Offspring Body Mass Research Articles

Prenatal Tobacco Exposure and Accelerated Offspring Weight and Body Mass Index Trajectories in the First 3 Years of Life

Background: Prenatal tobacco exposure (maternal active and passive smoking) has been associated with childhood obesity. It is unclear whether this is directly attributable to in utero exposure, with a graded effect across exposure groupings, or to associated lifestyle factors. Methods: In 971 maternal-offspring pairs from the GUSTO cohort, maternal plasma cotinine at 26-28 weeks' gestation and smoking history were used to categorise mothers into prenatal tobacco exposure groups. Offspring anthropometry was obtained longitudinally from birth and at ages 3, 6, 9, 12, 15, 18, 24, 36 months (m). Multiple linear regression, mixed linear models and counterfactual-based analysis were conducted, adjusting for ethnicity, maternal age, education, 1st trimester BMI, parity and gestational age. Findings: All results were compared with unexposed offspring (undetectable maternal cotinine and no history of tobacco exposure). Infants with low maternal cotinine (0·17-13·99 ng/ml) had a similar birthweight, while those with high maternal cotinine (≥14ng/ml) had a lower birthweight [β(95%CI) -162·0g (-291·8,-32·2)]. Low maternal cotinine was associated with higher offspring weight z-score at 18m [0·24 SDs (0·01,0·47)] and 36m [0·27 SDs (0·03,0·52)], and higher BMI z-score at 6m and across 15-36m [36m: 0·45 SDs (0·20,0·70)]. Over the 36m period high maternal cotinine was associated with accelerated gain in weight zscore [0·17 SDs/year (0·03,0·31)]. There was a dose-dependent BMI z-score acceleration, with offspring of mothers with low and high cotinine showing 0·09 (0·01,0·17) SDs/year and 0·17 (0·02,0·32) SDs/year gain, respectively. The association of prenatal tobacco exposure with 36m BMI was not explained by reduced breast-feeding, poor diet and increased screen time. Interpretation: Avoiding even low levels of prenatal tobacco exposure may reduce the risk of early childhood obesity. In utero programming by tobacco exposure directly influences childhood BMI rather than through unhealthy childhood lifestyle factors. Funding Statement: Singapore's National Medical Research Council and Singapore Institute for Clinical Sciences, A*STAR. Declaration of Interests: KMG is supported by the UK Medical Research Council (MC_UU_12011/4), the National Institute for Health Research (NIHR Senior Investigator (NF-SI-0515-10042) and the NIHR Southampton Biomedical Research Centre) and the European Union (Erasmus+ Programme Early Nutrition eAcademy Southeast Asia-573651-EPP-1-2016-1- DE-EPPKA2-CBHE-JP). KMG, Y-SC, and YSL have received reimbursement for speaking at conferences sponsored by companies selling nutritional products. KMG, S-YC and Y-SC are part of an academic consortium that has received research funding from Abbott Nutrition, Nestec and Danone. The other authors have no financial or personal conflict of interest to declare. Ethics Approval Statement: The study was ethically-approved by the Institutional Review Boards of the KK Women’s and Children’s Hospital, and the National University Health System. Informed written consent was obtained from all participants

Role of gestational weight gain, gestational diabetes, breastfeeding, and hypertension in mother-to-child obesity transmission.

Given the reported 30% prevalence of early-life obesity in the Western world, the nongenetic, maternally derived risk factors for excess body mass in offspring have been widely investigated recently. This review article aimed to analyze the results of 67 articles published from 2014 onwards that investigated causative non-genetic-based associations between maternal and infantile excess body mass. Excessive gestational weight gain was found to increase the incidence of excess body mass in offspring, reaching nearly 20% at 2 years of age. Furthermore, gestational diabetes mellitus (GDM) increases the risk of offspring that is large for gestational age. The offspring of mothers with GDM and mothers with dyslipidemia in the first trimester of pregnancy had higher rates of excess body mass. In addition, breastfeeding for a period of less than 6 months was one of the 4 factors that were most strongly associated with childhood obesity. Pregnancy-induced hypertension raises the risk of childhood obesity by 50%. In conclusion, excessive gestational weight gain, GDM, maternal dyslipidemia, breastfeeding for a period of less than 6 months, and hypertensive disorders of pregnancy are associated with maternal and childhood obesity and are perinatal risk factors of excess body mass in offspring. Their occurrence should be monitored and prevention of these factors should become the principal aim of obesity prevention programs for children. Occurrence of these factors may justify intense screening to diagnose early stages of metabolic disorders in offspring, even in adulthood. Further large-scale studies are warranted to draw a firm conclusion.

Associations of maternal gestational weight gain with the risk of offspring obesity and body mass index Z scores beyond the mean

PurposeWe examined the association of meeting the 2009 Institute of Medicine gestational weight gain (GWG) guidelines with offspring obesity and body mass index Z score (BMIZ) at age six overall and by maternal weight status. MethodsData were from the Infant Feeding Practices Survey II Study (2005–2007) and their Year Six Follow-Up Study (2012). Logistic regression and quantile regression models were used. ResultsEleven percent of children were obese. Children born to mothers who gained excessive weight during pregnancy had an increased risk of obesity as compared with those born to mothers who gained adequate weight (adjusted odds ratio: 1.67). The association was stronger among normal-weight mothers (adjusted odds ratio: 3.50). Inadequate GWG was not associated with offspring obesity overall or in subsamples by maternal prepregnancy BMI. Children born to mothers who gained excessive weight had higher BMIZ. This distributional association was more pronounced among normal-weight mothers. Children born to obese mothers who gained inadequate weight had lower BMIZ at some percentiles of the BMIZ distribution. ConclusionsExcessive GWG was associated with increased risk of offspring obesity and higher BMIZ at age six, whereas inadequate GWG was protective of high BMIZ among children born to obese mothers.

Maternal food supplementation and perceived predation risk modify egg composition and eggshell traits but not offspring condition

Mothers may vary resource allocation to eggs and embryos, which may affect offspring fitness and prepare them for future environmental conditions. The effects of food availability and predation risk on reproduction have been extensively studied, yet their simultaneous impacts on reproductive investment and offspring early life conditions are still unclear. We experimentally manipulated these key environmental elements using a 2×2 full factorial design in wild, free-living pied flycatchers (Ficedula hypoleuca), and measured egg composition, eggshell traits and offspring condition. Eggs laid in food-supplemented nests had larger yolks and thicker shells independently of predation risk, while eggs laid in nests exposed to predator cues had lower levels of immunoglobulins, independent of food supplementation. In nests without predator cues, shell biliverdin content was higher in eggs laid in food-supplemented nests. Incubation was 1day shorter in food-supplemented nests and shorter incubation periods were associated with higher hatching success, but there were no direct effects of maternal treatment on hatching success. To investigate the impact of maternal treatment (via egg composition) on the offspring, we performed full brood cross-fostering after hatching to unmanipulated nests. Maternal treatment did not significantly affect body mass and immunoglobulin levels of offspring. Our results suggest that although prenatal maternal cues affected egg composition, these egg-mediated effects may not have detectable consequences for offspring growth or immune capacity. Unpredictable environmental stressors may thus affect parental investment in the eggs, but parental care may level off costs and benefits of differential maternal egg allocation.

Maternal smoking during pregnancy and offspring body mass index and overweight: a systematic review and meta-analysis.

The present study aimed to conduct a systematic review and meta-analysis to evaluate the evidence on the association of maternal smoking during pregnancy with offspring body composition in childhood, adolescence and adulthood. MEDLINE, Web of Science and LILACS databases were searched. Reference lists were also screened. We included original studies, conducted in humans, that assessed the association of maternal smoking during pregnancy with offspring body mass index (BMI) and overweight in childhood, adolescence and adulthood, published through May 1st, 2018. A meta-analysis was used to estimate pooled effect sizes. The systematic review included 64 studies, of which 37 evaluated the association of maternal smoking during pregnancy with overweight, 13 with BMI, and 14 evaluated both outcomes. Of these 64 studies, 95 measures of effect were extracted and included in the meta-analysis. We verified that the quality of evidence across studies regarding maternal smoking in pregnancy and overweight and BMI of offspring to be moderate and low, respectively. Most studies (44 studies) were classified as moderate risk bias. Heterogeneity among studies included was high and, in the random-effects pooled analysis, maternal smoking during pregnancy increased the odds of offspring overweight (OR: 1.43, 95%CI: 1.35; 1.52) and mean difference of BMI (β: 0.31, 95%CI: 0.23; 0.39). In conclusion, offspring of mothers who smoked during pregnancy have higher odds of overweight and mean difference of BMI, and these associations persisted into adulthood.

Late-pregnancy dysglycemia in obese pregnancies after negative testing for gestational diabetes and risk of future childhood overweight: An interim analysis from a longitudinal mother-child cohort study.

BackgroundMaternal pre-conception obesity is a strong risk factor for childhood overweight. However, prenatal mechanisms and their effects in susceptible gestational periods that contribute to this risk are not well understood. We aimed to assess the impact of late-pregnancy dysglycemia in obese pregnancies with negative testing for gestational diabetes mellitus (GDM) on long-term mother–child outcomes.Methods and findingsThe prospective cohort study Programming of Enhanced Adiposity Risk in Childhood–Early Screening (PEACHES) (n = 1,671) enrolled obese and normal weight mothers from August 2010 to December 2015 with trimester-specific data on glucose metabolism including GDM status at the end of the second trimester and maternal glycated hemoglobin (HbA1c) at delivery as a marker for late-pregnancy dysglycemia (HbA1c ≥ 5.7% [39 mmol/mol]). We assessed offspring short- and long-term outcomes up to 4 years, and maternal glucose metabolism 3.5 years postpartum. Multivariable linear and log-binomial regression with effects presented as mean increments (Δ) or relative risks (RRs) with 95% confidence intervals (CIs) were used to examine the association between late-pregnancy dysglycemia and outcomes. Linear mixed-effects models were used to study the longitudinal development of offspring body mass index (BMI) z-scores. The contribution of late-pregnancy dysglycemia to the association between maternal pre-conception obesity and offspring BMI was estimated using mediation analysis. In all, 898 mother–child pairs were included in this unplanned interim analysis. Among obese mothers with negative testing for GDM (n = 448), those with late-pregnancy dysglycemia (n = 135, 30.1%) had higher proportions of excessive total gestational weight gain (GWG), excessive third-trimester GWG, and offspring with large-for-gestational-age birth weight than those without. Besides higher birth weight (Δ 192 g, 95% CI 100–284) and cord-blood C-peptide concentration (Δ 0.10 ng/ml, 95% CI 0.02–0.17), offspring of these women had greater weight gain during early childhood (Δ BMI z-score per year 0.18, 95% CI 0.06–0.30, n = 262) and higher BMI z-score at 4 years (Δ 0.58, 95% CI 0.18–0.99, n = 43) than offspring of the obese, GDM-negative mothers with normal HbA1c values at delivery. Late-pregnancy dysglycemia in GDM-negative mothers accounted for about one-quarter of the association of maternal obesity with offspring BMI at age 4 years (n = 151). In contrast, childhood BMI z-scores were not affected by a diagnosis of GDM in obese pregnancies (GDM-positive: 0.58, 95% CI 0.36–0.79, versus GDM-negative: 0.62, 95% CI 0.44–0.79). One mechanism triggering late-pregnancy dysglycemia in obese, GDM-negative mothers was related to excessive third-trimester weight gain (RR 1.72, 95% CI 1.12–2.65). Furthermore, in the maternal population, we found a 4-fold (RR 4.01, 95% CI 1.97–8.17) increased risk of future prediabetes or diabetes if obese, GDM-negative women had a high versus normal HbA1c at delivery (absolute risk: 43.2% versus 10.5%). There is a potential for misclassification bias as the predominantly used GDM test procedure changed over the enrollment period. Further studies are required to validate the findings and elucidate the possible third-trimester factors contributing to future mother–child health status.ConclusionsFindings from this interim analysis suggest that offspring of obese mothers treated because of a diagnosis of GDM appeared to have a better BMI outcome in childhood than those of obese mothers who—following negative GDM testing—remained untreated in the last trimester and developed dysglycemia. Late-pregnancy dysglycemia related to uncontrolled weight gain may contribute to the development of child overweight and maternal diabetes. Our data suggest that negative GDM testing in obese pregnancies is not an “all-clear signal” and should not lead to reduced attention and risk awareness of physicians and obese women. Effective strategies are needed to maintain third-trimester glycemic and weight gain control among otherwise healthy obese pregnant women.

Influence of family history on prognosis of spinal pain and the role of leisure time physical activity and body mass index: a prospective study using family-linkage data from the Norwegian HUNT study

ObjectivesTo investigate the influence of parental chronic spinal pain on prognosis of chronic spinal pain in adult offspring, and whether offspring physical activity level and body mass index (BMI) modified...

Maternal Physical Activity and Sex Impact Markers of Hepatic Mitochondrial Health.

Maternal exercise and physical activity during the gestational period can be protective against maternal high-fat diet-induced hepatic steatosis in older offspring. However, it is unknown whether these protective effects are seen in younger offspring. In this study, we investigated whether maternal physical activity would attenuate maternal western diet (WD)-induced steatosis in young adult rats. Female Wistar rats (7-8 wk of age) were randomized into WD (42% fat, 27% sucrose) or normal chow diet (ND), and further randomized into physical activity (RUN) or sedentary (SED) conditions for a total of four groups. Dams returned to ND/SED conditions after parturition. Postweaning, offspring were maintained in ND/SED conditions for 18 wk. Maternal WD-induced increases in male offspring body mass was attenuated in the WD/RUN offspring (P < 0.05). Maternal WD feeding significantly increased hepatic steatosis in male (but not female offspring), which was not attenuated by maternal RUN. However, maternal RUN increased (P < 0.05) hepatic markers of mitochondrial biogenesis and mitophagy (mitochondrial transcription factor A, peroxisome proliferator activator receptor γ, and nuclear factor E2-related factor 2) in all offspring and the mitophagy marker BCL2-interacting protein 3 in WD/RUN offspring. Interestingly, hepatic markers of de novo lipogenesis (fatty acid synthase and acetyl coenzyme A carboxylase), mitophagy (autophagy-related gene 12:5, BCL2-interacting protein 3, P62, and LC3 II/I), and mitochondria biogenesis/content (mitochondrial transcription factor A and OXPHOS-Complex II) were significantly increased in female versus male offspring. Although maternal physical activity did not attenuate maternal WD-induced hepatic steatosis as has been previously reported in older adult offspring, it did significantly increase hepatic markers of mitochondrial biogenesis and mitophagy. Furthermore, female offspring had elevated hepatic markers of mitochondrial health, possibly explaining why female rats are protected against maternal WD-induced hepatic steatosis. Future studies are warranted to shed light on the time line of hepatic steatosis development under the influence of maternal physical activity.

Maternal glycemic index and glycemic load in pregnancy and offspring metabolic health in childhood and adolescence-a cohort study of 68,471 mother-offspring dyads from the Danish National Birth Cohort.

High glycemic index (GI) and glycemic load (GL) as indicators of carbohydrate quality and quantity have been found to increase risk of metabolic outcomes in adults. Whether carbohydrate quality may influence metabolic programming already in early life is unknown. We examined the association of maternal GI and GL with offspring body mass index (BMI) in the first 7 years of life among 68,471 mother-offspring dyads from the Danish National Birth Cohort (DNBC). In a sub-cohort of offspring with clinical data (n = 1234) that included 608 dyads exposed to gestational diabetes mellitus (GDM), we also examined the relation to metabolic health at 9-16 years. Maternal GI and GL were quantified using a mid-pregnancy food frequency questionnaire. We used birth weight and length to calculate offspring's ponderal index. Age- and sex-specific BMI z scores at 5 mo, 12 mo, and 7 y were standardized against WHO reference data. In the clinical cohort, we quantified body composition, HOMA-IR, and HOMA-B. We used multivariable mixed linear and Poisson regression to model the associations. Median (IQR) of GI and GL were 83 (63-111) and 241 (180-333) g/day, respectively. We found that GI (Q4 vs. Q1:1.09, 95%CI: 1.03, 1.15) and GL (Q4 vs. Q1:1.10, 95%CI: 1.05, 1.16) modestly increased the relative risk of large-for gestational age (LGA). In the clinical sub-cohort, we observed a potential increase in offspring HOMA-IR, adiposity, and metabolic syndrome z score with higher maternal GI and GI. These associations were stronger among the GDM-exposed offspring, but the CI included the null value. We found associations of GI and GL in pregnancy with offspring LGA. Potential long-term benefits to offspring exposed to GDM need to be confirmed in larger, well-powered studies.

Long-Term Effects of Oral Antidiabetic Drugs During Pregnancy on Offspring: A Systematic Review and Meta-analysis of Follow-up Studies of RCTs.

IntroductionAntidiabetic drugs (OADs) are increasingly prescribed to treat hyperglycaemia during pregnancy in women with gestational diabetes mellitus (GDM) or polycystic ovary syndrome (PCOS), even though long-term effects on offspring are unknown. This systematic review summarises the evidence of follow-up studies of randomised controlled trials (RCTs) reporting on long-term effects of prenatal exposure to OADs on offspring.MethodsThe MEDLINE, EMBASE and CENTRAL databases were searched from inception to April 2018 for the concepts antidiabetic agents and prenatal exposure (or pregnancy and offspring/child) in combination with an RCT search filter. RCTs evaluating post-neonatal health effects in offspring and comparing maternal treatment with an OAD with no treatment, placebo, an alternative OAD or insulin during pregnancy were eligible for inclusion. Two independent researchers selected, extracted and assessed the data. Meta-analyses were performed using a random effects model and the Cochrane Collaboration’s risk of bias tool was used for quality assessment.ResultsTen studies were included, with a maximal follow-up duration of 9 years, comprising 778 children of mothers with GDM or PCOS who were randomised to either metformin or insulin/placebo during pregnancy. Meta-analysis showed that children prenatally exposed to metformin were heavier compared to controls (standardised mean difference (SMD) 0.26 [95% CI 0.11–0.41]), but not taller (SMD 0.10 [95% CI −0.14–0.33]). Additionally, offspring body mass index (BMI) z scores did not differ according to metformin exposure (mean difference 0.30 [95% CI −0.01–0.61]). Individual small studies reported that prenatal exposure to metformin was associated with greater mid-upper arm, head and waist circumferences, biceps skinfolds, waist-to-height ratio, more arm fat, higher fasting glucose, ferritin and lower LDL cholesterol in offspring.ConclusionPrenatal exposure to metformin is associated with increased offspring weight, but not with height or BMI. Larger follow-up studies are needed to confirm and look into the implications of these findings.Plain Language SummaryPlain language summary available for this article.Electronic supplementary materialThe online version of this article (10.1007/s13300-018-0479-0) contains supplementary material, which is available to authorized users.

Maternal smoking and low family income during pregnancy as predictors of the relationship between depression and adiposity in young adults

There is an increasing incidence of overweight/obesity and mental health disorders in young adults and the two conditions often coexist. We aimed to investigate the influence of antenatal and postnatal factors that may underlie this association with a focus on maternal prenatal smoking, socio-economic status and gender. Data from the Western Australian Pregnancy Cohort (Raine) Study (women enrolled 1989-1991) including 1056 offspring aged 20 years (cohort recalled 2010-2012) were analyzed (2015-2016) using multivariable models for associations between offspring depression scores (DASS-21 Depression-scale) and body mass index (BMI), adjusting for pregnancy and early life factors and offspring behaviours. There was a significant positive relationship between offspring depression-score and BMI independent of gender and other psychosocial covariates. There was a significant interaction between maternal prenatal smoking and depression-score (interaction coefficient=0.096; 95% CI: 0.006, 0.19, P=0.037), indicating the relationship between depression-score and BMI differed according to maternal prenatal smoking status. In offspring of maternal prenatal smokers, a positive association between BMI and depression-score (coefficient=0.133; 95% CI: 0.05, 0.21, P=0.001) equated to 1.1 kg/m2 increase in BMI for every 1standard deviation (8 units) increase in depression-score. Substituting low family income during pregnancy for maternal prenatal smoking in the interaction (interaction coefficient=0.091; 95% CI: 0.01, 0.17, P=0.027) showed a positive association between BMI and depression score only among offspring of mothers with a low family income during pregnancy (coefficient=0.118; 95% CI: 0.06, 0.18, P<0.001). There were no significant effects of gender on these associations. Whilst further studies are needed to determine whether these associations are supported in other populations, they suggest potentially important maternal behavioural and socio-economic factors that identify individuals vulnerable to the coexistence of obesity and depression in early adulthood.

Differences in maternal smoking across successive pregnancies - dose-dependent relation to BMI z-score in the offspring: an individual patient data (IPD) meta-analysis.

Uncontrolled family factors may bias the estimation of the association between maternal smoking during pregnancy and offspring body mass index (BMI). The objective was to assess if there is an association between maternal smoking during pregnancy and offspring BMI z-score independent of factors in the siblings' shared environment and if such association is linear. We performed an individual patient data meta-analysis using five studies providing sibling data (45,299 children from 14,231 families). In a multi-level model, separating within-family and between-family effects and with random intercept for families, we analysed the dose-response association between maternal number of cigarettes per day during pregnancy and offspring's BMI z-score using B-splines to allow for non-linear associations. A linear within-family effect for number of cigarettes smoked in the range from 1 to 30 cigarettes per day on the offspring's BMI z-score was observed. Each additional cigarette per day between sibling pregnancies resulted in an increase in BMI z-score of 0.007 (95% CI [0.006, 0.009]). A between family-effect emerged only with doses ≥25 cigarettes per day. The number of cigarettes mothers smoke per day during pregnancy is positively associated with offspring BMI z-score even among siblings, suggesting that the association is not entirely explained by confounding by family factors.

Thermal plasticity due to parental and early-life environments in the jacky dragon (Amphibolurus muricatus).

Developmental plasticity creates marked variation in individual phenotypes when the environment is patchy, such as when the thermal environment varies. Plasticity may occur in response to the environment experienced during an individual's lifetime or to the environment experienced by parents (transgenerational plasticity), and may be adaptive if it enhances fitness. In particular, plasticity in thermal traits, such as preferred temperatures and thermal limits, may improve performance and fitness based on temperatures in the local environment. This study examined the influence of parental and offspring thermal environments (duration of access to a basking lamp) on offspring thermal traits (preferred temperatures and panting threshold) in jacky dragons (Agamidae: Amphibolurus muricatus). Long-bask parental environments led, indirectly, to higher preferred temperatures of offspring due to increased offspring body mass compared to offspring of short-bask parents. The increase in median temperature preference was associated with a higher voluntary minimum body temperature and a narrower preference range, suggesting tradeoffs in thermal behavior and a matching of offspring preferences to the parental environment. Parental thermal treatment did not influence offspring panting threshold. Instead, the panting threshold tended to be higher in offspring that were reared in the long-bask treatment compared to those in the short-bask treatment, suggesting longer basking environments increased thermal tolerance. Parental and offspring thermal environment did not exhibit any interactive effect on thermal traits. The results indicate that thermal environments experienced by lizards can have both transgenerational and within-generation impacts on thermal traits, thus influencing how populations respond to fluctuating or changing climates.

Parental chronic widespread pain and the association with chronic widespread pain in adult offspring: Family-linkage data from the Norwegian HUNT Study.

Individuals experiencing chronic widespread pain (CWP) have greater disability and poorer quality of life compared to those with other chronic painful conditions; although research identifying risk factors for CWP is lacking. We aimed to investigate whether parental CWP increases the risk of offspring CWP, and if offspring body mass index (BMI) and leisure time physical activity modify this association. We included 6589 parent-offspring trios participating in the Norwegian HUNT Study in 1995-1997 and 2006-2008. Logistic regression was used to calculate adjusted odd ratios (ORs) (95% confidence intervals, CIs) as estimates of relative risk for offspring CWP. We analysed the joint effect of parental CWP and offspring BMI or leisure time physical activity on offspring risk of CWP and calculated the relative excess risk due to interaction (RERI). In total, 886 (13.5%) offspring developed CWP during follow-up. Having one (OR=1.23, 95% CI, 1.05-1.44) or both parents with CWP (OR=1.89, 95% CI, 1.50-2.38) increased the risk of offspring CWP. In analyses of joint effects, ORs were 1.84 (95% CI, 1.31-2.56) and 3.35 (95% CI, 1.94-5.77) in normal weight and obese offspring, respectively, when both parents had CWP. The estimate of RERI suggested some synergistic effect (RERI=1.19, 95% CI, -0.68 to 3.05), although precision was low. Risk of CWP was similar in active (OR=2.05, 95% CI, 1.56-2.70) and inactive (OR=1.96, 95% CI, 1.31-2.91) offspring when both parents had CWP. Parental CWP increases the risk of CWP in adult offspring, particularly if both parents have CWP and offspring are obese. This highlights a familial predisposition for CWP and an important target group for preventive measures. The parent-offspring transmission of CWP is stronger in obese offspring (particularly when both parents have CWP). This study is the first to investigate the interaction between modifiable lifestyle factors, familial factors and CWP.

Maternal intake of omega-3 and omega-6 polyunsaturated fatty acids during mid-pregnancy is inversely associated with linear growth

This study investigates relations of maternal N-3 and N-6 polyunsaturated fatty acids (PUFA) intake during pregnancy with offspring body mass index (BMI), height z-score and metabolic risk (fasting glucose, C-peptide, leptin, lipid profile) during peripuberty (8-14 years) among 236 mother-child pairs in Mexico. We used food frequency questionnaire data to quantify trimester-specific intake of N-3 alpha-linolenic acid, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA); N-6 linoleic acid and arachidonic acid (AA); and N-6:N-3 (AA:EPA+DHA), which accounts for the fact that the two PUFA families have opposing effects on physiology. Next, we used multivariable linear regression models that accounted for maternal education and parity, and child's age, sex and pubertal status, to examine associations of PUFA intake with the offspring outcomes. In models where BMI z-score was the outcome, we also adjusted for height z-score. We found that higher second trimester intake of EPA, DHA and AA were associated with lower offspring BMI and height z-score. For example, each 1-s.d. increment in second trimester EPA intake corresponded with 0.25 (95% CI: 0.03, 0.47) z-scores lower BMI and 0.20 (0.05, 0.36) z-scores lower height. Accounting for height z-score in models where BMI z-score was the outcome attenuated estimates [e.g., EPA: -0.16 (-0.37, 0.05)], suggesting that this relationship was driven by slower linear growth rather than excess adiposity. Maternal PUFA intake was not associated with the offspring metabolic biomarkers. Our findings suggest that higher PUFA intake during mid-pregnancy is associated with lower attained height in offspring during peripuberty. Additional research is needed to elucidate mechanisms and to confirm findings in other populations.

Do paternal semen parameters influence the birth weight or BMI of the offspring? A study from the Utah Population Database.

To study the role of individual semen parameters on the offspring birth weight and body mass index (BMI) from a population of men evaluated in an assisted reproduction technology (ART) clinic compared to fertile controls. We performed a retrospective study using a cohort with fertile, age-matched controls of men evaluated with semen analysis at the University of Utah Andrology Clinic from 1996 to 2011 and Intermountain Healthcare from 2002 to 2011. We use the offspring from both our sub-fertile cohort and controls using the Utah Population Database. The two main outcomes of interest were offspring birth weight and adolescent BMI. The offspring of men with impaired sperm parameters had significantly lower birth weight compared to fertile control offspring. Low-concentration offspring weighed 158g less (95% CI - 278~- 38; p = 0.01), low total count weighed 172g less (95% CI - 294~- 51; p = 0.005), and low total motility weighed 155g less (95% CI - 241~- 69; p < 0.001) compared to those of the controls. When we controlled for the use of ART within the sub-fertile group, we found that there was a significant trend of increasing birth weight across levels of total motile count and total sperm count compared to the azoospermic group. We did not find any consistent significant differences between the subject and control adolescence BMI based on semen parameters. Despite limitations within our population-based dataset, we found that poor quality semen analysis parameters pointed towards an association with low birth weight in the offspring of sub-fertile men compared to the offspring of normal fertile controls. However, in contrast to studies of ART effects on offspring, we did not find evidence of long-term associations between semen quality and offspring BMI.

Effect of maternal glycemia and weight status on offspring birth measures and BMI-z among Chinese population in the first year

To investigate the effects of maternal fasting plasma glucose (FPG) and pre-pregnancy weight status (PPWS) on offspring birth measures and body mass index z-score (BMI-z) in the first year, we conducted a prospective study of 1,096 mother-infant dyads in Guangdong, China, 2014–2015. Multivariate logistic regression was used to test independent/interaction associations of maternal FPG and PPWS with macrosomia/large for gestational age (LGA). Association of PPWS and FPG with offspring BMI-z in the first year was assessed by the linear mixed effects models. For each 1-mmol/L increase in FPG, the risk of macrosomia and LGA was elevated by 2.74 and 2.01 (95% CI: 1.85, 7.60 and 1.54, 5.88), respectively. No main effect of PPWS or interaction association of FPG and PPWS on macrosomia/LGA was observed (P > 0.05). A relation between maternal FPG and PPWS was detected (P < 0.05). Infants of Q5 FPG mothers, those who were born to OWO mothers, had a 0.35 increase in the BMI-z (95% CI: 0.16, 0.55) compared with infants of NW mothers. In conclusion, maternal FPG is positively associated with macrosomia/LGA. Maternal PPWS and FPG considerably interacted for the association with the risk of offspring high BMI-z in the first year.

Among‐individual heterogeneity in maternal behaviour and physiology affects reproductive allocation and offspring life‐history traits in the garter snake Thamnophis elegans

Accumulating evidence suggests that within‐individual plasticity of behavioural and physiological traits is limited, resulting in stable among‐individual differences in these aspects of the phenotype. Furthermore, these traits often covary within individuals, resulting in a continuum of correlated phenotypic variation among individuals within populations and species. This heterogeneity, in turn, affects individual fitness and can have cross‐generational effects. Patterns of trait covariation, among‐individual differences, and subsequent fitness consequences have long been recognized in reptiles. Here, we provide a test of patterns of among‐individual heterogeneity in behaviour and physiology and subsequent effects on reproduction and offspring fitness in the garter snake Thamnophis elegans. We find that measures of activity levels vary among individuals and are consistent within individuals in reproductive female snakes, indicating stable behavioural phenotypes. Blood hormone and glucose concentrations are not as stable within individuals, indicating that these traits do not describe consistent physiological phenotypes. Nonetheless, the major axes of variation in maternal traits describe behavioural and physiological phenotypes that interact to predict offspring body condition and mass at birth. This differential allocation of energy to offspring, in turn, strongly influences subsequent offspring growth and survival. This pattern suggests the potential for strong selection on phenotypes defined by behaviour–physiology interactions.

Maternal viral mimetic administration at the beginning of fetal hypothalamic nuclei development accelerates puberty in female rat offspring

This study aimed to investigate the effects of maternal viral infection during a critical time window of fetal hypothalamic development on timing of puberty in the female offspring. For that purpose, a viral mimetic (i.e., synthetic double-strand RNA, namely, polyinosinic-polycytidylic acid, poly (I:C)) or saline was injected (i.p.) to the pregnant rats during the beginning (day 12 of pregnancy, n = 5 for each group) or at the end of this time window (day 14 of pregnancy, n = 5 for each group). Four study groups were formed from the female pups (n = 9-10 pups/group). Following weaning of pups, vaginal opening and vaginal smearing was studied daily until 2 sequential estrous cycles were observed. During the second diestrus phase, blood samples were taken for progesterone, leptin, corticosterone, follicle-stimulating hormone, and luteinizing hormone. Maternal poly (I:C) injection on day 12 of pregnancy increased body mass and reduced the time to puberty in the female offspring. Neither poly (I:C) nor timing of injection affected other parameters studied (p > 0.05). It has been shown for the first time that maternal viral infection during the beginning of fetal hypothalamic development might hasten puberty by increasing body mass in rat offspring.

Major histocompatibility complex genes partly explain early survival in house sparrows

Environmental factors and genetic incompatibilities between parents have been suggested as important determinants for embryonic mortality and survival. The genetic set-up of the immune system, specifically the highly polymorphic major histocompatibility complex (MHC) may also influence individual resistance to infections. MHC proteins are important for an appropriate adaptive immune response and enable T-cells to separate ‘self’ from ‘non-self’. Here we investigate the importance of MHC functional diversity for early development in birds, more specifically, if offspring survival and body mass or size depends on number of different functional MHC alleles, specific functional MHC alleles or similarity of MHC alleles in the parents. Unhatched eggs are common in clutches of many bird species. In house sparrows (Passer domesticus), embryo and nestling mortality can exceed 50%. To control for environmental factors, our study was carried out on an aviary population. We found that one specific functional MHC allele was associated with reduced nestling survival, which was additionally supported by lower body mass and a smaller tarsus when nestlings have been 6 days old. Another allele was positively associated with tarsus length at a later nestling stage (nestlings 12 days old). These results indicate that MHC alleles might influence pathogen resistance or susceptibility.