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1. Investigating the determinants of macular pigment including response to supplementation

Author: Lowry, E. S.
Subjects: 617.7
Abstract: A growing interest in macular pigment has highlighted the need for further investigation into environmental and genetic factors which may influence individual density and whether these levels can be increased. This thesis has aimed to address these fundamental questions through a systematic review of the current literature, a cross-sectional analysis of environmental and genetic factors associated with macular pigment and a randomised, placebo-controlled trial using a lutein and zeaxanthin supplement. Environmental and genetic factors affecting individual ability to respond were also investigated. Integral to macular pigment research is the ability to accurately measure macular pigment in vivo. This thesis also aimed to assess repeatability of the widely used HFP method, and to compare this technique to fundus reflectometry using the Viscucam 200. A statistically significant increase in serum lutein and macular pigment in response to supplementation was demonstrated by both the systematic review and randomised, placebo-controlled trial within this thesis. Both studies also show great variability in the response of macular pigment. When associations with macular pigment and serum carotenoid concentrations were examined cross-sectionally, established relationships were replicated with regards to baseline and environmental determinants of serum lutein and macular pigment. PTe taster status was not significantly associated with dietary intake of lutein and zeaxanthin. With regards to measurement of macular pigment, measures taken by the. Visucam 200 were found to be repeatable but not comparable to HFP using the MPS 1000. This thesis demonstrated good repeatability of the MPS 1000 over both short and longer-term periods making it useful for cross-sectional and longitudinal studies . To conclude, environmental and genetic factors found to be significantly associated with baseline macular pigment in previous studies have been replicated in the current study and new association identified, including environmental and genetic factors associated with macular response. Newly identified associations warrant further investigation.
Published: 2014

2. Adverse childhood experiences, social participation and multimorbidity risk in Europe

Author: Deschenes, S, primary, Simmons, C, additional, Elsden, E, additional, McInerney, A, additional, Lowry, E, additional, and Rodrigues, R, additional
Published: 2023
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3. Truths : talks with a boy concerning himself.

Author: Lowry, E. B. (Edith Belle), 1878-1945. and Lowry, E. B. (Edith Belle), 1878-1945.
Published: 1911

4. Improving Struggling Readers’ Literacy Skills through Talk about Text

Author: Hemphill, Lowry E., primary, Kim, James, additional, and Troyer, Margaret, additional
Published: 2019
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5. An investigation of depression and inflammation as potential mediators linking adverse childhood experiences with cognitive decline in adulthood: results from a prospective cohort study

Author: Lowry, E., primary, Mc Inerney, A., additional, Schmitz, N., additional, and Deschenes, S., additional
Published: 2022
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6. The relationship of life-course patterns of adiposity with type 2 diabetes, depression, and their comorbidity in the Northern Finland Birth Cohort 1966

Author: Choudhary, P. (Priyanka), Ronkainen, J. (Justiina), Nedelec, R. (Rozenn), Tolvanen, M. (Mimmi), Lowry, E. (Estelle), Miettunen, J. (Jouko), Järvelin, M.-R. (Marjo-Riitta), Sebert, S. (Sylvain), Choudhary, P. (Priyanka), Ronkainen, J. (Justiina), Nedelec, R. (Rozenn), Tolvanen, M. (Mimmi), Lowry, E. (Estelle), Miettunen, J. (Jouko), Järvelin, M.-R. (Marjo-Riitta), and Sebert, S. (Sylvain)
Abstract: Objectives: Type 2 diabetes (T2D) and comorbid depression challenges clinical management particularly in individuals with overweight. We aim to explore the shared etiology, via lifecourse adiposity, between T2D and depression. Methods: We used data from birth until 46years from Northern Finland Birth Cohort 1966 (n = 6,372; 53.8% females). We conducted multivariate analyses on three outcomes: T2D (4.2%), depression (19.2%) and as comorbidity (1.8%). We conducted (i) Path analysis to clarify time-dependent body mass index (BMI) related pathways, including BMI polygenic risk scores (PRS); and (ii) Cox regression models to assess whether reduction of overweight between 7years and 31years influence T2D, depression and/or comorbidity. The models were tested for covariation with sex, education, smoking, physical activity, and diet score. Results: The odd ratios (OR) of T2D in individuals with depression was 1.68 [95% confidence interval (CI): 1.34–2.11], and no change in estimate was observed when adjusted for covariates. T2D and comorbidity showed similar patterns of relationships in the path analyses (P < 0.001). The genetic risk for obesity (PRS BMI) did not show direct effect on T2D or comorbidity in adulthood but indirectly through measures of adiposity in early childhood and mid-adulthood in the path analysis (P < 0.001). Having early-onset of overweight at 7years and 31years showed highest risk of T2D (OR 3.8, 95%CI 2.4–6.1) and comorbidity (OR 5.0, 95%CI 2.7–9.5), with mild-to-moderate attenuation with adjustments. Depression showed no significant associations. Conclusions: We found evidence for overweight since childhood as a risk factor for T2D and co-morbidity between T2D and depression, influenced moderately by lifestyle factors in later life. However, no shared early life adiposity related risk factors were observed between T2D and depression when assessed independently in this Finnish setting.
Published: 2022

7. Maternal haemoglobin levels in pregnancy and child DNA methylation:a study in the pregnancy and childhood epigenetics consortium

Author: Ronkainen, J. (Justiina), Heiskala, A. (Anni), Vehmeijer, F. O. (Florianne O. L.), Lowry, E. (Estelle), Caramaschi, D. (Doretta), Estrada Gutierrez, G. (Guadalupe), Heiss, J. A. (Jonathan A.), Hummel, N. (Nadine), Keikkala, E. (Elina), Kvist, T. (Tuomas), Kupsco, A. (Allison), Melton, P. E. (Phillip E.), Pesce, G. (Giancarlo), Soomro, M. H. (Munawar H.), Vives-Usano, M. (Marta), Baiz, N. (Nour), Binder, E. (Elisabeth), Czamara, D. (Darina), Guxens, M. (Mònica), Mustaniemi, S. (Sanna), London, S. J. (Stephanie J.), Rauschert, S. (Sebastian), Vääräsmäki, M. (Marja), Vrijheid, M. (Martine), Ziegler, A.-G. (Anette-G.), Annesi-Maesano, I. (Isabella), Bustamante, M. (Mariona), Huang, R.-C. (Rae-Chi), Hummel, S. (Sandra), Just, A. C. (Allan C.), Kajantie, E. (Eero), Lahti, J. (Jari), Lawlor, D. (Deborah), Räikkönen, K. (Katri), Järvelin, M.-R. (Marjo-Riitta), Felix, J. F. (Janine F.), Sebert, S. (Sylvain), Ronkainen, J. (Justiina), Heiskala, A. (Anni), Vehmeijer, F. O. (Florianne O. L.), Lowry, E. (Estelle), Caramaschi, D. (Doretta), Estrada Gutierrez, G. (Guadalupe), Heiss, J. A. (Jonathan A.), Hummel, N. (Nadine), Keikkala, E. (Elina), Kvist, T. (Tuomas), Kupsco, A. (Allison), Melton, P. E. (Phillip E.), Pesce, G. (Giancarlo), Soomro, M. H. (Munawar H.), Vives-Usano, M. (Marta), Baiz, N. (Nour), Binder, E. (Elisabeth), Czamara, D. (Darina), Guxens, M. (Mònica), Mustaniemi, S. (Sanna), London, S. J. (Stephanie J.), Rauschert, S. (Sebastian), Vääräsmäki, M. (Marja), Vrijheid, M. (Martine), Ziegler, A.-G. (Anette-G.), Annesi-Maesano, I. (Isabella), Bustamante, M. (Mariona), Huang, R.-C. (Rae-Chi), Hummel, S. (Sandra), Just, A. C. (Allan C.), Kajantie, E. (Eero), Lahti, J. (Jari), Lawlor, D. (Deborah), Räikkönen, K. (Katri), Järvelin, M.-R. (Marjo-Riitta), Felix, J. F. (Janine F.), and Sebert, S. (Sylvain)
Abstract: Altered maternal haemoglobin levels during pregnancy are associated with pre-clinical and clinical conditions affecting the fetus. Evidence from animal models suggests that these associations may be partially explained by differential DNA methylation in the newborn with possible long-term consequences. To test this in humans, we meta-analyzed the epigenome-wide associations of maternal haemoglobin levels during pregnancy with offspring DNA methylation in 3,967 newborn cord blood and 1,534 children and 1,962 adolescent whole-blood samples derived from 10 cohorts. DNA methylation was measured using Illumina Infinium Methylation 450K or MethylationEPIC arrays covering 450,000 and 850,000 methylation sites, respectively. There was no statistical support for the association of maternal haemoglobin levels with offspring DNA methylation either at individual methylation sites or clustered in regions. For most participants, maternal haemoglobin levels were within the normal range in the current study, whereas adverse perinatal outcomes often arise at the extremes. Thus, this study does not rule out the possibility that associations with offspring DNA methylation might be seen in studies with more extreme maternal haemoglobin levels.
Published: 2022

8. The Lively Art of "Manhattan Transfer"

Author: Lowry, E. D.
Published: 1969
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9. DNA methylation signatures of aggression and closely related constructs: A meta-analysis of epigenome-wide studies across the lifespan

Author: Dongen, J. Van, Hagenbeek, F.A., Suderman, M., Roetman, P.J., Sugden, K., Chiocchetti, A.G., Ismail, K., Mulder, R.H., Hafferty, J.D., Adams, M.J., Walker, R.M., Morris, S.W., Lahti, J., Küpers, L.K., Escaramis, G., Alemany, S., Bonder, M. Jan, Meijer, M., Ip, H.F., Jansen, R., Baselmans, B.M.L., Parmar, P., Lowry, E., Streit, F., Sirignano, L., Send, T.S., Frank, J., Jylhävä, J., Wang, Y., Mishra, P.P., Colins, O.F., Corcoran, D.L., Poulton, R., Mill, J., Hannon, E., Arseneault, L., Korhonen, T., Vuoksimaa, E., Felix, J.F., Bakermans-Kranenburg, M.J., Campbell, A., Czamara, D., Binder, E., Corpeleijn, E., Gonzalez, J.R., Grazuleviciene, R., Gutzkow, K.B., Evandt, J., Vafeiadi, M., Klein, M., Meer, D. van der, Ligthart, L., Kluft, C., Davies, G.E., Hakulinen, C., Keltikangas-Järvinen, L., Franke, B., Freitag, C.M., Konrad, K., Hervas, A., Fernández-Rivas, A., Vetro, A., Raitakari, O., Lehtimäki, T., Vermeiren, R., Strandberg, T., Räikkönen, K., Snieder, H., Witt, S.H., Deuschle, M., Pedersen, N.L., Hägg, S., Sunyer, J., Franke, L., Kaprio, J., Ollikainen, M., Moffitt, T.E., Tiemeier, H., van, I.M.H., Relton, C., Vrijheid, M., Sebert, S., Jarvelin, M.R., Caspi, A., Evans, K.L., McIntosh, A.M., Bartels, M., Boomsma, D.I., Dongen, J. Van, Hagenbeek, F.A., Suderman, M., Roetman, P.J., Sugden, K., Chiocchetti, A.G., Ismail, K., Mulder, R.H., Hafferty, J.D., Adams, M.J., Walker, R.M., Morris, S.W., Lahti, J., Küpers, L.K., Escaramis, G., Alemany, S., Bonder, M. Jan, Meijer, M., Ip, H.F., Jansen, R., Baselmans, B.M.L., Parmar, P., Lowry, E., Streit, F., Sirignano, L., Send, T.S., Frank, J., Jylhävä, J., Wang, Y., Mishra, P.P., Colins, O.F., Corcoran, D.L., Poulton, R., Mill, J., Hannon, E., Arseneault, L., Korhonen, T., Vuoksimaa, E., Felix, J.F., Bakermans-Kranenburg, M.J., Campbell, A., Czamara, D., Binder, E., Corpeleijn, E., Gonzalez, J.R., Grazuleviciene, R., Gutzkow, K.B., Evandt, J., Vafeiadi, M., Klein, M., Meer, D. van der, Ligthart, L., Kluft, C., Davies, G.E., Hakulinen, C., Keltikangas-Järvinen, L., Franke, B., Freitag, C.M., Konrad, K., Hervas, A., Fernández-Rivas, A., Vetro, A., Raitakari, O., Lehtimäki, T., Vermeiren, R., Strandberg, T., Räikkönen, K., Snieder, H., Witt, S.H., Deuschle, M., Pedersen, N.L., Hägg, S., Sunyer, J., Franke, L., Kaprio, J., Ollikainen, M., Moffitt, T.E., Tiemeier, H., van, I.M.H., Relton, C., Vrijheid, M., Sebert, S., Jarvelin, M.R., Caspi, A., Evans, K.L., McIntosh, A.M., Bartels, M., and Boomsma, D.I.
Abstract: Item does not contain fulltext, DNA methylation profiles of aggressive behavior may capture lifetime cumulative effects of genetic, stochastic, and environmental influences associated with aggression. Here, we report the first large meta-analysis of epigenome-wide association studies (EWAS) of aggressive behavior (N = 15,324 participants). In peripheral blood samples of 14,434 participants from 18 cohorts with mean ages ranging from 7 to 68 years, 13 methylation sites were significantly associated with aggression (alpha = 1.2 × 10(-7); Bonferroni correction). In cord blood samples of 2425 children from five cohorts with aggression assessed at mean ages ranging from 4 to 7 years, 83% of these sites showed the same direction of association with childhood aggression (r = 0.74, p = 0.006) but no epigenome-wide significant sites were found. Top-sites (48 at a false discovery rate of 5% in the peripheral blood meta-analysis or in a combined meta-analysis of peripheral blood and cord blood) have been associated with chemical exposures, smoking, cognition, metabolic traits, and genetic variation (mQTLs). Three genes whose expression levels were associated with top-sites were previously linked to schizophrenia and general risk tolerance. At six CpGs, DNA methylation variation in blood mirrors variation in the brain. On average 44% (range = 3-82%) of the aggression-methylation association was explained by current and former smoking and BMI. These findings point at loci that are sensitive to chemical exposures with potential implications for neuronal functions. We hope these results to be a starting point for studies leading to applications as peripheral biomarkers and to reveal causal relationships with aggression and related traits.
Published: 2021

10. DNA methylation signatures of aggression and closely related constructs: A meta-analysis of epigenome-wide studies across the lifespan

Author: Dongen, J. (Jenny) van, Hagenbeek, F.A. (Fiona A.), Suderman, M.J. (Matthew J.), Roetman, P.J. (Peter J.), Sugden, K. (Karen), Chiocchetti, A.G. (Andreas G.), Ismail, K. (Khadeeja), Mulder, R.H. (Rosa), Hafferty, J.D. (Jonathan D.), Adams, M.J. (Mark J.), Walker, R.M. (Rosie M.), Morris, S.W. (Stewart W.), Lahti, J. (Jari), Küpers, A.M. (Marlijn), Escaramis, G. (Georgia), Alemany, S. (Silvia), Jan Bonder, M. (Marc), Meijer, M. (Mandy), Ip, H.F. (Hill F.), Jansen, R. (Rick), Baselmans, B.M.L. (Bart M. L.), Parmar, P. (Priyanka), Lowry, E. (Estelle), Streit, F. (Fabian), Sirignano, L. (Lea), Send, T.S. (Tabea S.), Frank, J. (Josef), Jylhävä, J. (Juulia), Wang, Y. (Yunzhang), Mishra, P.P. (Pashupati Prasad), Colins, O.F. (Olivier F.), Corcoran, D.L. (David L.), Poulton, R. (Richie), Mill, J. (Jonathan), Hannon, E. (Eilis), Arseneault, L. (Louise), Korhonen, T. (Tellervo), Vuoksimaa, E. (Eero), Felix, J.F. (Janine), Bakermans-Kranenburg, M.J. (Marian), Campbell, A. (Archie), Czamara, D. (Darina), Binder, E.B. (Elisabeth), Corpeleijn, E. (Eva), Gonzalez, J.R. (Juan R.), Grazuleviciene, R. (Regina), Gutzkow, K.B. (Kristine B.), Evandt, J. (Jorunn), Vafeiadi, M. (Marina), Klein, M. (Marieke), van der Meer, D. (Dennis), Ligthart, L. (Lannie), Kluft, C. (Cornelis), Davies, G.E. (Gareth E.), Hakulinen, C. (Christian), Keltikangas-Järvinen, L. (Liisa), Franke, B. (Barbara), Freitag, C.M. (Christine), Konrad, K. (Kerstin), Hervas, A. (Amaia), Fernández-Rivas, A. (Aranzazu), Vetro, A. (Agnes), Raitakari, O. (Olli), Lehtimäki, T. (Terho), Vermeiren, R.R.J.M. (Robert R.J.M.), Strandberg, T. (Timo), Räikkönen, K. (Katri), Snieder, H. (Harold), Witt, S.H. (Stephanie H), Deuschle, M. (Michael), Pedersen, N.L. (Nancy), Hägg, S. (Sara), Sunyer, J. (Jordi), Franke, L. (Lude), Kaprio, J. (Jaakko), Ollikainen, M. (Miina), Moffitt, T.E. (Terrie E.), Tiemeier, H.W. (Henning), IJzendoorn, M.H. (Rien) van, Relton, C.L. (Caroline), Vrijheid, M. (Martine), Sebert, S. (Sylvain), Jarvelin, M.-R. (Marjo-Riitta), Caspi, A. (Avshalom), Evans, K.L. (Kathryn L.), McIntosh, A.M. (Andrew), Bartels, M. (Meike), Boomsma, D.I. (Dorret I.), Dongen, J. (Jenny) van, Hagenbeek, F.A. (Fiona A.), Suderman, M.J. (Matthew J.), Roetman, P.J. (Peter J.), Sugden, K. (Karen), Chiocchetti, A.G. (Andreas G.), Ismail, K. (Khadeeja), Mulder, R.H. (Rosa), Hafferty, J.D. (Jonathan D.), Adams, M.J. (Mark J.), Walker, R.M. (Rosie M.), Morris, S.W. (Stewart W.), Lahti, J. (Jari), Küpers, A.M. (Marlijn), Escaramis, G. (Georgia), Alemany, S. (Silvia), Jan Bonder, M. (Marc), Meijer, M. (Mandy), Ip, H.F. (Hill F.), Jansen, R. (Rick), Baselmans, B.M.L. (Bart M. L.), Parmar, P. (Priyanka), Lowry, E. (Estelle), Streit, F. (Fabian), Sirignano, L. (Lea), Send, T.S. (Tabea S.), Frank, J. (Josef), Jylhävä, J. (Juulia), Wang, Y. (Yunzhang), Mishra, P.P. (Pashupati Prasad), Colins, O.F. (Olivier F.), Corcoran, D.L. (David L.), Poulton, R. (Richie), Mill, J. (Jonathan), Hannon, E. (Eilis), Arseneault, L. (Louise), Korhonen, T. (Tellervo), Vuoksimaa, E. (Eero), Felix, J.F. (Janine), Bakermans-Kranenburg, M.J. (Marian), Campbell, A. (Archie), Czamara, D. (Darina), Binder, E.B. (Elisabeth), Corpeleijn, E. (Eva), Gonzalez, J.R. (Juan R.), Grazuleviciene, R. (Regina), Gutzkow, K.B. (Kristine B.), Evandt, J. (Jorunn), Vafeiadi, M. (Marina), Klein, M. (Marieke), van der Meer, D. (Dennis), Ligthart, L. (Lannie), Kluft, C. (Cornelis), Davies, G.E. (Gareth E.), Hakulinen, C. (Christian), Keltikangas-Järvinen, L. (Liisa), Franke, B. (Barbara), Freitag, C.M. (Christine), Konrad, K. (Kerstin), Hervas, A. (Amaia), Fernández-Rivas, A. (Aranzazu), Vetro, A. (Agnes), Raitakari, O. (Olli), Lehtimäki, T. (Terho), Vermeiren, R.R.J.M. (Robert R.J.M.), Strandberg, T. (Timo), Räikkönen, K. (Katri), Snieder, H. (Harold), Witt, S.H. (Stephanie H), Deuschle, M. (Michael), Pedersen, N.L. (Nancy), Hägg, S. (Sara), Sunyer, J. (Jordi), Franke, L. (Lude), Kaprio, J. (Jaakko), Ollikainen, M. (Miina), Moffitt, T.E. (Terrie E.), Tiemeier, H.W. (Henning), IJzendoorn, M.H. (Rien) van, Relton, C.L. (Caroline), Vrijheid, M. (Martine), Sebert, S. (Sylvain), Jarvelin, M.-R. (Marjo-Riitta), Caspi, A. (Avshalom), Evans, K.L. (Kathryn L.), McIntosh, A.M. (Andrew), Bartels, M. (Meike), and Boomsma, D.I. (Dorret I.)
Abstract: DNA methylation profiles of aggressive behavior may capture lifetime cumulative effects of genetic, stochastic, and environmental influences associated with aggression. Here, we report the first large meta-analysis of epigenome-wide association studies (EWAS) of aggressive behavior (N = 15,324 participants). In peripheral blood samples of 14,434 participants from 18 cohorts with mean ages ranging from 7 to 68 years, 13 methylation sites were significantly associated with aggression (alpha = 1.2 × 10−7; Bonferroni correction). In cord blood samples of 2425 children from five cohorts with aggression assessed at mean ages ranging from 4 to 7 years, 83% of these sites showed the same direction of association with childhood aggression (r = 0.74, p = 0.006) but no epigenome-wide significant sites were found. Top-sites (48
Published: 2021
Full Text: View/download PDF

11. Maternal haemoglobin levels in pregnancy and child DNA methylation: a study in the pregnancy and childhood epigenetics consortium

Author: Ronkainen, J. (Justiina), Heiskala, A. (Anni), Vehmeijer, F.O.L. (Florianne O.L.), Lowry, E. (Estelle), Caramaschi, D. (Doretta), Estrada Gutierrez, G. (Guadalupe), Heiss, J.A. (Jonathan A.), Hummel, N. (Nadine), Keikkala, E. (Elina), Kvist, T. (Tuomas), Kupsco, A. (Allison), Melton, P.E. (Phillip E.), Pesce, G. (Giancarlo), Soomro, M.H. (Munawar H.), Vives-Usano, M. (Marta), Baïz, N. (Nour), Binder, E.B. (Elisabeth), Czamara, D. (Darina), Guxens Junyent, M. (Mònica), Mustaniemi, S. (Sanna), London, S.J. (Stephanie J.), Rauschert, S. (Sebastian), Vääräsmäki, M. (Marja), Vrijheid, M. (Martine), Ziegler, A.-G. (Anette-G.), Annesi-Maesano, I. (Isabella), Bustamante, M. (Mariona), Huang, R.-C. (Rae-Chi), Hummel, S. (Sandra), Just, A.C. (Allan C.), Kajantie, E. (Eero), Lahti, J. (Jari), Lawlor, D. (Deborah), Räikkönen, K. (Katri), Järvelin, M.-R. (Marjo-Riitta), Felix, J.F. (Janine), Sebert, S. (Sylvain), Ronkainen, J. (Justiina), Heiskala, A. (Anni), Vehmeijer, F.O.L. (Florianne O.L.), Lowry, E. (Estelle), Caramaschi, D. (Doretta), Estrada Gutierrez, G. (Guadalupe), Heiss, J.A. (Jonathan A.), Hummel, N. (Nadine), Keikkala, E. (Elina), Kvist, T. (Tuomas), Kupsco, A. (Allison), Melton, P.E. (Phillip E.), Pesce, G. (Giancarlo), Soomro, M.H. (Munawar H.), Vives-Usano, M. (Marta), Baïz, N. (Nour), Binder, E.B. (Elisabeth), Czamara, D. (Darina), Guxens Junyent, M. (Mònica), Mustaniemi, S. (Sanna), London, S.J. (Stephanie J.), Rauschert, S. (Sebastian), Vääräsmäki, M. (Marja), Vrijheid, M. (Martine), Ziegler, A.-G. (Anette-G.), Annesi-Maesano, I. (Isabella), Bustamante, M. (Mariona), Huang, R.-C. (Rae-Chi), Hummel, S. (Sandra), Just, A.C. (Allan C.), Kajantie, E. (Eero), Lahti, J. (Jari), Lawlor, D. (Deborah), Räikkönen, K. (Katri), Järvelin, M.-R. (Marjo-Riitta), Felix, J.F. (Janine), and Sebert, S. (Sylvain)
Abstract: Altered maternal haemoglobin levels during pregnancy are associated with pre-clinical and clinical conditions affecting the fetus. Evidence from animal models suggests that these associations may be partially explained by differential DNA methylation in the newborn with possible long-term consequences. To test this in humans, we meta-analyzed the epigenome-wide associations of maternal haemoglobin levels during pregnancy with offspring DNA methylation in 3,967 newborn cord blood and 1,534 children and 1,962 adolescent whole-blood samples derived from 10 cohorts. DNA methylation was measured using Illumina Infinium Methylation 450K or MethylationEPIC arrays covering 450,000 and 850,000 methylation sites, respectively. There was no statistical support for the association of maternal haemoglobin levels with offspring DNA methylation either at individual methylation sites or clustered in regions. For most participants, maternal haemoglobin levels were within the normal range in the current study, whereas adverse perinatal outcomes often arise at the extremes. Thus, this study does not rule out the possibility that associations with offspring DNA methylation might be seen in studies with more extreme maternal haemoglobin levels.
Published: 2021
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12. DNA methylation signatures of aggression and closely related constructs:a meta-analysis of epigenome-wide studies across the lifespan

Author: van Dongen, J. (Jenny), Hagenbeek, F. A. (Fiona A.), Suderman, M. (Matthew), Roetman, P. J. (Peter J.), Sugden, K. (Karen), Chiocchetti, A. G. (Andreas G.), Ismail, K. (Khadeeja), Mulder, R. H. (Rosa H.), Hafferty, J. D. (Jonathan D.), Adams, M. J. (Mark J.), Walker, R. M. (Rosie M.), Morris, S. W. (Stewart W.), Lahti, J. (Jari), Kupers, L. K. (Leanne K.), Escaramis, G. (Georgia), Alemany, S. (Silvia), Bonder, M. J. (Marc Jan), Meijer, M. (Mandy), Ip, H. F. (Hill F.), Jansen, R. (Rick), Baselmans, B. M. (Bart M. L.), Parmar, P. (Priyanka), Lowry, E. (Estelle), Streit, F. (Fabian), Sirignano, L. (Lea), Send, T. S. (Tabea S.), Frank, J. (Josef), Jylhava, J. (Juulia), Wang, Y. (Yunzhang), Mishra, P. P. (Pashupati Prasad), Colins, O. F. (Olivier F.), Corcoran, D. L. (David L.), Poulton, R. (Richie), Mill, J. (Jonathan), Hannon, E. (Eilis), Arseneault, L. (Louise), Korhonen, T. (Tellervo), Vuoksimaa, E. (Eero), Felix, J. F. (Janine F.), Bakermans-Kranenburg, M. J. (Marian J.), Campbell, A. (Archie), Czamara, D. (Darina), Binder, E. (Elisabeth), Corpeleijn, E. (Eva), Gonzalez, J. R. (Juan R.), Grazuleviciene, R. (Regina), Gutzkow, K. B. (Kristine B.), Evandt, J. (Jorunn), Vafeiadi, M. (Marina), Klein, M. (Marieke), van der Meer, D. (Dennis), Ligthart, L. (Lannie), Kluft, C. (Cornelis), Davies, G. E. (Gareth E.), Hakulinen, C. (Christian), Keltikangas-Jarvinen, L. (Liisa), Franke, B. (Barbara), Freitag, C. M. (Christine M.), Konrad, K. (Kerstin), Hervas, A. (Amaia), Fernandez-Rivas, A. (Aranzazu), Vetro, A. (Agnes), Raitakari, O. (Olli), Lehtimaki, T. (Terho), Vermeiren, R. (Robert), Strandberg, T. (Timo), Raikkonen, K. (Katri), Snieder, H. (Harold), Witt, S. H. (Stephanie H.), Deuschle, M. (Michael), Pedersen, N. L. (Nancy L.), Hagg, S. (Sara), Sunyer, J. (Jordi), Franke, L. (Lude), Kaprio, J. (Jaakko), Ollikainen, M. (Miina), Moffitt, T. E. (Terrie E.), Tiemeier, H. (Henning), van IJzendoorn, M. H. (Marinus H.), Relton, C. (Caroline), Vrijheid, M. (Martine), Sebert, S. (Sylvain), Järvelin, M.-R. (Marjo-Riitta), Caspi, A. (Avshalom), Evans, K. L. (Kathryn L.), McIntosh, A. M. (Andrew M.), Bartels, M. (Meike), Boomsma, D. I. (Dorret, I), van Dongen, J. (Jenny), Hagenbeek, F. A. (Fiona A.), Suderman, M. (Matthew), Roetman, P. J. (Peter J.), Sugden, K. (Karen), Chiocchetti, A. G. (Andreas G.), Ismail, K. (Khadeeja), Mulder, R. H. (Rosa H.), Hafferty, J. D. (Jonathan D.), Adams, M. J. (Mark J.), Walker, R. M. (Rosie M.), Morris, S. W. (Stewart W.), Lahti, J. (Jari), Kupers, L. K. (Leanne K.), Escaramis, G. (Georgia), Alemany, S. (Silvia), Bonder, M. J. (Marc Jan), Meijer, M. (Mandy), Ip, H. F. (Hill F.), Jansen, R. (Rick), Baselmans, B. M. (Bart M. L.), Parmar, P. (Priyanka), Lowry, E. (Estelle), Streit, F. (Fabian), Sirignano, L. (Lea), Send, T. S. (Tabea S.), Frank, J. (Josef), Jylhava, J. (Juulia), Wang, Y. (Yunzhang), Mishra, P. P. (Pashupati Prasad), Colins, O. F. (Olivier F.), Corcoran, D. L. (David L.), Poulton, R. (Richie), Mill, J. (Jonathan), Hannon, E. (Eilis), Arseneault, L. (Louise), Korhonen, T. (Tellervo), Vuoksimaa, E. (Eero), Felix, J. F. (Janine F.), Bakermans-Kranenburg, M. J. (Marian J.), Campbell, A. (Archie), Czamara, D. (Darina), Binder, E. (Elisabeth), Corpeleijn, E. (Eva), Gonzalez, J. R. (Juan R.), Grazuleviciene, R. (Regina), Gutzkow, K. B. (Kristine B.), Evandt, J. (Jorunn), Vafeiadi, M. (Marina), Klein, M. (Marieke), van der Meer, D. (Dennis), Ligthart, L. (Lannie), Kluft, C. (Cornelis), Davies, G. E. (Gareth E.), Hakulinen, C. (Christian), Keltikangas-Jarvinen, L. (Liisa), Franke, B. (Barbara), Freitag, C. M. (Christine M.), Konrad, K. (Kerstin), Hervas, A. (Amaia), Fernandez-Rivas, A. (Aranzazu), Vetro, A. (Agnes), Raitakari, O. (Olli), Lehtimaki, T. (Terho), Vermeiren, R. (Robert), Strandberg, T. (Timo), Raikkonen, K. (Katri), Snieder, H. (Harold), Witt, S. H. (Stephanie H.), Deuschle, M. (Michael), Pedersen, N. L. (Nancy L.), Hagg, S. (Sara), Sunyer, J. (Jordi), Franke, L. (Lude), Kaprio, J. (Jaakko), Ollikainen, M. (Miina), Moffitt, T. E. (Terrie E.), Tiemeier, H. (Henning), van IJzendoorn, M. H. (Marinus H.), Relton, C. (Caroline), Vrijheid, M. (Martine), Sebert, S. (Sylvain), Järvelin, M.-R. (Marjo-Riitta), Caspi, A. (Avshalom), Evans, K. L. (Kathryn L.), McIntosh, A. M. (Andrew M.), Bartels, M. (Meike), and Boomsma, D. I. (Dorret, I)
Abstract: DNA methylation profiles of aggressive behavior may capture lifetime cumulative effects of genetic, stochastic, and environmental influences associated with aggression. Here, we report the first large meta-analysis of epigenome-wide association studies (EWAS) of aggressive behavior (N = 15,324 participants). In peripheral blood samples of 14,434 participants from 18 cohorts with mean ages ranging from 7 to 68 years, 13 methylation sites were significantly associated with aggression (alpha = 1.2 × 10−7; Bonferroni correction). In cord blood samples of 2425 children from five cohorts with aggression assessed at mean ages ranging from 4 to 7 years, 83% of these sites showed the same direction of association with childhood aggression (r = 0.74, p = 0.006) but no epigenome-wide significant sites were found. Top-sites (48 at a false discovery rate of 5% in the peripheral blood meta-analysis or in a combined meta-analysis of peripheral blood and cord blood) have been associated with chemical exposures, smoking, cognition, metabolic traits, and genetic variation (mQTLs). Three genes whose expression levels were associated with top-sites were previously linked to schizophrenia and general risk tolerance. At six CpGs, DNA methylation variation in blood mirrors variation in the brain. On average 44% (range = 3–82%) of the aggression–methylation association was explained by current and former smoking and BMI. These findings point at loci that are sensitive to chemical exposures with potential implications for neuronal functions. We hope these results to be a starting point for studies leading to applications as peripheral biomarkers and to reveal causal relationships with aggression and related traits.
Published: 2021

13. Early origins of cardiometabolic risk factors:life course epidemiology and pathways

Author: Sebert, S. (Sylvain), Järvelin, M. (Marjo-Riitta), Lowry, E. (Estelle), Choudhary, P. (Priyanka), Sebert, S. (Sylvain), Järvelin, M. (Marjo-Riitta), Lowry, E. (Estelle), and Choudhary, P. (Priyanka)
Abstract: Non-communicable diseases, chiefly cardiovascular diseases and type 2 diabetes (T2D), are major causes of mortality and morbidity worldwide. The literature expands on multifactorial risks that extend beyond biological dimension, including interplays with social, psychological and environmental factors, setting in place the foundations for shaping future health outcomes. However, the link between genetic and environmental causative mechanisms and temporal trajectories since gestation is poorly understood. In this thesis, a holistic approach was achieved by assessing the: 1) Variations in DNA methylation at the GFI1 locus in relation to smoking to build the epigenetic link, mediating the latent association of maternal smoking on offspring’s cardiometabolic health in adulthood; 2) Synergy between maternal prenatal biological, psychological and social factors in cumulatively influencing offspring’s birth outcomes and; 3) Early origins of T2D tracked through longitudinal risk of adiposity and modulating associations of lifestyle factors. Studies were primarily conducted in the Northern Finland Birth Cohorts 1966 and 1986, and multiple cohorts were included in studiesI & II to enable robustness and generalizability. The first study showed associations of the hypomethylation of epigenetic sites at the GFI1 locus, associated with fetal exposures to maternal smoking, on adult triglyceride, adiposity, and blood pressure levels. The second study yielded a four factor structure between the biopsychosocial variables thata clustered into biological and psychosocial factors and showed comparable associations with birth outcomes. The third study provided clear evidence that in a contemporary birth cohort, lower birth weight remains a major risk for T2D. Overweight patterns in childhood associated with increased risks of developing T2D when continued into adulthood. This research serves as a proof of concept for the ongoing debate of the lifecourse consequences of early, Tiivistelmä Pitkäaikaissairaudet, kuten sydän- ja verisuonisairaudet sekä tyypin 2 diabetes ovat maailmanlaajuisesti merkittäviä sairastavuuden ja kuolleisuuden taustatekijöitä. Biologisia tekijöitä laajemmalle ulottuvat monitekijäiset riskit ovat saaneet kirjallisuudessa paljon huomiota. Näihin riskeihin kuuluvat esimerkiksi sosiaalisten, psykologisten ja ympäristötekijöiden väliset vuorovaikutukset, jotka luovat perustaa myöhemmin elämässä kohdattaville terveysongelmille. Raskausaikana syntyviä perinnöllisiä ja ympäristöllisiä mekanismeja ymmärretään huonommin. Tämä väitöskirja keskittyi kokonaisvaltaisen lähestymisen kautta-seuraaviin kokonaisuuksiin: 1) tupakointiin liittyvä DNA-metylaatio vaihtelu GFI1-geenin alueella. Tämä epigeneettinen linkki välittää äidin raskausajan tupakoinnin vaikutuksia syntyvän lapsen aikuisiän sydän- ja verisuonisairauksien puhkeamisriskiin, 2) Raskausajan biologisten, psykologisten ja sosiaalisten tekijöiden kumulatiivinen vaikutus syntyvän lapsen terveyteen, sekä, 3) Tyypin 2 diabeteksen varhainen puhkeaminen pitkäaikaisen lihavuuden sekä elämäntyyliin liittyvien tekijöiden kautta. Tutkimuksen aineistona käytettiin Pohjois-Suomen syntymäkohortteja 1966 ja 1986, ja lisäksi osajulkaisuissa I ja II käytettiin useiden muiden kohorttien aineistoja tulosten validointiin. Ensimmäisessä osajulkaisussa havaittiin, että sikiöaikana tupakoinnille altistuneiden lasten GFI1-geenissä oli vähemmän metyloituneita kohtia verrattuna tupakoimattomien äitien lapsiin. GFI1-geenin metylaatio assosioi myös aikuisiän triglyseridiarvojen, lihavuuden ja verenpaineen kanssa. Toisessa osajulkaisussa löydettiin nelitekijäinen mekanismi, joka ryhmittyi biologisiin ja psykososiaalisiin tekijöihin, joiden vaikutukset puolestaan olivat pääosin yhdenmukaisia kahdessa etnisesti erilaisessa populaatiossa. Kolmannessa osajulkaisussa osoitettiin, että matala syntymäpaino on yhä merkittävä tyypin 2 diabeteksen riskitekijä. Lisäksi lapsuudesta aikuisuuteen jatkuva lihavu
Published: 2021

14. Rapid Systematic Review Exploring Historical and Present Day National and International Governance during Pandemics: Review Protocol

Author: Lowry, E, Taddese, H, and Bowman, LR
Abstract: Introduction Pandemics have plagued mankind since records began, and while non-communicable disease pandemics are more common in high-income nations, infectious disease pandemics continue to affect all countries worldwide. To mitigate impact, national pandemic preparedness and response policies remain crucial. And in response to emerging pathogens of pandemic potential, public health policies must be both dynamic and adaptive. Yet, this process of policy change and adaptation remains opaque. Accordingly, this rapid systematic review will synthesise and analyse evaluative policy literature to develop a roadmap of policy changes that have occurred after each pandemic event, throughout both the 20th and 21st Century, in order to better inform future policy development. Methods and Analysis A rapid systematic review will be conducted to assimilate and synthesise both peer-reviewed articles and grey literature that document the then current pandemic preparedness policy, and the subsequent changes to that policy, across high-, middle- and low-income countries. The rapid review will follow the PRISMA guidelines, and the literature search will be performed across five relevant databases, as well as various government websites to scan for grey literature. Articles will be screen against pre-agreed inclusion/ exclusion criteria, and data will be extracted using a pre-defined charting table. Ethics and Dissemination All data rely on secondary, publicly available data sources; therefore no ethical clearance is required. Upon completion, the results of this study will be disseminated via the Imperial College London Community and published in an open access, peer-reviewed journal.
Published: 2020

15. Could vitamin D reduce obesity-associated inflammation?:observational and Mendelian randomization study

Author: Palaniswamy, S. (Saranya), Gill, D. (Dipender), De Silva, N. M. (N. Maneka), Lowry, E. (Estelle), Jokelainen, J. (Jari), Karhu, T. (Toni), Mutt, S. J. (Shivaprakash J.), Dehghan, A. (Abbas), Sliz, E. (Eeva), Chasman, D. I. (Daniel I.), Timonen, M. (Markku), Viinamäki, H. (Heimo), Keinänen-Kiukaanniemi, S. (Sirkka), Hyppönen, E. (Elina), Herzig, K.-H. (Karl-Heinz), Sebert, S. (Sylvain), and Järvelin, M.-R. (Marjo-Riitta)
Subjects: BMI, obesity, 25(OH)D, inflammation, Mendelian randomization, mediation, vitamin D
Abstract: Background: Obesity is associated with inflammation but the role of vitamin D in this process is not clear. Objectives: We aimed to assess the associations between serum 25-hydroxyvitamin D [25(OH)D], BMI, and 16 inflammatory biomarkers, and to assess the role of vitamin D as a potential mediator in the association between higher BMI and inflammation. Methods: Northern Finland Birth Cohort 1966 (NFBC1966) 31-y data on 3586 individuals were analyzed to examine the observational associations between BMI, 25(OH)D, and 16 inflammatory biomarkers. Multivariable regression analyses and 2-sample regression-based Mendelian randomization (MR) mediation analysis were performed to assess any role of vitamin D in mediating a causal effect of BMI on inflammatory biomarkers [soluble intercellular adhesion molecule 1 (sICAM-1), high sensitivity C-reactive protein (hs-CRP), and α1-acid glycoprotein (AGP)] for which observational associations were detected. For MR, genome-wide association study summary results ranging from 5163 to 806,834 individuals were used for biomarkers, 25(OH)D, and BMI. Findings were triangulated with a literature review of vitamin D supplementation trials. Results: In NFBC1966, mean BMI (kg/m²) was 24.8 (95% CI: 24.7, 25.0) and mean 25(OH)D was 50.3 nmol/L (95% CI: 49.8, 50.7 nmol/L). Inflammatory biomarkers correlated as 4 independent clusters: interleukins, adhesion molecules, acute-phase proteins, and chemokines. BMI was positively associated with 9 inflammatory biomarkers and inversely with 25(OH)D (false discovery rate < 0.05). 25(OH)D was inversely associated with sICAM-1, hs-CRP, and AGP, which were positively associated with BMI. The MR analyses showed causal association of BMI on these 3 inflammatory biomarkers. There was no observational or MR evidence that circulating 25(OH)D concentrations mediated the association between BMI and these 3 inflammatory markers. Review of randomized controlled trials (RCTs) supported our findings showing no impact of vitamin D supplementation on inflammatory biomarkers. Conclusions: The findings from our observational study and causal MR analyses, together with data from RCTs, do not support a beneficial role of vitamin D supplementation on obesity-related inflammation.
Published: 2020

16. Understanding the cumulative risk of maternal prenatal biopsychosocial factors on birth weight:a DynaHEALTH study on two birth cohorts

Author: Parmar, P. (Priyanka), Lowry, E. (Estelle), Vehmeijer, F. (Florianne), El Marroun, H. (Hanan), Lewin, A. (Alex), Tolvanen, M. (Mimmi), Tzala, E. (Evangelia), Ala-Mursula, L. (Leena), Herzig, K.-H. (Karl-Heinz), Miettunen, J. (Jouko), Prokopenko, I. (Inga), Rautio, N. (Nina), Jaddoe, V. W. (Vincent W. V.), Järvelin, M.-R. (Marjo-Riitta), Felix, J. (Janine), and Sebert, S. (Sylvain)
Subjects: Child health, Ageing, Birth defects, Disability, Birth weight, Epidemiology of chronic non communicable diseases, Diabetes, Life course epidemiology, Cohort studies, Maternal health, Biostatistics, Cardiovascular disease
Abstract: Background: There are various maternal prenatal biopsychosocial (BPS) predictors of birth weight, making it difficult to quantify their cumulative relationship. Methods: We studied two birth cohorts: Northern Finland Birth Cohort 1986 (NFBC1986) born in 1985–1986 and the Generation R Study (from the Netherlands) born in 2002–2006. In NFBC1986, we selected variables depicting BPS exposure in association with birth weight and performed factor analysis to derive latent constructs representing the relationship between these variables. In Generation R, the same factors were generated weighted by loadings of NFBC1986. Factor scores from each factor were then allocated into tertiles and added together to calculate a cumulative BPS score. In all cases, we used regression analyses to explore the relationship with birth weight corrected for sex and gestational age and additionally adjusted for other factors. Results: Factor analysis supported a four-factor structure, labelled closely to represent their characteristics as ‘Factor1-BMI’ (body mass index), ‘Factor2-DBP’ (diastolic blood pressure), ‘Factor3-Socioeconomic-Obstetric-Profile’ and ‘Factor4-Parental-Lifestyle’. In both cohorts, ‘Factor1-BMI’ was positively associated with birth weight, whereas other factors showed negative association. ‘Factor3-Socioeconomic-Obstetric-Profile’ and ‘Factor4-Parental-Lifestyle’ had the greatest effect size, explaining 30% of the variation in birth weight. Associations of the factors with birth weight were largely driven by ‘Factor1-BMI’. Graded decrease in birth weight was observed with increasing cumulative BPS score, jointly evaluating four factors in both cohorts. Conclusion: Our study is a proof of concept for maternal prenatal BPS hypothesis, highlighting the components snowball effect on birth weight in two different European birth cohorts.
Published: 2020

17. Early exposure to social disadvantages and later life body mass index beyond genetic predisposition in three generations of Finnish birth cohorts

Author: Lowry, E. (Estelle), Rautio, N. (Nina), Wasenius, N. (Niko), Bond, T. A. (Tom A.), Lahti, J. (Jari), Tzoulaki, I. (Ioanna), Dehghan, A. (Abbas), Heiskala, A. (Anni), Ala-Mursula, L. (Leena), Miettunen, J. (Jouko), Eriksson, J. (Johan), Järvelin, M.-R. (Marjo-Riitta), Sebert, S. (Sylvain), Lowry, E. (Estelle), Rautio, N. (Nina), Wasenius, N. (Niko), Bond, T. A. (Tom A.), Lahti, J. (Jari), Tzoulaki, I. (Ioanna), Dehghan, A. (Abbas), Heiskala, A. (Anni), Ala-Mursula, L. (Leena), Miettunen, J. (Jouko), Eriksson, J. (Johan), Järvelin, M.-R. (Marjo-Riitta), and Sebert, S. (Sylvain)
Abstract: Background: The study aimed to explore the association between early life and life-course exposure to social disadvantage and later life body mass index (BMI) accounting for genetic predisposition and maternal BMI. Methods: We studied participants of Helsinki Birth Cohort Study born in 1934–1944 (HBCS1934–1944, n = 1277) and Northern Finland Birth Cohorts born in 1966 and 1986 (NFBC1966, n = 5807, NFBC1986, n = 6717). Factor analysis produced scores of social disadvantage based on social and economic elements in early life and adulthood/over the life course, and was categorized as high, intermediate and low. BMI was measured at 62 years in HBCS1934–1944, at 46 years in NFBC1966 and at 16 years in NFBC1986. Multivariable linear regression analysis was used to explore associations between social disadvantages and BMI after adjustments for polygenic risk score for BMI (PRS BMI), maternal BMI and sex. Results: The association between exposure to high early social disadvantage and increased later life BMI persisted after adjustments (β = 0.79, 95% CI, 0.33, 1.25, p < 0.001) in NFBC1966. In NFBC1986 this association was attenuated by PRS BMI (p = 0.181), and in HBCS1934–1944 there was no association between high early social disadvantage and increased later life BMI (β 0.22, 95% CI −0.91,1.35, p = 0.700). In HBCS1934–1944 and NFBC1966, participants who had reduced their exposure to social disadvantage during the life-course had lower later life BMI than those who had increased their exposure (β − 1.34, [−2.37,−0.31], p = 0.011; β − 0.46, [−0.89,−0.03], p = 0.038, respectively). Conclusions: High social disadvantage in early life appears to be associated with higher BMI in later life. Reducing exposure to social disadvantage during the life-course may be a potential pathway for obesity reduction.
Published: 2020

18. Understanding the cumulative risk of maternal prenatal biopsychosocial factors on birth weight: A DynaH

Author: Parmar, P. (Priyanka), Lowry, E. (Estelle), Vehmeijer, F.O.L. (Florianne O.L.), El Marroun, H. (Hanan), Lewin, A. (Alex), Tolvanen, M. (Mimmi), Tzala, E. (Evangelia), Ala-Mursula, L. (Leena), Herzig, K.H., Miettunen, J. (Jouko), Prokopenko, I. (Inga), Rautio, N. (Nina), Jaddoe, V.W.V. (Vincent), Järvelin, M.-R. (Marjo-Riitta), Felix, J.F. (Janine), Sebert, S. (Sylvain), Parmar, P. (Priyanka), Lowry, E. (Estelle), Vehmeijer, F.O.L. (Florianne O.L.), El Marroun, H. (Hanan), Lewin, A. (Alex), Tolvanen, M. (Mimmi), Tzala, E. (Evangelia), Ala-Mursula, L. (Leena), Herzig, K.H., Miettunen, J. (Jouko), Prokopenko, I. (Inga), Rautio, N. (Nina), Jaddoe, V.W.V. (Vincent), Järvelin, M.-R. (Marjo-Riitta), Felix, J.F. (Janine), and Sebert, S. (Sylvain)
Abstract: Background: There are various maternal prenatal biopsychosocial (BPS) predictors of birth weight, making it difficult to quantify their cumulative relationship. Methods: We studied two birth cohorts: Northern Finland Birth Cohort 1986 (NFBC1986) born in 1985-1986 and the Generation R Study (from the Netherlands) born in 2002-2006. In NFBC1986, we selected variables depicting BPS exposure in association with birth weight and performed factor analysis to derive latent constructs representing the relationship between these variables. In Generation R, the same factors were generated weighted by loadings of NFBC1986. Factor scores from each factor were then allocated into tertiles and added together to calculate a cumulative BPS score. In all cases, we used regression analyses to explore the relationship with birth weight corrected for sex and gestational age and additionally adjusted for other factors. Results: Factor analysis supported a four-factor structure, labelled closely to represent their characteristics as â € Factor1-BMI' (body mass index), â € Factor2-DBP' (diastolic blood pressure), â € Factor3-Socioeconomic-Obstetric-Profile' and â € Factor4-Parental-Lifestyle'. In both cohorts, â € Factor1-BMI' was positively associated with birth weight, whereas other factors showed negative association. â € Factor3-Socioeconomic-Obstetric-Profile' and â € Factor4-Parental-Lifestyle' had the greatest effect size, explaining 30% of the variation in birth weight. Associations of the factors with birth weight were largely driven by â € Factor1-BMI'. Graded decrease in birth weight was observed with increasing cumulative BPS score, jointly evaluating four factors in both cohorts. Conclusion: Our study is a proof of concept for maternal prenatal BPS hypothesis, highlighting the components snowball effect on birth weight in two different European birth cohorts.
Published: 2020
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19. Novel loci for childhood body mass index and shared heritability with adult cardiometabolic traits.

Author: Vogelezang, S, Bradfield, JP, Ahluwalia, TS, Curtin, JA, Lakka, TA, Grarup, N, Scholz, M, van der Most, PJ, Monnereau, C, Stergiakouli, E, Heiskala, A, Horikoshi, M, Fedko, IO, Vilor-Tejedor, N, Cousminer, DL, Standl, M, Wang, CA, Viikari, J, Geller, F, Íñiguez, C, Pitkänen, N, Chesi, A, Bacelis, J, Yengo, L, Torrent, M, Ntalla, I, Helgeland, Ø, Selzam, S, Vonk, JM, Zafarmand, MH, Heude, B, Farooqi, IS, Alyass, A, Beaumont, RN, Have, CT, Rzehak, P, Bilbao, JR, Schnurr, TM, Barroso, I, Bønnelykke, K, Beilin, LJ, Carstensen, L, Charles, M-A, Chawes, B, Clément, K, Closa-Monasterolo, R, Custovic, A, Eriksson, JG, Escribano, J, Groen-Blokhuis, M, Grote, V, Gruszfeld, D, Hakonarson, H, Hansen, T, Hattersley, AT, Hollensted, M, Hottenga, J-J, Hyppönen, E, Johansson, S, Joro, R, Kähönen, M, Karhunen, V, Kiess, W, Knight, BA, Koletzko, B, Kühnapfel, A, Landgraf, K, Langhendries, J-P, Lehtimäki, T, Leinonen, JT, Li, A, Lindi, V, Lowry, E, Bustamante, M, Medina-Gomez, C, Melbye, M, Michaelsen, KF, Morgen, CS, Mori, TA, Nielsen, TRH, Niinikoski, H, Oldehinkel, AJ, Pahkala, K, Panoutsopoulou, K, Pedersen, O, Pennell, CE, Power, C, Reijneveld, SA, Rivadeneira, F, Simpson, A, Sly, Peter, Stokholm, J, Teo, KK, Thiering, E, Timpson, NJ, Uitterlinden, AG, van Beijsterveldt, CEM, van Schaik, BDC, Vaudel, M, Verduci, E, Vinding, RK, Vogel, M, Zeggini, E, Sebert, S, Lind, MV, Brown, CD, Santa-Marina, L, Reischl, E, Frithioff-Bøjsøe, C, Meyre, D, Wheeler, E, Ong, K, Nohr, EA, Vrijkotte, TGM, Koppelman, GH, Plomin, R, Njølstad, PR, Dedoussis, GD, Froguel, P, Sørensen, TIA, Jacobsson, B, Freathy, RM, Zemel, BS, Raitakari, O, Vrijheid, M, Feenstra, B, Lyytikäinen, L-P, Snieder, H, Kirsten, H, Holt, PG, Heinrich, J, Widén, E, Sunyer, J, Boomsma, DI, Järvelin, M-R, Körner, A, Davey Smith, G, Holm, J-C, Atalay, M, Murray, C, Bisgaard, H, McCarthy, MI, Early Growth Genetics Consortium, Jaddoe, VWV, Grant, SFA, Felix, JF, Vogelezang, S, Bradfield, JP, Ahluwalia, TS, Curtin, JA, Lakka, TA, Grarup, N, Scholz, M, van der Most, PJ, Monnereau, C, Stergiakouli, E, Heiskala, A, Horikoshi, M, Fedko, IO, Vilor-Tejedor, N, Cousminer, DL, Standl, M, Wang, CA, Viikari, J, Geller, F, Íñiguez, C, Pitkänen, N, Chesi, A, Bacelis, J, Yengo, L, Torrent, M, Ntalla, I, Helgeland, Ø, Selzam, S, Vonk, JM, Zafarmand, MH, Heude, B, Farooqi, IS, Alyass, A, Beaumont, RN, Have, CT, Rzehak, P, Bilbao, JR, Schnurr, TM, Barroso, I, Bønnelykke, K, Beilin, LJ, Carstensen, L, Charles, M-A, Chawes, B, Clément, K, Closa-Monasterolo, R, Custovic, A, Eriksson, JG, Escribano, J, Groen-Blokhuis, M, Grote, V, Gruszfeld, D, Hakonarson, H, Hansen, T, Hattersley, AT, Hollensted, M, Hottenga, J-J, Hyppönen, E, Johansson, S, Joro, R, Kähönen, M, Karhunen, V, Kiess, W, Knight, BA, Koletzko, B, Kühnapfel, A, Landgraf, K, Langhendries, J-P, Lehtimäki, T, Leinonen, JT, Li, A, Lindi, V, Lowry, E, Bustamante, M, Medina-Gomez, C, Melbye, M, Michaelsen, KF, Morgen, CS, Mori, TA, Nielsen, TRH, Niinikoski, H, Oldehinkel, AJ, Pahkala, K, Panoutsopoulou, K, Pedersen, O, Pennell, CE, Power, C, Reijneveld, SA, Rivadeneira, F, Simpson, A, Sly, Peter, Stokholm, J, Teo, KK, Thiering, E, Timpson, NJ, Uitterlinden, AG, van Beijsterveldt, CEM, van Schaik, BDC, Vaudel, M, Verduci, E, Vinding, RK, Vogel, M, Zeggini, E, Sebert, S, Lind, MV, Brown, CD, Santa-Marina, L, Reischl, E, Frithioff-Bøjsøe, C, Meyre, D, Wheeler, E, Ong, K, Nohr, EA, Vrijkotte, TGM, Koppelman, GH, Plomin, R, Njølstad, PR, Dedoussis, GD, Froguel, P, Sørensen, TIA, Jacobsson, B, Freathy, RM, Zemel, BS, Raitakari, O, Vrijheid, M, Feenstra, B, Lyytikäinen, L-P, Snieder, H, Kirsten, H, Holt, PG, Heinrich, J, Widén, E, Sunyer, J, Boomsma, DI, Järvelin, M-R, Körner, A, Davey Smith, G, Holm, J-C, Atalay, M, Murray, C, Bisgaard, H, McCarthy, MI, Early Growth Genetics Consortium, Jaddoe, VWV, Grant, SFA, and Felix, JF
Abstract: The genetic background of childhood body mass index (BMI), and the extent to which the well-known associations of childhood BMI with adult diseases are explained by shared genetic factors, are largely unknown. We performed a genome-wide association study meta-analysis of BMI in 61,111 children aged between 2 and 10 years. Twenty-five independent loci reached genome-wide significance in the combined discovery and replication analyses. Two of these, located near NEDD4L and SLC45A3, have not previously been reported in relation to either childhood or adult BMI. Positive genetic correlations of childhood BMI with birth weight and adult BMI, waist-to-hip ratio, diastolic blood pressure and type 2 diabetes were detected (Rg ranging from 0.11 to 0.76, P-values <0.002). A negative genetic correlation of childhood BMI with age at menarche was observed. Our results suggest that the biological processes underlying childhood BMI largely, but not completely, overlap with those underlying adult BMI. The well-known observational associations of BMI in childhood with cardio-metabolic diseases in adulthood may reflect partial genetic overlap, but in light of previous evidence, it is also likely that they are explained through phenotypic continuity of BMI from childhood into adulthood.
Published: 2020

20. Novel loci for childhood body mass index and shared heritability with adult cardiometabolic traits

Author: Vogelezang, S. (Suzanne), Bradfield, J. P. (Jonathan P.), Ahluwalia, T. S. (Tarunveer S.), Curtin, J. A. (John A.), Lakka, T. A. (Timo A.), Grarup, N. (Niels), Scholz, M. (Markus), van der Most, P. J. (Peter J.), Monnereau, C. (Claire), Stergiakouli, E. (Evie), Heiskala, A. (Anni), Horikoshi, M. (Momoko), Fedko, I. O. (Iryna O.), Vilor-Tejedor, N. (Natalia), Cousminer, D. L. (Diana L.), Standl, M. (Marie), Wang, C. A. (Carol A.), Viikari, J. (Jorma), Geller, F. (Frank), iniguez, C. (Carmen), Pitkanen, N. (Niina), Chesi, A. (Alessandra), Bacelis, J. (Jonas), Yengo, L. (Loic), Torrent, M. (Maties), Ntalla, I. (Ioanna), Helgeland, O. (Oyvind), Selzam, S. (Saskia), Vonk, J. M. (Judith M.), Zafarmand, M. H. (Mohammed H.), Heude, B. (Barbara), Farooqi, I. S. (Ismaa Sadaf), Alyass, A. (Akram), Beaumont, R. N. (Robin N.), Have, C. T. (Christian T.), Rzehak, P. (Peter), Bilbao, J. R. (Jose Ramon), Schnurr, T. M. (Theresia M.), Barroso, I. (Ines), Bonnelykke, K. (Klaus), Beilin, L. J. (Lawrence J.), Carstensen, L. (Lisbeth), Charles, M.-A. (Marie-Aline), Chawes, B. (Bo), Clement, K. (Karine), Closa-Monasterolo, R. (Ricardo), Custovic, A. (Adnan), Eriksson, J. G. (Johan G.), Escribano, J. (Joaquin), Groen-Blokhuis, M. (Maria), Grote, V. (Veit), Gruszfeld, D. (Dariusz), Hakonarson, H. (Hakon), Hansen, T. (Torben), Hattersley, A. T. (Andrew T.), Hollensted, M. (Mette), Hottenga, J.-J. (Jouke-Jan), Hypponen, E. (Elina), Johansson, S. (Stefan), Joro, R. (Raimo), Kahonen, M. (Mika), Karhunen, V. (Ville), Kiess, W. (Wieland), Knight, B. A. (Bridget A.), Koletzko, B. (Berthold), Kuehnapfel, A. (Andreas), Landgraf, K. (Kathrin), Langhendries, J.-P. (Jean-Paul), Lehtimaki, T. (Terho), Leinonen, J. T. (Jaakko T.), Li, A. (Aihuali), Lindi, V. (Virpi), Lowry, E. (Estelle), Bustamante, M. (Mariona), Medina-Gomez, C. (Carolina), Melbye, M. (Mads), Michaelsen, K. F. (Kim F.), Morgen, C. S. (Camilla S.), Mori, T. A. (Trevor A.), Nielsen, T. R. (Tenna R. H.), Niinikoski, H. (Harri), Oldehinkel, A. J. (Albertine J.), Pahkala, K. (Katja), Panoutsopoulou, K. (Kalliope), Pedersen, O. (Oluf), Pennell, C. E. (Craig E.), Power, C. (Christine), Reijneveld, S. A. (Sijmen A.), Rivadeneira, F. (Fernando), Simpson, A. (Angela), Sly, P. D. (Peter D.), Stokholm, J. (Jakob), Teo, K. K. (Kook K.), Thiering, E. (Elisabeth), Timpson, N. J. (Nicholas J.), Uitterlinden, A. G. (Andre G.), van Beijsterveldt, C. E. (Catharina E. M.), van Schaik, B. D. (Barbera D. C.), Vaudel, M. (Marc), Verduci, E. (Elvira), Vinding, R. K. (Rebecca K.), Vogel, M. (Mandy), Zeggini, E. (Eleftheria), Sebert, S. (Sylvain), Lind, M. V. (Mads V.), Brown, C. D. (Christopher D.), Santa-Marina, L. (Loreto), Reischl, E. (Eva), Frithioff-Bojsoe, C. (Christine), Meyre, D. (David), Wheeler, E. (Eleanor), Ong, K. (Ken), Nohr, E. A. (Ellen A.), Vrijkotte, T. G. (Tanja G. M.), Koppelman, G. H. (Gerard H.), Plomin, R. (Robert), Njolstad, P. R. (Pal R.), Dedoussis, G. D. (George D.), Froguel, P. (Philippe), Sorensen, T. I. (Thorkild I. A.), Jacobsson, B. (Bo), Freathy, R. M. (Rachel M.), Zemel, B. S. (Babette S.), Raitakari, O. (Olli), Vrijheid, M. (Martine), Feenstra, B. (Bjarke), Lyytikainen, L.-P. (Leo-Pekka), Snieder, H. (Harold), Kirsten, H. (Holger), Holt, P. G. (Patrick G.), Heinrich, J. (Joachim), Widen, E. (Elisabeth), Sunyer, J. (Jordi), Boomsma, D. I. (Dorret I.), Jarvelin, M.-R. (Marjo-Riitta), Koerner, A. (Antje), Davey Smith, G. (George), Holm, J.-C. (Jens-Christian), Atalay, M. (Mustafa), Murray, C. (Clare), Bisgaard, H. (Hans), McCarthy, M. I. (Mark I.), Jaddoe, V. W. (Vincent W. V.), Grant, S. F. (Struan F. A.), Felix, J. F. (Janine F.), Vogelezang, S. (Suzanne), Bradfield, J. P. (Jonathan P.), Ahluwalia, T. S. (Tarunveer S.), Curtin, J. A. (John A.), Lakka, T. A. (Timo A.), Grarup, N. (Niels), Scholz, M. (Markus), van der Most, P. J. (Peter J.), Monnereau, C. (Claire), Stergiakouli, E. (Evie), Heiskala, A. (Anni), Horikoshi, M. (Momoko), Fedko, I. O. (Iryna O.), Vilor-Tejedor, N. (Natalia), Cousminer, D. L. (Diana L.), Standl, M. (Marie), Wang, C. A. (Carol A.), Viikari, J. (Jorma), Geller, F. (Frank), iniguez, C. (Carmen), Pitkanen, N. (Niina), Chesi, A. (Alessandra), Bacelis, J. (Jonas), Yengo, L. (Loic), Torrent, M. (Maties), Ntalla, I. (Ioanna), Helgeland, O. (Oyvind), Selzam, S. (Saskia), Vonk, J. M. (Judith M.), Zafarmand, M. H. (Mohammed H.), Heude, B. (Barbara), Farooqi, I. S. (Ismaa Sadaf), Alyass, A. (Akram), Beaumont, R. N. (Robin N.), Have, C. T. (Christian T.), Rzehak, P. (Peter), Bilbao, J. R. (Jose Ramon), Schnurr, T. M. (Theresia M.), Barroso, I. (Ines), Bonnelykke, K. (Klaus), Beilin, L. J. (Lawrence J.), Carstensen, L. (Lisbeth), Charles, M.-A. (Marie-Aline), Chawes, B. (Bo), Clement, K. (Karine), Closa-Monasterolo, R. (Ricardo), Custovic, A. (Adnan), Eriksson, J. G. (Johan G.), Escribano, J. (Joaquin), Groen-Blokhuis, M. (Maria), Grote, V. (Veit), Gruszfeld, D. (Dariusz), Hakonarson, H. (Hakon), Hansen, T. (Torben), Hattersley, A. T. (Andrew T.), Hollensted, M. (Mette), Hottenga, J.-J. (Jouke-Jan), Hypponen, E. (Elina), Johansson, S. (Stefan), Joro, R. (Raimo), Kahonen, M. (Mika), Karhunen, V. (Ville), Kiess, W. (Wieland), Knight, B. A. (Bridget A.), Koletzko, B. (Berthold), Kuehnapfel, A. (Andreas), Landgraf, K. (Kathrin), Langhendries, J.-P. (Jean-Paul), Lehtimaki, T. (Terho), Leinonen, J. T. (Jaakko T.), Li, A. (Aihuali), Lindi, V. (Virpi), Lowry, E. (Estelle), Bustamante, M. (Mariona), Medina-Gomez, C. (Carolina), Melbye, M. (Mads), Michaelsen, K. F. (Kim F.), Morgen, C. S. (Camilla S.), Mori, T. A. (Trevor A.), Nielsen, T. R. (Tenna R. H.), Niinikoski, H. (Harri), Oldehinkel, A. J. (Albertine J.), Pahkala, K. (Katja), Panoutsopoulou, K. (Kalliope), Pedersen, O. (Oluf), Pennell, C. E. (Craig E.), Power, C. (Christine), Reijneveld, S. A. (Sijmen A.), Rivadeneira, F. (Fernando), Simpson, A. (Angela), Sly, P. D. (Peter D.), Stokholm, J. (Jakob), Teo, K. K. (Kook K.), Thiering, E. (Elisabeth), Timpson, N. J. (Nicholas J.), Uitterlinden, A. G. (Andre G.), van Beijsterveldt, C. E. (Catharina E. M.), van Schaik, B. D. (Barbera D. C.), Vaudel, M. (Marc), Verduci, E. (Elvira), Vinding, R. K. (Rebecca K.), Vogel, M. (Mandy), Zeggini, E. (Eleftheria), Sebert, S. (Sylvain), Lind, M. V. (Mads V.), Brown, C. D. (Christopher D.), Santa-Marina, L. (Loreto), Reischl, E. (Eva), Frithioff-Bojsoe, C. (Christine), Meyre, D. (David), Wheeler, E. (Eleanor), Ong, K. (Ken), Nohr, E. A. (Ellen A.), Vrijkotte, T. G. (Tanja G. M.), Koppelman, G. H. (Gerard H.), Plomin, R. (Robert), Njolstad, P. R. (Pal R.), Dedoussis, G. D. (George D.), Froguel, P. (Philippe), Sorensen, T. I. (Thorkild I. A.), Jacobsson, B. (Bo), Freathy, R. M. (Rachel M.), Zemel, B. S. (Babette S.), Raitakari, O. (Olli), Vrijheid, M. (Martine), Feenstra, B. (Bjarke), Lyytikainen, L.-P. (Leo-Pekka), Snieder, H. (Harold), Kirsten, H. (Holger), Holt, P. G. (Patrick G.), Heinrich, J. (Joachim), Widen, E. (Elisabeth), Sunyer, J. (Jordi), Boomsma, D. I. (Dorret I.), Jarvelin, M.-R. (Marjo-Riitta), Koerner, A. (Antje), Davey Smith, G. (George), Holm, J.-C. (Jens-Christian), Atalay, M. (Mustafa), Murray, C. (Clare), Bisgaard, H. (Hans), McCarthy, M. I. (Mark I.), Jaddoe, V. W. (Vincent W. V.), Grant, S. F. (Struan F. A.), and Felix, J. F. (Janine F.)
Abstract: The genetic background of childhood body mass index (BMI), and the extent to which the well-known associations of childhood BMI with adult diseases are explained by shared genetic factors, are largely unknown. We performed a genome-wide association study meta-analysis of BMI in 61,111 children aged between 2 and 10 years. Twenty-five independent loci reached genome-wide significance in the combined discovery and replication analyses. Two of these, located near NEDD4L and SLC45A3, have not previously been reported in relation to either childhood or adult BMI. Positive genetic correlations of childhood BMI with birth weight and adult BMI, waist-to-hip ratio, diastolic blood pressure and type 2 diabetes were detected (Rg ranging from 0.11 to 0.76, P-values <0.002). A negative genetic correlation of childhood BMI with age at menarche was observed. Our results suggest that the biological processes underlying childhood BMI largely, but not completely, overlap with those underlying adult BMI. The well-known observational associations of BMI in childhood with cardio-metabolic diseases in adulthood may reflect partial genetic overlap, but in light of previous evidence, it is also likely that they are explained through phenotypic continuity of BMI from childhood into adulthood.
Published: 2020

21. Understanding the cumulative risk of maternal prenatal biopsychosocial factors on birth weight: a DynaHEALTH study on two birth cohorts

Author: Parmar, P, Lowry, E, Vehmeijer, Florianne, El Marroun, Hanan, Lewin, A, Tolvanen, M, Tzala, E, Ala-Mursula, L, Herzig, KH, Miettunen, J, Prokopenko, I, Rautio, N, Jaddoe, Vincent, Jarvelin, M R R, Felix, Janine, Sebert, S, Parmar, P, Lowry, E, Vehmeijer, Florianne, El Marroun, Hanan, Lewin, A, Tolvanen, M, Tzala, E, Ala-Mursula, L, Herzig, KH, Miettunen, J, Prokopenko, I, Rautio, N, Jaddoe, Vincent, Jarvelin, M R R, Felix, Janine, and Sebert, S
Published: 2020

22. DRUG BURDEN INDEX, PHYSICAL FUNCTION AND ADVERSE OUTCOMES IN OLDER HOSPITALISED PATIENTS: O17

Author: Lowry, E., Woodman, R. J., Soiza, R. L., and Mangoni, A. A.
Published: 2011

23. GWAS on longitudinal growth traits reveals different genetic factors influencing infant, child, and adult BMI

Author: Couto Alves, A, De Silva, NMG, Karhunen, V, Sovio, U, Das, S, Taal, HR, Warrington, NM, Lewin, AM, Kaakinen, M, Cousminer, DL, Thiering, E, Timpson, NJ, Bond, TA, Lowry, E, Brown, CD, Estivill, X, Lindi, V, Bradfield, JP, Geller, F, Speed, D, Coin, LJM, Loh, M, Barton, SJ, Beilin, LJ, Bisgaard, H, Bønnelykke, K, Alili, R, Hatoum, IJ, Schramm, K, Cartwright, R, Charles, M, Salerno, V, Clément, K, Claringbould, AAJ, BIOS Consortium, van Duijn, CM, Moltchanova, E, Eriksson, JG, Elks, C, Feenstra, B, Flexeder, C, Franks, S, Frayling, TM, Freathy, RM, Elliott, P, Widén, E, Hakonarson, H, Hattersley, AT, Rodriguez, A, Banterle, M, Heinrich, J, Heude, B, Holloway, JW, Hofman, A, Hyppönen, E, Inskip, H, Kaplan, LM, Hedman, AK, Läärä, E, Prokisch, H, Grallert, H, Lakka, TA, Lawlor, DA, Melbye, M, Ahluwalia, TS, Marinelli, M, Millwood, IY, Palmer, LJ, Pennell, CE, Perry, JR, Ring, SM, Savolainen, MJ, Rivadeneira, F, Standl, M, Sunyer, J, Tiesler, CMT, Uitterlinden, AG, Schierding, W, O’Sullivan, JM, Prokopenko, I, Herzig, K, Smith, GD, O'Reilly, P, Felix, JF, Buxton, JL, Blakemore, AIF, Ong, KK, Jaddoe, VWV, Grant, SFA, Sebert, S, McCarthy, MI, Järvelin, M., and Early Growth Genetics (EGG) Consortium
Abstract: Copyright © 2019 The Authors. Early childhood growth patterns are associated with adult health, yet the genetic factors and the developmental stages involved are not fully understood. Here, we combine genome-wide association studies with modeling of longitudinal growth traits to study the genetics of infant and child growth, followed by functional, pathway, genetic correlation, risk score, and colocalization analyses to determine how developmental timings, molecular pathways, and genetic determinants of these traits overlap with those of adult health. We found a robust overlap between the genetics of child and adult body mass index (BMI), with variants associated with adult BMI acting as early as 4 to 6 years old. However, we demonstrated a completely distinct genetic makeup for peak BMI during infancy, influenced by variation at the LEPR/LEPROT locus. These findings suggest that different genetic factors control infant and child BMI. In light of the obesity epidemic, these findings are important to inform the timing and targets of prevention strategies.
Published: 2019

24. Understanding the complexity of glycaemic health:systematic bio-psychosocial modelling of fasting glucose in middle-age adults; a DynaHEALTH study

Author: Lowry, E. (Estelle), Rautio, N. (Nina), Karhunen, V. (Ville), Miettunen, J. (Jouko), Ala-Mursula, L. (Leena), Auvinen, J. (Juha), Keinänen-Kiukaanniemi, S. (Sirkka), Puukka, K. (Katri), Prokopenko, I. (Inga), Herzig, K.-H. (Karl-Heinz), Lewin, A. (Alexandra), Sebert, S. (Sylvain), and Järvelin, M.-R. (Marjo-Riitta)
Abstract: Background: The prevention of the risk of type 2 diabetes (T2D) is complicated by multidimensional interplays between biological and psychosocial factors acting at the individual level. To address the challenge we took a systematic approach, to explore the bio-psychosocial predictors of blood glucose in mid-age. Methods: Based on the 31-year and 46-year follow-ups (5,078 participants, 43% male) of Northern Finland Birth Cohort 1966, we used a systematic strategy to select bio-psychosocial variables at 31 years to enable a data-driven approach. As selection criteria, the variable must be (i) a component of the metabolic syndrome or an indicator of psychosocial health using WHO guidelines, (ii) easily obtainable in general health check-ups and (iii) associated with fasting blood glucose at 46 years (P
Published: 2019

25. Cohort Profile: The DynaHEALTH consortium - A European consortium for a life-course bio-psychosocial model of healthy ageing of glucose homeostasis

Author: Sebert, S. (Sylvain), Lowry, E. (Estelle), Aumüller, N. (Nicole), Bermúdez, M.G. (Mercedes G.), Bjerregaard, L.G. (Lise G.), Rooij, S.R. (Susanne) de, De Silva, M. (Maneka), El Marroun, H. (Hanan), Hummel, N. (Nadine), Juola, T. (Teija), Mason, G. (Giacomo), Much, D. (D), Oliveros, E. (Elena), Poupakis, S. (Stavros), Rautio, N. (Nina), Schwarzfischer, P. (Phillipp), Tzala, E. (Evangelia), Uhl, O. (Olaf), Van De Beek, C. (Cornelieke), Vehmeijer, F.O.L. (Florianne O.L.), Verdejo-Román, J. (Juan), Wasenius, N. (Niko), Webster, C. (Claire), Ala-Mursula, L. (Leena), Herzig, K.H., Keinanen-Kiukaanniemi, S. (Sirkka), Miettunen, J. (Jouko), Baker, J.L. (Jennifer L.), Campoy, C. (Cristina), Conti, G. (Gabriella), Hagen, K. (Knut), Hummel, S. (Sandra), Jaddoe, V.W.V. (Vincent), Koletzko, B. (Berthold), Lewin, A. (Alex), Rodriguez-Palermo, M. (Maria), Roseboom, T.J. (Tessa), Rueda, R. (Ricardo), Evans, J. (Jonathan Mark), Felix, J.F. (Janine), Prokopenko, I. (Inga), Sørensen, T.I.A. (Thorkild I. A.), Järvelin, M.-R. (Marjo-Riitta), Sebert, S. (Sylvain), Lowry, E. (Estelle), Aumüller, N. (Nicole), Bermúdez, M.G. (Mercedes G.), Bjerregaard, L.G. (Lise G.), Rooij, S.R. (Susanne) de, De Silva, M. (Maneka), El Marroun, H. (Hanan), Hummel, N. (Nadine), Juola, T. (Teija), Mason, G. (Giacomo), Much, D. (D), Oliveros, E. (Elena), Poupakis, S. (Stavros), Rautio, N. (Nina), Schwarzfischer, P. (Phillipp), Tzala, E. (Evangelia), Uhl, O. (Olaf), Van De Beek, C. (Cornelieke), Vehmeijer, F.O.L. (Florianne O.L.), Verdejo-Román, J. (Juan), Wasenius, N. (Niko), Webster, C. (Claire), Ala-Mursula, L. (Leena), Herzig, K.H., Keinanen-Kiukaanniemi, S. (Sirkka), Miettunen, J. (Jouko), Baker, J.L. (Jennifer L.), Campoy, C. (Cristina), Conti, G. (Gabriella), Hagen, K. (Knut), Hummel, S. (Sandra), Jaddoe, V.W.V. (Vincent), Koletzko, B. (Berthold), Lewin, A. (Alex), Rodriguez-Palermo, M. (Maria), Roseboom, T.J. (Tessa), Rueda, R. (Ricardo), Evans, J. (Jonathan Mark), Felix, J.F. (Janine), Prokopenko, I. (Inga), Sørensen, T.I.A. (Thorkild I. A.), and Järvelin, M.-R. (Marjo-Riitta)
Published: 2019
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26. GWAS on longitudinal growth traits reveals different genetic factors influencing infant, child, and adult BMI

Author: Alves, AC, De Silva, NMG, Karhunen, V, Sovio, U, Das, S, Taal, HR, Warrington, NM, Lewin, AM, Kaakinen, M, Cousminer, DL, Thiering, E, Timpson, NJ, Bond, TA, Lowry, E, Brown, CD, Estivill, X, Lindi, V, Bradfield, JP, Geller, F, Speed, D, Coin, LJM, Loh, M, Barton, SJ, Beilin, LJ, Bisgaard, H, Bonnelykke, K, Alili, R, Hatoum, IJ, Schramm, K, Cartwright, R, Charles, M-A, Salerno, V, Clement, K, Claringbould, AAJ, van Duijn, CM, Moltchanova, E, Eriksson, JG, Elks, C, Feenstra, B, Flexeder, C, Franks, S, Frayling, TM, Freathy, RM, Elliott, P, Widen, E, Hakonarson, H, Hattersley, AT, Rodriguez, A, Banterle, M, Heinrich, J, Heude, B, Holloway, JW, Hofman, A, Hypponen, E, Inskip, H, Kaplan, LM, Hedman, AK, Laara, E, Prokisch, H, Grallert, H, Lakka, TA, Lawlor, DA, Melbye, M, Ahluwalia, TS, Marinelli, M, Millwood, IY, Palmer, LJ, Pennell, CE, Perry, JR, Ring, SM, Savolainen, MJ, Rivadeneira, F, Standl, M, Sunyer, J, Tiesler, CMT, Uitterlinden, AG, Schierding, W, O'Sullivan, JM, Prokopenko, I, Herzig, K-H, Smith, GD, O'Reilly, P, Felix, JF, Buxton, JL, Blakemore, AIF, Ong, KK, Jaddoe, VWV, Grant, SFA, Sebert, S, McCarthy, MI, Jarvelin, M-R, Alves, AC, De Silva, NMG, Karhunen, V, Sovio, U, Das, S, Taal, HR, Warrington, NM, Lewin, AM, Kaakinen, M, Cousminer, DL, Thiering, E, Timpson, NJ, Bond, TA, Lowry, E, Brown, CD, Estivill, X, Lindi, V, Bradfield, JP, Geller, F, Speed, D, Coin, LJM, Loh, M, Barton, SJ, Beilin, LJ, Bisgaard, H, Bonnelykke, K, Alili, R, Hatoum, IJ, Schramm, K, Cartwright, R, Charles, M-A, Salerno, V, Clement, K, Claringbould, AAJ, van Duijn, CM, Moltchanova, E, Eriksson, JG, Elks, C, Feenstra, B, Flexeder, C, Franks, S, Frayling, TM, Freathy, RM, Elliott, P, Widen, E, Hakonarson, H, Hattersley, AT, Rodriguez, A, Banterle, M, Heinrich, J, Heude, B, Holloway, JW, Hofman, A, Hypponen, E, Inskip, H, Kaplan, LM, Hedman, AK, Laara, E, Prokisch, H, Grallert, H, Lakka, TA, Lawlor, DA, Melbye, M, Ahluwalia, TS, Marinelli, M, Millwood, IY, Palmer, LJ, Pennell, CE, Perry, JR, Ring, SM, Savolainen, MJ, Rivadeneira, F, Standl, M, Sunyer, J, Tiesler, CMT, Uitterlinden, AG, Schierding, W, O'Sullivan, JM, Prokopenko, I, Herzig, K-H, Smith, GD, O'Reilly, P, Felix, JF, Buxton, JL, Blakemore, AIF, Ong, KK, Jaddoe, VWV, Grant, SFA, Sebert, S, McCarthy, MI, and Jarvelin, M-R
Abstract: Early childhood growth patterns are associated with adult health, yet the genetic factors and the developmental stages involved are not fully understood. Here, we combine genome-wide association studies with modeling of longitudinal growth traits to study the genetics of infant and child growth, followed by functional, pathway, genetic correlation, risk score, and colocalization analyses to determine how developmental timings, molecular pathways, and genetic determinants of these traits overlap with those of adult health. We found a robust overlap between the genetics of child and adult body mass index (BMI), with variants associated with adult BMI acting as early as 4 to 6 years old. However, we demonstrated a completely distinct genetic makeup for peak BMI during infancy, influenced by variation at the LEPR/LEPROT locus. These findings suggest that different genetic factors control infant and child BMI. In light of the obesity epidemic, these findings are important to inform the timing and targets of prevention strategies.
Published: 2019

27. Maternal hemoglobin associates with preterm delivery and small for gestational age in two Finnish birth cohorts

Author: Ronkainen, J. (Justiina), Lowry, E. (Estelle), Heiskala, A. (Anni), Uusitalo, I. (Iida), Koivunen, P. (Peppi), Kajantie, E. (Eero), Vääräsmäki, M. (Marja), Järvelin, M.-R. (Marjo-Riitta), Sebert, S. (Sylvain), Ronkainen, J. (Justiina), Lowry, E. (Estelle), Heiskala, A. (Anni), Uusitalo, I. (Iida), Koivunen, P. (Peppi), Kajantie, E. (Eero), Vääräsmäki, M. (Marja), Järvelin, M.-R. (Marjo-Riitta), and Sebert, S. (Sylvain)
Abstract: Objective: To test whether maternal hemoglobin during pregnancy associates with offspring perinatal outcomes in a developed country. Changes in maternal hemoglobin concentration during pregnancy are partly physiological phenomena reflecting alterations of maternal blood volume. Especially hemoglobin measures outside the physiological range may influence maternal health and fetal growth with long-lasting consequences. Study design: We studied an unselected sample drawn from two regional birth cohorts born 20 years apart: The Northern Finland Birth Cohorts 1966 and 1986. These are two mother-and-child population-based birth cohorts together comprising 21,710 mothers and their children. After exclusions, the sample size of the current study was 20,554. Concentrations of maternal hemoglobin at first and last antenatal visits were categorized as low (lowest 10%), medium (reference) or high (highest 10%). Multinomial logistic regression analyses for categories of maternal hemoglobin and perinatal outcomes such as preterm delivery and full-term small and large for gestational age were conducted with adjustments for maternal cofactors. Results: Low maternal hemoglobin at early pregnancy associated with decreased risk of full-term small for gestational age (adjusted OR 0.73, 95% CI [0.58, 0.93], p = 0.010). At late pregnancy, low maternal hemoglobin associated with increased risk of preterm delivery (adjusted OR 1.60, 95% CI [1.26, 2.02], p < 0.0005) whereas high maternal hemoglobin associated with increased risk of full-term small for gestational age (adjusted OR 1.29, 95% CI [1.07, 1.56], p = 0.009). Maternal hemoglobin did not show constant association with risk of large for gestational age. Conclusion: The results from this study support evidence that both low and high maternal hemoglobin associate with adverse perinatal outcomes. Low maternal hemoglobin associated with preterm delivery and high with full-term small for gestational age. Association was mainly
Published: 2019

28. GWAS on longitudinal growth traits reveals different genetic factors influencing infant, child, and adult BMI

Author: Alves, A. C. (Alexessander Couto), De Silva, N. M. (N. Maneka G.), Karhunen, V. (Ville), Sovio, U. (Ulla), Das, S. (Shikta), Taal, H. R. (H. Rob), Warrington, N. M. (Nicole M.), Lewin, A. M. (Alexandra M.), Kaakinen, M. (Marika), Cousminer, D. L. (Diana L.), Thiering, E. (Elisabeth), Timpson, N. J. (Nicholas J.), Bond, T. A. (Tom A.), Lowry, E. (Estelle), Brown, C. D. (Christopher D.), Estivill, X. (Xavier), Lindi, V. (Virpi), Bradfield, J. P. (Jonathan P.), Geller, F. (Frank), Speed, D. (Doug), Coin, L. J. (Lachlan J. M.), Loh, M. (Marie), Barton, S. J. (Sheila J.), Beilin, L. J. (Lawrence J.), Bisgaard, H. (Hans), Bonnelykke, K. (Klaus), Alili, R. (Rohia), Hatoum, I. J. (Ida J.), Schramm, K. (Katharina), Cartwright, R. (Rufus), Charles, M.-A. (Marie-Aline), Salerno, V. (Vincenzo), Clement, K. (Karine), Claringbould, A. A. (Annique A. J.), van Duijn, C. M. (Cornelia M.), Moltchanova, E. (Elena), Eriksson, J. G. (Johan G.), Elks, C. (Cathy), Feenstra, B. (Bjarke), Flexeder, C. (Claudia), Franks, S. (Stephen), Frayling, T. M. (Timothy M.), Freathy, R. M. (Rachel M.), Elliott, P. (Paul), Widen, E. (Elisabeth), Hakonarson, H. (Hakon), Hattersley, A. T. (Andrew T.), Rodriguez, A. (Alina), Banterle, M. (Marco), Heinrich, J. (Joachim), Heude, B. (Barbara), Holloway, J. W. (John W.), Hofman, A. (Albert), Hypponen, E. (Elina), Inskip, H. (Hazel), Kaplan, L. M. (Lee M.), Hedman, A. K. (Asa K.), Läärä, E. (Esa), Prokisch, H. (Holger), Grallert, H. (Harald), Lakka, T. A. (Timo A.), Lawlor, D. A. (Debbie A.), Melbye, M. (Mads), Ahluwalia, T. S. (Tarunveer S.), Marinelli, M. (Marcella), Millwood, I. Y. (Iona Y.), Palmer, L. J. (Lyle J.), Pennell, C. E. (Craig E.), Perry, J. R. (John R.), Ring, S. M. (Susan M.), Savolainen, M. J. (Markku J.), Rivadeneira, F. (Fernando), Standl, M. (Marie), Sunyer, J. (Jordi), Tiesler, C. M. (Carla M. T.), Uitterlinden, A. G. (Andre G.), Schierding, W. (William), O'Sullivan, J. M. (Justin M.), Prokopenko, I. (Inga), Herzig, K.-H. (Karl-Heinz), Smith, G. D. (George Davey), O'Reilly, P. (Paul), Felix, J. F. (Janine F.), Buxton, J. L. (Jessica L.), Blakemore, A. I. (Alexandra I. F.), Ong, K. K. (Ken K.), Jaddoe, V. W. (Vincent W. V.), Grant, S. F. (Struan F. A.), Sebert, S. (Sylvain), McCarthy, M. I. (Mark I.), Jarvelin, M.-R. (Marjo-Riitta), Alves, A. C. (Alexessander Couto), De Silva, N. M. (N. Maneka G.), Karhunen, V. (Ville), Sovio, U. (Ulla), Das, S. (Shikta), Taal, H. R. (H. Rob), Warrington, N. M. (Nicole M.), Lewin, A. M. (Alexandra M.), Kaakinen, M. (Marika), Cousminer, D. L. (Diana L.), Thiering, E. (Elisabeth), Timpson, N. J. (Nicholas J.), Bond, T. A. (Tom A.), Lowry, E. (Estelle), Brown, C. D. (Christopher D.), Estivill, X. (Xavier), Lindi, V. (Virpi), Bradfield, J. P. (Jonathan P.), Geller, F. (Frank), Speed, D. (Doug), Coin, L. J. (Lachlan J. M.), Loh, M. (Marie), Barton, S. J. (Sheila J.), Beilin, L. J. (Lawrence J.), Bisgaard, H. (Hans), Bonnelykke, K. (Klaus), Alili, R. (Rohia), Hatoum, I. J. (Ida J.), Schramm, K. (Katharina), Cartwright, R. (Rufus), Charles, M.-A. (Marie-Aline), Salerno, V. (Vincenzo), Clement, K. (Karine), Claringbould, A. A. (Annique A. J.), van Duijn, C. M. (Cornelia M.), Moltchanova, E. (Elena), Eriksson, J. G. (Johan G.), Elks, C. (Cathy), Feenstra, B. (Bjarke), Flexeder, C. (Claudia), Franks, S. (Stephen), Frayling, T. M. (Timothy M.), Freathy, R. M. (Rachel M.), Elliott, P. (Paul), Widen, E. (Elisabeth), Hakonarson, H. (Hakon), Hattersley, A. T. (Andrew T.), Rodriguez, A. (Alina), Banterle, M. (Marco), Heinrich, J. (Joachim), Heude, B. (Barbara), Holloway, J. W. (John W.), Hofman, A. (Albert), Hypponen, E. (Elina), Inskip, H. (Hazel), Kaplan, L. M. (Lee M.), Hedman, A. K. (Asa K.), Läärä, E. (Esa), Prokisch, H. (Holger), Grallert, H. (Harald), Lakka, T. A. (Timo A.), Lawlor, D. A. (Debbie A.), Melbye, M. (Mads), Ahluwalia, T. S. (Tarunveer S.), Marinelli, M. (Marcella), Millwood, I. Y. (Iona Y.), Palmer, L. J. (Lyle J.), Pennell, C. E. (Craig E.), Perry, J. R. (John R.), Ring, S. M. (Susan M.), Savolainen, M. J. (Markku J.), Rivadeneira, F. (Fernando), Standl, M. (Marie), Sunyer, J. (Jordi), Tiesler, C. M. (Carla M. T.), Uitterlinden, A. G. (Andre G.), Schierding, W. (William), O'Sullivan, J. M. (Justin M.), Prokopenko, I. (Inga), Herzig, K.-H. (Karl-Heinz), Smith, G. D. (George Davey), O'Reilly, P. (Paul), Felix, J. F. (Janine F.), Buxton, J. L. (Jessica L.), Blakemore, A. I. (Alexandra I. F.), Ong, K. K. (Ken K.), Jaddoe, V. W. (Vincent W. V.), Grant, S. F. (Struan F. A.), Sebert, S. (Sylvain), McCarthy, M. I. (Mark I.), and Jarvelin, M.-R. (Marjo-Riitta)
Abstract: Early childhood growth patterns are associated with adult health, yet the genetic factors and the developmental stages involved are not fully understood. Here, we combine genome-wide association studies with modeling of longitudinal growth traits to study the genetics of infant and child growth, followed by functional, pathway, genetic correlation, risk score, and colocalization analyses to determine how developmental timings, molecular pathways, and genetic determinants of these traits overlap with those of adult health. We found a robust overlap between the genetics of child and adult body mass index (BMI), with variants associated with adult BMI acting as early as 4 to 6 years old. However, we demonstrated a completely distinct genetic makeup for peak BMI during infancy, influenced by variation at the LEPR/LEPROT locus. These findings suggest that different genetic factors control infant and child BMI. In light of the obesity epidemic, these findings are important to inform the timing and targets of prevention strategies.
Published: 2019

29. Cohort profile:the DynaHEALTH consortium – a European consortium for a life-course bio-psychosocial model of healthy ageing of glucose homeostasis

Author: Sebert, S. (Sylvain), Lowry, E. (Estelle), Aumüller, N. (Nicole), Bermúdez, M. G. (Mercedes G), Bjerregaard, L. G. (Lise G), de Rooij, S. R. (Susanne R), De Silva, M. (Maneka), El Marroun, H. (Hanan), Hummel, N. (Nadine), Juola, T. (Teija), Mason, G. (Giacomo), Much, D. (Daniela), Oliveros, E. (Elena), Poupakis, S. (Stavros), Rautio, N. (Nina), Schwarzfischer, P. (Phillipp), Tzala, E. (Evangelia), Uhl, O. (Olaf), van de Beek, C. (Cornelieke), Vehmeijer, F. (Florianne), Verdejo-Román, J. (Juan), Wasenius, N. (Niko), Webster, C. (Claire), Ala-Mursula, L. (Leena), Herzig, K.-H. (Karl-Heinz), Keinänen-Kiukaanniemi, S. (Sirkka), Miettunen, J. (Jouko), Baker, J. L. (Jennifer L), Campoy, C. (Cristina), Conti, G. (Gabriella), Eriksson, J. G. (Johan G), Hummel, S. (Sandra), Jaddoe, V. (Vincent), Koletzko, B. (Berthold), Lewin, A. (Alex), Rodriguez-Palermo, M. (Maria), Roseboom, T. (Tessa), Rueda, R. (Ricardo), Evans, J. (Jayne), Felix, J. F. (Janine F), Prokopenko, I. (Inga), Sørensen, T. I. (Thorkild IA), Järvelin, M.-R. (Marjo-Riitta), Sebert, S. (Sylvain), Lowry, E. (Estelle), Aumüller, N. (Nicole), Bermúdez, M. G. (Mercedes G), Bjerregaard, L. G. (Lise G), de Rooij, S. R. (Susanne R), De Silva, M. (Maneka), El Marroun, H. (Hanan), Hummel, N. (Nadine), Juola, T. (Teija), Mason, G. (Giacomo), Much, D. (Daniela), Oliveros, E. (Elena), Poupakis, S. (Stavros), Rautio, N. (Nina), Schwarzfischer, P. (Phillipp), Tzala, E. (Evangelia), Uhl, O. (Olaf), van de Beek, C. (Cornelieke), Vehmeijer, F. (Florianne), Verdejo-Román, J. (Juan), Wasenius, N. (Niko), Webster, C. (Claire), Ala-Mursula, L. (Leena), Herzig, K.-H. (Karl-Heinz), Keinänen-Kiukaanniemi, S. (Sirkka), Miettunen, J. (Jouko), Baker, J. L. (Jennifer L), Campoy, C. (Cristina), Conti, G. (Gabriella), Eriksson, J. G. (Johan G), Hummel, S. (Sandra), Jaddoe, V. (Vincent), Koletzko, B. (Berthold), Lewin, A. (Alex), Rodriguez-Palermo, M. (Maria), Roseboom, T. (Tessa), Rueda, R. (Ricardo), Evans, J. (Jayne), Felix, J. F. (Janine F), Prokopenko, I. (Inga), Sørensen, T. I. (Thorkild IA), and Järvelin, M.-R. (Marjo-Riitta)
Published: 2019

30. Association of maternal prenatal smoking GFI1-locus and cardio-metabolic phenotypes in 18,212 adults

Author: Parmar, P, Lowry, E, Cugliari, G, Kähönen, M, Hurme, M, Lehtimäki, T, Lääketieteen ja biotieteiden tiedekunta - Faculty of Medicine and Life Sciences, and Tampere University
Subjects: Biolääketieteet - Biomedicine, Syöpätaudit - Cancers, Naisten- ja lastentaudit - Gynaecology and paediatrics
Published: 2018

31. Association of maternal prenatal smoking GFI1-locus and cardio-metabolic phenotypes in 18,212 adults

Author: Parmar, P. (Priyanka), Lowry, E. (Estelle), Cugliari, G. (Giovanni), Suderman, M.J. (Matthew J.), Wilson, R. (Rory), Karhunen, V. (Ville), Andrew, T. (Toby), Wiklund, P. (Petri), Wielscher, M. (Matthias), Guarrera, S. (Simonetta), Teumer, A. (Alexander), Lehne, B. (Benjamin), Milani, L. (Lili), de Klein, N. (Niek), Mishra, P.P. (Pashupati P.), Melton, P.E. (Phillip E.), Mandaviya, P.R. (Pooja), Kasela, S. (Silva), Nano, J. (Jana), Zhang, W. (Weihua), Zhang, Y. (Yan), Uitterlinden, A.G. (André), Peters, A. (Annette), Schöttker, B. (Ben), Gieger, C. (Christian), Anderson, D. (Denise), Boomsma, D.I. (Dorret I.), Grabe, H.J. (Hans Jörgen), Panico, S. (Salvatore), Veldink, J.H. (Jan), Meurs, J.B.J. (Joyce) van, Berg, L.H. (Leonard) van den, Beilin, L.J. (Lawrence), Franke, L. (Lude), Loh, M. (Marie), Greevenbroek, M.M. van, Nauck, M. (Matthias), Kähönen, M. (Mika), Hurme, M. (Mikko), Raitakari, O. (Olli), Franco, O.H. (Oscar), Slagboom, P.E. (Eline), van der Harst, P. (Pim), Kunze, S. (Sonja), Felix, S.B. (Stephan), Zhang, T. (Tao), Chen, W. (Wei), Mori, T.A. (Trevor A.), Bonnefond, A. (Amélie), Heijmans, B.T. (Bastiaan T.), Muka, T. (Taulant), Kooner, J.S. (Jaspal S.), Fischer, K. (Krista), Waldenberger, M. (Melanie), Froguel, P. (Philippe), Huang, R.-C. (Rae-Chi), Lehtimäki, T. (Terho), Rathmann, W. (Wolfgang), Relton, C.L. (Caroline), Matullo, G., Brenner, H. (Hermann), Verweij, N. (Niek), Li, S. (Shengxu), Chambers, J.C. (John C.), Järvelin, M.-R. (Marjo-Riitta), Sebert, S. (Sylvain), Parmar, P. (Priyanka), Lowry, E. (Estelle), Cugliari, G. (Giovanni), Suderman, M.J. (Matthew J.), Wilson, R. (Rory), Karhunen, V. (Ville), Andrew, T. (Toby), Wiklund, P. (Petri), Wielscher, M. (Matthias), Guarrera, S. (Simonetta), Teumer, A. (Alexander), Lehne, B. (Benjamin), Milani, L. (Lili), de Klein, N. (Niek), Mishra, P.P. (Pashupati P.), Melton, P.E. (Phillip E.), Mandaviya, P.R. (Pooja), Kasela, S. (Silva), Nano, J. (Jana), Zhang, W. (Weihua), Zhang, Y. (Yan), Uitterlinden, A.G. (André), Peters, A. (Annette), Schöttker, B. (Ben), Gieger, C. (Christian), Anderson, D. (Denise), Boomsma, D.I. (Dorret I.), Grabe, H.J. (Hans Jörgen), Panico, S. (Salvatore), Veldink, J.H. (Jan), Meurs, J.B.J. (Joyce) van, Berg, L.H. (Leonard) van den, Beilin, L.J. (Lawrence), Franke, L. (Lude), Loh, M. (Marie), Greevenbroek, M.M. van, Nauck, M. (Matthias), Kähönen, M. (Mika), Hurme, M. (Mikko), Raitakari, O. (Olli), Franco, O.H. (Oscar), Slagboom, P.E. (Eline), van der Harst, P. (Pim), Kunze, S. (Sonja), Felix, S.B. (Stephan), Zhang, T. (Tao), Chen, W. (Wei), Mori, T.A. (Trevor A.), Bonnefond, A. (Amélie), Heijmans, B.T. (Bastiaan T.), Muka, T. (Taulant), Kooner, J.S. (Jaspal S.), Fischer, K. (Krista), Waldenberger, M. (Melanie), Froguel, P. (Philippe), Huang, R.-C. (Rae-Chi), Lehtimäki, T. (Terho), Rathmann, W. (Wolfgang), Relton, C.L. (Caroline), Matullo, G., Brenner, H. (Hermann), Verweij, N. (Niek), Li, S. (Shengxu), Chambers, J.C. (John C.), Järvelin, M.-R. (Marjo-Riitta), and Sebert, S. (Sylvain)
Abstract: Background: DNA methylation at the GFI1-locus has been repeatedly associated with exposure to smoking from the foetal period onwards. We explored whether DNA methylation may be a mechanism that links exposure to maternal prenatal smoking with offspring's adult cardio-metabolic health. Methods: We meta-analysed the association between DNA methylation at GFI1-locus with maternal prenatal smoking, adult own smoking, and cardio-metabolic phenotypes in 22 population-based studies from Europe, Australia, and USA (n = 18,212). DNA methylation at the GFI1-locus was measured in whole-blood. Multivariable regression models were fitted to examine its association with exposure to prenatal and own adult smoking. DNA methylation levels were analysed in relation to body mass index (BMI), waist circumference (WC), fasting glucose (FG), high-density lipoprotein cholesterol (HDL—C), triglycerides (TG), diastolic, and systolic blood pressure (BP). Findings: Lower DNA methylation at three out of eight GFI1-CpGs was associated with exposure to maternal prenatal smoking, whereas, all eight CpGs were associated with adult own smoking. Lower DNA methylation at cg14179389, the strongest maternal prenatal smoking locus, was associated with increased WC and BP when adjusted for sex, age, and adult smoking with Bonferroni-corrected P < 0·012. In contrast, lower DNA methylation at cg09935388, the strongest adult own smoking locus, was associated with decreased BMI, WC, and BP (adjusted 1 × 10−7 < P < 0.01). Similarly, lower DNA methylation at cg12876356, cg18316974, cg09662411, and cg18146737 was associated with decreased BMI and WC (5 × 10−8 < P < 0.001). Lower DNA methylation at all the CpGs was consistently associated with higher TG levels. Interpretation: Epigenetic changes at the GFI1 were linked to smoking exposure in-utero/in-adulthood and robustly associated with cardio-metabolic risk factors. Fund: European Union's Horizon 2020 research and innovation programme under grant agreement no
Published: 2018
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32. Early motor developmental milestones and schizotypy in the Northern Finland Birth Cohort Study 1966

Author: Filatova, S. (Svetlana), Koivumaa-Honkanen, H. (Heli), Khandaker, G. M. (Golam M.), Lowry, E. (Estelle), Nordström, T. (Tanja), Hurtig, T. (Tuula), Moilanen, K. (Kristiina), Miettunen, J. (Jouko), Filatova, S. (Svetlana), Koivumaa-Honkanen, H. (Heli), Khandaker, G. M. (Golam M.), Lowry, E. (Estelle), Nordström, T. (Tanja), Hurtig, T. (Tuula), Moilanen, K. (Kristiina), and Miettunen, J. (Jouko)
Abstract: Delayed motor developmental milestones have been reported to be associated with schizophrenia in previous studies, but no study has examined the relationship between early motor developmental milestones and schizotypy. We have examined this relationship in a prospective birth cohort. In the Northern Finland Birth Cohort 1966, data on 9 early motor developmental milestones were collected prospectively from visits to child welfare centers, and data on adult schizotypy were collected through a questionnaire (N = 4557–4674). Positive schizotypy was measured by the Perceptual Aberration Scale (PAS), negative schizotypy was measured by Physical Anhedonia Scale (PhAS) and Social Anhedonia Scale (SAS). Three related scales were included: Schizoidia Scale (SCHD), Hypomanic Personality Scale (HPS), and Bipolar II Scale (BIP2). We examined the milestone–schizotypy associations before and after excluding cases of schizophrenia from this population-based sample. Hierarchical regression analyses adjusted for covariates and separately for both genders were performed. In men, each extra month of delay in achievement of touching thumb with index finger, sitting unsupported, standing up, walking with support, or walking unsupported was associated with an increase in PAS, PhAS, or SCHD scores, or decrease in BIP2 score (P < 0.05). In women, each extra month of delay in achievement of turning from back to tummy was associated with an increase in PhAS and SAS scores (P < 0.05). Schizotypy is associated with delayed motor developmental milestones in early-life, but there is some heterogeneity with regards to types of milestones and gender. These findings suggest delayed motor development confers risk across the continuum of schizophrenia syndrome.
Published: 2018

33. Association of maternal prenatal smoking GFI1-locus and cardiometabolic phenotypes in 18,212 adults

Author: Parmar, P, Lowry, E, Cugliari, G, Suderman, M, Wilson, R, Karhunen, V, Andrew, T, Wiklund, P, Wielscher, M, Guarrera, S, Teumer, A, Lehne, B, Milani, L, de Klein, N, Mishra, PP, Melton, PE, Mandaviya, Pooja, Kasela, S, Nano, Jana, Zhang, WH, Zhang, Y, Uitterlinden, André, Peters, A, Schottker, B, Gieger, C, Anderson, D, Boomsma, DI, Grabe, HJ, Panico, S, Veldink, JH, van Meurs, Joyce, Berg, L, Beilin, LJ, Franke, L, Loh, M, van Greevenbroek, MMJ, Nauck, M, Kahonen, M, Hurme, MA, Raitakari, OT, Franco Duran, OH, Slagboom, PE (Eline), van der Harst, P, Kunze, S, Felix, SB, Zhang, T, Chen, W, Mori, TA, Bonnefond, A, Heijmans, BT, Muka, Taulant, Kooner, JS, Fischer, K, Waldenberger, M, Froguel, P, Huang, RC, Lehtimaki, T, Rathmann, W, Relton, CL, Matullo, G, Brenner, H, Verweij, N, Li, SX, Chambers, JC, Jarvelin, MR, Sebert, S, Parmar, P, Lowry, E, Cugliari, G, Suderman, M, Wilson, R, Karhunen, V, Andrew, T, Wiklund, P, Wielscher, M, Guarrera, S, Teumer, A, Lehne, B, Milani, L, de Klein, N, Mishra, PP, Melton, PE, Mandaviya, Pooja, Kasela, S, Nano, Jana, Zhang, WH, Zhang, Y, Uitterlinden, André, Peters, A, Schottker, B, Gieger, C, Anderson, D, Boomsma, DI, Grabe, HJ, Panico, S, Veldink, JH, van Meurs, Joyce, Berg, L, Beilin, LJ, Franke, L, Loh, M, van Greevenbroek, MMJ, Nauck, M, Kahonen, M, Hurme, MA, Raitakari, OT, Franco Duran, OH, Slagboom, PE (Eline), van der Harst, P, Kunze, S, Felix, SB, Zhang, T, Chen, W, Mori, TA, Bonnefond, A, Heijmans, BT, Muka, Taulant, Kooner, JS, Fischer, K, Waldenberger, M, Froguel, P, Huang, RC, Lehtimaki, T, Rathmann, W, Relton, CL, Matullo, G, Brenner, H, Verweij, N, Li, SX, Chambers, JC, Jarvelin, MR, and Sebert, S
Published: 2018

34. 106 Early stage mycosis fungoides has a mutanome distinct from Sezary Syndrome

Author: de Masson, A., primary, Lowry, E., additional, Elco, C., additional, Tangrea, M., additional, Thorner, A., additional, Nag, A., additional, Clark, R., additional, and Kupper, T., additional
Published: 2018
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35. 110 Tumor clone frequency is a robust predictor of progression and survival in patients with Stage IB mycosis fungoides

Author: de Masson, A., primary, O'Malley, J., additional, Elco, C., additional, Garcia, S., additional, Divito, S., additional, Lowry, E., additional, Teague, J., additional, LeBoeuf, N.R., additional, Robins, H., additional, Clark, R., additional, and Kupper, T., additional
Published: 2018
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36. 481 Benign T cells drive visible inflammation in cutaneous T cell lymphoma

Author: Vieyra-Garcia, P., primary, O'Malley, J., additional, Crouch, J., additional, Seger, E., additional, Teague, J., additional, Lowry, E., additional, Gehad, A., additional, Kupper, T., additional, Wolf, P., additional, and Clark, R., additional
Published: 2018
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37. 458 CD8+ T cell skin infiltration predicts disease progression in CTCL patients

Author: Seger, E., primary, O'Malley, J., additional, de Masson, A., additional, Teague, J., additional, Lowry, E., additional, Gehad, A., additional, Vromans, A., additional, Kupper, T., additional, and Clark, R., additional
Published: 2018
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38. Potential determinants of vitamin D in Finnish adults:a cross-sectional study from the Northern Finland birth cohort 1966

Author: Palaniswamy, S. (Saranya), Hyppönen, E. (Elina), Williams, D. M. (Dylan M), Jokelainen, J. (Jari), Lowry, E. (Estelle), Keinänen-Kiukaanniemi, S. (Sirkka), Herzig, K.-H. (Karl-Heinz), Järvelin, M.-R. (Marjo-Riitta), Sebert, S. (Sylvain), Palaniswamy, S. (Saranya), Hyppönen, E. (Elina), Williams, D. M. (Dylan M), Jokelainen, J. (Jari), Lowry, E. (Estelle), Keinänen-Kiukaanniemi, S. (Sirkka), Herzig, K.-H. (Karl-Heinz), Järvelin, M.-R. (Marjo-Riitta), and Sebert, S. (Sylvain)
Abstract: Objective: Evidence from randomised controlled trials suggests that vitamin D may reduce multimorbidity, but very few studies have investigated specific determinants of vitamin D2 and D3 (two isoforms of 25-hydroxyvitamin D). The aim of the study was to investigate the determinants of vitamin D2 and D3 and to identify the risk factors associated with hypovitaminosis D. Design: Cross-sectional study. Setting: Northern Finland Birth Cohort 1966. Participants: 2374 male and 2384 female participants with data on serum 25(OH)D₂ and 25(OH)D₃ concentrations measured at 31 years of age (1997), together with comprehensive measures of daylight, anthropometric, social, lifestyle and contraceptive cofactors. Methods: We assessed a wide range of potential determinants prior to a nationwide fortification programme introduced in Finland. The determinants of 25(OH)D₂, 25(OH)D₃ and 25(OH)D concentrations were analysed by linear regression and risk factors for being in lower tertile of 25(OH)D concentration by ordinal logistic regression. Results: At the time of sampling, 72% of the participants were vitamin D sufficient (≥50 nmol/L). Low sunlight exposure period (vs high) was associated positively with 25(OH)D₂ and negatively with 25(OH)D₃ concentrations. Use of oral contraceptives (vs nonusers) was associated with an increase of 0.17 nmol/L (95% CI 0.08 to 0.27) and 0.48 nmol/L (95% CI 0.41 to 0.56) in 25(OH)D₂ and 25(OH)D₃ concentrations. Sex, season, latitude, alcohol consumption and physical activity were the factors most strongly associated with 25(OH)D concentration. Risk factors for low vitamin D status were low sunlight exposure defined by time of sampling, residing in northern latitudes, obesity, higher waist circumference, low physical activity and unhealthy diet. Conclusions: We demonstrate some differential associations of environmental and lifestyle factors with 25(OH)D₂ and 25(OH)D₃ raising important questions related to personalised healthcare. Future strateg
Published: 2017

39. Can The Doctors Work The Insurance Act?

Author: Lowry, E. W.
Published: 1912

40. Cast Iron in Its Relation to the Automotive Industry

Author: Lowry, E. J.
Published: 1927

41. 314 Preferential expression of PD-1 on malignant T cells of CTCL may underlie disease worsening in patients undergoing anti-PD1 therapy

Author: O'Malley, J.T., primary, Gehad, A., additional, Lowry, E., additional, Teague, J., additional, LeBoeuf, N., additional, Kupper, T., additional, and Clark, R., additional
Published: 2017
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42. Promoting a Good Death for Persons With Dementia in Nursing Facilities

Author: David Lindeman, Lowry E, Burck, Marcia Sue DeWolf Bosek, and Lisa P. Gwyther
Subjects: Male, Attitude to Death, media_common.quotation_subject, Decision Making, Holistic Health, Disease, Nurse Administrator, Dignity, Nursing, Alzheimer Disease, Cause of Death, Surveys and Questionnaires, Health care, Humans, Medicine, Dementia, Family, Qualitative Research, Aged, Quality of Health Care, media_common, Terminal Care, business.industry, Family caregivers, Health Policy, General Medicine, medicine.disease, United States, Nursing Homes, Issues, ethics and legal aspects, Caregivers, Telephone interview, Female, business, Law, Good death, Needs Assessment, Total Quality Management
Abstract: The experience of dying from Alzheimer's disease (AD) in a nursing home setting is a poorly understood phenomenon. Fifty-seven family member caregivers of persons with Alzheimer's disease, who had died as a resident in a national nursing home chain, participated in a structured telephone interview. Despite the belief that their loved one had died with dignity, 16 out of 57 (28%) family member caregivers believed that their loved one had not experienced a good death. This article reviews the definition of a good death and the six themes of a good death found in the literature: pain and symptom management; clear decision making; preparation for death; completion; contributing to others; and affirmation of the whole person. Five standards for evaluating the quality of an anticipated death are discussed in relation to the experiences of the persons with AD. Finally, recommendations for how nurse administrators and other members of the healthcare team can promote a positive death experience for a person with AD are proposed.
Published: 2003

43. 459 Understanding benign T-cell infiltration in mycosis fungoides: Malignant clones are not alone

Author: Vieyra-Garcia, P.A., primary, O’Malley, J.T., additional, Teague, J., additional, Lowry, E., additional, Clark, R., additional, and Wolf, P., additional
Published: 2016
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44. Water Use and Management in the Bakken Shale Oil Play in North Dakota

Author: Horner, R. M., primary, Harto, C. B., additional, Jackson, R. B., additional, Lowry, E. R., additional, Brandt, A. R., additional, Yeskoo, T. W., additional, Murphy, D. J., additional, and Clark, C. E., additional
Published: 2016
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