSurfer 7. We used Pearson correlations and partial correlations with adjustments to test associations between the AUCgluc and offspring hypothalamic brain volumes. We found that higher maternal AUCgluc was associated with greater total offspring hypothalamic volume (r = 0.30; p = 0.006). In comparison, no other brain region was significantly correlated with the maternal AUCgluc. Correlations remain significant when adjusted for maternal or offspring’s variables. Overall, we found that higher maternal glycemic response following OGTT in pregnancy appears associated with larger offspring hypothalamic volume. Our results suggest that prenatal exposure to hyperglycemia may lead to hypothalamic programming.

Brain development and face morphology are related through underlying biological mechanisms, namely embryonic neuroectodermal processes. This study examined whether the facial parameters identified in children can help understand the neurodevelopmental impact of prenatal exposures on child behavior. We studied 9- to 10-year-old children of European descent from Generation R Study (N = 2,779) with three-dimensional face photographs. With an AI model of a 3D graph autoencoder, each facial shape was compressed into 200 traits representing facial morphology. We examined associations of traits with internalizing and externalizing behaviors and attention problems. Next, select prenatal substance and micronutrient exposures were related to facial traits using adjusted linear regression analyses. We identified a robust association between one specific facial trait and attention problem scores (β = −1.47, p = 0.038). This trait features chin retrusion, mild nasal contour variation, nose tip protrusion, and overall facial asymmetry. Higher prenatal vitamin D and folic acid concentrations were associated with more facial curvature (β = 0.0001, 95%CI: 0.00001 to 0.0002, p = 0.002; and β = 0.0003, 95%CI: 0.00002 to 0.0005, p = 0.03 accordingly), while prenatal tobacco smoking showed a negative association both until the mother became aware of pregnancy (β = −0.008, 95%CI: −0.0135 to −0.0014, p = 0.02) and throughout pregnancy (β = −0.006, 95%CI: −0.0113 to −0.0005, p = 0.03). Findings suggest that facial morphology may serve as a marker of impaired neuroectodermal development. Leveraging its association with attention problems enabled a robust examination of prenatal exposures’ impact. The associations of maternal smoking, vitamin D, and folic acid concentrations with facial morphology provide insights into the origins of neurodevelopment.

Early life stress (ELS) increases the risk of metabolic disorders such as obesity, as well as neuropsychiatric conditions including depression. Adolescence represents a critical window for metabolic programming, particularly under the influence of ELS and poor dietary habits. Animal models of ELS, such as maternal separation (MS180), induce long-term alterations in hypothalamic-pituitary-adrenal (HPA) axis function, glucose metabolism, and emotionality; however, it remains unclear whether this paradigm increases vulnerability to a chronic metabolic challenge. The aim of this study was to evaluate the effects of MS180 on male rats provided with mild fructose in drinking water starting at postnatal day (P) 21. Control and MS180 (3 h daily, from postnatal day 1 to day 14) rats were given a choice of normal water or a 10% fructose solution for 10 weeks, with standard animal facility-reared (STD) animals serving as controls. Innate emotionality was assessed using the forced swimming test. Animals were implanted with a jugular vein catheter and we evaluated fasting glucose, glucose tolerance, and baseline corticosterone (CORT) levels after one week. Our findings showed that only MS180 + Fructose rats showed a decrease in swimming and increased immobility in the forced swimming test, and previously reported effects of MS180 were only observed when performing simple comparisons. MS180 also increased body weight gain, caloric intake, impaired glucose tolerance, and elevated baseline CORT levels; however, these effects were not exacerbated by fructose. These findings suggest that even low-level fructose exposure during periadolescence may exacerbate behavioral, but not metabolic, vulnerabilities induced by ELS.

Obesity and overweight in pregnant women increase pregnancy and neonatal morbidity with a risk of metabolic syndrome for children in later life. Maternal preconceptional bariatric surgery reduces maternal and paediatric outcomes but may induce fetal nutritional deficiencies and intrauterine growth restriction through placental reprogramming. The aim of this study was to describe feto-placental unit modifications induced by obesity, and the effect of bariatric surgery performed before gestation, on a diet-induced obese rat model. One month after surgery, rats of ‘control’, ‘obese’ and ‘bariatric surgery’ groups were mated and then sacrificed at D19 of gestation. Clinical description, immuno-histochemistry and molecular analyses were performed on feto-placental units. Obesity induces placental modifications including lipid accumulations, increased inflammation and oxidative stress. Some of these modifications are partially restored by maternal preconceptional bariatric surgery. On the other hand, a reduction in the expression of markers of glucose transport, insulin function and amino acid transport, after bariatric surgery was observed. This phenotype may lead to fetal caloric restriction, adoption of a ‘thrifty phenotype’ and subsequently fetal growth restriction. These preliminary findings highlight the importance of a close follow-up of women who have undergone bariatric surgery and their children.

The prenatal period, childhood, and adolescence are critical periods of development characterized by high plasticity. As an extension of the Developmental Origins of Health and Disease (DOHaD) paradigm, known as Origins of Paternal Health and Disease (POHaD), recent studies in rodents provide evidence that paternal obesity is associated not only with infertility but also with an increased risk of metabolic disorders in the offspring. In rodents, litter size reduction is used to induce lactational overfeeding by increasing the amount of breast milk to pups, which causes metabolic and reproductive disorders in adulthood. This work evaluated the metabolic and reproductive alterations in the offspring of males raised in normal or small litter (SL) in the prepubertal period and in adult life. The results show that paternal obesity due to early overfeeding affects the offspring in a sex-specific manner. During the prepubertal period, male offspring of SL fathers showed decreased Lee index, tibia length, and HDL plasma levels, and increased weight of gastrocnemius muscle, while female offspring of SL fathers only showed reduced HDL plasma levels. In adulthood, male offspring of overfed males showed glucose intolerance and reduced food intake and triglycerides plasma levels, signs of metabolic dysfunction. Female offspring of overfed males showed delayed puberty onset and higher prevalence of infertile periods in the estrous cycles, indicating a potential susceptibility to reproductive dysfunction. The results of the current study show that paternal obesity due to early overfeeding affects energy balance and reproduction of their offspring in a sex-specific manner.

Studies have linked lower birth weight to development of radiographic osteoarthritis (OA). We examined early life factors in relation to subsequent knee pain among individuals with radiographic OA. 143 participants from the UK Hertfordshire Cohort study were included. Birth weight and weight at one year (WA1) were ascertained from health ledgers and used to derive conditional infant weight gain (CIWG). At baseline and follow-up, heath questionnaires (including knee pain) and knee radiographs were collected. Only those with radiographic knee OA at baseline were analysed. Logistic regression was used to examine early life factors in relation to pain. Pain at follow-up was common (men 41.3%, women 50%). Greater WA1 and greater CIWG were related to reduced risk of knee pain at follow-up after adjustment for sex and follow-up time. CIWG was protective against knee pain at follow-up, with this association attenuated after adjustment for follow-up osteophyte score. Validation in larger studies is required.

Micro- and nanoplastics (MNPs) pollution has become a global environmental concern due to its widespread presence and diverse sources. These tiny plastic particles, originating from industrial processes, plastic waste degradation, and consumer products, have infiltrated various ecosystems, food chains, and even human tissues. Recent studies indicate that MNPs are not only pervasive in air, water, and soil but also accumulate in the human body through ingestion, inhalation, and dermal exposure. However, the implications of MNPs exposure, particularly during pregnancy, remain poorly understood. Of critical concern is the potential transfer of MNPs and their associated chemical additives across the placental barrier, posing risks to fetal development. In this review, we comprehensively analyze mainstream technologies used for detecting and characterizing MNPs, including spectroscopy- and microscopy-based approaches, as well as emerging detection methods. We also examine recent findings on the toxicity of MNP-associated chemicals, such as endocrine-disrupting compounds and heavy metals, which may have long-term effects on human health. Particular emphasis is placed on how maternal exposure to MNPs could impact offspring development, potentially leading to neurodevelopmental disorders, metabolic disturbances, and immune system dysregulation. Despite growing concerns, research gaps persist regarding the precise mechanisms through which MNPs influence maternal and fetal health. The findings recommend for further multidisciplinary research to assess the long-term consequences of prenatal MNPs exposure. Addressing these uncertainties is crucial for informing public health policies, mitigating risks, and ensuring the well-being of pregnant women and future generations.

Breastfeeding is a critical component of infant nutrition, and breastfed infants are less likely to become stunted or obese reducing the risk of non-communicable diseases in adult life. Optimal breastfeeding practices remain a challenge worldwide; as adolescents are the mothers and fathers of tomorrow, integrating DOHaD-informed knowledge into school curricula is called for. However, research indicates adolescents have low awareness of the importance of the first 1000 days of life, only see specific elements as relevant to them, and gender-related differences exist in their comprehension. This study evaluated the impact on adolescents of an in-class presentation on parenting and the benefits of breastfeeding in high schools in 5 African countries. Pre- and post-intervention questionnaires were completed by 345 pupils (182 girls, 163 boys, mean age 17.9 years). Analysis indicated the education session impacted pupils’ perceptions of parenting and changed which aspects of breastfeeding they viewed as most and least interesting. A statistically significant difference was evident between genders on the importance of cost-benefits; more boys saw relevance for fathers that no cost is incurred for formula. Boys also ranked the potential to reduce diabetes healthcare costs in adult life higher than girls. Girls preferentially ranked breastfed babies crying less, being easier to feed at night, and diaper changing being less gross as benefits for fathers. School-based education can engage adolescents and impact knowledge and attitudes about breastfeeding. Awareness of differences in girls’ and boys’ perceptions of relevance will enable educational content to be targeted to attract and inform both genders.

Developmental programming has emerged as one of the major biological principles and biomedical issues of this century because of its potential for long-term, even transgenerational, effects on the health and productivity of offspring. Livestock models have been widely used to establish the mechanisms of developmental programming in fetuses and offspring, and accordingly present data with dual benefits; both serving animal agricultural purposes and providing insights for biomedical applications. Livestock models have furthered our understanding of how developmental processes can influence postnatal health and productivity in the short- and long-term. In addition, because livestock are key to agricultural sustainability and food security, studies in livestock contribute to human livelihood. In this review, we will focus on the influence of maternal nutrition in livestock models on developmental outcomes. Maternal nutritional models include global nutrient intake (over- and under-nutrition) and supplementation of specific macro and micronutrients. Specifically, we will review the effects of maternal nutrition on: placental function, key metabolic tissues of the fetus/offspring (visceral tissues, skeletal muscle, and immune system), genetics, epigenetics, and transgenerational programming, parturition, and the underlying mechanism of developmental programming. Lastly, we will focus on gaps in knowledge and future research directions.

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.

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.

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.

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) 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.

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.