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The Roles of Maternal and Child Nutrition in Fetal Alcohol Spectrum Disorders (FASD): From Mechanistic Insights to Opportunities for Intervention

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Public Health".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 39865

Special Issue Editor

Dr. Robert Colin Carter

E-Mail Website
Guest Editor
Institute of Human Nutrition and Departments of Emergency Medicine and Pediatrics, Columbia University Irving Medical Center, New York, NY, USA
Interests: alcohol-related teratology; prenatal nutrition; iron; one-carbon nutrients; child growth; neurodevelopment

Special Issue Information

Dear Colleagues,

Despite extensive prevention efforts worldwide, fetal alcohol spectrum disorders (FASD) remain the most common preventable cause of neurodevelopmental delay worldwide. Both animal models and human cohort studies have demonstrated important roles of nutrition in the teratogenesis of prenatal alcohol exposure. Chronic alcohol use has been shown to alter nutrient absorption, metabolism, and utilization in non-pregnant adults, and recent studies have begun to elucidate how such alterations may play mechanistic roles in FASD. Animal models have demonstrated the potential for alterations in prenatal and/or postnatal nutrition to modify the teratogenic effects of prenatal alcohol exposure, leading to recent FASD nutritional intervention studies in humans. This special issue of Nutrients showcases important known and novel roles of maternal, fetal, and postnatal nutrition in FASD, with an emphasis on mechanistic insights and nutritional interventions.

Dr. Robert Colin Carter
Guest Editor

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Keywords

  • fetal alcohol spectrum disorders
  • prenatal alcohol exposure
  • prenatal nutrition
  • neurodevelopment
  • child growth
  • nutritional interventions

Published Papers (15 papers)

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16 pages, 292 KiB  
Article
Fetal Alcohol-Related Postnatal Growth Restriction Is Independent of Infant Feeding Practices and Postnatal Alcohol Exposure in a Prospective South African Birth Cohort
by Alexia C. Edwards, Sandra W. Jacobson, Marjanne Senekal, Neil C. Dodge, Christopher D. Molteno, Ernesta M. Meintjes, Joseph L. Jacobson and R. Colin Carter
Nutrients 2023, 15(9), 2018; https://0-doi-org.brum.beds.ac.uk/10.3390/nu15092018 - 22 Apr 2023
Cited by 1 | Viewed by 1144
Abstract
Prenatal alcohol exposure (PAE) causes growth restriction that worsens in the first year of life. However, the roles of postnatal nutrition in fetal alcohol growth restriction and the impact of postnatal alcohol exposure via breastmilk on growth remain unknown. We aimed to compare [...] Read more.
Prenatal alcohol exposure (PAE) causes growth restriction that worsens in the first year of life. However, the roles of postnatal nutrition in fetal alcohol growth restriction and the impact of postnatal alcohol exposure via breastmilk on growth remain unknown. We aimed to compare infant feeding practices during the first 6.5 months of life between heavy drinkers and abstainers/light drinkers, to examine whether these practices play confounding roles in fetal alcohol growth restriction, and to determine the impact of postnatal alcohol exposure via breastmilk on growth. Eighty-seven heavy-drinking pregnant women and 71 abstainers/light drinkers (controls) were recruited prenatally from antenatal clinics in Cape Town, South Africa. Demographic background and alcohol, cigarette, marijuana, and methamphetamine use during pregnancy were assessed pre- and postnatally. Infant feeding practices were assessed at 6.5 months postpartum using the USDA Infant Feeding Questionnaire. Infant weight, length, and head circumference were measured at 2 weeks, 6.5 and 12 months, and 5 years. Neither prenatal nor postnatal alcohol consumption was related to the duration of breastfeeding, exclusive breastfeeding, exclusive formula, or mixed feeding. Complementary feeding practices were remarkably similar between exposure groups. PAE was related to all postnatal anthropometry measures at all age points, independent of infant feeding practices. Postnatal alcohol exposure via breastmilk was unrelated to any anthropometry outcome after control for PAE. In conclusion, fetal alcohol-related postnatal growth restriction was not attributable to differences in postnatal infant feeding practices or postnatal alcohol exposure and is thus likely a direct teratogenic effect of PAE. Full article
(This article belongs to the Special Issue The Roles of Maternal and Child Nutrition in Fetal Alcohol Spectrum Disorders (FASD): From Mechanistic Insights to Opportunities for Intervention)
23 pages, 3816 KiB  
Article
Untargeted Metabolome Analysis of Alcohol-Exposed Pregnancies Reveals Metabolite Differences That Are Associated with Infant Birth Outcomes
by Julie M. Hasken, Marlene M. de Vries, Anna-Susan Marais, Philip A. May, Charles D. H. Parry, Soraya Seedat, Sandra M. Mooney and Susan M. Smith
Nutrients 2022, 14(24), 5367; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14245367 - 17 Dec 2022
Cited by 1 | Viewed by 1907
Abstract
Prenatal alcohol exposure can produce offspring growth deficits and is a leading cause of neurodevelopmental disability. We used untargeted metabolomics to generate mechanistic insight into how alcohol impairs fetal development. In the Western Cape Province of South Africa, 52 women between gestational weeks [...] Read more.
Prenatal alcohol exposure can produce offspring growth deficits and is a leading cause of neurodevelopmental disability. We used untargeted metabolomics to generate mechanistic insight into how alcohol impairs fetal development. In the Western Cape Province of South Africa, 52 women between gestational weeks 5–36 (mean 18.5 ± 6.5) were recruited, and they provided a finger-prick fasting bloodspot that underwent mass spectrometry. Metabolomic data were analyzed using partial least squares-discriminant analyses (PLS-DA) to identify metabolites that correlated with alcohol exposure and infant birth outcomes. Women who consumed alcohol in the past seven days were distinguished by a metabolite profile that included reduced sphingomyelins, cholesterol, and pregnenolones, and elevated fatty acids, acyl and amino acyl carnitines, and androsterones. Using PLS-DA, 25 of the top 30 metabolites differentiating maternal groups were reduced by alcohol with medium-chain free fatty acids and oxidized sugar derivatives having the greatest influence. A separate ortho-PLS-DA analysis identified a common set of 13 metabolites that were associated with infant length, weight, and head circumference. These included monoacylglycerols, glycerol-3-phosphate, and unidentified metabolites, and most of their associations were negative, implying they represent processes having adverse consequences for fetal development. Full article
(This article belongs to the Special Issue The Roles of Maternal and Child Nutrition in Fetal Alcohol Spectrum Disorders (FASD): From Mechanistic Insights to Opportunities for Intervention)
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21 pages, 327 KiB  
Article
Mediating and Moderating Effects of Iron Homeostasis Alterations on Fetal Alcohol-Related Growth and Neurobehavioral Deficits
by R. Colin Carter, Neil C. Dodge, Christopher D. Molteno, Ernesta M. Meintjes, Joseph L. Jacobson and Sandra W. Jacobson
Nutrients 2022, 14(20), 4432; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14204432 - 21 Oct 2022
Cited by 5 | Viewed by 1711
Abstract
We have previously demonstrated prenatal alcohol exposure (PAE)-related alterations in maternal and infant iron homeostasis. Given that early iron deficiency and PAE both lead to growth restriction and deficits in recognition memory and processing speed, we hypothesized that PAE-related iron homeostasis alterations may [...] Read more.
We have previously demonstrated prenatal alcohol exposure (PAE)-related alterations in maternal and infant iron homeostasis. Given that early iron deficiency and PAE both lead to growth restriction and deficits in recognition memory and processing speed, we hypothesized that PAE-related iron homeostasis alterations may mediate and/or moderate effects of PAE on growth and neurobehavior. We examined this hypothesis in a prenatally recruited, prospective longitudinal birth cohort [87 mother-infant pairs with heavy prenatal alcohol exposure (mean = 7.2 drinks/occasion on 1.4 days/week); 71 controls], with serial growth measures and infant neurobehavioral assessments. PAE was related to growth restriction at 2 weeks and 5 years, and, in infancy, poorer visual recognition memory, slower processing speed, lower complexity of symbolic play, and higher emotionality and shyness on a parental report temperament scale. Lower maternal hemoglobin-to-log(ferritin) ratio, which we have shown to be associated with PAE, appeared to exacerbate PAE-related 2-week head circumference reductions, and elevated maternal ferritin, which we have shown to be associated with PAE, appeared to exacerbate PAE-related visual recognition memory deficits. In causal inference analyses, PAE-related elevations in maternal ferritin and hemoglobin:log(ferritin) appeared to statistically mediate 22.6–82.3% of PAE-related growth restriction. These findings support potential mechanistic roles of iron homeostasis alterations in fetal alcohol spectrum disorders (FASD). Full article
(This article belongs to the Special Issue The Roles of Maternal and Child Nutrition in Fetal Alcohol Spectrum Disorders (FASD): From Mechanistic Insights to Opportunities for Intervention)
16 pages, 1282 KiB  
Article
Dietary Intake Patterns and Lifestyle Behaviors of Pregnant Women Living in a Manitoba First Nations Community: Implications for Fetal Alcohol Spectrum Disorder
by Olena Kloss, Marie Jebb, Linda Chartrand, Albert E. Chudley, Michael N. A. Eskin and Miyoung Suh
Nutrients 2022, 14(15), 3233; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14153233 - 07 Aug 2022
Cited by 1 | Viewed by 2292
Abstract
The information on the nutrition status of women at-risk of carrying a child with fetal alcohol spectrum disorder (FASD) is scarce, particularly in the First Nations population living on reserve. This study examined and compared nutrition status, dietary intake, and lifestyle patterns of [...] Read more.
The information on the nutrition status of women at-risk of carrying a child with fetal alcohol spectrum disorder (FASD) is scarce, particularly in the First Nations population living on reserve. This study examined and compared nutrition status, dietary intake, and lifestyle patterns of pregnant at-risk, defined as those who consume alcoholic drink during the current pregnancy, and non-at-risk women living in northern Manitoban community. Thirty-seven pregnant, First Nations women (at-risk n = 15; non-at-risk, n = 22) were recruited to participate in the study. A questionnaire, presented in paper and iPad formats, collected information on participants’ demographics, dietary intake, lifestyle, pregnancy outcomes, and maternal health. A food frequency questionnaire and 24-h recall were used to determine nutrient intake. Nutrient values were assessed using Dietary Reference Intakes (DRI). At-risk and non-at-risk women were below the Canada Food Guide serving size recommended for Vegetable and Fruit, Grain, and Milk Products with 93%, 92%, and 93% of participants not meeting the recommendations, respectively. Women met the recommendations for vitamins A, B1, B12, C, niacin, choline, as well as calcium, and zinc. Sixty eight percentage (%) of participants did not meet the recommendations for folate and iron, and 97% for docosahexaenoic acid (DHA). Significant differences were observed between non-at-risk and at-risk women for mean % DRI intakes of vitamin C (313 ± 224 vs. 172 ± 81 mg/day), niacin (281 ± 123 vs. 198 ± 80 mg/day), folate (70 ± 38 vs. 10 ± 22 mcg/day), and iron (101 ± 74 vs. 74 ± 30 mg/day). The findings of this study lay a fundamental premise for the development of community nutrition programs, nutrition education, and nutrition intervention, such as community specific prenatal supplementation. These will assist in ensuring adequate maternal nutrient intake and benefit families and communities in Northern Manitoba with and without alcohol insult. Full article
(This article belongs to the Special Issue The Roles of Maternal and Child Nutrition in Fetal Alcohol Spectrum Disorders (FASD): From Mechanistic Insights to Opportunities for Intervention)
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19 pages, 2003 KiB  
Article
Choline Supplementation Modifies the Effects of Developmental Alcohol Exposure on Immune Responses in Adult Rats
by Jessica A. Baker, Kristen R. Breit, Tamara S. Bodnar, Joanne Weinberg and Jennifer D. Thomas
Nutrients 2022, 14(14), 2868; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14142868 - 13 Jul 2022
Cited by 7 | Viewed by 2800
Abstract
Prenatal alcohol exposure can disrupt the development of numerous systems, including the immune system. Indeed, alterations in cytokine levels may contribute to the neuropathological, behavioral, and cognitive problems, and other adverse outcomes observed in individuals with fetal alcohol spectrum disorders. Importantly, supplementation with [...] Read more.
Prenatal alcohol exposure can disrupt the development of numerous systems, including the immune system. Indeed, alterations in cytokine levels may contribute to the neuropathological, behavioral, and cognitive problems, and other adverse outcomes observed in individuals with fetal alcohol spectrum disorders. Importantly, supplementation with the essential nutrient choline can improve performance in hippocampal-dependent behaviors; thus, the present study examined the effects of choline on plasma and hippocampal cytokines in adult rats exposed to ethanol in early development. From postnatal day (PD) 4–9 (third trimester equivalent), pups received ethanol (5.25 g/kg/day) or Sham intubations. Subjects were treated with choline chloride (100 mg/kg/day) or saline from PD10–30. On PD60, plasma and hippocampal tissue was collected before and after an immune challenge (lipopolysaccharide (LPS); 50 ug/kg). Prior to the immune challenge, ethanol-exposed subjects showed an overall increase in hippocampal pro-inflammatory cytokines, an effect mitigated by choline supplementation. In contrast, in the plasma, choline reduced LPS-related increases in pro-inflammatory markers, particularly in ethanol-exposed subjects. Thus, early choline supplementation may modify both brain and peripheral inflammation. These results suggest that early choline can mitigate some long-term effects of ethanol exposure on hippocampal inflammation, which may contribute to improved hippocampal function, and could also influence peripheral immune responses that may impact overall health. Full article
(This article belongs to the Special Issue The Roles of Maternal and Child Nutrition in Fetal Alcohol Spectrum Disorders (FASD): From Mechanistic Insights to Opportunities for Intervention)
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18 pages, 2758 KiB  
Article
Brain Iron and Mental Health Symptoms in Youth with and without Prenatal Alcohol Exposure
by Daphne Nakhid, Carly A. McMorris, Hongfu Sun, Ben Gibbard, Christina Tortorelli and Catherine Lebel
Nutrients 2022, 14(11), 2213; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14112213 - 26 May 2022
Cited by 3 | Viewed by 2220
Abstract
Prenatal alcohol exposure (PAE) negatively affects brain development and increases the risk of poor mental health. We investigated if brain volumes or magnetic susceptibility, an indirect measure of brain iron, were associated with internalizing or externalizing symptoms in youth with and without PAE. [...] Read more.
Prenatal alcohol exposure (PAE) negatively affects brain development and increases the risk of poor mental health. We investigated if brain volumes or magnetic susceptibility, an indirect measure of brain iron, were associated with internalizing or externalizing symptoms in youth with and without PAE. T1-weighted and quantitative susceptibility mapping (QSM) MRI scans were collected for 19 PAE and 40 unexposed participants aged 7.5–15 years. Magnetic susceptibility and volume of basal ganglia and limbic structures were extracted using FreeSurfer. Internalizing and Externalizing Problems were assessed using the Behavioural Assessment System for Children (BASC-2-PRS). Susceptibility in the nucleus accumbens was negatively associated with Internalizing Problems, while amygdala susceptibility was positively associated with Internalizing Problems across groups. PAE moderated the relationship between thalamus susceptibility and internalizing symptoms as well as the relationship between putamen susceptibility and externalizing symptoms. Brain volume was not related to internalizing or externalizing symptoms. These findings highlight that brain iron is related to internalizing and externalizing symptoms differently in some brain regions for youth with and without PAE. Atypical iron levels (high or low) may indicate mental health issues across individuals, and iron in the thalamus may be particularly important for behavior in individuals with PAE. Full article
(This article belongs to the Special Issue The Roles of Maternal and Child Nutrition in Fetal Alcohol Spectrum Disorders (FASD): From Mechanistic Insights to Opportunities for Intervention)
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14 pages, 2351 KiB  
Article
Postnatal Choline Supplementation Rescues Deficits in Synaptic Plasticity Following Prenatal Ethanol Exposure
by Erin L. Grafe, Mira M. M. Wade, Claire E. Hodson, Jennifer D. Thomas and Brian R. Christie
Nutrients 2022, 14(10), 2004; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14102004 - 10 May 2022
Cited by 8 | Viewed by 2112
Abstract
Prenatal ethanol exposure (PNEE) is a leading cause of neurodevelopmental impairments, yet treatments for individuals with PNEE are limited. Importantly, postnatal supplementation with the essential nutrient choline can attenuate some adverse effects of PNEE on cognitive development; however, the mechanisms of action for [...] Read more.
Prenatal ethanol exposure (PNEE) is a leading cause of neurodevelopmental impairments, yet treatments for individuals with PNEE are limited. Importantly, postnatal supplementation with the essential nutrient choline can attenuate some adverse effects of PNEE on cognitive development; however, the mechanisms of action for choline supplementation remain unclear. This study used an animal model to determine if choline supplementation could restore hippocampal synaptic plasticity that is normally impaired by prenatal alcohol. Throughout gestation, pregnant Sprague Dawley rats were fed an ethanol liquid diet (35.5% ethanol-derived calories). Offspring were injected with choline chloride (100 mg/kg/day) from postnatal days (PD) 10–30, and then used for in vitro electrophysiology experiments as juveniles (PD 31–35). High-frequency conditioning stimuli were used to induce long-term potentiation (LTP) in the medial perforant path input to the dentate gyrus of the hippocampus. PNEE altered synaptic transmission in female offspring by increasing excitability, an effect that was mitigated with choline supplementation. In contrast, PNEE juvenile males had decreased LTP compared to controls, and this was rescued by choline supplementation. These data demonstrate sex-specific changes in plasticity following PNEE, and provide evidence that choline-related improvements in cognitive functioning may be due to its positive impact on hippocampal synaptic physiology. Full article
(This article belongs to the Special Issue The Roles of Maternal and Child Nutrition in Fetal Alcohol Spectrum Disorders (FASD): From Mechanistic Insights to Opportunities for Intervention)
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12 pages, 619 KiB  
Article
Nutritionists’ Practices and Knowledge about the Risks of Alcohol Consumption during Pregnancy: An Israeli Survey
by Liat Hen-Herbst, Meital Ron El Levin, Yehuda Senecky, Sigal Frishman and Andrea Berger
Nutrients 2022, 14(9), 1885; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14091885 - 29 Apr 2022
Cited by 2 | Viewed by 1938
Abstract
Fetal alcohol spectrum disorders (FASDs) are lifelong disabilities and the leading preventable cause of developmental disabilities. Antenatal care providers may influence pregnant women’s dietary practices and their awareness of the risks of alcohol consumption during pregnancy. This study aimed to assess nutritionists’ self-reported [...] Read more.
Fetal alcohol spectrum disorders (FASDs) are lifelong disabilities and the leading preventable cause of developmental disabilities. Antenatal care providers may influence pregnant women’s dietary practices and their awareness of the risks of alcohol consumption during pregnancy. This study aimed to assess nutritionists’ self-reported knowledge about the risks of drinking alcohol during pregnancy, professional practices in this respect, and self-perceived competence to assess and guide women about alcohol consumption during pregnancy in Israel. A sample of 526 professional nutritionists completed an anonymous online questionnaire. Results showed significant differences between the nutritionists’ knowledge and professional practices scores. About 349 (66.3%) of the sample agreed (to any degree) that they did not have enough knowledge to guide pregnant women regarding drinking alcohol. The number of years of experience, combined with self-perceived competence and the mean knowledge score, explained 18% of the variance in professional practices. Nutritionists and other health professionals may have a crucial role in preventing FASD and should prioritize appropriate screening for prenatal alcohol use. Eliminating alcohol consumption at any point in pregnancy would reduce the risk for FASDs. Full article
(This article belongs to the Special Issue The Roles of Maternal and Child Nutrition in Fetal Alcohol Spectrum Disorders (FASD): From Mechanistic Insights to Opportunities for Intervention)
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18 pages, 2181 KiB  
Article
Prenatal Choline Supplementation Alters One Carbon Metabolites in a Rat Model of Periconceptional Alcohol Exposure
by Sarah E. Steane, Vinod Kumar, James S. M. Cuffe, Karen M. Moritz and Lisa K. Akison
Nutrients 2022, 14(9), 1874; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14091874 - 29 Apr 2022
Cited by 2 | Viewed by 3067
Abstract
Prenatal alcohol exposure disturbs fetal and placental growth and can alter DNA methylation (DNAm). Supplementation with the methyl donor choline can increase fetal and placental growth and restore DNAm, suggesting converging effects on one-carbon metabolism (1CM). We investigated the impact of periconceptional ethanol [...] Read more.
Prenatal alcohol exposure disturbs fetal and placental growth and can alter DNA methylation (DNAm). Supplementation with the methyl donor choline can increase fetal and placental growth and restore DNAm, suggesting converging effects on one-carbon metabolism (1CM). We investigated the impact of periconceptional ethanol (PCE) exposure and prenatal choline supplementation on 1CM in maternal, placental, and fetal compartments. Female Sprague Dawley rats were given a liquid diet containing 12.5% ethanol (PCE) or 0% ethanol (control) for 4 days before and 4 days after conception. Dams were then placed on chow with different concentrations of choline (1.6 g, 2.6 g, or 7.2 g choline/kg chow). Plasma and tissues were collected in late gestation for the analysis of 1CM components by means of mass spectrometry and real-time PCR. PCE reduced placental components of 1CM, particularly those relating to folate metabolism, resulting in a 3–7.5-fold reduction in the ratio of s-adenosylmethionine:s-adenosylhomocysteine (SAM:SAH) (p < 0.0001). Choline supplementation increased placental 1CM components and the SAM:SAH ratio (3.5–14.5-fold, p < 0.0001). In the maternal and fetal compartments, PCE had little effect, whereas choline increased components of 1CM. This suggests that PCE impairs fetal development via altered placental 1CM, highlighting its role in modulating nutritional inputs to optimize fetal development. Full article
(This article belongs to the Special Issue The Roles of Maternal and Child Nutrition in Fetal Alcohol Spectrum Disorders (FASD): From Mechanistic Insights to Opportunities for Intervention)
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18 pages, 1998 KiB  
Article
Gestational Iron Supplementation Improves Fetal Outcomes in a Rat Model of Prenatal Alcohol Exposure
by Kaylee K. Helfrich, Nipun Saini, Sze Ting Cecilia Kwan, Olivia C. Rivera, Rachel Hodges and Susan M. Smith
Nutrients 2022, 14(8), 1653; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14081653 - 15 Apr 2022
Cited by 6 | Viewed by 2355
Abstract
Prenatal alcohol exposure causes neurodevelopmental disability and is associated with a functional iron deficiency in the fetus and neonate, even when the mother consumes an apparently iron-adequate diet. Here, we test whether gestational administration of the clinically relevant iron supplement Fer-In-Sol mitigates alcohol’s [...] Read more.
Prenatal alcohol exposure causes neurodevelopmental disability and is associated with a functional iron deficiency in the fetus and neonate, even when the mother consumes an apparently iron-adequate diet. Here, we test whether gestational administration of the clinically relevant iron supplement Fer-In-Sol mitigates alcohol’s adverse impacts upon the fetus. Pregnant Long-Evans rats consumed an iron-adequate diet and received 5 g/kg alcohol by gavage for 7 days in late pregnancy. Concurrently, some mothers received 6 mg/kg oral iron. We measured maternal and fetal weights, hematology, tissue iron content, and oxidative damage on gestational day 20.5. Alcohol caused fetal anemia, decreased fetal body and brain weight, increased hepatic iron content, and modestly elevated hepatic malondialdehyde (p’s < 0.05). Supplemental iron normalized this brain weight reduction in alcohol-exposed males (p = 0.154) but not female littermates (p = 0.031). Iron also reversed the alcohol-induced fetal anemia and normalized both red blood cell numbers and hematocrit (p’s < 0.05). Iron had minimal adverse effects on the mother or fetus. These data show that gestational iron supplementation improves select fetal outcomes in prenatal alcohol exposure (PAE) including brain weight and hematology, suggesting that this may be a clinically feasible approach to improve prenatal iron status and fetal outcomes in alcohol-exposed pregnancies. Full article
(This article belongs to the Special Issue The Roles of Maternal and Child Nutrition in Fetal Alcohol Spectrum Disorders (FASD): From Mechanistic Insights to Opportunities for Intervention)
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17 pages, 2496 KiB  
Article
Aging-Related Behavioral, Adiposity, and Glucose Impairments and Their Association following Prenatal Alcohol Exposure in the C57BL/6J Mouse
by Susan M. Smith, Eneda Pjetri, Walter B. Friday, Brandon H. Presswood, Dane K. Ricketts, Kathleen R. Walter and Sandra M. Mooney
Nutrients 2022, 14(7), 1438; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14071438 - 30 Mar 2022
Cited by 4 | Viewed by 2016
Abstract
People that experience prenatal alcohol exposure (PAE) may have behavioral and metabolic impairments, and it is unclear whether these remain stable or change with age. We assessed behavioral and metabolic endpoints across the lifespan in a mouse model of fetal alcohol spectrum disorder [...] Read more.
People that experience prenatal alcohol exposure (PAE) may have behavioral and metabolic impairments, and it is unclear whether these remain stable or change with age. We assessed behavioral and metabolic endpoints across the lifespan in a mouse model of fetal alcohol spectrum disorder (FASD). Pregnant C57BL/6J mice received alcohol (ALC; 3 g/kg) or maltose-dextrin (control, CON) daily from embryonic day 8.5 to 17.5. Offspring were tested on accelerating rotarod, Y-maze, novel object recognition, and fear conditioning at 6 weeks and 10 and 17 months; females were also tested at 24 months. Body composition, fasting glucose, and glucose clearance were assessed at 18 months. Female but not male ALC mice had greater adiposity than age-matched CON from 7 months onward. At 18 months, male but not female ALC mice had reduced glucose clearance and ALC mice were more likely to have elevated fasting glucose. In the rotarod training session, ALC females performed worse than CON. In the Y-maze, significant exposure-age interactions affected ALC performance in both sexes versus age-match CON. For fear conditioning, all animals acquired the task and froze more at older ages. In both the context and cued tasks, there were exposure-age interactions and ALC animals frozen less than CON at 10 months. Correlation analysis revealed that fasting glucose and glucose clearance correlated with % of body fat in ALC but not in CON mice. Additionally, glucose intolerance and % body fat negatively correlated with performance in the rotarod, context learning, and novel object recognition tasks in ALC but not CON mice. All mice exhibit worsening of behavioral performance as they age, and PAE did not further exacerbate this. ALC but not CON mice displayed adiposity and glucose intolerance that correlate with their cognitive impairments, suggesting that these may be mechanistically related in PAE. Findings emphasize that FASD should be considered a whole-body disorder. Full article
(This article belongs to the Special Issue The Roles of Maternal and Child Nutrition in Fetal Alcohol Spectrum Disorders (FASD): From Mechanistic Insights to Opportunities for Intervention)
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21 pages, 3381 KiB  
Article
Untargeted Metabolome Analysis Reveals Reductions in Maternal Hepatic Glucose and Amino Acid Content That Correlate with Fetal Organ Weights in a Mouse Model of Fetal Alcohol Spectrum Disorders
by Nipun Saini, Manjot S. Virdee, Kaylee K. Helfrich, Sze Ting Cecilia Kwan, Sandra M. Mooney and Susan M. Smith
Nutrients 2022, 14(5), 1096; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14051096 - 05 Mar 2022
Cited by 6 | Viewed by 2176
Abstract
Prenatal alcohol exposure (PAE) causes fetal growth restrictions. A major driver of fetal growth deficits is maternal metabolic disruption; this is under-investigated following PAE. Untargeted metabolomics on the dam and fetus exposed to alcohol (ALC) revealed that the hepatic metabolome of ALC and [...] Read more.
Prenatal alcohol exposure (PAE) causes fetal growth restrictions. A major driver of fetal growth deficits is maternal metabolic disruption; this is under-investigated following PAE. Untargeted metabolomics on the dam and fetus exposed to alcohol (ALC) revealed that the hepatic metabolome of ALC and control (CON) dams were distinct, whereas that of ALC and CON fetuses were similar. Alcohol reduced maternal hepatic glucose content and enriched essential amino acid (AA) catabolites, N-acetylated AA products, urea content, and free fatty acids. These alterations suggest an attempt to minimize the glucose gap by increasing gluconeogenesis using AA and glycerol. In contrast, ALC fetuses had unchanged glucose and AA levels, suggesting an adequate draw of maternal nutrients, despite intensified stress on ALC dams. Maternal metabolites including glycolytic intermediates, AA catabolites, urea, and one-carbon-related metabolites correlated with fetal liver and brain weights, whereas lipid metabolites correlated with fetal body weight, indicating they may be drivers of fetal weight outcomes. Together, these data suggest that ALC alters maternal hepatic metabolic activity to limit glucose availability, thereby switching to alternate energy sources to meet the high-energy demands of pregnancy. Their correlation with fetal phenotypic outcomes indicates the influence of maternal metabolism on fetal growth and development. Full article
(This article belongs to the Special Issue The Roles of Maternal and Child Nutrition in Fetal Alcohol Spectrum Disorders (FASD): From Mechanistic Insights to Opportunities for Intervention)
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Review

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16 pages, 1160 KiB  
Review
Fetal Alcohol Spectrum Disorder and Iron Homeostasis
by Regan Bradley, Koffi L. Lakpa, Michael Burd, Sunil Mehta, Maja Z. Katusic and Jacob R. Greenmyer
Nutrients 2022, 14(20), 4223; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14204223 - 11 Oct 2022
Cited by 6 | Viewed by 2759
Abstract
Prenatal alcohol exposure results in a spectrum of behavioral, cognitive, and morphological abnormalities collectively referred to as fetal alcohol spectrum disorder (FASD). FASD presents with significant phenotypic variability and may be modified by gestational variables such as maternal nutritional status. Iron serves a [...] Read more.
Prenatal alcohol exposure results in a spectrum of behavioral, cognitive, and morphological abnormalities collectively referred to as fetal alcohol spectrum disorder (FASD). FASD presents with significant phenotypic variability and may be modified by gestational variables such as maternal nutritional status. Iron serves a critical function in the development of and processes within central nervous system (CNS) structures. Gestational iron deficiency alters CNS development and may contribute to neurodevelopmental impairment in FASD. This review explores the relationship between iron deficiency and fetal alcohol spectrum disorder as described in small animal and human studies. Consideration is given to the pathophysiologic mechanisms linking iron homeostasis and prenatal alcohol exposure. Existing data suggest that iron deficiency contributes to the severity of FASD and provide a mechanistic explanation linking these two conditions. Full article
(This article belongs to the Special Issue The Roles of Maternal and Child Nutrition in Fetal Alcohol Spectrum Disorders (FASD): From Mechanistic Insights to Opportunities for Intervention)
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25 pages, 441 KiB  
Review
Prenatal and Postnatal Choline Supplementation in Fetal Alcohol Spectrum Disorder
by Abigail M. Ernst, Blake A. Gimbel, Erik de Water, Judith K. Eckerle, Joshua P. Radke, Michael K. Georgieff and Jeffrey R. Wozniak
Nutrients 2022, 14(3), 688; https://0-doi-org.brum.beds.ac.uk/10.3390/nu14030688 - 06 Feb 2022
Cited by 20 | Viewed by 8341
Abstract
Fetal alcohol spectrum disorder (FASD) is common and represents a significant public health burden, yet very few interventions have been tested in FASD. Cognitive deficits are core features of FASD, ranging from broad intellectual impairment to selective problems in attention, executive functioning, memory, [...] Read more.
Fetal alcohol spectrum disorder (FASD) is common and represents a significant public health burden, yet very few interventions have been tested in FASD. Cognitive deficits are core features of FASD, ranging from broad intellectual impairment to selective problems in attention, executive functioning, memory, visual–perceptual/motor skills, social cognition, and academics. One potential intervention for the cognitive impairments associated with FASD is the essential nutrient choline, which is known to have numerous direct effects on brain and cognition in both typical and atypical development. We provide a summary of the literature supporting the use of choline as a neurodevelopmental intervention in those affected by prenatal alcohol. We first discuss how alcohol interferes with normal brain development. We then provide a comprehensive overview of the nutrient choline and discuss its role in typical brain development and its application in the optimization of brain development following early insult. Next, we review the preclinical literature that provides evidence of choline’s potential as an intervention following alcohol exposure. Then, we review a handful of existing human studies of choline supplementation in FASD. Lastly, we conclude with a review of practical considerations in choline supplementation, including dose, formulation, and feasibility in children. Full article
(This article belongs to the Special Issue The Roles of Maternal and Child Nutrition in Fetal Alcohol Spectrum Disorders (FASD): From Mechanistic Insights to Opportunities for Intervention)

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11 pages, 1429 KiB  
Brief Report
Untargeted and Targeted Blood Lipidomic Signature Profile of Gestational Alcohol Exposure
by Vishal D. Naik and Jayanth Ramadoss
Nutrients 2023, 15(6), 1411; https://0-doi-org.brum.beds.ac.uk/10.3390/nu15061411 - 15 Mar 2023
Cited by 2 | Viewed by 1339
Abstract
Alcohol consumption has a close relationship with blood lipid levels in a nonpregnant state, with a myriad of effects on the liver; however, little is known about the interaction of alcohol and lipids in the context of fetal alcohol spectrum disorders (FASD). We [...] Read more.
Alcohol consumption has a close relationship with blood lipid levels in a nonpregnant state, with a myriad of effects on the liver; however, little is known about the interaction of alcohol and lipids in the context of fetal alcohol spectrum disorders (FASD). We herein aimed to determine the effect of alcohol on the lipid profile in a pregnant rat model, with a focus on FASD. Dry blood spots (50 µL) were obtained from rat maternal blood collected on gestational day (GD) 20, two hours after the last binge alcohol exposure (4.5 g/kg, GD 5–10; 6 g/kg, GD 11–20). The samples were then analyzed using high-throughput untargeted and targeted lipid profiling via liquid chromatography-tandem mass spectrometry (LC-MS/MS). In untargeted lipidomics, 73 of 315 identified lipids were altered in the alcohol group compared to the pair-fed controls; 67 were downregulated and 6 were upregulated. In targeted analysis, 57 of the 260 studied lipid subspecies were altered, including Phosphatidylcholine (PC), Phosphatidylethanolamine (PE), Phosphatidylglycerol (PG), Phosphatidic Acid (PA), Phosphatidylinositol (PI), and Phosphatidylserine (PS); 36 of these were downregulated and 21 lipid subspecies were upregulated. These findings suggest alcohol-induced dysregulation of lipids in the maternal blood of rats and provide novel insights into possible FASD mechanisms. Full article
(This article belongs to the Special Issue The Roles of Maternal and Child Nutrition in Fetal Alcohol Spectrum Disorders (FASD): From Mechanistic Insights to Opportunities for Intervention)
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