Offspring Cognition Research Articles

Effects of prenatal exposure to silver nanoparticles on spatial cognition and hippocampal neurodevelopment in rats

BackgroundSilver nanoparticles (Ag-NPs) are among the most commonly used nanomaterials and may be exposed to human and ecosystem. Prior in vitro study showed that Ag-NPs compromised neurodevelopment of PC12 cells. This study aims to investigate the effect of prenatal exposure to Ag-NPs on spatial cognition and hippocampal neurodevelopment in rats. MethodsPregnant rats were exposed by intraperitoneal injection to various solutions during pregnancy, including vehicle (water and glycerol mixture, 1:1 in volume), uncoated Ag-NPs (0.427mg Ag perg rat), polyvinylpyrrolidine (PVP)-coated Ag-NPs (0.407mg Ag perg rat), silver nitrate (0.013mg Ag+ and 0.007mg NO3+ per g rat) and sodium nitrate (0.007mg NO3+ perg rat). Pregnant rats without any injection were used as blank control. Male offspring at postnatal day 35 (PND35) were randomly selected for Morris Water Maze (MWM) test. After the MWM test, the rats were decapitated and hippocampus were collected for analysis of tissue structure, silver content, GAP-43 mRNA and protein expressions. ResultsFor the spatial learning in MWM test, since the third test day, the escape latency of rats in the uncoated Ag-NPs group was significantly higher than those in the other groups. The behaviors of rats were not significantly different among the other groups. The averaged silver content in the hippocampus of rats in the uncoated Ag-NPs group was 17.51μg/g, significantly higher than those in the other groups. The hippocampal structure in rats of the uncoated Ag-NPs group was deformed as compared to those in the other groups. Compared with the rats in blank and vehicle controls, the levels of GAP-43 mRNA and protein in the uncoated Ag-NPs, PVP-coated Ag-NPs, silver nitrate and sodium nitrate groups were all significantly decreased. The levels of GAP-43 mRNA and protein of rats in the uncoated Ag-NPs group was significantly lower than those in the later three groups, while there was no significant difference among the later three groups. ConclusionsMaternal exposure to uncoated Ag-NPs during pregnancy impaired spatial cognition in rat offspring. GAP-43 reduction might be involved in the cognitive impairment. The toxicity was mainly associated with release of silver ion. Coating with PVP reduced the toxicity of Ag-NPs.

Fœtal impact of glucocorticoids in the programming of the disease

Epidemiological and experimental evidence suggests that an adverse fetal environment permanently “programmes” physiology leading to increased risks of cardiometabolic and neuropsychiatric disorders in later life. We originally hypothesised that fetal glucocorticoid overexposure might underpin this link. In genetically identical rodents, prenatal stress, glucocorticoid overexposure or inhibition/knockout of 11s-hydroxysteroid dehydrogenase type 2 (11β-HSD2), the feto-placental “barrier” to maternal glucocorticoids, reduces birth weight and causes permanent hypertension, hyperglycaemia, increased hypothalamic-pituitary-adrenal (HPA) axis activity and anxiety-related behaviours in adult offspring. The phenotype persists into a second generation and transmits via male and female lines. This implies epigenetic mediation, a mechanism emerging for HPA axis and metabolic programming. However, whilst first and second generation phenotypes are similar, the molecular mechanisms and epigenetic markers differ in each generation, implying strong selection on phenotype but weighing against neo-Lamarckian notions of ‘epigenetic inheritance’. Glucocorticoid programming appears of clinical relevance. In humans, placental 11β-HSD2 activity correlates directly with birth weight and inversely with infant blood pressure. Moreover, low birth weight babies have higher plasma cortisol levels throughout adult life, indicating HPA programming. Indeed, maternal glucocorticoid therapy or ingestion of liquorice (which inhibits 11β-HSD) alters offspring cognition, behaviour and HPA axis function. Stress has similar effects since the offspring of women pregnant during and directly exposed to the 9.11.2001 atrocity and who developed PTSD exhibit neuroendocrine changes but only if exposure was in the third trimester. Furthermore, exposure to the Nazi Holocaust exerted permanent effects upon glucocorticoid levels and steroid metabolism, effects dependent upon the age at exposure. The second (unexposed) generation also shows altered cortisol levels and metabolism, again with discordance in detail between generations. Overall, the data suggest that developmental exposure to excess glucocorticoids/stress programmes peripheral and CNS functions in adult life, predisposing to affective and other pathology, and these effects may impact on a subsequent generation. Any core mechanistic role for epigenetic processes in such early environment-induced effects is attractive but remains to be unequivocally established.

Maternal omega-3 fatty acid supplementation on vitamin B12 rich diet improves brain omega-3 fatty acids, neurotrophins and cognition in the Wistar rat offspring

The consequences of wide spread vegetarianism due to low vitamin B12 on brain development and functioning is gaining importance. However, there are no studies which have evaluated exclusively vitamin B12 supplementation during pregnancy on brain growth. A series of our animal studies have documented adverse effects of maternal micronutrient imbalance on brain neurotrophins and its amelioration by omega-3 fatty acids. Therefore, the present study investigated the effect of maternal supplementation with vitamin B12 alone and B12 plus omega-3 fatty acid on pup brain fatty acids and neurotrophins at birth and 3 mo of age. Pregnant Wistar rats and their male offspring were assigned to 3 dietary groups: Control (normal vitamin B12 (25 μg/kg), vitamin B12 supplemented (BS) (50 μg/kg), vitamin B12 supplemented with omega-3 fatty acid (BSO) till 3 month of age. Maternal vitamin B12 supplementation (BS) increased brain BDNF (protein and mRNA) and DHA levels in pups at birth and in the hippocampus at 3 month of age (BDNF only). These effects were further enhanced by omega-3 fatty acid supplementation to vitamin B12 supplemented group. The spatial memory performance was found to be enhanced in BSO group which was characterised by less number of errors in radial eight arm maze. Our results indicate that a combination of omega-3 fatty acid and vitamin B12 enriched diet may exert beneficial effects on synaptic plasticity and cognition, which may prove beneficial for mental health, particularly in preventing neurocognitive disorders.

Maternal iron levels early in pregnancy are not associated with offspring IQ score at age 8, findings from a Mendelian randomization study

Background/Objectives:Iron is fundamental to many basic biological functions, and animal studies suggest that iron deficiency early in life can have a lasting impact on the developing brain.Subjects/Methods:We used a population-based cohort of mothers and their children to assess the effect of iron status among pregnant women on the cognitive ability of their offspring. But to avoid the inherent confounding that occurs within observational epidemiology studies we examined the association of maternal genotype at single-nucleotide polymorphisms in the genes HFE (rs1799945) and (rs1800562), TF (rs3811647) and TMPRSS6 (rs1800562), which are related to iron, haemoglobin or transferrin levels, on their child's cognitive test scores at age 8.Results:We found strong associations between HFE and TMPRSS6 genotypes and mother's haemoglobin levels early in pregnancy (P-values are all ⩽4.1 × 10−5) and a genetic score comprised of alleles at these loci was even more strongly associated with haemoglobin levels (P=3.0 × 10−18), suggesting that this was a good instrument to use to look at the effect of prenatal iron levels on offspring cognition. However, mother's genotype at the above loci was not associated with offspring IQ at age 8.Conclusions:We therefore concluded that there is no evidence of an effect of exposure to low levels of iron (within the normal range) in pregnancy on offspring cognition at age 8. However, pregnant women in the UK with low haemoglobin levels are prescribed iron supplements and so we were unable to look at the effect of iron deficiency in our study.

Mother's milk programs offspring's cognition

A study finds that immune factors transmitted through breast milk regulate the cognitive function of offspring. Changes in milk composition alter hippocampal development and have effects on memory that last into adulthood.

Parental longevity is associated with cognition and brain ageing in middle-aged offspring

offspring of long-lived individuals have lower risk for dementia. We examined the relation between parental longevity and cognition and subclinical markers of brain ageing in community-dwelling adult offspring. offspring participants with both parents in the Framingham Heart Study, aged ≥55 years and dementia-free underwent baseline and repeat neuropsychological (NP) testing and brain magnetic resonance imaging (MRI). Parental longevity was defined as having at least one parent survive to age ≥85 years. To test the association between parental longevity and measures of cognition and brain volumes, we used multivariable linear and logistic regression adjusting for age, sex, education and time to NP testing or brain MRI. of 728 offspring (mean age 66 years, 54% women), 407 (56%) had ≥1 parent achieve longevity. In cross-sectional analysis, parental longevity was associated with better scores on attention (beta 0.21 ± 0.08, P = 0.006) and a lower odds of extensive white matter hyperintensity on brain MRI (odds ratio 0.59, 95% CI: 0.38, 0.92, P = 0.019). The association with white matter hyperintensity was no longer significant in models adjusted for cardiovascular risk factors and disease. In longitudinal analysis (6.7 ± 1.7 years later), offspring with parental longevity had slower decline in attention (0.18 ± 0.08, P = 0.038), executive function (beta 0.19 ± 0.09, P = 0.031) and visual memory (beta -0.18 ± 0.08, P = 0.023), and less increase in temporal horn volume (beta -0.25 ± 0.09, P = 0.005). The associations persisted in fully adjusted models. parental longevity is associated with better brain ageing in middle-aged offspring.

Prenatal alcohol exposure and offspring cognition and school performance. A ‘Mendelian randomization’ natural experiment

Background There is substantial debate as to whether moderate alcohol use during pregnancy could have subtle but important effects on offspring, by impairing later cognitive function and thus school performance. The authors aimed to investigate the unconfounded effect of moderately increased prenatal alcohol exposure on cognitive/educational performance.Methods We used mother-offspring pairs participating in the Avon Longitudinal Study of Parents and Children (ALSPAC) and performed both conventional observational analyses and Mendelian randomization using an ADH1B variant (rs1229984) associated with reduced alcohol consumption. Women of White European origin with genotype and self-reported prenatal alcohol consumption, whose offspring’s IQ score had been assessed in clinic (N = 4061 pairs) or Key Stage 2 (KS2) academic achievement score was available through linkage to the National Pupil Database (N = 6268), contributed to the analyses.Results Women reporting moderate drinking before and during early pregnancy were relatively affluent compared with women reporting lighter drinking, and their children had higher KS2 and IQ scores. In contrast, children whose mothers’ genotype predisposes to lower consumption or abstinence during early pregnancy had higher KS2 scores (mean difference +1.7, 95% confidence interval +0.4, +3.0) than children of mothers whose genotype predisposed to heavier drinking, after adjustment for population stratification.Conclusions Better offspring cognitive/educational outcomes observed in association with prenatal alcohol exposure presumably reflected residual confounding by factors associated with social position and maternal education. The unconfounded Mendelian randomization estimates suggest a small but potentially important detrimental effect of small increases in prenatal alcohol exposure, at least on educational outcomes.

Associations of Maternal Weight Gain in Pregnancy With Offspring Cognition in Childhood and Adolescence

Nutrition in utero and during early infancy is critical for normal development and cognition. It is still unclear whether less drastic undernutrition that affects gestational weight gain (GWG), but does not necessarily cause weight loss, is related to offspring long-term cognition. This study was designed to examine the association of GWG with a child’s School Entry Assessment (SEA) scores at age 4 years, IQ at age 8 years, and school final examination results at age 16 years. The Avon Longitudinal Study of Parents and Children is a prospective, population-based birth cohort study that recruited 14,541 pregnant women with expected delivery dates between April 1991 and December 1992. Analyses included only women with complete GWG data (n = 12,484) and with term deliveries (n = 12,449). Maternal GWG was determined as a measure of “less than recommended,” “as recommended,” and “more than recommended,” based on the 2009 Institute of Medicine recommendations, in which the recommended weight gain varies depending on prepregnancy body mass index. Pregnancy weight measurements were used to develop a linear spline multilevel model relating weight to gestational age. This model was then used to predict each woman’s weight at 0 weeks’ gestation (prepregnancy weight) and GWG/wk from 0 to 18, 18 to 28, and 28 weeks to delivery. Outcomes included SEA scores at age 4 years, cognitive function at age 8 years using the Wechsler Intelligence Scale for Children from which IQs are derived, and results of General Certificate of Secondary Education examinations at age 16 years. Multivariable logistic and linear regression models were created, with model 1 adjusted for gestational age, maternal age, age at outcome assessment, and sex. Model 2, the main model, was adjusted for the confounders in model 1 and prepregnancy body mass index, maternal smoking during pregnancy, parity, mode of delivery, and maternal education. Interactions between being overweight/obese before pregnancy and GWG and their association with outcomes were also assessed. Compared with women who gained as recommended (reference group), those who gained less than recommended were slightly older (28.7 ± 4.7 vs 29.0 ± 4.9 years) and more likely to smoke, be from a manual social class, be multiparous, and have babies with a lower mean birth weight (3511.4 ± 445.2 vs 3333.4 ± 445.4 g). Compared with the reference group, those who gained more than recommended were slightly younger (28.7 ± 4.7 vs 27.9 ± 4.6 years), were less likely to smoke, were less educated, and were more likely to be nulliparous, have a cesarean delivery, and have heavier offspring (3511.4 ± 445.2 vs 3639.6 ± 481.1 g). Compared with the reference group, offspring of women who gained less than recommended had lower mean SEA scores, even after adjusting for confounders, with mean differences of SEA scores in model 1 and model 2 of −0.100 and −0.075, respectively (95% confidence intervals [CIs], −0.155 to −0.046 and −0.127 to −0.013, respectively). No association was found between less than recommended GWG and offspring IQ, nor was there strong evidence found for associations of more than recommended GWG with SEA scores or IQs. More than recommended GWG was associated with decreased odds of obtaining adequate final examination results in model 1 (OR, 0.89; 95% CI, 0.79–1.00), but this was attenuated after adjusting for confounders in model 2 (OR, 1.00; 95% CI, 0.88–1.14). Both less and more than recommended GWGs were associated with greater odds of low General Certificate of Secondary Education achievement. Gestational weight gain in all 3 periods of pregnancy was positively associated with IQs in models 1 and 2. The magnitudes of these associations were modest and unlikely to have major importance for individuals. At a population level, modest shifts in the distribution of educational attainment could be important. The results indicate the importance of defining optimal GWG, which is a complex process involving many competing risks.

Commentary: Can maternal-paternal comparisons contribute to our understanding of maternal pre-pregnancy obesity and its association with offspring cognitive outcomes?

In this issue of the IJE, Casas and colleagues 1 report associations of maternal pre-pregnancy obesity with lower infant cognitive development scores in two European cohorts, RHEA and INMA. This was observed after extensive confounder adjustment (in particular, multiple indicators of socioeconomic position) and results were replicated across the two cohorts, reflecting two important methodological strengths of the paper. This paper is timely as it contributes to a body of literature on maternal obesity and offspring cognitive ability that is currently sparse and relatively inconclusive. Although independent associations have been reported in several previous studies, inconsistent 2 and predominantly null 3 associations have also been observed when multiple cohorts have been investigated simultaneously. Nevertheless, the persisting associations observed independently of a comprehensive range of sociodemographic and postnatal factors, here and elsewhere, raise the question as to whether maternal obesity might adversely affect cognitive development in offspring via intrauterine mechanisms. In the presence of escalating rates of obesity worldwide, this association warrants further study since, if causal, this would clearly be an increasing public health concern. A crucial step in investigating the association of maternal obesity with offspring cognitive development, above and beyond replication of results, is to disentangle adjusted associations that are due to intrauterine mechanisms from those that reflect residual cofounding by postnatal, socioeconomic and familial factors not fully captured by the measured confounders. As can be seen from the results in the main paper and supplementary information, maternal obesity and lower infant cognitive scores were both associated with less favourable sociodemographic factors in this study (lower parental education, lower occupational social class, shorter breastfeeding duration etc.). Furthermore, confounder associations (namely, with infant cognitive scores) appeared stronger in RHEA, compared with INMA. Since the unadjusted association for maternal obesity and infant cognition was also substantially larger in RHEA (6.00, vs 3.37 in INMA), and this reduced markedly, resulting in similar effect sizes across the cohorts following confounder adjustment, confounding factors therefore appear to account for a substantial proportion of the observed relationship between maternal obesity and offspring cognition, at least at the unadjusted level. Given the known difficulties in fully capturing confounding, particularly socioeconomic,

Cognitive ability in old age may be determined in the womb

Commentary on: Tuovinen S, Raikkonen K, Kajantie E, et al. Hypertensive disorders in pregnancy and cognitive decline in the offspring up to old age. Neurology 2012;79:1578–82.[OpenUrl][1][CrossRef][2] In the past few...

Associations of maternal weight gain in pregnancy with offspring cognition in childhood and adolescence: findings from the Avon Longitudinal Study of Parents and Children.

An association of gestational weight gain (GWG) with offspring cognition has been postulated. We used data from the Avon Longitudinal Study of Parents and Children, a United Kingdom prospective cohort (1990 through the present) with a median of 10 maternal weight measurements in pregnancy. These were used to allocate participants to 2009 Institute of Medicine weight-gain categories and in random effect linear spline models. Outcomes were School Entry Assessment score (age, 4 years; n = 5,832), standardized intelligence quotient assessed by Wechsler Intelligence Scale for Children (age, 8 years; n = 5,191), and school final-examination results (age, 16 years; n = 7,339). Offspring of women who gained less weight than recommended had a 0.075 standard deviation lower mean School Entry Assessment score (95% confidence interval: −0.127, −0.023) and were less likely to achieve adequate final-examination results (odds ratio = 0.88, 95% confidence interval: 0.78, 0.99) compared with offspring of women who gained as recommended. GWG in early pregnancy (defined as 0–18 weeks on the basis of a knot point at 18 weeks) and midpregnancy (defined as 18–28 weeks on the basis of knot points at 18 and 28 weeks) was positively associated with School Entry Assessment score and intelligence quotient. GWG in late pregnancy (defined as 28 weeks onward on the basis of a knot point at 28 weeks) was positively associated with offspring intelligence quotient and with increased odds of offspring achieving adequate final-examination results in mothers who were overweight prepregnancy. Findings support small positive associations between GWG and offspring cognitive development, which may have lasting effects on educational attainment up to age 16 years.

Prenatal stress disturbs hippocampal KIF17 and NR2B in spatial cognition in male offspring

Numerous studies have demonstrated that prenatal stress disturbs the hippocampal-mediated learning and memory processes in offspring. The underlying mechanisms for this effect, however, remain vague. It is well documented that N-methyl-D-aspartate (NMDA) receptors play a pivotal role in learning and memory, which are related to dynamically trafficking and regulating NMDA receptors by their response motor proteins. Over the past few years, increasing numbers of studies have elucidated that hippocampal-mediated learning and memory are regulated by KIF17 (kinesin superfamily motor protein 17), which specifically transports and regulates the NMDA receptor subunit NR2B in hippocampal neurons. The present study shows the influence of prenatal stress on KIF17 and NR2B expression and hippocampal NR2A/NR2B ratio partially reflecting function of KIF17, using mice as models. It was found that prenatal stress significantly decreased the hippocampal KIF17 and NR2B level in offspring at postnatal stages of 3 weeks and 9 weeks. Moreover, hippocampal KIF17 in the prenatally stressed pups continued to be weakened even after serial Morris water maze trainings, but not NR2B. Finally, the synaptic NR2A/NR2B level was upregulated in offspring exposed to prenatal stress, which revealed the dysfunction of KIF17. Thus, we conclude that prenatal stress leads to long-lasting deterioration of the expression and function of hippocampal KIF17 in offspring, which may be related to deficits of spatial cognition caused by prenatal stress. These data underpin the hypotheses that a physiopathology of neurodevelopmental origin in early life leads to defects in learning and memory in later life.

Fetal Alcohol Exposure and IQ at Age 8: Evidence from a Population-Based Birth-Cohort Study

BackgroundObservational studies have generated conflicting evidence on the effects of moderate maternal alcohol consumption during pregnancy on offspring cognition mainly reflecting problems of confounding. Among mothers who drink during pregnancy fetal alcohol exposure is influenced not only by mother’s intake but also by genetic variants carried by both the mother and the fetus. Associations between children’s cognitive function and both maternal and child genotype at these loci can shed light on the effects of maternal alcohol consumption on offspring cognitive development.MethodsWe used a large population based study of women recruited during pregnancy to determine whether genetic variants in alcohol metabolising genes in this cohort of women and their children were related to the child’s cognitive score (measured by the Weschler Intelligence Scale) at age 8.FindingsWe found that four genetic variants in alcohol metabolising genes in 4167 children were strongly related to lower IQ at age 8, as was a risk allele score based on these 4 variants. This effect was only seen amongst the offspring of mothers who were moderate drinkers (1–6 units alcohol per week during pregnancy (per allele effect estimates were −1.80 (95% CI = −2.63 to −0.97) p = 0.00002, with no effect among children whose mothers abstained during pregnancy (0.16 (95%CI = −1.05 to 1.36) p = 0.80), p-value for interaction = 0.009). A further genetic variant associated with alcohol metabolism in mothers was associated with their child’s IQ, but again only among mothers who drank during pregnancy.

Maternal Stress and Child Outcomes: Evidence from Siblings.

We study how maternal stress affects offspring outcomes. We find that in-utero exposure to elevated levels of the stress hormone cortisol negatively affects offspring cognition, health and educational attainment. These findings are based on comparisons between siblings which limits variation to short-lived shocks and controls for unobserved differences between mothers that could bias estimates. Our results are consistent with recent experimental results in the neurobiological literature linking exogenous exposure to stress hormones in-utero with declines in offspring cognitive, behavioral and motor development. Moreover, we find that not only are mothers with low levels of human capital characterized by higher and more variable cortisol levels, but that the negative impact of elevated cortisol on their offspring is greater. These results suggest that maternal stress may play a role in the intergenerational persistence of poverty.

042 A critical analysis of studies of antiepileptic drugs (AEDs) and pregnancy. Maternal safety is neglected

Guidelines for AEDs during pregnancy emphasise dangers of polytherapy and sodium valproate. I evaluate 1651 articles on AEDs and pregnancy since 1970, identified through a PubMed search. All studies are...

Associations of Existing Diabetes, Gestational Diabetes, and Glycosuria with Offspring IQ and Educational Attainment: The Avon Longitudinal Study of Parents and Children

Introduction. Results from studies examining associations of maternal diabetes in pregnancy with offspring cognitive outcomes have been inconclusive. Methods. We used data from the Avon Longitudinal Study of Parents and Children, a UK prospective pregnancy cohort. Outcomes were School Entry Assessment (SEA) scores (age 4, N = 6, 032) and WISC-III IQ (age 8, N = 5, 282–5,307) and General Certificate of Secondary Education (GCSE) results (age 16, N = 7, 615). Results. Existing diabetes, gestational diabetes, and, to a lesser extent, glycosuria were associated with lower offspring SEA scores (age 4), IQ (age 8), and GCSE results (age 16) even when adjusting for offspring sex, maternal age, prepregnancy BMI, smoking in pregnancy, parity, caesarean section, maternal education, and occupational social class. Offspring of mothers with existing diabetes had a threefold risk of achieving no GCSEs graded A*-C, whilst offspring of women with gestational diabetes had, on average, a five point lower IQ compared to offspring of women with no diabetes or glycosuria. Conclusions. Maternal diabetes in pregnancy is consistently associated with lower offspring cognition and educational attainment though confidence intervals were wide. The weaker associations with glycosuria suggest a dose-dependent adverse association with IQ.

P1-427 Associations of maternal weight gain in pregnancy with offspring cognition throughout childhood and adolescence

IntroductionBasic science evidence suggests that gestational weight gain (GWG) may influence offspring cognitive development. However, this relationship has not been investigated in human population studies.MethodsData from the ALSPAC, a UK...

Prenatal betamethasone exposure has sex specific effects in reversal learning and attention in juvenile baboons

We investigated effects of 3 weekly courses of fetal betamethasone (βM) on motivation and cognition in juvenile baboon offspring utilizing the Cambridge Neuropsychological Test Automated Battery. Pregnant baboons (Papio species) received 2 injections of saline control or 175 μg/kg βM 24 hours apart at 0.6, 0.65, and 0.7 gestation. Offspring (saline control female, n = 7 and saline control male, n = 6; βM female [FβM], n = 7 and βM male [MβM], n = 5) were studied at 2.6-3.2 years with a progressive ratio test for motivation, simple discriminations and reversals for associative learning and rule change plasticity, and an intra/extradimensional set-shifting test for attention allocation. βM exposure decreased motivation in both sexes. In intra/extradimensional testing, FβM made more errors in the simple discrimination reversal (mean difference of errors [FβM - MβM] = 20.2 ± 9.9; P ≤ .05), compound discrimination (mean difference of errors = 36.3 ± 17.4; P ≤ .05), and compound reversal (mean difference of errors = 58 ± 23.6; P < .05) stages as compared to the MβM offspring. This central nervous system developmental programming adds growing concerns of long-term effects of repeated fetal synthetic glucocorticoid exposure. In summary, behavioral effects observed show sex-specific differences in resilience to multiple fetal βM exposures.

Tu-S9:3 Omega-3 fatty acids and fatal arrhythmias

Conflicting evidence concerning possible harm from mercury (Hg) in regard to offspring cognition if the woman eats fish has prompted this study to examine evidence from a British pre-birth cohort to investigate the relationship between the two.Pregnant women (median prenatal blood mercury 1.86 μg/L) resident in the study area with delivery between April 1991 and December 1992 were followed up and verbal, performance and total intelligence quotient (IQ) of 2062 offspring were measured at age 8. Analysis treated IQ as (a) continuous and (b) the lowest 25% of the distribution. Multiple and logistic regression analyses took account of social and demographic variables. Stratification considered children of fish eaters separately.Before adjustment, mean full-scale IQ increased with increasing Hg (change with 1SD of Hg = +2.02; 95%CI +1.40,+2.64 IQ points; P < 0.0001); after adjustment effect size was reduced although still positive (+0.61;95%CI -0.06,+1.29 IQ points; P = 0.073). The adjusted positive relationship was stronger when fish-eating mothers were considered separately (+0.84:95%CI +0.13,+1.56 IQ points; P = 0.021) in comparison with the outcomes for non-fish eaters, where the adjusted relationship was negative (-2.22;95%CI -5.00,+0.56 IQ points; P = 0.117). The binary outcome showed a similar pattern with the adjusted OR for non-fish-eaters 1.79 (95%CI 1.10,2.93; P = 0.019) per SD of Hg, significantly different from that for fish consumers (0.94;95%CI:0.82,1.08)(Pinteraction<0.05). There were no differences between the sexes in the associations, nor did the level of the mother’s blood selenium change the effect sizes.The relationship between intrauterine exposure to mercury and offspring IQ appears to be benign provided the mother consumes fish.

Effect of repeating administration of antenatal betamethasone on cognition in mice offspring

Effect of repeating administration of antenatal betamethasone on cognition in mice offspring