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1.
Alcohol Clin Exp Res. 2018 Jun 5. doi: 10.1111/acer.13808. [Epub ahead of print]

Alcohol-Related Alterations in Placental Imprinted Gene Expression in Humans Mediate Effects of Prenatal Alcohol Exposure on Postnatal Growth.

Author information

1
Division of Pediatric Emergency Medicine and Institute for Human Nutrition, Columbia University Medical Center, New York, New York.
2
Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, New York.
3
Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, Michigan.
4
National Health Laboratory Service, Groote Schuur Hospital, Cape Town, South Africa.
5
the Departments of Human Biology and of Psychiatry and Mental Health, University of Cape Town Faculty of Health Sciences, Cape Town, South Africa.

Abstract

BACKGROUND:

A growing body of evidence in animal models has implicated alcohol-induced alterations in epigenetic programming as an important mechanism in fetal alcohol spectrum disorders (FASD). Imprinted genes, a subset of epigenetically regulated genes that are sensitive to the prenatal environment, are chiefly involved in growth and neurobehavior. We tested the hypothesis that alterations in placental imprinted gene expression mediate fetal alcohol growth restriction.

METHODS:

Placental expression of 109 genes previously shown to be imprinted and expressed in the placenta was assessed using the NanoString™ nCounter Analysis System in flash-frozen samples from 34 heavy drinkers and 31 control women in Cape Town, South Africa, from whom prospective pregnancy alcohol consumption data had been obtained. Length/height, weight, and head circumference were measured at 6.5 and 12 months and at an FASD diagnostic clinic (at ages 1.1 to 4.6 years) that we organized. Imprinted gene expression between exposed and control placentas was compared using the limma R package. The relation of alcohol exposure to World Health Organization length-for-age z-scores was examined before and after inclusion of expression for each alcohol-related imprinted gene, using hierarchical mixed regression models with repeated measures.

RESULTS:

Heavy drinkers averaged 8 standard drinks on 2 to 3 days/wk (vs. 0 for controls). Prenatal alcohol exposure was associated with smaller length/height and weight during the postnatal period. Heavy exposure was related to alterations in expression of 11 of 93 expressed imprinted genes, including increased expression of 5 genes found to be negatively associated with growth and decreased expression of 3 genes positively associated with growth. Alcohol-related alterations in expression of 5 genes statistically mediated the effect of prenatal alcohol exposure on length.

CONCLUSIONS:

These findings identify alcohol-related alterations in placental imprinted gene expression as potential biomarkers of adverse effect in FASD and suggest that these alterations may play a mechanistic role in fetal alcohol growth restriction. Future studies are needed to determine whether alterations in imprinted gene expression also mediate FASD neurobehavioral deficits and whether such alterations are amenable to intervention.

KEYWORDS:

Fetal Alcohol Spectrum Disorders; Gene Expression; Genomic Imprinting; Growth Restriction; Placenta; Prenatal Alcohol Exposure

2.
Alcohol Clin Exp Res. 2018 Jul;42(7):1327-1341. doi: 10.1111/acer.13769. Epub 2018 Jun 15.

Efficacy of Maternal Choline Supplementation During Pregnancy in Mitigating Adverse Effects of Prenatal Alcohol Exposure on Growth and Cognitive Function: A Randomized, Double-Blind, Placebo-Controlled Clinical Trial.

Author information

1
Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, Michigan.
2
Department of Human Biology, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
3
Department of Psychiatry and Mental Health, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
4
Division of Pediatric Emergency Medicine, Morgan Stanley Children's Hospital of New York, New York, New York.
5
Institute for Human Nutrition, Columbia University Medical Center, New York, New York.
6
Department of Psychology, University of Delaware, Newark, Delaware.
7
Department of Psychology, University of Wollongong, New South Wales, Australia.
8
Department of Pediatrics, Sanford School of Medicine, University of South Dakota, Sioux Falls, South Dakota.
9
College of Medicine, University of Arizona, Tucson, Arizona.
10
Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, North Carolina.
11
MRC/UCT Medical Imaging Research Unit, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
12
Division of Gastroenterology, Hepatology and Nutrition, Center for Nutrition, Boston Children's Hospital/Harvard Medical School, Boston, Massachusetts.

Abstract

BACKGROUND:

We recently demonstrated the acceptability and feasibility of a randomized, double-blind choline supplementation intervention for heavy drinking women during pregnancy. In this study, we report our results relating to the efficacy of this intervention in mitigating adverse effects of prenatal alcohol exposure (PAE) on infant growth and cognitive function.

METHODS:

Sixty-nine Cape Coloured (mixed ancestry) heavy drinkers in Cape Town, South Africa, recruited in mid-pregnancy, were randomly assigned to receive a daily oral dose of either 2 g of choline or placebo from time of enrollment until delivery. Each dose consisted of an individually wrapped packet of powder that, when mixed with water, produced a sweet tasting grape-flavored drink. The primary outcome, eyeblink conditioning (EBC), was assessed at 6.5 months. Somatic growth was measured at birth, 6.5, and 12 months, recognition memory and processing speed on the Fagan Test of Infant Intelligence, at 6.5 and 12 months.

RESULTS:

Infants born to choline-treated mothers were more likely to meet criterion for conditioning on EBC than the placebo group. Moreover, within the choline arm, degree of maternal adherence to the supplementation protocol strongly predicted EBC performance. Both groups were small at birth, but choline-treated infants showed considerable catch-up growth in weight and head circumference at 6.5 and 12 months. At 12 months, the infants in the choline treatment arm had higher novelty preference scores, indicating better visual recognition memory.

CONCLUSIONS:

This exploratory study is the first to provide evidence that a high dose of choline administered early in pregnancy can mitigate adverse effects of heavy PAE on EBC, postnatal growth, and cognition in human infants. These findings are consistent with studies of alcohol-exposed animals that have demonstrated beneficial effects of choline supplementation on classical conditioning, learning, and memory.

KEYWORDS:

Choline Supplementation; Eyeblink Conditioning; Fetal Alcohol Spectrum Disorders; Fetal Alcohol Syndrome; Growth; Prenatal Alcohol Exposure

PMID:
29750367
PMCID:
PMC6028282
[Available on 2019-07-01]
DOI:
10.1111/acer.13769
Icon for Wiley
3.
Alcohol Clin Exp Res. 2018 Jul;42(7):1315-1326. doi: 10.1111/acer.13768. Epub 2018 Jun 13.

Feasibility and Acceptability of Maternal Choline Supplementation in Heavy Drinking Pregnant Women: A Randomized, Double-Blind, Placebo-Controlled Clinical Trial.

Author information

1
Department of Psychiatry and Behavioral Neurosciences , Wayne State University School of Medicine, Detroit, Michigan.
2
Department of Human Biology , Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
3
Department of Psychiatry and Mental Health , Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
4
Division of Pediatric Emergency Medicine , Morgan Stanley Children's Hospital of New York, New York, New York.
5
Institute for Human Nutrition , Columbia University Medical Center, New York, New York.
6
MRC/UCT Medical Imaging Research Unit , Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
7
Division of Nutrition , Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
8
Nutrition Research Institute , University of North Carolina at Chapel Hill, Kannapolis, North Carolina.
9
Division of Gastroenterology, Hepatology and Nutrition , Center for Nutrition, Boston Children's Hospital/Harvard Medical School, Boston, Massachusetts.

Abstract

BACKGROUND:

Choline, an essential nutrient, serves as a methyl-group donor for DNA methylation and is a constituent of the neurotransmitter acetylcholine and a precursor to major components of cell membranes. Findings from animal studies suggest that choline supplementation during pregnancy can mitigate adverse effects of prenatal alcohol exposure on growth and neurocognitive function. We conducted a randomized, double-blind exploratory trial to examine feasibility and acceptability of a choline supplementation intervention during pregnancy.

METHODS:

Seventy heavy drinkers, recruited in mid-pregnancy, were randomly assigned to receive a daily oral dose of 2 g of choline or a placebo from time of enrollment until delivery. Each dose consisted of an individually wrapped packet of powder that, when mixed with water, produced a sweet tasting grape-flavored drink. Adherence was assessed by collecting used and unused drink packets on a monthly basis and tabulating the number used. Side effects were assessed in monthly interviews. Blood samples obtained at enrollment and at 4 and 12 weeks after randomization were assayed for plasma choline concentration.

RESULTS:

Adherence was good-to-excellent (median doses taken = 74.0%; interquartile range = 53.9 to 88.7%) and was not related to a range of sociodemographic characteristics or to alcohol consumption ascertained using a timeline follow-back interview. By 4 weeks, plasma choline concentrations were significantly higher in the choline supplementation than the placebo arm, and this group difference continued to be evident at 12 weeks. The only side effect was a small increase in nausea/dyspepsia. No effects were seen for diarrhea, vomiting, muscle stiffness, blood pressure, or body odor changes.

CONCLUSIONS:

This study demonstrated that a choline supplementation program with very heavy drinkers during pregnancy is feasible even among highly disadvantaged, poorly educated women. The broad acceptability of this intervention is indicated by our finding that adherence was not related to maternal education, intellectual function, depression, nutritional status, or alcohol use.

KEYWORDS:

Adherence; Feasibility; Fetal Alcohol Spectrum Disorders; Fetal Alcohol Syndrome; Maternal Choline Supplementation; Prenatal Alcohol Exposure

PMID:
29750366
PMCID:
PMC6028314
[Available on 2019-07-01]
DOI:
10.1111/acer.13768
Icon for Wiley
4.
Front Neuroanat. 2018 Jan 12;11:132. doi: 10.3389/fnana.2017.00132. eCollection 2017.

Reductions in Corpus Callosum Volume Partially Mediate Effects of Prenatal Alcohol Exposure on IQ.

Author information

1
Department of Human Biology, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
2
Department of Psychiatry and Mental Health, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
3
Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, MI, United States.
4
MRC/UCT Medical Imaging Research Unit, Division of Biomedical Engineering, Department of Human Biology, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.

Abstract

Disproportionate volume reductions in the basal ganglia, corpus callosum (CC) and hippocampus have been reported in children with prenatal alcohol exposure (PAE). However, few studies have investigated these reductions in high prevalence communities, such as the Western Cape Province of South Africa, and only one study made use of manual tracing, the gold standard of volumetric analysis. The present study examined the effects of PAE on subcortical neuroanatomy using manual tracing and the relation of volumetric reductions in these regions to IQ and performance on the California Verbal Learning Test-Children's Version (CVLT-C), a list learning task sensitive to PAE. High-resolution T1-weighted images were acquired, using a sequence optimized for morphometric neuroanatomical analysis, on a Siemens 3T Allegra MRI scanner from 71 right-handed, 9- to 11-year-old children [9 fetal alcohol syndrome (FAS), 19 partial FAS (PFAS), 24 non-syndromal heavily exposed (HE) and 19 non-exposed controls]. Frequency of maternal drinking was ascertained prospectively during pregnancy using timeline follow-back interviews. PAE was examined in relation to volumes of the CC and left and right caudate nuclei, nucleus accumbens and hippocampi. All structures were manually traced using Multitracer. Higher levels of PAE were associated with reductions in CC volume after adjustment for TIV. Although the effect of PAE on CC was confounded with smoking and lead exposure, additional analyses showed that it was not accounted for by these exposures. Amongst dysmorphic children, smaller CC was associated with poorer IQ and CVLT-C scores and statistically mediated the effect of PAE on IQ. In addition, higher levels of PAE were associated with bilateral volume reductions in caudate nuclei and hippocampi, effects that remained significant after control for TIV, child sex and age, socioeconomic status, maternal smoking during pregnancy, and childhood lead exposure. These data confirm previous findings showing that PAE is associated with decreases in subcortical volumes and is the first study to show that decreases in callosal volume may play a role in fetal alcohol-related impairment in cognitive function seen in childhood.

KEYWORDS:

IQ; MRI; corpus callosum; fetal alcohol spectrum disorders; subcortical volumes

5.
Front Hum Neurosci. 2018 Jan 8;11:627. doi: 10.3389/fnhum.2017.00627. eCollection 2017.

Altered Parietal Activation during Non-symbolic Number Comparison in Children with Prenatal Alcohol Exposure.

Author information

1
Division of Biomedical Engineering, Department of Human Biology, University of Cape Town, Cape Town, South Africa.
2
Department of Human Biology, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
3
Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, MI, United States.
4
Department of Psychiatry and Mental Health, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.

Abstract

Number processing is a cognitive domain particularly sensitive to prenatal alcohol exposure, which relies on intact parietal functioning. Alcohol-related alterations in brain activation have been found in the parietal lobe during symbolic number processing. However, the effects of prenatal alcohol exposure on the neural correlates of non-symbolic number comparison and the numerical distance effect have not been investigated. Using functional magnetic resonance imaging (fMRI), we examined differences in brain activation associated with prenatal alcohol exposure in five parietal regions involved in number processing during a non-symbolic number comparison task with varying degrees of difficulty. fMRI results are presented for 27 Cape Colored children (6 fetal alcohol syndome (FAS)/partial FAS, 5 heavily exposed (HE) non-sydromal, 16 controls; mean age ± SD = 11.7 ± 1.1 years). Fetal alcohol exposure was assessed by interviewing mothers using a timeline follow-back approach. Separate subject analyses were performed in each of five regions of interest, bilateral horizontal intraparietal sulci (IPS), bilateral posterior superior parietal lobules (PSPL), and left angular gyrus (left AG), using the general linear model with predictors for number comparison and difficulty level. Mean percent signal change for each predictor was extracted for each subject for each region to examine group differences and associations with continuous measures of alcohol exposure. Although groups did not differ in performance, controls activated the right PSPL more during non-symbolic number comparison than exposed children, but this was not significant after controlling for maternal smoking, and the right IPS more than children with fetal alcohol syndrome (FAS) or partial FAS. More heavily exposed children recruited the left AG to a greater extent as task difficulty increased, possibly to compensate, in part, for impairments in function in the PSPL and IPS. Notably, in non-syndromal heavily exposed children activation was impaired in the right PSPL, but spared in the right IPS. These results extend previous findings of poor right IPS recruitment during symbolic number processing in FAS/PFAS, indicating that mental representation of relative quantity is affected by prenatal alcohol exposure for both symbolic and non-symbolic representations of quantity.

KEYWORDS:

arithmetic deficits; fMRI; fetal alcohol spectrum disorders; fetal alcohol syndrome; intraparietal sulci; non-symbolic number processing; numerical distance effect; parietal lobe

6.
Neurotoxicol Teratol. 2017 Nov;64:73-78. doi: 10.1016/j.ntt.2017.10.007. Epub 2017 Oct 24.

Alcohol use among Inuit pregnant women: Validity of alcohol ascertainment measures over time.

Author information

1
Department of Psychiatry, McGill University, Montreal, QC, Canada; Douglas Mental Health University Institute, Montreal, QC, Canada. Electronic address: marilyn.fortin@douglas.mcgill.ca.
2
School of Psychology, Université Laval, Québec, QC, Canada; Population Health and Optimal Health Practices Branch, CHU de Québec Research Centre, Québec, QC, Canada.
3
Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, MI, USA.
4
Population Health and Optimal Health Practices Branch, CHU de Québec Research Centre, Québec, QC, Canada; Department of Paediatrics, Centre mère-enfant Soleil, CHU de Québec, Université Laval, Québec, QC, Canada.

Abstract

BACKGROUND:

Frequency and quantity of alcohol consumed by women are two important indicators of the risks associated with drinking during pregnancy. Some studies have compared the validity of maternal alcohol report obtained during and after pregnancy. However, to date none have examined alcohol use in a Native Canadian population, such as the Inuit. Effective measurement methods are necessary to better understand why children from some communities seem at increased risk of alcohol-related neurodevelopmental disorders.

METHODS:

Prospective and retrospective drinking interviews were obtained from a sub-sample of 67 women included in the Nunavik Child Development Study (NCDS), Nunavik, Canada (1995-2010; N=248). Number of days of alcohol consumption and binge drinking (five drinks or more per episode) across pregnancy as well as ounces of absolute alcohol per day and per drinking day among users were collected using timeline follow-back interviews administered both during pregnancy and again 11years after delivery. Consistency of alcohol reports over time, as well as significant differences for alcohol quantities described by users between interviews were examined. Sociodemographic characteristics associated with alcohol use reports were also assessed.

RESULTS:

The proportion of positive reports of alcohol and binge drinking during pregnancy was higher when women were interviewed prospectively during pregnancy than retrospectively. We observed a fair to moderate agreement of alcohol report between interview periods. By contrast, the number of binge drinking days during pregnancy was slightly higher among alcohol users when documented retrospectively.

CONCLUSIONS:

Our findings endorse the conclusion that prospective alcohol measures provide more reliable ascertainment and likely generate more valid information about the proportion of children prenatally exposed to alcohol in the Inuit population.

KEYWORDS:

Alcohol; Binge drinking; Indigenous; Inuit; Longitudinal studies; Measures; Pregnancy; Pregnant women; Prenatal alcohol exposure; Prospective and retrospective alcohol ascertainment

PMID:
29079497
DOI:
10.1016/j.ntt.2017.10.007
[Indexed for MEDLINE]
Icon for Elsevier Science
7.
Neurotoxicol Teratol. 2018 Jan - Feb;65:51-59. doi: 10.1016/j.ntt.2017.10.005. Epub 2017 Oct 22.

Prenatal methamphetamine exposure is associated with reduced subcortical volumes in neonates.

Author information

1
Department of Human Biology, Faculty of Health Sciences, University of Cape Town, South Africa. Electronic address: Fleur.Warton@uct.ac.za.
2
Department of Human Biology, Faculty of Health Sciences, University of Cape Town, South Africa; MRC/UCT Medical Imaging Research Unit, Division of Biomedical Engineering, Faculty of Health Sciences, University of Cape Town, South Africa.
3
Department of Human Biology, Faculty of Health Sciences, University of Cape Town, South Africa.
4
Department of Psychiatry and Mental Health, Faculty of Health Sciences, University of Cape Town, South Africa.
5
Child Development Research Unit, Department of Human Biology, University of Cape Town, South Africa.
6
Division of Pediatric Emergency Medicine, Columbia University Medical Center, New York, NY, USA.
7
Athinoula A. Martinos Centre for Biomedical Imaging, Massachusetts General Hospital, Charlestown, MA, USA.
8
Department of Pediatrics, McGill University, Montreal Children's Hospital, Montreal, Canada.
9
Department of Human Biology, Faculty of Health Sciences, University of Cape Town, South Africa; Department of Psychiatry and Mental Health, Faculty of Health Sciences, University of Cape Town, South Africa; Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, MI, USA.

Abstract

OBJECTIVES:

Prenatal exposure to methamphetamine is associated with a range of neuropsychological, behavioural and cognitive deficits. A small number of imaging studies suggests that these may be mediated by neurostructural changes, including reduced volumes of specific brain regions. This study investigated potential volumetric changes in the brains of neonates with prenatal methamphetamine exposure. To our knowledge no previous studies have examined methamphetamine effects on regional brain volumes at this age.

STUDY DESIGN:

Mothers were recruited antenatally and interviewed regarding methamphetamine use during pregnancy. Mothers in the exposure group reported using methamphetamine≥twice/month during pregnancy; control infants had no exposure to methamphetamine or other drugs and minimal exposure to alcohol. MRI scans were performed in the first postnatal month, following which anatomical images were processed using FreeSurfer. Subcortical and cerebellar regions were manually segmented and their volumes determined using FreeView. Pearson correlations were used to analyse potential associations between methamphetamine exposure and regional volumes. The associations between methamphetamine exposure and regional volumes were then examined adjusting for potential confounding variables.

RESULTS:

Methamphetamine exposure was associated with reduced left and right caudate and thalamus volumes. The association in the right caudate remained significant following adjustment for potential confounding variables.

CONCLUSIONS:

Our findings showing reduced caudate and thalamus volumes in neonates with prenatal methamphetamine exposure are consistent with previous findings in older exposed children, and demonstrate that these changes are already detectable in neonates. Continuing research is warranted to examine whether reduced subcortical volumes are predictive of cognitive, behavioural and affective impairment in older children.

KEYWORDS:

Caudate nucleus; Magnetic resonance imaging; Neonate; Prenatal methamphetamine exposure; Regional brain volumes; Thalamus

PMID:
29069607
PMCID:
PMC5803390
[Available on 2019-01-01]
DOI:
10.1016/j.ntt.2017.10.005
Icon for Elsevier Science
8.
Metab Brain Dis. 2018 Apr;33(2):507-522. doi: 10.1007/s11011-017-0135-9. Epub 2017 Oct 23.

Prenatal methamphetamine exposure is associated with corticostriatal white matter changes in neonates.

Author information

1
Department of Human Biology, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa. fleur.warton@gmail.com.
2
Department of Human Biology, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
3
MRC/UCT Medical Imaging Research Unit, Division of Biomedical Engineering, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
4
African Institute for Mathematical Sciences, Cape Town, South Africa.
5
Scientific and Statistical Computing Core, National Institutes of Health, Bethesda, MD, USA.
6
Department of Psychiatry and Mental Health, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
7
Department of Pediatrics, Montreal Children's Hospital, McGill University, Montreal, Canada.
8
ACSENT Laboratory, Department of Psychology, University of Cape Town, Cape Town, South Africa.
9
Athinoula A. Martinos Centre for Biomedical Imaging, Massachusetts General Hospital, Charlestown, MA, USA.
10
Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, MI, USA.

Abstract

Diffusion tensor imaging (DTI) studies have shown that prenatal exposure to methamphetamine is associated with alterations in white matter microstructure, but to date no tractography studies have been performed in neonates. The striato-thalamo-orbitofrontal circuit and its associated limbic-striatal areas, the primary circuit responsible for reinforcement, has been postulated to be dysfunctional in drug addiction. This study investigated potential white matter changes in the striatal-orbitofrontal circuit in neonates with prenatal methamphetamine exposure. Mothers were recruited antenatally and interviewed regarding methamphetamine use during pregnancy, and DTI sequences were acquired in the first postnatal month. Target regions of interest were manually delineated, white matter bundles connecting pairs of targets were determined using probabilistic tractography in AFNI-FATCAT, and fractional anisotropy (FA) and diffusion measures were determined in white matter connections. Regression analysis showed that increasing methamphetamine exposure was associated with reduced FA in several connections between the striatum and midbrain, orbitofrontal cortex, and associated limbic structures, following adjustment for potential confounding variables. Our results are consistent with previous findings in older children and extend them to show that these changes are already evident in neonates. The observed alterations are likely to play a role in the deficits in attention and inhibitory control frequently seen in children with prenatal methamphetamine exposure.

KEYWORDS:

Corticostriatal white matter; Diffusion tensor imaging; Magnetic resonance imaging; Neonate; Prenatal methamphetamine exposure

PMID:
29063448
PMCID:
PMC5866741
[Available on 2019-04-01]
DOI:
10.1007/s11011-017-0135-9
Icon for Springer
9.
Alcohol Clin Exp Res. 2017 Dec;41(12):2114-2127. doi: 10.1111/acer.13504. Epub 2017 Oct 31.

Maternal Alcohol Use and Nutrition During Pregnancy: Diet and Anthropometry.

Author information

1
Columbia University Medical Center, New York City, New York.
2
University of Cape Town Faculty of Health Sciences, Cape Town, South Africa.
3
Wayne State University School of Medicine, Detroit, Michigan.
4
Boston Children's Hospital, Boston, Massachusetts.

Abstract

BACKGROUND:

Despite known risks of prenatal nutritional deficiencies and studies documenting increased prevalence of poor dietary intake among nonpregnant alcohol abusers, the nutritional status of heavy drinking pregnant women remains largely unstudied. Animal models have found interactions between prenatal ethanol exposure and micronutrients, such as choline, folate, B12, and iron, and human studies have reported that lower maternal weight and body mass confer increased fetal alcohol-related risk.

METHODS:

One hundred and twenty-three heavy drinking Cape Coloured pregnant women and 83 abstaining controls were recruited at their first antenatal clinic visit. At 3 prenatal study visits, each gravida was interviewed about alcohol, smoking, and drug use and weight, height, and arm skinfolds were measured. Dietary intakes of energy, protein, fat, and major micronutrients were assessed from three 24-hour recall interviews.

RESULTS:

The majority of women gained less than the recommended 0.42 kg/wk during pregnancy. Whereas methamphetamine use was associated with smaller biceps skinfolds, an indicator of body fat, alcohol consumption was not related to any anthropometric indicator. Alcohol was related to higher intake of phosphorus, choline, and vitamins B12 and D. Alcohol, cigarette, and methamphetamine use were related to lower vitamin C intake. Insufficient intake was reported by >85% of women for 10 of 22 key nutrients, and >50% for an additional 3 nutrients.

CONCLUSIONS:

Alcohol consumption during pregnancy was not associated with meaningful changes in diet or anthropometric measures in this population, suggesting that poor nutrition among drinkers does not confound the extensively reported effects of prenatal alcohol exposure on growth and neurobehavior. The poor gestational weight gain and high rates of insufficient intake for several nutrients in both the alcohol-exposed and control groups are also of public health importance.

KEYWORDS:

Alcohol Consumption During Pregnancy; Anthropometry; Diet; Fetal Alcohol Spectrum Disorders; Nutrition

PMID:
28940428
DOI:
10.1111/acer.13504
[Indexed for MEDLINE]
Icon for Wiley
10.
Hum Brain Mapp. 2017 Oct;38(10):5217-5233. doi: 10.1002/hbm.23726. Epub 2017 Jul 22.

Localized reductions in resting-state functional connectivity in children with prenatal alcohol exposure.

Author information

1
MRC/UCT Medical Imaging Research Unit, Division of Biomedical Engineering, University of Cape Town, South Africa.
2
Department of Human Biology, University of Cape Town, South Africa.
3
African Institute for Mathematical Sciences, South Africa.
4
Scientific and Statistical Computing Core, National Institutes of Health, Bethesda, Maryland.
5
Department of Psychiatry and Mental Health, University of Cape Town, South Africa.
6
Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, Michigan.
7
Department of Biomedical Engineering, New Jersey Institute of Technology, Newark, New Jersey.

Abstract

Fetal alcohol spectrum disorders (FASD) are characterized by impairment in cognitive function that may or may not be accompanied by craniofacial anomalies, microcephaly, and/or growth retardation. Resting-state functional MRI (rs-fMRI), which examines the low-frequency component of the blood oxygen level dependent (BOLD) signal in the absence of an explicit task, provides an efficient and powerful mechanism for studying functional brain networks even in low-functioning and young subjects. Studies using independent component analysis (ICA) have identified a set of resting-state networks (RSNs) that have been linked to distinct domains of cognitive and perceptual function, which are believed to reflect the intrinsic functional architecture of the brain. This study is the first to examine resting-state functional connectivity within these RSNs in FASD. Rs-fMRI scans were performed on 38 children with FASD (19 with either full fetal alcohol syndrome (FAS) or partial FAS (PFAS), 19 nonsyndromal heavily exposed (HE)), and 19 controls, mean age 11.3 ± 0.9 years, from the Cape Town Longitudinal Cohort. Nine resting-state networks were generated by ICA. Voxelwise group comparison between a combined FAS/PFAS group and controls revealed localized dose-dependent functional connectivity reductions in five regions in separate networks: anterior default mode, salience, ventral and dorsal attention, and R executive control. The former three also showed lower connectivity in the HE group. Gray matter connectivity deficits in four of the five networks appear to be related to deficits in white matter tracts that provide intra-RSN connections. Hum Brain Mapp 38:5217-5233, 2017.

KEYWORDS:

fetal alcohol spectrum disorders; fractional amplitude of low-frequency fluctuation; regional homogeneity; resting-state functional MRI; resting-state functional connectivity

PMID:
28734059
DOI:
10.1002/hbm.23726
[Indexed for MEDLINE]
Icon for Wiley
11.
Alcohol Clin Exp Res. 2017 Aug;41(8):1471-1483. doi: 10.1111/acer.13429. Epub 2017 Jul 10.

Facial Curvature Detects and Explicates Ethnic Differences in Effects of Prenatal Alcohol Exposure.

Author information

1
Nuffield Department of Obstetrics and Gynaecology , University of Oxford, Oxford, United Kingdom.
2
Big Data Institute , University of Oxford, Oxford, UK.
3
Department of Medical and Molecular Genetics , Indiana University School of Medicine, Indianapolis, Indiana.
4
Department of Psychiatry and Behavioral Neurosciences , Wayne State University School of Medicine, Detroit, Michigan.
5
Departments of Human Biology and of Psychiatry and Mental Health , University of Cape Town Faculty of Health Sciences, Cape Town, South Africa.
6
Sanford Research and Department of Pediatrics , Sanford School of Medicine, University of South Dakota, Sioux Falls, South Dakota.
7
Developmental Cognitive Neuroimaging Laboratory , Children's Hospital Los Angeles, Los Angeles, California.
8
Department of Psychiatry and Behavioral Sciences , Emory University School of Medicine, Atlanta, Georgia.
9
Department of Psychiatry , University of Minnesota, Minneapolis, Minnesota.
10
Department of Psychology , San Diego State University, San Diego, California.
11
Department of Pediatrics , School of Medicine, UCSD, San Diego, California.

Abstract

BACKGROUND:

Our objective is to help clinicians detect the facial effects of prenatal alcohol exposure by developing computer-based tools for screening facial form.

METHODS:

All 415 individuals considered were evaluated by expert dysmorphologists and categorized as (i) healthy control (HC), (ii) fetal alcohol syndrome (FAS), or (iii) heavily prenatally alcohol exposed (HE) but not clinically diagnosable as FAS; 3D facial photographs were used to build models of facial form to support discrimination studies. Surface curvature-based delineations of facial form were introduced.

RESULTS:

(i) Facial growth in FAS, HE, and control subgroups is similar in both cohorts. (ii) Cohort consistency of agreement between clinical diagnosis and HC-FAS facial form classification is lower for midline facial regions and higher for nonmidline regions. (iii) Specific HC-FAS differences within and between the cohorts include: for HC, a smoother philtrum in Cape Coloured individuals; for FAS, a smoother philtrum in Caucasians; for control-FAS philtrum difference, greater homogeneity in Caucasians; for control-FAS face difference, greater homogeneity in Cape Coloured individuals. (iv) Curvature changes in facial profile induced by prenatal alcohol exposure are more homogeneous and greater in Cape Coloureds than in Caucasians. (v) The Caucasian HE subset divides into clusters with control-like and FAS-like facial dysmorphism. The Cape Coloured HE subset is similarly divided for nonmidline facial regions but not clearly for midline structures. (vi) The Cape Coloured HE subset with control-like facial dysmorphism shows orbital hypertelorism.

CONCLUSIONS:

Facial curvature assists the recognition of the effects of prenatal alcohol exposure and helps explain why different facial regions result in inconsistent control-FAS discrimination rates in disparate ethnic groups. Heavy prenatal alcohol exposure can give rise to orbital hypertelorism, supporting a long-standing suggestion that prenatal alcohol exposure at a particular time causes increased separation of the brain hemispheres with a concomitant increase in orbital separation.

KEYWORDS:

3D Face Analysis; Facial Curvature; Facial Dysmorphism; Fetal Alcohol Spectrum Disorders

PMID:
28608920
PMCID:
PMC5563255
DOI:
10.1111/acer.13429
[Indexed for MEDLINE]
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12.
Cereb Cortex. 2018 Feb 1;28(2):688. doi: 10.1093/cercor/bhw357.

Erratum to: "Functional MRI of Human Eyeblink Classical Conditioning in Children with Fetal Alcohol Spectrum Disorders".

Author information

1
Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.
2
University of Cape Town, Faculty of Health Sciences, Observatory, Western Cape 7925, South Africa.
3
University of Delaware, Newark, DE 19716, USA.
4
Wayne State University, School of Medicine, Detroit, MI 48207, USA.
5
Children's Hospital Los Angeles and University of Southern California, Los Angeles, CA 90027, USA.
13.
Alcohol Clin Exp Res. 2017 May;41(5):965-975. doi: 10.1111/acer.13363. Epub 2017 Apr 3.

Heavy Prenatal Alcohol Exposure is Related to Smaller Corpus Callosum in Newborn MRI Scans.

Author information

1
Department of Psychiatry and Behavioral Neurosciences , Wayne State University School of Medicine, Detroit, Michigan.
2
Department of Human Biology , Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
3
Department of Psychiatry and Mental Health , Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
4
Montreal Children's Hospital , Montreal, Quebec, Canada.
5
Department of Pediatrics , Sanford School of Medicine, University of South Dakota, Sioux Falls, South Dakota.
6
College of Medicine , University of Arizona, Tucson, Arizona.
7
Division of Molecular Biology and Human Genetics , Stellenbosch University, Faculty of Medicine and Health Sciences, Cape Town, South Africa.
8
Scientific and Statistical Computing Core , National Institutes of Health, Bethesda, Maryland.
9
Department of Psychology , University of Cape Town, Cape Town, South Africa.
10
Division of Pediatric Emergency Medicine , Morgan Stanley Children's Hospital of New York, Columbia University Medical Center, New York, New York.
11
Department of Pediatrics , Boston Children's Hospital/Harvard Medical School, Boston, Massachusetts.
12
Department of Radiology , Massachusetts General Hospital, Boston, Massachusetts.
13
MRC/UCT Medical Imaging Research Unit , Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.

Abstract

BACKGROUND:

Magnetic resonance imaging (MRI) studies have consistently demonstrated disproportionately smaller corpus callosa in individuals with a history of prenatal alcohol exposure (PAE) but have not previously examined the feasibility of detecting this effect in infants. Tissue segmentation of the newborn brain is challenging because analysis techniques developed for the adult brain are not directly transferable, and segmentation for cerebral morphometry is difficult in neonates, due to the latter's incomplete myelination. This study is the first to use volumetric structural MRI to investigate PAE effects in newborns using manual tracing and to examine the cross-sectional area of the corpus callosum (CC).

METHODS:

Forty-three nonsedated infants born to 32 Cape Coloured heavy drinkers and 11 controls recruited prospectively during pregnancy were scanned using a custom-designed birdcage coil for infants, which increases signal-to-noise ratio almost 2-fold compared to the standard head coil. Alcohol use was ascertained prospectively during pregnancy, and fetal alcohol spectrum disorders diagnosis was conducted by expert dysmorphologists. Data were acquired using a multi-echo FLASH protocol adapted for newborns, and a knowledge-based procedure was used to hand-segment the neonatal brains.

RESULTS:

CC was disproportionately smaller in alcohol-exposed neonates than controls after controlling for intracranial volume. By contrast, CC area was unrelated to infant sex, gestational age, age at scan, or maternal smoking, marijuana, or methamphetamine use during pregnancy.

CONCLUSIONS:

Given that midline craniofacial anomalies have been recognized as a hallmark of fetal alcohol syndrome in humans and animal models since this syndrome was first identified, the CC deficit identified here in newborns may support early identification of a range of midline structural impairments. Smaller CC during the newborn period may provide an early indicator of fetal alcohol-related cognitive deficits that have been linked to this critically important brain structure in childhood and adolescence.

KEYWORDS:

Corpus Callosum; Fetal Alcohol Spectrum Disorders; Fetal Alcohol Syndrome; Manual Tracing; Neonatal Brain MRI; Prenatal Alcohol Exposure

PMID:
28247416
PMCID:
PMC5404976
DOI:
10.1111/acer.13363
[Indexed for MEDLINE]
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14.
Cereb Cortex. 2017 Jul 1;27(7):3752-3767. doi: 10.1093/cercor/bhw273.

Functional MRI of Human Eyeblink Classical Conditioning in Children with Fetal Alcohol Spectrum Disorders.

Author information

1
Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA.
2
University of Cape Town, Faculty of Health Sciences, Observatory, Western Cape 7925, South Africa.
3
University of Delaware, Newark, DE 19716, USA.
4
Wayne State University, School of Medicine, Detroit, MI 48207, USA.
5
Children's Hospital Los Angeles andUniversity of Southern California, Los Angeles, CA 90027, USA.

Abstract

Prenatal alcohol exposure has been linked to a broad range of developmental deficits, with eyeblink classical conditioning (EBC) among the most sensitive endpoints. This fMRI study compared EBC-related brain activity in 47 children with fetal alcohol syndrome (FAS), partial FAS (PFAS), heavily exposed (HE) non-syndromal children, and healthy controls. All of the children had previously participated in two EBC studies conducted as part of our longitudinal study of fetal alcohol spectrum disorders. Although learning-related behavioral differences were seen in all groups during the scans, controls showed more conditioned responses (CR) than the alcohol-exposed groups. Despite lower conditioning levels relative to controls, the exposed groups exhibited extensive cerebellar activations. Specifically, children with FAS/PFAS showed increased activation of cerebellar lobule VI in session 2, while HE children showed increased activation in session 1. Continuous measures of prenatal alcohol use correlated with learning-related activations in cerebellum and frontal cortices. Only controls showed significant cerebellar activation-CR correlations in the deep nuclei and lateral lobule VI, suggesting that these key regions supporting EBC may be functionally disorganized in alcohol-exposed children. These findings are the first to characterize abnormalities in brain function associated with the behavioral conditioning deficits seen in children with prenatal alcohol exposure.

KEYWORDS:

cerebellar volume; cerebellum; fetal alcohol syndrome; gray matter volume; learning; prenatal alcohol exposure; white matter volume

PMID:
28169393
PMCID:
PMC6075216
DOI:
10.1093/cercor/bhw273
[Indexed for MEDLINE]
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15.
Alcohol Clin Exp Res. 2017 Feb;41(2):334-344. doi: 10.1111/acer.13307. Epub 2017 Jan 11.

Differential Recruitment of Brain Regions During Response Inhibition in Children Prenatally Exposed to Alcohol.

Author information

1
Department of Psychiatry and Behavioral Neurosciences , Wayne State University School of Medicine, Detroit, Michigan.
2
Department of Human Biology , University of Cape Town Faculty of Health Sciences, Cape Town, South Africa.
3
Department of Psychiatry and Mental Health , University of Cape Town Faculty of Health Sciences, Cape Town, South Africa.

Abstract

BACKGROUND:

Response inhibition is a distinct aspect of executive function that is frequently impaired in children with fetal alcohol spectrum disorders (FASD). We used a Go/NoGo (GNG) task in a functional MRI protocol to investigate differential activation of brain regions in the response inhibition network in children diagnosed with full or partial fetal alcohol syndrome (FAS/PFAS), compared with healthy controls.

METHODS:

A rapid, event-related task with 120 Go and 60 NoGo trials was used to study children aged 8 to 12 years-8 with FAS/PFAS, 17 controls. Letters were projected sequentially, with Go and NoGo trials randomly interspersed across the task. BOLD signal in the whole brain was contrasted for the correct NoGo minus correct Go trials between the FAS/PFAS and control groups.

RESULTS:

Compared to the FAS/PFAS group, controls showed greater activation of the inferior frontal and anterior cingulate network linked to response inhibition in typically developing children. By contrast, the FAS/PFAS group showed greater BOLD response in dorsolateral prefrontal cortex and other middle prefrontal regions, suggesting compensation for inefficient function of pathways that normally mediate inhibitory processing. All group differences were significant after control for potential confounding variables. None of the effects of prenatal alcohol exposure on activation of the regions associated with response inhibition were attributable to the effects of this exposure on IQ.

CONCLUSIONS:

This is the first FASD GNG study in which all participants in the exposed group met criteria for a diagnosis of full FAS or PFAS. Although FASD is frequently comorbid with attention deficit hyperactivity disorder, the pattern of brain activation seen in these disorders differs, suggesting that different neural pathways mediate response inhibition in FASD and that different interventions for FASD are, therefore, warranted.

KEYWORDS:

Fetal Alcohol Syndrome; Functional Magnetic Resonance Imaging; Go/NoGo; Prenatal Alcohol Exposure; Response Inhibition

PMID:
28075019
PMCID:
PMC5272840
DOI:
10.1111/acer.13307
[Indexed for MEDLINE]
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16.
17.
Alcohol Clin Exp Res. 2017 Jan;41(1):96-106. doi: 10.1111/acer.13263. Epub 2016 Dec 7.

An ERP Study of Response Inhibition in the Auditory Domain in Children with Fetal Alcohol Spectrum Disorders.

Author information

1
MRC/UCT Medical Imaging Research Unit, Department of Human Biology, University of Cape Town, Cape Town, South Africa.
2
Department of Psychiatry and Behavioural Neurosciences, Wayne State University School of Medicine, Detroit, Michigan.
3
Departments of Human Biology and Psychiatry and Mental Health, University of Cape Town, Cape Town, South Africa.
4
Department of Psychiatry and Mental Health, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.

Abstract

BACKGROUND:

Previous event-related potential (ERP) studies of response inhibition in children with fetal alcohol spectrum disorder (FASD) have used a visual Go/NoGo task to study the impact of prenatal alcohol exposure on response inhibition. No studies exist using auditory versions of the task; thus, it is unclear how the deficits observed in visual tasks translate into the auditory domain.

METHODS:

This study examined ERPs using an auditory Go/NoGo paradigm in a sample of 35 school-age children-18 with heavy prenatal alcohol exposure and 17 normally developing controls.

RESULTS:

Alcohol-exposed children performed as well as controls in terms of inhibiting their responses; however, their reaction times were significantly slower under the Go condition. As in the ERP visual Go/NoGo task previously administered to these children, group differences were seen in early perceptual processing, specifically related to stimulus discrimination, with a decrease in P2 amplitude in the alcohol-exposed group. The control group exhibited greater N2 amplitude in the NoGo compared to the Go condition while the alcohol-exposed group did not, suggesting a group difference in the neural substrates underlying conflict monitoring. The alcohol-exposed group demonstrated longer latency P3 with reduced amplitude, suggesting poorer allocation of attention. The alcohol-exposed group also exhibited a late positive component (LPC) similar to the one observed in the previous visual ERP study. This LPC may indicate compensatory neurophysiological function related to resetting of attentional control networks in preparation for the next trial. None of the ERP outcomes in this study were related to potential confounders which included cognitive and socioeconomic measures as well as ADHD diagnosis.

CONCLUSIONS:

The observed ERP group differences point to elements of perceptual and attentional processing likely to be involved in the performance deficits often observed in children with FASD. We also observed changes in ERPs related to conflict monitoring/response inhibition, highlighting fetal alcohol-related effects on how the brain responds when there is need to identify and respond to environmental cues by switching away from a prepotent motor response to an inhibited state.

KEYWORDS:

Event-Related Potentials; Fetal Alcohol Spectrum Disorders; Fetal Alcohol Syndrome; Go/NoGo; Prenatal Alcohol Exposure; Response Inhibition

PMID:
27925227
PMCID:
PMC5205560
DOI:
10.1111/acer.13263
[Indexed for MEDLINE]
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18.
Environ Int. 2016 Oct;95:144-51. doi: 10.1016/j.envint.2016.08.010. Epub 2016 Aug 27.

Altered fine motor function at school age in Inuit children exposed to PCBs, methylmercury, and lead.

Author information

1
Département de psychologie, Université de Montréal, Montréal, Québec, Canada; Centre de recherche du CHU de Québec, Québec, Québec, Canada.
2
Centre de recherche du CHU de Québec, Québec, Québec, Canada; Université Laval, Québec, Québec, Canada.
3
Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, MI, USA.
4
Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, MI, USA. Electronic address: joseph.jacobson@wayne.edu.

Abstract

BACKGROUND:

Motor deficits have frequently been reported in methylmercury (MeHg) poisoning in adults. However, whether exposure to neurotoxic contaminants from environmental sources early in life is associated with neuromotor impairments has received relatively little attention. This study examines the relation of developmental exposure to MeHg, polychlorinated biphenyls (PCBs), and lead to motor function in school-age Inuit children exposed through their traditional diet.

METHODS:

In a prospective study in Nunavik, children (mean age=11.3years) were assessed on a battery of fine motor tasks, namely the Stanford-Binet Copying subtest (N=262), the Santa Ana Form Board, and the Finger Tapping Test (N=215). The relation of mercury (Hg; as an index of MeHg exposure), PCB congener 153 (PCB153), and lead concentrations in cord and current blood samples to task performance was examined using linear regression analyses.

RESULTS:

After adjustment for potential confounders and control for the other contaminants, higher current PCB concentrations were associated with poorer Santa Ana Form Board and Finger Tapping performance. Results were virtually identical when PCB153 was replaced by other PCB congeners. Higher current Hg levels were independently associated with poorer Finger Tapping performance.

CONCLUSIONS:

This is the first prospective longitudinal study in children to provide evidence of neuromotor impairments associated with postnatal exposure to seafood contaminants from environmental sources. Fine motor speed appears particularly sensitive to the effects of postnatal PCB exposure, which is unusually high in this population. Results with postnatal MeHg are concordant with previous cross-sectional studies with children and adults.

KEYWORDS:

Contaminants; Lead; Mercury; Neurotoxicity; Polychlorinated biphenyls; Postnatal

PMID:
27575364
PMCID:
PMC5035542
DOI:
10.1016/j.envint.2016.08.010
[Indexed for MEDLINE]
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19.
Pediatrics. 2016 Aug;138(2). pii: e20160775. doi: 10.1542/peds.2016-0775. Epub 2016 Jul 8.

Fetal Alcohol Growth Restriction and Cognitive Impairment.

Author information

1
Division of Pediatric Emergency Medicine, Morgan Stanley Children's Hospital of New York, Columbia University Medical Center, New York, New York; rcolincarter@gmail.com.
2
Departments of Psychiatry and Mental Health, and Human Biology, University of Cape Town Faculty of Health Sciences, Cape Town, South Africa; and Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, Michigan.
3
Departments of Psychiatry and Mental Health, and.
4
Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, Michigan.
5
Human Biology, University of Cape Town Faculty of Health Sciences, Cape Town, South Africa; and.

Abstract

BACKGROUND:

Although both fetal and long-term growth restriction are well documented in fetal alcohol spectrum disorders, effects on pattern of growth trajectory have not been characterized. Furthermore, the degree to which growth trajectories are related to fetal alcohol-related neurocognitive deficits is unknown.

METHODS:

Ninety-three heavy drinking pregnant women and 64 controls were recruited at initiation of prenatal care in Cape Town, South Africa. Small for gestational age (SGA) was defined as birth weight <10th percentile. Length/height, weight, and head circumference were measured at 6.5 and 12 months and 5, 9, and 13 years. Four growth trajectories were identified: SGA with long-term postnatal growth restriction (length/height-for-age <10th percentile through 13 years); SGA with catch-up growth; no SGA or postnatal growth restriction; and late-onset postnatal stunting. IQ was assessed at 5 and 10 years, and learning, memory, and executive function at 10 years.

RESULTS:

Children born SGA with postnatal growth restriction were most heavily exposed. Exposure was intermediate for those born SGA with catch-up growth and lowest for those without prenatal or postnatal growth restriction. Effects on neurocognition were strongest in children with both prenatal and long-term growth restriction, more moderate in those with fetal growth restriction and postnatal catch-up, and weakest in those without growth restriction.

CONCLUSIONS:

These findings validate the use of growth restriction in the diagnosis of fetal alcohol spectrum disorders and identify growth trajectory as a biomarker of which heavily exposed children are at greatest risk for cognitive developmental deficits.

PMID:
27401098
PMCID:
PMC4960732
DOI:
10.1542/peds.2016-0775
[Indexed for MEDLINE]
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20.
Int J Psychophysiol. 2016 Aug;106:106-14. doi: 10.1016/j.ijpsycho.2016.06.009. Epub 2016 Jun 18.

An ERP study of recognition memory for concrete and abstract pictures in school-aged children.

Author information

1
Département de psychologie, Université de Montréal, Montréal, QC, Canada.
2
Université Laval, Québec, QC, Canada; Centre de recherche du CHU de Québec, Québec, QC, Canada.
3
Boston Children's Hospital, Boston, MA, USA.
4
Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, MI, USA.
5
Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, MI, USA. Electronic address: joseph.jacobson@wayne.edu.

Abstract

Recognition memory for concrete, nameable pictures is typically faster and more accurate than for abstract pictures. A dual-coding account for these findings suggests that concrete pictures are processed into verbal and image codes, whereas abstract pictures are encoded in image codes only. Recognition memory relies on two successive and distinct processes, namely familiarity and recollection. Whether these two processes are similarly or differently affected by stimulus concreteness remains unknown. This study examined the effect of picture concreteness on visual recognition memory processes using event-related potentials (ERPs). In a sample of children involved in a longitudinal study, participants (N=96; mean age=11.3years) were assessed on a continuous visual recognition memory task in which half the pictures were easily nameable, everyday concrete objects, and the other half were three-dimensional abstract, sculpture-like objects. Behavioral performance and ERP correlates of familiarity and recollection (respectively, the FN400 and P600 repetition effects) were measured. Behavioral results indicated faster and more accurate identification of concrete pictures as "new" or "old" (i.e., previously displayed) compared to abstract pictures. ERPs were characterized by a larger repetition effect, on the P600 amplitude, for concrete than for abstract images, suggesting a graded recollection process dependent on the type of material to be recollected. Topographic differences were observed within the FN400 latency interval, especially over anterior-inferior electrodes, with the repetition effect more pronounced and localized over the left hemisphere for concrete stimuli, potentially reflecting different neural processes underlying early processing of verbal/semantic and visual material in memory.

KEYWORDS:

Abstract; Children; Concrete; Event-related potentials; Familiarity; Recognition memory

PMID:
27329352
PMCID:
PMC4966662
DOI:
10.1016/j.ijpsycho.2016.06.009
[Indexed for MEDLINE]
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