Journal of Developmental Origins of Health and Disease最新文献

{"title":"Relationships between the maternal prenatal diet and epigenetic state in infants: a systematic review of human studies.","authors":"Kathya K Fernando, Jeffrey M Craig, Samantha L Dawson","doi":"10.1017/S2040174423000211","DOIUrl":"10.1017/S2040174423000211","url":null,"abstract":"<p><p>Most human studies investigating the relationship between maternal diet in pregnancy and infant epigenetic state have focused on macro- and micro-nutrient intake, rather than the whole diet. This makes it difficult to translate the evidence into practical prenatal dietary recommendations.To review the evidence on how the prenatal diet relates to the epigenetic state of infants measured in the first year of life via candidate gene or genome-wide approaches.Following the PRISMA guidelines, this systematic literature search was completed in August 2020, and updated in August 2021 and April 2022. Studies investigating dietary supplementation were excluded. Risk of bias was assessed, and the certainty of results was analysed with consideration of study quality and validity.Seven studies were included, encompassing 6852 mother-infant dyads. One study was a randomised controlled trial and the remaining six were observational studies. There was heterogeneity in dietary exposure measures. Three studies used an epigenome-wide association study (EWAS) design and four focused on candidate genes from cord blood samples. All studies showed inconsistent associations between maternal dietary measures and DNA methylation in infants. Effect sizes of maternal diet on DNA methylation ranged from very low (< 1%) to high (> 10%). All studies had limitations and were assessed as having moderate to high risk of bias.The evidence presented here provides very low certainty that dietary patterns in pregnancy relate to epigenetic state in infants. We recommend that future studies maximise sample sizes and optimise and harmonise methods of dietary measurement and pipelines of epigenetic analysis.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"14 4","pages":"540-555"},"PeriodicalIF":1.8,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10235131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential long consequences from internal and external ecology: loss of gut microbiota antifragility in children from an industrialized population compared with an indigenous rural lifestyle.","authors":"Isaac G-Santoyo,&nbsp;Elvia Ramírez-Carrillo,&nbsp;Jonathan Dominguez Sanchez,&nbsp;Oliver López-Corona","doi":"10.1017/S2040174423000144","DOIUrl":"10.1017/S2040174423000144","url":null,"abstract":"<p><p>Human health is strongly mediated by the gut microbiota ecosystem, which, in turn, depends not only on its state but also on its dynamics and how it responds to perturbations. Healthy microbiota ecosystems tend to be in criticality and antifragile dynamics corresponding to a maximum complexity configuration, which may be assessed with information and network theory analysis. Under this complex system perspective, we used a new analysis of published data to show that a children's population with an industrialized urban lifestyle from Mexico City exhibits informational and network characteristics similar to parasitized children from a rural indigenous population in the remote mountainous region of Guerrero, México. We propose then, that in this critical age for gut microbiota maturation, the industrialized urban lifestyle could be thought of as an external perturbation to the gut microbiota ecosystem, and we show that it produces a similar loss in criticality/antifragility as the one observed by internal perturbation due to parasitosis by the helminth <i>A. lumbricoides.</i> Finally, several general complexity-based guidelines to prevent or restore gut ecosystem antifragility are discussed.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"14 4","pages":"469-480"},"PeriodicalIF":1.7,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9503803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship between insulin and Netrin-1/DCC guidance cue pathway regulation in the prefrontal cortex of rodents exposed to prenatal dietary restriction.","authors":"Aashita Batra, Santiago Cuesta, Marcio Bonesso Alves, Jose Maria Restrepo, Michel Giroux, Daniela Pereira Laureano, Amanda Brondani Mucellini Lovato, Patrícia Maidana Miguel, Tania Diniz Machado, Roberta Dalle Molle, Cecilia Flores, Patricia Pelufo Silveira","doi":"10.1017/S204017442300017X","DOIUrl":"10.1017/S204017442300017X","url":null,"abstract":"<p><p>Fetal restriction (FR) alters insulin sensitivity, but it is unknown how the metabolic profile associated with restriction affects development of the dopamine (DA) system and DA-related behaviors. The Netrin-1/DCC guidance cue system participates in maturation of the mesocorticolimbic DA circuitry. Therefore, our objective was to identify if FR modifies Netrin-1/DCC receptor protein expression in the prefrontal cortex (PFC) at birth and mRNA in adulthood in rodent males. We used cultured HEK293 cells to assess if levels of miR-218, microRNA regulator of DCC, are sensitive to insulin. To assess this, pregnant dams were subjected to a 50% FR diet from gestational day 10 until birth. Medial PFC (mPFC) DCC/Netrin-1 protein expression was measured at P0 at baseline and <i>Dcc</i>/<i>Netrin</i>-1 mRNA levels were quantified in adults 15 min after a saline/insulin injection. miR-218 levels in HEK-293 cells were measured in response to insulin exposure. At P0, Netrin-1 levels are downregulated in FR animals in comparison to controls. In adult rodents, insulin administration results in an increase in <i>Dcc</i> mRNA levels in control but not FR rats. In HEK293 cells, there is a positive correlation between insulin concentration and miR-218 levels. Since miR-218 is a <i>Dcc</i> gene expression regulator and our in vitro results show that insulin regulates miR-218 levels, we suggest that FR-induced changes in insulin sensitivity could be affecting <i>Dcc</i> expression via miR-218, impacting DA system maturation and organization. As fetal adversity is linked to nonadaptive behaviors later in life, this may contribute to early identification of vulnerability to chronic diseases associated with fetal adversity.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"14 4","pages":"501-507"},"PeriodicalIF":1.8,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10988268/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9766859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lifetime caffeine and adolescent nicotine exposure in mice: effects on anxiety-like behavior and reward.","authors":"Ana Carolina Dutra-Tavares,&nbsp;Anderson Ribeiro-Carvalho,&nbsp;Fernanda Nunes,&nbsp;Ulisses Cesar Araújo,&nbsp;Vitor Bruno,&nbsp;Tania Marcourakis,&nbsp;Claudio C Filgueiras,&nbsp;Alex C Manhães,&nbsp;Yael Abreu-Villaça","doi":"10.1017/S2040174423000077","DOIUrl":"https://doi.org/10.1017/S2040174423000077","url":null,"abstract":"<p><p>Caffeine consumption occurs throughout life, while nicotine use typically begins during adolescence, the period when caffeine-nicotine epidemiological association begins in earnest. Despite that, few studies in animal models parallel the pattern of coexposure that occurs in humans. Therefore, the neurobehavioral consequences of the association between these drugs remain unclear. Here, we exposed Swiss mice to lifetime caffeine. Caffeine solutions of 0.1 g/L (CAF0.1), 0.3 g/L (CAF0.3), or water (CTRL) were used as the sole liquid source, being offered to progenitors until weaning and, after that, directly to the offspring until the last day of adolescent behavioral evaluation. The open field test was used to evaluate acute effects of nicotine, of lifetime caffeine and of their interaction on locomotion and anxiety-like behavior, while the conditioned place preference test was used to assess the impact of caffeine on nicotine (0.5 mg/Kg, i.p.) reward. Frontal cerebral cortex dopamine content, dopamine turnover, and norepinephrine levels, as well as hippocampal serotonin 1A receptor expression were assessed. CAF0.3 mice exhibited an increase in anxiety-like behavior when compared to CAF0.1 and CTRL ones, but nicotine coexposure mitigated the anxiogenic-like caffeine-induced effect. Distinctively, caffeine had no effect on locomotion and failed to interfere with both nicotine-induced hyperactivity and place preference. There were no significant effects on dopaminergic and serotonergic markers. In conclusion, although caffeine did not affect nicotine reward, considering the strong association between anxiety disorders and tobacco consumption, caffeine-induced anxiety-like behavior advises limiting its consumption during development, including adolescence, as caffeine could be a risk factor to nicotine use.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"14 3","pages":"362-370"},"PeriodicalIF":1.7,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9938319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Attenuated glucose-stimulated insulin secretion during an acute IGF-1 LR3 infusion into fetal sheep does not persist in isolated islets.","authors":"Alicia White, Jane Stremming, Laura D Brown, Paul J Rozance","doi":"10.1017/S2040174423000090","DOIUrl":"10.1017/S2040174423000090","url":null,"abstract":"<p><p>Insulin-like growth factor-1 (IGF-1) is a critical fetal growth hormone that has been proposed as a therapy for intrauterine growth restriction. We previously demonstrated that a 1-week IGF-1 LR3 infusion into fetal sheep reduces <i>in vivo</i> and <i>in vitro</i> insulin secretion suggesting an intrinsic islet defect. Our objective herein was to determine whether this intrinsic islet defect was related to chronicity of exposure. We therefore tested the effects of a 90-min IGF-1 LR3 infusion on fetal glucose-stimulated insulin secretion (GSIS) and insulin secretion from isolated fetal islets. We first infused late gestation fetal sheep (<i>n</i> = 10) with either IGF-1 LR3 (IGF-1) or vehicle control (CON) and measured basal insulin secretion and <i>in vivo</i> GSIS utilizing a hyperglycemic clamp. We then isolated fetal islets immediately following a 90-min IGF-1 or CON <i>in vivo</i> infusion and exposed them to glucose or potassium chloride to measure <i>in vitro</i> insulin secretion (IGF-1, <i>n</i> = 6; CON, <i>n</i> = 6). Fetal plasma insulin concentrations decreased with IGF-1 LR3 infusion (<i>P</i> < 0.05), and insulin concentrations during the hyperglycemic clamp were 66% lower with IGF-1 LR3 infusion compared to CON (<i>P</i> < 0.0001). Insulin secretion in isolated fetal islets was not different based on infusion at the time of islet collection. Therefore, we speculate that while acute IGF-1 LR3 infusion may directly suppress insulin secretion, the fetal β-cell <i>in vitro</i> retains the ability to recover GSIS. This may have important implications when considering the long-term effects of treatment modalities for fetal growth restriction.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"14 3","pages":"353-361"},"PeriodicalIF":1.7,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10205682/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9619847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of maternal preterm birth with subsequent risk for type 2 diabetes in women from the women's health initiative.","authors":"Aaron Holman-Vittone, Brian Monahan, Erin S LeBlanc, Simin Liu, Rami Nassir, Nazmus Saquib, Peter F Schnatz, Aladdin H Shadyab, Rachel Sinkey, Jean Wactawski-Wende, Robert A Wild, Lisa Chasan-Taber, JoAnn E Manson, Cassandra N Spracklen","doi":"10.1017/S2040174423000089","DOIUrl":"10.1017/S2040174423000089","url":null,"abstract":"<p><p>Preterm birth has been associated with insulin resistance and beta-cell dysfunction, a hallmark characteristic of type 2 diabetes. However, studies investigating the relationship between a personal history of being born preterm and type 2 diabetes are sparse. We sought to investigate the potential association between a personal history of being born preterm and risk for type 2 diabetes in a racially and ethnically diverse population. Baseline and incident data (>16 years of follow-up) from the Women's Health Initiative (<i>n</i> = 85,356) were used to examine the association between personal history of being born preterm (born 1910-1940s) and prevalent (baseline enrollment; cross-sectional) or incident (prospective cohort) cases of type 2 diabetes. Logistic and Cox proportional hazards regression models were used to estimate odds and hazards ratios. Being born preterm was significantly, positively associated with odds for prevalent type 2 diabetes at enrollment (adjOR = 1.79, 95% CI 1.43-2.24; <i>P</i> < 0.0001). Stratified regression models suggested the positive associations at baseline were consistent across race and ethnicity groups. However, being born preterm was not significantly associated with risk for incident type 2 diabetes. Regression models stratified by age at enrollment suggest the relationship between being born preterm and type 2 diabetes persists only among younger age groups. Preterm birth was associated with higher risk of type 2 diabetes but only in those diagnosed with type 2 diabetes prior to study enrollment, suggesting the association between preterm birth and type 2 diabetes may exist at earlier age of diagnosis but wane over time.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"14 3","pages":"333-340"},"PeriodicalIF":1.7,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10205667/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9619845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Placental nanoparticle gene therapy normalizes gene expression changes in the fetal liver associated with fetal growth restriction in a fetal sex-specific manner.","authors":"Rebecca L Wilson, Kendal K Stephens, Helen N Jones","doi":"10.1017/S2040174423000016","DOIUrl":"10.1017/S2040174423000016","url":null,"abstract":"<p><p>Fetal growth restriction (FGR) is associated with increased risk of developing non-communicable diseases. We have a placenta-specific nanoparticle gene therapy protocol that increases placental expression of <i>human insulin-like growth factor 1</i> (<i>hIGF1</i>), for the treatment of FGR <i>in utero</i>. We aimed to characterize the effects of FGR on hepatic gluconeogenesis pathways during early stages of FGR establishment, and determine whether placental nanoparticle-mediated <i>hIGF1</i> therapy treatment could resolve differences in the FGR fetus. Female Hartley guinea pigs (dams) were fed either a Control or Maternal Nutrient Restriction (MNR) diet using established protocols. At GD30-33, dams underwent ultrasound guided, transcutaneous, intraplacental injection of <i>hIGF1</i> nanoparticle or PBS (sham) and were sacrificed 5 days post-injection. Fetal liver tissue was fixed and snap frozen for morphology and gene expression analysis. In female and male fetuses, liver weight as a percentage of body weight was reduced by MNR, and not changed with <i>hIGF1</i> nanoparticle treatment. In female fetal livers, expression of <i>hypoxia inducible factor 1</i> (<i>Hif1α</i>) and <i>tumor necrosis factor</i> (<i>Tnfα</i>) were increased in MNR compared to Control, but reduced in MNR + <i>hIGF1</i> compared to MNR. In male fetal liver, MNR increased expression of <i>Igf1</i> and decreased expression of <i>Igf2</i> compared to Control. <i>Igf1</i> and <i>Igf2</i> expression was restored to Control levels in the MNR + <i>hIGF1</i> group. This data provides further insight into the sex-specific mechanistic adaptations seen in FGR fetuses and demonstrates that disruption to fetal developmental mechanisms may be returned to normal by treatment of the placenta.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"14 3","pages":"325-332"},"PeriodicalIF":1.7,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10947591/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9563880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prenatal dietary patterns in relation to adolescent offspring adiposity and adipokines in a Mexico City cohort.","authors":"Erica Fossee, Astrid N Zamora, Karen E Peterson, Alejandra Cantoral, Wei Perng, Martha M Téllez-Rojo, Libni A Torres-Olascoaga, Erica C Jansen","doi":"10.1017/S2040174422000678","DOIUrl":"10.1017/S2040174422000678","url":null,"abstract":"<p><p>Maternal diet during pregnancy has been associated with obesity among offspring. The extent to which trimester-specific dietary patterns are associated with markers of adiposity during adolescence remains unclear. We examined associations between prenatal diet patterns with adolescent offspring measures of adiposity and adipokines in 384 mother-adolescent dyads from the Mexico City ELEMENT cohort. Trimester-specific diet patterns were derived from principal component analysis of food frequency questionnaire data. Adolescent anthropometry and serum leptin and adiponectin were measured at 10-17 years. Three maternal diet patterns were identified: Prudent Diet (PD), high in fish and vegetables, the High Meat and Fat Diet (HMFD), high in pork and processed meats, and the Transitioning Mexican Diet (TMD), high in corn tortillas and sugar-sweetened beverages. Multiple linear regression was used to estimate sex-stratified associations among quartiles of diet patterns with adiposity and adipokines, adjusting for maternal marital status, education, and parity. First trimester TMD was associated with greater anthropometric measures and higher leptin in females, while third trimester HMFD was associated higher body fat percentage, triceps thickness, waist circumference, and leptin, but lower adiponectin among males. Contrary to expectation, there were positive associations between the trimester 1 PD pattern and anthropometric measurements in females, and for trimester 2 HMFD and TMD patterns with adipokines among males. Findings suggest maternal diet patterns may influence offspring adiposity markers during adolescence in a sex-specific manner.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"14 3","pages":"371-380"},"PeriodicalIF":1.7,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10202837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9584850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiovascular and renal profiles in rat offspring that do not undergo catch-up growth after exposure to maternal protein restriction.","authors":"Ryan J Wood-Bradley,&nbsp;Sarah L Henry,&nbsp;Roger G Evans,&nbsp;John F Bertram,&nbsp;Luise A Cullen-McEwen,&nbsp;James A Armitage","doi":"10.1017/S2040174422000666","DOIUrl":"https://doi.org/10.1017/S2040174422000666","url":null,"abstract":"<p><p>Maternal protein restriction is often associated with structural and functional sequelae in offspring, particularly affecting growth and renal-cardiovascular function. However, there is little understanding as to whether hypertension and kidney disease occur because of a primary nephron deficit or whether controlling postnatal growth can result in normal renal-cardiovascular phenotypes. To investigate this, female Sprague-Dawley rats were fed either a low-protein (LP, 8.4% protein) or normal-protein (NP, 19.4% protein) diet prior to mating and until offspring were weaned at postnatal day (PN) 21. Offspring were then fed a non 'growth' (4.6% fat) which ensured that catch-up growth did not occur. Offspring growth was determined by weight and dual energy X-ray absorptiometry. Nephron number was determined at PN21 using the disector-fractionator method. Kidney function was measured at PN180 and PN360 using clearance methods. Blood pressure was measured at PN360 using radio-telemetry. Body weight was similar at PN1, but by PN21 LP offspring were 39% smaller than controls (P_diet < 0.001). This difference was due to proportional changes in lean muscle, fat, and bone content. LP offspring remained smaller than NP offspring until PN360. In LP offspring, nephron number was 26% less in males and 17% less in females, than NP controls (P_diet < 0.0004). Kidney function was similar across dietary groups and sexes at PN180 and PN360. Blood pressure was similar in LP and NP offspring at PN360. These findings suggest that remaining on a slow growth trajectory after exposure to a suboptimal intrauterine environment does not lead to the development of kidney dysfunction and hypertension.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"14 3","pages":"426-436"},"PeriodicalIF":1.7,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9921230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations between maternal folate status and choline intake during pregnancy and neurodevelopment at 3-4 years of age in the Alberta Pregnancy Outcomes and Nutrition (APrON) study.","authors":"Nathalie Irvine, Gillian England-Mason, Catherine J Field, Nicole Letourneau, Rhonda C Bell, Gerald F Giesbrecht, David W Kinniburgh, Amy M MacDonald, Jonathan W Martin, Deborah Dewey","doi":"10.1017/S2040174423000041","DOIUrl":"10.1017/S2040174423000041","url":null,"abstract":"<p><p>Folate and choline are methyl donor nutrients that may play a role in fetal brain development. Animal studies have reported that prenatal folate and choline supplementation are associated with better cognitive outcomes in offspring and that these nutrients may interact and affect brain development. Human studies that have investigated associations between maternal prenatal folate or choline levels and neurodevelopmental outcomes have reported contradictory findings and no human studies have examined the potential interactive effect of folate and choline on children's neurodevelopment. During the second trimester of pregnancy, maternal red blood cell folate was measured from blood samples and choline intake was estimated using a 24-h dietary recall in 309 women in the APrON cohort. At 3-5 years of age, their children's neurodevelopment was assessed using the Wechsler Preschool and Primary Scales of Intelligence - Fourth Edition^CND, NEPSY-II language and memory subtests, four behavioral executive function tasks, and the Movement Assessment Battery for Children - Second Edition. Adjusted regressions revealed no associations between maternal folate and choline levels during pregnancy and most of the child outcomes. On the Dimensional Change Card Sort, an executive function task, there was an interaction effect; at high levels of choline intake (i.e., 1 SD above the mean; 223.03 mg/day), higher maternal folate status was associated with decreased odds of receiving a passing score (β = -0.44; 95%CI -0.81, -0.06). In conclusion, maternal folate status and choline intake during the second trimester of pregnancy were not associated with children's intelligence, language, memory, or motor outcomes at 3-4 years of age; however, their interaction may have an influence children's executive functions.</p>","PeriodicalId":49167,"journal":{"name":"Journal of Developmental Origins of Health and Disease","volume":"14 3","pages":"402-414"},"PeriodicalIF":1.7,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10202845/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9921701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}