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1. Maternal and fetal genetic contribution to gestational weight gain

Author

Warrington, N.M. (N. M.), Richmond, R.C. (Rebecca C.), Fenstra, B. (B.), Myhre, R. (Ronny), Gaillard, R. (Romy), Paternoster, L. (L.), Wang, C.A. (C. A.), Beaumont, R.N. (R. N.), Das, S. (Shikta), Murcia, M. (Mario), Barton, S.J. (Sheila), Espinosa, A. (A.), Thiering, E. (Elisabeth), Atalay, M. (Mustafa), Pitkanen, N. (Niina), Ntalla, I. (Ioanna), Jonsson, A.E. (A. E.), Freathy, R.M. (Rachel), Karhunen, V. (V.), Tiesler, C.M.T. (C. M.T.), Allard, C. (Catherine), Crawford, A. (A.), Ring, S.M. (Susan), Melbye, M. (Mads), Magnus, P. (Per), Rivadeneira, F. (F.), Skotte, L. (L.), Hansen, T. (Torben), Marsh, J.A. (Julie), Guxens Junyent, M. (Mònica), Holloway, J.W. (J. W.), Grallert, H. (Harald), Jaddoe, V.W.V. (Vincent), Lowe, W.L. (W. L.), Roumeliotaki, T. (Theano), Hattersley, A.T. (Andrew), Lindi, V. (Virpi), Pahkala, K. (Katja), Panoutsopoulou, K. (K.), Standl, M. (M.), Flexeder, C. (Claudia), Bouchard, L. (Luigi), Aagaard Nohr, E. (E.), Santa-Marina, L. (Loreto), Kogevinas, M. (Manolis), Niinikoski, H. (H.), Dedoussis, G.V. (George), Heinrich, J. (J.), Reynolds, R.M. (Rebecca), Lakka, T.A. (Timo), Zeggini, E. (Eleftheria), Raitakari, O.T. (O. T.), Chatzi, L. (Leda), Inskip, H.M. (Hazel), Bustamante, M. (Mariona), Hivert, M.-F. (Marie-France), Jarvelin, M.-R. (M. R.), Sørensen, T.I.A. (Thorkild), Pennell, C.E. (Craig), Felix, J.F. (J. F.), Jacobsson, B. (B.), Geller, F. (Frank), Evans, D.M. (D. M.), Lawlor, D.A. (D. A.), Warrington, N.M. (N. M.), Richmond, R.C. (Rebecca C.), Fenstra, B. (B.), Myhre, R. (Ronny), Gaillard, R. (Romy), Paternoster, L. (L.), Wang, C.A. (C. A.), Beaumont, R.N. (R. N.), Das, S. (Shikta), Murcia, M. (Mario), Barton, S.J. (Sheila), Espinosa, A. (A.), Thiering, E. (Elisabeth), Atalay, M. (Mustafa), Pitkanen, N. (Niina), Ntalla, I. (Ioanna), Jonsson, A.E. (A. E.), Freathy, R.M. (Rachel), Karhunen, V. (V.), Tiesler, C.M.T. (C. M.T.), Allard, C. (Catherine), Crawford, A. (A.), Ring, S.M. (Susan), Melbye, M. (Mads), Magnus, P. (Per), Rivadeneira, F. (F.), Skotte, L. (L.), Hansen, T. (Torben), Marsh, J.A. (Julie), Guxens Junyent, M. (Mònica), Holloway, J.W. (J. W.), Grallert, H. (Harald), Jaddoe, V.W.V. (Vincent), Lowe, W.L. (W. L.), Roumeliotaki, T. (Theano), Hattersley, A.T. (Andrew), Lindi, V. (Virpi), Pahkala, K. (Katja), Panoutsopoulou, K. (K.), Standl, M. (M.), Flexeder, C. (Claudia), Bouchard, L. (Luigi), Aagaard Nohr, E. (E.), Santa-Marina, L. (Loreto), Kogevinas, M. (Manolis), Niinikoski, H. (H.), Dedoussis, G.V. (George), Heinrich, J. (J.), Reynolds, R.M. (Rebecca), Lakka, T.A. (Timo), Zeggini, E. (Eleftheria), Raitakari, O.T. (O. T.), Chatzi, L. (Leda), Inskip, H.M. (Hazel), Bustamante, M. (Mariona), Hivert, M.-F. (Marie-France), Jarvelin, M.-R. (M. R.), Sørensen, T.I.A. (Thorkild), Pennell, C.E. (Craig), Felix, J.F. (J. F.), Jacobsson, B. (B.), Geller, F. (Frank), Evans, D.M. (D. M.), and Lawlor, D.A. (D. A.)

Abstract

Background:Clinical recommendations to limit gestational weight gain (GWG) imply high GWG is causally related to adverse outcomes in mother or offspring, but GWG is the sum of several inter-related complex phenotypes (maternal fat deposition and vascular expansion, placenta, amniotic fluid and fetal growth). Understanding the genetic contribution to GWG could help clarify the potential effect of its different components on maternal and offspring health. Here we explore the genetic contribution to total, early and late GWG.Participants and methods:A genome-wide association study was used to identify maternal and fetal variants contributing to GWG in up to 10 543 mothers and 16 317 offspring of European origin, with replication in 10 660 mothers and 7561 offspring. Additional analyses determined the proportion of variability in GWG from maternal and fetal common genetic variants and the overlap of established genome-wide significant variants for phenotypes relevant to GWG (for example, maternal body mass index (BMI) and glucose, birth weight).Results:Approximately 20% of the variability in GWG was tagged by common maternal genetic variants, and the fetal genome made a surprisingly minor contribution to explain variation in GWG. Variants near the pregnancy-specific beta-1 glycoprotein 5 (PSG5) gene reached genome-wide significance (P=1.71 × 10 â '8) for total GWG in the offspring genome, but did not replicate. Some established variants associated with increased BMI, fasting glucose and type 2 diabetes were associated with lower early, and higher later GWG. Maternal variants related to higher systolic blood pressure were related to lower late GWG. Established maternal and fetal birth weight variants were largely unrelated to GWG.Conclusions:We found a modest contribution of maternal common variants to GWG and some overlap of maternal BMI, glucose and type 2 diabetes variants with GWG. These findings suggest that associations between GWG and later offspring/maternal outc

Published
2018
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2. Maternal and fetal genetic contribution to gestational weight gain

Author

Warrington, N. M. (N. M.), Richmond, R. (R.), Fenstra, B. (B.), Myhre, R. (R.), Gaillard, R. (R.), Paternoster, L. (L.), Wang, C. A. (C. A.), Beaumont, R. N. (R. N.), Das, S. (S.), Murcia, M. (M.), Barton, S. J. (S. J.), Espinosa, A. (A.), Thiering, E. (E.), Atalay, M. (M.), Pitkanen, N. (N.), Ntalla, I. (I.), Jonsson, A. E. (A. E.), Freathy, R. (R.), Karhunen, V. (V.), Tiesler, C. M. (C. M. T.), Allard, C. (C.), Crawford, A. (A.), Ring, S. M. (S. M.), Melbye, M. (M.), Magnus, P. (P.), Rivadeneira, F. (F.), Skotte, L. (L.), Hansen, T. (T.), Marsh, J. (J.), Guxens, M. (M.), Holloway, J. W. (J. W.), Grallert, H. (H.), Jaddoe, V. W. (V. W. V.), Lowe, W. L. (W. L.), Roumeliotaki, T. (T.), Hattersley, A. T. (A. T.), Lindi, V. (V.), Pahkala, K. (K.), Panoutsopoulou, K. (K.), Standl, M. (M.), Flexeder, C. (C.), Bouchard, L. (L.), Aagaard Nohr, E. (E.), Santa Marina, L. (L.), Kogevinas, M. (M.), Niinikoski, H. (H.), Dedoussis, G. (G.), Heinrich, J. (J.), Reynolds, R. M. (R. M.), Lakka, T. (T.), Zeggini, E. (E.), Raitakari, O. T. (O. T.), Chatzi, L. (L.), Inskip, H. M. (H. M.), Bustamante, M. (M.), Hivert, M.-F. (M-F), Järvelin, M.-R. (M-R), Sorensen, T. I. (T. I. A.), Pennell, C. (C.), Felix, J. F. (J. F.), Jacobsson, B. (B.), Geller, F. (F.), Evans, D. M. (D. M.), Lawlor, D. A. (D. A.), Warrington, N. M. (N. M.), Richmond, R. (R.), Fenstra, B. (B.), Myhre, R. (R.), Gaillard, R. (R.), Paternoster, L. (L.), Wang, C. A. (C. A.), Beaumont, R. N. (R. N.), Das, S. (S.), Murcia, M. (M.), Barton, S. J. (S. J.), Espinosa, A. (A.), Thiering, E. (E.), Atalay, M. (M.), Pitkanen, N. (N.), Ntalla, I. (I.), Jonsson, A. E. (A. E.), Freathy, R. (R.), Karhunen, V. (V.), Tiesler, C. M. (C. M. T.), Allard, C. (C.), Crawford, A. (A.), Ring, S. M. (S. M.), Melbye, M. (M.), Magnus, P. (P.), Rivadeneira, F. (F.), Skotte, L. (L.), Hansen, T. (T.), Marsh, J. (J.), Guxens, M. (M.), Holloway, J. W. (J. W.), Grallert, H. (H.), Jaddoe, V. W. (V. W. V.), Lowe, W. L. (W. L.), Roumeliotaki, T. (T.), Hattersley, A. T. (A. T.), Lindi, V. (V.), Pahkala, K. (K.), Panoutsopoulou, K. (K.), Standl, M. (M.), Flexeder, C. (C.), Bouchard, L. (L.), Aagaard Nohr, E. (E.), Santa Marina, L. (L.), Kogevinas, M. (M.), Niinikoski, H. (H.), Dedoussis, G. (G.), Heinrich, J. (J.), Reynolds, R. M. (R. M.), Lakka, T. (T.), Zeggini, E. (E.), Raitakari, O. T. (O. T.), Chatzi, L. (L.), Inskip, H. M. (H. M.), Bustamante, M. (M.), Hivert, M.-F. (M-F), Järvelin, M.-R. (M-R), Sorensen, T. I. (T. I. A.), Pennell, C. (C.), Felix, J. F. (J. F.), Jacobsson, B. (B.), Geller, F. (F.), Evans, D. M. (D. M.), and Lawlor, D. A. (D. A.)

Abstract

Background: Clinical recommendations to limit gestational weight gain (GWG) imply high GWG is causally related to adverse outcomes in mother or offspring, but GWG is the sum of several inter-related complex phenotypes (maternal fat deposition and vascular expansion, placenta, amniotic fluid and fetal growth). Understanding the genetic contribution to GWG could help clarify the potential effect of its different components on maternal and offspring health. Here we explore the genetic contribution to total, early and late GWG. Participants and methods: A genome-wide association study was used to identify maternal and fetal variants contributing to GWG in up to 10 543 mothers and 16 317 offspring of European origin, with replication in 10 660 mothers and 7561 offspring. Additional analyses determined the proportion of variability in GWG from maternal and fetal common genetic variants and the overlap of established genome-wide significant variants for phenotypes relevant to GWG (for example, maternal body mass index (BMI) and glucose, birth weight). Results: Approximately 20% of the variability in GWG was tagged by common maternal genetic variants, and the fetal genome made a surprisingly minor contribution to explain variation in GWG. Variants near the pregnancy-specific beta-1 glycoprotein 5 (PSG5) gene reached genome-wide significance (P=1.71 × 10−8) for total GWG in the offspring genome, but did not replicate. Some established variants associated with increased BMI, fasting glucose and type 2 diabetes were associated with lower early, and higher later GWG. Maternal variants related to higher systolic blood pressure were related to lower late GWG. Established maternal and fetal birth weight variants were largely unrelated to GWG. Conclusions: We found a modest contribution of maternal common variants to GWG and some overlap of maternal BMI, glucose and type 2 diabetes variants with GWG. These findings suggest that associations between GWG and later offspring

Published
2018

3. Maternal and fetal genetic contribution to gestational weight gain

Author

Warrington, N M, Richmond, R, Fenstra, B, Myhre, R, Gaillard, R, Paternoster, L, Wang, C A, Beaumont, R N, Das, S, Murcia, M, Barton, S J, Espinosa, A, Thiering, E, Atalay, M, Pitkänen, N, Ntalla, I, Jonsson, A E, Freathy, R, Karhunen, V, Tiesler, C M T, Allard, C, Crawford, A, Ring, S M, Melbye, M, Magnus, P, Rivadeneira, F, Skotte, L, Hansen, T, Marsh, J, Guxens, M, Holloway, J W, Grallert, H, Jaddoe, V W V, Lowe, W L, Roumeliotaki, T, Hattersley, A T, Lindi, V, Pahkala, K, Panoutsopoulou, K, Standl, M, Flexeder, C, Bouchard, L, Aagaard Nohr, E, Marina, L Santa, Kogevinas, M, Niinikoski, H, Dedoussis, G, Heinrich, J, Reynolds, R M, Lakka, T, Zeggini, E, Raitakari, O T, Chatzi, L, Inskip, H M, Bustamante, M, Hivert, M-F, Jarvelin, M-R, Sørensen, T I A, Pennell, C, Felix, J F, Jacobsson, B, Geller, F, Evans, D M, Lawlor, D A, Warrington, N M, Richmond, R, Fenstra, B, Myhre, R, Gaillard, R, Paternoster, L, Wang, C A, Beaumont, R N, Das, S, Murcia, M, Barton, S J, Espinosa, A, Thiering, E, Atalay, M, Pitkänen, N, Ntalla, I, Jonsson, A E, Freathy, R, Karhunen, V, Tiesler, C M T, Allard, C, Crawford, A, Ring, S M, Melbye, M, Magnus, P, Rivadeneira, F, Skotte, L, Hansen, T, Marsh, J, Guxens, M, Holloway, J W, Grallert, H, Jaddoe, V W V, Lowe, W L, Roumeliotaki, T, Hattersley, A T, Lindi, V, Pahkala, K, Panoutsopoulou, K, Standl, M, Flexeder, C, Bouchard, L, Aagaard Nohr, E, Marina, L Santa, Kogevinas, M, Niinikoski, H, Dedoussis, G, Heinrich, J, Reynolds, R M, Lakka, T, Zeggini, E, Raitakari, O T, Chatzi, L, Inskip, H M, Bustamante, M, Hivert, M-F, Jarvelin, M-R, Sørensen, T I A, Pennell, C, Felix, J F, Jacobsson, B, Geller, F, Evans, D M, and Lawlor, D A

Abstract

BACKGROUND: Clinical recommendations to limit gestational weight gain (GWG) imply high GWG is causally related to adverse outcomes in mother or offspring, but GWG is the sum of several inter-related complex phenotypes (maternal fat deposition and vascular expansion, placenta, amniotic fluid and fetal growth). Understanding the genetic contribution to GWG could help clarify the potential effect of its different components on maternal and offspring health. Here we explore the genetic contribution to total, early and late GWG.PARTICIPANTS AND METHODS: A genome-wide association study was used to identify maternal and fetal variants contributing to GWG in up to 10 543 mothers and 16 317 offspring of European origin, with replication in 10 660 mothers and 7561 offspring. Additional analyses determined the proportion of variability in GWG from maternal and fetal common genetic variants and the overlap of established genome-wide significant variants for phenotypes relevant to GWG (for example, maternal body mass index (BMI) and glucose, birth weight).RESULTS: Approximately 20% of the variability in GWG was tagged by common maternal genetic variants, and the fetal genome made a surprisingly minor contribution to explain variation in GWG. Variants near the pregnancy-specific beta-1 glycoprotein 5 (PSG5) gene reached genome-wide significance (P=1.71 × 10-8) for total GWG in the offspring genome, but did not replicate. Some established variants associated with increased BMI, fasting glucose and type 2 diabetes were associated with lower early, and higher later GWG. Maternal variants related to higher systolic blood pressure were related to lower late GWG. Established maternal and fetal birth weight variants were largely unrelated to GWG.CONCLUSIONS: We found a modest contribution of maternal common variants to GWG and some overlap of maternal BMI, glucose and type 2 diabetes variants with GWG. These findings suggest that associations between GWG and late

Published
2018

4. Smoking and pregnancy-related pelvic pain

Author

Biering, K, Aagaard Nohr, E, Olsen, J, Andersen, Anne-Marie Nybo, Juhl, Mette, Biering, K, Aagaard Nohr, E, Olsen, J, Andersen, Anne-Marie Nybo, and Juhl, Mette

Abstract

To investigate possible associations between smoking and pregnancy-related pelvic pain.

Published
2010

7. Influences of childhood family factors on depressive symptoms in adolescence and early adulthood: A Danish longitudinal study.

Author

Poulsen PH, Biering K, Winding TN, Aagaard Nohr E, and Andersen JH

Subjects
Adolescent, Denmark epidemiology, Family, Female, Humans, Longitudinal Studies, Male, Prospective Studies, Risk Factors, Socioeconomic Factors, Young Adult, Adverse Childhood Experiences statistics & numerical data, Depression epidemiology
Abstract

Aims: The study examined the timing of family socio-economic factors during early (aged 0-8 years) and late (aged 9-14 years) childhood, as well as psychosocial variables in relation to depressive symptoms at the ages of 15, 18 and 21. Methods: This prospective cohort study included 3014 young people from western Denmark. Exposure variables were equivalised household income (income), mother's educational level and mother's labour market participation (LMP), derived from registers and self-reported variables family functioning, subjective social status and negative life events. The outcome variable was depressive symptoms. Associations were analysed using logistic regression, adjusted for other exposure variables and sex. Results: In early childhood, mother's low LMP was associated with higher risk of depressive symptoms at the age of 15, whereas mother's low educational level and lower income was associated with higher risk of depressive symptoms at the age of 21. In late childhood, lower income, mother's low educational level and mother's low LMP was associated with higher risk of depressive symptoms at the ages of 15 and 21. Poorer family functioning was associated with depressive symptoms at the age of 15-21, with estimates ranging from 1.8 to 2.6. Reporting two or more negative life events were associated with depressive symptoms at the ages of 15 and 18. Conclusions: Timing of low income, mother's low educational level and mother's low LMP during childhood in relation to future depressive symptoms in the offspring appears to be of some importance in this Danish youth cohort. Family functioning and negative life events were the most stable risk factors for depressive symptoms. Results should, however, be interpreted with caution due to the risk of reverse causality.

Published
2020
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8. Maternal and fetal genetic contribution to gestational weight gain.

Author

Warrington NM, Richmond R, Fenstra B, Myhre R, Gaillard R, Paternoster L, Wang CA, Beaumont RN, Das S, Murcia M, Barton SJ, Espinosa A, Thiering E, Atalay M, Pitkänen N, Ntalla I, Jonsson AE, Freathy R, Karhunen V, Tiesler CMT, Allard C, Crawford A, Ring SM, Melbye M, Magnus P, Rivadeneira F, Skotte L, Hansen T, Marsh J, Guxens M, Holloway JW, Grallert H, Jaddoe VWV, Lowe WL Jr, Roumeliotaki T, Hattersley AT, Lindi V, Pahkala K, Panoutsopoulou K, Standl M, Flexeder C, Bouchard L, Aagaard Nohr E, Marina LS, Kogevinas M, Niinikoski H, Dedoussis G, Heinrich J, Reynolds RM, Lakka T, Zeggini E, Raitakari OT, Chatzi L, Inskip HM, Bustamante M, Hivert MF, Jarvelin MR, Sørensen TIA, Pennell C, Felix JF, Jacobsson B, Geller F, Evans DM, and Lawlor DA

Subjects
Female, Genome-Wide Association Study, Gestational Weight Gain physiology, Humans, Pregnancy physiology, Pregnancy statistics & numerical data, Fetus physiology, Gestational Weight Gain genetics, Pregnancy genetics
Abstract

Background: Clinical recommendations to limit gestational weight gain (GWG) imply high GWG is causally related to adverse outcomes in mother or offspring, but GWG is the sum of several inter-related complex phenotypes (maternal fat deposition and vascular expansion, placenta, amniotic fluid and fetal growth). Understanding the genetic contribution to GWG could help clarify the potential effect of its different components on maternal and offspring health. Here we explore the genetic contribution to total, early and late GWG., Participants and Methods: A genome-wide association study was used to identify maternal and fetal variants contributing to GWG in up to 10 543 mothers and 16 317 offspring of European origin, with replication in 10 660 mothers and 7561 offspring. Additional analyses determined the proportion of variability in GWG from maternal and fetal common genetic variants and the overlap of established genome-wide significant variants for phenotypes relevant to GWG (for example, maternal body mass index (BMI) and glucose, birth weight)., Results: Approximately 20% of the variability in GWG was tagged by common maternal genetic variants, and the fetal genome made a surprisingly minor contribution to explain variation in GWG. Variants near the pregnancy-specific beta-1 glycoprotein 5 (PSG5) gene reached genome-wide significance (P=1.71 × 10 -8 ) for total GWG in the offspring genome, but did not replicate. Some established variants associated with increased BMI, fasting glucose and type 2 diabetes were associated with lower early, and higher later GWG. Maternal variants related to higher systolic blood pressure were related to lower late GWG. Established maternal and fetal birth weight variants were largely unrelated to GWG., Conclusions: We found a modest contribution of maternal common variants to GWG and some overlap of maternal BMI, glucose and type 2 diabetes variants with GWG. These findings suggest that associations between GWG and later offspring/maternal outcomes may be due to the relationship of maternal BMI and diabetes with GWG.

Published
2018
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9. Smoking and pregnancy-related pelvic pain.

Author

Biering K, Aagaard Nohr E, Olsen J, Hjollund JO, Nybo Andersen AM, and Juhl M

Subjects
Adult, Body Mass Index, Case-Control Studies, Female, Humans, Parity, Pregnancy, Risk Factors, Young Adult, Pelvic Pain etiology, Pregnancy Complications etiology, Smoking adverse effects
Abstract

Objective: To investigate possible associations between smoking and pregnancy-related pelvic pain., Design: Nested case-control study., Setting: Denmark 2000-2001., Population: The Danish National Birth Cohort., Methods: The women were interviewed twice in pregnancy and twice after childbirth. The first pregnancy interview provided information on smoking and possible confounding factors,whereas the first interview after birth addressed case identification.Cases (n = 2302) were defined on the basis of self-reported pelvic pain, and controls were selected among women who did not report pelvic pain (n = 2692). Logistic regression analysis was used to estimate associations between smoking and pelvic pain., Main Outcome Measure: Pregnancy-related pelvic pain., Results: Compared with non-smokers, women who smoked during pregnancy had an adjusted odds ratio of 1.2 (1.0-1.4) for overall pelvic pain, similar to women who stopped smoking in early pregnancy 1.3 (1.1-1.7). The equivalent adjusted odds ratio for severe pelvic pain was 1.2 (1.0-1.5) for smokers, and 1.5 (1.2-1.9)for women who stopped smoking. Smoking intensity, measured as number of cigarettes smoked per day, was associated with pelvic pain in a dose-response pattern. Information about smoking was collected prospectively, which makes it unlikely that differential recall alone explains the results., Conclusions: Smoking was associated with pregnancy-related pelvic pain, with a dose-response pattern between reported smoking intensity and pelvic pain. These findings suggest a possible new risk factor for a common ailment during pregnancy

Published
2010
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10. Incidence and prevalence of keratoconus in Denmark.

Author

Nielsen K, Hjortdal J, Aagaard Nohr E, and Ehlers N

Subjects
Denmark epidemiology, Humans, Incidence, Middle Aged, Prevalence, Registries, Hospitalization statistics & numerical data, Keratoconus epidemiology, Keratoconus therapy
Abstract

Purpose: To estimate the prevalence and incidence of hospitalized keratoconus (KC) in Denmark., Methods: Data extracts from the National Patient Registry under the National Board of Health (which covers the entire Danish population) were analysed., Results: The prevalence of KC was estimated at 86 patients per 100,000 residents and the incidence at 1.3 per 100 000 per year., Conclusion: KC is rather widespread in Denmark, with more than 4600 affected individuals.

Published
2007
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