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1. Impact of maternal body mass index and gestational weight gain on pregnancy complications: an individual participant data meta‐analysis of European, North American and Australian cohorts

Author: Santos, S, Voerman, E, Amiano, P, Barros, H, Beilin, LJ, Bergström, A, Charles, M‐A, Chatzi, L, Chevrier, C, Chrousos, GP, Corpeleijn, E, Costa, O, Costet, N, Crozier, S, Devereux, G, Doyon, M, Eggesbø, M, Fantini, MP, Farchi, S, Forastiere, F, Georgiu, V, Godfrey, KM, Gori, D, Grote, V, Hanke, W, Hertz‐Picciotto, I, Heude, B, Hivert, M‐F, Hryhorczuk, D, Huang, R‐C, Inskip, H, Karvonen, AM, Kenny, LC, Koletzko, B, Küpers, LK, Lagström, H, Lehmann, I, Magnus, P, Majewska, R, Mäkelä, J, Manios, Y, McAuliffe, FM, McDonald, SW, Mehegan, J, Melén, E, Mommers, M, Morgen, CS, Moschonis, G, Murray, D, Chaoimh, C Ní, Nohr, EA, Andersen, A‐M Nybo, Oken, E, Oostvogels, AJJM, Pac, A, Papadopoulou, E, Pekkanen, J, Pizzi, C, Polanska, K, Porta, D, Richiardi, L, Rifas‐Shiman, SL, Roeleveld, N, Ronfani, L, Santos, AC, Standl, M, Stigum, H, Stoltenberg, C, Thiering, E, Thijs, C, Torrent, M, Tough, SC, Trnovec, T, Turner, S, Gelder, MMHJ, Rossem, L, Berg, A, Vrijheid, M, Vrijkotte, TGM, West, J, Wijga, AH, Wright, J, Zvinchuk, O, Sørensen, TIA, Lawlor, DA, Gaillard, R, and Jaddoe, VWV
Subjects: Obesity, Contraception/Reproduction, Diabetes, Preterm, Low Birth Weight and Health of the Newborn, Infant Mortality, Cardiovascular, Clinical Research, Perinatal Period - Conditions Originating in Perinatal Period, Prevention, Nutrition, Pediatric, Aetiology, 3.1 Primary prevention interventions to modify behaviours or promote wellbeing, 2.1 Biological and endogenous factors, Prevention of disease and conditions, and promotion of well-being, Metabolic and endocrine, Reproductive health and childbirth, Good Health and Well Being, Adult, Australia, Birth Weight, Body Mass Index, Cohort Studies, Europe, Female, Gestational Age, Gestational Weight Gain, Humans, Infant, Newborn, North America, Odds Ratio, Overweight, Pregnancy, Pregnancy Complications, Risk Factors, Birthweight, body mass index, pregnancy complications, preterm birth, weight gain, Medical and Health Sciences, Obstetrics & Reproductive Medicine
Abstract: ObjectiveTo assess the separate and combined associations of maternal pre-pregnancy body mass index (BMI) and gestational weight gain with the risks of pregnancy complications and their population impact.DesignIndividual participant data meta-analysis of 39 cohorts.SettingEurope, North America, and Oceania.Population265 270 births.MethodsInformation on maternal pre-pregnancy BMI, gestational weight gain, and pregnancy complications was obtained. Multilevel binary logistic regression models were used.Main outcome measuresGestational hypertension, pre-eclampsia, gestational diabetes, preterm birth, small and large for gestational age at birth.ResultsHigher maternal pre-pregnancy BMI and gestational weight gain were, across their full ranges, associated with higher risks of gestational hypertensive disorders, gestational diabetes, and large for gestational age at birth. Preterm birth risk was higher at lower and higher BMI and weight gain. Compared with normal weight mothers with medium gestational weight gain, obese mothers with high gestational weight gain had the highest risk of any pregnancy complication (odds ratio 2.51, 95% CI 2.31- 2.74). We estimated that 23.9% of any pregnancy complication was attributable to maternal overweight/obesity and 31.6% of large for gestational age infants was attributable to excessive gestational weight gain.ConclusionsMaternal pre-pregnancy BMI and gestational weight gain are, across their full ranges, associated with risks of pregnancy complications. Obese mothers with high gestational weight gain are at the highest risk of pregnancy complications. Promoting a healthy pre-pregnancy BMI and gestational weight gain may reduce the burden of pregnancy complications and ultimately the risk of maternal and neonatal morbidity.Tweetable abstractPromoting a healthy body mass index and gestational weight gain might reduce the population burden of pregnancy complications.
Published: 2019

2. Autism risk associated with parental age and with increasing difference in age between the parents

Author: Sandin, S, Schendel, D, Magnusson, P, Hultman, C, Surén, P, Susser, E, Grønborg, T, Gissler, M, Gunnes, N, Gross, R, Henning, M, Bresnahan, M, Sourander, A, Hornig, M, Carter, K, Francis, R, Parner, E, Leonard, H, Rosanoff, M, Stoltenberg, C, and Reichenberg, A
Published: 2016
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3. Within-sibship genome-wide association analyses decrease bias in estimates of direct genetic effects

Author: Howe, LJ, Nivard, MG, Morris, TT, Hansen, AF, Rasheed, H, Cho, Y, Chittoor, G, Ahlskog, R, Lind, PA, Palviainen, T, van der Zee, MD, Cheesman, R, Mangino, M, Wang, Y, Li, S, Klaric, L, Ratliff, SM, Bielak, LF, Nygaard, M, Giannelis, A, Willoughby, EA, Reynolds, CA, Balbona, JV, Andreassen, OA, Ask, H, Baras, A, Bauer, CR, Boomsma, DI, Campbell, A, Campbell, H, Chen, Z, Christofidou, P, Corfield, E, Dahm, CC, Dokuru, DR, Evans, LM, de Geus, EJC, Giddaluru, S, Gordon, SD, Harden, KP, Hill, WD, Hughes, A, Kerr, SM, Kim, Y, Kweon, H, Latvala, A, Lawlor, DA, Li, L, Lin, K, Magnus, P, Magnusson, PKE, Mallard, TT, Martikainen, P, Mills, MC, Njolstad, PR, Overton, JD, Pedersen, NL, Porteous, DJ, Reid, J, Silventoinen, K, Southey, MC, Stoltenberg, C, Tucker-Drob, EM, Wright, MJ, Hewitt, JK, Keller, MC, Stallings, MC, Lee, JJ, Christensen, K, Kardia, SLR, Peyser, PA, Smith, JA, Wilson, JF, Hopper, JL, Hagg, S, Spector, TD, Pingault, J-B, Plomin, R, Havdahl, A, Bartels, M, Martin, NG, Oskarsson, S, Justice, AE, Millwood, IY, Hveem, K, Naess, O, Willer, CJ, Asvold, BO, Koellinger, PD, Kaprio, J, Medland, SE, Walters, RG, Benjamin, DJ, Turley, P, Evans, DM, Smith, GD, Hayward, C, Brumpton, B, Hemani, G, Davies, NM, Howe, LJ, Nivard, MG, Morris, TT, Hansen, AF, Rasheed, H, Cho, Y, Chittoor, G, Ahlskog, R, Lind, PA, Palviainen, T, van der Zee, MD, Cheesman, R, Mangino, M, Wang, Y, Li, S, Klaric, L, Ratliff, SM, Bielak, LF, Nygaard, M, Giannelis, A, Willoughby, EA, Reynolds, CA, Balbona, JV, Andreassen, OA, Ask, H, Baras, A, Bauer, CR, Boomsma, DI, Campbell, A, Campbell, H, Chen, Z, Christofidou, P, Corfield, E, Dahm, CC, Dokuru, DR, Evans, LM, de Geus, EJC, Giddaluru, S, Gordon, SD, Harden, KP, Hill, WD, Hughes, A, Kerr, SM, Kim, Y, Kweon, H, Latvala, A, Lawlor, DA, Li, L, Lin, K, Magnus, P, Magnusson, PKE, Mallard, TT, Martikainen, P, Mills, MC, Njolstad, PR, Overton, JD, Pedersen, NL, Porteous, DJ, Reid, J, Silventoinen, K, Southey, MC, Stoltenberg, C, Tucker-Drob, EM, Wright, MJ, Hewitt, JK, Keller, MC, Stallings, MC, Lee, JJ, Christensen, K, Kardia, SLR, Peyser, PA, Smith, JA, Wilson, JF, Hopper, JL, Hagg, S, Spector, TD, Pingault, J-B, Plomin, R, Havdahl, A, Bartels, M, Martin, NG, Oskarsson, S, Justice, AE, Millwood, IY, Hveem, K, Naess, O, Willer, CJ, Asvold, BO, Koellinger, PD, Kaprio, J, Medland, SE, Walters, RG, Benjamin, DJ, Turley, P, Evans, DM, Smith, GD, Hayward, C, Brumpton, B, Hemani, G, and Davies, NM
Abstract: Estimates from genome-wide association studies (GWAS) of unrelated individuals capture effects of inherited variation (direct effects), demography (population stratification, assortative mating) and relatives (indirect genetic effects). Family-based GWAS designs can control for demographic and indirect genetic effects, but large-scale family datasets have been lacking. We combined data from 178,086 siblings from 19 cohorts to generate population (between-family) and within-sibship (within-family) GWAS estimates for 25 phenotypes. Within-sibship GWAS estimates were smaller than population estimates for height, educational attainment, age at first birth, number of children, cognitive ability, depressive symptoms and smoking. Some differences were observed in downstream SNP heritability, genetic correlations and Mendelian randomization analyses. For example, the within-sibship genetic correlation between educational attainment and body mass index attenuated towards zero. In contrast, analyses of most molecular phenotypes (for example, low-density lipoprotein-cholesterol) were generally consistent. We also found within-sibship evidence of polygenic adaptation on taller height. Here, we illustrate the importance of family-based GWAS data for phenotypes influenced by demographic and indirect genetic effects.
Published: 2022

4. The Autism Birth Cohort: a paradigm for gene–environment–timing research

Author: Stoltenberg, C, Schjølberg, S, Bresnahan, M, Hornig, M, Hirtz, D, Dahl, C, Lie, K K, Reichborn-Kjennerud, T, Schreuder, P, Alsaker, E, Øyen, A-S, Magnus, P, Surén, P, Susser, E, and Lipkin, W I
Published: 2010
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5. Degree of fetal growth restriction associated with schizophrenia risk in a national cohort

Author: Eide, M. G., Moster, D., Irgens, L. M., Reichborn-Kjennerud, T., Stoltenberg, C., Skjærven, R., Susser, E., and Abel, K.
Published: 2013

6. Remission, continuation and incidence of eating disorders during early pregnancy: a validation study in a population-based birth cohort

Author: Watson, H. J., Von Holle, A., Hamer, R. M., Berg, C. Knoph, Torgersen, L., Magnus, P., Stoltenberg, C., Sullivan, P., Reichborn-Kjennerud, T., and Bulik, C. M.
Published: 2013

7. The effect of recurrent miscarriage and infertility on the risk of pre-eclampsia

Author: Trogstad, L, Magnus, P, Moffett, A, and Stoltenberg, C
Published: 2009

8. Changes in parental smoking during pregnancy and risks of adverse birth outcomes and childhood overweight in Europe and North America: An individual participant data meta-analysis of 229,000 singleton births

Author: Philips, E.M. Santos, S. Trasande, L. Aurrekoetxea, J.J. Barros, H. von Berg, A. Bergström, A. Bird, P.K. Brescianini, S. Chaoimh, C.N. Charles, M.-A. Chatzi, L. Chevrier, C. Chrousos, G.P. Costet, N. Criswell, R. Crozier, S. Eggesbø, M. Fantini, M.P. Farchi, S. Forastiere, F. van Gelder, M.M.H.J. Georgiu, V. Godfrey, K.M. Gori, D. Hanke, W. Heude, B. Hryhorczuk, D. Iñiguez, C. Inskip, H. Karvonen, A.M. Kenny, L.C. Kull, I. Lawlor, D.A. Lehmann, I. Magnus, P. Manios, Y. Melén, E. Mommers, M. Morgen, C.S. Moschonis, G. Murray, D. Nohr, E.A. Nybo Andersen, A.-M. Oken, E. Oostvogels, A.J.J.M. Papadopoulou, E. Pekkanen, J. Pizzi, C. Polanska, K. Porta, D. Richiardi, L. Rifas-Shiman, S.L. Roeleveld, N. Rusconi, F. Santos, A.C. Sørensen, T.I.A. Standl, M. Stoltenberg, C. Sunyer, J. Thiering, E. Thijs, C. Torrent, M. Vrijkotte, T.G.M. Wright, J. Zvinchuk, O. Gaillard, R. Jaddoe, V.W.V.
Abstract: Background Fetal smoke exposure is a common and key avoidable risk factor for birth complications and seems to influence later risk of overweight. It is unclear whether this increased risk is also present if mothers smoke during the first trimester only or reduce the number of cigarettes during pregnancy, or when only fathers smoke. We aimed to assess the associations of parental smoking during pregnancy, specifically of quitting or reducing smoking and maternal and paternal smoking combined, with preterm birth, small size for gestational age, and childhood overweight. Methods and findings We performed an individual participant data meta-analysis among 229,158 families from 28 pregnancy/birth cohorts from Europe and North America. All 28 cohorts had information on maternal smoking, and 16 also had information on paternal smoking. In total, 22 cohorts were population-based, with birth years ranging from 1991 to 2015. The mothers’ median age was 30.0 years, and most mothers were medium or highly educated. We used multilevel binary logistic regression models adjusted for maternal and paternal sociodemographic and lifestyle-related characteristics. Compared with nonsmoking mothers, maternal first trimester smoking only was not associated with adverse birth outcomes but was associated with a higher risk of childhood overweight (odds ratio [OR] 1.17 [95% CI 1.02–1.35], P value = 0.030). Children from mothers who continued smoking during pregnancy had higher risks of preterm birth (OR 1.08 [95% CI 1.02–1.15], P value = 0.012), small size for gestational age (OR 2.15 [95% CI 2.07–2.23], P value < 0.001), and childhood overweight (OR 1.42 [95% CI 1.35–1.48], P value < 0.001). Mothers who reduced the number of cigarettes between the first and third trimester, without quitting, still had a higher risk of small size for gestational age. However, the corresponding risk estimates were smaller than for women who continued the same amount of cigarettes throughout pregnancy (OR 1.89 [95% CI 1.52–2.34] instead of OR 2.20 [95% CI 2.02–2.42] when reducing from 5–9 to ≤4 cigarettes/day; OR 2.79 [95% CI 2.39–3.25] and OR 1.93 [95% CI 1.46–2.57] instead of OR 2.95 [95% CI 2.75–3.15] when reducing from ≥10 to 5–9 and ≤4 cigarettes/day, respectively [P values < 0.001]). Reducing the number of cigarettes during pregnancy did not affect the risks of preterm birth and childhood overweight. Among nonsmoking mothers, paternal smoking was associated with childhood overweight (OR 1.21 [95% CI 1.16–1.27], P value < 0.001) but not with adverse birth outcomes. Limitations of this study include the self-report of parental smoking information and the possibility of residual confounding. As this study only included participants from Europe and North America, results need to be carefully interpreted regarding other populations. Conclusions We observed that as compared to nonsmoking during pregnancy, quitting smoking in the first trimester is associated with the same risk of preterm birth and small size for gestational age, but with a higher risk of childhood overweight. Reducing the number of cigarettes, without quitting, has limited beneficial effects. Paternal smoking seems to be associated, independently of maternal smoking, with the risk of childhood overweight. Population strategies should focus on parental smoking prevention before or at the start, rather than during, pregnancy. © 2020 Philips et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Published: 2020

9. Changes in parental smoking during pregnancy and risks of adverse birth outcomes and childhood overweight in Europe and North America

Author: Philips, E.M. (Elise), Santos, S.M.S. (Susana), Trasande, L. (Leonardo), Aurrekoetxea, J.J. (Juan José), Barros, A.I. (Ana), Berg, A. (Andrea) von, Bergström, A. (Anna), Bird, P.K. (Philippa K.), Brescianini, S. (Sonia), Ní Chaoimh, C. (Carol), Charles, M.A., Chatzi, L. (Leda), Chevrier, C. (Cécile), Chrousos, G.P., Costet, N. (Nathalie), Criswell, R. (Rachel), Crozier, S. (Sarah), Eggesbø, M. (Merete), Fantini, M.P. (Maria), Farchi, S. (Sara), Forastiere, F. (Francesco), van Gelder, M.M.H.J. (Marleen M H J), Georgiu, V. (Vagelis), Godfrey, N., Gori, D. (Davide), Hanke, W. (Wojciech), Heude, B. (Barbara), Hryhorczuk, D.O. (Daniel), Iñiguez, C. (Carmen), Inskip, H.M. (Hazel), Karvonen, S.L., Kenny, L.C. (Louise C.), Kull, C.A. (Christian), Lawlor, D.A. (Debbie), Lehmann, I. (Irina), Magnus, P. (Per), Manios, Y., Melén, E. (Erik), Mommers, M. (Monique), Morgen, C.S. (Camilla S.), Moschonis, G. (George), Murray, D. (Deirdre), Nohr, C. (Christian), Nybo Andersen, A.-M. (Anne-Marie), Oken, E. (Emily), Oostvogels, A.J.J.M. (Adriëtte J J M), Papadopoulou, E. (Eleni), Pekkanen, J. (Juha), Pizzi, C. (Costanza), Polanska, K. (Kinga), Porta, D. (Daniela), Richiardi, L. (Lorenzo), Rifas-Shiman, S.L. (Sheryl), Roeleveld, N. (Nel), Rusconi, F. (Franca), Santos, A.C. (Ana Cristina), Sørensen, T.I.A. (Thorkild), Standl, M. (Marie), Stoltenberg, C. (Camilla), Sunyer, J. (Jordi), Thiering, E. (Elisabeth), Thijs, C. (Carel), Torrent, M. (Maties), Vrijkotte, T.G.M. (Tanja), Wright, J. (John), Zvinchuk, O. (Oleksandr), Gaillard, R. (Romy), Jaddoe, V.W.V. (Vincent), Philips, E.M. (Elise), Santos, S.M.S. (Susana), Trasande, L. (Leonardo), Aurrekoetxea, J.J. (Juan José), Barros, A.I. (Ana), Berg, A. (Andrea) von, Bergström, A. (Anna), Bird, P.K. (Philippa K.), Brescianini, S. (Sonia), Ní Chaoimh, C. (Carol), Charles, M.A., Chatzi, L. (Leda), Chevrier, C. (Cécile), Chrousos, G.P., Costet, N. (Nathalie), Criswell, R. (Rachel), Crozier, S. (Sarah), Eggesbø, M. (Merete), Fantini, M.P. (Maria), Farchi, S. (Sara), Forastiere, F. (Francesco), van Gelder, M.M.H.J. (Marleen M H J), Georgiu, V. (Vagelis), Godfrey, N., Gori, D. (Davide), Hanke, W. (Wojciech), Heude, B. (Barbara), Hryhorczuk, D.O. (Daniel), Iñiguez, C. (Carmen), Inskip, H.M. (Hazel), Karvonen, S.L., Kenny, L.C. (Louise C.), Kull, C.A. (Christian), Lawlor, D.A. (Debbie), Lehmann, I. (Irina), Magnus, P. (Per), Manios, Y., Melén, E. (Erik), Mommers, M. (Monique), Morgen, C.S. (Camilla S.), Moschonis, G. (George), Murray, D. (Deirdre), Nohr, C. (Christian), Nybo Andersen, A.-M. (Anne-Marie), Oken, E. (Emily), Oostvogels, A.J.J.M. (Adriëtte J J M), Papadopoulou, E. (Eleni), Pekkanen, J. (Juha), Pizzi, C. (Costanza), Polanska, K. (Kinga), Porta, D. (Daniela), Richiardi, L. (Lorenzo), Rifas-Shiman, S.L. (Sheryl), Roeleveld, N. (Nel), Rusconi, F. (Franca), Santos, A.C. (Ana Cristina), Sørensen, T.I.A. (Thorkild), Standl, M. (Marie), Stoltenberg, C. (Camilla), Sunyer, J. (Jordi), Thiering, E. (Elisabeth), Thijs, C. (Carel), Torrent, M. (Maties), Vrijkotte, T.G.M. (Tanja), Wright, J. (John), Zvinchuk, O. (Oleksandr), Gaillard, R. (Romy), and Jaddoe, V.W.V. (Vincent)
Abstract: BACKGROUND: Fetal smoke exposure is a common and key avoidable risk factor for birth complications and seems to influence later risk of overweight. It is unclear whether this increased risk is also present if mothers smoke during the first trimester only or reduce the number of cigarettes during pregnancy, or when only fathers smoke. We aimed to assess the associations of parental smoking during pregnancy, specifically of quitting or reducing smoking and maternal and paternal smoking combined, with preterm birth, small size for gestational age, and childhood overweight. METHODS AND FINDINGS: We performed an individual participant data meta-analysis among 229,158 families from 28 pregnancy/birth cohorts from Europe and North America. All 28 cohorts had information on maternal smoking, and 16 also had information on paternal smoking. In total, 22 cohorts were population-based, with birth years ranging from 1991 to 2015. The mothers' median age was 30.0 years, and most mothers were medium or highly educated. We used multilevel binary logistic regression models adjusted for maternal and paternal sociodemographic and lifestyle-related characteristics. Compared with nonsmoking mothers, maternal first trimester smoking only was not associated with adverse birth outcomes but was associated with a higher risk of childhood overweight (odds ratio [OR] 1.17 [95% CI 1.02-1.35], P value = 0.030). Children from mothers who continued smoking during pregnancy had higher risks of preterm birth (OR 1.08 [95% CI 1.02-1.15], P value = 0.012), small size for gestational age (OR 2.15 [95% CI 2.07-2.23], P value < 0.001), and childhood overweight (OR 1.42 [95% CI 1.35-1.48], P value < 0.001). Mothers who reduced the number of cigarettes between the first and third trimester, without quitting, still had a higher risk of small size for gestational age. However, the corresponding risk estimates were smaller than for women who continued the same amount of cigarettes throughout pregnancy (OR 1.
Published: 2020
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10. Parental occupational exposure to pesticides, animals and organic dust and risk of childhood leukemia and central nervous system tumors: Findings from the International Childhood Cancer Cohort Consortium (I4C)

Author: Patel, DM, Jones, RR, Booth, BJ, Olsson, AC, Kromhout, H, Straif, K, Vermeulen, R, Tikellis, G, Paltiel, O, Golding, J, Northstone, K, Stoltenberg, C, Haberg, SE, Schuz, J, Friesen, MC, Ponsonby, A-L, Lemeshow, S, Linet, MS, Magnus, P, Olsen, J, Olsen, SF, Dwyer, T, Stayner, LT, Ward, MH, Patel, DM, Jones, RR, Booth, BJ, Olsson, AC, Kromhout, H, Straif, K, Vermeulen, R, Tikellis, G, Paltiel, O, Golding, J, Northstone, K, Stoltenberg, C, Haberg, SE, Schuz, J, Friesen, MC, Ponsonby, A-L, Lemeshow, S, Linet, MS, Magnus, P, Olsen, J, Olsen, SF, Dwyer, T, Stayner, LT, and Ward, MH
Abstract: Parental occupational exposures to pesticides, animals and organic dust have been associated with an increased risk of childhood cancer based mostly on case-control studies. We prospectively evaluated parental occupational exposures and risk of childhood leukemia and central nervous system (CNS) tumors in the International Childhood Cancer Cohort Consortium. We pooled data on 329,658 participants from birth cohorts in five countries (Australia, Denmark, Israel, Norway and United Kingdom). Parental occupational exposures during pregnancy were estimated by linking International Standard Classification of Occupations-1988 job codes to the ALOHA+ job exposure matrix. Risk of childhood (<15 years) acute lymphoblastic leukemia (ALL; n = 129), acute myeloid leukemia (AML; n = 31) and CNS tumors (n = 158) was estimated using Cox proportional hazards models to generate hazard ratios (HR) and 95% confidence intervals (CI). Paternal exposures to pesticides and animals were associated with increased risk of childhood AML (herbicides HR = 3.22, 95% CI = 0.97-10.68; insecticides HR = 2.86, 95% CI = 0.99-8.23; animals HR = 3.89, 95% CI = 1.18-12.90), but not ALL or CNS tumors. Paternal exposure to organic dust was positively associated with AML (HR = 2.38 95% CI = 1.12-5.07), inversely associated with ALL (HR = 0.55, 95% CI = 0.31-0.99) and not associated with CNS tumors. Low exposure prevalence precluded evaluation of maternal pesticide and animal exposures; we observed no significant associations with organic dust exposure. This first prospective analysis of pooled birth cohorts and parental occupational exposures provides evidence for paternal agricultural exposures as childhood AML risk factors. The different risks for childhood ALL associated with maternal and paternal organic dust exposures should be investigated further.
Published: 2020

11. Changes in parental smoking during pregnancy and risks of adverse birth outcomes and childhood overweight in Europe and North America: An individual participant data meta-analysis of 229,000 singleton births

Author: Philips, E.M., Santos, S., Trasande, L., Aurrekoetxea, J.J., Barros, H., von Berg, A., Bergström, A., Bird, P.K., Brescianini, S., Ní Chaoimh, C., Charles, M.-A., Chatzi, L., Chevrier, C., Chrousos, G.P., Costet, N., Criswell, R., Crozier, S., Eggesbø, M., Fantini, M.P., Farchi, S., Forastiere, F., van Gelder, M.M.H.J., Georgiu, V., Godfrey, K.M., Gori, D., Hanke, W., Heude, B., Hryhorczuk, D., Iñiguez, C., Inskip, H., Karvonen, A.M., Kenny, L.C., Kull, I., Lawlor, D.A., Lehmann, Irina, Magnus, P., Manios, Y., Melén, E., Mommers, M., Morgen, C.S., Moschonis, G., Murray, D., Nohr, E.A., Nybo Andersen, A.-M., Oken, E., Oostvogels, A.J.J.M., Papadopoulou, E., Pekkanen, J., Pizzi, C., Polanska, K., Porta, D., Richiardi, L., Rifas‐Shiman, S.L., Roeleveld, N., Rusconi, F., Santos, A.C., Sørensen, T.I.A., Standl, M., Stoltenberg, C., Sunyer, J., Thiering, E., Thijs, C., Torrent, M., Vrijkotte, T.G.M., Wright, J., Zvinchuk, O., Gaillard, R., Jaddoe, V.W.V., Philips, E.M., Santos, S., Trasande, L., Aurrekoetxea, J.J., Barros, H., von Berg, A., Bergström, A., Bird, P.K., Brescianini, S., Ní Chaoimh, C., Charles, M.-A., Chatzi, L., Chevrier, C., Chrousos, G.P., Costet, N., Criswell, R., Crozier, S., Eggesbø, M., Fantini, M.P., Farchi, S., Forastiere, F., van Gelder, M.M.H.J., Georgiu, V., Godfrey, K.M., Gori, D., Hanke, W., Heude, B., Hryhorczuk, D., Iñiguez, C., Inskip, H., Karvonen, A.M., Kenny, L.C., Kull, I., Lawlor, D.A., Lehmann, Irina, Magnus, P., Manios, Y., Melén, E., Mommers, M., Morgen, C.S., Moschonis, G., Murray, D., Nohr, E.A., Nybo Andersen, A.-M., Oken, E., Oostvogels, A.J.J.M., Papadopoulou, E., Pekkanen, J., Pizzi, C., Polanska, K., Porta, D., Richiardi, L., Rifas‐Shiman, S.L., Roeleveld, N., Rusconi, F., Santos, A.C., Sørensen, T.I.A., Standl, M., Stoltenberg, C., Sunyer, J., Thiering, E., Thijs, C., Torrent, M., Vrijkotte, T.G.M., Wright, J., Zvinchuk, O., Gaillard, R., and Jaddoe, V.W.V.
Abstract: Background Fetal smoke exposure is a common and key avoidable risk factor for birth complications and seems to influence later risk of overweight. It is unclear whether this increased risk is also present if mothers smoke during the first trimester only or reduce the number of cigarettes during pregnancy, or when only fathers smoke. We aimed to assess the associations of parental smoking during pregnancy, specifically of quitting or reducing smoking and maternal and paternal smoking combined, with preterm birth, small size for gestational age, and childhood overweight. Methods and findings We performed an individual participant data meta-analysis among 229,158 families from 28 pregnancy/birth cohorts from Europe and North America. All 28 cohorts had information on maternal smoking, and 16 also had information on paternal smoking. In total, 22 cohorts were population-based, with birth years ranging from 1991 to 2015. The mothers’ median age was 30.0 years, and most mothers were medium or highly educated. We used multilevel binary logistic regression models adjusted for maternal and paternal sociodemographic and lifestyle-related characteristics. Compared with nonsmoking mothers, maternal first trimester smoking only was not associated with adverse birth outcomes but was associated with a higher risk of childhood overweight (odds ratio [OR] 1.17 [95% CI 1.02–1.35], P value = 0.030). Children from mothers who continued smoking during pregnancy had higher risks of preterm birth (OR 1.08 [95% CI 1.02–1.15], P value = 0.012), small size for gestational age (OR 2.15 [95% CI 2.07–2.23], P value < 0.001), and childhood overweight (OR 1.42 [95% CI 1.35–1.48], P value < 0.001). Mothers who reduced the number of cigarettes between the first and third trimester, without quitting, still had a higher risk of small size for gestational age. However, the corresponding risk estimates were smaller than for women who continued the same amount of cigarettes throughout preg
Published: 2020

12. Diet and vitamin D status among pregnant Pakistani women in Oslo

Author: Henriksen, C., Brunvand, L., Stoltenberg, C., Trygg, K., Haug, E., and Pedersen, J.I.
Subjects: Pakistanis in foreign countries -- Health aspects, Pregnant women -- Physiological aspects, Vitamin D deficiency -- Analysis, Norway -- Health aspects
Abstract: A comparative study of the diet and nutritional status of 38 pregnant Pakistani immigrant women and equal numbers of Norwegian pregnant women in Oslo, Norway, revealed lack of exposure to the sun and deficient vitamin D intake as the main causes of vitamin D deficiency in the Pakistani women. While the serum levels of 25-hydroxy-vitamin D3 was lower than prescribed safe levels, the serum parathyroid hormone quantity was considerably higher than desired in the immigrant women.
Published: 1995

13. Back-neck pain and symptoms of anxiety and depression: a population-based twin study

Author: REICHBORN-KJENNERUD, T., STOLTENBERG, C., TAMBS, K., ROYSAMB, E., KRINGLEN, E., TORGERSEN, S., and HARRIS, J. R.
Published: 2002

14. Impact of maternal body mass index and gestational weight gain on pregnancy complications: an individual participant data meta-analysis of European, North American and Australian cohorts

Author: Santos, S. Voerman, E. Amiano, P. Barros, H. Beilin, L.J. Bergström, A. Charles, M.-A. Chatzi, L. Chevrier, C. Chrousos, G.P. Corpeleijn, E. Costa, O. Costet, N. Crozier, S. Devereux, G. Doyon, M. Eggesbø, M. Fantini, M.P. Farchi, S. Forastiere, F. Georgiu, V. Godfrey, K.M. Gori, D. Grote, V. Hanke, W. Hertz-Picciotto, I. Heude, B. Hivert, M.-F. Hryhorczuk, D. Huang, R.-C. Inskip, H. Karvonen, A.M. Kenny, L.C. Koletzko, B. Küpers, L.K. Lagström, H. Lehmann, I. Magnus, P. Majewska, R. Mäkelä, J. Manios, Y. McAuliffe, F.M. McDonald, S.W. Mehegan, J. Melén, E. Mommers, M. Morgen, C.S. Moschonis, G. Murray, D. Ní Chaoimh, C. Nohr, E.A. Nybo Andersen, A.-M. Oken, E. Oostvogels, A.J.J.M. Pac, A. Papadopoulou, E. Pekkanen, J. Pizzi, C. Polanska, K. Porta, D. Richiardi, L. Rifas-Shiman, S.L. Roeleveld, N. Ronfani, L. Santos, A.C. Standl, M. Stigum, H. Stoltenberg, C. Thiering, E. Thijs, C. Torrent, M. Tough, S.C. Trnovec, T. Turner, S. van Gelder, M.M.H.J. van Rossem, L. von Berg, A. Vrijheid, M. Vrijkotte, T.G.M. West, J. Wijga, A.H. Wright, J. Zvinchuk, O. Sørensen, T.I.A. Lawlor, D.A. Gaillard, R. Jaddoe, V.W.V.
Abstract: Objective: To assess the separate and combined associations of maternal pre-pregnancy body mass index (BMI) and gestational weight gain with the risks of pregnancy complications and their population impact. Design: Individual participant data meta-analysis of 39 cohorts. Setting: Europe, North America, and Oceania. Population: 265 270 births. Methods: Information on maternal pre-pregnancy BMI, gestational weight gain, and pregnancy complications was obtained. Multilevel binary logistic regression models were used. Main outcome measures: Gestational hypertension, pre-eclampsia, gestational diabetes, preterm birth, small and large for gestational age at birth. Results: Higher maternal pre-pregnancy BMI and gestational weight gain were, across their full ranges, associated with higher risks of gestational hypertensive disorders, gestational diabetes, and large for gestational age at birth. Preterm birth risk was higher at lower and higher BMI and weight gain. Compared with normal weight mothers with medium gestational weight gain, obese mothers with high gestational weight gain had the highest risk of any pregnancy complication (odds ratio 2.51, 95% CI 2.31– 2.74). We estimated that 23.9% of any pregnancy complication was attributable to maternal overweight/obesity and 31.6% of large for gestational age infants was attributable to excessive gestational weight gain. Conclusions: Maternal pre-pregnancy BMI and gestational weight gain are, across their full ranges, associated with risks of pregnancy complications. Obese mothers with high gestational weight gain are at the highest risk of pregnancy complications. Promoting a healthy pre-pregnancy BMI and gestational weight gain may reduce the burden of pregnancy complications and ultimately the risk of maternal and neonatal morbidity. Tweetable abstract: Promoting a healthy body mass index and gestational weight gain might reduce the population burden of pregnancy complications. © 2019 Royal College of Obstetricians and Gynaecologists
Published: 2019

15. Discovery of the first genome-wide significant risk loci for attention deficit/hyperactivity disorder

Author: Demontis, D, Walters, R, Martin, J, Mattheisen, M, Als, T, Agerbo, E, Baldursson, G, Belliveau, R, Bybjerg-Grauholm, J, Baekvad-Hansen, M, Cerrato, F, Chambert, K, Churchhouse, C, Dumont, A, Eriksson, N, Gandal, M, Goldstein, J, Grasby, K, Grove, J, Gudmundsson, O, Hansen, C, Hauberg, M, Hollegaard, M, Howrigan, D, Huang, H, Maller, J, Martin, A, Martin, N, Moran, J, Pallesen, J, Palmer, D, Pedersen, C, Pedersen, M, Poterba, T, Poulsen, J, Ripke, S, Robinson, E, Satterstrom, F, Stefansson, H, Stevens, C, Turley, P, Walters, G, Won, H, Wright, M, Andreassen, O, Asherson, P, Burton, C, Boomsma, D, Cormand, B, Dalsgaard, S, Franke, B, Gelernter, J, Geschwind, D, Hakonarson, H, Haavik, J, Kranzler, H, Kuntsi, J, Langley, K, Lesch, K, Middeldorp, C, Reif, A, Rohde, L, Roussos, P, Schachar, R, Sklar, P, Sonuga-Barke, E, Sullivan, P, Thapar, A, Tung, J, Waldman, I, Medland, S, Stefansson, K, Nordentoft, M, Hougaard, D, Werge, T, Mors, O, Mortensen, P, Daly, M, Faraone, S, Borglum, A, Neale, B, Albayrak, O, Anney, R, Arranz, M, Banaschewski, T, Bau, C, Biederman, J, Buitelaar, J, Casas, M, Charach, A, Crosbie, J, Dempfle, A, Doyle, A, Ebstein, R, Elia, J, Freitag, C, Focker, M, Gill, M, Grevet, E, Hawi, Z, Hebebrand, J, Herpertz-Dahlmann, B, Hervas, A, Hinney, A, Hohmann, S, Holmans, P, Hutz, M, Ickowitz, A, Johansson, S, Kent, L, Kittel-Schneider, S, Lambregts-Rommelse, N, Lehmkuhl, G, Loo, S, McGough, J, Meyer, J, Mick, E, Middletion, F, Miranda, A, Mota, N, Mulas, F, Mulligan, A, Nelson, F, Nguyen, T, Oades, R, O'Donovan, M, Owen, M, Palmason, H, Ramos-Quiroga, J, Renner, T, Ribases, M, Rietschel, M, Rivero, O, Romanos, J, Romanos, M, Rothenberger, A, Royers, H, Sanchez-Mora, C, Scherag, A, Schimmelmann, B, Schafer, H, Sergeant, J, Sinzig, J, Smalley, S, Steinhausen, H, Thompson, M, Todorov, A, Vasquez, A, Walitza, S, Wang, Y, Warnke, A, Williams, N, Witt, S, Yang, L, Zayats, T, Zhang-James, Y, Smith, G, Davies, G, Ehli, E, Evans, D, Fedko, I, Greven, C, Groen-Blokhuis, M, Guxens, M, Hammerschlag, A, Hartman, C, Heinrich, J, Hottenga, J, Hudziak, J, Jugessur, A, Kemp, J, Krapohl, E, Murcia, M, Myhre, R, Nolte, I, Nyholt, D, Ormel, J, Ouwens, K, Pappa, I, Pennell, C, Plomin, R, Ring, S, Standl, M, Stergiakouli, E, St Pourcain, B, Stoltenberg, C, Sunyer, J, Thiering, E, Tiemeier, H, Tiesler, C, Timpson, N, Trzaskowski, M, van der Most, P, Vilor-Tejedor, N, Wang, C, Whitehouse, A, Zhao, H, Agee, M, Alipanahi, B, Auton, A, Bell, R, Bryc, K, Elson, S, Fontanillas, P, Furlotte, N, Hinds, D, Hromatka, B, Huber, K, Kleinman, A, Litterman, N, McIntyre, M, Mountain, J, Northover, C, Pitts, S, Sathirapongsasuti, J, Sazonova, O, Shelton, J, Shringarpure, S, Tian, C, Vacic, V, Wilson, C, ADHD Working Grp Psychiat Genomics, Early Lifecourse Genetic, 23andMe Res Team, Institute for Molecular Medicine Finland, Centre of Excellence in Complex Disease Genetics, Psychiatrie & Neuropsychologie, RS: MHeNs - R3 - Neuroscience, Psychiatry, ADHD Working Group of the Psychiatric Genomics Consortium (PGC), 23andme Research Team, University of St Andrews. Cellular Medicine Division, University of St Andrews. Institute of Behavioural and Neural Sciences, University of St Andrews. School of Medicine, Child and Adolescent Psychiatry / Psychology, Erasmus MC other, Interdisciplinary Centre Psychopathology and Emotion regulation (ICPE), Life Course Epidemiology (LCE), Clinical Neuropsychology, Biological Psychology, APH - Health Behaviors & Chronic Diseases, APH - Mental Health, Amsterdam Neuroscience - Mood, Anxiety, Psychosis, Stress & Sleep, APH - Personalized Medicine, Clinical Child and Family Studies, LEARN! - Child rearing, and APH - Methodology
Subjects: Netherlands Twin Register (NTR), Male, Trastorns per dèficit d'atenció amb hiperactivitat en els infants, LD SCORE REGRESSION, Medizin, Genome-wide association study, US CHILDREN, Genoma humà, Attention deficit disorder with hyperactivity in children, Medical and Health Sciences, Cohort Studies, 0302 clinical medicine, 2.1 Biological and endogenous factors, POLYGENIC RISK, Aetiology, Child, IDENTIFIES 11, SEXUAL-BEHAVIOR, Early Lifecourse & Genetic Epidemiology (EAGLE) Consortium, Pediatric, 0303 health sciences, education.field_of_study, Genome, Genetic Predisposition to Disease/genetics, 1184 Genetics, developmental biology, physiology, Brain, 3rd-DAS, Single Nucleotide, Biological Sciences, Polymorphism, Single Nucleotide/genetics, 3. Good health, Mental Health, Meta-analysis, Child, Preschool, Genetic Loci/genetics, Genome-Wide Association Study/methods, Trastorns per dèficit d'atenció amb hiperactivitat en els adults, Attention Deficit Disorder (ADD), Female, Attention Deficit Disorder with Hyperactivity/genetics, RC0321 Neuroscience. Biological psychiatry. Neuropsychiatry, SDG 4 - Quality Education, Clinical psychology, Risk, Adolescent, DEFICIT HYPERACTIVITY DISORDER, Concordance, Population, PROVIDES INSIGHTS, QH426 Genetics, Biology, Quantitative trait locus, Brain/physiology, Polymorphism, Single Nucleotide, 23andMe Research Team, behavioral disciplines and activities, Gene Expression Regulation/genetics, Article, 150 000 MR Techniques in Brain Function, GENETIC ARCHITECTURE, 03 medical and health sciences, All institutes and research themes of the Radboud University Medical Center, Clinical Research, Behavioral and Social Science, mental disorders, medicine, Genetics, Attention deficit hyperactivity disorder, Humans, Genetic Predisposition to Disease, Polymorphism, education, Preschool, QH426, 030304 developmental biology, Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7], ASSOCIATION METAANALYSIS, Prevention, Human Genome, Case-control study, MAJOR DEPRESSION, medicine.disease, Attention Deficit Hyperactivity Disorder (ADHD), Genetic architecture, Brain Disorders, ADHD Working Group of the Psychiatric Genomics Consortium, Gene Expression Regulation, Attention Deficit Disorder with Hyperactivity, Genetic Loci, RC0321, Attention deficit disorder with hyperactivity in adults, 3111 Biomedicine, 030217 neurology & neurosurgery, Genome-Wide Association Study, Developmental Biology
Abstract: Attention deficit/hyperactivity disorder (ADHD) is a highly heritable childhood behavioral disorder affecting 5% of children and 2.5% of adults. Common genetic variants contribute substantially to ADHD susceptibility, but no variants have been robustly associated with ADHD. We report a genome-wide association meta-analysis of 20,183 individuals diagnosed with ADHD and 35,191 controls that identifies variants surpassing genome-wide significance in 12 independent loci, finding important new information about the underlying biology of ADHD. Associations are enriched in evolutionarily constrained genomic regions and loss-of-function intolerant genes and around brain-expressed regulatory marks. Analyses of three replication studies: a cohort of individuals diagnosed with ADHD, a self-reported ADHD sample and a meta-analysis of quantitative measures of ADHD symptoms in the population, support these findings while highlighting study-specific differences on genetic overlap with educational attainment. Strong concordance with GWAS of quantitative population measures of ADHD symptoms supports that clinical diagnosis of ADHD is an extreme expression of continuous heritable traits. Postprint
Published: 2019
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16. Association of Gestational Weight Gain With Adverse Maternal and Infant Outcomes

Author: LifeCycle Project-Maternal Obesity Childhood Outcomes Study Group Voerman, E. Santos, S. Inskip, H. Amiano, P. Barros, H. Charles, M.-A. Chatzi, L. Chrousos, G.P. Corpeleijn, E. Crozier, S. Doyon, M. Eggesbø, M. Fantini, M.P. Farchi, S. Forastiere, F. Georgiu, V. Gori, D. Hanke, W. Hertz-Picciotto, I. Heude, B. Hivert, M.-F. Hryhorczuk, D. Iñiguez, C. Karvonen, A.M. Küpers, L.K. Lagström, H. Lawlor, D.A. Lehmann, I. Magnus, P. Majewska, R. Mäkelä, J. Manios, Y. Mommers, M. Morgen, C.S. Moschonis, G. Nohr, E.A. Nybo Andersen, A.-M. Oken, E. Pac, A. Papadopoulou, E. Pekkanen, J. Pizzi, C. Polanska, K. Porta, D. Richiardi, L. Rifas-Shiman, S.L. Roeleveld, N. Ronfani, L. Santos, A.C. Standl, M. Stigum, H. Stoltenberg, C. Thiering, E. Thijs, C. Torrent, M. Trnovec, T. van Gelder, M.M.H.J. van Rossem, L. von Berg, A. Vrijheid, M. Wijga, A. Zvinchuk, O. Sørensen, T.I.A. Godfrey, K. Jaddoe, V.W.V. Gaillard, R.
Abstract: Importance: Both low and high gestational weight gain have been associated with adverse maternal and infant outcomes, but optimal gestational weight gain remains uncertain and not well defined for all prepregnancy weight ranges. Objectives: To examine the association of ranges of gestational weight gain with risk of adverse maternal and infant outcomes and estimate optimal gestational weight gain ranges across prepregnancy body mass index categories. Design, Setting, and Participants: Individual participant-level meta-analysis using data from 196 670 participants within 25 cohort studies from Europe and North America (main study sample). Optimal gestational weight gain ranges were estimated for each prepregnancy body mass index (BMI) category by selecting the range of gestational weight gain that was associated with lower risk for any adverse outcome. Individual participant-level data from 3505 participants within 4 separate hospital-based cohorts were used as a validation sample. Data were collected between 1989 and 2015. The final date of follow-up was December 2015. Exposures: Gestational weight gain. Main Outcomes and Measures: The main outcome termed any adverse outcome was defined as the presence of 1 or more of the following outcomes: preeclampsia, gestational hypertension, gestational diabetes, cesarean delivery, preterm birth, and small or large size for gestational age at birth. Results: Of the 196 670 women (median age, 30.0 years [quartile 1 and 3, 27.0 and 33.0 years] and 40 937 were white) included in the main sample, 7809 (4.0%) were categorized at baseline as underweight (BMI
Published: 2019

17. Maternal body mass index, gestational weight gain, and the risk of overweight and obesity across childhood: An individual participant data meta-analysis

Author: Voerman, E. Santos, S. Golab, B.P. Amiano, P. Ballester, F. Barros, H. Bergström, A. Charles, M.-A. Chatzi, L. Chevrier, C. Chrousos, G.P. Corpeleijn, E. Costet, N. Crozier, S. Devereux, G. Eggesbø, M. Ekström, S. Fantini, M.P. Farchi, S. Forastiere, F. Georgiu, V. Godfrey, K.M. Gori, D. Grote, V. Hanke, W. Hertz-Picciotto, I. Heude, B. Hryhorczuk, D. Huang, R.-C. Inskip, H. Iszatt, N. Karvonen, A.M. Kenny, L.C. Koletzko, B. Küpers, L.K. Lagström, H. Lehmann, I. Magnus, P. Majewska, R. Mäkelä, J. Manios, Y. McAuliffe, F.M. McDonald, S.W. Mehegan, J. Mommers, M. Morgen, C.S. Mori, T.A. Moschonis, G. Murray, D. Chaoimh, C.N. Nohr, E.A. Andersen, A.-M.N. Oken, E. Oostvogels, A.J.J.M. Pac, A. Papadopoulou, E. Pekkanen, J. Pizzi, C. Polanska, K. Porta, D. Richiardi, L. Rifas-Shiman, S.L. Ronfani, L. Santos, A.C. Standl, M. Stoltenberg, C. Thiering, E. Thijs, C. Torrent, M. Tough, S.C. Trnovec, T. Turner, S. van Rossem, L. von Berg, A. Vrijheid, M. Vrijkotte, T.G.M. West, J. Wijga, A. Wright, J. Zvinchuk, O. Sørensen, T.I.A. Lawlor, D.A. Gaillard, R. Jaddoe, V.W.V. and Voerman, E. Santos, S. Golab, B.P. Amiano, P. Ballester, F. Barros, H. Bergström, A. Charles, M.-A. Chatzi, L. Chevrier, C. Chrousos, G.P. Corpeleijn, E. Costet, N. Crozier, S. Devereux, G. Eggesbø, M. Ekström, S. Fantini, M.P. Farchi, S. Forastiere, F. Georgiu, V. Godfrey, K.M. Gori, D. Grote, V. Hanke, W. Hertz-Picciotto, I. Heude, B. Hryhorczuk, D. Huang, R.-C. Inskip, H. Iszatt, N. Karvonen, A.M. Kenny, L.C. Koletzko, B. Küpers, L.K. Lagström, H. Lehmann, I. Magnus, P. Majewska, R. Mäkelä, J. Manios, Y. McAuliffe, F.M. McDonald, S.W. Mehegan, J. Mommers, M. Morgen, C.S. Mori, T.A. Moschonis, G. Murray, D. Chaoimh, C.N. Nohr, E.A. Andersen, A.-M.N. Oken, E. Oostvogels, A.J.J.M. Pac, A. Papadopoulou, E. Pekkanen, J. Pizzi, C. Polanska, K. Porta, D. Richiardi, L. Rifas-Shiman, S.L. Ronfani, L. Santos, A.C. Standl, M. Stoltenberg, C. Thiering, E. Thijs, C. Torrent, M. Tough, S.C. Trnovec, T. Turner, S. van Rossem, L. von Berg, A. Vrijheid, M. Vrijkotte, T.G.M. West, J. Wijga, A. Wright, J. Zvinchuk, O. Sørensen, T.I.A. Lawlor, D.A. Gaillard, R. Jaddoe, V.W.V.
Abstract: Background Maternal obesity and excessive gestational weight gain may have persistent effects on offspring fat development. However, it remains unclear whether these effects differ by severity of obesity, and whether these effects are restricted to the extremes of maternal body mass index (BMI) and gestational weight gain. We aimed to assess the separate and combined associations of maternal BMI and gestational weight gain with the risk of overweight/obesity throughout childhood, and their population impact. Methods and findings We conducted an individual participant data meta-analysis of data from 162,129 mothers and their children from 37 pregnancy and birth cohort studies from Europe, North America, and Australia. We assessed the individual and combined associations of maternal pre-pregnancy BMI and gestational weight gain, both in clinical categories and across their full ranges, with the risks of overweight/obesity in early (2.0–5.0 years), mid (5.0–10.0 years) and late childhood (10.0–18.0 years), using multilevel binary logistic regression models with a random intercept at cohort level adjusted for maternal sociodemographic and lifestyle-related characteristics. We observed that higher maternal pre-pregnancy BMI and gestational weight gain both in clinical categories and across their full ranges were associated with higher risks of childhood overweight/obesity, with the strongest effects in late childhood (odds ratios [ORs] for overweight/obesity in early, mid, and late childhood, respectively: OR 1.66 [95% CI: 1.56, 1.78], OR 1.91 [95% CI: 1.85, 1.98], and OR 2.28 [95% CI: 2.08, 2.50] for maternal overweight; OR 2.43 [95% CI: 2.24, 2.64], OR 3.12 [95% CI: 2.98, 3.27], and OR 4.47 [95% CI: 3.99, 5.23] for maternal obesity; and OR 1.39 [95% CI: 1.30, 1.49], OR 1.55 [95% CI: 1.49, 1.60], and OR 1.72 [95% CI: 1.56, 1.91] for excessive gestational weight gain). The proportions of childhood overweight/obesity prevalence attributable to maternal overweight, materna
Published: 2019

18. Impact of maternal body mass index and gestational weight gain on pregnancy complications: an individual participant data meta-analysis of European, North American and Australian cohorts

Author: Santos, S., Santos, S., Voerman, E., Amiano, P., Barros, H., Beilin, L. J., Bergstrom, A., Charles, M-A, Chatzi, L., Chevrier, C., Chrousos, G. P., Corpeleijn, E., Costa, O., Costet, N., Crozier, S., Devereux, G., Doyon, M., Eggesbo, M., Fantini, M. P., Farchi, S., Forastiere, F., Georgiu, V., Godfrey, K. M., Gori, D., Grote, V., Hanke, W., Hertz-Picciotto, I., Heude, B., Hivert, M-F, Hryhorczuk, D., Huang, R-C, Inskip, H., Karvonen, A. M., Kenny, L. C., Koletzko, B., Kupers, L. K., Lagstrom, H., Lehmann, I., Magnus, P., Majewska, R., Makela, J., Manios, Y., McAuliffe, F. M., McDonald, S. W., Mehegan, J., Melen, E., Mommers, M., Morgen, C. S., Moschonis, G., Murray, D., Ni Chaoimh, C., Nohr, E. A., Andersen, A-M Nybo, Oken, E., Oostvogels, A. J. J. M., Pac, A., Papadopoulou, E., Pekkanen, J., Pizzi, C., Polanska, K., Porta, D., Richiardi, L., Rifas-Shiman, S. L., Roeleveld, N., Ronfani, L., Santos, A. C., Standl, M., Stigum, H., Stoltenberg, C., Thiering, E., Thijs, C., Torrent, M., Tough, S. C., Trnovec, T., Turner, S., van Gelder, M. M. H. J., van Rossem, L., von Berg, A., Vrijheid, M., Vrijkotte, T. G. M., West, J., Wijga, A. H., Wright, J., Zvinchuk, O., Sorensen, T. I. A., Lawlor, D. A., Gaillard, R., Jaddoe, V. W. V., Santos, S., Santos, S., Voerman, E., Amiano, P., Barros, H., Beilin, L. J., Bergstrom, A., Charles, M-A, Chatzi, L., Chevrier, C., Chrousos, G. P., Corpeleijn, E., Costa, O., Costet, N., Crozier, S., Devereux, G., Doyon, M., Eggesbo, M., Fantini, M. P., Farchi, S., Forastiere, F., Georgiu, V., Godfrey, K. M., Gori, D., Grote, V., Hanke, W., Hertz-Picciotto, I., Heude, B., Hivert, M-F, Hryhorczuk, D., Huang, R-C, Inskip, H., Karvonen, A. M., Kenny, L. C., Koletzko, B., Kupers, L. K., Lagstrom, H., Lehmann, I., Magnus, P., Majewska, R., Makela, J., Manios, Y., McAuliffe, F. M., McDonald, S. W., Mehegan, J., Melen, E., Mommers, M., Morgen, C. S., Moschonis, G., Murray, D., Ni Chaoimh, C., Nohr, E. A., Andersen, A-M Nybo, Oken, E., Oostvogels, A. J. J. M., Pac, A., Papadopoulou, E., Pekkanen, J., Pizzi, C., Polanska, K., Porta, D., Richiardi, L., Rifas-Shiman, S. L., Roeleveld, N., Ronfani, L., Santos, A. C., Standl, M., Stigum, H., Stoltenberg, C., Thiering, E., Thijs, C., Torrent, M., Tough, S. C., Trnovec, T., Turner, S., van Gelder, M. M. H. J., van Rossem, L., von Berg, A., Vrijheid, M., Vrijkotte, T. G. M., West, J., Wijga, A. H., Wright, J., Zvinchuk, O., Sorensen, T. I. A., Lawlor, D. A., Gaillard, R., and Jaddoe, V. W. V.
Abstract: Objective To assess the separate and combined associations of maternal pre-pregnancy body mass index (BMI) and gestational weight gain with the risks of pregnancy complications and their population impact. Design Individual participant data meta-analysis of 39 cohorts. Setting Europe, North America, and Oceania. Population 265 270 births. Methods Information on maternal pre-pregnancy BMI, gestational weight gain, and pregnancy complications was obtained. Multilevel binary logistic regression models were used. Main outcome measures Gestational hypertension, pre-eclampsia, gestational diabetes, preterm birth, small and large for gestational age at birth. Results Higher maternal pre-pregnancy BMI and gestational weight gain were, across their full ranges, associated with higher risks of gestational hypertensive disorders, gestational diabetes, and large for gestational age at birth. Preterm birth risk was higher at lower and higher BMI and weight gain. Compared with normal weight mothers with medium gestational weight gain, obese mothers with high gestational weight gain had the highest risk of any pregnancy complication (odds ratio 2.51, 95% CI 2.31- 2.74). We estimated that 23.9% of any pregnancy complication was attributable to maternal overweight/obesity and 31.6% of large for gestational age infants was attributable to excessive gestational weight gain. Conclusions Maternal pre-pregnancy BMI and gestational weight gain are, across their full ranges, associated with risks of pregnancy complications. Obese mothers with high gestational weight gain are at the highest risk of pregnancy complications. Promoting a healthy pre-pregnancy BMI and gestational weight gain may reduce the burden of pregnancy complications and ultimately the risk of maternal and neonatal morbidity.
Published: 2019

19. The Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia: design, results and future prospects

Author: Middeldorp, CM, Mahajan, A, Horikoshi, M, Robertson, NR, Beaumont, RN, Bradfield, JP, Bustamante, M, Cousminer, DL, Day, FR, De Silva, NM, Guxens, M, Mook-Kanamori, DO, St Pourcain, B, Warrington, NM, Adair, LS, Ahlqvist, E, Ahluwalia, TS, Almgren, P, Ang, W, Atalay, M, Auvinen, J, Bartels, M, Beckmann, JS, Bilbao, JR, Bond, T, Borja, JB, Cavadino, A, Charoen, P, Chen, Z, Coin, L, Cooper, C, Curtin, JA, Custovic, A, Das, S, Davies, GE, Dedoussis, GV, Duijts, L, Eastwood, PR, Eliasen, AU, Elliott, P, Eriksson, JG, Estivill, X, Fadista, J, Fedko, IO, Frayling, TM, Gaillard, R, Gauderman, WJ, Geller, F, Gilliland, F, Gilsanz, V, Granell, R, Grarup, N, Groop, L, Hadley, D, Hakonarson, H, Hansen, T, Hartman, CA, Hattersley, AT, Hayes, MG, Hebebrand, J, Heinrich, J, Helgeland, O, Henders, AK, Henderson, J, Henriksen, TB, Hirschhorn, JN, Hivert, M-F, Hocher, B, Holloway, JW, Holt, P, Hottenga, J-J, Hypponen, E, Iniguez, C, Johansson, S, Jugessur, A, Kahonen, M, Kalkwarf, HJ, Kaprio, J, Karhunen, V, Kemp, JP, Kerkhof, M, Koppelman, GH, Korner, A, Kotecha, S, Kreiner-Moller, E, Kulohoma, B, Kumar, A, Kutalik, Z, Lahti, J, Lappe, JM, Larsson, H, Lehtimaki, T, Lewin, AM, Li, J, Lichtenstein, P, Lindgren, CM, Lindi, V, Linneberg, A, Liu, X, Liu, J, Lowe, WL, Lundstrom, S, Lyytikainen, L-P, Ma, RCW, Mace, A, Magi, R, Magnus, P, Mamun, AA, Mannikko, M, Martin, NG, Mbarek, H, McCarthy, NS, Medland, SE, Melbye, M, Melen, E, Mohlke, KL, Monnereau, C, Morgen, CS, Morris, AP, Murray, JC, Myhre, R, Najman, JM, Nivard, MG, Nohr, EA, Nolte, IM, Ntalla, I, O'Reilly, P, Oberfield, SE, Oken, E, Oldehinkel, AJ, Pahkala, K, Palviainen, T, Panoutsopoulou, K, Pedersen, O, Pennell, CE, Pershagen, G, Pitkanen, N, Plomin, R, Power, C, Prasad, RB, Prokopenko, I, Pulkkinen, L, Raikkonen, K, Raitakari, OT, Reynolds, RM, Richmond, RC, Rivadeneira, F, Rodriguez, A, Rose, RJ, Salem, R, Santa-Marina, L, Saw, S-M, Schnurr, TM, Scott, JG, Selzam, S, Shepherd, JA, Simpson, A, Skotte, L, Sleiman, PMA, Snieder, H, Sorensen, TIA, Standl, M, Steegers, EAP, Strachan, DP, Straker, L, Strandberg, T, Taylor, M, Teo, Y-Y, Thiering, E, Torrent, M, Tyrrell, J, Uitterlinden, AG, van Beijsterveldt, T, van der Most, PJ, van Duijn, CM, Viikari, J, Vilor-Tejedor, N, Vogelezang, S, Vonk, JM, Vrijkotte, TGM, Vuoksimaa, E, Wang, CA, Watkins, WJ, Wichmann, H-E, Willemsen, G, Williams, GM, Wilson, JF, Wray, NR, Xu, S, Xu, C-J, Yaghootkar, H, Yi, L, Zafarmand, MH, Zeggini, E, Zemel, BS, Hinney, A, Lakka, TA, Whitehouse, AJO, Sunyer, J, Widen, EE, Feenstra, B, Sebert, S, Jacobsson, B, Njolstad, PR, Stoltenberg, C, Smith, GD, Lawlor, DA, Paternoster, L, Timpson, NJ, Ong, KK, Bisgaard, H, Bonnelykke, K, Jaddoe, VWV, Tiemeier, H, Jarvelin, M-R, Evans, DM, Perry, JRB, Grant, SFA, Boomsma, DI, Freathy, RM, McCarthy, MI, Felix, JF, Middeldorp, CM, Mahajan, A, Horikoshi, M, Robertson, NR, Beaumont, RN, Bradfield, JP, Bustamante, M, Cousminer, DL, Day, FR, De Silva, NM, Guxens, M, Mook-Kanamori, DO, St Pourcain, B, Warrington, NM, Adair, LS, Ahlqvist, E, Ahluwalia, TS, Almgren, P, Ang, W, Atalay, M, Auvinen, J, Bartels, M, Beckmann, JS, Bilbao, JR, Bond, T, Borja, JB, Cavadino, A, Charoen, P, Chen, Z, Coin, L, Cooper, C, Curtin, JA, Custovic, A, Das, S, Davies, GE, Dedoussis, GV, Duijts, L, Eastwood, PR, Eliasen, AU, Elliott, P, Eriksson, JG, Estivill, X, Fadista, J, Fedko, IO, Frayling, TM, Gaillard, R, Gauderman, WJ, Geller, F, Gilliland, F, Gilsanz, V, Granell, R, Grarup, N, Groop, L, Hadley, D, Hakonarson, H, Hansen, T, Hartman, CA, Hattersley, AT, Hayes, MG, Hebebrand, J, Heinrich, J, Helgeland, O, Henders, AK, Henderson, J, Henriksen, TB, Hirschhorn, JN, Hivert, M-F, Hocher, B, Holloway, JW, Holt, P, Hottenga, J-J, Hypponen, E, Iniguez, C, Johansson, S, Jugessur, A, Kahonen, M, Kalkwarf, HJ, Kaprio, J, Karhunen, V, Kemp, JP, Kerkhof, M, Koppelman, GH, Korner, A, Kotecha, S, Kreiner-Moller, E, Kulohoma, B, Kumar, A, Kutalik, Z, Lahti, J, Lappe, JM, Larsson, H, Lehtimaki, T, Lewin, AM, Li, J, Lichtenstein, P, Lindgren, CM, Lindi, V, Linneberg, A, Liu, X, Liu, J, Lowe, WL, Lundstrom, S, Lyytikainen, L-P, Ma, RCW, Mace, A, Magi, R, Magnus, P, Mamun, AA, Mannikko, M, Martin, NG, Mbarek, H, McCarthy, NS, Medland, SE, Melbye, M, Melen, E, Mohlke, KL, Monnereau, C, Morgen, CS, Morris, AP, Murray, JC, Myhre, R, Najman, JM, Nivard, MG, Nohr, EA, Nolte, IM, Ntalla, I, O'Reilly, P, Oberfield, SE, Oken, E, Oldehinkel, AJ, Pahkala, K, Palviainen, T, Panoutsopoulou, K, Pedersen, O, Pennell, CE, Pershagen, G, Pitkanen, N, Plomin, R, Power, C, Prasad, RB, Prokopenko, I, Pulkkinen, L, Raikkonen, K, Raitakari, OT, Reynolds, RM, Richmond, RC, Rivadeneira, F, Rodriguez, A, Rose, RJ, Salem, R, Santa-Marina, L, Saw, S-M, Schnurr, TM, Scott, JG, Selzam, S, Shepherd, JA, Simpson, A, Skotte, L, Sleiman, PMA, Snieder, H, Sorensen, TIA, Standl, M, Steegers, EAP, Strachan, DP, Straker, L, Strandberg, T, Taylor, M, Teo, Y-Y, Thiering, E, Torrent, M, Tyrrell, J, Uitterlinden, AG, van Beijsterveldt, T, van der Most, PJ, van Duijn, CM, Viikari, J, Vilor-Tejedor, N, Vogelezang, S, Vonk, JM, Vrijkotte, TGM, Vuoksimaa, E, Wang, CA, Watkins, WJ, Wichmann, H-E, Willemsen, G, Williams, GM, Wilson, JF, Wray, NR, Xu, S, Xu, C-J, Yaghootkar, H, Yi, L, Zafarmand, MH, Zeggini, E, Zemel, BS, Hinney, A, Lakka, TA, Whitehouse, AJO, Sunyer, J, Widen, EE, Feenstra, B, Sebert, S, Jacobsson, B, Njolstad, PR, Stoltenberg, C, Smith, GD, Lawlor, DA, Paternoster, L, Timpson, NJ, Ong, KK, Bisgaard, H, Bonnelykke, K, Jaddoe, VWV, Tiemeier, H, Jarvelin, M-R, Evans, DM, Perry, JRB, Grant, SFA, Boomsma, DI, Freathy, RM, McCarthy, MI, and Felix, JF
Abstract: The impact of many unfavorable childhood traits or diseases, such as low birth weight and mental disorders, is not limited to childhood and adolescence, as they are also associated with poor outcomes in adulthood, such as cardiovascular disease. Insight into the genetic etiology of childhood and adolescent traits and disorders may therefore provide new perspectives, not only on how to improve wellbeing during childhood, but also how to prevent later adverse outcomes. To achieve the sample sizes required for genetic research, the Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia were established. The majority of the participating cohorts are longitudinal population-based samples, but other cohorts with data on early childhood phenotypes are also involved. Cohorts often have a broad focus and collect(ed) data on various somatic and psychiatric traits as well as environmental factors. Genetic variants have been successfully identified for multiple traits, for example, birth weight, atopic dermatitis, childhood BMI, allergic sensitization, and pubertal growth. Furthermore, the results have shown that genetic factors also partly underlie the association with adult traits. As sample sizes are still increasing, it is expected that future analyses will identify additional variants. This, in combination with the development of innovative statistical methods, will provide detailed insight on the mechanisms underlying the transition from childhood to adult disorders. Both consortia welcome new collaborations. Policies and contact details are available from the corresponding authors of this manuscript and/or the consortium websites.
Published: 2019

20. Association of gestational weight gain with adverse maternal and infant outcomes

Author: Voerman, E., Santos, S., Inskip, H., Amiano, P., Barros, H., Charles, M.-A., Chatzi, L., Chrousos, G.P., Corpeleijn, E., Crozier, S., Doyon, M., Eggesbø, M., Fantini, M.P., Farchi, S., Forastiere, F., Georgiu, V., Gori, D., Hanke, W., Hertz-Picciotto, I., Heude, B., Hivert, M.-F., Hryhorczuk, D., Iniguez, C., Karvonen, A.M., Kupers, L.K., Lagström, H., Lawlor, D.A., Lehmann, Irina, Magnus, P., Majewska, R., Mäkelä, J., Manios, Y., Mommers, M., Morgen, C.S., Moschonis, G., Nohr, E.A., Nybo Andersen, A.-M., Oken, E., Pac, A., Papadopoulou, E., Pekkanen, J., Pizzi, C., Polanska, K., Porta, D., Richiardi, L., Rifas-Shiman, S.-L., Roeleveld, N., Ronfani, L., Santos, A.C., Standl, M., Stigum, H., Stoltenberg, C., Thiering, E., Thijs, C., Torrent, M., Trnovec, T., van Gelder, M.M.H.J., van Rossem, L., von Berg, A., Vijheid, M., Wijga, A., Zvinchuk, O., Sørensen, T.I.A., Godfrey, K., Jaddoe, V.W.V., Gaillard, R., Voerman, E., Santos, S., Inskip, H., Amiano, P., Barros, H., Charles, M.-A., Chatzi, L., Chrousos, G.P., Corpeleijn, E., Crozier, S., Doyon, M., Eggesbø, M., Fantini, M.P., Farchi, S., Forastiere, F., Georgiu, V., Gori, D., Hanke, W., Hertz-Picciotto, I., Heude, B., Hivert, M.-F., Hryhorczuk, D., Iniguez, C., Karvonen, A.M., Kupers, L.K., Lagström, H., Lawlor, D.A., Lehmann, Irina, Magnus, P., Majewska, R., Mäkelä, J., Manios, Y., Mommers, M., Morgen, C.S., Moschonis, G., Nohr, E.A., Nybo Andersen, A.-M., Oken, E., Pac, A., Papadopoulou, E., Pekkanen, J., Pizzi, C., Polanska, K., Porta, D., Richiardi, L., Rifas-Shiman, S.-L., Roeleveld, N., Ronfani, L., Santos, A.C., Standl, M., Stigum, H., Stoltenberg, C., Thiering, E., Thijs, C., Torrent, M., Trnovec, T., van Gelder, M.M.H.J., van Rossem, L., von Berg, A., Vijheid, M., Wijga, A., Zvinchuk, O., Sørensen, T.I.A., Godfrey, K., Jaddoe, V.W.V., and Gaillard, R.
Abstract: Importance Both low and high gestational weight gain have been associated with adverse maternal and infant outcomes, but optimal gestational weight gain remains uncertain and not well defined for all prepregnancy weight ranges.Objectives To examine the association of ranges of gestational weight gain with risk of adverse maternal and infant outcomes and estimate optimal gestational weight gain ranges across prepregnancy body mass index categories.Design, Setting, and Participants Individual participant-level meta-analysis using data from 196 670 participants within 25 cohort studies from Europe and North America (main study sample). Optimal gestational weight gain ranges were estimated for each prepregnancy body mass index (BMI) category by selecting the range of gestational weight gain that was associated with lower risk for any adverse outcome. Individual participant-level data from 3505 participants within 4 separate hospital-based cohorts were used as a validation sample. Data were collected between 1989 and 2015. The final date of follow-up was December 2015.Exposures Gestational weight gain.Main Outcomes and Measures The main outcome termed any adverse outcome was defined as the presence of 1 or more of the following outcomes: preeclampsia, gestational hypertension, gestational diabetes, cesarean delivery, preterm birth, and small or large size for gestational age at birth.Results Of the 196 670 women (median age, 30.0 years [quartile 1 and 3, 27.0 and 33.0 years] and 40 937 were white) included in the main sample, 7809 (4.0%) were categorized at baseline as underweight (BMI <18.5); 133 788 (68.0%), normal weight (BMI, 18.5-24.9); 38 828 (19.7%), overweight (BMI, 25.0-29.9); 11 992 (6.1%), obesity grade 1 (BMI, 30.0-34.9); 3284 (1.7%), obesity grade 2 (BMI, 35.0-39.9); and 969 (0.5%), obesity grade 3 (BMI, ≥40.0). Overall, any adverse outcome occurred in 37.2% (n = 73 161) of women, ranging fro
Published: 2019

21. Maternal body mass index, gestational weight gain, and the risk of overweight and obesity across childhood: An individual participant data meta-analysis

Author: Voerman, E., Santos, S., Patro Golab, B., Amiano, P., Ballester, F., Barros, H., Bergström, A., Charles, M.-A., Chatzi, L., Chevrier, C., Chrousos, G.P., Corpeleijn, E., Costet, N., Crozier, S., Devereux, G., Eggesbø, M., Ekström, S., Fantini, M.P., Farchi, S., Forastiere, F., Georgiu, V., Godfrey, K.M., Gori, D., Grote, V., Hanke, W., Hertz-Picciotto, I., Heude, B., Hryhorczuk, D., Huang, R.-C., Inskip, H., Iszatt, N., Karvonen, A.M., Kenny, L.C., Koletzko, B., Küpers, L.K., Lagström, H., Lehmann, Irina, Magnus, P., Majewska, R., Mäkelä, J., Manios, Y., McAuliffe, F.M., McDonald, S.W., Mehegan, J., Mommers, M., Morgen, C.S., Mori, T.A., Moschonis, G., Murray, D., Ní Chaoimh, C., Nohr, E.A., Nybo Andersen, A.-M., Oken, E., Oostvogels, A.J.J.M., Pac, A., Papadopoulou, E., Pekkanen, J., Pizzi, C., Polanska, K., Porta, D., Richiardi, L., Rifas-Shiman, S.-L., Ronfani, L., Santos, A.C., Standl, M., Stoltenberg, C., Thiering, E., Thijs, C., Torrent, M., Tough, S.C., Trnovec, T., Turner, S., van Rossem, L., von Berg, A., Vrijheid, M., Vrijkotte, T.G.M., West, J., Wijga, A., Wright, J., Zvinchuk, O., Sørensen, T.I.A., Lawlor, D.A., Gaillard, R., Jaddoe, V.W.V., Voerman, E., Santos, S., Patro Golab, B., Amiano, P., Ballester, F., Barros, H., Bergström, A., Charles, M.-A., Chatzi, L., Chevrier, C., Chrousos, G.P., Corpeleijn, E., Costet, N., Crozier, S., Devereux, G., Eggesbø, M., Ekström, S., Fantini, M.P., Farchi, S., Forastiere, F., Georgiu, V., Godfrey, K.M., Gori, D., Grote, V., Hanke, W., Hertz-Picciotto, I., Heude, B., Hryhorczuk, D., Huang, R.-C., Inskip, H., Iszatt, N., Karvonen, A.M., Kenny, L.C., Koletzko, B., Küpers, L.K., Lagström, H., Lehmann, Irina, Magnus, P., Majewska, R., Mäkelä, J., Manios, Y., McAuliffe, F.M., McDonald, S.W., Mehegan, J., Mommers, M., Morgen, C.S., Mori, T.A., Moschonis, G., Murray, D., Ní Chaoimh, C., Nohr, E.A., Nybo Andersen, A.-M., Oken, E., Oostvogels, A.J.J.M., Pac, A., Papadopoulou, E., Pekkanen, J., Pizzi, C., Polanska, K., Porta, D., Richiardi, L., Rifas-Shiman, S.-L., Ronfani, L., Santos, A.C., Standl, M., Stoltenberg, C., Thiering, E., Thijs, C., Torrent, M., Tough, S.C., Trnovec, T., Turner, S., van Rossem, L., von Berg, A., Vrijheid, M., Vrijkotte, T.G.M., West, J., Wijga, A., Wright, J., Zvinchuk, O., Sørensen, T.I.A., Lawlor, D.A., Gaillard, R., and Jaddoe, V.W.V.
Abstract: BackgroundMaternal obesity and excessive gestational weight gain may have persistent effects on offspring fat development. However, it remains unclear whether these effects differ by severity of obesity, and whether these effects are restricted to the extremes of maternal body mass index (BMI) and gestational weight gain. We aimed to assess the separate and combined associations of maternal BMI and gestational weight gain with the risk of overweight/obesity throughout childhood, and their population impact. Methods and findingsWe conducted an individual participant data meta-analysis of data from 162,129 mothers and their children from 37 pregnancy and birth cohort studies from Europe, North America, and Australia. We assessed the individual and combined associations of maternal pre-pregnancy BMI and gestational weight gain, both in clinical categories and across their full ranges, with the risks of overweight/obesity in early (2.0–5.0 years), mid (5.0–10.0 years) and late childhood (10.0–18.0 years), using multilevel binary logistic regression models with a random intercept at cohort level adjusted for maternal sociodemographic and lifestyle-related characteristics. We observed that higher maternal pre-pregnancy BMI and gestational weight gain both in clinical categories and across their full ranges were associated with higher risks of childhood overweight/obesity, with the strongest effects in late childhood (odds ratios [ORs] for overweight/obesity in early, mid, and late childhood, respectively: OR 1.66 [95% CI: 1.56, 1.78], OR 1.91 [95% CI: 1.85, 1.98], and OR 2.28 [95% CI: 2.08, 2.50] for maternal overweight; OR 2.43 [95% CI: 2.24, 2.64], OR 3.12 [95% CI: 2.98, 3.27], and OR 4.47 [95% CI: 3.99, 5.23] for maternal obesity; and OR 1.39 [95% CI: 1.30, 1.49], OR 1.55 [95% CI: 1.49, 1.60], and OR 1.72 [95% CI: 1.56, 1.91] for excessive gestational weight gain). The proportions of childhood overweight/obesity prevalence attributable to maternal overweight, maternal
Published: 2019

22. Impact of maternal body mass index and gestational weight gain on pregnancy complications:an individual participant data meta-analysis of European, North American and Australian cohorts

Author: Santos, S., Voerman, E., Amiano, P., Barros, H., Beilin, L. J., Bergstrom, A., Charles, M-A, Chatzi, L., Chevrier, C., Chrousos, G. P., Corpeleijn, E., Costa, O., Costet, N., Crozier, S., Devereux, G., Doyon, M., Eggesbo, M., Fantini, M. P., Farchi, S., Forastiere, F., Georgiu, V., Godfrey, K. M., Gori, D., Grote, V., Hanke, W., Hertz-Picciotto, I., Heude, B., Hivert, M-F, Hryhorczuk, D., Huang, R-C, Inskip, H., Karvonen, A. M., Kenny, L. C., Koletzko, B., Kupers, L. K., Lagstrom, H., Lehmann, I., Magnus, P., Majewska, R., Makela, J., Manios, Y., McAuliffe, F. M., McDonald, S. W., Mehegan, J., Melen, E., Mommers, M., Morgen, C. S., Moschonis, G., Murray, D., Ni Chaoimh, C., Nohr, E. A., Andersen, A-M Nybo, Oken, E., Oostvogels, A. J. J. M., Pac, A., Papadopoulou, E., Pekkanen, J., Pizzi, C., Polanska, K., Porta, D., Richiardi, L., Rifas-Shiman, S. L., Roeleveld, N., Ronfani, L., Santos, A. C., Standl, M., Stigum, H., Stoltenberg, C., Thiering, E., Thijs, C., Torrent, M., Tough, S. C., Trnovec, T., Turner, S., van Gelder, M. M. H. J., van Rossem, L., von Berg, A., Vrijheid, M., Vrijkotte, T. G. M., West, J., Wijga, A. H., Wright, J., Zvinchuk, O., Sørensen, T. I. A., Lawlor, D. A., Gaillard, R., Jaddoe, V. W. V., Santos, S., Voerman, E., Amiano, P., Barros, H., Beilin, L. J., Bergstrom, A., Charles, M-A, Chatzi, L., Chevrier, C., Chrousos, G. P., Corpeleijn, E., Costa, O., Costet, N., Crozier, S., Devereux, G., Doyon, M., Eggesbo, M., Fantini, M. P., Farchi, S., Forastiere, F., Georgiu, V., Godfrey, K. M., Gori, D., Grote, V., Hanke, W., Hertz-Picciotto, I., Heude, B., Hivert, M-F, Hryhorczuk, D., Huang, R-C, Inskip, H., Karvonen, A. M., Kenny, L. C., Koletzko, B., Kupers, L. K., Lagstrom, H., Lehmann, I., Magnus, P., Majewska, R., Makela, J., Manios, Y., McAuliffe, F. M., McDonald, S. W., Mehegan, J., Melen, E., Mommers, M., Morgen, C. S., Moschonis, G., Murray, D., Ni Chaoimh, C., Nohr, E. A., Andersen, A-M Nybo, Oken, E., Oostvogels, A. J. J. M., Pac, A., Papadopoulou, E., Pekkanen, J., Pizzi, C., Polanska, K., Porta, D., Richiardi, L., Rifas-Shiman, S. L., Roeleveld, N., Ronfani, L., Santos, A. C., Standl, M., Stigum, H., Stoltenberg, C., Thiering, E., Thijs, C., Torrent, M., Tough, S. C., Trnovec, T., Turner, S., van Gelder, M. M. H. J., van Rossem, L., von Berg, A., Vrijheid, M., Vrijkotte, T. G. M., West, J., Wijga, A. H., Wright, J., Zvinchuk, O., Sørensen, T. I. A., Lawlor, D. A., Gaillard, R., and Jaddoe, V. W. V.
Published: 2019

23. The Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia: design, results and future prospects

Author: Middeldorp, C.M., Felix, J.F., Mahajan, A., Ahluwalia, T.S., Auvinen, J., Bartels, M., Bilbao, J.R., Bisgaard, H., Bønnelykke, K., Boomsma, D.I., Bradfield, J.P., Bustamante, M., Chen, Z., Curtin, J.A., Custovic, A., Smith, G.D., Davies, G.E., Duijts, L., Eastwood, Peter, Eliasen, A.U., Estivill, X., Evans, D.M., Fedko, I.O., Gauderman, W.J., Gilliland, F., Granell, R., Grant, S.F.A., Guxens, M., Hakonarson, H., Hartman, C.A., Heinrich, J., Henders, A.K., Henderson, J., Holt, P., Hottenga, J.J., Hyppönen, E., Iñíguez, C., Jacobsson, B., Jaddoe, V.W.V., Järvelin, M.R., Jugessur, A., Kähönen, M., Kaprio, J., Karhunen, V., Kemp, J.P., Koppelman, G.H., Kumar, A., Lahti, J., Larsson, H., Lawlor, D.A., Lehtimäki, T., Li, J., Lichtenstein, P., Lundström, S., Lyytikäinen, L.P., Magnus, P., Mamun, A.A., Mannikko, M., Martin, N.G., Mbarek, H., Medland, S.E., Melén, E., Najman, J.M., Nivard, M.G., Nolte, I.M., Oldehinkel, A.J., Pahkala, K., Palviainen, T., Paternoster, L., Pennell, C.E., Pershagen, G., Pitkänen, N., Plomin, R., Pourcain, B.S., Power, C., Pulkkinen, L., Räikkönen, K., Raitakari, O.T., Richmond, R.C., Rivadeneira, F., Rose, R.J., Santa-Marina, L., Scott, J.G., Sebert, S., Selzam, S., Simpson, A., Sleiman, P.M.A., Snieder, H., Standl, M., Stoltenberg, C., Strachan, D.P., Straker, Leon, Strandberg, T., Sunyer, J., Thiering, E., Tiemeier, H., Timpson, N.J., Torrent, M., Uitterlinden, A.G., Middeldorp, C.M., Felix, J.F., Mahajan, A., Ahluwalia, T.S., Auvinen, J., Bartels, M., Bilbao, J.R., Bisgaard, H., Bønnelykke, K., Boomsma, D.I., Bradfield, J.P., Bustamante, M., Chen, Z., Curtin, J.A., Custovic, A., Smith, G.D., Davies, G.E., Duijts, L., Eastwood, Peter, Eliasen, A.U., Estivill, X., Evans, D.M., Fedko, I.O., Gauderman, W.J., Gilliland, F., Granell, R., Grant, S.F.A., Guxens, M., Hakonarson, H., Hartman, C.A., Heinrich, J., Henders, A.K., Henderson, J., Holt, P., Hottenga, J.J., Hyppönen, E., Iñíguez, C., Jacobsson, B., Jaddoe, V.W.V., Järvelin, M.R., Jugessur, A., Kähönen, M., Kaprio, J., Karhunen, V., Kemp, J.P., Koppelman, G.H., Kumar, A., Lahti, J., Larsson, H., Lawlor, D.A., Lehtimäki, T., Li, J., Lichtenstein, P., Lundström, S., Lyytikäinen, L.P., Magnus, P., Mamun, A.A., Mannikko, M., Martin, N.G., Mbarek, H., Medland, S.E., Melén, E., Najman, J.M., Nivard, M.G., Nolte, I.M., Oldehinkel, A.J., Pahkala, K., Palviainen, T., Paternoster, L., Pennell, C.E., Pershagen, G., Pitkänen, N., Plomin, R., Pourcain, B.S., Power, C., Pulkkinen, L., Räikkönen, K., Raitakari, O.T., Richmond, R.C., Rivadeneira, F., Rose, R.J., Santa-Marina, L., Scott, J.G., Sebert, S., Selzam, S., Simpson, A., Sleiman, P.M.A., Snieder, H., Standl, M., Stoltenberg, C., Strachan, D.P., Straker, Leon, Strandberg, T., Sunyer, J., Thiering, E., Tiemeier, H., Timpson, N.J., Torrent, M., and Uitterlinden, A.G.
Abstract: The impact of many unfavorable childhood traits or diseases, such as low birth weight and mental disorders, is not limited to childhood and adolescence, as they are also associated with poor outcomes in adulthood, such as cardiovascular disease. Insight into the genetic etiology of childhood and adolescent traits and disorders may therefore provide new perspectives, not only on how to improve wellbeing during childhood, but also how to prevent later adverse outcomes. To achieve the sample sizes required for genetic research, the Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia were established. The majority of the participating cohorts are longitudinal population-based samples, but other cohorts with data on early childhood phenotypes are also involved. Cohorts often have a broad focus and collect(ed) data on various somatic and psychiatric traits as well as environmental factors. Genetic variants have been successfully identified for multiple traits, for example, birth weight, atopic dermatitis, childhood BMI, allergic sensitization, and pubertal growth. Furthermore, the results have shown that genetic factors also partly underlie the association with adult traits. As sample sizes are still increasing, it is expected that future analyses will identify additional variants. This, in combination with the development of innovative statistical methods, will provide detailed insight on the mechanisms underlying the transition from childhood to adult disorders. Both consortia welcome new collaborations. Policies and contact details are available from the corresponding authors of this manuscript and/or the consortium websites.
Published: 2019

24. Gestational weight gain charts for different body mass index groups for women in Europe, North America, and Oceania

Author: Santos, S. Eekhout, I. Voerman, E. Gaillard, R. Barros, H. Charles, M.-A. Chatzi, L. Chevrier, C. Chrousos, G.P. Corpeleijn, E. Costet, N. Crozier, S. Doyon, M. Eggesbø, M. Fantini, M.P. Farchi, S. Forastiere, F. Gagliardi, L. Georgiu, V. Godfrey, K.M. Gori, D. Grote, V. Hanke, W. Hertz-Picciotto, I. Heude, B. Hivert, M.-F. Hryhorczuk, D. Huang, R.-C. Inskip, H. Jusko, T.A. Karvonen, A.M. Koletzko, B. Küpers, L.K. Lagström, H. Lawlor, D.A. Lehmann, I. Lopez-Espinosa, M.-J. Magnus, P. Majewska, R. Mäkelä, J. Manios, Y. McDonald, S.W. Mommers, M. Morgen, C.S. Moschonis, G. Murínová, L. Newnham, J. Nohr, E.A. Andersen, A.-M.N. Oken, E. Oostvogels, A.J.J.M. Pac, A. Papadopoulou, E. Pekkanen, J. Pizzi, C. Polanska, K. Porta, D. Richiardi, L. Rifas-Shiman, S.L. Roeleveld, N. Santa-Marina, L. Santos, A.C. Smit, H.A. Sørensen, T.I.A. Standl, M. Stanislawski, M. Stoltenberg, C. Thiering, E. Thijs, C. Torrent, M. Tough, S.C. Trnovec, T. Van Gelder, M.M.H.J. Van Rossem, L. Von Berg, A. Vrijheid, M. Vrijkotte, T.G.M. Zvinchuk, O. Van Buuren, S. Jaddoe, V.W.V.
Abstract: Background: Gestational weight gain differs according to pre-pregnancy body mass index and is related to the risks of adverse maternal and child health outcomes. Gestational weight gain charts for women in different pre-pregnancy body mass index groups enable identification of women and offspring at risk for adverse health outcomes. We aimed to construct gestational weight gain reference charts for underweight, normal weight, overweight, and grades 1, 2 and 3 obese women and to compare these charts with those obtained in women with uncomplicated term pregnancies. Methods: We used individual participant data from 218,216 pregnant women participating in 33 cohorts from Europe, North America, and Oceania. Of these women, 9065 (4.2%), 148,697 (68.1%), 42,678 (19.6%), 13,084 (6.0%), 3597 (1.6%), and 1095 (0.5%) were underweight, normal weight, overweight, and grades 1, 2, and 3 obese women, respectively. A total of 138, 517 women from 26 cohorts had pregnancies with no hypertensive or diabetic disorders and with term deliveries of appropriate for gestational age at birth infants. Gestational weight gain charts for underweight, normal weight, overweight, and grade 1, 2, and 3 obese women were derived by the Box-Cox t method using the generalized additive model for location, scale, and shape. Results: We observed that gestational weight gain strongly differed per maternal pre-pregnancy body mass index group. The median (interquartile range) gestational weight gain at 40 weeks was 14.2 kg (11.4-17.4) for underweight women, 14.5 kg (11.5-17.7) for normal weight women, 13.9 kg (10.1-17.9) for overweight women, and 11.2 kg (7.0-15.7), 8.7 kg (4.3-13.4) and 6.3 kg (1.9-11.1) for grades 1, 2, and 3 obese women, respectively. The rate of weight gain was lower in the first half than in the second half of pregnancy. No differences in the patterns of weight gain were observed between cohorts or countries. Similar weight gain patterns were observed in mothers without pregnancy complications. Conclusions: Gestational weight gain patterns are strongly related to pre-pregnancy body mass index. The derived charts can be used to assess gestational weight gain in etiological research and as a monitoring tool for weight gain during pregnancy in clinical practice. © 2018 The Author(s).
Published: 2018

25. Gestational weight gain charts for different body mass index groups for women in Europe, North America, and Oceania

Author: Santos, S. (Susana), Eekhout, I. (Iris), Voerman, E. (Ellis), Gaillard, R. (Romy), Barros, A.I. (Ana), Charles, M.A., Chatzi, L. (Leda), Chevrier, C. (Cécile), Chrousos, G.P. (George P.), Corpeleijn, W.E. (Willemijn), Costet, N. (Nathalie), Crozier, S. (Sarah), Doyon, M. (Myriam), Eggesbø, M. (Merete), Fantini, M.P. (Maria), Farchi, S. (Sara), Forastiere, F. (Francesco), Gagliardi, L. (Luigi), Georgiu, V. (Vagelis), Godfrey, K.M. (Keith M.), Gori, D. (Davide), Grote, V. (Veit), Hanke, W. (Wojciech), Hertz-Picciotto, I. (Irva), Heude, B. (Barbara), Hivert, M.-F. (Marie-France), Hryhorczuk, D.O. (Daniel), Huang, R.-C. (Rae-Chi), Inskip, H.M. (Hazel), Jusko, T.A. (Todd A), Karvonen, A.M. (Anne M.), Koletzko, B. (Berthold), Küpers, A.M. (Marlijn), Lagström, H. (Hanna), Lawlor, D.A. (Debbie A.), Lehmann, I. (Irina), Lopez-Espinosa, M.-J. (Maria-Jose), Magnus, P. (Per), Majewska, R. (Renata), Mäkelä, J. (Johanna), Manios, Y., McDonald, S.W. (Sheila W.), Mommers, M. (Monique), Morgen, C.S. (Camilla S.), Moschonis, G., Murinova, L.P. (Lubica Palkovicova), Newnham, J.P. (John), Nohr, C. (Christian), Andersen, A-M.N. (Anne-Marie Nybo), Oken, E. (Emily), Oostvogels, A.J.J.M. (Adriëtte J. J. M.), Pac, A. (Agnieszka), Papadopoulou, E. (Eleni), Pekkanen, J. (Juha), Pizzi, C. (Costanza), Polanska, K. (Kinga), Porta, D. (Daniela), Richiardi, L. (Lorenzo), Rifas-Shiman, S.L. (Sheryl), Roeleveld, N. (Nel), Santa-Marina, L. (Loreto), Santos, A.C. (Ana Cristina), Smit, H.A. (Henriëtte), Sørensen, T.I.A. (Thorkild), Standl, M. (Marie), Stanislawski, M. (Maggie), Stoltenberg, C. (Camilla), Thiering, E. (Elisabeth), Thijs, C. (Carel), Torrent, M. (Maties), Tough, S.C. (Suzanne C.), Trnovec, T. (Tomáš), Van Gelder, M.M.H.J. (Marleen M. H. J.), Rossem, L. (Lenie) van, Berg, A. (Andrea) von, Vrijheid, M. (Martine), Vrijkotte, T.G.M. (Tanja), Zvinchuk, O. (Oleksandr), Buuren, S. (Stef) van, Jaddoe, V.W.V. (Vincent), Santos, S. (Susana), Eekhout, I. (Iris), Voerman, E. (Ellis), Gaillard, R. (Romy), Barros, A.I. (Ana), Charles, M.A., Chatzi, L. (Leda), Chevrier, C. (Cécile), Chrousos, G.P. (George P.), Corpeleijn, W.E. (Willemijn), Costet, N. (Nathalie), Crozier, S. (Sarah), Doyon, M. (Myriam), Eggesbø, M. (Merete), Fantini, M.P. (Maria), Farchi, S. (Sara), Forastiere, F. (Francesco), Gagliardi, L. (Luigi), Georgiu, V. (Vagelis), Godfrey, K.M. (Keith M.), Gori, D. (Davide), Grote, V. (Veit), Hanke, W. (Wojciech), Hertz-Picciotto, I. (Irva), Heude, B. (Barbara), Hivert, M.-F. (Marie-France), Hryhorczuk, D.O. (Daniel), Huang, R.-C. (Rae-Chi), Inskip, H.M. (Hazel), Jusko, T.A. (Todd A), Karvonen, A.M. (Anne M.), Koletzko, B. (Berthold), Küpers, A.M. (Marlijn), Lagström, H. (Hanna), Lawlor, D.A. (Debbie A.), Lehmann, I. (Irina), Lopez-Espinosa, M.-J. (Maria-Jose), Magnus, P. (Per), Majewska, R. (Renata), Mäkelä, J. (Johanna), Manios, Y., McDonald, S.W. (Sheila W.), Mommers, M. (Monique), Morgen, C.S. (Camilla S.), Moschonis, G., Murinova, L.P. (Lubica Palkovicova), Newnham, J.P. (John), Nohr, C. (Christian), Andersen, A-M.N. (Anne-Marie Nybo), Oken, E. (Emily), Oostvogels, A.J.J.M. (Adriëtte J. J. M.), Pac, A. (Agnieszka), Papadopoulou, E. (Eleni), Pekkanen, J. (Juha), Pizzi, C. (Costanza), Polanska, K. (Kinga), Porta, D. (Daniela), Richiardi, L. (Lorenzo), Rifas-Shiman, S.L. (Sheryl), Roeleveld, N. (Nel), Santa-Marina, L. (Loreto), Santos, A.C. (Ana Cristina), Smit, H.A. (Henriëtte), Sørensen, T.I.A. (Thorkild), Standl, M. (Marie), Stanislawski, M. (Maggie), Stoltenberg, C. (Camilla), Thiering, E. (Elisabeth), Thijs, C. (Carel), Torrent, M. (Maties), Tough, S.C. (Suzanne C.), Trnovec, T. (Tomáš), Van Gelder, M.M.H.J. (Marleen M. H. J.), Rossem, L. (Lenie) van, Berg, A. (Andrea) von, Vrijheid, M. (Martine), Vrijkotte, T.G.M. (Tanja), Zvinchuk, O. (Oleksandr), Buuren, S. (Stef) van, and Jaddoe, V.W.V. (Vincent)
Abstract: Background: Gestational weight gain differs according to pre-pregnancy body mass index and is related to the risks of adverse maternal and child health outcomes. Gestational weight gain charts for women in different pre-pregnancy body mass index groups enable identification of women and offspring at risk for adverse health outcomes. We aimed to construct gestational weight gain reference charts for underweight, normal weight, overweight, and grades 1, 2 and 3 obese women and to compare these charts with those obtained in women with uncomplicated term pregnancies. Methods: We used individual participant data from 218,216 pregnant women participating in 33 cohorts from Europe, North America, and Oceania. Of these women, 9065 (4.2%), 148,697 (68.1%), 42,678 (19.6%), 13,084 (6.0%), 3597 (1.6%), and 1095 (0.5%) were underweight, normal weight, overweight, and grades 1, 2, and 3 obese women, respectively. A total of 138, 517 women from 26 cohorts had pregnancies with no hypertensive or diabetic disorders and with term deliveries of appropriate for gestational age at birth infants. Gestational weight gain charts for underweight, normal weight, overweight, and grade 1, 2, and 3 obese women were derived by the Box-Cox t method using the generalized additive model for location, scale, and shape. Results: We observed that gestational weight gain strongly differed per maternal pre-pregnancy body mass index group. The median (interquartile range) gestational weight gain at 40 weeks was 14.2 kg (11.4-17.4) for underweight women, 14.5 kg (11.5-17.7) for normal weight women, 13.9 kg (10.1-17.9) for overweight women, and 11.2 kg (7.0-15.7), 8.7 kg (4.3-13.4) and 6.3 kg (1.9-11.1) for grades 1, 2, and 3 obese women, respectively. The rate of weight gain was lower in the first half than in the second half of pregnancy. No differences in the patterns of weight gain were observed between cohorts or countries. Similar weight gain patterns were observed in mothers without pregnancy compli
Published: 2018
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26. Gestational weight gain charts for different body mass index groups for women in Europe, North America, and Oceania

Author: Santos, S., Eekhout, I., Voerman, I., Gaillard, R., Barros, H., Charles, M.-A., Chatzi, L., Chevrier, C., Chrousos, G.P., Corpeleijn, E., Costet, N., Crozier, S., Doyon, M., Eggesbø, M., Fantini, M.P., Farchi, S., Forastiere, F., Gagliardi, L., Georgiu, V., Godfrey, K.M., Gori, D., Grote, V., Hanke, W., Hertz-Picciotto, I., Heude, B., Hivert, M.-F., Hryhorczuk, D., Huang, R.-C., Inskip, H., Jusko, T.A., Karvonen, A.M., Koletzko, B., Küpers, L.K., Lagström, H., Lawlor, D.A., Lehmann, Irina, Lopez-Espinosa, M.-J., Magnus, P., Majewska, R., Mäkelä, J., Manios, Y., McDonald, S.W., Mommers, M., Morgen, C.S., Moschonis, G., Murínová, L., Newnham, J., Nohr, E.A., Nybo Andersen, A.-M., Oken, E., Oostvogels, A.J.J.M., Pac, A., Papadopoulou, E., Pekkanen, J., Pizzi, C., Polanska, K., Porta, D., Richiardi, L., Rifas-Shiman, S.-L., Roeleveld, N., Santa-Marina, L., Santos, A.C., Smit, H.A., Sørensen, T.I.A., Standl, M., Stanislawski, M., Stoltenberg, C., Thiering, E., Thijs, C., Torrent, M., Tough, S.C., Trnovec, T., van Gelder, M.M.H.J., van Rossem, L., von Berg, A., Vrijheid, M., Vrijkotte, T.G.M., Zvinchuk, O., van Buuren, S., Jaddoe, V.W.V., Santos, S., Eekhout, I., Voerman, I., Gaillard, R., Barros, H., Charles, M.-A., Chatzi, L., Chevrier, C., Chrousos, G.P., Corpeleijn, E., Costet, N., Crozier, S., Doyon, M., Eggesbø, M., Fantini, M.P., Farchi, S., Forastiere, F., Gagliardi, L., Georgiu, V., Godfrey, K.M., Gori, D., Grote, V., Hanke, W., Hertz-Picciotto, I., Heude, B., Hivert, M.-F., Hryhorczuk, D., Huang, R.-C., Inskip, H., Jusko, T.A., Karvonen, A.M., Koletzko, B., Küpers, L.K., Lagström, H., Lawlor, D.A., Lehmann, Irina, Lopez-Espinosa, M.-J., Magnus, P., Majewska, R., Mäkelä, J., Manios, Y., McDonald, S.W., Mommers, M., Morgen, C.S., Moschonis, G., Murínová, L., Newnham, J., Nohr, E.A., Nybo Andersen, A.-M., Oken, E., Oostvogels, A.J.J.M., Pac, A., Papadopoulou, E., Pekkanen, J., Pizzi, C., Polanska, K., Porta, D., Richiardi, L., Rifas-Shiman, S.-L., Roeleveld, N., Santa-Marina, L., Santos, A.C., Smit, H.A., Sørensen, T.I.A., Standl, M., Stanislawski, M., Stoltenberg, C., Thiering, E., Thijs, C., Torrent, M., Tough, S.C., Trnovec, T., van Gelder, M.M.H.J., van Rossem, L., von Berg, A., Vrijheid, M., Vrijkotte, T.G.M., Zvinchuk, O., van Buuren, S., and Jaddoe, V.W.V.
Abstract: BackgroundGestational weight gain differs according to pre-pregnancy body mass index and is related to the risks of adverse maternal and child health outcomes. Gestational weight gain charts for women in different pre-pregnancy body mass index groups enable identification of women and offspring at risk for adverse health outcomes. We aimed to construct gestational weight gain reference charts for underweight, normal weight, overweight, and grades 1, 2 and 3 obese women and to compare these charts with those obtained in women with uncomplicated term pregnancies.MethodsWe used individual participant data from 218,216 pregnant women participating in 33 cohorts from Europe, North America, and Oceania. Of these women, 9065 (4.2%), 148,697 (68.1%), 42,678 (19.6%), 13,084 (6.0%), 3597 (1.6%), and 1095 (0.5%) were underweight, normal weight, overweight, and grades 1, 2, and 3 obese women, respectively. A total of 138, 517 women from 26 cohorts had pregnancies with no hypertensive or diabetic disorders and with term deliveries of appropriate for gestational age at birth infants. Gestational weight gain charts for underweight, normal weight, overweight, and grade 1, 2, and 3 obese women were derived by the Box-Cox t method using the generalized additive model for location, scale, and shape.ResultsWe observed that gestational weight gain strongly differed per maternal pre-pregnancy body mass index group. The median (interquartile range) gestational weight gain at 40 weeks was 14.2 kg (11.4–17.4) for underweight women, 14.5 kg (11.5–17.7) for normal weight women, 13.9 kg (10.1–17.9) for overweight women, and 11.2 kg (7.0–15.7), 8.7 kg (4.3–13.4) and 6.3 kg (1.9–11.1) for grades 1, 2, and 3 obese women, respectively. The rate of weight gain was lower in the first half than in the second half of pregnancy. No differences in the patterns of weight gain were observed between cohorts or countries. Similar weight gain pat
Published: 2018

27. Gestational weight gain charts for different body mass index groups for women in Europe, North America, and Oceania

Author: Moreira da Silva Santos, Susana, Eekhout, I, Voerman, Ellis, Gaillard, Romy, Barros, H, Charles, MA, Chatzi, L, Chevrier, C, Chrousos, GP, Corpeleijn, E, Costet, N, Crozier, S, Doyon, M, Eggesbo, M, Fantini, MP, Farchi, S, Forastiere, F, Gagliardi, L, Georgiu, V, Godfrey, KM, Gori, D, Grote, V, Hanke, W, Hertz-Picciotto, I, Heude, B, Hivert, MF, Hryhorczuk, D, Huang, RC, Inskip, H, Jusko, TA, Karvonen, AM, Koletzko, B, Kupers, LK, Lagstrom, H, Lawlor, DA, Lehmann, I, Lopez-Espinosa, MJ, Magnus, P, Majewska, R, Makela, J, Manios, Y, McDonald, SW, Mommers, M, Morgen, CS, Moschonis, G, Murinova, L, Newnham, J, Nohr, EA, Andersen, AMN, Oken, E, Oostvogels, A, Pac, A, Papadopoulou, E, Pekkanen, J, Pizzi, C, Polanska, K, Porta, D, Richiardi, L, Rifas-Shiman, SL, Roeleveld, N, Santa-Marina, L, dos Santos, AC, Smit, HA, Sorensen, TIA, Standl, M, Stanislawski, M, Stoltenberg, C, Thiering, E, Thijs, C, Torrent, M, Tough, SC, Trnovec, T, Gelder, M, Rossem, L, Berg, A, Vrijheid, M, Vrijkotte, TGM, Zvinchuk, O, van Buuren, S, Jaddoe, Vincent, Moreira da Silva Santos, Susana, Eekhout, I, Voerman, Ellis, Gaillard, Romy, Barros, H, Charles, MA, Chatzi, L, Chevrier, C, Chrousos, GP, Corpeleijn, E, Costet, N, Crozier, S, Doyon, M, Eggesbo, M, Fantini, MP, Farchi, S, Forastiere, F, Gagliardi, L, Georgiu, V, Godfrey, KM, Gori, D, Grote, V, Hanke, W, Hertz-Picciotto, I, Heude, B, Hivert, MF, Hryhorczuk, D, Huang, RC, Inskip, H, Jusko, TA, Karvonen, AM, Koletzko, B, Kupers, LK, Lagstrom, H, Lawlor, DA, Lehmann, I, Lopez-Espinosa, MJ, Magnus, P, Majewska, R, Makela, J, Manios, Y, McDonald, SW, Mommers, M, Morgen, CS, Moschonis, G, Murinova, L, Newnham, J, Nohr, EA, Andersen, AMN, Oken, E, Oostvogels, A, Pac, A, Papadopoulou, E, Pekkanen, J, Pizzi, C, Polanska, K, Porta, D, Richiardi, L, Rifas-Shiman, SL, Roeleveld, N, Santa-Marina, L, dos Santos, AC, Smit, HA, Sorensen, TIA, Standl, M, Stanislawski, M, Stoltenberg, C, Thiering, E, Thijs, C, Torrent, M, Tough, SC, Trnovec, T, Gelder, M, Rossem, L, Berg, A, Vrijheid, M, Vrijkotte, TGM, Zvinchuk, O, van Buuren, S, and Jaddoe, Vincent
Published: 2018

28. Common colorectal cancer risk alleles contribute to the multiple colorectal adenoma phenotype, but do not influence colonic polyposis in FAP

Author: Cheng, T. H. T., Gorman, M., Martin, L., Barclay, E., Casey, G., Newcomb, P. A., Conti, D. V., Schumacher, F. R., Gallinger, S., Lindor, N. M., Hopper, J., Jenkins, M., Hunter, D. J., Kraft, P., Jacobs, K. B., Cox, D. G., Yeager, M., Hankinson, S. E., Wacholder, S., Wang, Z., Welch, R., Hutchinson, A., Wang, J., Yu, K., Chatterjee, N., Orr, N., Willett, W. C., Colditz, G. A., Ziegler, R. G., Berg, C. D., Buys, S. S., McCarty, C. A., Feigelson, H. S., Calle, E. E., Thun, M. J., Hayes, R. B., Tucker, M., Gerhard, D. S., Fraumeni, J. F., Jr., Hoover, R. N., Thomas, G., Chanock, S. J., Ciampa, J., Gonzalez-Bosquet, J., Berndt, S., Amundadottir, L., Diver, W. R., Albanes, D., Virtamo, J., Weinstein, S. J., Cancel-Tassin, G., Cussenot, O., Valeri, A., Andriole, G. L., Crawford, E. D., Haiman, C. A., Henderson, B., Kolonel, L., March, L. L., Siddiq, A., Riboli, E., Key, T. J., Kaaks, R., Isaacs, W., Isaacs, S., Wiley, K. E., Gronberg, H., Wiklund, F., Stattin, P., Xu, J., Zheng, S. L., Sun, J., Vatten, L. J., Hveem, K., Kumle, M., Purdue, M. P., Johansson, M., Zelenika, D., Toro, J. R., Scelo, G., Moore, L. E., Prokhortchouk, E., Wu, X., Kiemeney, L. A., Gaborieau, V., Chow, W. -H., Zaridze, D., Matveev, V., Lubinski, J., Trubicka, J., Szeszenia-Dabrowska, N., Lissowska, J., Rudnai, P., Fabianova, E., Bucur, A., Bencko, V., Foretova, L., Janout, V., Boffetta, P., Colt, J. S., Davis, F. G., Schwartz, K. L., Banks, R. E., Selby, P. J., Harnden, P., Hsing, A. W., Grubb, R. L., III, Boeing, H., Vineis, P., Clavel-Chapelon, F., Palli, D., Tumino, R., Krogh, V., Panico, S., Duell, E. J., Quirós, J. R., Sanchez, M. -J., Navarro, C., Ardanaz, E., Dorronsoro, M., Khaw, K. -T., Allen, N. E., Bueno-de-Mesquita, H. B., Peeters, P. H. M., Trichopoulos, D., Linseisen, J., Ljungberg, B., Overvad, K., Tjønnel, Romieu, I., Mukeria, A., Shangina, O., Stevens, V. L., Gapstur, S. M., Pharoah, P. D., Easton, D. F., Njølstad, I., Tell, G. S., Stoltenberg, C., Kumar, R., Koppova, K., Benhamou, S., Oosterwijk, E., Vermeulen, S. H., Aben, K. K. H., Van Der Marel, S. L., Ye, Y., Wood, C. G., Pu, X., Mazur, A. M., Boulygina, E. S., Chekanov, N. N., Foglio, M., Lechner, D., Gut, I., Heath, S., Blanche, H., Skryabin, K. G., McKay, J. D., Rothman, N., Lathrop, M., Brennan, P., Saunders, B., Thomas, H., Clark, S., Tomlinson, I., and Cheng, T.H.T. and Gorman, M. and Martin, L. and Barclay, E. and Casey, G. and Newcomb, P.A. and Conti, D.V. and Schumacher, F.R. and Gallinger, S. and Lindor, N.M. and Hopper, J. and Jenkins, M. and Hunter, D.J. and Kraft, P. and Jacobs, K.B. and Cox, D.G. and Yeager, M. and Hankinson, S.E. and Wacholder, S. and Wang, Z. and Welch, R. and Hutchinson, A. and Wang, J. and Yu, K. and Chatterjee, N. and Orr, N. and Willett, W.C. and Colditz, G.A. and Ziegler, R.G. and Berg, C.D. and Buys, S.S. and McCarty, C.A. and Feigelson, H.S. and Calle, E.E. and Thun, M.J. and Hayes, R.B. and Tucker, M. and Gerhard, D.S. and Fraumeni, J.F., Jr. and Hoover, R.N. and Thomas, G. and Chanock, S.J. and Ciampa, J. and Gonzalez-Bosquet, J. and Berndt, S. and Amundadottir, L. and Diver, W.R. and Albanes, D. and Virtamo, J. and Weinstein, S.J. and Cancel-Tassin, G. and Cussenot, O. and Valeri, A. and Andriole, G.L. and Crawford, E.D. and Haiman, C.A. and Henderson, B. and Kolonel, L. and Marchand, L.L. and Siddiq, A. and Riboli, E. and Key, T.J. and Kaaks, R. and Isaacs, W. and Isaacs, S. and Wiley, K.E. and Gronberg, H. and Wiklund, F. and Stattin, P. and Xu, J. and Zheng, S.L. and Sun, J. and Vatten, L.J. and Hveem, K. and Kumle, M. and Purdue, M.P. and Johansson, M. and Zelenika, D. and Toro, J.R. and Scelo, G. and Moore, L.E. and Prokhortchouk, E. and Wu, X. and Kiemeney, L.A. and Gaborieau, V. and Chow, W.-H. and Zaridze, D. and Matveev, V. and Lubinski, J. and Trubicka, J. and Szeszenia-Dabrowska, N. and Lissowska, J. and Rudnai, P. and Fabianova, E. and Bucur, A. and Bencko, V. and Foretova, L. and Janout, V. and Boffetta, P. and Colt, J.S. and Davis, F.G. and Schwartz, K.L. and Banks, R.E. and Selby, P.J. and Harnden, P. and Hsing, A.W. and Grubb, R.L., III and Boeing, H. and Vineis, P. and Clavel-Chapelon, F. and Palli, D. and Tumino, R. and Krogh, V. and Panico, S. and Duell, E.J. and Quirós, J.R. and Sanchez, M.-J. and Navarro, C. and Ardanaz, E. and Dorronsoro, M. and Khaw, K.-T. and Allen, N.E. and Bueno-de-Mesquita, H.B. and Peeters, P.H.M. and Trichopoulos, D. and Linseisen, J. and Ljungberg, B. and Overvad, K. and Tjønneland, A. and Romieu, I. and Mukeria, A. and Shangina, O. and Stevens, V.L. and Gapstur, S.M. and Pharoah, P.D. and Easton, D.F. and Njølstad, I. and Tell, G.S. and Stoltenberg, C. and Kumar, R. and Koppova, K. and Benhamou, S. and Oosterwijk, E. and Vermeulen, S.H. and Aben, K.K.H. and Van Der Marel, S.L. and Ye, Y. and Wood, C.G. and Pu, X. and Mazur, A.M. and Boulygina, E.S. and Chekanov, N.N. and Foglio, M. and Lechner, D. and Gut, I. and Heath, S. and Blanche, H. and Skryabin, K.G. and McKay, J.D. and Rothman, N. and Lathrop, M. and Brennan, P. and Saunders, B. and Thomas, H. and Clark, S. and Tomlinson, I.
Subjects: Male, pathogenesi, genetic association, phenotype, Adenomatous Polyposis Coli Protein, colorectal cancer, Colorectal Neoplasm, cancer risk, gene frequency, Polymorphism, Single Nucleotide, Article, DNA glycosyltransferase, adult, DNA glycosylase MutY, colon polyposi, single nucleotide polymorphism, genetic variability, middle aged, controlled study, Genetic Predisposition to Disease, human, DNA Glycosylase, Germ-Line Mutation, Aged, colorectal adenoma, Allele, modifier gene, Genes, Modifier, disease predisposition, APC protein, human, major clinical study, digestive system diseases, human tissue, APC protein, female, priority journal, Adenomatous Polyposis Coli, germline mutation, familial colon polyposi, adenoma, single nucleotide polymorphism, Adenoma, genetic, genetic predisposition
Abstract: The presence of multiple (5-100) colorectal adenomas suggests an inherited predisposition, but the genetic aetiology of this phenotype is undetermined if patients test negative for Mendelian polyposis syndromes such as familial adenomatous polyposis (FAP) and MUTYH-associated polyposis (MAP). We investigated whether 18 common colorectal cancer (CRC) predisposition single-nucleotide polymorphisms (SNPs) could help to explain some cases with multiple adenomas who phenocopied FAP or MAP, but had no pathogenic APC or MUTYH variant. No multiple adenoma case had an outlying number of CRC SNP risk alleles, but multiple adenoma patients did have a significantly higher number of risk alleles than population controls (P = 5.7 × 10-7). The association was stronger in those with ≥ 10 adenomas. The CRC SNPs accounted for 4.3% of the variation in multiple adenoma risk, with three SNPs (rs6983267, rs10795668, rs3802842) explaining 3.0% of the variation. In FAP patients, the CRC risk score did not differ significantly from the controls, as we expected given the overwhelming effect of pathogenic germline APC variants on the phenotype of these cases. More unexpectedly, we found no evidence that the CRC SNPs act as modifier genes for the number of colorectal adenomas in FAP patients. In conclusion, common colorectal tumour risk alleles contribute to the development of multiple adenomas in patients without pathogenic germline APC or MUTYH variants. This phenotype may have 'polygenic' or monogenic origins. The risk of CRC in relatives of multiple adenoma cases is probably much lower for cases with polygenic disease, and this should be taken into account when counselling such patients. © 2015 Macmillan Publishers Limited All rights reserved.
Published: 2015

29. Rates, distribution and implications of postzygotic mosaic mutations in autism spectrum disorder

Author: Lim, Elaine T., Uddin, Mohammed, De Rubeis, Silvia, Chan, Yingleong, Kamumbu, Anne S., Zhang, Xiaochang, D'Gama, Alissa M., Kim, Sonia N., Hill, Robert Sean, Goldberg, Arthur P., Poultney, Christopher, Minshew, Nancy J., Kushima, Itaru, Aleksic, Branko, Ozaki, Norio, Parellada, Mara, Arango, Celso, Penzol, Maria J., Carracedo, Angel, Kolevzon, Alexander, Hultman, Christina M., Weiss, Lauren A., Fromer, Menachem, Chiocchetti, Andreas G., Freitag, Christine M., Church, George M., Scherer, Stephen W., Buxbaum, Joseph D., Walsh, Christopher A, Aleksic, B, Anney, R, Barbosa, M, Barrett, J, Betancur, C, Bishop, S, Brusco, A, Buxbaum, Jd, Carracedo, A, Chiocchetti, Ag, Chung, Bhy, Cook, E, Coon, H, Cutler, Dj, Daly, M, De Rubeis, S, Doan, R, Fernández-Prieto, M, Ferrero, Gb, Freitag, Cm, Fromer, M, Gargus, J, Geschwind, D, Gill, M, Gómez-Guerrero, L, Hansen-Kiss, E, He, X, Herman, G, Hertz-Picciotto, I, Hultman, C, Iliadou, B, Ionita-Laza, I, Jugessur, A, Knudsen, Gp, Kolevzon, A, Kosmicki, J, Kushima, I, Lee, Sl, Lehner, T, Lennertz, S, Lim, E, Maciel, P, Magnus, P, Manoach, D, Minshew, N, Morrow, E, Mulle, J, Neale, B, Ozaki, N, Palotie, A, Parellada, M, Passos-Bueno, Mr, Pericak-Vance, M, Persico, A, Pessah, I, Reichenberg, A, Reichert, J, Renieri, A, Robinson, E, Samocha, K, Sanders, S, Sandin, S, Santangelo, Sl, Satterstrom, K, Schafer, C, Schellenberg, G, Scherer, S, Senthil, G, Silva, M, Singh, T, Siper, Pm, Soares, G, Stevens, C, Stoltenberg, C, Surén, P, Sutcliffe, Js, Szatmari, P, Tassone, F, Thurm, A, Walsh, C, Weiss, L, Werling, D, Willsey, J, Xu, X, Yu, Tw, Yuen, R, Zwick, Me., Howard Hughes Medical Institute [Boston] (HHMI), Howard Hughes Medical Institute (HHMI)-Harvard Medical School [Boston] (HMS), Boston Children's Hospital, Harvard Medical School [Boston] (HMS), Broad Institute of MIT and Harvard (BROAD INSTITUTE), Harvard Medical School [Boston] (HMS)-Massachusetts Institute of Technology (MIT)-Massachusetts General Hospital [Boston], Harvard University [Cambridge], Mohammed Bin Rashid University of Medicine and Health Sciences (MBRU), Icahn School of Medicine at Mount Sinai [New York] (MSSM), University of Pittsburgh (PITT), Pennsylvania Commonwealth System of Higher Education (PCSHE), Nagoya University, Hospital General Universitario 'Gregorio Marañón' [Madrid], Universidad Complutense de Madrid = Complutense University of Madrid [Madrid] (UCM), Centro de Investigación Biomédica en Red Salud Mental [Madrid] (CIBER-SAM), Universidade de Santiago de Compostela [Spain] (USC ), CIBER de Enfermedades Raras (CIBERER), Fundación Pública Galega Medicina Xenómica - SERGAS [Santiago de Compostela, Spain] (Grupo de Medicina Xenómica), CIBER de Enfermedades Raras (CIBERER)-Universidade de Santiago de Compostela [Spain] (USC ), King Abdulaziz University, Karolinska Institutet [Stockholm], University of California [San Francisco] (UCSF), University of California, Goethe-University Frankfurt am Main, Génétique de l'autisme = Genetics of Autism (NPS-01), Neurosciences Paris Seine (NPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), The Hospital for sick children [Toronto] (SickKids), University of Toronto, McLaughlin Centre for Population Health Risk Assessment, University of Ottawa [Ottawa], Autism Sequencing Consortium: Branko Aleksic, Richard Anney, Mafalda Barbosa, Jeffrey Barrett, Catalina Betancur, Somer Bishop, Alfredo Brusco, Joseph D Buxbaum, Angel Carracedo, Andreas G Chiocchetti, Brian H Y Chung, Edwin Cook, Hilary Coon, David J Cutler, Mark Daly, Silvia De Rubeis, Ryan Doan, Montserrat Fernández-Prieto, Giovanni Battista Ferrero, Christine M Freitag, Menachem Fromer, Jay Gargus, Dan Geschwind, Michael Gill, Lorena Gómez-Guerrero, Emily Hansen-Kiss, Xin He, Gail Herman, Irva Hertz-Picciotto, Christina Hultman, Bozenna Iliadou, Iuliana Ionita-Laza, Anil Jugessur, Gun Peggy Knudsen, Alexander Kolevzon, Jack Kosmicki, Itaru Kushima, S L Lee, Thomas Lehner, Savannah Lennertz, Elaine Lim, Patricia Maciel, Per Magnus, Dara Manoach, Nancy Minshew, Eric Morrow, Jennifer Mulle, Benjamin Neale, Norio Ozaki, Aarno Palotie, Mara Parellada, Maria Rita Passos-Bueno, Margaret Pericak-Vance, Antonio Persico, Isaac Pessah, Avi Reichenberg, Jennifer Reichert, Alessandra Renieri, Elise Robinson, Kaitlin Samocha, Stephan Sanders, Sven Sandin, Susan L Santangelo, Kyle Satterstrom, Chad Schafer, Gerry Schellenberg, Stephen Scherer, Geetha Senthil, Marisol Silva, Tarjinder Singh, Paige M Siper, Gabriela Soares, Christine Stevens, Camilla Stoltenberg, Pål Surén, James S Sutcliffe, Peter Szatmari, Flora Tassone, Audrey Thurm, Christopher Walsh, Lauren Weiss, Donna Werling, Jeremy Willsey, Xinyi Xu, Timothy W Yu, Ryan Yuen, Michael E Zwick., University of California [San Francisco] (UC San Francisco), University of California (UC), Neuroscience Paris Seine (NPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), and Betancur, Catalina
Subjects: 0301 basic medicine, Proband, Nonsynonymous substitution, Autism Spectrum Disorder, Databases, Genetic, Genetic Predisposition to Disease, Genetic Variation, Humans, Mosaicism, Mutation, Missense, Zygote, Neuroscience (all), Mutation, Missense, Epigenetics of autism, Biology, [SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human genetics, medicine.disease_cause, Article, 03 medical and health sciences, Genetic variation, mental disorders, Databases, Genetic, medicine, Missense mutation, Heritability of autism, MESH: Genetic Variation, MESH: Databases, Genetic, Genetics, MESH: Autism Spectrum Disorder, MESH: Mutation, Missense, [SDV.GEN]Life Sciences [q-bio]/Genetics, MESH: Humans, General Neuroscience, MESH: Genetic Predisposition to Disease, medicine.disease, 030104 developmental biology, [SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human genetics, Autism spectrum disorder, MESH: Zygote, MESH: Mosaicism
Abstract: International audience; We systematically analyzed postzygotic mutations (PZMs) in whole-exome sequences from the largest collection of trios (5,947) with autism spectrum disorder (ASD) available, including 282 unpublished trios, and performed resequencing using multiple independent technologies. We identified 7.5% of de novo mutations as PZMs, 83.3% of which were not described in previous studies. Damaging, nonsynonymous PZMs within critical exons of prenatally expressed genes were more common in ASD probands than controls (P < 1 × 10-6), and genes carrying these PZMs were enriched for expression in the amygdala (P = 5.4 × 10-3). Two genes (KLF16 and MSANTD2) were significantly enriched for PZMs genome-wide, and other PZMs involved genes (SCN2A, HNRNPU and SMARCA4) whose mutation is known to cause ASD or other neurodevelopmental disorders. PZMs constitute a significant proportion of de novo mutations and contribute importantly to ASD risk.
Published: 2017
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30. A Genome-Wide Association Meta-Analysis of Attention-Deficit/Hyperactivity Disorder Symptoms in Population-Based Pediatric Cohorts

Author: Middeldorp, C., Hammerschlag, A., Ouwens, K., Groen-Blokhuis, M., St Pourcain, B., Greven, C., Pappa, I., Tiesler, C., Ang, W., Nolte, I., Vilor-Tejedor, N., Bacelis, J., Ebejer, J., Zhao, H., Davies, G., Ehli, E., Evans, D., Fedko, I., Guxens, M., Hottenga, J., Hudziak, J., Jugessur, A., Kemp, J., Krapohl, E., Martin, N., Murcia, M., Myhre, R., Ormel, J., Ring, S., Standl, M., Stergiakouli, E., Stoltenberg, C., Thiering, E., Timpson, N., Trzaskowski, M., van der Most, P., Wang, C., EArly Genetics and Lifecourse Epidemiology (EAGLE) Consortium, Psychiatric Genomics Consortium ADHD Working Group, Nyholt, D., Medland, S., Neale, B., Jacobsson, B., Sunyer, J., Hartman, C., Whitehouse, A., Pennell, C., Heinrich, J., Plomin, R., Smith, G., Tiemeier, H., Posthuma, D., Boomsma, D., Epidemiology, Child and Adolescent Psychiatry / Psychology, Psychiatry, Life Course Epidemiology (LCE), Interdisciplinary Centre Psychopathology and Emotion regulation (ICPE), Human genetics, IOO, Amsterdam Neuroscience - Complex Trait Genetics, Child Psychiatry, EMGO+ - Mental Health, Amsterdam Neuroscience - Mood, Anxiety, Psychosis, Stress & Sleep, Biological Psychology, and Complex Trait Genetics
Subjects: 0301 basic medicine, Male, Netherlands Twin Register (NTR), attention problems, Population/methods, CHILDHOOD, Adhd Symptoms, Gwa, Snp Heritability, Attention Problems, Meta-analysis, Genome-wide association study, CHILDREN, Cohort Studies, 0302 clinical medicine, Developmental and Educational Psychology, GENETIC INFLUENCES, NETHERLANDS TWIN REGISTER, Child, Genetics, RISK, education.field_of_study, Genetics, Population/methods, 3. Good health, Psychiatry and Mental health, PERSONALITY CONSORTIUM, Female, Psychology, Attention Deficit Disorder with Hyperactivity/genetics, Adolescent, DEFICIT HYPERACTIVITY DISORDER, Population, Single-nucleotide polymorphism, GWA, PROFILE, Genetic correlation, ADHD symptoms, Article, 150 000 MR Techniques in Brain Function, SNP heritability, BEHAVIOR PROBLEMS, 03 medical and health sciences, SDG 3 - Good Health and Well-being, medicine, SNP, Attention deficit hyperactivity disorder, ADHD, Humans, education, Genetic association, Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7], Heritability, medicine.disease, meta-analysis, 030104 developmental biology, Genetics, Population, Trastorn per dèficit d'atenció amb hiperactivitat, Attention Deficit Disorder with Hyperactivity, Case-Control Studies, 030217 neurology & neurosurgery, Genètica, Genome-Wide Association Study
Abstract: OBJECTIVE: The aims of this study were to elucidate the influence of common genetic variants on childhood attention-deficit/hyperactivity disorder (ADHD) symptoms, to identify genetic variants that explain its high heritability, and to investigate the genetic overlap of ADHD symptom scores with ADHD diagnosis. METHOD: Within the EArly Genetics and Lifecourse Epidemiology (EAGLE) consortium, genome-wide single nucleotide polymorphisms (SNPs) and ADHD symptom scores were available for 17,666 children (
Published: 2016
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31. Prenatal fever and autism risk

Author: Hornig, M, primary, Bresnahan, M A, additional, Che, X, additional, Schultz, A F, additional, Ukaigwe, J E, additional, Eddy, M L, additional, Hirtz, D, additional, Gunnes, N, additional, Lie, K K, additional, Magnus, P, additional, Mjaaland, S, additional, Reichborn-Kjennerud, T, additional, Schjølberg, S, additional, Øyen, A-S, additional, Levin, B, additional, Susser, E S, additional, Stoltenberg, C, additional, and Lipkin, W I, additional
Published: 2017
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32. Pooling birth cohorts in allergy and asthma: European union-funded initiatives-a MeDALL, CHICOS, ENRIECO, and GALEN joint paper: CHICOS study group ENRIECO study group GA2LEN study group

Author: Bousquet, Jean, Anto, Josep, Sunyer, Jordi, Nieuwenhuijsen, Mark, Vrijheid, Martine, Keil, Thomas, Akdis, M., Auffray, C., Postma, D. S., Valenta, R., Haahtela, T., Cambon-Thomsen, A., Lambrecht, B. N., Akdis, C. A., Annesi-Maesano, I., Arno, A., Bachert, C., Ballester, F., Basagana, X., Baumgartner, U., Bindslev-Jensen, C., Brunekreef, B., Chatzi, L., Eller, E., Forastiere, F., Garcia-Aymerich, J., Guerra, S., Gehring, U., Hammad, H., Heinrich, J., Hohmann, C., Kauffmann, F., Kerkhof, M., Kogevinas, M., Koppelman, G. H., Kowalski, M. L., Kull, I., Lau, S., Lodrup-Carlsen, K. C., Lupinek, C., Maier, D., Makela, M. J., Martinez, F. D., Momas, I., Nawijn, M. C., Neubauer, A., Oddie, S., Palkonen, S., Reitamo, S., Rial-Sebbag, E., Salapatas, M., Siroux, V., Smagghe, D., Smit, H. A., Torrent, M., Toskala, E., van Oosterhout, A. J. M., Varaso, R., von Hertzen, L., Wickman, M., Wijmenga, C., Zuberbier, T., Burney, P. G., Van Cauwenberge, P., Bonini, S., Fokkens, W. J., Kramer, U., Mullol, J., Nizankowska-Mogilnicka, E., Papadopoulos, N., Alm, B., Alm, J., Arshad, S. H., Bravi, F., Canonica, G. W., Custovic, A., Dubakiene, R., Fantini, M. P., Gjomarkaj, M., Halken, S., Host, A., Howarth, P., Kuehni, C., Lotvall, J., Mommers, M., Porta, D., Radon, K., Ring, J., Roberts, G., Schünemann, H. J., Simpson, A., Szczecklik, A., Thijs, C., Todo-Bom, A., Valovirta, E., van Steen, K., Von Berg, A., von Mutius, E., Wahn, U., Wennergren, G., Wijga, A. H., Zock, J. P., Duijts, L., Jaddoe, V., Lawlor, D., Lucas, P., Magnus, P., Merletti, F., Nybo Andersen, A. M., Raat, H., Stoltenberg, C., Casas, M., Bergström, A., Carmichael, A., Chen, C. -M., Cordier, S., Eggesbø, M., Fernández, M. F., Fernández-Somoano, A., Grazuleviciene, R., Karvonen, A. M., Koppen, G., Krämer, U., Kuehni, C. E., Majewska, R., Patelarou, E., Skaalum Petersen, M., Pierik, F. H., Polanska, K., Richiardi, L., Santos, A. C., Slama, R., Sram, R. J., Tischer, C., Toft, G., Trnovec, T., Vandentorren, S., Vardavas, C., Vrijkotte, T. G. M., Wilhelm, M., Bousquet, Jean, Anto, Josep, Sunyer, Jordi, Nieuwenhuijsen, Mark, Vrijheid, Martine, Keil, Thoma, Akdis, M., Auffray, C., Postma, D.S., Valenta, R., Haahtela, T., Cambon-Thomsen, A., Lambrecht, B.N., Akdis, C.A., Annesi-Maesano, I., Arno, A., Bachert, C., Ballester, F., Basagana, X., Baumgartner, U., Bindslev-Jensen, C., Brunekreef, B., Chatzi, L., Eller, E., Forastiere, F., Garcia-Aymerich, J., Guerra, S., Gehring, U., Hammad, H., Heinrich, J., Hohmann, C., Kauffmann, F., Kerkhof, M., Kogevinas, M., Koppelman, G.H., Kowalski, M.L., Kull, I., Lau, S., Lodrup-Carlsen, K.C., Lupinek, C., Maier, D., Makela, M.J., Martinez, F.D., Momas, I., Nawijn, M.C., Neubauer, A., Oddie, S., Palkonen, S., Reitamo, S., Rial-Sebbag, E., Salapatas, M., Siroux, V., Smagghe, D., Smit, H.A., Torrent, M., Toskala, E., van Oosterhout, A.J.M., Varaso, R., von Hertzen, L., Wickman, M., Wijmenga, C., Zuberbier, T., Burney, P.G., Van Cauwenberge, P., Bonini, S., Fokkens, W.J., Kramer, U., Mullol, J., Nizankowska-Mogilnicka, E., Papadopoulos, N., Alm, B., Alm, J., Arshad, S.H., Bravi, F., Canonica, G.W., Custovic, A., Dubakiene, R., Fantini, M.P., Gjomarkaj, M., Halken, S., Host, A., Howarth, P., Kuehni, C., Lotvall, J., Mommers, M., Porta, D., Radon, K., Ring, J., Roberts, G., Schünemann, H.J., Simpson, A., Szczecklik, A., Thijs, C., Todo-Bom, A., Valovirta, E., van Steen, K., Von Berg, A., von Mutius, E., Wahn, U., Wennergren, G., Wijga, A.H., Zock, J.P., Duijts, L., Jaddoe, V., Lawlor, D., Lucas, P., Magnus, P., Merletti, F., Nybo Andersen, A.M., Raat, H., Stoltenberg, C., Casas, M., Bergström, A., Carmichael, A., Chen, C.-M., Cordier, S., Eggesbø, M., Fernández, M.F., Fernández-Somoano, A., Grazuleviciene, R., Karvonen, A.M., Koppen, G., Krämer, U., Kuehni, C.E., Majewska, R., Patelarou, E., Skaalum Petersen, M., Pierik, F.H., Polanska, K., Richiardi, L., Santos, A.C., Slama, R., Sram, R.J., Tischer, C., Toft, G., Trnovec, T., Vandentorren, S., Vardavas, C., Vrijkotte, T.G.M., and Wilhelm, M.
Subjects: Allergy, Risk Factor, Immunology, CHICOS, Longitudinal Studie, Environmental Exposure, Asthma, Europe, MeDALL, ENRIECO, Hypersensitivity, Multicenter Studies as Topic, Immunology and Allergy, European Union, Cohort Studie, Birth cohort, Human
Abstract: Long-term birth cohort studies are essential to understanding the life course and childhood predictors of allergy and the complex interplay between genes and the environment (including lifestyle and socioeconomic determinants). Over 100 cohorts focusing on asthma and allergy have been initiated in the world over the past 30 years. Since 2004, several research initiatives funded under the EU Framework Program for Research and Technological Development FP6-FP7 have attempted to identify, compare, and evaluate pooling data from existing European birth cohorts (GA2LEN: Global Allergy and European Network, FP6; ENRIECO: Environmental Health Risks in European Birth Cohorts, FP7; CHICOS: Developing a Child Cohort Research Strategy for Europe, FP7; MeDALL: Mechanisms of the Development of ALLergy, FP7). However, there is a general lack of knowledge about these initiatives and their potentials. The aim of this paper is to review current and past EU-funded projects in order to make a summary of their goals and achievements and to suggest future research needs of these European birth cohort networks. © 2012 S. Karger AG, Basel.
Published: 2013

33. Genome-wide association study of renal cell carcinoma identifiestwo susceptibility loci on 2p21 and 11q13.3

Author: Purdue MP, Johansson M, Zelenika D, Toro JR, Scelo G, Moore LE, Prokhortchouk E, Wu X, Kiemeney LA, Gaborieau V, Jacobs KB, Chow WH, Zaridze D, Matveev V, Lubinski J, Trubicka J, Szeszenia Dabrowska N, Lissowska J, Rudnai P, Fabianova E, Bucur A, Bencko V, Foretova L, Janout V, Boffetta P, Colt JS, Davis FG, Schwartz KL, Banks RE, Selby PJ, Harnden P, Berg CD, Hsing AW, Grubb RL 3rd, Boeing H, Vineis P, Clavel Chapelon F, Palli D, Tumino R, Krogh V, Duell EJ, Quirós JR, Sanchez MJ, Navarro C, Ardanaz E, Dorronsoro M, Khaw KT, Allen NE, Bueno de Mesquita HB, Peeters PH, Trichopoulos D, Linseisen J, Ljungberg B, Overvad K, Tjønneland A, Romieu I, Riboli E, Mukeria A, Shangina O, Stevens VL, Thun MJ, Diver WR, Gapstur SM, Pharoah PD, Easton DF, Albanes D, Weinstein SJ, Virtamo J, Vatten L, Hveem K, Njølstad I, Tell GS, Stoltenberg C, Kumar R, Koppova K, Cussenot O, Benhamou S, Oosterwijk E, Vermeulen SH, Aben KK, van der Marel SL, Ye Y, Wood CG, Pu X, Mazur AM, Boulygina ES, Chekanov NN, Foglio M, Lechner D, Gut I, Heath S, Blanche H, Hutchinson A, Thomas G, Wang Z, Yeager M, Fraumeni JF Jr, Skryabin KG, McKay JD, Rothman N, Chanock SJ, Lathrop M, Brennan P., PANICO, SALVATORE, Purdue, Mp, Johansson, M, Zelenika, D, Toro, Jr, Scelo, G, Moore, Le, Prokhortchouk, E, Wu, X, Kiemeney, La, Gaborieau, V, Jacobs, Kb, Chow, Wh, Zaridze, D, Matveev, V, Lubinski, J, Trubicka, J, Szeszenia Dabrowska, N, Lissowska, J, Rudnai, P, Fabianova, E, Bucur, A, Bencko, V, Foretova, L, Janout, V, Boffetta, P, Colt, J, Davis, Fg, Schwartz, Kl, Banks, Re, Selby, Pj, Harnden, P, Berg, Cd, Hsing, Aw, Grubb RL, 3rd, Boeing, H, Vineis, P, Clavel Chapelon, F, Palli, D, Tumino, R, Krogh, V, Panico, Salvatore, Duell, Ej, Quirós, Jr, Sanchez, Mj, Navarro, C, Ardanaz, E, Dorronsoro, M, Khaw, Kt, Allen, Ne, Bueno de Mesquita, Hb, Peeters, Ph, Trichopoulos, D, Linseisen, J, Ljungberg, B, Overvad, K, Tjønneland, A, Romieu, I, Riboli, E, Mukeria, A, Shangina, O, Stevens, Vl, Thun, Mj, Diver, Wr, Gapstur, Sm, Pharoah, Pd, Easton, Df, Albanes, D, Weinstein, Sj, Virtamo, J, Vatten, L, Hveem, K, Njølstad, I, Tell, G, Stoltenberg, C, Kumar, R, Koppova, K, Cussenot, O, Benhamou, S, Oosterwijk, E, Vermeulen, Sh, Aben, Kk, van der Marel, Sl, Ye, Y, Wood, Cg, Pu, X, Mazur, Am, Boulygina, E, Chekanov, Nn, Foglio, M, Lechner, D, Gut, I, Heath, S, Blanche, H, Hutchinson, A, Thomas, G, Wang, Z, Yeager, M, Fraumeni JF, Jr, Skryabin, Kg, Mckay, Jd, Rothman, N, Chanock, Sj, Lathrop, M, and Brennan, P.
Published: 2011

34. On Positive Value of Information in Risk Sharing

Author: Denderski, P.R., Stoltenberg, C., and Economics
Published: 2015

35. A Genome-Wide Association Meta-Analysis of Attention-Deficit/Hyperactivity Disorder Symptoms in Population-Based Pediatric Cohorts

Author: Middeldorp, C.M., Hammerschlag, A.R., Ouwens, K.G., Groen-Blokhuis, M.M., Pourcain, B. St, Greven, C.U., Pappa, I., Tiesler, C.M., Ang, W., Nolte, I.M., Vilor-Tejedor, N., Bacelis, J., Ebejer, J.L., Zhao, H., Davies, G.E., Ehli, E.A., Evans, D.M., Fedko, I.O., Guxens, M., Hottenga, J.J., Hudziak, J.J., Jugessur, A., Kemp, J.P., Krapohl, E., Martin, N.G., Murcia, M., Myhre, R., Ormel, J., Ring, S.M., Standl, M., Stergiakouli, E., Stoltenberg, C., Thiering, E., Timpson, N.J., Trzaskowski, M., Most, P.J. van der, Wang, C., Nyholt, D.R., Medland, S.E., Neale, B., Jacobsson, B., Sunyer, J., Hartman, C.A., Whitehouse, A.J.O., Pennell, C.E., Heinrich, J., Plomin, R., Smith, G., Tiemeier, H., Posthuma, D., Boomsma, D.I., Middeldorp, C.M., Hammerschlag, A.R., Ouwens, K.G., Groen-Blokhuis, M.M., Pourcain, B. St, Greven, C.U., Pappa, I., Tiesler, C.M., Ang, W., Nolte, I.M., Vilor-Tejedor, N., Bacelis, J., Ebejer, J.L., Zhao, H., Davies, G.E., Ehli, E.A., Evans, D.M., Fedko, I.O., Guxens, M., Hottenga, J.J., Hudziak, J.J., Jugessur, A., Kemp, J.P., Krapohl, E., Martin, N.G., Murcia, M., Myhre, R., Ormel, J., Ring, S.M., Standl, M., Stergiakouli, E., Stoltenberg, C., Thiering, E., Timpson, N.J., Trzaskowski, M., Most, P.J. van der, Wang, C., Nyholt, D.R., Medland, S.E., Neale, B., Jacobsson, B., Sunyer, J., Hartman, C.A., Whitehouse, A.J.O., Pennell, C.E., Heinrich, J., Plomin, R., Smith, G., Tiemeier, H., Posthuma, D., and Boomsma, D.I.
Abstract: Contains fulltext : 165989.pdf (publisher's version ) (Closed access), OBJECTIVE: The aims of this study were to elucidate the influence of common genetic variants on childhood attention-deficit/hyperactivity disorder (ADHD) symptoms, to identify genetic variants that explain its high heritability, and to investigate the genetic overlap of ADHD symptom scores with ADHD diagnosis. METHOD: Within the EArly Genetics and Lifecourse Epidemiology (EAGLE) consortium, genome-wide single nucleotide polymorphisms (SNPs) and ADHD symptom scores were available for 17,666 children (<13 years of age) from nine population-based cohorts. SNP-based heritability was estimated in data from the three largest cohorts. Meta-analysis based on genome-wide association (GWA) analyses with SNPs was followed by gene-based association tests, and the overlap in results with a meta-analysis in the Psychiatric Genomics Consortium (PGC) case-control ADHD study was investigated. RESULTS: SNP-based heritability ranged from 5% to 34%, indicating that variation in common genetic variants influences ADHD symptom scores. The meta-analysis did not detect genome-wide significant SNPs, but three genes, lying close to each other with SNPs in high linkage disequilibrium (LD), showed a gene-wide significant association (p values between 1.46 x 10(-6) and 2.66 x 10(-6)). One gene, WASL, is involved in neuronal development. Both SNP- and gene-based analyses indicated overlap with the PGC meta-analysis results with the genetic correlation estimated at 0.96. CONCLUSION: The SNP-based heritability for ADHD symptom scores indicates a polygenic architecture, and genes involved in neurite outgrowth are possibly involved. Continuous and dichotomous measures of ADHD appear to assess a genetically common phenotype. A next step is to combine data from population-based and case-control cohorts in genetic association studies to increase sample size and to improve statistical power for identifying genetic variants.
Published: 2016

36. A Genome-Wide Association Meta-Analysis of Attention-Deficit/Hyperactivity Disorder Symptoms in Population-Based Pediatric Cohorts

Author: Middeldorp, C.M. (Christel), Hammerschlag, A.R. (Anke R.), Ouwens, K.G. (Klaasjan), Groen-Blokhuis, M. (Maria), St Pourcain, B. (Beate), Greven, C.U. (Corina U.), Pappa, M. (Magda), Tiesler, C.M.T. (Carla M.T.), Ang, W.Q. (Wei), Nolte, I.M. (Ilja), Vilor-Tejedor, N. (Natàlia), Bacelis, J. (Jonas), Ebejer, J.L. (Jane L.), Zhao, H. (Huiying), Davies, G.E. (Gareth), Ehli, E.A. (Erik), Evans, D.M. (David), Fedko, I.O. (Iryna O.), Guxens Junyent, M. (Mònica), Hottenga, J.J. (Jouke Jan), Hudziak, J.J. (James), Juqessur, A. (Astanand), Kemp, J.P. (John), Krapohl, E. (Eva), Martin, N.G. (Nicholas), Murcia, M. (Mario), Myhre, R. (Ronny), Ormel, J. (Johan), Ring, S.M. (Susan), Standl, E. (Eberhard), Stergiakouli, E. (Evangelia), Stoltenberg, C. (Camilla), Thiering, E. (Elisabeth), Timpson, N.J. (Nicholas), Trzaskowski, M. (Maciej), Most, P.J. (Peter) van der, Wang, C.A. (Carol A.), Nyholt, D.R. (Dale), Medland, S.E. (Sarah), Neale, B.M. (Benjamin), Jacobsson, B. (Bo), Sunyer, J. (Jordi), Hartman, C.A. (C.), Whitehouse, A.J.O. (Andrew), Pennell, C.E. (Craig), Heinrich, J. (Joachim), Plomin, R. (Robert), Smith, A.V. (Davey), Tiemeier, H.W. (Henning), Posthuma, D. (Danielle), Boomsma, D.I. (Dorret), Middeldorp, C.M. (Christel), Hammerschlag, A.R. (Anke R.), Ouwens, K.G. (Klaasjan), Groen-Blokhuis, M. (Maria), St Pourcain, B. (Beate), Greven, C.U. (Corina U.), Pappa, M. (Magda), Tiesler, C.M.T. (Carla M.T.), Ang, W.Q. (Wei), Nolte, I.M. (Ilja), Vilor-Tejedor, N. (Natàlia), Bacelis, J. (Jonas), Ebejer, J.L. (Jane L.), Zhao, H. (Huiying), Davies, G.E. (Gareth), Ehli, E.A. (Erik), Evans, D.M. (David), Fedko, I.O. (Iryna O.), Guxens Junyent, M. (Mònica), Hottenga, J.J. (Jouke Jan), Hudziak, J.J. (James), Juqessur, A. (Astanand), Kemp, J.P. (John), Krapohl, E. (Eva), Martin, N.G. (Nicholas), Murcia, M. (Mario), Myhre, R. (Ronny), Ormel, J. (Johan), Ring, S.M. (Susan), Standl, E. (Eberhard), Stergiakouli, E. (Evangelia), Stoltenberg, C. (Camilla), Thiering, E. (Elisabeth), Timpson, N.J. (Nicholas), Trzaskowski, M. (Maciej), Most, P.J. (Peter) van der, Wang, C.A. (Carol A.), Nyholt, D.R. (Dale), Medland, S.E. (Sarah), Neale, B.M. (Benjamin), Jacobsson, B. (Bo), Sunyer, J. (Jordi), Hartman, C.A. (C.), Whitehouse, A.J.O. (Andrew), Pennell, C.E. (Craig), Heinrich, J. (Joachim), Plomin, R. (Robert), Smith, A.V. (Davey), Tiemeier, H.W. (Henning), Posthuma, D. (Danielle), and Boomsma, D.I. (Dorret)
Abstract: Objective The aims of this study were to elucidate the influence of common genetic variants on childhood attention-deficit/hyperactivity disorder (ADHD) symptoms, to identify genetic variants that explain its high heritability, and to investigate the genetic overlap of ADHD symptom scores with ADHD diagnosis. Method Within the EArly Genetics and Lifecourse Epidemiology (EAGLE) consortium, genome-wide single nucleotide polymorphisms (SNPs) and ADHD symptom scores were available for 17,666 children (<13 years of age) from nine population-based cohorts. SNP-based heritability was estimated in data from the three largest cohorts. Meta-analysis based on genome-wide association (GWA) analyses with SNPs was followed by gene-based association tests, and the overlap in results with a meta-analysis in the Psychiatric Genomics Consortium (PGC) case-control ADHD study was investigated. Results SNP-based heritability ranged from 5% to 34%, indicating that variation in common genetic variants influences ADHD symptom scores. The meta-analysis did not detect genome-wide significant SNPs, but three genes, lying close to each other with SNPs in high linkage disequilibrium (LD), showed a gene-wide significant association (p values between 1.46 × 10−6 and 2.66 × 10−6). One gene, WASL, is involved in neuronal development. Both SNP- and gene-based analyses indicated overlap with the PGC meta-analysis results with the genetic correlation estimated at 0.96. Conclusion The SNP-based heritability for ADHD symptom scores indicates a polygenic architecture, and genes involved in neurite outgrowth are possibly involved. Continuous and dichotomous measures of ADHD appear to assess a genetically common phenotype. A next step is to combine data from population-based and case-control cohorts in genetic association studies to increase sample size and to improve statistical power for identifying genetic variants.
Published: 2016
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37. Folic Acid Supplementation and Interpregnancy Interval

Author: Nilsen, R.M., Mastroiacovo, P., Gunnes, N., Alsaker, E.R., Bjorke-Monsen, A.L., Eussen, S.J.P.M., Haugen, M., Johannessen, A., Meltzer, H.M., Stoltenberg, C., Ueland, P.M., Vollset, S.E., Epidemiologie, RS: CAPHRI School for Public Health and Primary Care, and RS: CAPHRI - Nutritional and Molecular Epidemiology
Abstract: Background Maternal folic acid supplementation between subsequent pregnancies may be important to reduce the risk of low folate status associated with short interpregnancy intervals. We examined how the prevalence of preconception folic acid use for a given pregnancy in Norwegian women varied according to the time interval from the previous pregnancy. Methods Analysis was based on 48 855 pairs of pregnancies with the second pregnancy included in the Norwegian Mother and Child Cohort Study (birth years 1999-2009). Interpregnancy interval was defined as the time from birth of a child to the conception of the subsequent sibling. Preconception folic acid use was defined as any use of folic acid-containing supplements within the last 4 weeks before the second pregnancy. Results The prevalence of preconception folic acid use was 31%. Among women with a term birth (>= 37 weeks) in the previous pregnancy (92%), those with interpregnancy intervals = 49 months were associated with up to 35% lower prevalence of preconception folic acid use for the second pregnancy, relative to the reference group (13-24 months). The low use in short intervals was mainly attributable to lower proportion of planned pregnancies and fewer women with higher education. Among women with a preterm birth (
Published: 2014

38. The autism birth cohort (ABC): A study of autism spectrum disorders in MoBa

Author: Surén, P., Schjølberg, S., Anne-Siri Øyen, Lie, K. K., Hornig, M., Bresnahan, M., Bakke, T., Roth, C., Alsaker, E., Schreuder, P., Stenberg, N., Reichborn-Kjennerud, T., Hirtz, D., Susser, E., Magnus, P., Lipkin, W. I., and Stoltenberg, C.
Subjects: genetic structures, mental disorders, VDP::Medisinske fag: 700::Helsefag: 800::Epidemiologi medisinsk og odontologisk statistikk: 803, VDP::Midical sciences: 700::Health sciences: 800::Epidemiology, medical and dental statistics: 803, behavioral disciplines and activities
Abstract: Background: Autism spectrum disorders (ASDs) are characterized by persistent deficits in social communication and interaction and restricted, repetitive patterns of behavior, interests or activities. In most cases, the cause of ASD is likely to be a combination of genetic predisposition and environmental exposures occurring in fetal life or early infancy. Consequently, a prospective pregnancy cohort like MoBa represents an ideal platform for studies of ASDs in children. Methods: The Autism Birth Cohort (ABC) Study has identified potential ASD cases in MoBa through questionnaire- based screening, parental and professional referrals, and linkages to the Norwegian Patient Register. ASD diagnoses have been ascertained through in-person clinical assessments and medical record reviews. Current results: By the end of 2012, the ABC Study had identified 518 ASD cases in MoBa. The ASD prevalence in school-age children is 0.7-0.8%, which is in line with nationwide estimates for Norway. The most important source of ASD case identification was registry linkages, while only a minority was detected through early screening. Published findings show that screening at 18 months misses the majority of ASD cases. Analyses of risk factors for ASDs have shown that maternal use of folic acid supplements in early pregnancy may lower the child’s risk of developing ASDs and that paternal obesity appears to increase the child’s risk of ASDs. Future plans: ASD case identification will continue through annual registry linkages and subsequent reviews of medical records. Analyses of plasma samples and RNA samples will be conducted to investigate prenatal and perinatal microbial exposures, innate immune and inflammatory responses, biomarkers of autism risk, and exposures to xenobiotics. Analyses of deciduous teeth will also investigate the effect of medications and environmental toxins. Exome sequencing of DNA from ASD cases and their parents is ongoing, and will elucidate the role of de novo DNA mutations in the pathogenesis of ASDs. Future epidemiological analyses will explore the results of the 36-month screening for ASDs, the diagnostic stability and developmental trajectories in ASD children, and psychiatric and medical comorbidities in ASDs. publishedVersion
Published: 2014

39. Birthweight and Childhood Cancer: Preliminary Findings from the International Childhood Cancer Cohort Consortium (I4C)

Author: Paltiel, O, Tikellis, G, Linet, M, Golding, J, Lemeshow, S, Phillips, G, Lamb, K, Stoltenberg, C, Haberg, SE, Strom, M, Granstrom, C, Northstone, K, Klebanoff, M, Ponsonby, A-L, Milne, E, Pedersen, M, Kogevinas, M, Ha, E, Dwyer, T, Paltiel, O, Tikellis, G, Linet, M, Golding, J, Lemeshow, S, Phillips, G, Lamb, K, Stoltenberg, C, Haberg, SE, Strom, M, Granstrom, C, Northstone, K, Klebanoff, M, Ponsonby, A-L, Milne, E, Pedersen, M, Kogevinas, M, Ha, E, and Dwyer, T
Abstract: BACKGROUND: Evidence relating childhood cancer to high birthweight is derived primarily from registry and case-control studies. We aimed to investigate this association, exploring the potential modifying roles of age at diagnosis and maternal anthropometrics, using prospectively collected data from the International Childhood Cancer Cohort Consortium. METHODS: We pooled data on infant and parental characteristics and cancer incidence from six geographically and temporally diverse member cohorts [the Avon Longitudinal Study of Parents and Children (UK), the Collaborative Perinatal Project (USA), the Danish National Birth Cohort (Denmark), the Jerusalem Perinatal Study (Israel), the Norwegian Mother and Child Cohort Study (Norway), and the Tasmanian Infant Health Survey (Australia)]. Birthweight metrics included a continuous measure, deciles, and categories (≥ 4.0 vs. < 4.0 kilogram). Childhood cancer (377 cases diagnosed prior to age 15 years) risk was analysed by type (all sites, leukaemia, acute lymphoblastic leukaemia, and non-leukaemia) and age at diagnosis. We estimated hazard ratios (HR) and 95% confidence intervals (CI) from Cox proportional hazards models stratified by cohort. RESULTS: A linear relationship was noted for each kilogram increment in birthweight adjusted for gender and gestational age for all cancers [HR = 1.26; 95% CI 1.02, 1.54]. Similar trends were observed for leukaemia. There were no significant interactions with maternal pre-pregnancy overweight or pregnancy weight gain. Birthweight ≥ 4.0 kg was associated with non-leukaemia cancer among children diagnosed at age ≥ 3 years [HR = 1.62; 95% CI 1.06, 2.46], but not at younger ages [HR = 0.7; 95% CI 0.45, 1.24, P for difference = 0.02]. CONCLUSION: Childhood cancer incidence rises with increasing birthweight. In older children, cancers other than leukaemia are particularly related to high birthweight. Maternal adiposity, currently widespread, was not demonstrated to substantially modify these
Published: 2015

40. Psychosocial factors associated with bulimia nervosa during pregnancy: An internal validation study

Author: Watson, Hunna, Von Holle, A., Knoph, C., Hamer, R., Torgersen, L., Reichborn-Kjennerud, T., Stoltenberg, C., Magnus, P., Bulik, C., Watson, Hunna, Von Holle, A., Knoph, C., Hamer, R., Torgersen, L., Reichborn-Kjennerud, T., Stoltenberg, C., Magnus, P., and Bulik, C.
Abstract: Objective The aim of this paper was to internally validate previously reported relations (Knoph Berg et al., Aust N Z J Psychiatry, 42, 396–404, 2008) between psychosocial factors and bulimia nervosa (BN) outcomes during pregnancy. Method This study is based on the Norwegian Mother and Child Cohort Study (MoBa) conducted by the Norwegian Institute of Public Health. Participants were women enrolled during pregnancy (N?=?69,030). Internal validity was evaluated by way of bootstrapped parameter estimates using the overall sample and a split sample calibration approach. Results Bootstrap bias estimates were below the problematic threshold, and extend earlier findings (Knoph Berg et al., Aust N Z J Psychiatry, 42, 396–404, 2008) by providing support for the validity of the models at the population level of all pregnant women in Norway. Bootstrap risk ratios indicated that prevalence, incidence, and remission of BN during pregnancy were significantly associated with psychosocial factors. The split sample procedure showed that the models developed on the training sample did not predict risks in the validation sample. Discussion This study characterizes associations between psychosocial exposures and BN outcomes among pregnant women in Norway. Women with lifetime and current self-reported psychosocial adversities were at a much higher risk for BN during pregnancy. Psychosocial factors were associated with BN remission during pregnancy, inviting the prospect of enhancing therapeutic interventions. We consider the findings in the context of reproducibility in science. © 2014 Wiley Periodicals, Inc. (Int J Eat Disord 2015; 48:654–662)
Published: 2015

41. ViPAR: a software platform for the Virtual Pooling and Analysis of Research Data

Author: Carter, Kim W, primary, Carter, KW, additional, Francis, RW, additional, Bresnahan, M, additional, Gissler, M, additional, Grønborg, TK, additional, Gross, R, additional, Gunnes, N, additional, Hammond, G, additional, Hornig, M, additional, Hultman, CM, additional, Huttunen, J, additional, Langridge, A, additional, Leonard, H, additional, Newman, S, additional, Parner, ET, additional, Petersson, G, additional, Reichenberg, A, additional, Sandin, S, additional, Schendel, DE, additional, Schalkwyk, L, additional, Sourander, A, additional, Steadman, C, additional, Stoltenberg, C, additional, Suominen, A, additional, Surén, P, additional, Susser, E, additional, Sylvester Vethanayagam, A, additional, and Yusof, Z, additional
Published: 2015
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42. Autism risk associated with parental age and with increasing difference in age between the parents

Author: Sandin, S, primary, Schendel, D, additional, Magnusson, P, additional, Hultman, C, additional, Surén, P, additional, Susser, E, additional, Grønborg, T, additional, Gissler, M, additional, Gunnes, N, additional, Gross, R, additional, Henning, M, additional, Bresnahan, M, additional, Sourander, A, additional, Hornig, M, additional, Carter, K, additional, Francis, R, additional, Parner, E, additional, Leonard, H, additional, Rosanoff, M, additional, Stoltenberg, C, additional, and Reichenberg, A, additional
Published: 2015
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43. Foreldres utdanning og spedbarnsdødelighet 1967-98

Author: Amtzen, A., Samuelsen, S.O., Bakketeig, Leiv S., and Stoltenberg, C.
Published: 2004

44. The return-to-work process of individuals sick-listed because of whiplash-associated disorder:a three-year follow-up study in a Danish cohort of long-term sickness absentees

Author: Biering-Sørensen, Sarah, Møller, Anne, Stoltenberg, C., Holm, J.W., Skov, P.G., Biering-Sørensen, Sarah, Møller, Anne, Stoltenberg, C., Holm, J.W., and Skov, P.G.
Published: 2014

45. Eating disorders, pregnancy, and the postpartum period: Findings from the Norwegian Mother and Child Cohort Study (MoBa)

Author: Watson, Hunna, Torgersen, L., Zerwas, S., Reichborn-Kjennerud, T., Knoph, C., Stoltenberg, C., Siega-Riz, A.M., von Holle, A., Hamer, R., Meltzer, H., Ferguson, E., Haugen, M., Magnus, P., Kuhns, R., Bulik, C., Watson, Hunna, Torgersen, L., Zerwas, S., Reichborn-Kjennerud, T., Knoph, C., Stoltenberg, C., Siega-Riz, A.M., von Holle, A., Hamer, R., Meltzer, H., Ferguson, E., Haugen, M., Magnus, P., Kuhns, R., and Bulik, C.
Abstract: This review summarizes studies on eating disorders in pregnancy and the postpartum period that have been conducted as part of the broader Norwegian Mother and Child Cohort Study (MoBa). Prior to the 2000s, empirical literature on eating disorders in pregnancy was sparse and consisted mostly of studies in small clinical samples. MoBa has contributed to a new era of research by making population-based and large sample research possible. To date, MoBa has led to 19 eating disorder studies on diverse questions including the prevalence, course, and risk correlates of eating disorders during pregnancy and the postpartum. The associations between eating disorder exposure and pregnancy, birth and obstetric outcomes, and maternal and offspring health and well-being, have also been areas of focus. The findings indicate that eating disorders in pregnancy are relatively common and appear to confer health risks to mother and her child related to sleep, birth outcomes, maternal nutrition, and child feeding and eating.
Published: 2014

46. Parental Obesity and Risk of Autism Spectrum Disorder

Author: Suren, P., primary, Gunnes, N., additional, Roth, C., additional, Bresnahan, M., additional, Hornig, M., additional, Hirtz, D., additional, Lie, K. K., additional, Lipkin, W. I., additional, Magnus, P., additional, Reichborn-Kjennerud, T., additional, Schjolberg, S., additional, Susser, E., additional, Oyen, A.-S., additional, Smith, G. D., additional, and Stoltenberg, C., additional
Published: 2014
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47. Male-mediated infertility in sons of building painters and gardeners:a nationwide register-based follow-up study

Author: Ramlau-Hansen, C H, Stoltenberg, C D G, Hougaard, K S, Parner, E T, Toft, G, Thulstrup, A M, Hansen, J, Bonde, J P, Ramlau-Hansen, C H, Stoltenberg, C D G, Hougaard, K S, Parner, E T, Toft, G, Thulstrup, A M, Hansen, J, and Bonde, J P
Abstract: To investigate whether sons of gardeners and building painters have increased risk of infertility in comparison with sons of bricklayers, carpenters and electricians.
Published: 2012

48. Genome-wide association study of renal cell carcinoma identifies two susceptibility loci on 2p21 and 11q13.3

Author: Purdue, M.P., Johansson, M., Zelenika, D., Toro, J.R., Scelo, G., Moore, L.E., Prokhortchouk, E., Wu, X., Kiemeney, L.A.L.M., Gaborieau, V., Jacobs, K.B., Chow, W.H., Zaridze, D., Matveev, V., Lubinski, J., Trubicka, J., Szeszenia-Dabrowska, N., Lissowska, J., Rudnai, P., Fabianova, E., Bucur, A., Bencko, V., Foretova, L., Janout, V., Boffetta, P., Colt, J.S., Davis, F.G., Schwartz, K.L., Banks, R.E., Selby, P.J., Harnden, P., Berg, C.D., Hsing, A.W., Grubb, R.L. 3rd, Boeing, H., Vineis, P., Clavel-Chapelon, F., Palli, D., Tumino, R., Krogh, V., Panico, S., Duell, E.J., Quiros, J.R., Sanchez, M.J., Navarro, C, Ardanaz, E., Dorronsoro, M., Khaw, K.T., Allen, N.E., Bueno-De-Mesquita, H.B., Peeters, P.H.M., Trichopoulos, D., Linseisen, J., Ljungberg, B, Overvad, K., Tjonneland, A., Romieu, I., Riboli, E., Mukeria, A., Shangina, O., Stevens, V.L., Thun, M.J., Diver, W.R., Gapstur, S.M., Pharoah, P.D., Easton, D.F., Albanes, D., Weinstein, S.J., Virtamo, J., Vatten, L., Hveem, K., Njolstad, I., Tell, G.S., Stoltenberg, C., Kumar, R., Koppova, K., Cussenot, O., Benhamou, S., Oosterwijk, E., Vermeulen, H.H.M., Aben, K.K.H., Marel, S.L. van der, Ye, Y., Wood, C.G., Pu, X., Mazur, A.M., Boulygina, E.S., Chekanov, N.N., Foglio, M., Lechner, D., Gut, I, Heath, S., Blanche, H., Hutchinson, A., Thomas, G., Wang, Z., Yeager, M., Fraumeni, J.F. Jr., Skryabin, K.G., McKay, J.D., Purdue, M.P., Johansson, M., Zelenika, D., Toro, J.R., Scelo, G., Moore, L.E., Prokhortchouk, E., Wu, X., Kiemeney, L.A.L.M., Gaborieau, V., Jacobs, K.B., Chow, W.H., Zaridze, D., Matveev, V., Lubinski, J., Trubicka, J., Szeszenia-Dabrowska, N., Lissowska, J., Rudnai, P., Fabianova, E., Bucur, A., Bencko, V., Foretova, L., Janout, V., Boffetta, P., Colt, J.S., Davis, F.G., Schwartz, K.L., Banks, R.E., Selby, P.J., Harnden, P., Berg, C.D., Hsing, A.W., Grubb, R.L. 3rd, Boeing, H., Vineis, P., Clavel-Chapelon, F., Palli, D., Tumino, R., Krogh, V., Panico, S., Duell, E.J., Quiros, J.R., Sanchez, M.J., Navarro, C, Ardanaz, E., Dorronsoro, M., Khaw, K.T., Allen, N.E., Bueno-De-Mesquita, H.B., Peeters, P.H.M., Trichopoulos, D., Linseisen, J., Ljungberg, B, Overvad, K., Tjonneland, A., Romieu, I., Riboli, E., Mukeria, A., Shangina, O., Stevens, V.L., Thun, M.J., Diver, W.R., Gapstur, S.M., Pharoah, P.D., Easton, D.F., Albanes, D., Weinstein, S.J., Virtamo, J., Vatten, L., Hveem, K., Njolstad, I., Tell, G.S., Stoltenberg, C., Kumar, R., Koppova, K., Cussenot, O., Benhamou, S., Oosterwijk, E., Vermeulen, H.H.M., Aben, K.K.H., Marel, S.L. van der, Ye, Y., Wood, C.G., Pu, X., Mazur, A.M., Boulygina, E.S., Chekanov, N.N., Foglio, M., Lechner, D., Gut, I, Heath, S., Blanche, H., Hutchinson, A., Thomas, G., Wang, Z., Yeager, M., Fraumeni, J.F. Jr., Skryabin, K.G., and McKay, J.D.
Abstract: Contains fulltext : 97937.pdf (publisher's version ) (Closed access), We conducted a two-stage genome-wide association study of renal cell carcinoma (RCC) in 3,772 affected individuals (cases) and 8,505 controls of European background from 11 studies and followed up 6 SNPs in 3 replication studies of 2,198 cases and 4,918 controls. Two loci on the regions of 2p21 and 11q13.3 were associated with RCC susceptibility below genome-wide significance. Two correlated variants (r(2) = 0.99 in controls), rs11894252 (P = 1.8 x 10) and rs7579899 (P = 2.3 x 10), map to EPAS1 on 2p21, which encodes hypoxia-inducible-factor-2 alpha, a transcription factor previously implicated in RCC. The second locus, rs7105934, at 11q13.3, contains no characterized genes (P = 7.8 x 10(1)). In addition, we observed a promising association on 12q24.31 for rs4765623, which maps to SCARB1, the scavenger receptor class B, member 1 gene (P = 2.6 x 10). Our study reports previously unidentified genomic regions associated with RCC risk that may lead to new etiological insights.
Published: 2011

49. Remission, continuation and incidence of eating disorders during early pregnancy: a validation study in a population-based birth cohort

Author: Watson, H. J., primary, Von Holle, A., additional, Hamer, R. M., additional, Knoph Berg, C., additional, Torgersen, L., additional, Magnus, P., additional, Stoltenberg, C., additional, Sullivan, P., additional, Reichborn-Kjennerud, T., additional, and Bulik, C. M., additional
Published: 2012
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50. Prenatal fever and autism risk

Author: Hornig, M, Bresnahan, M A, Che, X, Schultz, A F, Ukaigwe, J E, Eddy, M L, Hirtz, D, Gunnes, N, Lie, K K, Magnus, P, Mjaaland, S, Reichborn-Kjennerud, T, Schjølberg, S, Øyen, A-S, Levin, B, Susser, E S, Stoltenberg, C, and Lipkin, W I
Abstract: Some studies suggest that prenatal infection increases risk of autism spectrum disorders (ASDs). This study was undertaken in a prospective cohort in Norway to examine whether we could find evidence to support an association of the prenatal occurrence of fever, a common manifestation of infection, with ASD risk. Prospective questionnaires provided maternal exposure data; case status was established from clinical assessments and registry linkages. In a large, prospectively ascertained cohort of pregnant mothers and their offspring, we examined infants born ⩾32 weeks for associations between fever exposure in each trimester and ASD risk using logistic regression. Maternal exposure to second-trimester fever was associated with increased ASD risk, adjusting for presence of fever in other trimesters and confounders (adjusted odds ratio (aOR), 1.40; 95% confidence interval, 1.09–1.79), with a similar, but nonsignificant, point estimate in the first trimester. Risk increased markedly with exposure to three or more fever episodes after 12 weeks' gestation (aOR, 3.12; 1.28–7.63). ASD risk appears to increase with maternal fever, particularly in the second trimester. Risk magnified dose dependently with exposure to multiple fevers after 12 weeks' gestation. Our findings support a role for gestational maternal infection and innate immune responses to infection in the pathogenesis of at least some cases of ASD.
Published: 2018
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