Browsing by Subject "MATERNAL SMOKING"

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  • Ananth, Cande V.; Keyes, Katherine M.; Hamilton, Ava; Gissler, Mika; Wu, Chunsen; Liu, Shiliang; Luque-Fernandez, Miguel Angel; Skjaerven, Rolv; Williams, Michelle A.; Tikkanen, Minna; Cnattingius, Sven (2015)
    Background Although rare, placental abruption is implicated in disproportionately high rates of perinatal morbidity and mortality. Understanding geographic and temporal variations may provide in-sights into possible amenable factors of abruption. We examined abruption frequencies by maternal age, delivery year, and maternal birth cohorts over three decades across seven countries. Methods Women that delivered in the US (n = 863,879; 1979-10), Canada (4 provinces, n = 5,407,463; 1982-11), Sweden (n = 3,266,742; 1978-10), Denmark (n = 1,773,895; 197808), Norway (n = 1,780,271, 1978-09), Finland (n = 1,411,867; 1987-10), and Spain (n = 6,151,508; 1999-12) were analyzed. Abruption diagnosis was based on ICD coding. Rates were modeled using Poisson regression within the framework of an age-period-cohort analysis, and multi-level models to examine the contribution of smoking in four countries. Results Abruption rates varied across the seven countries (3-10 per 1000), Maternal age showed a consistent J-shaped pattern with increased rates at the extremes of the age distribution. In comparison to births in 2000, births after 2000 in European countries had lower abruption rates; in the US there was an increase in rate up to 2000 and a plateau thereafter. No birth cohort effects were evident. Changes in smoking prevalence partially explained the period effect in the US (P = 0.01) and Sweden (P <0.01). Conclusions There is a strong maternal age effect on abruption. While the abruption rate has plateaued since 2000 in the US, all other countries show declining rates. These findings suggest considerable variation in abruption frequencies across countries; differences in the distribution of risk factors, especially smoking, may help guide policy to reduce abruption rates.
  • Philips, Elise M.; Santos, Susana; Trasande, Leonardo; Aurrekoetxea, Juan J.; Barros, Henrique; von Berg, Andrea; Bergstroem, Anna; Bird, Philippa K.; Brescianini, Sonia; Chaoimh, Carol Ni; Charles, Marie-Aline; Chatzi, Leda; Chevrier, Cecile; Chrousos, George P.; Costet, Nathalie; Criswell, Rachel; Crozier, Sarah; Eggesbo, Merete; Fantini, Maria Pia; Farchi, Sara; Forastiere, Francesco; van Gelder, Marleen M. H. J.; Georgiu, Vagelis; Godfrey, Keith M.; Gori, Davide; Hanke, Wojciech; Heude, Barbara; Hryhorczuk, Daniel; Iniguez, Carmen; Inskip, Hazel; Karvonen, Anne M.; Kenny, Louise C.; Kull, Inger; Lawlor, Debbie A.; Lehmann, Irina; Magnus, Per; Manios, Yannis; Melen, Erik; Mommers, Monique; Morgen, Camilla S.; Moschonis, George; Murray, Deirdre; Nohr, Ellen A.; Andersen, Anne-Marie Nybo; Oken, Emily; Oostvogels, Adriette J. J. M.; Papadopoulou, Eleni; Pekkanen, Juha; Pizzi, Costanza; Polanska, Kinga; Porta, Daniela; Richiardi, Lorenzo; Rifas-Shiman, Sheryl L.; Roeleveld, Nel; Rusconi, Franca; Santos, Ana C.; Sorensen, Thorkild I. A.; Standl, Marie; Stoltenberg, Camilla; Sunyer, Jordi; Thiering, Elisabeth; Thijs, Carel; Torrent, Maties; Vrijkotte, Tanja G. M.; Wright, John; Zvinchuk, Oleksandr; Gaillard, Romy; Jaddoe, Vincent W. V. (2020)
    Author summaryWhy was this study done? Maternal smoking during pregnancy is an important risk factor for various birth complications and childhood overweight. It is not clear whether this increased risk is also present if mothers smoke during the first trimester only or reduce the number of cigarettes during pregnancy. The associations of paternal smoking with birth and childhood outcomes also remain unknown. What did the researchers do and find? We conducted an individual participant data meta-analysis using data from 229,158 families from 28 pregnancy and birth cohorts from Europe and North America to assess the associations of parental smoking during pregnancy, specifically of quitting or reducing smoking and maternal and paternal smoking combined, with preterm birth, small size for gestational age, and childhood overweight. We observed that smoking in the first trimester only did not increase the risk of preterm birth and small size for gestational age but was associated with a higher risk of childhood overweight, as compared to nonsmoking. Reducing the number of cigarettes during pregnancy, without quitting, was still associated with higher risks of these adverse outcomes. Paternal smoking seems to be associated, independently of maternal smoking, with the risks of childhood overweight. What do these findings mean? Population strategies should focus on parental smoking prevention before or at the start of, rather than during, pregnancy. Future studies are needed to assess the specific associations of smoking in the preconception and childhood periods with offspring outcomes. Background Fetal smoke exposure is a common and key avoidable risk factor for birth complications and seems to influence later risk of overweight. It is unclear whether this increased risk is also present if mothers smoke during the first trimester only or reduce the number of cigarettes during pregnancy, or when only fathers smoke. We aimed to assess the associations of parental smoking during pregnancy, specifically of quitting or reducing smoking and maternal and paternal smoking combined, with preterm birth, small size for gestational age, and childhood overweight. Methods and findings We performed an individual participant data meta-analysis among 229,158 families from 28 pregnancy/birth cohorts from Europe and North America. All 28 cohorts had information on maternal smoking, and 16 also had information on paternal smoking. In total, 22 cohorts were population-based, with birth years ranging from 1991 to 2015. The mothers' median age was 30.0 years, and most mothers were medium or highly educated. We used multilevel binary logistic regression models adjusted for maternal and paternal sociodemographic and lifestyle-related characteristics. Compared with nonsmoking mothers, maternal first trimester smoking only was not associated with adverse birth outcomes but was associated with a higher risk of childhood overweight (odds ratio [OR] 1.17 [95% CI 1.02-1.35],Pvalue = 0.030). Children from mothers who continued smoking during pregnancy had higher risks of preterm birth (OR 1.08 [95% CI 1.02-1.15],Pvalue = 0.012), small size for gestational age (OR 2.15 [95% CI 2.07-2.23],Pvalue <0.001), and childhood overweight (OR 1.42 [95% CI 1.35-1.48],Pvalue <0.001). Mothers who reduced the number of cigarettes between the first and third trimester, without quitting, still had a higher risk of small size for gestational age. However, the corresponding risk estimates were smaller than for women who continued the same amount of cigarettes throughout pregnancy (OR 1.89 [95% CI 1.52-2.34] instead of OR 2.20 [95% CI 2.02-2.42] when reducing from 5-9 to = 10 to 5-9 and
  • Felix, Janine F.; Joubert, Bonnie R.; Baccarelli, Andrea A.; Sharp, Gemma C.; Almqvist, Catarina; Annesi-Maesano, Isabella; Arshad, Hasan; Baiz, Nour; Bakermans-Kranenburg, Marian J.; Bakulski, Kelly M.; Binder, Elisabeth B.; Bouchard, Luigi; Breton, Carrie V.; Brunekreef, Bert; Brunst, Kelly J.; Burchard, Esteban G.; Bustamante, Mariona; Chatzi, Leda; Munthe-Kaas, Monica Cheng; Corpeleijn, Eva; Czamara, Darina; Dabelea, Dana; Smith, George Davey; De Boever, Patrick; Duijts, Liesbeth; Dwyer, Terence; Eng, Celeste; Eskenazi, Brenda; Everson, Todd M.; Falahi, Fahimeh; Fallin, M. Daniele; Farchi, Sara; Fernandez, Mariana F.; Gao, Lu; Gaunt, Tom R.; Ghantous, Akram; Gillman, Matthew W.; Gonseth, Semira; Grote, Veit; Gruzieva, Olena; Haberg, Siri E.; Herceg, Zdenko; Hivert, Marie-France; Holland, Nina; Holloway, John W.; Hoyo, Cathrine; Hu, Donglei; Huang, Rae-Chi; Huen, Karen; Jarvelin, Marjo-Riitta; Jima, Dereje D.; Just, Allan C.; Karagas, Margaret R.; Karlsson, Robert; Karmaus, Wilfried; Kechris, Katerina J.; Kere, Juha; Kogevinas, Manolis; Koletzko, Berthold; Koppelman, Gerard H.; Kupers, Leanne K.; Ladd-Acosta, Christine; Lahti, Jari; Lambrechts, Nathalie; Langie, Sabine A. S.; Lie, Rolv T.; Liu, Andrew H.; Magnus, Maria C.; Magnus, Per; Maguire, Rachel L.; Marsit, Carmen J.; McArdle, Wendy; Melen, Erik; Melton, Phillip; Murphy, Susan K.; Nawrot, Tim S.; Nistico, Lorenza; Nohr, Ellen A.; Nordlund, Bjorn; Nystad, Wenche; Oh, Sam S.; Oken, Emily; Page, Christian M.; Perron, Patrice; Pershagen, Goran; Pizzi, Costanza; Plusquin, Michelle; Räikkönen, Katri; Reese, Sarah E.; Reischl, Eva; Richiardi, Lorenzo; Ring, Susan; Roy, Ritu P.; Rzehak, Peter; Schoeters, Greet; Schwartz, David A.; Sebert, Sylvain; Snieder, Harold; Sorensen, Thorkild I. A.; Starling, Anne P.; Sunyer, Jordi; ATaylor, Jack; Tiemeier, Henning; Ullemar, Vilhelmina; Vafeiadi, Marina; Van Ijzendoorn, Marinus H.; Vonk, Judith M.; Vriens, Annette; Vrijheid, Martine; Wang, Pei; Wiemels, Joseph L.; Wilcox, Allen J.; Wright, Rosalind J.; Xu, Cheng-Jian; Xu, Zongli; Yang, Ivana V.; Yousefi, Paul; Zhang, Hongmei; Zhang, Weiming; Zhao, Shanshan; Agha, Golareh; Relton, Caroline L.; Jaddoe, Vincent W. V.; London, Stephanie J. (2018)
  • Merid, Simon Kebede; Novoloaca, Alexei; Sharp, Gemma C.; Kupers, Leanne K.; Kho, Alvin T.; Roy, Ritu; Gao, Lu; Annesi-Maesano, Isabella; Jain, Pooja; Plusquin, Michelle; Kogevinas, Manolis; Allard, Catherine; Vehmeijer, Florianne O.; Kazmi, Nabila; Salas, Lucas A.; Rezwan, Faisal I.; Zhang, Hongmei; Sebert, Sylvain; Czamara, Darina; Rifas-Shiman, Sheryl L.; Melton, Phillip E.; Lawlor, Debbie A.; Pershagen, Goran; Breton, Carrie V.; Huen, Karen; Baiz, Nour; Gagliardi, Luigi; Nawrot, Tim S.; Corpeleijn, Eva; Perron, Patrice; Duijts, Liesbeth; Nohr, Ellen Aagaard; Bustamante, Mariona; Ewart, Susan L.; Karmaus, Wilfried; Zhao, Shanshan; Page, Christian M.; Herceg, Zdenko; Jarvelin, Marjo-Riitta; Lahti, Jari; Baccarelli, Andrea A.; Anderson, Denise; Kachroo, Priyadarshini; Relton, Caroline L.; Bergstrom, Anna; Eskenazi, Brenda; Soomro, Munawar Hussain; Vineis, Paolo; Snieder, Harold; Bouchard, Luigi; Jaddoe, Vincent W.; Sorensen, Thorkild I. A.; Vrijheid, Martine; Arshad, S. Hasan; Holloway, John W.; Haberg, Siri E.; Magnus, Per; Dwyer, Terence; Binder, Elisabeth B.; DeMeo, Dawn L.; Vonk, Judith M.; Newnham, John; Tantisira, Kelan G.; Kull, Inger; Wiemels, Joseph L.; Heude, Barbara; Sunyer, Jordi; Nystad, Wenche; Munthe-Kaas, Monica C.; Raikkonen, Katri; Oken, Emily; Huang, Rae-Chi; Weiss, Scott T.; Anto, Josep Maria; Bousquet, Jean; Kumar, Ashish; Soderhall, Cilla; Almqvist, Catarina; Cardenas, Andres; Gruzieva, Olena; Xu, Cheng-Jian; Reese, Sarah E.; Kere, Juha; Brodin, Petter; Solomon, Olivia; Wielscher, Matthias; Holland, Nina; Ghantous, Akram; Hivert, Marie-France; Felix, Janine F.; Koppelman, Gerard H.; London, Stephanie J.; Melen, Erik (2020)
    Background Preterm birth and shorter duration of pregnancy are associated with increased morbidity in neonatal and later life. As the epigenome is known to have an important role during fetal development, we investigated associations between gestational age and blood DNA methylation in children. Methods We performed meta-analysis of Illumina's HumanMethylation450-array associations between gestational age and cord blood DNA methylation in 3648 newborns from 17 cohorts without common pregnancy complications, induced delivery or caesarean section. We also explored associations of gestational age with DNA methylation measured at 4-18 years in additional pediatric cohorts. Follow-up analyses of DNA methylation and gene expression correlations were performed in cord blood. DNA methylation profiles were also explored in tissues relevant for gestational age health effects: fetal brain and lung. Results We identified 8899 CpGs in cord blood that were associated with gestational age (range 27-42 weeks), at Bonferroni significance, P <1.06 x 10(- 7), of which 3343 were novel. These were annotated to 4966 genes. After restricting findings to at least three significant adjacent CpGs, we identified 1276 CpGs annotated to 325 genes. Results were generally consistent when analyses were restricted to term births. Cord blood findings tended not to persist into childhood and adolescence. Pathway analyses identified enrichment for biological processes critical to embryonic development. Follow-up of identified genes showed correlations between gestational age and DNA methylation levels in fetal brain and lung tissue, as well as correlation with expression levels. Conclusions We identified numerous CpGs differentially methylated in relation to gestational age at birth that appear to reflect fetal developmental processes across tissues. These findings may contribute to understanding mechanisms linking gestational age to health effects.
  • Kaminen-Ahola, Nina (2020)
    Fetal alcohol spectrum disorders (FASD) are a consequence of prenatal alcohol exposure. The etiology of the complex FASD phenotype with growth deficit, birth defects and neurodevelopmental impairments is under extensive research. Both genetic and environmental factors contribute to the wide phenotype: chromosomal rearrangements, risk and protective alleles, environmental‐induced epigenetic alterations as well as gene‐environment interactions are all involved. Understanding the molecular mechanisms of prenatal alcohol exposure can provide tools for prevention or intervention of the alcohol‐induced developmental disorders in the future. By revealing the alcohol‐induced genetic and epigenetic alterations which associate with the variable FASD phenotypes, it is possible to identify biomarkers for the disorder. This would enable early diagnoses and personalized support for development of the affected child.
  • Psychiat Genomics Consortium; Czamara, Darina; Eraslan, Goekcen; Page, Christian M.; Lahti, Jari; Lahti-Pulkkinen, Marius; Hämäläinen, Esa; Kajantie, Eero; Laivuori, Hannele; Villa, Pia M.; Reynolds, Rebecca M.; Nystad, Wenche; Håberg, Siri E.; London, Stephanie J.; O'Donnell, Kieran J.; Garg, Elika; Meaney, Michael J.; Entringer, Sonja; Wadhwa, Pathik D.; Buss, Claudia; Jones, Meaghan J.; Lin, David T. S.; MacIsaac, Julie L.; Kobor, Michael S.; Koen, Nastassja; Zar, Heather J.; Koenen, Karestan C.; Dalvie, Shareefa; Stein, Dan J.; Kondofersky, Ivan; Mueller, Nikola S.; Theis, Fabian J.; Raikkonen, Katri; Binder, Elisabeth B. (2019)
    Epigenetic processes, including DNA methylation (DNAm), are among the mechanisms allowing integration of genetic and environmental factors to shape cellular function. While many studies have investigated either environmental or genetic contributions to DNAm, few have assessed their integrated effects. Here we examine the relative contributions of prenatal environmental factors and genotype on DNA methylation in neonatal blood at variably methylated regions (VMRs) in 4 independent cohorts (overall n = 2365). We use Akaike's information criterion to test which factors best explain variability of methylation in the cohort-specific VMRs: several prenatal environmental factors (E), genotypes in cis (G), or their additive (G + E) or interaction (GxE) effects. Genetic and environmental factors in combination best explain DNAm at the majority of VMRs. The CpGs best explained by either G, G + E or GxE are functionally distinct. The enrichment of genetic variants from GxE models in GWAS for complex disorders supports their importance for disease risk.
  • Näsänen-Gilmore, Pieta; Sipola-Leppänen, Marika; Tikanmäki, Marjaana; Matinolli, Hanna-Maria; Eriksson, Johan G.; Järvelin, Marjo-Riitta; Vääräsmäki, Marja; Hovi, Petteri; Kajantie, Eero (2018)
    Very preterm birth, before the gestational age (GA) of 32 weeks, increases the risk of obstructed airflow in adulthood. We examined whether all preterm births (GA= 37 weeks). Preterm birth was associated with poorer lung function. Mean differences between individuals born early preterm versus full-term were -0.23 standard deviation (SD) (95% confidence interval (CI): -0.40, -0.05)) for forced vital capacity z-score (zFVC), -0.44 SD (95% CI -0.64, -0.25) for forced expiratory volume z-score (zFEV1), and -0.29 SD (95% CI -0.47, -0.10) for zFEV1/FVC. For late preterm, mean differences with full-term controls were -0.02 SD (95% CI -0.17, 0.13), -0.12 SD (95% CI -0.29, 0.04) and -0.13 SD (95% CI -0.29, 0.02) for zFVC, zFEV1, and zFEV1/FVC, respectively. Examination of finer GA subgroups suggested an inverse non-linear association between lung function and GA, with the greatest impact on zFEV1 for those born extremely preterm. The subgroup means were GA= 37weeks): 0.02 SD. Corresponding means for zFEV1/FVC were -1.79, -0.44, -0.47, -0.48, -0.29, and -0.02. Adjustment for maternal pregnancy conditions and socioeconomic and lifestyle factors had no major impact on the relationship. Preterm birth is associated with airflow limitation in adult life. The association appears to be attributable predominantly to those born most immature, with only a modest decrease among those born preterm at later gestational ages.
  • Kupers, Leanne K.; Monnereau, Claire; Sharp, Gemma C.; Yousefi, Paul; Salas, Lucas A.; Ghantous, Akram; Page, Christian M.; Reese, Sarah E.; Wilcox, Allen J.; Czamara, Darina; Starling, Anne P.; Novoloaca, Alexei; Lent, Samantha; Roy, Ritu; Hoyo, Cathrine; Breton, Carrie; Allard, Catherine; Just, Allan C.; Bakulski, Kelly M.; Holloway, John W.; Everson, Todd M.; Xu, Cheng-Jian; Huang, Rae-Chi; van der Plaat, Diana A.; Wielscher, Matthias; Merid, Simon Kebede; Ullemar, Vilhelmina; Rezwan, Faisal; Lahti, Jari; van Dongen, Jenny; Langie, Sabine A. S.; Richardson, Tom G.; Magnus, Maria C.; Nohr, Ellen A.; Xu, Zongli; Duijts, Liesbeth; Zhao, Shanshan; Zhang, Weiming; Plusquin, Michelle; DeMeo, Dawn L.; Solomon, Olivia; Heimovaara, Joosje H.; Jima, Dereje D.; Gao, Lu; Bustamante, Mariona; Perron, Patrice; Wright, Robert O.; Hertz-Picciotto, Irva; Zhang, Hongmei; Karagas, Margaret R.; Gehring, Ulrike; Marsit, Carmen J.; Beilin, Lawrence J.; Vonk, Judith M.; Jarvelin, Marjo-Riitta; Bergstrom, Anna; Ortqvist, Anne K.; Ewart, Susan; Villa, Pia M.; Moore, Sophie E.; Willemsen, Gonneke; Standaert, Arnout R. L.; Haberg, Siri E.; Sorensen, Thorkild I. A.; Taylor, Jack A.; Räikkönen, Katri; Yang, Ivana; Kechris, Katerina; Nawrot, Tim S.; Silver, Matt J.; Gong, Yun Yun; Richiardi, Lorenzo; Kogevinas, Manolis; Litonjua, Augusto A.; Eskenazi, Brenda; Huen, Karen; Mbarek, Hamdi; Maguire, Rachel L.; Dwyer, Terence; Vrijheid, Martine; Bouchard, Luigi; Baccarelli, Andrea A.; Croen, Lisa A.; Karmaus, Wilfried; Anderson, Denise; de Vries, Maaike; Sebert, Sylvain; Kere, Juha; Karlsson, Robert; Arshad, Syed Hasan; Hämäläinen, Esa; Routledge, Michael N.; Boomsma, Dorret; Feinberg, Andrew P.; Newschaffer, Craig J.; Govarts, Eva; Moisse, Matthieu; Fallin, M. Daniele; Melen, Erik; Prentice, Andrew M.; Kajantie, Eero; Almqvist, Catarina; Oken, Emily; Dabelea, Dana; Boezen, H. Marike; Melton, Phillip E.; Wright, Rosalind J.; Koppelman, Gerard H.; Trevisi, Letizia; Hivert, Marie-France; Sunyer, Jordi; Munthe-Kaas, Monica C.; Murphy, Susan K.; Corpeleijn, Eva; Wiemels, Joseph; Holland, Nina; Herceg, Zdenko; Binder, Elisabeth B.; Smith, George Davey; Jaddoe, Vincent W. V.; Lie, Rolv T.; Nystad, Wenche; London, Stephanie J.; Lawlor, Debbie A.; Relton, Caroline L.; Snieder, Harold; Felix, Janine F. (2019)
    Birthweight is associated with health outcomes across the life course, DNA methylation may be an underlying mechanism. In this meta-analysis of epigenome-wide association studies of 8,825 neonates from 24 birth cohorts in the Pregnancy And Childhood Epigenetics Consortium, we find that DNA methylation in neonatal blood is associated with birthweight at 914 sites, with a difference in birthweight ranging from -183 to 178 grams per 10% increase in methylation (P-Bonferroni <1.06 x 10(-7)). In additional analyses in 7,278 participants,
  • Leivonen, Susanna; Scharf, Jeremiah M.; Mathews, Carol A.; Chudal, Roshan; Gyllenberg, David; Sucksdorff, Dan; Suominen, Auli; Voutilainen, Arja; Brown, Alan S.; Sourander, Andre (2017)
    Objective: To determine the associations between maternal and paternal psychiatric diagnoses and Tourette syndrome (TS)/chronic tic disorder (CT) in a nationwide study. Method: This nested case-control study linked data derived from three national registers. All singletons born and diagnosed with TS/CT in Finland between January 1991 and December 2010 were identified (n = 1,120) and matched to four controls (n = 4,299). Conditional logistic regression was used to examine the associations between parental psychopathology and TS/CT. Results: Altogether, 24.9% of patients with TS/CT and 12.00/0 of controls had a mother with a psychiatric diagnosis. Similarly, 17.9% and 12.9% had a father with a psychiatric diagnosis. Any maternal and any paternal psychiatric diagnosis was associated with offspring TS/CT (odds ratio [OR] 2.3; 95% CI 1.9-2.7 and OR 1.2; 95% CI 1.01-1.5, respectively). The association between maternal psychiatric diagnosis and TS/CT was stronger than that between paternal psychiatric diagnosis and TS/CT (p Conclusion: Parental psychiatric diagnoses (especially in the mother) are associated with diagnosed offspring TS/CT. Further studies are required before the results can be generalized to all children with TS/CT. The associations between maternal psychiatric disorders and TS may reflect both maternal specific environmental and/or genetic influences.
  • Sourander, Andre; Sucksdorff, Minna; Chudal, Roshan; Surcel, Helja-Marja; Hinkka-Yli-Salomaki, Susanna; Gyllenberg, David; Cheslack-Postava, Keely; Brown, Alan S. (2019)
    OBJECTIVES: An association between maternal smoking during pregnancy and offspring attention-deficit/hyperactivity disorder (ADHD) has been shown across several studies based on self-reports. No previous studies have investigated the association of nicotine exposure measured by cotinine levels during pregnancy and offspring ADHD. METHODS: In this population-based study, 1079 patients born between 1998 and 1999 and diagnosed with ADHD according to the International Classification of Diseases and 1079 matched controls were identified from Finnish nationwide registers. Maternal cotinine levels were measured by using quantitative immunoassays from maternal serum specimens collected during the first and second trimesters of pregnancy and archived in the national biobank. RESULTS: There was a significant association between increasing log-transformed maternal cotinine levels and offspring ADHD. The odds ratio was 1.09 (95% confidence interval [CI] 1.06-1.12) when adjusting for maternal socioeconomic status, maternal age, maternal psychopathology, paternal age, paternal psychopathology, and child's birth weight for gestational age. In the categorical analyses with cotinine levels in 3 groups, heavy nicotine exposure (cotinine level >50 ng/mL) was associated with offspring ADHD, with an odds ratio of 2.21 (95% CI 1.63-2.99) in the adjusted analyses. Analyses by deciles of cotinine levels revealed that the adjusted odds for offspring ADHD in the highest decile was 3.34 (95% CI 2.02-5.52). CONCLUSIONS: The study reveals an association with and a dose-response relationship between nicotine exposure during pregnancy and offspring ADHD. Future studies incorporating maternal smoking and environmental, genetic, and epigenetic factors are warranted.
  • Tikanmaki, Marjaana; Tammelin, Tuija; Vaarasmaki, Marja; Sipola-Leppänen, Marika; Miettola, Satu; Pouta, Anneli; Jarvelin, Marjo-Riitta; Kajantie, Eero (2017)
    Background: Lower levels of physical activity and cardiorespiratory fitness are key risk factors of chronic adult diseases. Physical activity and cardiorespiratory fitness are predicted by birth weight, but the underlying parental and pregnancy-related factors remain largely unknown. We examined how prenatal determinants are associated with physical activity and cardiorespiratory fitness in adolescence. Methods: Of the 16-year-old members of the population-based Northern Finland Birth Cohort 1986 (NFBC 1986), 6682 singletons with no major physical disability reported their amount of physical activity outside school hours, and 4706 completed a submaximal cycle ergometer test assessing cardiorespiratory fitness. Physical activity was expressed as metabolic equivalent hours per week (METh/week) and cardiorespiratory fitness as peak oxygen uptake (ml center dot kg(-1)center dot min(-1)). Prenatal determinants included birth weight, length of gestation, mother's and father's body mass index (BMI), maternal gestational diabetes mellitus (GDM), and maternal hypertension and smoking during pregnancy. Data were analyzed by multiple linear regression. Results: A higher birth weight and longer length of gestation predicted lower levels of physical activity and cardiorespiratory fitness at 16 years, although the association between length of gestation and physical activity was inverse U-shaped. Mother's or father's overweight or obesity before pregnancy were associated with lower levels of their offspring's physical activity and fitness in adolescence. Adjusting for maternal pregnancy disorders and the adolescent's own BMI attenuated the associations with the mother's but not the father's overweight/obesity. Furthermore, maternal GDM predicted lower cardiorespiratory fitness. Conclusions: A high birth weight and parental overweight/obesity are associated with lower levels of both physical activity and cardiorespiratory fitness in adolescence, while maternal GDM and longer length of gestation are associated with lower cardiorespiratory fitness. Both long and short lengths of gestation predict low physical activity.
  • Tsai, Pei-Chien; Glastonbury, Craig A.; Eliot, Melissa N.; Bollepalli, Sailalitha; Yet, Idil; Castillo-Fernandez, Juan E.; Carnero-Montoro, Elena; Hardiman, Thomas; Martin, Tiphaine C.; Vickers, Alice; Mangino, Massimo; Ward, Kirsten; Pietilaeinen, Kirsi H.; Deloukas, Panos; Spector, Tim D.; Vinuela, Ana; Loucks, Eric B.; Ollikainen, Miina; Kelsey, Karl T.; Small, Kerrin S.; Bell, Jordana T. (2018)
    Background: Tobacco smoking is a risk factor for multiple diseases, including cardiovascular disease and diabetes. Many smoking-associated signals have been detected in the blood methylome, but the extent to which these changes are widespread to metabolically relevant tissues, and impact gene expression or metabolic health, remains unclear. Methods: We investigated smoking-associated DNA methylation and gene expression variation in adipose tissue biopsies from 542 healthy female twins. Replication, tissue specificity, and longitudinal stability of the smoking-associated effects were explored in additional adipose, blood, skin, and lung samples. We characterized the impact of adipose tissue smoking methylation and expression signals on metabolic disease risk phenotypes, including visceral fat. Results: We identified 42 smoking-methylation and 42 smoking-expression signals, where five genes (AHRR, CYP1A1, CYP1B1, CYTL1, F2RL3) were both hypo-methylated and upregulated in current smokers. CYP1A1 gene expression achieved 95% prediction performance of current smoking status. We validated and replicated a proportion of the signals in additional primary tissue samples, identifying tissue-shared effects. Smoking leaves systemic imprints on DNA methylation after smoking cessation, with stronger but shorter-lived effects on gene expression. Metabolic disease risk traits such as visceral fat and android-to-gynoid ratio showed association with methylation at smoking markers with functional impacts on expression, such as CYP1A1, and at tissue-shared smoking signals, such as NOTCH1. At smoking-signals, BHLHE40 and AHRR DNA methylation and gene expression levels in current smokers were predictive of future gain in visceral fat upon smoking cessation. Conclusions: Our results provide the first comprehensive characterization of coordinated DNA methylation arid gene expression markers of smoking in adipose tissue. The findings relate to human metabolic health and give insights into understanding the widespread health consequence of smoking outside of the lung.
  • Filatova, S.; Gyllenberg, D.; Sillanmäki, L.; Suominen, A.; Hinkka-Yli-Salomäki, S.; Kaljonen, A.; Kerkelä, M.; Keski-Säntti, M.; Ristikari, T.; Lagström, H.; Hurtig, T.; Miettunen, J.; Surcel, H.-M.; Veijola, J.; Gissler, M.; Sourander, A. (2019)
    Background: Psychiatric disorders tend to be developmental, and longitudinal settings are required to examine predictors of psychiatric phenomena. Replicating and combining data and results from different birth cohorts, which are a source of reliable data, can make research even more valuable. The Finnish Psychiatric Birth Cohort Consortium (PSYCOHORTS) project combines birth cohorts in Finland. Aim: The aim of this paper is to introduce content, plans and perspectives of the PSYCOHORTS project that brings together researchers from Finland. In addition, we illustrate an example of data harmonization using available data on causes of death. Content: PSYCOHORTS includes eight Finnish birth cohorts. The project has several plans: to harmonize different data from birth cohorts, to incorporate biobanks into psychiatric birth cohort research, to apply multigenerational perspectives, to integrate longitudinal patterns of marginalization and inequality in mental health, and to utilize data in health economics research. Data on causes of death, originally obtained from Finnish Cause of Death register, were harmonized across the six birth cohorts using SAS macro facility. Results: Harmonization of the cause of death data resulted in a total of 21,993 observations from 1965 to 2015. For example, the percentage of deaths due to suicide and the sequelae of intentional self-harm was 14% and alcohol-related diseases, including accidental poisoning by alcohol, was 13%. Conclusions: PSYCOHORTS lays the foundation for complex examinations of psychiatric disorders that is based on compatible datasets, use of biobanks and multigenerational approach to risk factors, and extensive data on marginalization and inequality.