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Martins-Silva T, Bauer A, Matijasevich A, Munhoz TN, Barros AJD, Santos IS, Tovo-Rodrigues L, Murray J. Early risk factors for conduct problem trajectories from childhood to adolescence: the 2004 Pelotas (BRAZIL) Birth Cohort. Eur Child Adolesc Psychiatry 2024; 33:881-895. [PMID: 37097345 PMCID: PMC10126565 DOI: 10.1007/s00787-023-02178-9] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/14/2022] [Accepted: 02/23/2023] [Indexed: 04/26/2023]
Abstract
Conduct problems are associated with an increased risk of a wide range of physical, mental, and social problems. However, there is still uncertainty about how early risk factors differentiate different developmental patterns of conduct problems and whether findings replicate across diverse social contexts. We aimed to identify developmental trajectories of conduct problems, and test early risk factors, in the 2004 Pelotas Birth Cohort in Brazil. Conduct problems were measured at ages 4, 6, 11, and 15 years from caregiver reports on the Child Behaviour Checklist (CBCL) and Strengths and Difficulties Questionnaire (SDQ). Conduct problem trajectories were estimated using group-based semi-parametric modeling (n = 3938). Multinomial logistic regression was used to examine associations between early risk factors and conduct problem trajectories. We identified four trajectories: three with elevated conduct problems, including early-onset persistent (n = 150; 3.8%), adolescence-onset (n = 286; 17.3%), and childhood-limited (n = 697; 17.7%), and one with low conduct problems (n = 2805; 71.2%). The three elevated conduct problem trajectories were associated with a wide range of sociodemographic risk factors, prenatal smoking, maternal mental health, harsh parenting, childhood trauma, and child neurodevelopmental risk factors. Early-onset persistent conduct problems were particularly associated with trauma, living without a father figure, and attention difficulties. The four trajectories of conduct problems from ages 4 to 15 years in this Brazilian cohort have similar longitudinal patterns to those identified in high-income countries. The results confirm previous longitudinal research and developmental taxonomic theories on the etiology of conduct problems in a Brazilian sample.
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Affiliation(s)
- Thais Martins-Silva
- Human Development and Violence Research Centre (DOVE), Federal University of Pelotas, Pelotas, Brazil
- Post-Graduate Program in Epidemiology, Federal University of Pelotas, Pelotas, Brazil
| | - Andreas Bauer
- Human Development and Violence Research Centre (DOVE), Federal University of Pelotas, Pelotas, Brazil
- Post-Graduate Program in Epidemiology, Federal University of Pelotas, Pelotas, Brazil
| | - Alicia Matijasevich
- Post-Graduate Program in Epidemiology, Federal University of Pelotas, Pelotas, Brazil
- Departamento de Medicina Preventiva, Faculdade de Medicina FMUSP, Universidade de São Paulo, São Paulo, Brazil
| | - Tiago N Munhoz
- Post-Graduate Program in Epidemiology, Federal University of Pelotas, Pelotas, Brazil
| | - Aluísio J D Barros
- Post-Graduate Program in Epidemiology, Federal University of Pelotas, Pelotas, Brazil
- International Center for Equity in Health, Federal University of Pelotas, Pelotas, Brazil
| | - Iná S Santos
- Post-Graduate Program in Epidemiology, Federal University of Pelotas, Pelotas, Brazil
- Postgraduate Program in Pediatrics and Child Health, School of Medicine, Pontifical Catholic University of Rio Grande Do Sul, Porto Alegre, Brazil
| | - Luciana Tovo-Rodrigues
- Human Development and Violence Research Centre (DOVE), Federal University of Pelotas, Pelotas, Brazil
- Post-Graduate Program in Epidemiology, Federal University of Pelotas, Pelotas, Brazil
| | - Joseph Murray
- Human Development and Violence Research Centre (DOVE), Federal University of Pelotas, Pelotas, Brazil.
- Post-Graduate Program in Epidemiology, Federal University of Pelotas, Pelotas, Brazil.
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Schmidt RA, Wey TW, Harding KD, Fortier I, Atkinson S, Tough S, Letourneau N, Knight JA, Fraser WD, Bocking A. A harmonized analysis of five Canadian pregnancy cohort studies: exploring the characteristics and pregnancy outcomes associated with prenatal alcohol exposure. BMC Pregnancy Childbirth 2023; 23:128. [PMID: 36855094 PMCID: PMC9972615 DOI: 10.1186/s12884-023-05447-2] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/03/2022] [Accepted: 02/14/2023] [Indexed: 03/02/2023] Open
Abstract
BACKGROUND As a teratogen, alcohol exposure during pregnancy can impact fetal development and result in adverse birth outcomes. Despite the clinical and social importance of prenatal alcohol use, limited routinely collected information or epidemiological data exists in Canada. The aim of this study was to pool data from multiple Canadian cohort studies to identify sociodemographic characteristics before and during pregnancy that were associated with alcohol consumption during pregnancy and to assess the impact of different patterns of alcohol use on birth outcomes. METHODS We harmonized information collected (e.g., pregnant women's alcohol intake, infants' gestational age and birth weight) from five Canadian pregnancy cohort studies to consolidate a large sample (n = 11,448). Risk factors for any alcohol use during pregnancy, including any alcohol use prior to pregnancy recognition, and binge drinking, were estimated using binomial regressions including fixed effects of pregnancy cohort membership and multiple maternal risk factors. Impacts of alcohol use during pregnancy on birth outcomes (preterm birth and low birth weight for gestational) were also estimated using binomial regression models. RESULTS In analyses adjusting for multiple risk factors, women's alcohol use during pregnancy, both any use and any binge drinking, was associated with drinking prior to pregnancy, smoking during pregnancy, and white ethnicity. Higher income level was associated with any drinking during pregnancy. Neither drinking during pregnancy nor binge drinking during pregnancy was significantly associated with preterm delivery or low birth weight for gestational age in our sample. CONCLUSIONS Pooling data across pregnancy cohort studies allowed us to create a large sample of Canadian women and investigate the risk factors for alcohol consumption during pregnancy. We suggest that future pregnancy and birth cohorts should always include questions related to the frequency and amount of alcohol consumed before and during pregnancy that are prospectively harmonized to support data reusability and collaborative research.
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Affiliation(s)
- Rose A. Schmidt
- grid.17063.330000 0001 2157 2938Dalla Lana School of Public Health, University of Toronto, Toronto, ON Canada ,grid.155956.b0000 0000 8793 5925Institute for Mental Health Policy Research, Centre for Addiction and Mental Health (CAMH), Toronto, ON Canada
| | - Tina W. Wey
- grid.63984.300000 0000 9064 4811Research Institute of the McGill University Health Centre, Montreal, QC Canada
| | - Kelly D. Harding
- Canada Fetal Alcohol Spectrum Disorder Research Network, Vancouver, BC Canada ,grid.258970.10000 0004 0469 5874Department of Psychology, Laurentian University, Sudbury, ON Canada
| | - Isabel Fortier
- grid.63984.300000 0000 9064 4811Research Institute of the McGill University Health Centre, Montreal, QC Canada
| | - Stephanie Atkinson
- grid.25073.330000 0004 1936 8227Department of Pediatrics, McMaster University, Hamilton, ON Canada
| | - Suzanne Tough
- grid.22072.350000 0004 1936 7697Owerko Centre at the Alberta Children’s Hospital Research Institute, University of Calgary, Calgary, AB Canada ,grid.22072.350000 0004 1936 7697Cumming School of Medecine, University of Calgary, Calgary, AB Canada
| | - Nicole Letourneau
- grid.22072.350000 0004 1936 7697Owerko Centre at the Alberta Children’s Hospital Research Institute, University of Calgary, Calgary, AB Canada
| | - Julia A. Knight
- grid.17063.330000 0001 2157 2938Dalla Lana School of Public Health, University of Toronto, Toronto, ON Canada ,grid.250674.20000 0004 0626 6184Lunenfeld-Tanenbaum Research Institute, Sinai Health, Toronto, ON Canada
| | - William D. Fraser
- grid.86715.3d0000 0000 9064 6198Department of Obstetrics and Gynecology, University of Sherbrooke, Sherbrooke, QC Canada
| | - Alan Bocking
- grid.17063.330000 0001 2157 2938Department of Obstetrics and Gynecology, University of Toronto, Toronto, ON Canada
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Genetic Influences on Fetal Alcohol Spectrum Disorder. Genes (Basel) 2023; 14:genes14010195. [PMID: 36672936 PMCID: PMC9859092 DOI: 10.3390/genes14010195] [Citation(s) in RCA: 12] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/09/2022] [Revised: 01/06/2023] [Accepted: 01/10/2023] [Indexed: 01/14/2023] Open
Abstract
Fetal alcohol spectrum disorder (FASD) encompasses the range of deleterious outcomes of prenatal alcohol exposure (PAE) in the affected offspring, including developmental delay, intellectual disability, attention deficits, and conduct disorders. Several factors contribute to the risk for and severity of FASD, including the timing, dose, and duration of PAE and maternal factors such as age and nutrition. Although poorly understood, genetic factors also contribute to the expression of FASD, with studies in both humans and animal models revealing genetic influences on susceptibility. In this article, we review the literature related to the genetics of FASD in humans, including twin studies, candidate gene studies in different populations, and genetic testing identifying copy number variants. Overall, these studies suggest different genetic factors, both in the mother and in the offspring, influence the phenotypic outcomes of PAE. While further work is needed, understanding how genetic factors influence FASD will provide insight into the mechanisms contributing to alcohol teratogenicity and FASD risk and ultimately may lead to means for early detection and intervention.
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Haan E, Westmoreland KE, Schellhas L, Sallis HM, Taylor G, Zuccolo L, Munafò MR. Prenatal smoking, alcohol and caffeine exposure and offspring externalizing disorders: a systematic review and meta-analysis. Addiction 2022; 117:2602-2613. [PMID: 35385887 DOI: 10.1111/add.15858] [Citation(s) in RCA: 8] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/03/2021] [Accepted: 02/09/2022] [Indexed: 12/14/2022]
Abstract
BACKGROUND AND AIMS Several studies have indicated an association between maternal prenatal substance use and offspring externalizing disorders; however, it is uncertain whether this relationship is causal. We conducted a systematic review to determine: (1) if the literature supports a causal role of maternal prenatal substance use on offspring externalizing disorders diagnosis and (2) whether these associations differ across externalizing disorders. METHODS We searched Web of Science, Embase, PsycINFO and Medline databases. Risk of bias assessment was conducted using the Newcastle-Ottawa Scale (NOS), and where possible meta-analysis was conducted for studies classed as low risk of bias. We included studies of any design that examined prenatal smoking, alcohol or caffeine use. Studies in non-English language, fetal alcohol syndrome and comorbid autism spectrum disorders were excluded. Participants in the included studies were mothers and their offspring. Measurements included prenatal smoking, alcohol or caffeine use as an exposure, and diagnosis of attention-deficit hyperactivity disorder (ADHD), conduct disorder (CD) and oppositional defiant disorder (ODD) in offspring as an outcome. RESULTS We included 63 studies, 46 of which investigated smoking and ADHD. All studies were narratively synthesized, and seven studies on smoking and ADHD were meta-analysed. The largest meta-analysis based on genetically sensitive design included 1 011 546 participants and did not find evidence for an association [odds ratio (OR)1-9 cigarettes = 0.90, 95% confidence interval (CI) = 0.83-1.11; OR > 10 cigarettes = 1.04, 95% CI = 0.79-1.36). Studies on alcohol exposure in all the outcomes reported inconsistent findings and no strong conclusions on causality can be made. Studies on caffeine exposure were mainly limited to ADHD and these studies do not support a causal effect. CONCLUSIONS There appears to be no clear evidence to support a causal relationship between maternal prenatal smoking and offspring attention-deficit hyperactivity disorder. Findings with alcohol and caffeine exposures and conduct disorder and oppositional-defiant disorder need more research, using more genetically sensitive designs.
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Affiliation(s)
- Elis Haan
- School of Psychological Science, University of Bristol, Bristol, UK
- MRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK
| | | | - Laura Schellhas
- School of Psychological Science, University of Bristol, Bristol, UK
- MRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK
| | - Hannah M Sallis
- School of Psychological Science, University of Bristol, Bristol, UK
- MRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK
| | - Gemma Taylor
- Addiction and Mental Health Group (AIM), Department of Psychology, University of Bath, Bath, UK
| | - Luisa Zuccolo
- MRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK
- Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK
| | - Marcus R Munafò
- School of Psychological Science, University of Bristol, Bristol, UK
- MRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK
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Okulicz-Kozaryn K. Is Public Health Response to the Phenomenon of Alcohol Use during Pregnancy Adequate to the Polish Women’s Needs? INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH 2022; 19:ijerph19084552. [PMID: 35457420 PMCID: PMC9025347 DOI: 10.3390/ijerph19084552] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Subscribe] [Scholar Register] [Received: 02/17/2022] [Revised: 04/01/2022] [Accepted: 04/06/2022] [Indexed: 11/16/2022]
Abstract
Due to the risks it poses to a child’s health, drinking alcohol during pregnancy is a serious problem that the public health sector is struggling to deal with. The reasons why women who do not have alcohol problems do not give up drinking alcohol completely during pregnancy are still poorly understood. And the knowledge available about them does not translate into communication strategies in Poland. The analysis of standards and examples of good practice allows to formulate proposals for improving the quality and effectiveness of social campaigns addressed to the general population and women of childbearing age in order to reduce the risk associated with the prenatal exposure to alcohol.
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Affiliation(s)
- Katarzyna Okulicz-Kozaryn
- Institute of Mother and Child, 01-211 Warsaw, Poland;
- National Centre for Prevention of Addictions, 02-776 Warsaw, Poland
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Brunst KJ, Hsu HHL, Zhang L, Zhang X, Carroll KN, Just A, Coull BA, Kloog I, Wright RO, Baccarelli AA, Wright RJ. Prenatal particulate matter exposure and mitochondrial mutational load at the maternal-fetal interface: Effect modification by genetic ancestry. Mitochondrion 2022; 62:102-110. [PMID: 34785263 PMCID: PMC9175302 DOI: 10.1016/j.mito.2021.11.003] [Citation(s) in RCA: 8] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/06/2021] [Revised: 10/26/2021] [Accepted: 11/08/2021] [Indexed: 12/30/2022]
Abstract
Prenatal ambient particulate matter (PM2.5) exposure impacts infant development and alters placental mitochondrial DNA abundance. We investigated whether the timing of PM2.5 exposure predicts placental mitochondrial mutational load using NextGen sequencing in 283 multi-ethnic mother-infant dyads. We observed increased PM2.5exposure, particularly during mid- to late-pregnancy and among genes coding for NADH dehydrogenase and subunits of ATP synthase, was associated with a greater amount of nonsynonymous mutations. The strongest associations were observed for participants of African ancestry. Further work is needed to tease out the role of mitochondrial genetics and its impact on offspring development and emerging disease disparities.
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Affiliation(s)
- Kelly J Brunst
- Department of Environmental and Public Health Sciences, University of Cincinnati College of Medicine, 160 Panzeca Way, Cincinnati, OH 45267, USA.
| | - Hsiao-Hsien Leon Hsu
- Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, 17 East 102(nd) St. New York, NY 10029, USA.
| | - Li Zhang
- Department of Environmental and Public Health Sciences, University of Cincinnati College of Medicine, 160 Panzeca Way, Cincinnati, OH 45267, USA.
| | - Xiang Zhang
- Department of Environmental and Public Health Sciences, University of Cincinnati College of Medicine, 160 Panzeca Way, Cincinnati, OH 45267, USA.
| | - Kecia N Carroll
- Kravis Children's Hospital, Department of Pediatrics, Icahn School of Medicine at Mount Sinai, 17 East 102(nd) St. New York, NY 10029, USA; Institute for Exposomic Research, Icahn School of Medicine at Mount Sinai, 17 East 102(nd) St., New York, NY 10029, USA.
| | - Allan Just
- Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, 17 East 102(nd) St. New York, NY 10029, USA
| | - Brent A Coull
- Department of Biostatistics, Harvard T.H. Chan School of Public Health, 655 Huntington Ave., Boston, MA 02115, USA.
| | - Itai Kloog
- Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, 17 East 102(nd) St. New York, NY 10029, USA; Department of Geography and Environmental Development, Ben-Gurion University of the Negev, P.O.B 653, Beer Sheva, Israel.
| | - Robert O Wright
- Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, 17 East 102(nd) St. New York, NY 10029, USA; Institute for Exposomic Research, Icahn School of Medicine at Mount Sinai, 17 East 102(nd) St., New York, NY 10029, USA.
| | - Andrea A Baccarelli
- Department of Environmental Health Sciences, Mailman School of Public Health, Columbia University Medical Center, 722 W 168(th) St. New York, NY 10032, USA.
| | - Rosalind J Wright
- Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, 17 East 102(nd) St. New York, NY 10029, USA; Institute for Exposomic Research, Icahn School of Medicine at Mount Sinai, 17 East 102(nd) St., New York, NY 10029, USA.
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Haan E, Sallis HM, Ystrom E, Njølstad PR, Andreassen OA, Reichborn-Kjennerud T, Munafò MR, Havdahl A, Zuccolo L. Maternal and offspring genetic risk score analyses of fetal alcohol exposure and attention-deficit hyperactivity disorder risk in offspring. Alcohol Clin Exp Res 2021; 45:2090-2102. [PMID: 34486127 PMCID: PMC9293034 DOI: 10.1111/acer.14692] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/12/2021] [Revised: 08/04/2021] [Accepted: 08/05/2021] [Indexed: 12/02/2022]
Abstract
Background Studies investigating the effects of prenatal alcohol exposure on childhood attention‐deficit hyperactivity disorder (ADHD) symptoms using conventional observational designs have reported inconsistent findings, which may be affected by unmeasured confounding and maternal and fetal ability to metabolize alcohol. We used genetic variants from the alcohol metabolizing genes, alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), as proxies for fetal alcohol exposure to investigate their association with risk of offspring ADHD symptoms around age 7–8 years. Methods We used data from 3 longitudinal pregnancy cohorts: Avon Longitudinal Study of Parents and Children (ALSPAC), Generation R study (GenR), and the Norwegian Mother, Father and Child Cohort study (MoBa). Genetic risk scores (GRS) for alcohol use and metabolism using 36 single nucleotide polymorphisms (SNPs) from ADH and ALDH genes were calculated for mothers (NALSPAC = 8196; NMOBA = 13,614), fathers (NMOBA = 13,935), and offspring (NALSPAC=8,237; NMOBA=14,112; NGENR=2,661). Associations between maternal GRS and offspring risk of ADHD symptoms were tested in the full sample to avoid collider bias. Offspring GRS analyses were stratified by maternal drinking status. Results The pooled estimate in maternal GRS analyses adjusted for offspring GRS in ALSPAC and MoBa was OR = 0.99, 95%CI 0.97–1.02. The pooled estimate in offspring GRS analyses stratified by maternal drinking status across all the cohorts was as follows: ORDRINKING = 0.98, 95% CI 0.94–1.02; ORNO DRINKING = 0.99, 95% CI 0.97–1.02. These findings remained similar after accounting for maternal genotype data in ALSPAC and maternal and paternal genotype data in MoBa. Conclusions We did not find evidence for a causal effect of fetal alcohol exposure on risk of ADHD symptoms in offspring. The results may be affected by limited power to detect small effects and outcome assessment.
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Affiliation(s)
- Elis Haan
- School of Psychological Science, University of Bristol, Bristol, UK.,MRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK
| | - Hannah M Sallis
- School of Psychological Science, University of Bristol, Bristol, UK.,MRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK
| | - Eivind Ystrom
- Department of Psychology, PROMENTA Research Center, University of Oslo, Oslo, Norway.,Department of Mental Disorders, Norwegian Institute of Public Health, Oslo, Norway
| | - Pål Rasmus Njølstad
- Department of Clinical Science, Center for Diabetes Research, University of Bergen, Bergen, Norway.,Department of Pediatrics and Adolescents, Haukeland University Hospital, Bergen, Norway
| | - Ole A Andreassen
- NORMENT Centre, Institute of Clinical Medicine, University of Oslo, Oslo, Norway.,Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway
| | - Ted Reichborn-Kjennerud
- Department of Mental Disorders, Norwegian Institute of Public Health, Oslo, Norway.,Institute of Clinical Medicine, University of Oslo, Oslo, Norway
| | - Marcus R Munafò
- School of Psychological Science, University of Bristol, Bristol, UK.,MRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK
| | - Alexandra Havdahl
- Department of Psychology, PROMENTA Research Center, University of Oslo, Oslo, Norway.,Department of Mental Disorders, Norwegian Institute of Public Health, Oslo, Norway.,Nic Waals Institute, Lovisenberg Diaconal Hospital, Oslo, Norway
| | - Luisa Zuccolo
- MRC Integrative Epidemiology Unit, University of Bristol, Bristol, UK.,Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK
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Brunst KJ, Zhang L, Zhang X, Baccarelli AA, Bloomquist T, Wright RJ. Associations Between Maternal Lifetime Stress and Placental Mitochondrial DNA Mutations in an Urban Multiethnic Cohort. Biol Psychiatry 2021; 89:570-578. [PMID: 33229036 PMCID: PMC7889635 DOI: 10.1016/j.biopsych.2020.09.013] [Citation(s) in RCA: 10] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/10/2019] [Revised: 09/08/2020] [Accepted: 09/10/2020] [Indexed: 02/06/2023]
Abstract
BACKGROUND Disrupted placental functioning due to stress can have lifelong implications. Cumulative stress and trauma are likely to have lasting impacts on maternal physiological functioning and offspring development, resulting in increased risk for later-life complex disorders for which racial disparities exist. METHODS This study examined the association between maternal lifetime stress and placental mitochondrial DNA mutational load in an urban multiethnic cohort. Maternal lifetime exposure to stressful events was assessed using the validated Life Stressor Checklist-Revised. Whole mitochondrial DNA sequencing was performed and mutations were determined for 365 placenta samples with complete exposure and covariate data. Multivariable regression was used to model maternal lifetime stress in relation to placental mitochondrial DNA mutational load. Racial/ethnic differences were examined by cross-product terms and contrast statements. Gene-wise analyses were conducted. RESULTS We identified 13,189 heteroplasmies (Phred score > 10,000, minor allele frequency < 0.5, number of mutant reads > 1). Women experiencing increased psychosocial stress over their lifetime exhibited a higher number of total placental mitochondrial mutations (β = .23, 95% confidence interval = .03 to .42) and heteroplasmic mutations (β = .18, 95% confidence interval = .05 to .31) but not homoplasmic mutations (β = -.008, 95% confidence interval = -.03 to .01); the strongest associations were observed among Black women and genes coding for NADH dehydrogenase and cytochrome c oxidase subunits. CONCLUSIONS Cumulative maternal lifetime stress is associated with a greater mitochondrial mutational load, particularly among Black women. The impact of racial/ethnic differences in mutational load on placental function directly affecting offspring development and/or leading to chronic disease disparities warrants further investigation.
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Affiliation(s)
- Kelly J. Brunst
- University of Cincinnati, College of Medicine, Department of Environmental and Public Health Sciences, 160 Panzeca Way, Cincinnati, OH 45267
| | - Li Zhang
- University of Cincinnati, College of Medicine, Department of Environmental and Public Health Sciences, 160 Panzeca Way, Cincinnati, OH 45267
| | - Xiang Zhang
- University of Cincinnati, College of Medicine, Department of Environmental and Public Health Sciences, 160 Panzeca Way, Cincinnati, OH 45267
| | - Andrea A. Baccarelli
- Columbia University, Mailman School of Public Health, Department of Environmental Health Sciences, 722 West 168 Street, New York, NY 10032
| | - Tessa Bloomquist
- Columbia University, Mailman School of Public Health, Department of Environmental Health Sciences, 722 West 168 Street, New York, NY 10032
| | - Rosalind J. Wright
- Icahn School of Medicine at Mount Sinai, Department of Pediatrics and Department of Environmental Medicine & Public Health, 1 Gustave L. Levy Place, New York, NY 10029
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Mamluk L, Jones T, Ijaz S, Edwards HB, Savović J, Leach V, Moore THM, von Hinke S, Lewis SJ, Donovan JL, Lawlor DA, Davey Smith G, Fraser A, Zuccolo L. Evidence of detrimental effects of prenatal alcohol exposure on offspring birthweight and neurodevelopment from a systematic review of quasi-experimental studies. Int J Epidemiol 2021; 49:1972-1995. [PMID: 31993631 PMCID: PMC7825937 DOI: 10.1093/ije/dyz272] [Citation(s) in RCA: 24] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Revised: 11/25/2019] [Accepted: 01/08/2020] [Indexed: 12/19/2022] Open
Abstract
BACKGROUND Systematic reviews of prenatal alcohol exposure effects generally only include conventional observational studies. However, estimates from such studies are prone to confounding and other biases. OBJECTIVES To systematically review the evidence on the effects of prenatal alcohol exposure from randomized controlled trials (RCTs) and observational designs using alternative analytical approaches to improve causal inference. SEARCH STRATEGY Medline, Embase, Web of Science, PsychINFO from inception to 21 June 2018. Manual searches of reference lists of retrieved papers. SELECTION CRITERIA RCTs of interventions to stop/reduce drinking in pregnancy and observational studies using alternative analytical methods (quasi-experimental studies e.g. Mendelian randomization and natural experiments, negative control comparisons) to determine the causal effects of prenatal alcohol exposure on pregnancy and longer-term offspring outcomes in human studies. DATA COLLECTION AND ANALYSIS One reviewer extracted data and another checked extracted data. Risk of bias was assessed using customized risk of bias tools. A narrative synthesis of findings was carried out and a meta-analysis for one outcome. MAIN RESULTS Twenty-three studies were included, representing five types of study design, including 1 RCT, 9 Mendelian randomization and 7 natural experiment studies, and reporting on over 30 outcomes. One study design-outcome combination included enough independent results to meta-analyse. Based on evidence from several studies, we found a likely causal detrimental role of prenatal alcohol exposure on cognitive outcomes, and weaker evidence for a role in low birthweight. CONCLUSION None of the included studies was judged to be at low risk of bias in all domains, results should therefore be interpreted with caution. SYSTEMATIC REVIEW REGISTRATION This study is registered with PROSPERO, registration number CRD42015015941.
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Affiliation(s)
- Loubaba Mamluk
- MRC Integrative Epidemiology Unit, Department of Population Health Sciences, University of Bristol, Bristol, UK
- Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK
- NIHR ARC West, University Hospitals Bristol NHS Foundation Trust, Bristol, UK
| | - Timothy Jones
- Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK
- NIHR ARC West, University Hospitals Bristol NHS Foundation Trust, Bristol, UK
| | - Sharea Ijaz
- Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK
- NIHR ARC West, University Hospitals Bristol NHS Foundation Trust, Bristol, UK
| | - Hannah B Edwards
- Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK
- NIHR ARC West, University Hospitals Bristol NHS Foundation Trust, Bristol, UK
| | - Jelena Savović
- Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK
- NIHR ARC West, University Hospitals Bristol NHS Foundation Trust, Bristol, UK
| | - Verity Leach
- Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK
- NIHR ARC West, University Hospitals Bristol NHS Foundation Trust, Bristol, UK
| | - Theresa H M Moore
- Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK
- NIHR ARC West, University Hospitals Bristol NHS Foundation Trust, Bristol, UK
| | - Stephanie von Hinke
- Department of Economics, School of Economics, Finance and Management, University of Bristol, Bristol, UK
| | - Sarah J Lewis
- Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK
| | - Jenny L Donovan
- Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK
- NIHR ARC West, University Hospitals Bristol NHS Foundation Trust, Bristol, UK
| | - Deborah A Lawlor
- MRC Integrative Epidemiology Unit, Department of Population Health Sciences, University of Bristol, Bristol, UK
- Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK
- NIHR ARC West, University Hospitals Bristol NHS Foundation Trust, Bristol, UK
- NIHR Bristol Biomedical Research Centre, University Hospitals Bristol NHS Foundation Trust, University of Bristol, Bristol, UK
| | - George Davey Smith
- MRC Integrative Epidemiology Unit, Department of Population Health Sciences, University of Bristol, Bristol, UK
- Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK
- NIHR Bristol Biomedical Research Centre, University Hospitals Bristol NHS Foundation Trust, University of Bristol, Bristol, UK
| | - Abigail Fraser
- MRC Integrative Epidemiology Unit, Department of Population Health Sciences, University of Bristol, Bristol, UK
- Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK
- NIHR Bristol Biomedical Research Centre, University Hospitals Bristol NHS Foundation Trust, University of Bristol, Bristol, UK
| | - Luisa Zuccolo
- MRC Integrative Epidemiology Unit, Department of Population Health Sciences, University of Bristol, Bristol, UK
- Department of Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK
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10
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Diemer EW, Labrecque JA, Neumann A, Tiemeier H, Swanson SA. Mendelian randomisation approaches to the study of prenatal exposures: A systematic review. Paediatr Perinat Epidemiol 2021; 35:130-142. [PMID: 32779786 PMCID: PMC7891574 DOI: 10.1111/ppe.12691] [Citation(s) in RCA: 11] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/10/2020] [Revised: 04/30/2020] [Accepted: 05/05/2020] [Indexed: 12/11/2022]
Abstract
BACKGROUND Mendelian randomisation (MR) designs apply instrumental variable techniques using genetic variants to study causal effects. MR is increasingly used to evaluate the role of maternal exposures during pregnancy on offspring health. OBJECTIVES We review the application of MR to prenatal exposures and describe reporting of methodologic challenges in this area. DATA SOURCES We searched PubMed, EMBASE, Medline Ovid, Cochrane Central, Web of Science, and Google Scholar. STUDY SELECTION AND DATA EXTRACTION Eligible studies met the following criteria: (a) a maternal pregnancy exposure; (b) an outcome assessed in offspring of the pregnancy; and (c) a genetic variant or score proposed as an instrument or proxy for an exposure. SYNTHESIS We quantified the frequency of reporting of MR conditions stated, techniques used to examine assumption plausibility, and reported limitations. RESULTS Forty-three eligible studies were identified. When discussing challenges or limitations, the most common issues described were known potential biases in the broader MR literature, including population stratification (n = 29), weak instrument bias (n = 18), and certain types of pleiotropy (n = 30). Of 22 studies presenting point estimates for the effect of exposure, four defined their causal estimand. Twenty-four studies discussed issues unique to prenatal MR, including selection on pregnancy (n = 1) and pleiotropy via postnatal exposure (n = 10) or offspring genotype (n = 20). CONCLUSIONS Prenatal MR studies frequently discuss issues that affect all MR studies, but rarely discuss problems specific to the prenatal context, including selection on pregnancy and effects of postnatal exposure. Future prenatal MR studies should report and attempt to falsify their assumptions, with particular attention to issues specific to prenatal MR. Further research is needed to evaluate the impacts of biases unique to prenatal MR in practice.
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Affiliation(s)
- Elizabeth W. Diemer
- Department of Child and Adolescent PsychiatryErasmus MCRotterdamThe Netherlands
| | | | - Alexander Neumann
- Department of Child and Adolescent PsychiatryErasmus MCRotterdamThe Netherlands,Lady Davis Institute for Medical ResearchJewish General HospitalMontrealQCCanada
| | - Henning Tiemeier
- Department of Child and Adolescent PsychiatryErasmus MCRotterdamThe Netherlands,Department of Social and Behavioral ScienceHarvard T.H. Chan School of Public HealthBostonMAUSA
| | - Sonja A. Swanson
- Department of EpidemiologyErasmus MCRotterdamThe Netherlands,Department of EpidemiologyHarvard T.H. Chan School of Public HealthBostonMAUSA
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11
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Madarnas C, Villalba NM, Soriano D, Brusco A. Anxious Behavior of Adult CD1 Mice Perinatally Exposed to Low Concentrations of Ethanol Correlates With Morphological Changes in Cingulate Cortex and Amygdala. Front Behav Neurosci 2020; 14:92. [PMID: 32636737 PMCID: PMC7319189 DOI: 10.3389/fnbeh.2020.00092] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/15/2019] [Accepted: 05/14/2020] [Indexed: 01/12/2023] Open
Abstract
Perinatal ethanol (EtOH) exposure is associated with high incidence of behavioral disorders such as depression and anxiety. The cerebral areas related with these consequences involve the corticolimbic system, in particular the prefrontal cortex, hippocampus, amygdala, and cingulate cortex, although the latter has not been thoroughly studied yet. Different animal models of prenatal or perinatal EtOH exposure have reported morphofunctional alterations in the central nervous system, which could explain behavioral disorders along life; these results focus on youth and adolescents and are still controversial. In the light of these inconclusive results, the aim of this work was to analyze adult behavior in CD1 mice perinatally exposed to low concentrations of EtOH (PEE) during gestation and lactation, and describe the morphology of the cingulate cortex and amygdala with a view to establishing structure/function/behavior correlations. Primiparous CD1 female mice were exposed to EtOH 6% v/v for 20 days prior to mating and continued drinking EtOH 6% v/v during pregnancy and lactation. After weaning, male pups were fed food and water ad libitum until 77 days of age, when behavioral and morphological studies were performed. Mouse behavior was analyzed through light–dark box and open field tests. Parameters related to anxious behavior and locomotor activity revealed anxiogenic behavior in PEE mice. After behavioral studies, mice were perfused and neurons, axons, serotonin transporter, 5HT, CB1 receptor (CB1R) and 5HT1A receptor (5HT1AR) were studied by immunofluorescence and immunohistochemistry in brain sections containing cingulate cortex and amygdala. Cingulate cortex and amygdala cytoarchitecture were preserved in adult PEE mice, although a smaller number of neurons was detected in the amygdala. Cingulate cortex axons demonstrated disorganized radial distribution and reduced area. Serotonergic and endocannabinoid systems, both involved in anxious behavior, showed differential expression. Serotonergic afferents were lower in both brain areas of PEE animals, while 5HT1AR expression was lower in the cingulate cortex and higher in the amygdala. The expression of CB1R was lower only in the amygdala. In sum, EtOH exposure during early brain development induces morphological changes in structures of the limbic system and its neuromodulation, which persist into adulthood and may be responsible for anxious behavior.
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Affiliation(s)
- Catalina Madarnas
- Instituto de Biología Celular y Neurociencia (IBCN), Universidad de Buenos Aires, CONICET, Buenos Aires, Argentina
| | - Nerina Mariel Villalba
- Instituto de Biología Celular y Neurociencia (IBCN), Universidad de Buenos Aires, CONICET, Buenos Aires, Argentina
| | - Delia Soriano
- Instituto de Biología Celular y Neurociencia (IBCN), Universidad de Buenos Aires, CONICET, Buenos Aires, Argentina.,Facultad de Medicina, Departamento de Biología Celular, Histología, Embriología y Genética, Universidad de Buenos Aires, Buenos Aires, Argentina
| | - Alicia Brusco
- Instituto de Biología Celular y Neurociencia (IBCN), Universidad de Buenos Aires, CONICET, Buenos Aires, Argentina.,Facultad de Medicina, Departamento de Biología Celular, Histología, Embriología y Genética, Universidad de Buenos Aires, Buenos Aires, Argentina
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12
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Easey KE, Timpson NJ, Munafò MR. Association of Prenatal Alcohol Exposure and Offspring Depression: A Negative Control Analysis of Maternal and Partner Consumption. Alcohol Clin Exp Res 2020; 44:1132-1140. [PMID: 32315093 PMCID: PMC7341445 DOI: 10.1111/acer.14324] [Citation(s) in RCA: 12] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/07/2019] [Accepted: 03/04/2020] [Indexed: 11/28/2022]
Abstract
BACKGROUND Previous research has suggested that intrauterine alcohol exposure is associated with a variety of adverse outcomes in offspring. However, few studies have investigated its association with offspring internalizing disorders in late adolescence. METHODS Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC), we investigated the associations of maternal drinking in pregnancy with offspring depression at age 18 and 24 (n = 13,480). We also examined partner drinking as a negative control for intrauterine exposure for comparison. RESULTS Offspring of mothers that consumed any alcohol at 18 weeks gestation were at increased risk of having a diagnosis of depression (fully adjusted model: OR 1.17, 95% CI 1.02 to 1.34), but there was no clear evidence of association between partners' alcohol consumption at 18 weeks gestation during pregnancy and increased risk of offspring depression (fully adjusted model: OR 0.87, 95% CI 0.74 to 1.01). Postestimation tests found a positive difference between the association of maternal and partner alcohol use on offspring depression, showing a stronger association for maternal compared with partner alcohol use (OR 1.41, CI 1.07 to 1.84). CONCLUSIONS Maternal drinking in pregnancy was associated with increased risk of offspring depression at age 18. Residual confounding may explain this association, but the negative control comparison of paternal drinking provides some evidence that it may be causal, and this warrants further investigation.
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Affiliation(s)
- Kayleigh E. Easey
- UK Centre for Tobacco and Alcohol StudiesSchool of Psychological ScienceUniversity of BristolBristolUK
- MRC Integrative Epidemiology UnitUniversity of BristolBristolUK
- Bristol Medical SchoolUniversity of BristolBristolUK
| | - Nicholas J. Timpson
- MRC Integrative Epidemiology UnitUniversity of BristolBristolUK
- Bristol Medical SchoolUniversity of BristolBristolUK
| | - Marcus R. Munafò
- UK Centre for Tobacco and Alcohol StudiesSchool of Psychological ScienceUniversity of BristolBristolUK
- MRC Integrative Epidemiology UnitUniversity of BristolBristolUK
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13
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McQuire C, Daniel R, Hurt L, Kemp A, Paranjothy S. The causal web of foetal alcohol spectrum disorders: a review and causal diagram. Eur Child Adolesc Psychiatry 2020; 29:575-594. [PMID: 30648224 PMCID: PMC7250957 DOI: 10.1007/s00787-018-1264-3] [Citation(s) in RCA: 34] [Impact Index Per Article: 6.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/22/2018] [Accepted: 12/05/2018] [Indexed: 12/21/2022]
Abstract
Foetal alcohol spectrum disorders (FASDs) are a leading cause of developmental disability. Prenatal alcohol use is the sole necessary cause of FASD, but it is not always sufficient. Multiple factors influence a child's susceptibility to FASD following prenatal alcohol exposure. Much of the FASD risk factor literature has been limited to discussions of association, rather than causation. While knowledge of predictor variables is important for identifying who is most at risk of FASD and for targeting interventions, causal knowledge is important for identifying effective mechanisms for prevention and intervention programmes. We conducted a systematic search and narrative synthesis of the evidence and used this to create a causal diagram (directed acyclic graph; DAG) to describe the causal pathways to FASD. Our results show that the aetiology of FASD is multifaceted and complex. FASD risk is determined by a range of lifestyle, sociodemographic, maternal, social, gestational, and genetic factors. The causal diagram that we present in this review provides a comprehensive summary of causal risk factors for FASD and can be used as a tool to inform data collection and statistical modelling strategies to minimise bias in future studies of FASD.
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Affiliation(s)
- Cheryl McQuire
- Population Health Sciences, Bristol Medical School, University of Bristol, Canynge Hall, 39 Whatley Road, Bristol, BS8 2PS, UK.
| | - R. Daniel
- Division of Population Medicine, Cardiff University, 3rd Floor, Neuadd Meirionnydd, Heath Park, Cardiff, CF14 4YS UK
| | - L. Hurt
- Division of Population Medicine, Cardiff University, 3rd Floor, Neuadd Meirionnydd, Heath Park, Cardiff, CF14 4YS UK
| | - A. Kemp
- Division of Population Medicine, Cardiff University, 3rd Floor, Neuadd Meirionnydd, Heath Park, Cardiff, CF14 4YS UK
| | - S. Paranjothy
- Division of Population Medicine, Cardiff University, 3rd Floor, Neuadd Meirionnydd, Heath Park, Cardiff, CF14 4YS UK
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14
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Cantacorps L, Alfonso-Loeches S, Guerri C, Valverde O. Long-term epigenetic changes in offspring mice exposed to alcohol during gestation and lactation. J Psychopharmacol 2019; 33:1562-1572. [PMID: 31210079 DOI: 10.1177/0269881119856001] [Citation(s) in RCA: 12] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]
Abstract
BACKGROUND Alcohol exposure impairs brain development and leads to a range of behavioural and cognitive dysfunctions, termed as foetal alcohol spectrum disorders. Although different mechanisms have been proposed to participate in foetal alcohol spectrum disorders, the molecular insights of such effects are still uncertain. Using a mouse model of foetal alcohol spectrum disorder, we have previously shown that maternal binge-like alcohol drinking causes persistent effects on motor, cognitive and emotional-related behaviours associated with neuroimmune dysfunctions. AIMS In this study, we sought to evaluate whether the long-term behavioural alterations found in offspring with early exposure to alcohol are associated with epigenetic changes in the hippocampus and prefrontal cortex. METHODS Pregnant C57BL/6 female mice underwent a model procedure for binge alcohol drinking throughout both the gestation and lactation periods. Subsequently, adult offspring were assessed for their cognitive function in a reversal learning task and brain areas were extracted for epigenetic analyses. RESULTS The results demonstrated that early binge alcohol exposure induces long-term behavioural effects along with alterations in histone acetylation (histone H4 lysine 5 and histone H4 lysine 12) in the hippocampus and prefrontal cortex. The epigenetic effects were linked with an imbalance in histone acetyltransferase activity that was found to be increased in the prefrontal cortex of mice exposed to alcohol. CONCLUSIONS In conclusion, our results reveal that maternal binge-like alcohol consumption induces persistent epigenetic modifications, effects that might be associated with the long-term cognitive and behavioural impairments observed in foetal alcohol spectrum disorder models.
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Affiliation(s)
- Lídia Cantacorps
- Neurobiology of Behaviour Research Group (GReNeC-NeuroBio), Universitat Pompeu Fabra (UPF), Barcelona, Spain
| | - Silvia Alfonso-Loeches
- Molecular and Cellular Pathology of Alcohol, Prince Felipe Research Centre, Valencia, Spain
| | - Consuelo Guerri
- Molecular and Cellular Pathology of Alcohol, Prince Felipe Research Centre, Valencia, Spain
| | - Olga Valverde
- Neurobiology of Behaviour Research Group (GReNeC-NeuroBio), Universitat Pompeu Fabra (UPF), Barcelona, Spain.,Neuroscience Research Programme, IMIM-Hospital del Mar Research Institute, Barcelona, Spain
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15
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de Diego I, Müller-Eigner A, Peleg S. The Brain Epigenome Goes Drunk: Alcohol Consumption Alters Histone Acetylation and Transcriptome. Trends Biochem Sci 2019; 45:93-95. [PMID: 31767183 DOI: 10.1016/j.tibs.2019.11.002] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/24/2019] [Revised: 11/05/2019] [Accepted: 11/06/2019] [Indexed: 10/25/2022]
Abstract
Recent studies demonstrated that alcohol consumption can induce epigenetic changes in the brain, although the exact mechanism underlying such changes remained unclear. Now, a report by Mews et al. shows a direct link between alcohol consumption and histone acetylation changes in the brain, which are mediated by the neuronal acetyl-CoA synthase, ACSS2.
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Affiliation(s)
- Irene de Diego
- Epigenetics, Metabolism, and Longevity, Independent Research Group, Leibniz Institute for Farm Animal Biology (FBN), 18196, Dummerstorf, Germany
| | - Annika Müller-Eigner
- Epigenetics, Metabolism, and Longevity, Independent Research Group, Leibniz Institute for Farm Animal Biology (FBN), 18196, Dummerstorf, Germany
| | - Shahaf Peleg
- Epigenetics, Metabolism, and Longevity, Independent Research Group, Leibniz Institute for Farm Animal Biology (FBN), 18196, Dummerstorf, Germany; Laboratory for Metabolism and Epigenetics in Brain Aging, Institute of Neuroregeneration and Neurorehabilitation, Qingdao University, Qingdao, China.
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16
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Light drinking during pregnancy: Social advantages explain positive correlates with child and early adolescent adjustment. Addict Behav 2019; 98:106003. [PMID: 31415972 DOI: 10.1016/j.addbeh.2019.05.027] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/14/2019] [Revised: 05/05/2019] [Accepted: 05/23/2019] [Indexed: 11/20/2022]
Abstract
Maternal heavy alcohol use during pregnancy is harmful to offspring's health and adjustment. However, findings from studies on lower levels of prenatal drinking are mixed; a few even predict positive cognitive and psychosocial outcomes. Given that alcohol is a neurotoxin and teratogen, scholars question developmental benefits and point to residual confounding as a potential explanation, particularly as light drinkers are positively selected with respect to health and socioeconomic status. Using prospective, intergenerational data from the nationally-representative Millennium Cohort Study (MCS) in the United Kingdom, we studied associations between mother's drinking during pregnancy and children's cognitive and psychosocial outcomes at ages 3, 5, 7, 11, and 14 years (n = 10,454). We included early life confounders (e.g., maternal education, health, smoking) and mother's cognitive ability, and assessed robustness of relationships across outcomes and alternate drinking classifications. Results of a series of multivariable regression models found no association between light drinking and cognitive and psychosocial outcomes up to and including the age of 14, after controlling for key confounders. Light drinking during pregnancy was linked to higher socioeconomic advantages (e.g., mothers' higher education, professional/managerial occupation, home ownership, cognitive scores), which together accounted for positive associations between light drinking and children's outcomes. Mother's cognitive ability was an especially important confounder.
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17
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Perinatal maternal mental health and infant socio-emotional development: A growth curve analysis using the MPEWS cohort. Infant Behav Dev 2019; 57:101336. [PMID: 31404801 DOI: 10.1016/j.infbeh.2019.101336] [Citation(s) in RCA: 22] [Impact Index Per Article: 3.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/18/2019] [Revised: 06/21/2019] [Accepted: 06/24/2019] [Indexed: 12/17/2022]
Abstract
Pregnancy and the early post partum period are widely understood as a critical period for the infant's emotional development and the earliest influence shaping social interaction. The present study aims to understand the potential influence of both antenatal and postnatal maternal anxiety and depressive symptoms on socio-emotional outcomes in offspring aged 12 months. The study used longitudinal data from a prospective cohort study on Australian pregnant women and their children. Data were available for 282 mothers and their children. Maternal depressive and anxiety symptoms were measured in early pregnancy, trimester three of pregnancy, six and 12 months postpartum. Social and emotional development in children was measured using the Brief Infant and Toddler Social Emotional Assessment (BITSEA) at 12 months. Using growth curve analysis of 4 waves of repeated measurement to examine intercept and slope, we found that both initial maternal depression and anxiety symptom levels, and the growth of these symptoms over time, predicted more problems with children's social and emotional development. In the final model anxiety accounted for 19% of the variance in child socio-emotional problems and depression 23% of variance. The results emphasise the importance of perinatal maternal mental health as a potential risk factor for child development. This carries important implications for policy development, such as the need to build early identification and early intervention models in to the current clinical practice for perinatal care, specifically, to develop targeted screening, assessment and interventions to address maternal mental health issues for at-risk parents during pregnancy, and continuing monitoring of young children whose mothers have experienced perinatal mental health difficulties.
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18
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Collier AD, Halkina V, Min SS, Roberts MY, Campbell SD, Camidge K, Leibowitz SF. Embryonic Ethanol Exposure Affects the Early Development, Migration, and Location of Hypocretin/Orexin Neurons in Zebrafish. Alcohol Clin Exp Res 2019; 43:1702-1713. [PMID: 31206717 PMCID: PMC6677602 DOI: 10.1111/acer.14126] [Citation(s) in RCA: 20] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/07/2019] [Accepted: 06/03/2019] [Indexed: 01/15/2023]
Abstract
BACKGROUND Embryonic ethanol (EtOH) exposure is known to increase alcohol drinking later in life and have long-term effects on neurochemical systems in the brain. With zebrafish having marked advantages for elucidating neural mechanisms underlying brain disorders, we recently tested and showed in these fish, similar to rodents, that low-dose embryonic EtOH stimulates voluntary consumption of EtOH while increasing expression of hypocretin/orexin (hcrt) neurons, a neuropeptide that promotes consummatory and reward-related behaviors. The goal of the present study was to characterize how embryonic EtOH affects early development of the hcrt system and produces persistent changes at older ages that may contribute to this increase in EtOH consumption. METHODS We utilized live imaging and Imaris software to investigate how low-dose embryonic EtOH (0.5%), administered from 22 to 24 hours postfertilization, affects specific properties of hcrt neurons in hcrt:EGFP transgenic zebrafish at different ages. RESULTS Time-lapse imaging from 24 to 28 hpf showed that embryonic EtOH increased the number of hcrt neurons, reduced the speed, straightness, and displacement of their migratory paths, and altered their direction early in development. At older ages up to 6 dpf, the embryonic EtOH-induced increase in hcrt neurons was persistent, and the neurons became more widely dispersed. These effects of embryonic EtOH were found to be asymmetric, occurring predominantly on the left side of the brain, and at 6 dpf, they resulted in marked changes in the anatomical location of the hcrt neurons, with some detected outside their normal position in the anterior hypothalamus again primarily on the left side. CONCLUSIONS Our findings demonstrate that low-dose embryonic EtOH has diverse, persistent, and asymmetric effects on the early development of hypothalamic hcrt neurons, which lead to abnormalities in their ultimate location that may contribute to behavioral disturbances, including an increase in EtOH consumption.
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Affiliation(s)
- Adam D. Collier
- Laboratory of Behavioral Neurobiology, The Rockefeller University, New York, NY
| | - Viktoriya Halkina
- Laboratory of Behavioral Neurobiology, The Rockefeller University, New York, NY
| | - Soe S. Min
- Laboratory of Behavioral Neurobiology, The Rockefeller University, New York, NY
| | - Mia Y. Roberts
- Laboratory of Behavioral Neurobiology, The Rockefeller University, New York, NY
| | | | - Kaylin Camidge
- Laboratory of Behavioral Neurobiology, The Rockefeller University, New York, NY
| | - Sarah F. Leibowitz
- Laboratory of Behavioral Neurobiology, The Rockefeller University, New York, NY
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19
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Huybrechts KF, Bateman BT, Hernández-Díaz S. Use of real-world evidence from healthcare utilization data to evaluate drug safety during pregnancy. Pharmacoepidemiol Drug Saf 2019; 28:906-922. [PMID: 31074570 PMCID: PMC6823105 DOI: 10.1002/pds.4789] [Citation(s) in RCA: 88] [Impact Index Per Article: 14.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/22/2019] [Revised: 03/25/2019] [Accepted: 03/27/2019] [Indexed: 12/16/2022]
Abstract
PURPOSE Because preapproval clinical trials typically exclude pregnant women, the evidence on drug safety during pregnancy required to inform drug labeling must come from postapproval controlled observational studies. Common designs have included pregnancy registries and case-control studies. Recently, pregnancy cohorts nested within healthcare utilization databases are increasingly being used. Despite clear advantages, these databases share some important limitations that may threaten the validity of studies emerging from them. METHODS This paper describes the distinctive methodological aspects of conducting drug safety studies in healthcare utilization databases with special emphasis on design and analytic approaches to minimize biases. RESULTS We describe considerations for study design, cohort definition, and follow-up. We then address issues related to exposure ascertainment based on prescription fills, including the importance of the etiologically relevant window and of properly accounting for preterm births. This is followed by a discussion of advantages and challenges when ascertaining maternal and infant outcomes based on secondary data. We then explore useful approaches to address confounding within the context of pregnancy research and of the potential for selection bias when restricting the cohort to live births. Finally, we consider issues related to external validity and statistical significance. The examples are mainly drawn from a pregnancy cohort nested in the Medicaid Analytic Extract. CONCLUSIONS The approaches presented provide guidance regarding the important methodological considerations that need to be attended to in order to generate valid, minimally biased risk when using large healthcare utilization databases for drug safety surveillance in pregnancy.
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Affiliation(s)
- Krista F Huybrechts
- Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts
| | - Brian T Bateman
- Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts
- Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts
| | - Sonia Hernández-Díaz
- Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts
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20
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Fairchild G, Hawes DJ, Frick PJ, Copeland WE, Odgers CL, Franke B, Freitag CM, De Brito SA. Conduct disorder. Nat Rev Dis Primers 2019; 5:43. [PMID: 31249310 DOI: 10.1038/s41572-019-0095-y] [Citation(s) in RCA: 191] [Impact Index Per Article: 31.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Accepted: 05/17/2019] [Indexed: 02/06/2023]
Abstract
Conduct disorder (CD) is a common and highly impairing psychiatric disorder that usually emerges in childhood or adolescence and is characterized by severe antisocial and aggressive behaviour. It frequently co-occurs with attention-deficit/hyperactivity disorder (ADHD) and often leads to antisocial personality disorder in adulthood. CD affects ~3% of school-aged children and is twice as prevalent in males than in females. This disorder can be subtyped according to age at onset (childhood-onset versus adolescent-onset) and the presence or absence of callous-unemotional traits (deficits in empathy and guilt). The aetiology of CD is complex, with contributions of both genetic and environmental risk factors and different forms of interplay among the two (gene-environment interaction and correlation). In addition, CD is associated with neurocognitive impairments; smaller grey matter volume in limbic regions such as the amygdala, insula and orbitofrontal cortex, and functional abnormalities in overlapping brain circuits responsible for emotion processing, emotion regulation and reinforcement-based decision-making have been reported. Lower hypothalamic-pituitary-adrenal axis and autonomic reactivity to stress has also been reported. Management of CD primarily involves parent-based or family-based psychosocial interventions, although stimulants and atypical antipsychotics are sometimes used, especially in individuals with comorbid ADHD.
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Affiliation(s)
| | - David J Hawes
- School of Psychology, University of Sydney, Sydney, New South Wales, Australia
| | - Paul J Frick
- Department of Psychology, Louisiana State University, Baton Rouge, LA, USA and Institute for Learning Science and Teacher Education, Australian Catholic University, Brisbane, Queensland, Australia
| | | | - Candice L Odgers
- Department of Psychological Science, School of Social Ecology, University of California, Irvine, CA, USA
| | - Barbara Franke
- Departments of Human Genetics and Psychiatry, Radboud University Medical Center, Nijmegen, the Netherlands
| | - Christine M Freitag
- Department of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy, University Hospital Frankfurt, Goethe University, Frankfurt am Main, Germany
| | - Stephane A De Brito
- School of Psychology and Centre for Human Brain Health, University of Birmingham, Birmingham, UK
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21
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Easey KE, Dyer ML, Timpson NJ, Munafò MR. Prenatal alcohol exposure and offspring mental health: A systematic review. Drug Alcohol Depend 2019; 197:344-353. [PMID: 30827758 PMCID: PMC6446223 DOI: 10.1016/j.drugalcdep.2019.01.007] [Citation(s) in RCA: 51] [Impact Index Per Article: 8.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/26/2018] [Revised: 11/26/2018] [Accepted: 01/08/2019] [Indexed: 11/22/2022]
Abstract
BACKGROUND High levels of alcohol use in pregnancy have been shown to be associated with negative physical health consequences in offspring. However, the literature is less clear on the association of alcohol use in pregnancy and offspring mental health, specifically for low levels of prenatal alcohol exposure. We conducted a systematic review to evaluate studies examining this association. METHODS Studies were identified by searching PsycINFO, PubMed and Web of Science, and were included if they examined alcohol use during pregnancy as an exposure and offspring mental health at age 3 or older as an outcome. We excluded non-English language publications and studies of fetal alcohol syndrome. RESULTS Thirty-three studies were included and were categorized by mental health outcomes: anxiety/depression, emotional problems, total internalizing problems, total problem score, and conduct disorder. Over half of the analyses reported a positive association of prenatal alcohol exposure and offspring mental health problems. CONCLUSIONS Our review suggests that maternal alcohol use during pregnancy is associated with offspring mental health problems, even at low to moderate levels of alcohol use. Future investigation using methods that allow stronger causal inference is needed to further investigate if these associations shown are causal.
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Affiliation(s)
- Kayleigh E Easey
- UK Centre for Tobacco and Alcohol Studies, School of Psychological Science, University of Bristol, UK; MRC Integrative Epidemiology Unit, University of Bristol, UK.
| | - Maddy L Dyer
- UK Centre for Tobacco and Alcohol Studies, School of Psychological Science, University of Bristol, UK; MRC Integrative Epidemiology Unit, University of Bristol, UK
| | - Nicholas J Timpson
- MRC Integrative Epidemiology Unit, University of Bristol, UK; Population Health Sciences, Bristol Medical School, University of Bristol, UK
| | - Marcus R Munafò
- UK Centre for Tobacco and Alcohol Studies, School of Psychological Science, University of Bristol, UK; MRC Integrative Epidemiology Unit, University of Bristol, UK
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22
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Sakano M, Mukherjee R, Turk J. Behaviour and adaptive functioning in children and young people with fetal alcohol spectrum disorders: a UK study. ADVANCES IN DUAL DIAGNOSIS 2019. [DOI: 10.1108/add-10-2018-0016] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/29/2022]
Abstract
Purpose
The purpose of this paper is to explore the profiles of behaviours and adaptive functioning in the UK children and young people with fetal alcohol spectrum disorders.
Design/methodology/approach
Data of 106 participants registered from 2005 to 2015 were extracted from a clinic database. In total, 99 individuals with confirmed prenatal alcohol exposure (PAE), aged from 5 to 25 years, were analysed using scaled scores of the Vineland Adaptive Behavior Scales-Second Edition (VABS-II), and the Developmental Behaviour Checklist-Primary Carer Version (DBC-P) and Teacher Version (DBC-T). Differences due to age, gender, IQ and family structure (adopted/living with birth parents) were also explored.
Findings
The mean composite adaptive behaviour score on the VABS-II was classified as “low” at 68.2 (SD=8.5), with the socialisation domain being the most impaired. Significantly lower VABS-II composite scores were found in individuals with lower IQ’s, older ages and in males. Disruptive behaviours were the most commonly observed on the DBCs, whereas primary carers scored significantly higher than teachers across all subscales. IQ, age and gender were not associated with the total percentile scores of both DBCs. Adoption made no differences compared to living with birth parents.
Research limitations/implications
Future studies would replicate these findings in a larger sample size including individuals without PAE and those living with birth parents.
Originality/value
This study is the first UK report that examines this issue.
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Abstract
BACKGROUND The alcohol industry recognizes children and pregnant women as population sub-groups vulnerable to the effects of alcohol marketing. Research indicates that heavy alcohol users are also potentially vulnerable to alcohol marketing. The purpose of the current study is to determine if sub-groups defined by psychological characteristics should be classified as potentially vulnerable as well. METHODS College students (n = 326) from two northeast schools were recruited to complete a survey containing questions on demographics, alcohol use, and psychological characteristics (alcohol expectancies, alcohol dependence, sensation seeking traits, and past delinquent behaviors). Additionally, after viewing each of five alcohol ads (4 television and 1 magazine), participants answered questions about their perceptions of alcohol consumption, responsible drinking, excessive drinking, and appeal of the ads. Main effects were assessed using hierarchical linear modeling, with adjustment for age, sex, race, ethnicity, and AUDIT score. RESULTS Alcohol expectancies (p < .001), particularly the social and physical pleasure and social expressiveness sub-scales, and sensation seeking traits (p = .002) were positively associated with alcohol ad appeal. Alcohol dependence symptoms, specifically impaired control and tolerance, were positively associated with perceptions of responsible drinking (p = .035), even though mean perceived number of drinks consumed met the definition of binge drinking. CONCLUSIONS Individuals with positive alcohol expectancies, sensation seeking traits, and alcohol dependence may be vulnerable to alcohol advertising and marketing. Because alcohol advertising often contains content that can serve as a cue or reinforce to drink, specific regulations may be needed to prevent alcohol-related harm from occurring in these sub-populations.
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Affiliation(s)
- Jonathan K Noel
- a Department of Health Science , Johnson & Wales University , Providence , RI , USA
| | - Ziming Xuan
- b Department of Community Health Sciences , Boston University School of Public Health , Boston , MA , USA
| | - Thomas F Babor
- c Department of Community Medicine and Health Care , University of Connecticut School of Medicine , Farmington , CT , USA
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24
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Ren Y, Yao X, Liu Y, Liu S, Li X, Huang Q, Liu F, Li N, Lu Y, Yuan Z, Li S, Xiang H. Outdoor air pollution pregnancy exposures are associated with behavioral problems in China's preschoolers. ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH INTERNATIONAL 2019; 26:2397-2408. [PMID: 30467751 DOI: 10.1007/s11356-018-3715-2] [Citation(s) in RCA: 19] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 09/13/2018] [Accepted: 11/07/2018] [Indexed: 05/22/2023]
Abstract
There are mounting evidences indicated that maternal exposure to outdoor air pollutants in pregnancy affects children's neural development, but the researches on children's behavioral difficulties are seldom. We explored the association between maternal exposure to outdoor air pollution during different trimesters of pregnancy and the prevalence of behavioral difficulties among 657 preschool children aged 3-4 from three kindergartens in Wuhan, China. This is a cross-sectional study. Children's behavioral difficulties were assessed by the Strengths and Difficulties Questionnaire (SDQ) (reported by parents). Maternal exposure to outdoor air pollutants during pregnancy were estimated based on the daily average measured concentration levels from ground monitoring stations. Potential confounding factors including children-related, maternal, and socio-economic status (SES) were adjusted in the study. We calculated the prevalence of each type of behavioral difficulties and used binary logistic regression method to estimate the crude odds ratio (cOR), adjusted odds ratio (aOR), and corresponding 95% confidence intervals (95% CIs) for 1 μg/m3 increase in each air pollutant during every exposure window in single- and two-pollutant models. The prevalence of participants' total behavioral difficulties was 9.6%. In single-pollutant models, during full gestation, positive associations were observed between exposure to NO2 (aOR = 1.204, 95% CI 1.042, 1.392), particle matter (PM)10 (aOR = 1.070, 95% CI 1.018, 1.125), PM2.5 (aOR = 1.095, 95% CI 1.021, 1.176) and total difficulties, exposure to PM10 (aOR = 1.040, 95% CI 1.001, 1.081), PM2.5 (aOR = 1.053, 95% CI 1.000, 1.109) and prosocial behavior, respectively. In the first trimester, exposure to SO2 (aOR = 1.047, 95% CI 1.009, 1.086), NO2 (aOR = 1.039, 95% CI 1.013, 1.066), PM10 (aOR = 1.013, 95% CI 1.004, 1.023), and PM2.5 (aOR = 1.016, 95% CI 1.004, 1.028) were all positively associated with total difficulties. The associations between second and third trimesters' exposure to all pollutants and outcomes were not statistically significant. However, in the two-pollutant models, second trimester exposure to PM2.5 (aOR = 1.078, 95%CI 1.023, 1.137) was positively associated with total behavioral difficulties after adjusting for PM10. Exposure to outdoor air pollutants SO2, NO2, PM10, and PM2.5 during pregnancy may be associated with behavioral difficulties, especially in the first trimester.
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Affiliation(s)
- Yunzhao Ren
- School of Health Sciences, Wuhan University, 115# Donghu Road, Wuhan, 430071, Hubei, China
| | - Xing Yao
- School of Health Sciences, Wuhan University, 115# Donghu Road, Wuhan, 430071, Hubei, China
| | - Yisi Liu
- Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, 1959 NE Pacific Street, Seattle, WA, 98195, USA
| | - Suyang Liu
- School of Health Sciences, Wuhan University, 115# Donghu Road, Wuhan, 430071, Hubei, China
- Global Health Institute, Wuhan University, 115# Donghu Road, Wuhan, 430071, China
| | - Xiao Li
- Gilead Sciences Inc, 333 Lakeside Drive, Foster City, CA, 94404, USA
| | - Qing Huang
- School of Health Sciences, Wuhan University, 115# Donghu Road, Wuhan, 430071, Hubei, China
| | - Feifei Liu
- School of Health Sciences, Wuhan University, 115# Donghu Road, Wuhan, 430071, Hubei, China
| | - Na Li
- School of Health Sciences, Wuhan University, 115# Donghu Road, Wuhan, 430071, Hubei, China
| | - Yuanan Lu
- Environmental Health Laboratory, Department of Public Health Sciences, University of Hawaii at Manoa, 1960 East-West Rd, Biomed Bldg, D105, Honolulu, HI, 96822, USA
| | - Zhanpeng Yuan
- School of Health Sciences, Wuhan University, 115# Donghu Road, Wuhan, 430071, Hubei, China
| | - Shiyue Li
- School of Health Sciences, Wuhan University, 115# Donghu Road, Wuhan, 430071, Hubei, China.
| | - Hao Xiang
- School of Health Sciences, Wuhan University, 115# Donghu Road, Wuhan, 430071, Hubei, China.
- Global Health Institute, Wuhan University, 115# Donghu Road, Wuhan, 430071, China.
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25
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Schoeps A, Peterson ER, Mia Y, Waldie KE, Underwood L, D'Souza S, Morton SMB. Prenatal alcohol consumption and infant and child behavior: Evidence from the Growing Up in New Zealand Cohort. Early Hum Dev 2018; 123:22-29. [PMID: 30036725 DOI: 10.1016/j.earlhumdev.2018.06.011] [Citation(s) in RCA: 15] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/13/2018] [Revised: 06/26/2018] [Accepted: 06/27/2018] [Indexed: 01/16/2023]
Abstract
BACKGROUND High levels of alcohol exposure during pregnancy can damage developing brains and influence child behavior and learning. AIM To examine the effects of lower levels of alcohol and very early exposure to alcohol on infant temperament and child behavior. STUDY DESIGN, SUBJECTS, AND OUTCOME MEASURES The Growing Up in New Zealand study involves a prospective birth cohort of 6822 pregnant women of whom 6156 provided information on their child's temperament using the Infant Behavior Questionnaire-Revised (IBQ-R VSF) at 9 months and their child's behavior using the Strengths and Difficulties Questionnaire at 2 years. RESULTS A series of adjusted linear regression models controlling for socio-demographic factors found alcohol consumption during pregnancy was most consistently related to Lower Positive Affect, Affiliation/Regulation, and Orienting Capacity temperament scores. Mothers who stopped drinking after becoming aware of their pregnancy, but had an unplanned pregnancy (hence may have a baby exposed to alcohol for longer), also reported infants with lower Orienting Capacity, Affiliation/Regulation, and Fear temperament scores compared to those that did not drink. Children whose mothers drank four or more drinks per week during pregnancy were more likely to report their child as having conduct problems, with higher total difficulties scores at age 2. CONCLUSIONS Alcohol consumption during pregnancy has a negative effect especially on infant temperament, even if small amounts of alcohol are consumed. Our findings have implications for men and women who drink, medical professionals, and for the availability of contraception to those who drink, but do not plan to get pregnant.
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Affiliation(s)
- Anja Schoeps
- Institute of Public Health, University of Heidelberg, Im Neuenheimer Feld 324, 69120 Heidelberg, Germany.
| | - Elizabeth R Peterson
- School of Psychology, University of Auckland, Private Bag 92019, Auckland, New Zealand; Centre for Longitudinal Research - He Ara ki Mua, University of Auckland, Private Bag 92019, Auckland, New Zealand.
| | - Yasmine Mia
- School of Psychology, University of Auckland, Private Bag 92019, Auckland, New Zealand.
| | - Karen E Waldie
- School of Psychology, University of Auckland, Private Bag 92019, Auckland, New Zealand; Centre for Longitudinal Research - He Ara ki Mua, University of Auckland, Private Bag 92019, Auckland, New Zealand.
| | - Lisa Underwood
- Centre for Longitudinal Research - He Ara ki Mua, University of Auckland, Private Bag 92019, Auckland, New Zealand.
| | - Stephanie D'Souza
- School of Psychology, University of Auckland, Private Bag 92019, Auckland, New Zealand; Centre for Longitudinal Research - He Ara ki Mua, University of Auckland, Private Bag 92019, Auckland, New Zealand.
| | - Susan M B Morton
- Centre for Longitudinal Research - He Ara ki Mua, University of Auckland, Private Bag 92019, Auckland, New Zealand; School of Population Health, University of Auckland, Private Bag 92019, Auckland, New Zealand.
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26
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Bernhard A, Martinelli A, Ackermann K, Saure D, Freitag CM. Association of trauma, Posttraumatic Stress Disorder and Conduct Disorder: A systematic review and meta-analysis. Neurosci Biobehav Rev 2018; 91:153-169. [DOI: 10.1016/j.neubiorev.2016.12.019] [Citation(s) in RCA: 27] [Impact Index Per Article: 3.9] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/04/2016] [Revised: 11/28/2016] [Accepted: 12/19/2016] [Indexed: 11/30/2022]
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27
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Noor S, Milligan ED. Lifelong Impacts of Moderate Prenatal Alcohol Exposure on Neuroimmune Function. Front Immunol 2018; 9:1107. [PMID: 29910801 PMCID: PMC5992426 DOI: 10.3389/fimmu.2018.01107] [Citation(s) in RCA: 29] [Impact Index Per Article: 4.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/05/2017] [Accepted: 05/02/2018] [Indexed: 12/26/2022] Open
Abstract
In utero alcohol exposure is emerging as a major risk factor for lifelong aberrant neuroimmune function. Fetal alcohol spectrum disorder encompasses a range of behavioral and physiological sequelae that may occur throughout life and includes cognitive developmental disabilities as well as disease susceptibility related to aberrant immune and neuroimmune actions. Emerging data from clinical studies and findings from animal models support that very low to moderate levels of fetal alcohol exposure may reprogram the developing central nervous system leading to altered neuroimmune and neuroglial signaling during adulthood. In this review, we will focus on the consequences of low to moderate prenatal alcohol exposure (PAE) on neuroimmune interactions during early life and at different stages of adulthood. Data discussed here will include recent studies suggesting that while abnormal immune function is generally minimal under basal conditions, following pathogenic stimuli or trauma, significant alterations in the neuroimmune axis occur. Evidence from published reports will be discussed with a focus on observations that PAE may bias later-life peripheral immune responses toward a proinflammatory phenotype. The propensity for proinflammatory responses to challenges in adulthood may ultimately shape neuron–glial-immune processes suspected to underlie various neuropathological outcomes including chronic pain and cognitive impairment.
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Affiliation(s)
- Shahani Noor
- Department of Neurosciences, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, United States
| | - Erin D Milligan
- Department of Neurosciences, School of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, United States
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28
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Ogundele MO. Behavioural and emotional disorders in childhood: A brief overview for paediatricians. World J Clin Pediatr 2018; 7:9-26. [PMID: 29456928 PMCID: PMC5803568 DOI: 10.5409/wjcp.v7.i1.9] [Citation(s) in RCA: 160] [Impact Index Per Article: 22.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/27/2017] [Revised: 11/30/2017] [Accepted: 12/05/2017] [Indexed: 02/06/2023] Open
Abstract
Mental health problems in children and adolescents include several types of emotional and behavioural disorders, including disruptive, depression, anxiety and pervasive developmental (autism) disorders, characterized as either internalizing or externalizing problems. Disruptive behavioural problems such as temper tantrums, attention deficit hyperactivity disorder, oppositional, defiant or conduct disorders are the commonest behavioural problems in preschool and school age children. The routine Paediatric clinic or Family Medicine/General Practitioner surgery presents with several desirable characteristics that make them ideal for providing effective mental health services to children and adolescents. DSM-5 and ICD-10 are the universally accepted standard criteria for the classification of mental and behaviour disorders in childhood and adults. The age and gender prevalence estimation of various childhood behavioural disorders are variable and difficult to compare worldwide. A review of relevant published literature was conducted, including published meta-analyses and national guidelines. We searched for articles indexed by Ovid, PubMed, PubMed Medical Central, CINAHL, EMBASE, Database of Abstracts and Reviews, and the Cochrane Database of Systematic reviews and other online sources. The searches were conducted using a combination of search expressions including "childhood", "behaviour", "disorders" or "problems". Childhood behaviour and emotional problems with their related disorders have significant negative impacts on the individual, the family and the society. They are commonly associated with poor academic, occupational, and psychosocial functioning. It is important for all healthcare professionals, especially the Paediatricians to be aware of the range of presentation, prevention and management of the common mental health problems in children and adolescents.
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Affiliation(s)
- Michael O Ogundele
- Department of Community Paediatrics, NHS Fife, Glenwood Health Centre, Glenrothes KY6 1HK, United Kingdom
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29
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Comasco E, Rangmar J, Eriksson UJ, Oreland L. Neurological and neuropsychological effects of low and moderate prenatal alcohol exposure. Acta Physiol (Oxf) 2018; 222. [PMID: 28470828 DOI: 10.1111/apha.12892] [Citation(s) in RCA: 29] [Impact Index Per Article: 4.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/24/2017] [Revised: 02/17/2017] [Accepted: 04/27/2017] [Indexed: 01/18/2023]
Abstract
Several explanations for the diverse results in research on foetal alcohol spectrum disorders or alcohol-related neurodevelopmental disorder might be at hand: timing, amount and patterns of alcohol exposure, as well as complex epigenetic responses. The genetic background of the offspring and its interaction with other prenatal and post-natal environmental cues are likely also of importance. In the present report, key findings about the possible effects of low and moderate doses of maternal alcohol intake on the neuropsychological development of the offspring are reviewed and plausible mechanisms discussed. Special focus is put on the serotonergic system within developmental and gene-environment frameworks. The review also suggests guidelines for future studies and also summarizes some of to-be-answered questions of relevance to clinical practice. Contradictory findings and paucity of studies on the effects of exposure to low alcohol levels during foetal life for the offspring's neuropsychological development call for large prospective studies, as well as for studies including neuroimaging and multi-omics analyses to dissect the neurobiological underpinnings of alcohol exposure-related phenotypes and to identify biomarkers. Finally, it remains to be investigated whether any safe threshold of alcohol drinking during pregnancy can be identified.
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Affiliation(s)
- E. Comasco
- Department of Neuroscience; Uppsala University; Uppsala Sweden
| | - J. Rangmar
- Department of Psychology; University of Gothenburg; Gothenburg Sweden
| | - U. J. Eriksson
- Department of Medical Cell Biology; Uppsala University; Uppsala Sweden
| | - L. Oreland
- Department of Neuroscience; Uppsala University; Uppsala Sweden
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30
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Sharp GC, Arathimos R, Reese SE, Page CM, Felix J, Küpers LK, Rifas-Shiman SL, Liu C, Burrows K, Zhao S, Magnus MC, Duijts L, Corpeleijn E, DeMeo DL, Litonjua A, Baccarelli A, Hivert MF, Oken E, Snieder H, Jaddoe V, Nystad W, London SJ, Relton CL, Zuccolo L. Maternal alcohol consumption and offspring DNA methylation: findings from six general population-based birth cohorts. Epigenomics 2017; 10:27-42. [PMID: 29172695 PMCID: PMC5753623 DOI: 10.2217/epi-2017-0095] [Citation(s) in RCA: 44] [Impact Index Per Article: 5.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/07/2023] Open
Abstract
Aim: Alcohol consumption during pregnancy is sometimes associated with adverse outcomes in offspring, potentially mediated by epigenetic modifications. We aimed to investigate genome-wide DNA methylation in cord blood of newborns exposed to alcohol in utero. Materials & methods: We meta-analyzed information from six population-based birth cohorts within the Pregnancy and Childhood Epigenetics consortium. Results: We found no strong evidence of association at either individual CpGs or across larger regions of the genome. Conclusion: Our findings suggest no association between maternal alcohol consumption and offspring cord blood DNA methylation. This is in stark contrast to the multiple strong associations previous studies have found for maternal smoking, which is similarly socially patterned. However, it is possible that a combination of a larger sample size, higher doses, different timings of exposure, exploration of a different tissue and a more global assessment of genomic DNA methylation might show evidence of association.
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Affiliation(s)
- Gemma C Sharp
- MRC Integrative Epidemiology Unit, University of Bristol, Bristol, BS8 2BN, UK.,School of Social & Community Medicine, University of Bristol, Bristol, BS8 2BN, UK.,School of Oral & Dental Sciences, University of Bristol, Bristol, UK
| | - Ryan Arathimos
- MRC Integrative Epidemiology Unit, University of Bristol, Bristol, BS8 2BN, UK.,School of Social & Community Medicine, University of Bristol, Bristol, BS8 2BN, UK
| | - Sarah E Reese
- Division of Intramural Research, Department of Health & Human Services, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA
| | - Christian M Page
- Division for Mental & Physical Health, Department of Non-Communicable Diseases, Norwegian Institute of Public Health, Oslo, Norway.,Oslo Centre for Biostatistics & Epidemiology, Oslo University Hospital, Oslo, Norway
| | - Janine Felix
- The Generation R Study Group, Erasmus MC, University Medical Centre Rotterdam, Rotterdam, The Netherlands.,Department of Epidemiology, Erasmus MC, University Medical Centre Rotterdam, Rotterdam, The Netherlands.,Department of Pediatrics, Erasmus MC, University Medical Centre Rotterdam, Rotterdam, The Netherlands
| | - Leanne K Küpers
- MRC Integrative Epidemiology Unit, University of Bristol, Bristol, BS8 2BN, UK.,School of Social & Community Medicine, University of Bristol, Bristol, BS8 2BN, UK.,Department of Epidemiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
| | - Sheryl L Rifas-Shiman
- Department of Population Medicine, Harvard Medical School, Harvard Pilgrim Health Care Institute, Boston, MA, USA
| | - Chunyu Liu
- The Framingham Heart Study, Framingham, MA, USA.,The Population Sciences Branch, Division of Intramural Research, National Heart, Lung, & Blood Institute, Bethesda, MD, USA.,Department of Biostatistics, Boston University School of Public Health, 715 Albany St, Boston, MA, USA
| | | | - Kimberley Burrows
- MRC Integrative Epidemiology Unit, University of Bristol, Bristol, BS8 2BN, UK.,School of Social & Community Medicine, University of Bristol, Bristol, BS8 2BN, UK
| | - Shanshan Zhao
- Division of Intramural Research, Department of Health & Human Services, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA
| | - Maria C Magnus
- MRC Integrative Epidemiology Unit, University of Bristol, Bristol, BS8 2BN, UK.,School of Social & Community Medicine, University of Bristol, Bristol, BS8 2BN, UK.,Division for Mental & Physical Health, Department of Non-Communicable Diseases, Norwegian Institute of Public Health, Oslo, Norway
| | - Liesbeth Duijts
- The Generation R Study Group, Erasmus MC, University Medical Centre Rotterdam, Rotterdam, The Netherlands.,Department of Pediatrics, Division of Respiratory Medicine & Allergology, Erasmus MC, University Medical Centre Rotterdam, Rotterdam, The Netherlands.,Department of Pediatrics, Division of Neonatology, Erasmus MC, University Medical Centre Rotterdam, Rotterdam, The Netherlands
| | - Eva Corpeleijn
- Department of Epidemiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
| | - Dawn L DeMeo
- Channing Division of Network Medicine, Brigham & Women's Hospital, Harvard Medical School, Boston, MA, USA
| | - Augusto Litonjua
- Channing Division of Network Medicine, Brigham & Women's Hospital, Harvard Medical School, Boston, MA, USA
| | - Andrea Baccarelli
- Laboratory of Precision Environmental Biosciences, Columbia University Mailman School of Public Health, New York, NY, USA
| | - Marie-France Hivert
- Department of Population Medicine, Harvard Medical School, Harvard Pilgrim Health Care Institute, Boston, MA, USA.,Diabetes Unit, Massachusetts General Hospital, Boston, MA, USA
| | - Emily Oken
- Department of Population Medicine, Harvard Medical School, Harvard Pilgrim Health Care Institute, Boston, MA, USA
| | - Harold Snieder
- Department of Epidemiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
| | - Vincent Jaddoe
- The Generation R Study Group, Erasmus MC, University Medical Centre Rotterdam, Rotterdam, The Netherlands.,Department of Epidemiology, Erasmus MC, University Medical Centre Rotterdam, Rotterdam, The Netherlands.,Department of Pediatrics, Erasmus MC, University Medical Centre Rotterdam, Rotterdam, The Netherlands
| | - Wenche Nystad
- Division for Mental & Physical Health, Department of Non-Communicable Diseases, Norwegian Institute of Public Health, Oslo, Norway
| | - Stephanie J London
- Division of Intramural Research, Department of Health & Human Services, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA
| | - Caroline L Relton
- MRC Integrative Epidemiology Unit, University of Bristol, Bristol, BS8 2BN, UK.,School of Social & Community Medicine, University of Bristol, Bristol, BS8 2BN, UK
| | - Luisa Zuccolo
- MRC Integrative Epidemiology Unit, University of Bristol, Bristol, BS8 2BN, UK.,School of Social & Community Medicine, University of Bristol, Bristol, BS8 2BN, UK
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31
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Tiemeier H. A closer look at the fetal programming hypothesis with obstetric ultrasound. JORNAL DE PEDIATRIA (VERSÃO EM PORTUGUÊS) 2017. [DOI: 10.1016/j.jpedp.2017.04.010] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/16/2022] Open
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32
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Tiemeier H. A closer look at the fetal programming hypothesis with obstetric ultrasound. J Pediatr (Rio J) 2017; 93:437-438. [PMID: 28432862 DOI: 10.1016/j.jped.2017.04.001] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/13/2023] Open
Affiliation(s)
- Henning Tiemeier
- Erasmus Medical Center Rotterdam, Department of Child and Adolescent Psychiatry, Rotterdam, Netherlands.
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33
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Halliday JL, Muggli E, Lewis S, Elliott EJ, Amor DJ, O'Leary C, Donath S, Forster D, Nagle C, Craig JM, Anderson PJ. Alcohol consumption in a general antenatal population and child neurodevelopment at 2 years. J Epidemiol Community Health 2017; 71:990-998. [PMID: 28839077 DOI: 10.1136/jech-2017-209165] [Citation(s) in RCA: 16] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/07/2017] [Revised: 07/05/2017] [Accepted: 08/09/2017] [Indexed: 12/21/2022]
Abstract
BACKGROUND Prenatal alcohol exposure (PAE) is a community health problem with up to 50% of pregnant women drinking alcohol. The relationship between low or sporadic binge PAE and adverse child outcomes is not clear. This study examines the association between PAE in the general antenatal population and child neurodevelopment at 2 years, accounting for relevant contributing factors. METHODS This prospective population-based cohort recruited 1570 pregnant women, providing sociodemographic, psychological and lifestyle information and alcohol use for five time periods. PAE categories were 'low', 'moderate/high', 'binge', in trimester 1 or throughout pregnancy. Measures of cognitive, language and motor development (Bayley Scales of Infant and Toddler Development) were available for 554 children, while measures of sensory processing (Infant/Toddler Sensory Profile) and social-emotional development (Brief Infant Toddler Social Emotional Assessment) were available for 948. RESULTS A positive association in univariate analysis with low-level PAE throughout pregnancy and cognition (β=4.1, 95% CI -0.02 to 8.22, p=0.05) was attenuated by adjusting for environmental/social deprivation risk factors (β=3.06 (-1.19 to 7.30), p=0.16). Early binge drinking, plus continued PAE at lower levels, was associated with the child being more likely to score low in sensation avoidance (adjusted OR 1.88 (1.03 to 3.41), p=0.04). CONCLUSION Early binge exposure, followed by lower-level PAE, demonstrated an increase in sensation-avoiding behaviour. There were, however, no significant associations between PAE and neurodevelopment following adjustment for important confounders and modifiers. Follow-up is paramount to investigate subtle or later onset problems.
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Affiliation(s)
- Jane L Halliday
- Public Health Genetics, Murdoch Children's Research Institute, Parkville, Victoria, Australia.,Department of Paediatrics, The University of Melbourne, Melbourne, Victoria, Australia
| | - Evelyne Muggli
- Public Health Genetics, Murdoch Children's Research Institute, Parkville, Victoria, Australia.,Department of Paediatrics, The University of Melbourne, Melbourne, Victoria, Australia
| | - Sharon Lewis
- Public Health Genetics, Murdoch Children's Research Institute, Parkville, Victoria, Australia.,Department of Paediatrics, The University of Melbourne, Melbourne, Victoria, Australia
| | - Elizabeth J Elliott
- Public Health Genetics, Murdoch Children's Research Institute, Parkville, Victoria, Australia.,Paediatrics and Child Health, Children's Hospital Westmead, The University of Sydney, Sydney, New South Wales, Australia
| | - David J Amor
- Public Health Genetics, Murdoch Children's Research Institute, Parkville, Victoria, Australia.,Department of Paediatrics, The University of Melbourne, Melbourne, Victoria, Australia
| | - Colleen O'Leary
- Telethon Kids Institute, Perth, Western Australia, Australia
| | - Susan Donath
- Public Health Genetics, Murdoch Children's Research Institute, Parkville, Victoria, Australia.,Department of Paediatrics, The University of Melbourne, Melbourne, Victoria, Australia
| | - Della Forster
- School of Nursing and Midwifery, Judith Lumley Centre, SHE College, La Trobe University, Melbourne, Victoria, Australia.,Midwifery and Maternity Services Research Unit, The Royal Women's Hospital, Parkville, Victoria, Australia
| | - Cate Nagle
- Centre for Quality and Patient Safety Research, Deakin University, Geelong, Victoria, Australia.,Women's and Children's Division, Western Health, St Albans, Victoria, Australia
| | - Jeffrey M Craig
- Public Health Genetics, Murdoch Children's Research Institute, Parkville, Victoria, Australia.,Department of Paediatrics, The University of Melbourne, Melbourne, Victoria, Australia
| | - Peter J Anderson
- Public Health Genetics, Murdoch Children's Research Institute, Parkville, Victoria, Australia
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Dumas A, Toutain S, Simmat-Durand L. Alcohol Use During Pregnancy or Breastfeeding: A National Survey in France. J Womens Health (Larchmt) 2017; 26:798-805. [DOI: 10.1089/jwh.2016.6130] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/18/2023] Open
Affiliation(s)
- Agnès Dumas
- Centre for Research in Epidemiology and Population Health (CESP), INSERM U1018, Villejuif, France
- Institut Gustave Roussy, Villejuif, France
- Université Paris-Sud, Orsay, France
| | - Stéphanie Toutain
- Université Paris Descartes, Sorbonne Paris Cité, Paris, France
- Centre de Recherche Médecine, Sciences, Santé, Santé Mentale et Société (CERMES3), UMR CNRS 8211, INSERM U988, EHESS, Paris, France
| | - Laurence Simmat-Durand
- Université Paris Descartes, Sorbonne Paris Cité, Paris, France
- Centre de Recherche Médecine, Sciences, Santé, Santé Mentale et Société (CERMES3), UMR CNRS 8211, INSERM U988, EHESS, Paris, France
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Mahedy L, Hammerton G, Teyhan A, Edwards AC, Kendler KS, Moore SC, Hickman M, Macleod J, Heron J. Parental alcohol use and risk of behavioral and emotional problems in offspring. PLoS One 2017; 12:e0178862. [PMID: 28586358 PMCID: PMC5460848 DOI: 10.1371/journal.pone.0178862] [Citation(s) in RCA: 19] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/09/2016] [Accepted: 05/19/2017] [Indexed: 11/19/2022] Open
Abstract
OBJECTIVE The majority of studies that have examined parental alcohol use and offspring outcomes have either focused on exposure in the antenatal period or from clinical populations. This study sought to examine proximal and distal associations between parental alcohol use and offspring conduct problems and depressive symptoms in a population birth cohort. METHODS We used prospective data from a large UK based population cohort (ALSPAC) to investigate the association between parental alcohol use, measured in units, (assessed at ages 4 and 12 years) with childhood conduct trajectories, (assessed on six occasions from 4 to 13.5 years, n = 6,927), and adolescent depressive symptoms (assessed on four occasions from ~13 to ~18 years, n = 5,539). Heavy drinking was defined as ≥21 units per week in mothers and partners who drank 4+ units daily. RESULTS We found little evidence to support a dose response association between parental alcohol use and offspring outcomes. For example, we found insufficient evidence to support an association between maternal alcohol use at age 4 years and childhood conduct problems (childhood limited: OR = 1.00, 95% CI = .99, 1.01; adolescent onset: OR = 0.99, 95% CI = .98, 1.00; and early-onset persistent: OR = 0.99, 95% CI = .98, 1.00) per 1-unit change in maternal alcohol use compared to those with low levels of conduct problems. We also found insufficient evidence to support an association between maternal alcohol use at age 4 years and adolescent depressive symptoms (intercept: b = .001, 95% CI = -.01, .01, and slope: b = .003, 95% CI = -.03, .03) per 1-unit change in maternal alcohol use. Results remained consistent across amount of alcohol consumed (i.e., number of alcohol units or heavy alcohol use), parent (maternal self-reports or maternal reports of partner's alcohol use), and timing of alcohol use (assessed at age 4 or age 12 years). CONCLUSIONS There is no support for an association between parental alcohol use during childhood and conduct and emotional problems during childhood or adolescence.
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Affiliation(s)
- Liam Mahedy
- School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom
| | - Gemma Hammerton
- School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom
| | - Alison Teyhan
- School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom
| | - Alexis C. Edwards
- Department of Psychiatry and School of Medicine, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, Virginia, United States of America
| | - Kenneth S. Kendler
- Department of Psychiatry and School of Medicine, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, Virginia, United States of America
| | - Simon C. Moore
- School of Dentistry, College of Biomedical and Life Science, Cardiff University, Cardiff, United Kingdom
| | - Matthew Hickman
- School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom
| | - John Macleod
- School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom
| | - Jon Heron
- School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom
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Babor TF, Robaina K, Noel JK, Ritson EB. Vulnerability to alcohol-related problems: a policy brief with implications for the regulation of alcohol marketing. Addiction 2017; 112 Suppl 1:94-101. [PMID: 27922203 DOI: 10.1111/add.13626] [Citation(s) in RCA: 38] [Impact Index Per Article: 4.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/16/2023]
Abstract
BACKGROUND AND AIMS The concern that alcohol advertising can have detrimental effects on vulnerable viewers has prompted the development of codes of responsible advertising practices. This paper evaluates critically the concept of vulnerability as it applies to (1) susceptibility to alcohol-related harm and (2) susceptibility to the effects of marketing, and describes its implications for the regulation of alcohol marketing. METHOD We describe the findings of key published studies, review papers and expert reports to determine whether these two types of vulnerability apply to population groups defined by (1) age and developmental history; (2) personality characteristics; (3) family history of alcoholism; (4) female sex and pregnancy risk; and (5) history of alcohol dependence and recovery status. RESULTS Developmental theory and research suggest that groups defined by younger age, incomplete neurocognitive development and a history of alcohol dependence may be particularly vulnerable because of the disproportionate harm they experience from alcohol and their increased susceptibility to alcohol marketing. Children may be more susceptible to media imagery because they do not have the ability to compensate for biases in advertising portrayals and glamorized media imagery. CONCLUSION Young people and people with a history of alcohol dependence appear to be especially vulnerable to alcohol marketing, warranting the development of new content and exposure guidelines focused on protecting those groups to improve current self-regulation codes promoted by the alcohol industry. If adequate protections cannot be implemented through this mechanism, statutory regulations should be considered.
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Affiliation(s)
- Thomas F Babor
- Department of Community Medicine and Health Care, University of Connecticut School of Medicine, Farmington, CT, 06030, USA
| | - Katherine Robaina
- Department of Community Medicine and Health Care, University of Connecticut School of Medicine, Farmington, CT, 06030, USA
| | - Jonathan K Noel
- Department of Community Medicine and Health Care, University of Connecticut School of Medicine, Farmington, CT, 06030, USA
| | - E Bruce Ritson
- Department of Community Medicine and Health Care, University of Connecticut School of Medicine, Farmington, CT, 06030, USA
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Do EK, Latendresse SJ, Edwards AC, Kendler KS, Dick DM, York TP. Associations Between Gestational Age at Birth and Alcohol Use in the Avon Longitudinal Study of Parents and Children. Alcohol Clin Exp Res 2016; 40:1328-38. [PMID: 27155784 DOI: 10.1111/acer.13080] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/30/2015] [Accepted: 03/28/2016] [Indexed: 12/01/2022]
Abstract
BACKGROUND The relationship between gestational age at birth (GA) and alcohol use measures in early adulthood was examined in a large U.K. community-based birth cohort (Avon Longitudinal Study of Parents and Children). METHODS A series of linear and logistic regression models were used to test for main effects of a continuous measure of GA on a range of alcohol use measures, and moderation of these associations by sex. In addition, mediation analyses assessed the extent to which significant associations between GA and alcohol use operated indirectly, through influences of the parental environment and/or childhood measures of emotional and behavioral health (EBH). RESULTS Earlier GA significantly predicted never drinking by age 18, but was not associated with other measures of alcohol use behavior among young adult drinkers (i.e., Self-Rating of the Effects of Alcohol, Alcohol Use Disorders Identification Test, or DSM-IV-TR Criteria for Alcohol Dependence). The association between earlier GA and never drinking by age 18 was moderated by sex, such that females born early were less likely to have ever had a drink by age 18. In the full sample, childhood measures of EBH were found to mediate the association between earlier GA and never drinking by age 18. This association was not mediated by parenting factors. CONCLUSIONS Earlier GA is associated with never drinking alcohol in early adulthood, in females. Emotional and behavioral difficulties experienced in early childhood may mediate the relationship between earlier GA and never drinking by age 18.
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Affiliation(s)
- Elizabeth K Do
- Department of Psychiatry, Virginia Institute for Psychiatric and Behavioral Genetics, Center for Clinical and Translational Research, Virginia Commonwealth University, Richmond, Virginia
| | | | - Alexis C Edwards
- Department of Psychiatry, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, Virginia
| | - Kenneth S Kendler
- Department of Psychiatry, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, Virginia
| | - Danielle M Dick
- Departments of Psychology, African American Studies, and Human and Molecular Genetics, Virginia Commonwealth University, Richmond, Virginia
| | - Timothy P York
- Department of Human and Molecular Genetics, Virginia Institute for Psychiatric and Behavioral Genetics, Virginia Commonwealth University, Richmond, Virginia
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