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  • 1.
    Andersson, Ola
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, Pediatrics.
    Lindquist, Barbro
    Hosp Halland, Habilitat Ctr, Halmstad, Sweden..
    Lindgren, Magnus
    Lund Univ, Dept Psychol, Lund, Sweden..
    Stjernqvist, Karin
    Lund Univ, Dept Psychol, Lund, Sweden..
    Domellof, Magnus
    Umea Univ, Dept Clin Sci, Pediat Unit, Umea, Sweden..
    Hellström-Westas, Lena
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, Pediatrics.
    Effect of Delayed Cord Clamping on Neurodevelopment at 4 Years of Age A Randomized Clinical Trial2015In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 169, no 7, p. 631-638Article in journal (Refereed)
    Abstract [en]

    IMPORTANCE Prevention of iron deficiency in infancy may promote neurodevelopment. Delayuci umbilical cord clamping (CC) prevents iron deficiency at 4 to 6 months of age, but long-term effects after 12 months of age have not been reported. OBJECTIVE To investigate the effects of delayed CC compared with early CC on neurodevelopment at 4 years of age. DESIGN, SETTING, AND PARTICIPANTS Follow-up of a randomized clinical trial conducted from April 16, 2008, through May 21, 2010, at a Swedish county hospital. Children who were included in the original study (n = 382) as full-term infants born after a low-risk pregnancy were invited to return for follow-up at 4 years of age. Wechsler Preschool and Primary Scale of Intelligence (WPPSI-111) and Movement Assessment Battery for Children (Movement ABC) scores (collected between April 18, 2012, and July 5, 2013) were assessed by a blinded psychologist. Between April 11, 2012, and August 13, 2013, parents recorded their child's development using the Ages and Stages Questionnaire, Third Edition (ASQ) and behavior using the Strengths and Difficulties Questionnaire. All data were analyzed by intention to treat. INTERVENTIONS Randomization to delayed CC (>= 180 seconds after delivery) or early CC (<= 10 seconds after delivery). MAIN OUTCOMES AND MEASURES The main outcome was full-scale IQ as assessed by the were development as assessed by the scales from the WPPSI-III and Movement ABC, development as recorded using the ASQ, and behavior using the Strengths and Difficulties Questionnaire. RESULTS We assessed 263 children (68.8%). No differences were found in WPPSI-III scores between groups. Delayed CC improved the adjusted mean differences (AMDs) in the ASQ personal-social (AMD, 2.8; 95% Cl, 0.8-4.7) and fine-motor (AMD, 2.1; 95% Cl, 0.2-4.0) domains and the Strengths and Difficulties Questionnaire prosocial subscale (AMD, 0.5; 95% Cl, >0.0-0.9). Fewer children in the delayed-CC group had results below the cutoff in the ASQ fine-motor domain (11.0% vs 3.7%; P =.02) and the Movement ABC bicycle-trail task (12.9% vs 3.8%; P =.02). Boys who received delayed CC had significantly higher AMDs in the WPPSI-III processing-speed quotient (AMD, 4.2; 95% Cl, 0.8-7.6; P =.02), Movement ABC bicycle-trail task (AMD, 0.8; 95% Cl, 0.1-1.5; P =.03), and fine-motor (AMD, 4.7; 95% Cl, 1.0-8.4; P =.01) and personal-social (AMD, 4.9; 95% Cl, 1.6-8.3; P =.004) domains of the ASQ. CONCLUSIONS AND RELEVANCE Delayed CC compared with early CC improved scores in the fine-motor at 4 years of age, especially in boys, indicating that optimizing the time to CC may affect neurodevelopment in a low-risk population of children born in a high-income country.

  • 2. Andersson, Ola
    et al.
    Lindquist, Barbro
    Lindgren, Magnus
    Stjernqvist, Karin
    Domellöf, Magnus
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Hellstrom-Westas, Lena
    Effect of Delayed Cord Clamping on Neurodevelopment at 4 Years of Age: A Randomized Clinical Trial2015In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 169, no 7, p. 631-638Article in journal (Refereed)
    Abstract [en]

    IMPORTANCE Prevention of iron deficiency in infancy may promote neurodevelopment. Delayuci umbilical cord clamping (CC) prevents iron deficiency at 4 to 6 months of age, but long-term effects after 12 months of age have not been reported. OBJECTIVE To investigate the effects of delayed CC compared with early CC on neurodevelopment at 4 years of age. DESIGN, SETTING, AND PARTICIPANTS Follow-up of a randomized clinical trial conducted from April 16, 2008, through May 21, 2010, at a Swedish county hospital. Children who were included in the original study (n = 382) as full-term infants born after a low-risk pregnancy were invited to return for follow-up at 4 years of age. Wechsler Preschool and Primary Scale of Intelligence (WPPSI-111) and Movement Assessment Battery for Children (Movement ABC) scores (collected between April 18, 2012, and July 5, 2013) were assessed by a blinded psychologist. Between April 11, 2012, and August 13, 2013, parents recorded their child's development using the Ages and Stages Questionnaire, Third Edition (ASQ) and behavior using the Strengths and Difficulties Questionnaire. All data were analyzed by intention to treat. INTERVENTIONS Randomization to delayed CC (>= 180 seconds after delivery) or early CC (<= 10 seconds after delivery). MAIN OUTCOMES AND MEASURES The main outcome was full-scale IQ as assessed by the were development as assessed by the scales from the WPPSI-III and Movement ABC, development as recorded using the ASQ, and behavior using the Strengths and Difficulties Questionnaire. RESULTS We assessed 263 children (68.8%). No differences were found in WPPSI-III scores between groups. Delayed CC improved the adjusted mean differences (AMDs) in the ASQ personal-social (AMD, 2.8; 95% Cl, 0.8-4.7) and fine-motor (AMD, 2.1; 95% Cl, 0.2-4.0) domains and the Strengths and Difficulties Questionnaire prosocial subscale (AMD, 0.5; 95% Cl, >0.0-0.9). Fewer children in the delayed-CC group had results below the cutoff in the ASQ fine-motor domain (11.0% vs 3.7%; P =.02) and the Movement ABC bicycle-trail task (12.9% vs 3.8%; P =.02). Boys who received delayed CC had significantly higher AMDs in the WPPSI-III processing-speed quotient (AMD, 4.2; 95% Cl, 0.8-7.6; P =.02), Movement ABC bicycle-trail task (AMD, 0.8; 95% Cl, 0.1-1.5; P =.03), and fine-motor (AMD, 4.7; 95% Cl, 1.0-8.4; P =.01) and personal-social (AMD, 4.9; 95% Cl, 1.6-8.3; P =.004) domains of the ASQ. CONCLUSIONS AND RELEVANCE Delayed CC compared with early CC improved scores in the fine-motor at 4 years of age, especially in boys, indicating that optimizing the time to CC may affect neurodevelopment in a low-risk population of children born in a high-income country.

  • 3.
    Beckley, Amber L.
    et al.
    Stockholm University, Faculty of Social Sciences, Department of Sociology. Duke University, North Carolina.
    Caspi, Avshalom
    Broadbent, Jonathan
    Harrington, Honalee
    Houts, Renate M.
    Poulton, Richie
    Ramrakha, Sandhya
    Reuben, Aaron
    Moffitt, Terrie E.
    Association of Childhood Blood Lead Levels With Criminal Offending2018In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 172, no 2, p. 166-173Article in journal (Refereed)
    Abstract [en]

    Importance  Lead is a neurotoxin with well-documented effects on health. Research suggests that lead may be associated with criminal behavior. This association is difficult to disentangle from low socioeconomic status, a factor in both lead exposure and criminal offending.

    Objective  To test the hypothesis that a higher childhood blood lead level (BLL) is associated with greater risk of criminal conviction, recidivism (repeat conviction), conviction for violent offenses, and variety of self-reported criminal offending in a setting where BLL was not associated with low socioeconomic status.

    Design, Setting, and Participants  A total of 553 individuals participated in a prospective study based on a population-representative cohort born between April 1, 1972, and March 31, 1973, from New Zealand; the Dunedin Multidisciplinary Health and Development Study observed participants to age 38 years (December 2012). Statistical analysis was performed from November 10, 2016, to September 5, 2017.

    Exposures  Blood lead level measured at age 11 years.

    Main Outcomes and Measures  Official criminal conviction cumulative to age 38 years (data collected in 2013), single conviction or recidivism, conviction for nonviolent or violent crime, and self-reported variety of crime types at ages 15, 18, 21, 26, 32, and 38 years.

    Results  Participants included 553 individuals (255 female and 298 male participants) who had their blood tested for lead at age 11 years. The mean (SD) BLL at age 11 years was 11.01 (4.62) μg/dL. A total of 154 participants (27.8%) had a criminal conviction, 86 (15.6%) had recidivated, and 53 (9.6%) had a violent offense conviction. Variety scores for self-reported offending ranged from 0 to 10 offense types at each assessment; higher numbers indicated greater crime involvement. Self-reported offending followed the well-established age-crime curve (ie, the mean [SD] variety of self-reported offending increased from 1.99 [2.82] at age 15 years to its peak of 4.24 [3.15] at age 18 years and 4.22 [3.02] at age 21 years and declined thereafter to 1.10 [1.59] at age 38 years). Blood lead level was a poor discriminator between no conviction and conviction (area under the curve, 0.58). Overall, associations between BLL and conviction outcomes were weak. The estimated effect of BLL was lower for recidivism than for single convictions and lower for violent offending than for nonviolent offending. Sex-adjusted associations between BLL reached statistical significance for only 1 of the 6 self-reported offending outcomes at age 15 years (r = 0.10; 95% CI, 0.01-0.18; P = .02).

    Conclusions and Relevance  This study overcomes past limitations of studies of BLL and crime by studying the association in a place and time where the correlation was not confounded by childhood socioeconomic status. Findings failed to support a dose-response association between BLL and consequential criminal offending.

  • 4. Bolk, Jenny
    et al.
    Farooqi, Aijaz
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Hafstrom, Maria
    Aden, Ulrika
    Serenius, F.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Developmental Coordination Disorder and Its Association With Developmental Comorbidities at 6.5 Years in Apparently Healthy Children Born Extremely Preterm2018In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 172, no 8, p. 765-774Article in journal (Refereed)
    Abstract [en]

    IMPORTANCE There are concerns that apparently healthy extremely preterm children face a risk of developing motor impairments, such as developmental coordination disorder. OBJECTIVE To evaluate the prevalence of developmental coordination disorder and associated comorbidities in a national cohort of apparently healthy children born at 22 to 26 gestational weeks, compared alongside term-born peers. DESIGN, SETTING, AND PARTICIPANTS This prospective, population-based cohort study included all children who were consecutively born at 22 to 26 gestational weeks in Sweden from April 1, 2004, through March 31, 2007. At 6.5 years, 441 preterm children were evaluated alongside 371 controls. A total of 275 preterm children (62.4%) and 359 term-born children (96.8%) did not have neurodevelopmental disabilities. Motor assessments were completed for 229 of 275 preterm children (83.3%) and 344 of 359 (95.8%) term-born children, who composed the final study sample. MAIN OUTCOMES AND MEASURES Developmental coordination disorder was defined as a score of the fifth percentile or lower on the Movement Assessment Battery for Children-Second Edition scale, using control group scores. Assessment tools included the Wechsler Intelligence Scale for Children-Fourth Edition, the Brown Attention-Deficit Disorder Scales, the Five to Fifteen questionnaire, and the Strengths and Difficulties questionnaire. RESULTS Of the 229 extremely preterm children and 344 term-born controls who underwent motor assessments, 115 (50.2%) and 194 (56.4%) were boys, respectively. Developmental coordination disorder was present in 85 of 229 (37.1%) preterm children and in 19 of 344 controls (5.5%) (adjusted odds ratio [OR], 7.92; 99% CI, 3.69-17.20). When preterm children with developmental coordination disorder were compared with term-born peers, the risk was increased for total behavioral problems, internalizing, externalizing, attentional problems, hyperactivity, perceptual problems, executive dysfunction, and poor social skills, with adjusted ORs varying from 2.66 (99% CI, 1.09-6.48) for time concepts to 9.06 (99% CI, 3.60-22.8) for attentional problems (all P < .01). When preterm children with and without developmental coordination disorder were compared, preterm children with developmental coordination disorder had more behavioral problems; the adjusted OR for total behavioral problems was 2.71 (99% CI, 1.15-6.37); for externalizing problems, 2.80 (99% CI, 1.10-7.12); for inattention, 3.38 (99% CI, 1.39-8.18); and for combined attention/hyperactivity problems, 3.68 (99% CI, 1.47-9.16) (all P < .01). Parents underestimated the children's motor problems and only a few of the children had received psychological care or physiotherapy. CONCLUSIONS AND RELEVANCE Children who were born extremely preterm faced a high risk for developmental coordination disorder with associated comorbidities. Our findings support the importance of a structured follow-up of motor function, behavior, and cognition. 

  • 5.
    Bolk, Jenny
    et al.
    Soder Sjukhuset, Sachs Children & Youth Hosp, Stockholm, Sweden;Karolinska Inst, Dept Womens & Childrens Hlth, Tomtebodavagen 18a, S-17177 Stockholm, Sweden.
    Farooqi, Aijaz
    Univ Umea, Inst Clin Sci, Pediat Unit, Umea, Sweden.
    Hafstrom, Maria
    St Olavs Hosp, Dept Paediat, Trondheim, Norway;Norwegian Univ Sci & Technol Trondheim, Dept Lab Med Childrens & Womens Hlth, Trondheim, Norway;Univ Gothenburg, Inst Clin Sci, Queen Silvia Childrens Hosp, Dept Pediat, Gothenburg, Sweden.
    Aden, Ulrika
    Karolinska Inst, Dept Womens & Childrens Hlth, Tomtebodavagen 18a, S-17177 Stockholm, Sweden;Karolinska Univ Hosp, Stockholm, Sweden.
    Serenius, Fredrik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, Research group (Dept. of women´s and children´s health), Perinatal, Neonatal and Pediatric Cardiology Research. Univ Umeå, Inst Clin Sci, Pediat Unit, Umeå, Sweden.
    Developmental Coordination Disorder and Its Association With Developmental Comorbidities at 6.5 Years in Apparently Healthy Children Born Extremely Preterm2018In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 172, no 8, p. 765-774Article in journal (Refereed)
    Abstract [en]

    IMPORTANCE There are concerns that apparently healthy extremely preterm children face a risk of developing motor impairments, such as developmental coordination disorder.

    OBJECTIVE To evaluate the prevalence of developmental coordination disorder and associated comorbidities in a national cohort of apparently healthy children born at 22 to 26 gestational weeks, compared alongside term-born peers.

    DESIGN, SETTING, AND PARTICIPANTS This prospective, population-based cohort study included all children who were consecutively born at 22 to 26 gestational weeks in Sweden from April 1, 2004, through March 31, 2007. At 6.5 years, 441 preterm children were evaluated alongside 371 controls. A total of 275 preterm children (62.4%) and 359 term-born children (96.8%) did not have neurodevelopmental disabilities. Motor assessments were completed for 229 of 275 preterm children (83.3%) and 344 of 359 (95.8%) term-born children, who composed the final study sample. MAIN

    OUTCOMES AND MEASURES Developmental coordination disorder was defined as a score of the fifth percentile or lower on the Movement Assessment Battery for Children-Second Edition scale, using control group scores. Assessment tools included the Wechsler Intelligence Scale for Children-Fourth Edition, the Brown Attention-Deficit Disorder Scales, the Five to Fifteen questionnaire, and the Strengths and Difficulties questionnaire.

    RESULTS Of the 229 extremely preterm children and 344 term-born controls who underwent motor assessments, 115 (50.2%) and 194 (56.4%) were boys, respectively. Developmental coordination disorder was present in 85 of 229 (37.1%) preterm children and in 19 of 344 controls (5.5%) (adjusted odds ratio [OR], 7.92; 99% CI, 3.69-17.20). When preterm children with developmental coordination disorder were compared with term-born peers, the risk was increased for total behavioral problems, internalizing, externalizing, attentional problems, hyperactivity, perceptual problems, executive dysfunction, and poor social skills, with adjusted ORs varying from 2.66 (99% CI, 1.09-6.48) for time concepts to 9.06 (99% CI, 3.60-22.8) for attentional problems (all P < .01). When preterm children with and without developmental coordination disorder were compared, preterm children with developmental coordination disorder had more behavioral problems; the adjusted OR for total behavioral problems was 2.71 (99% CI, 1.15-6.37); for externalizing problems, 2.80 (99% CI, 1.10-7.12); for inattention, 3.38 (99% CI, 1.39-8.18); and for combined attention/hyperactivity problems, 3.68 (99% CI, 1.47-9.16) (all P < .01). Parents underestimated the children's motor problems and only a few of the children had received psychological care or physiotherapy.

    CONCLUSIONS AND RELEVANCE Children who were born extremely preterm faced a high risk for developmental coordination disorder with associated comorbidities. Our findings support the importance of a structured follow-up of motor function, behavior, and cognition.

  • 6.
    Bornehag, Carl-Gustaf
    et al.
    Karlstad University, Faculty of Health, Science and Technology (starting 2013), Department of Health Sciences (from 2013). Icahn School of Medicine at Mount Sinai.
    Lindh, C.
    Lunds universitet.
    Reichenberg, A.
    Mount Sinai School of Medicine, New York.
    Wikström, S.
    Örebro University.
    Unenge Hallerbäck, Maria
    Karlstad University, Faculty of Health, Science and Technology (starting 2013), Department of Health Sciences (from 2013).
    Evans, S. F.
    Icahn School of Medicine at Mount Sinai.
    Sathyanarayana, S.
    University of Washington, Seattle.
    Barrett, E. S.
    Rutgers School of Public Health, Piscataway, NJ.
    Nguyen, R. H. N.
    University of Minnesota.
    Bush, N. R.
    University of California, San Francisco.
    Swan, S. H.
    Icahn School of Medicine at Mount Sinai.
    Association of Prenatal Phthalate Exposure with Language Development in Early Childhood2018In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 172, no 12, p. 1169-1176Article in journal (Refereed)
    Abstract [en]

    Importance: Prenatal exposure to phthalates has been associated with neurodevelopmental outcomes, but little is known about the association with language development. Objective: To examine the association of prenatal phthalate exposure with language development in children in 2 population-based pregnancy cohort studies. Design, Setting, and Participants: Data for this study were obtained from the Swedish Environmental Longitudinal Mother and Child, Asthma and Allergy (SELMA) study conducted in prenatal clinics throughout Värmland county in Sweden and The Infant Development and the Environment Study (TIDES) conducted in 4 academic centers in the United States. Participants recruited into both studies were women in their first trimester of pregnancy who had literacy in Swedish (SELMA) or English or Spanish (TIDES). This study included mothers and their children from both the SELMA study (n = 963) and TIDES (n = 370) who had complete data on prenatal urinary phthalate metabolite levels, language delay, and modeled covariables. For SELMA, the data were collected from November 1, 2007, to June 30, 2013, and data analysis was conducted from November 1, 2016, to June 30, 2018. For TIDES, data collection began January 1, 2010, and ended March 29, 2016, and data analysis was performed from September 15, 2016, to June 30, 2018. Main Outcomes and Measures: Mothers completed a language development questionnaire that asked the number of words their children could understand or use at a median of 30 months of age (SELMA) and 37 months of age (TIDES). The responses were categorized as fewer than 25, 25 to 50, and more than 50 words, with 50 words or fewer classified as language delay. Results: In the SELMA study, 963 mothers, 455 (47.2%) girls, and 508 [52.8%] boys were included. In TIDES, 370 mothers, 185 (50.0%) girls, and 185 (50.0%) boys were included in this analysis. The prevalence of language delay was 10.0% in both SELMA (96 reported) and TIDES (37 reported), with higher rates of delay in boys than girls (SELMA: 69 [13.5%] vs 27 [6.0%]; TIDES: 12 [12.4%] vs 14 [7.6%]). In crude analyses, the metabolite levels of dibutyl phthalate and butyl benzyl phthalate were statistically significantly associated with language delay in both cohorts. In adjusted analyses, a doubling of prenatal exposure of dibutyl phthalate and butyl benzyl phthalate metabolites increased the odds ratio (OR) for language delay by approximately 25% to 40%, with statistically significant results in the SELMA study (dibutyl phthalate OR, 1.29 [95% CI, 1.03-1.63; P =.03]; butyl benzyl phthalate OR, 1.26 [95% CI, 1.07-1.49; P =.003]). A doubling of prenatal monoethyl phthalate exposure was associated with an approximately 15% increase in the OR for language delay in the SELMA study (OR, 1.14; 95% CI, 1.00-1.31; P =.05), but no such association was found in TIDES (OR, 0.98; 95% CI, 0.79-1.23). Conclusions and Relevance: In findings from this study, prenatal exposure to dibutyl phthalate and butyl benzyl phthalate was statistically significantly associated with language delay in children in both the SELMA study and TIDES. These findings, along with the prevalence of prenatal exposure to phthalates, the importance of language development, and the inconsistent results from a 2017 Danish study, suggest that the association of phthalates with language delay may warrant further examination.

  • 7.
    Bornehag, Carl-Gustaf
    et al.
    Department of Health, Karlstad University, Karlstad, Sweden; Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
    Lindh, Christian
    Laboratory Medicine, Lund University, Lund, Sweden.
    Reichenberg, Abraham
    Department of Psychiatry, Mount Sinai School of Medicine, New York, New York, USA.
    Wikström, Sverre
    Örebro University, School of Medical Sciences.
    Unenge Hallerback, Maria
    Department of Health, Karlstad University, Karlstad, Sweden.
    Evans, Sarah F.
    Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
    Sathyanarayana, Sheela
    Department of Pediatrics, University of Washington, Seattle, USA.
    Barrett, Emily S.
    Department of Epidemiology, Rutgers School of Public Health, Piscataway, New Jersey, USA.
    Nguyen, Ruby H. N.
    University of Minnesota, Minneapolis, Minnesota, USA.
    Bush, Nicole R.
    Department of Psychiatry and Pediatrics, Center for Health and Community, University of California, San Francisco, California, USA.
    Swan, Shanna H.
    Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
    Association of Prenatal Phthalate Exposure With Language Development in Early Childhood2018In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211Article in journal (Refereed)
    Abstract [en]

    Importance: Prenatal exposure to phthalates has been associated with neurodevelopmental outcomes, but little is known about the association with language development.

    Objective: To examine the association of prenatal phthalate exposure with language development in children in 2 population-based pregnancy cohort studies.

    Design, Setting, and Participants: Data for this study were obtained from the Swedish Environmental Longitudinal Mother and Child, Asthma and Allergy (SELMA) study conducted in prenatal clinics throughout Värmland county in Sweden and The Infant Development and the Environment Study (TIDES) conducted in 4 academic centers in the United States. Participants recruited into both studies were women in their first trimester of pregnancy who had literacy in Swedish (SELMA) or English or Spanish (TIDES). This study included mothers and their children from both the SELMA study (n = 963) and TIDES (n = 370) who had complete data on prenatal urinary phthalate metabolite levels, language delay, and modeled covariables. For SELMA, the data were collected from November 1, 2007, to June 30, 2013, and data analysis was conducted from November 1, 2016, to June 30, 2018. For TIDES, data collection began January 1, 2010, and ended March 29, 2016, and data analysis was performed from September 15, 2016, to June 30, 2018.

    Main Outcomes and Measures: Mothers completed a language development questionnaire that asked the number of words their children could understand or use at a median of 30 months of age (SELMA) and 37 months of age (TIDES). The responses were categorized as fewer than 25, 25 to 50, and more than 50 words, with 50 words or fewer classified as language delay.

    Results: In the SELMA study, 963 mothers, 455 (47.2%) girls, and 508 [52.8%] boys were included. In TIDES, 370 mothers, 185 (50.0%) girls, and 185 (50.0%) boys were included in this analysis. The prevalence of language delay was 10.0% in both SELMA (96 reported) and TIDES (37 reported), with higher rates of delay in boys than girls (SELMA: 69 [13.5%] vs 27 [6.0%]; TIDES: 12 [12.4%] vs 14 [7.6%]). In crude analyses, the metabolite levels of dibutyl phthalate and butyl benzyl phthalate were statistically significantly associated with language delay in both cohorts. In adjusted analyses, a doubling of prenatal exposure of dibutyl phthalate and butyl benzyl phthalate metabolites increased the odds ratio (OR) for language delay by approximately 25% to 40%, with statistically significant results in the SELMA study (dibutyl phthalate OR, 1.29 [95% CI, 1.03-1.63; P = .03]; butyl benzyl phthalate OR, 1.26 [95% CI, 1.07-1.49; P = .003]). A doubling of prenatal monoethyl phthalate exposure was associated with an approximately 15% increase in the OR for language delay in the SELMA study (OR, 1.14; 95% CI, 1.00-1.31; P = .05), but no such association was found in TIDES (OR, 0.98; 95% CI, 0.79-1.23).

    Conclusions and Relevance: In findings from this study, prenatal exposure to dibutyl phthalate and butyl benzyl phthalate was statistically significantly associated with language delay in children in both the SELMA study and TIDES. These findings, along with the prevalence of prenatal exposure to phthalates, the importance of language development, and the inconsistent results from a 2017 Danish study, suggest that the association of phthalates with language delay may warrant further examination.

  • 8.
    Bornehag, Carl-Gustaf
    et al.
    Karlstad University, Faculty of Health, Science and Technology (starting 2013), Department of Health Sciences (from 2013).
    Reichenber, A.
    Icahn School of Medicine at Mount Sinai, New York, NY, United States.
    Swan, S. H.
    Icahn School of Medicine at Mount Sinai, New York, NY, United States.
    Language Development of Young Children Is Not Linked to Phthalate Exposure: Reply2019In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 173, no 5, p. 499-499Article in journal (Other academic)
  • 9.
    Butwicka, Agnieszka
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden; Department of Child Psychiatry, Medical University of Warsaw, Warsaw, Poland; Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden.
    Olén, Ola
    Sachs' Children and Youth Hospital, Stockholm South General Hospital, Stockholm, Sweden; Department of Clinical Science and Education Södersjukhuset, Karolinska Institutet, Stockholm, Sweden; Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden; Unit of Biostatistics, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Larsson, Henrik
    Örebro University, School of Medical Sciences. Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.
    Halfvarson, Jonas
    Örebro University, School of Medical Sciences. Department of Gastroenterology.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden; Lung and Allergy Unit, Astrid Lindgren Children's Hospital, Stockholm, Sweden.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.
    Serlachius, Eva
    Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden; Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Frisén, Louise
    Stockholm Health Care Services, Stockholm County Council, Stockholm, Sweden; Centre for Psychiatry Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden; Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, United Kingdom; Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York.
    Association of Childhood-Onset Inflammatory Bowel Disease With Risk of Psychiatric Disorders and Suicide Attempt2019In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211Article in journal (Refereed)
    Abstract [en]

    Importance: Inflammatory bowel disease (IBD) has been associated with psychiatric morbidity in adults, although previous studies have not accounted for familial confounding. In children, IBD has an even more severe course, but the association between childhood-onset IBD and psychiatric morbidity remains unclear.

    Objective: To examine the risk of psychiatric morbidity in individuals with childhood-onset IBD, controlling for potential confounding shared between siblings.

    Design, Setting, and Participants: A population-based cohort study was conducted using data from the Swedish national health care and population registers of all children younger than 18 years born from 1973 to 2013. The study included 6464 individuals with a diagnosis of childhood-onset IBD (3228 with ulcerative colitis, 2536 with Crohn disease, and 700 with IBD unclassified) who were compared with 323 200 matched reference individuals from the general population and 6999 siblings of patients with IBD. Cox proportional hazards regression was used to estimate hazard ratios (HRs) with 95% CIs. Statistical analysis was performed from January 1, 1973, to December 1, 2013.

    Main Outcomes and Measures: The primary outcome was any psychiatric disorder and suicide attempt. Secondary outcomes were the following specific psychiatric disorders: psychotic, mood, anxiety, eating, personality, and behavioral disorders; substance misuse; attention-deficit/hyperactivity disorder; autism spectrum disorders; and intellectual disability.

    Results: The study included 6464 individuals with a diagnosis of childhood-onset IBD (2831 girls and 3633 boys; mean [SD] age at diagnosis of IBD, 13 [4] years). During a median follow-up time of 9 years, 1117 individuals with IBD (17.3%) received a diagnosis of any psychiatric disorder (incidence rate, 17.1 per 1000 person-years), compared with 38 044 of 323 200 individuals (11.8%) in the general population (incidence rate, 11.2 per 1000 person-years), corresponding to an HR of 1.6 (95% CI, 1.5-1.7), equaling 1 extra case of any psychiatric disorder per 170 person-years. Inflammatory bowel disease was significantly associated with suicide attempt (HR, 1.4; 95% CI, 1.2-1.7) as well as mood disorders (HR, 1.6; 95% CI, 1.4-1.7), anxiety disorders (HR, 1.9; 95% CI, 1.7-2.0) eating disorders (HR, 1.6; 95% CI, 1.3-2.0), personality disorders (HR, 1.4; 95% CI, 1.1-1.8), attention-deficit/hyperactivity disorder (HR, 1.2; 95% CI, 1.1-1.4), and autism spectrum disorders (HR, 1.4; 95% CI, 1.1-1.7) Results were similar for boys and girls. Hazard ratios for any psychiatric disorder were highest in the first year of follow-up but remained statistically significant after more than 5 years. Psychiatric disorders were particularly common for patients with very early-onset IBD (<6 years) and for patients with a parental psychiatric history. Results were largely confirmed by sibling comparison, with similar estimates noted for any psychiatric disorder (HR, 1.6; 95% CI, 1.5-1.8) and suicide attempt (HR, 1.7; 95% CI, 1.2-2.3).

    Conclusions and Relevance: Overall, childhood-onset IBD was associated with psychiatric morbidity, confirmed by between-sibling results. Particularly concerning is the increased risk of suicide attempt, suggesting that long-term psychological support be considered for patients with childhood-onset IBD.

  • 10.
    Bylund Grenklo, Tove
    et al.
    Karolinska Institutet, Stockholms Sjukhem.
    Kreicbergs, Ulrika
    Karolinska Institutet, Sophiahemmet.
    Hauksdóttir, Arna
    Island. Göteborgs universitet, Sverige..
    Valdimarsdóttir, Unnur A
    Island.
    Nyberg, Tommy
    Karolinska Institutet.
    Steineck, Gunnar
    Karolinska Institutet, Göteborgs universitet.
    Fürst, Carl Johan
    Karolinska Institutet, Stockholms Sjukhem.
    Self-injury in teenagers who lost a parent to cancer: a nationwide, population-based, long-term follow-up.2013In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 167, no 2, p. 133-140Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: To investigate the risk of self-injury in parentally cancer-bereaved youth compared with their nonbereaved peers.

    DESIGN: Population-based study of cancer-bereaved youth and a random sample of matched population controls.

    SETTING: Sweden in 2009 and 2010.

    PARTICIPANTS: A total of 952 youth (74.8%) confirmed to be eligible for the study returned the questionnaire: 622 (73.1%) of 851 eligible young adults who lost a parent to cancer between the ages of 13 and 16 years, in 2000 to 2003, and 330 (78.4%) of 451 nonbereaved peers.

    MAIN EXPOSURE: Cancer bereavement or nonbreavement during the teenage years.

    MAIN OUTCOME MEASURES: Unadjusted and adjusted odds ratios (ORs) of self-injury after January 1, 2000.

    RESULTS: Among cancer-bereaved youth, 120 (19.5%) reported self-injury compared with 35 (10.6%) of their nonbereaved peers, yielding an OR of 2.0 (95% CI, 1.4-3.0). After controlling for potential confounding factors in childhood (eg, having engaged in self-destructive behavior, having been bullied, having been sexually or physically abused, having no one to share joys and sorrows with, and sex), the adjusted OR was 2.3 (95% CI, 1.4-3.7). The OR for suicide attempts was 1.6 (95% CI, 0.8-3.0).

    CONCLUSIONS: One-fifth of cancer-bereaved youth reported self-injury, representing twice the odds for self-injury in their nonbereaved peers, regardless of any of the adjustments we made. Raised awareness on a broad basis in health care and allied disciplines would enable identification and support provision to this vulnerable group.

  • 11.
    Duberg, Anna
    et al.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Centre for Health Care Sciences, Örebro University Hospital, Örebro, Sweden; Örebro County Council, Örebro, Sweden.
    Hagberg, Lars
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Centre for Health Care Sciences, Örebro University Hospital, Örebro, Sweden; Örebro County Council, Örebro, Sweden.
    Sunvisson, Helena
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Möller, Margareta
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Örebro University Hospital, Örebro, Sweden.
    Influencing self-rated health among adolescent girls with dance intervention: a randomized controlled trial2013In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 167, no 1, p. 27-31Article in journal (Refereed)
    Abstract [en]

    Objective: To investigate whether dance intervention influenced self-rated health for adolescent girls with internalizing problems.

    Design: Randomized controlled intervention trial with follow-up measures at 8, 12, and 20 months after baseline.

    Setting: A Swedish city with a population of 130 000.

    Participants: Girls aged 13 to 18 years with internalizing problems, ie, stress and psychosomatic symptoms. A total of 59 girls were randomized to the intervention group and 53 were randomized to the control group.

    Intervention: The intervention comprised dance classes twice weekly during 8 months. Each dance class lasted 75 minutes and the focus was on the joy of movement, not on performance.

    Main Outcome Measures: Self-rated health was the primary outcome; secondary outcomes were adherence to and experience of the intervention.

    Results: The dance intervention group improved their self-rated health more than the control group at all follow-ups. At baseline, the mean score on a 5-point scale was 3.32 for the dance intervention group and 3.75 for the control group. The difference in mean change was 0.30 (95% CI, −0.01 to 0.61) at 8 months, 0.62 (95% CI, 0.25 to 0.99) at 12 months, and 0.40 (95% CI, 0.04 to 0.77) at 20 months. Among the girls in the intervention group, 67% had an attendance rate of 50% to 100%. A total of 91% of the girls rated the dance intervention as a positive experience.

    Conclusions: An 8-month dance intervention can improve self-rated health for adolescent girls with internalizing problems. The improvement remained a year after the intervention

  • 12.
    Fall, Tove
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular epidemiology.
    Lundholm, Cecilia
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Ortqvist, Anne K.
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Fall, Katja
    Orebro Univ Hosp, Clin Epidemiol & Biostat, Orebro, Sweden.;Univ Orebro, Sch Hlth & Med Sci, SE-70182 Orebro, Sweden..
    Fang, Fang
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Hedhammar, Ake
    Swedish Univ Agr Sci, Dept Clin Sci, Uppsala, Sweden..
    Kampe, Olle
    Karolinska Inst, Dept Med, Ctr Mol Med, Stockholm, Sweden..
    Ingelsson, Erik
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular epidemiology.
    Almqvist, Catarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.;Karolinska Univ Hosp, Astrid Lindgren Childrens Hosp, Lung & Allergy Unit, Stockholm, Sweden..
    Early Exposure to Dogs and Farm Animals and the Risk of Childhood Asthma2015In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 169, no 11, article id e153219Article in journal (Refereed)
    Abstract [en]

    IMPORTANCE The association between early exposure to animals and childhood asthma is not clear, and previous studies have yielded contradictory results. OBJECTIVE To determine whether exposure to dogs and farm animals confers a risk of asthma. DESIGN, SETTING AND PARTICIPANTS In a nationwide cohort study, the association between early exposure to dogs and farm animals and the risk of asthma was evaluated and included all children born in Sweden from January 1, 2001, to December 31, 2010 (N = 1 011 051), using registry data on dog and farm registration, asthma medication, diagnosis, and confounders for parents and their children. The association was assessed as the odds ratio (OR) for a current diagnosis of asthma at age 6 years for school-aged children and as the hazard ratio (HR) for incident asthma at ages 1 to 5 years for preschool-aged children. Data were analyzed from January 1, 2007, to September 30, 2012. EXPOSURES Living with a dog or farm animal. MAIN OUTCOMES AND MEASURES Childhood asthma diagnosis and medication used. RESULTS Of the 1 011 051 children born during the study period, 376 638 preschool-aged (53 460 [14.2%] exposed to dogs and 1729 [0.5%] exposed to farm animals) and 276 298 school-aged children (22 629 [8.2%] exposed to dogs and 958 [0.3%] exposed to farm animals) were included in the analyses. Of these, 18 799 children (5.0%) in the preschool-aged children's cohort experienced an asthmatic event before baseline, and 28 511 cases of asthma and 906 071 years at risk were recorded during follow-up (incidence rate, 3.1 cases per 1000 years at risk). In the school-aged children's cohort, 11 585 children (4.2%) experienced an asthmatic event during the seventh year of life. Dog exposure during the first year of life was associated with a decreased risk of asthma in school-aged children (OR, 0.87; 95% CI, 0.81-0.93) and in preschool-aged children 3 years or older (HR, 0.90; 95% CI, 0.83-0.99) but not in children younger than 3 years (HR, 1.03; 95% CI, 1.00-1.07). Results were comparable when analyzing only first-born children. Farm animal exposure was associated with a reduced risk of asthma in both school-aged children and preschool-aged children (OR, 0.48; 95% CI, 0.31-0.76, and HR, 0.69; 95% CI, 0.56-0.84), respectively. CONCLUSIONS AND RELEVANCE In this study, the data support the hypothesis that exposure to dogs and farm animals during the first year of life reduces the risk of asthma in children at age 6 years. This information might be helpful in decision making for families and physicians on the appropriateness and timing of early animal exposure.

  • 13.
    Fall, Tove
    et al.
    Department of Medical Sciences, Molecular Epidemiology and Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
    Lundholm, Cecilia
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Örtqvist, Anne K.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Orebro Univ Hosp, Orebro, Sweden.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Hedhammar, Åke
    Department of Clinical Sciences, Swedish University of Agricultural Sciences, Uppsala, Sweden .
    Kämpe, Olle
    Centre for Molecular Medicine, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden .
    Ingelsson, Erik
    Department of Medical Sciences, Molecular Epidemiology and Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Astrid Lindgren Children’s Hospital, Lung and Allergy Unit, Karolinska University Hospital, Stockholm, Sweden.
    Early Exposure to Dogs and Farm Animals and the Risk of Childhood Asthma2015In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 169, no 11, article id e153219Article in journal (Refereed)
    Abstract [en]

    IMPORTANCE: The association between early exposure to animals and childhood asthma is not clear, and previous studies have yielded contradictory results.

    OBJECTIVE: To determine whether exposure to dogs and farm animals confers a risk of asthma.

    DESIGN, SETTING AND PARTICIPANTS: In a nationwide cohort study, the association between early exposure to dogs and farm animals and the risk of asthma was evaluated and included all children born in Sweden from January 1, 2001, to December 31, 2010 (N = 1 011 051), using registry data on dog and farm registration, asthma medication, diagnosis, and confounders for parents and their children. The association was assessed as the odds ratio (OR) for a current diagnosis of asthma at age 6 years for school-aged children and as the hazard ratio (HR) for incident asthma at ages 1 to 5 years for preschool-aged children. Data were analyzed from January 1, 2007, to September 30, 2012.

    EXPOSURES: Living with a dog or farm animal.

    MAIN OUTCOMES AND MEASURES: Childhood asthma diagnosis and medication used.

    RESULTS: Of the 1 011 051 children born during the study period, 376 638 preschool-aged (53 460 [14.2%] exposed to dogs and 1729 [0.5%] exposed to farm animals) and 276 298 school-aged children (22 629 [8.2%] exposed to dogs and 958 [0.3%] exposed to farm animals) were included in the analyses. Of these, 18 799 children (5.0%) in the preschool-aged children's cohort experienced an asthmatic event before baseline, and 28 511 cases of asthma and 906 071 years at risk were recorded during follow-up (incidence rate, 3.1 cases per 1000 years at risk). In the school-aged children's cohort, 11 585 children (4.2%) experienced an asthmatic event during the seventh year of life. Dog exposure during the first year of life was associated with a decreased risk of asthma in school-aged children (OR, 0.87; 95% CI, 0.81-0.93) and in preschool-aged children 3 years or older (HR, 0.90; 95% CI, 0.83-0.99) but not in children younger than 3 years (HR, 1.03; 95% CI, 1.00-1.07). Results were comparable when analyzing only first-born children. Farm animal exposure was associated with a reduced risk of asthma in both school-aged children and preschool-aged children (OR, 0.48; 95% CI, 0.31-0.76, and HR, 0.69; 95% CI, 0.56-0.84), respectively.

    CONCLUSIONS AND RELEVANCE: In this study, the data support the hypothesis that exposure to dogs and farm animals during the first year of life reduces the risk of asthma in children at age 6 years. This information might be helpful in decision making for families and physicians on the appropriateness and timing of early animal exposure.

  • 14.
    Kantor, Elizabeth D.
    et al.
    Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, New York, USA; Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, Massachusetts, USA.
    Udumyan, Ruzan
    Örebro University, School of Medical Sciences.
    Giovannucci, Edward L.
    Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, Massachusetts, USA; Department of Nutrition, Harvard T. H. Chan School of Public Health, Boston, Massachusetts, USA; Channing Division of Network Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA.
    Valdimarsdottir, Unnur A.
    Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, Massachusetts, USA; Center of Public Health Sciences, Faculty of Medicine, School of Health Sciences, University of Iceland, Reykjavik, Iceland; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Signorello, Lisa B.
    Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, Massachusetts, USA; Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
    Montgomery, Scott
    Örebro University, School of Medical Sciences. Department of Epidemiology and Public Health, University College London, London, United Kingdom; Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
    Fall, Katja
    Örebro University, School of Medical Sciences. Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, Massachusetts, USA; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Association of Blood Marker of Inflammation in Late Adolescence With Premature Mortality2019In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211Article in journal (Refereed)
  • 15. Kassebaum, Nicholas
    et al.
    Kyu, Hmwe Hmwe
    Zoeckler, Leo
    Olsen, Helen Elizabeth
    Thomas, Katie
    Pinho, Christine
    Bhutta, Zulfiqar A
    Dandona, Lalit
    Ferrari, Alize
    Ghiwot, Tsegaye Tewelde
    Hay, Simon I
    Kinfu, Yohannes
    Liang, Xiaofeng
    Lopez, Alan
    Malta, Deborah Carvalho
    Mokdad, Ali H
    Naghavi, Mohsen
    Patton, George C
    Salomon, Joshua
    Sartorius, Benn
    Topor-Madry, Roman
    Vollset, Stein Emil
    Werdecker, Andrea
    Whiteford, Harvey A
    Abate, Kalkidan Hasen
    Abbas, Kaja
    Abreha Damtew, Solomon
    Ahmed, Muktar Beshir
    Akseer, Nadia
    Al-Raddadi, Rajaa
    Alemayohu, Mulubirhan Assefa
    Altirkawi, Khalid
    Abajobir, Amanuel Alemu
    Amare, Azmeraw T
    Antonio, Carl A T
    Ärnlöv, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Cardiovascular epidemiology.
    Artaman, Al
    Asayesh, Hamid
    Avokpaho, Euripide Frinel G Arthur
    Awasthi, Ashish
    Ayala Quintanilla, Beatriz Paulina
    Bacha, Umar
    Balem, Dimtsu
    Barac, Aleksandra
    Bärnighausen, Till Winfried
    Baye, Estifanos
    Bedi, Neeraj
    Bensenor, Isabela M
    Berhane, Adugnaw
    Bernabe, Eduardo
    Bernal, Oscar Alberto
    Beyene, Addisu Shunu
    Biadgilign, Sibhatu
    Bikbov, Boris
    Boyce, Cheryl Anne
    Brazinova, Alexandra
    Hailu, Gessessew Bugssa
    Carter, Austin
    Castañeda-Orjuela, Carlos A
    Catalá-López, Ferrán
    Charlson, Fiona J
    Chitheer, Abdulaal A
    Choi, Jee-Young Jasmine
    Ciobanu, Liliana G
    Crump, John
    Dandona, Rakhi
    Dellavalle, Robert P
    Deribew, Amare
    deVeber, Gabrielle
    Dicker, Daniel
    Betsu, Balem Balm
    Ding, Eric L
    Dubey, Manisha
    Endries, Amanuel Yesuf
    Erskine, Holly E
    Faraon, Emerito Jose Aquino
    Faro, Andre
    Farzadfar, Farshad
    Fernandes, Joao C
    Fijabi, Daniel Obadare
    Fitzmaurice, Christina
    Fleming, Thomas D
    Flor, Luisa Sorio
    Foreman, Kyle J
    Franklin, Richard C
    Fraser, Maya S
    Frostad, Joseph J
    Fullman, Nancy
    Gebregergs, Gebremedhin Berhe
    Gebru, Alemseged Aregay
    Geleijnse, Johanna M
    Gibney, Katherine B
    Gidey Yihdego, Mahari
    Ginawi, Ibrahim Abdelmageem Mohamed
    Gishu, Melkamu Dedefo
    Gizachew, Tessema Assefa
    Glaser, Elizabeth
    Gold, Audra L
    Goldberg, Ellen
    Gona, Philimon
    Goto, Atsushi
    Gugnani, Harish Chander
    Jiang, Guohong
    Gupta, Rajeev
    Tesfay, Fisaha Haile
    Hankey, Graeme J
    Havmoeller, Rasmus
    Hijar, Martha
    Horino, Masako
    Hosgood, H Dean
    Hu, Guoqing
    Jacobsen, Kathryn H
    Jakovljevic, Mihajlo B
    Jayaraman, Sudha P
    Jha, Vivekanand
    Jibat, Tariku
    Johnson, Catherine O
    Jonas, Jost
    Kasaeian, Amir
    Kawakami, Norito
    Keiyoro, Peter N
    Khalil, Ibrahim
    Khang, Young-Ho
    Khubchandani, Jagdish
    Ahmad Kiadaliri, Aliasghar A
    Kieling, Christian
    Kim, Daniel
    Kissoon, Niranjan
    Knibbs, Luke D
    Koyanagi, Ai
    Krohn, Kristopher J
    Kuate Defo, Barthelemy
    Kucuk Bicer, Burcu
    Kulikoff, Rachel
    Kumar, G Anil
    Lal, Dharmesh Kumar
    Lam, Hilton Y
    Larson, Heidi J
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Biochemial structure and function.
    Laryea, Dennis Odai
    Leung, Janni
    Lim, Stephen S
    Lo, Loon-Tzian
    Lo, Warren D
    Looker, Katharine J
    Lotufo, Paulo A
    Magdy Abd, Hassan
    El Razek, Razek
    Malekzadeh, Reza
    Markos Shifti, Desalegn
    Mazidi, Mohsen
    Meaney, Peter A
    Meles, Kidanu Gebremariam
    Memiah, Peter
    Mendoza, Walter
    Abera Mengistie, Mubarek
    Mengistu, Gebremichael Welday
    Mensah, George A
    Miller, Ted R
    Mock, Charles
    Mohammadi, Alireza
    Mohammed, Shafiu
    Monasta, Lorenzo
    Mueller, Ulrich
    Nagata, Chie
    Naheed, Aliya
    Nguyen, Grant
    Nguyen, Quyen Le
    Nsoesie, Elaine
    Oh, In-Hwan
    Okoro, Anselm
    Olusanya, Jacob Olusegun
    Olusanya, Bolajoko O
    Ortiz, Alberto
    Paudel, Deepak
    Pereira, David M
    Perico, Norberto
    Petzold, Max
    Phillips, Michael Robert
    Polanczyk, Guilherme V
    Pourmalek, Farshad
    Qorbani, Mostafa
    Rafay, Anwar
    Rahimi-Movaghar, Vafa
    Rahman, Mahfuzar
    Rai, Rajesh Kumar
    Ram, Usha
    Rankin, Zane
    Remuzzi, Giuseppe
    Renzaho, Andre M N
    Roba, Hirbo Shore
    Rojas-Rueda, David
    Ronfani, Luca
    Sagar, Rajesh
    Sanabria, Juan Ramon
    Kedir Mohammed, Muktar Sano
    Santos, Itamar S
    Satpathy, Maheswar
    Sawhney, Monika
    Schöttker, Ben
    Schwebel, David C
    Scott, James G
    Sepanlou, Sadaf G
    Shaheen, Amira
    Shaikh, Masood Ali
    She, June
    Shiri, Rahman
    Shiue, Ivy
    Sigfusdottir, Inga Dora
    Singh, Jasvinder
    Slipakit, Naris
    Smith, Alison
    Sreeramareddy, Chandrashekhar
    Stanaway, Jeffrey D
    Stein, Dan J
    Steiner, Caitlyn
    Sufiyan, Muawiyyah Babale
    Swaminathan, Soumya
    Tabarés-Seisdedos, Rafael
    Tabb, Karen M
    Tadese, Fentaw
    Tavakkoli, Mohammad
    Taye, Bineyam
    Teeple, Stephanie
    Tegegne, Teketo Kassaw
    Temam Shifa, Girma
    Terkawi, Adbullah Sulieman
    Thomas, Bernadette
    Thomson, Alan J
    Tobe-Gai, Ruoyan
    Tonelli, Marcello
    Tran, Bach Xuan
    Troeger, Christopher
    Ukwaja, Kingsley N
    Uthman, Olalekan
    Vasankari, Tommi
    Venketasubramanian, Narayanaswamy
    Vlassov, Vasiliy Victorovich
    Weiderpass, Elisabete
    Weintraub, Robert
    Gebrehiwot, Solomon Weldemariam
    Westerman, Ronny
    Williams, Hywel C
    Wolfe, Charles D A
    Woodbrook, Rachel
    Yano, Yuichiro
    Yonemoto, Naohiro
    Yoon, Seok-Jun
    Younis, Mustafa Z
    Yu, Chuanhua
    Zaki, Maysaa El Sayed
    Zegeye, Elias Asfaw
    Zuhlke, Liesl Joanna
    Murray, Christopher J L
    Vos, Theo
    Child and Adolescent Health From 1990 to 2015: Findings From the Global Burden of Diseases, Injuries, and Risk Factors 2015 Study2017In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 171, no 6, p. 573-592Article in journal (Refereed)
    Abstract [en]

    Importance: Comprehensive and timely monitoring of disease burden in all age groups, including children and adolescents, is essential for improving population health.

    Objective: To quantify and describe levels and trends of mortality and nonfatal health outcomes among children and adolescents from 1990 to 2015 to provide a framework for policy discussion.

    Evidence Review: Cause-specific mortality and nonfatal health outcomes were analyzed for 195 countries and territories by age group, sex, and year from 1990 to 2015 using standardized approaches for data processing and statistical modeling, with subsequent analysis of the findings to describe levels and trends across geography and time among children and adolescents 19 years or younger. A composite indicator of income, education, and fertility was developed (Socio-demographic Index [SDI]) for each geographic unit and year, which evaluates the historical association between SDI and health loss.

    Findings: Global child and adolescent mortality decreased from 14.18 million (95% uncertainty interval [UI], 14.09 million to 14.28 million) deaths in 1990 to 7.26 million (95% UI, 7.14 million to 7.39 million) deaths in 2015, but progress has been unevenly distributed. Countries with a lower SDI had a larger proportion of mortality burden (75%) in 2015 than was the case in 1990 (61%). Most deaths in 2015 occurred in South Asia and sub-Saharan Africa. Global trends were driven by reductions in mortality owing to infectious, nutritional, and neonatal disorders, which in the aggregate led to a relative increase in the importance of noncommunicable diseases and injuries in explaining global disease burden. The absolute burden of disability in children and adolescents increased 4.3% (95% UI, 3.1%-5.6%) from 1990 to 2015, with much of the increase owing to population growth and improved survival for children and adolescents to older ages. Other than infectious conditions, many top causes of disability are associated with long-term sequelae of conditions present at birth (eg, neonatal disorders, congenital birth defects, and hemoglobinopathies) and complications of a variety of infections and nutritional deficiencies. Anemia, developmental intellectual disability, hearing loss, epilepsy, and vision loss are important contributors to childhood disability that can arise from multiple causes. Maternal and reproductive health remains a key cause of disease burden in adolescent females, especially in lower-SDI countries. In low-SDI countries, mortality is the primary driver of health loss for children and adolescents, whereas disability predominates in higher-SDI locations; the specific pattern of epidemiological transition varies across diseases and injuries.

    Conclusions and Relevance: Consistent international attention and investment have led to sustained improvements in causes of health loss among children and adolescents in many countries, although progress has been uneven. The persistence of infectious diseases in some countries, coupled with ongoing epidemiologic transition to injuries and noncommunicable diseases, require all countries to carefully evaluate and implement appropriate strategies to maximize the health of their children and adolescents and for the international community to carefully consider which elements of child and adolescent health should be monitored.

  • 16. Kassebaum, Nicholas
    et al.
    Kyu, Hmwe Hmwe
    Zoeckler, Leo
    Olsen, Helen
    Thomas, Katie
    Pinho, Christine
    Bhutta, Zulfiqar
    Dandona, Lalit
    Ärnlöv, Johan
    Dalarna University, School of Education, Health and Social Studies, Medical Science. Uppsala universitet.
    Vos, Theo
    Child and adolescent health from 1990 to 2015: Findings from the Global Burden of Diseases, Injuries and Risk Factors 2015 study2017In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 171, no 6, p. 573-592Article in journal (Refereed)
    Abstract [en]

    Importance  Comprehensive and timely monitoring of disease burden in all age groups, including children and adolescents, is essential for improving population health.

    Objective  To quantify and describe levels and trends of mortality and nonfatal health outcomes among children and adolescents from 1990 to 2015 to provide a framework for policy discussion.

    Evidence Review  Cause-specific mortality and nonfatal health outcomes were analyzed for 195 countries and territories by age group, sex, and year from 1990 to 2015 using standardized approaches for data processing and statistical modeling, with subsequent analysis of the findings to describe levels and trends across geography and time among children and adolescents 19 years or younger. A composite indicator of income, education, and fertility was developed (Socio-demographic Index [SDI]) for each geographic unit and year, which evaluates the historical association between SDI and health loss.

    Findings  Global child and adolescent mortality decreased from 14.18 million (95% uncertainty interval [UI], 14.09 million to 14.28 million) deaths in 1990 to 7.26 million (95% UI, 7.14 million to 7.39 million) deaths in 2015, but progress has been unevenly distributed. Countries with a lower SDI had a larger proportion of mortality burden (75%) in 2015 than was the case in 1990 (61%). Most deaths in 2015 occurred in South Asia and sub-Saharan Africa. Global trends were driven by reductions in mortality owing to infectious, nutritional, and neonatal disorders, which in the aggregate led to a relative increase in the importance of noncommunicable diseases and injuries in explaining global disease burden. The absolute burden of disability in children and adolescents increased 4.3% (95% UI, 3.1%-5.6%) from 1990 to 2015, with much of the increase owing to population growth and improved survival for children and adolescents to older ages. Other than infectious conditions, many top causes of disability are associated with long-term sequelae of conditions present at birth (eg, neonatal disorders, congenital birth defects, and hemoglobinopathies) and complications of a variety of infections and nutritional deficiencies. Anemia, developmental intellectual disability, hearing loss, epilepsy, and vision loss are important contributors to childhood disability that can arise from multiple causes. Maternal and reproductive health remains a key cause of disease burden in adolescent females, especially in lower-SDI countries. In low-SDI countries, mortality is the primary driver of health loss for children and adolescents, whereas disability predominates in higher-SDI locations; the specific pattern of epidemiological transition varies across diseases and injuries.

    Conclusions and Relevance  Consistent international attention and investment have led to sustained improvements in causes of health loss among children and adolescents in many countries, although progress has been uneven. The persistence of infectious diseases in some countries, coupled with ongoing epidemiologic transition to injuries and noncommunicable diseases, require all countries to carefully evaluate and implement appropriate strategies to maximize the health of their children and adolescents and for the international community to carefully consider which elements of child and adolescent health should be monitored.

  • 17.
    KC, Ashish
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH), International Child Health and Nutrition. Health Section, United Nations Children’s Fund (UNICEF), Lalitpur, Nepal; Paropakar Maternity and Women’s Hospital, Kathmandu, Nepal.
    Rana, Nisha
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH), International Child Health and Nutrition. Paropakar Maternity and Women’s Hospital, Kathmandu, Nepal.
    Målqvist, Mats
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH), International Child Health and Nutrition.
    Jarawka Ranneberg, Linda
    epartment of Pediatrics, Hospital of Halland, Halmstad, Sweden.
    Subedi, Kalpana
    Paropakar Maternity and Women’s Hospital, Kathmandu, Nepal.
    Andersson, Ola
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, International Maternal and Child Health (IMCH), International Child Health and Nutrition.
    Effects of Delayed Umbilical Cord Clamping vs Early Clamping on Anemia in Infants at 8 and 12 Months: A Randomized Clinical Trial2017In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 171, no 3, p. 264-270Article in journal (Refereed)
    Abstract [en]

    Importance: Delayed umbilical cord clamping has been shown to improve iron stores in infants to 6 months of age. However, delayed cord clamping has not been shown to prevent iron deficiency or anemia after 6 months of age.

    Objective: To investigate the effects of delayed umbilical cord clamping, compared with early clamping, on hemoglobin and ferritin levels at 8 and 12 months of age in infants at high risk for iron deficiency anemia.

    Design, Setting, and Participants: This randomized clinical trial included 540 late preterm and term infants born vaginally at a tertiary hospital in Kathmandu, Nepal, from October 2 to November 21, 2014. Follow-up included blood levels of hemoglobin and ferritin at 8 and 12 months of age. Follow-up was completed on December 11, 2015. Analysis was based on intention to treat.

    Interventions: Infants were randomized to delayed umbilical cord clamping (≥180 seconds after delivery) or early clamping (≤60 seconds after delivery).

    Main Outcomes and Measures: Main outcomes included hemoglobin and anemia levels at 8 months of age with the power estimate based on the prevalence of anemia. Secondary outcomes included hemoglobin and anemia levels at 12 months of age and ferritin level, iron deficiency, and iron deficiency anemia at 8 and 12 months of age.

    Results: In this study of 540 infants (281 boys [52.0%] and 259 girls [48.0%]; mean [SD] gestational age, 39.2 [1.1] weeks), 270 each were randomized to the delayed and early clamping groups. At 8 months of age, 212 infants (78.5%) from the delayed group and 188 (69.6%) from the early clamping group returned for blood sampling. After multiple imputation analysis, infants undergoing delayed clamping had higher levels of hemoglobin (10.4 vs 10.2 g/dL; difference, 0.2 g/dL; 95% CI, 0.1 to 0.4 g/dL). Delayed cord clamping also reduced the prevalence of anemia (hemoglobin level <11.0 g/dL) at 8 months in 197 (73.0%) vs 222 (82.2%) infants (relative risk, 0.89; 95% CI, 0.81-0.98; number needed to treat [NNT], 11; 95% CI, 6-54). At 8 months, the risk for iron deficiency was reduced in the delayed clamping group in 60 (22.2%) vs 103 (38.1%) patients (relative risk, 0.58; 95% CI, 0.44-0.77; NNT, 6; 95% CI, 4-13). At 12 months, delayed cord clamping still resulted in a hemoglobin level of 0.3 (95% CI, 0.04-0.5) g/dL higher than in the early cord clamping group and a relative risk for anemia of 0.91 (95% CI, 0.84-0.98), resulting in a NNT of 12 (95% CI, 7-78).

    Conclusions and Relevance: Delayed cord clamping reduces anemia at 8 and 12 months of age in a high-risk population, which may have major positive effects on infants' health and development.

    Trial Registration: clinicaltrials.gov Identifier: NCT02222805.

  • 18.
    Kyu, Hmwe H
    et al.
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Pinho, Christine
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Wagner, Joseph A
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Brown, Jonathan C
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Bertozzi-Villa, Amelia
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Charlson, Fiona J
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Coffeng, Luc Edgar
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Dandona, Lalit
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Erskine, Holly E
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Ferrari, Alize J
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Fitzmaurice, Christina
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Fleming, Thomas D
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Forouzanfar, Mohammad H
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Graetz, Nicholas
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Guinovart, Caterina
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Haagsma, Juanita
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Higashi, Hideki
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Kassebaum, Nicholas J
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Larson, Heidi J
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Lim, Stephen S
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Mokdad, Ali H
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Moradi-Lakeh, Maziar
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Odell, Shaun V
    Univ Washington, Med Ctr, Seattle, WA 98195 USA.
    Roth, Gregory A
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Serina, Peter T
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Stanaway, Jeffrey D
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Misganaw, Awoke
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Whiteford, Harvey A
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Wolock, Timothy M
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Wulf Hanson, Sarah
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Abd-Allah, Foad
    Cairo Univ, Dept Neurol, Cairo, Egypt.
    Abera, Semaw Ferede
    Kilte Awlaelo Hlth & Demog Surveillance Site, Mekelle, Ethiopia.
    Abu-Raddad, Laith J
    Weill Cornell Med Coll Qatar, Infect Dis Epidemiol Grp, Doha, Qatar.
    AlBuhairan, Fadia S
    King Saud bin Abdulaziz Univ Hlth Sci, King Abdullah Specialized Childrens Hosp, Riyadh, Saudi Arabia.
    Amare, Azmeraw T
    Univ Groningen, Univ Med Ctr Groningen, Dept Epidemiol, Groningen, Netherlands.
    Antonio, Carl Abelardo T
    Univ Philippines, Coll Publ Hlth, Dept Hlth Policy & Adm, Manila, Philippines.
    Artaman, Al
    Barker-Collo, Suzanne L
    Univ Auckland, Sch Psychol, Auckland 1, New Zealand.
    Barrero, Lope H
    Pontificia Univ Javeriana, Sch Engn, Dept Ind Engn, Bogota, Colombia.
    Benjet, Corina
    Natl Inst Psychiat Ramon de la Fuente, Mexico City, DF, Mexico.
    Bensenor, Isabela M
    Univ Sao Paulo, Sao Paulo, Brazil.
    Bhutta, Zulfiqar A
    Aga Khan Univ, Med Ctr, Karachi, Pakistan.
    Bikbov, Boris
    AI Evdokimov Moscow State Univ Med & Dent, Moscow, Russia.
    Brazinova, Alexandra
    Int Neurotrama Res Org, Vienna, Austria.
    Campos-Nonato, Ismael
    Natl Inst Publ Hlth, Cuernavaca, Morelos, Mexico.
    Castañeda-Orjuela, Carlos A
    Inst Nacl Salud, Colombian Natl Hlth Observ, Bogota, Colombia.
    Catalá-López, Ferrán
    Ottawa Hosp Res Inst, Clin Epidemiol Program, Ottawa, ON, Canada.
    Chowdhury, Rajiv
    Univ Cambridge, Dept Publ Hlth & Primary Care, Cambridge, England.
    Cooper, Cyrus
    Univ Southampton, MRC Lifecourse Epidemiol Unit, Southampton, England.
    Crump, John A
    Univ Otago, Dunedin Sch Med, Ctr Int Hlth, Dunedin, New Zealand.
    Dandona, Rakhi
    Publ Hlth Fdn India, New Delhi, India.
    Degenhardt, Louisa
    Univ New S Wales, Natl Drug & Alcohol Res Ctr, Sydney, NSW, Australia.
    Dellavalle, Robert P
    Univ Colorado, Sch Med, Aurora, CO USA.
    Dharmaratne, Samath D
    Univ Peradeniya, Fac Med, Dept Community Med, Peradeniya, Sri Lanka.
    Faraon, Emerito Jose A
    Univ Philippines, Coll Publ Hlth, Dept Hlth Policy & Adm, Manila, Philippines.
    Feigin, Valery L
    Auckland Univ Technol, Natl Inst Stroke & Appl Neurosci, Auckland, New Zealand.
    Fürst, Thomas
    Univ London Imperial Coll Sci Technol & Med, Dept Infect Dis Epidemiol, London, England.
    Geleijnse, Johanna M
    Wageningen Univ, Div Human Nutr, NL-6700 AP Wageningen, Netherlands.
    Gessner, Bradford D
    Agence Med Prevent, Paris, France.
    Gibney, Katherine B
    Monash Univ, Dept Epidemiol & Prevent Med, Melbourne, Vic 3004, Australia.
    Goto, Atsushi
    Tokyo Womens Med Univ, Dept Publ Hlth, Tokyo, Japan.
    Gunnell, David
    Univ Bristol, Sch Social & Community Med, Bristol, England.
    Hankey, Graeme J
    Univ Western Australia, Sch Med & Pharmacol, Perth, WA 6009, Australia.
    Hay, Roderick J
    Int Fdn Dermatol, London, England.
    Hornberger, John C
    Cedar Associates, Menlo Pk, CA USA.
    Hosgood, H Dean
    Albert Einstein Coll Med, Bronx, NY 10467 USA.
    Hu, Guoqing
    Cent S Univ, Sch Publ Hlth, Dept Epidemiol & Hlth Stat, Changsha 410083, Peoples R China.
    Jacobsen, Kathryn H
    George Mason Univ, Fairfax, VA 22030 USA.
    Jayaraman, Sudha P
    Virginia Commonwealth Univ, Dept Surg, Richmond, VA 23284 USA.
    Jeemon, Panniyammakal
    Ctr Chron Dis Control, New Delhi, India.
    Jonas, Jost B
    Heidelberg Univ, Med Fac Mannheim, Dept Ophthalmol, Mannheim, Germany.
    Karch, André
    Helmholtz Ctr Infect Res, Epidemiol & Stat Methods Res Grp, Braunschweig, Germany.
    Kim, Daniel
    Northeastern Univ, Dept Hlth Sci, Boston, MA 02115 USA.
    Kim, Sungroul
    Soonchunhyang Univ, Seoul, South Korea.
    Kokubo, Yoshihiro
    Natl Cerebral & Cardiovasc Ctr, Dept Prevent Cardiol, Suita, Osaka, Japan.
    Kuate Defo, Barthelemy
    Univ Montreal, Sch Publ Hlth, Dept Social & Prevent Med, Montreal, PQ, Canada.
    Kucuk Bicer, Burcu
    Hacettepe Univ, Inst Publ Hlth, Ankara, Turkey.
    Kumar, G Anil
    Publ Hlth Fdn India, New Delhi, India.
    Larsson, Anders
    Uppsala Univ, Dept Med Sci, Uppsala, Sweden.
    Leasher, Janet L
    Nova SE Univ, Coll Optometry, Ft Lauderdale, FL 33314 USA.
    Leung, Ricky
    SUNY Albany, Rensselaer, NY USA.
    Li, Yongmei
    Genentech Inc, San Francisco, CA 94080 USA.
    Lipshultz, Steven E
    Wayne State Univ, Sch Med, Detroit, MI USA.
    Lopez, Alan D
    Univ Melbourne, Melbourne Sch Populat & Global Hlth, Melbourne, Vic, Australia.
    Lotufo, Paulo A
    Univ Sao Paulo, Sao Paulo, Brazil.
    Lunevicius, Raimundas
    Aintree Univ Hosp Natl Hlth Serv Fdn Trust, Liverpool, Merseyside, England.
    Lyons, Ronan A
    Swansea Univ, Farr Inst, Swansea, W Glam, Wales.
    Majdan, Marek
    Trnava Univ, Fac Hlth Sci & Social Work, Trnava, Slovakia.
    Malekzadeh, Reza
    Univ Tehran Med Sci, Digest Dis Res Inst, Tehran, Iran.
    Mashal, Taufiq
    Minist Publ Hlth, Kabul, Afghanistan.
    Mason-Jones, Amanda J
    Univ York, Dept Hlth Sci, York YO10 5DD, N Yorkshire, England.
    Melaku, Yohannes Adama
    Mekelle Univ, Coll Hlth Sci, Sch Publ Hlth, Mekelle, Ethiopia.
    Memish, Ziad A
    Saudi Minist Hlth, Riyadh, Saudi Arabia.
    Mendoza, Walter
    United Nations Populat Fund, Lima, Peru.
    Miller, Ted R
    Pacific Inst Res & Evaluat, Calverton, MD USA.
    Mock, Charles N
    Univ Washington, Harborview Injury Prevent & Res Ctr, Seattle, WA 98195 USA.
    Murray, Joseph
    Univ Cambridge, Dept Psychiat, Cambridge, England.
    Nolte, Sandra
    Charite, Ctr Internal Med & Dermatol, Dept Psychosomat Med, D-13353 Berlin, Germany.
    Oh, In-Hwan
    Kyung Hee Univ, Sch Med, Dept Prevent Med, Seoul, South Korea.
    Olusanya, Bolajoko Olubukunola
    Ctr Hlth Start Initiat, Ikoyi, Nigeria.
    Ortblad, Katrina F
    Harvard Univ, TH Chan Sch Publ Hlth, Boston, MA 02115 USA.
    Park, Eun-Kee
    Kosin Univ, Coll Med, Dept Med Humanities & Social Med, Busan, South Korea.
    Paternina Caicedo, Angel J
    Univ Cartagena, Cartagena, Colombia.
    Patten, Scott B
    Univ Calgary, Dept Community Hlth Sci, Calgary, AB, Canada.
    Patton, George C
    Univ Melbourne, Murdoch Childrens Res Inst, Melbourne, Vic, Australia.
    Pereira, David M
    Univ Porto, Fac Farm, Dept Quim, REQUIMTE LAQV,Lab Farmacognosia, Rua Campo Alegre 823, P-4100 Oporto, Portugal.
    Perico, Norberto
    Mario Negri Inst Pharmacol Res, Ist Ricovero & Cura Carattere Sci, Bergamo, Italy.
    Piel, Frédéric B
    Univ Oxford, Dept Zool, S Parks Rd, Oxford, England.
    Polinder, Suzanne
    Univ Med Ctr Rotterdam, Erasmus MC, Dept Publ Hlth, Rotterdam, Netherlands.
    Popova, Svetlana
    Univ Toronto, Ctr Addict & Mental Hlth, Toronto, ON, Canada.
    Pourmalek, Farshad
    Univ British Columbia, Sch Populat & Publ Hlth, Vancouver, BC V5Z 1M9, Canada.
    Quistberg, D Alex
    Univ Washington, Harborview Injury Prevent & Res Ctr, Seattle, WA 98195 USA.
    Remuzzi, Giuseppe
    Mario Negri Inst Pharmacol Res, Ist Ricovero & Cura Carattere Sci, Ctr Anna Maria Astori, Bergamo, Italy.
    Rodriguez, Alina
    Mid Sweden University, Faculty of Human Sciences, Department of Psychology. Univ London Imperial Coll Sci Technol & Med, Sch Publ Hlth, Dept Epidemiol & Biostat, London, England.
    Rojas-Rueda, David
    Barcelona Inst Global Hlth ISGlobal, Ctr Res Environm Epidemiol, Barcelona, Spain.
    Rothenbacher, Dietrich
    Univ Ulm, Inst Epidemiol & Med Biometry, D-89069 Ulm, Germany.
    Rothstein, David H
    Women & Childrens Hosp Buffalo, Dept Pediat Surg, Buffalo, NY USA.
    Sanabria, Juan
    Case Western Reserve Univ, Cleveland, OH 44106 USA.
    Santos, Itamar S
    Univ Sao Paulo, Dept Internal Med, Sao Paulo, Brazil.
    Schwebel, David C
    Univ Alabama Birmingham, Birmingham, AL USA.
    Sepanlou, Sadaf G
    Univ Tehran Med Sci, Digest Dis Res Inst, Tehran, Iran.
    Shaheen, Amira
    An Najah Natl Univ, Dept Publ Hlth, Nablus, Israel.
    Shiri, Rahman
    Finnish Inst Occupat Hlth, Helsinki, Finland.
    Shiue, Ivy
    Northumbria Univ, Hlth & Life Sci, Newcastle Upon Tyne NE1 8ST, Tyne & Wear, England.
    Skirbekk, Vegard
    Columbia Univ, New York, NY USA.
    Sliwa, Karen
    Univ Cape Town, Fac Hlth Sci, Hatter Inst Cardiovasc Res Africa, ZA-7925 Cape Town, South Africa.
    Sreeramareddy, Chandrashekhar T
    Int Med Univ, Dept Community Med, Kuala Lumpur 57000, Malaysia.
    Stein, Dan J
    Univ Cape Town, Dept Psychiat, ZA-7925 Cape Town, South Africa.
    Steiner, Timothy J
    Univ London Imperial Coll Sci Technol & Med, Div Brain Sci, London, England.
    Stovner, Lars Jacob
    Norwegian Univ Sci & Technol, Dept Neurosci, N-7034 Trondheim, Norway.
    Sykes, Bryan L
    Univ Calif Irvine, Dept Criminol Law & Soc, Irvine, CA USA.
    Tabb, Karen M
    Univ Illinois, Sch Social Work, Champaign, IL USA.
    Terkawi, Abdullah Sulieman
    Univ Virginia, Dept Anesthesiol, Charlottesville, VA USA.
    Thomson, Alan J
    Adapt Knowledge Management, Victoria, BC, Canada.
    Thorne-Lyman, Andrew L
    Harvard Univ, TH Chan Sch Publ Hlth, Dept Nutr, Boston, MA 02115 USA.
    Towbin, Jeffrey Allen
    Bonheur Childrens Hosp, Memphis, TN USA.
    Ukwaja, Kingsley Nnanna
    Fed Teaching Hosp, Dept Internal Med, Abakaliki, Nigeria.
    Vasankari, Tommi
    UKK Inst Hlth Promot Res, Tampere, Finland.
    Venketasubramanian, Narayanaswamy
    Raffles Hosp, Raffles Neurosci Ctr, Singapore, Singapore.
    Vlassov, Vasiliy Victorovich
    Natl Res Univ Higher Sch Econ, Moscow, Russia.
    Vollset, Stein Emil
    Norwegian Inst Publ Hlth, Oslo, Norway.
    Weiderpass, Elisabete
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.
    Weintraub, Robert G
    Univ Melbourne, Melbourne, Vic, Australia.
    Werdecker, Andrea
    Fed Inst Populat Res, German Natl Cohort, Competence Ctr Mortal Follow Up, Wiesbaden, Germany.
    Wilkinson, James D
    Wayne State Univ, Sch Med, Detroit, MI USA.
    Woldeyohannes, Solomon Meseret
    Univ Gondar, Inst Publ Hlth, Dept Epidemiol & Biostat, Gondar, Ethiopia.
    Wolfe, Charles D A
    Kings Coll London, Div Hlth & Social Care Res, London WC2R 2LS, England.
    Yano, Yuichiro
    Northwestern Univ, Dept Prevent Med, Chicago, IL 60611 USA.
    Yip, Paul
    Univ Hong Kong, Social Work & Social Adm Dept, Hong Kong, Hong Kong, Peoples R China.
    Yonemoto, Naohiro
    Natl Ctr Neurol & Psychiat, Kodaira, Tokyo, Japan.
    Yoon, Seok-Jun
    Korea Univ, Coll Med, Dept Prevent Med, Seoul 136705, South Korea.
    Younis, Mustafa Z
    Jackson State Univ, Jackson, MS USA.
    Yu, Chuanhua
    Wuhan Univ, Sch Publ Hlth, Dept Epidemiol & Biostat, Wuhan 430072, Peoples R China.
    El Sayed Zaki, Maysaa
    Mansoura Fac Med, Mansoura, Egypt.
    Naghavi, Mohsen
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Murray, Christopher J L
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Vos, Theo
    Univ Washington, Inst Hlth Metr & Evaluat, 2301 Fifth Ave,Ste 600, Seattle, WA 98121 USA.
    Global and National Burden of Diseases and Injuries Among Children and Adolescents Between 1990 and 2013: Findings From the Global Burden of Disease 2013 Study.2016In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 170, no 3, p. 267-287Article in journal (Refereed)
    Abstract [en]

    IMPORTANCE: The literature focuses on mortality among children younger than 5 years. Comparable information on nonfatal health outcomes among these children and the fatal and nonfatal burden of diseases and injuries among older children and adolescents is scarce.

    OBJECTIVE: To determine levels and trends in the fatal and nonfatal burden of diseases and injuries among younger children (aged <5 years), older children (aged 5-9 years), and adolescents (aged 10-19 years) between 1990 and 2013 in 188 countries from the Global Burden of Disease (GBD) 2013 study.

    EVIDENCE REVIEW: Data from vital registration, verbal autopsy studies, maternal and child death surveillance, and other sources covering 14 244 site-years (ie, years of cause of death data by geography) from 1980 through 2013 were used to estimate cause-specific mortality. Data from 35 620 epidemiological sources were used to estimate the prevalence of the diseases and sequelae in the GBD 2013 study. Cause-specific mortality for most causes was estimated using the Cause of Death Ensemble Model strategy. For some infectious diseases (eg, HIV infection/AIDS, measles, hepatitis B) where the disease process is complex or the cause of death data were insufficient or unavailable, we used natural history models. For most nonfatal health outcomes, DisMod-MR 2.0, a Bayesian metaregression tool, was used to meta-analyze the epidemiological data to generate prevalence estimates.

    FINDINGS: Of the 7.7 (95% uncertainty interval [UI], 7.4-8.1) million deaths among children and adolescents globally in 2013, 6.28 million occurred among younger children, 0.48 million among older children, and 0.97 million among adolescents. In 2013, the leading causes of death were lower respiratory tract infections among younger children (905 059 deaths; 95% UI, 810 304-998 125), diarrheal diseases among older children (38 325 deaths; 95% UI, 30 365-47 678), and road injuries among adolescents (115 186 deaths; 95% UI, 105 185-124 870). Iron deficiency anemia was the leading cause of years lived with disability among children and adolescents, affecting 619 (95% UI, 618-621) million in 2013. Large between-country variations exist in mortality from leading causes among children and adolescents. Countries with rapid declines in all-cause mortality between 1990 and 2013 also experienced large declines in most leading causes of death, whereas countries with the slowest declines had stagnant or increasing trends in the leading causes of death. In 2013, Nigeria had a 12% global share of deaths from lower respiratory tract infections and a 38% global share of deaths from malaria. India had 33% of the world's deaths from neonatal encephalopathy. Half of the world's diarrheal deaths among children and adolescents occurred in just 5 countries: India, Democratic Republic of the Congo, Pakistan, Nigeria, and Ethiopia.

    CONCLUSIONS AND RELEVANCE: Understanding the levels and trends of the leading causes of death and disability among children and adolescents is critical to guide investment and inform policies. Monitoring these trends over time is also key to understanding where interventions are having an impact. Proven interventions exist to prevent or treat the leading causes of unnecessary death and disability among children and adolescents. The findings presented here show that these are underused and give guidance to policy makers in countries where more attention is needed.

  • 19. Kyu, Hmwe H
    et al.
    Pinho, Christine
    Wagner, Joseph A
    Brown, Jonathan C
    Bertozzi-Villa, Amelia
    Charlson, Fiona J
    Coffeng, Luc Edgar
    Dandona, Lalit
    Erskine, Holly E
    Ferrari, Alize J
    Fitzmaurice, Christina
    Fleming, Thomas D
    Forouzanfar, Mohammad H
    Graetz, Nicholas
    Guinovart, Caterina
    Haagsma, Juanita
    Higashi, Hideki
    Kassebaum, Nicholas J
    Larson, Heidi J
    Lim, Stephen S
    Mokdad, Ali H
    Moradi-Lakeh, Maziar
    Odell, Shaun V
    Roth, Gregory A
    Serina, Peter T
    Stanaway, Jeffrey D
    Misganaw, Awoke
    Whiteford, Harvey A
    Wolock, Timothy M
    Wulf Hanson, Sarah
    Abd-Allah, Foad
    Abera, Semaw Ferede
    Abu-Raddad, Laith J
    AlBuhairan, Fadia S
    Amare, Azmeraw T
    Antonio, Carl Abelardo T
    Artaman, Al
    Barker-Collo, Suzanne L
    Barrero, Lope H
    Benjet, Corina
    Bensenor, Isabela M
    Bhutta, Zulfiqar A
    Bikbov, Boris
    Brazinova, Alexandra
    Campos-Nonato, Ismael
    Castañeda-Orjuela, Carlos A
    Catalá-López, Ferrán
    Chowdhury, Rajiv
    Cooper, Cyrus
    Crump, John A
    Dandona, Rakhi
    Degenhardt, Louisa
    Dellavalle, Robert P
    Dharmaratne, Samath D
    Faraon, Emerito Jose A
    Feigin, Valery L
    Fürst, Thomas
    Geleijnse, Johanna M
    Gessner, Bradford D
    Gibney, Katherine B
    Goto, Atsushi
    Gunnell, David
    Hankey, Graeme J
    Hay, Roderick J
    Hornberger, John C
    Hosgood, H Dean
    Hu, Guoqing
    Jacobsen, Kathryn H
    Jayaraman, Sudha P
    Jeemon, Panniyammakal
    Jonas, Jost B
    Karch, André
    Kim, Daniel
    Kim, Sungroul
    Kokubo, Yoshihiro
    Kuate Defo, Barthelemy
    Kucuk Bicer, Burcu
    Kumar, G Anil
    Larsson, Anders
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Biochemial structure and function.
    Leasher, Janet L
    Leung, Ricky
    Li, Yongmei
    Lipshultz, Steven E
    Lopez, Alan D
    Lotufo, Paulo A
    Lunevicius, Raimundas
    Lyons, Ronan A
    Majdan, Marek
    Malekzadeh, Reza
    Mashal, Taufiq
    Mason-Jones, Amanda J
    Melaku, Yohannes Adama
    Memish, Ziad A
    Mendoza, Walter
    Miller, Ted R
    Mock, Charles N
    Murray, Joseph
    Nolte, Sandra
    Oh, In-Hwan
    Olusanya, Bolajoko Olubukunola
    Ortblad, Katrina F
    Park, Eun-Kee
    Paternina Caicedo, Angel J
    Patten, Scott B
    Patton, George C
    Pereira, David M
    Perico, Norberto
    Piel, Frédéric B
    Polinder, Suzanne
    Popova, Svetlana
    Pourmalek, Farshad
    Quistberg, D Alex
    Remuzzi, Giuseppe
    Rodriguez, Alina
    Rojas-Rueda, David
    Rothenbacher, Dietrich
    Rothstein, David H
    Sanabria, Juan
    Santos, Itamar S
    Schwebel, David C
    Sepanlou, Sadaf G
    Shaheen, Amira
    Shiri, Rahman
    Shiue, Ivy
    Skirbekk, Vegard
    Sliwa, Karen
    Sreeramareddy, Chandrashekhar T
    Stein, Dan J
    Steiner, Timothy J
    Stovner, Lars Jacob
    Sykes, Bryan L
    Tabb, Karen M
    Terkawi, Abdullah Sulieman
    Thomson, Alan J
    Thorne-Lyman, Andrew L
    Towbin, Jeffrey Allen
    Ukwaja, Kingsley Nnanna
    Vasankari, Tommi
    Venketasubramanian, Narayanaswamy
    Vlassov, Vasiliy Victorovich
    Vollset, Stein Emil
    Weiderpass, Elisabete
    Weintraub, Robert G
    Werdecker, Andrea
    Wilkinson, James D
    Woldeyohannes, Solomon Meseret
    Wolfe, Charles D A
    Yano, Yuichiro
    Yip, Paul
    Yonemoto, Naohiro
    Yoon, Seok-Jun
    Younis, Mustafa Z
    Yu, Chuanhua
    El Sayed Zaki, Maysaa
    Naghavi, Mohsen
    Murray, Christopher J L
    Vos, Theo
    Global and National Burden of Diseases and Injuries Among Children and Adolescents Between 1990 and 2013: Findings From the Global Burden of Disease 2013 Study2016In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 170, no 3, p. 267-287Article, review/survey (Refereed)
    Abstract [en]

    Importance: The literature focuses on mortality among children younger than 5 years. Comparable information on nonfatal health outcomes among these children and the fatal and nonfatal burden of diseases and injuries among older children and adolescents is scarce.

    Objective: To determine levels and trends in the fatal and nonfatal burden of diseases and injuries among younger children (aged <5 years), older children (aged 5-9 years), and adolescents (aged 10-19 years) between 1990 and 2013 in 188 countries from the Global Burden of Disease (GBD) 2013 study.

    Evidence Review: Data from vital registration, verbal autopsy studies, maternal and child death surveillance, and other sources covering 14 244 site-years (ie, years of cause of death data by geography) from 1980 through 2013 were used to estimate cause-specific mortality. Data from 35 620 epidemiological sources were used to estimate the prevalence of the diseases and sequelae in the GBD 2013 study. Cause-specific mortality for most causes was estimated using the Cause of Death Ensemble Model strategy. For some infectious diseases (eg, HIV infection/AIDS, measles, hepatitis B) where the disease process is complex or the cause of death data were insufficient or unavailable, we used natural history models. For most nonfatal health outcomes, DisMod-MR 2.0, a Bayesian metaregression tool, was used to meta-analyze the epidemiological data to generate prevalence estimates.

    Findings: Of the 7.7 (95% uncertainty interval [UI], 7.4-8.1) million deaths among children and adolescents globally in 2013, 6.28 million occurred among younger children, 0.48 million among older children, and 0.97 million among adolescents. In 2013, the leading causes of death were lower respiratory tract infections among younger children (905 059 deaths; 95% UI, 810 304-998 125), diarrheal diseases among older children (38 325 deaths; 95% UI, 30 365-47 678), and road injuries among adolescents (115 186 deaths; 95% UI, 105 185-124 870). Iron deficiency anemia was the leading cause of years lived with disability among children and adolescents, affecting 619 (95% UI, 618-621) million in 2013. Large between-country variations exist in mortality from leading causes among children and adolescents. Countries with rapid declines in all-cause mortality between 1990 and 2013 also experienced large declines in most leading causes of death, whereas countries with the slowest declines had stagnant or increasing trends in the leading causes of death. In 2013, Nigeria had a 12% global share of deaths from lower respiratory tract infections and a 38% global share of deaths from malaria. India had 33% of the world's deaths from neonatal encephalopathy. Half of the world's diarrheal deaths among children and adolescents occurred in just 5 countries: India, Democratic Republic of the Congo, Pakistan, Nigeria, and Ethiopia.

    Conclusions and Relevance: Understanding the levels and trends of the leading causes of death and disability among children and adolescents is critical to guide investment and inform policies. Monitoring these trends over time is also key to understanding where interventions are having an impact. Proven interventions exist to prevent or treat the leading causes of unnecessary death and disability among children and adolescents. The findings presented here show that these are underused and give guidance to policy makers in countries where more attention is needed.

  • 20.
    Oberg, Anna Sara
    et al.
    Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, USA; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    D'Onofrio, Brian M.
    Department of Psychological and Brain Sciences, Indiana University, Bloomington, USA.
    Rickert, Martin E.
    Department of Psychological and Brain Sciences, Indiana University, Bloomington, USA.
    Hernandez-Diaz, Sonia
    Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, USA.
    Ecker, Jeffrey L.
    Department of Obstetrics and Gynecology, Massachusetts General Hospital, Harvard Medical School, Boston, USA.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Astrid Lindgren Children’s Hospital, Karolinska University Hospital, Stockholm, Sweden.
    Larsson, Henrik
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Lichtenstein, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Bateman, Brian T
    Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, USA; Department of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, USA.
    Association of Labor Induction With Offspring Risk of Autism Spectrum Disorders2016In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 170, no 9, article id e160965Article in journal (Refereed)
    Abstract [en]

    Importance: Induction of labor is a frequently performed obstetrical intervention. It would thus be of great concern if reported associations between labor induction and offspring risk of autism spectrum disorders (ASD) reflected causal influence.

    Objective: To assess the associations of labor induction with ASD, comparing differentially exposed relatives (siblings and cousins discordant for induction).

    Design, setting, and participants: Follow-up of all live births in Sweden between 1992 and 2005, defined in the Medical Birth Register. The register was linked to population registers of familial relations, inpatient and outpatient visits, and education records. Diagnoses of ASD were from 2001 through 2013, and data were analyzed in the 2015-2016 year.

    EXPOSURES: Induction of labor.

    MAIN OUTCOMES AND MEASURES: Autism spectrum disorders identified by diagnoses from inpatient and outpatient records between 2001 and 2013. Hazard ratios (HRs) quantified the association between labor induction and offspring ASD. In addition to considering a wide range of measured confounders, comparison of exposure-discordant births to the same woman allowed additional control for all unmeasured factors shared by siblings.

    RESULTS: The full cohort included 1 362 950 births, of which 22 077 offspring (1.6%) were diagnosed with ASD by ages 8 years through 21 years. In conventional models of the full cohort, associations between labor induction and offspring ASD were attenuated but remained statistically significant after adjustment for measured potential confounders (HR, 1.19; 95% CI, 1.13-1.24). When comparison was made within siblings whose births were discordant with respect to induction, thus accounting for all environmental and genetic factors shared by siblings, labor induction was no longer associated with offspring ASD (HR, 0.99; 95% CI, 0.88-1.10).

    CONCLUSIONS AND RELEVANCE: In this nationwide sample of live births we observed no association between induction of labor and offspring ASD within sibling comparison. Our findings suggest that concern for ASD should not factor into the clinical decision about whether to induce labor.

  • 21. Persson, Martina
    et al.
    Shah, Prakesh S.
    Rusconi, Franca
    Reichman, Brian
    Modi, Neena
    Kusuda, Satoshi
    Lehtonen, Liisa
    Håkansson, Stellan
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Yang, Junmin
    Isayama, Tetsuya
    Beltempo, Marc
    Lee, Shoo
    Norman, Mikael
    Association of Maternal Diabetes With Neonatal Outcomes of Very Preterm and Very Low-Birth-Weight Infants: an International Cohort Study2018In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 172, no 9, p. 867-875Article in journal (Refereed)
    Abstract [en]

    IMPORTANCE: Diabetes in pregnancy is associated with a 2-times to 3-times higher rate of very preterm birth than in women without diabetes. Very preterm infants are at high risk of death and severe morbidity. The association of maternal diabetes with these risks is unclear.

    OBJECTIVE: To determine the associations between maternal diabetes and in-hospital mortality, as well as neonatal morbidity in very preterm infants with a birth weight of less than 1500 g.

    DESIGN, SETTING, AND PARTICIPANTS: This retrospective cohort study was conducted at 7 national networks in high-income countries that are part of the International Neonatal Network for Evaluating Outcomes in Neonates and used prospectively collected data on 76 360 very preterm, singleton infants without malformations born between January 1, 2007, and December 31, 2015, at 24 to 31 weeks' gestation with birth weights of less than 1500 g, 3280 (4.3%) of whom were born to diabetic mothers. EXPOSURES Any type of diabetes during pregnancy.

    MAIN OUTCOMES AND MEASURES: The primary outcome was in-hospital mortality. The secondary outcomes were severe neonatal morbidities, including intraventricular hemorrhages of grade 3 to 4, cystic periventricular leukomalacia, retinopathy of prematurity needing treatment and bronchopulmonary dysplasia, and other morbidities, including respiratory distress, treated patent ductus arteriosus, and necrotizing enterocolitis. Odds ratios (ORs) with 95% confidence intervals were estimated, adjusted for potential confounders, and stratified by gestational age (GA), sex, and network.

    RESULTS: The mean (SD) birth weight of offspring born to mothers with diabetes was significantly higher at 1081 (262) g than in offspring born to mothers without diabetes (mean [SD] birth weight, 1027 [270] g). Of 76 360 infants, 25 962 (34%) and 33 598 (44%) were born before 28 weeks of gestation to mothers with and without diabetes, respectively. Mothers with diabetes were older and had more hypertensive disorders, antenatal steroid treatments, and deliveries by cesarean delivery than mothers without diabetes. Infants of mothers with diabetes were born at a later GA than infants of mothers without diabetes. In-hospital mortality (6.6% vs 8.3%) and the composite of mortality and severe morbidity (31.6% vs 40.6%) were lower in infants of mothers with diabetes. However, in adjusted analyses, no significant differences in in-hospital mortality (adjusted OR, 1.16 (95% CI, 0.97-1.39) or the composite of mortality and severe morbidity (adjusted OR, 0.99 (95% CI, 0.88-1.10) were observed. With few exceptions, outcomes of infants born to mothers with and without diabetes were similar regardless of infant sex, GA, or country of birth.

    CONCLUSIONS AND RELEVANCE: In high-resource settings, maternal diabetes is not associated with an increased risk of in-hospital mortality or severe morbidity in very preterm infants with a birth weight of fewer than 1500 g.

  • 22.
    Serenius, Fredrik
    et al.
    Uppsala University, Sweden; Umeå University, Sweden.
    Ewald, Uwe
    Uppsala University, Sweden.
    Farooqi, Aijaz
    Umeå University, Sweden.
    Fellman, Vineta
    Lund University, Sweden.
    Hafstrom, Maria
    University of Gothenburg, Sweden; St Olavs Hospital Trondheim, Norway; Norwegian University of Science and Technology, Norway.
    Hellgren, Kerstin
    Karolinska Institute, Sweden.
    Marsal, Karel
    Lund University, Sweden.
    Ohlin, Andreas
    University of Örebro, Sweden.
    Olhager, Elisabeth
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences. Region Östergötland, Center of Paediatrics and Gynaecology and Obstetrics, Department of Paediatrics in Linköping.
    Stjernqvist, Karin
    Lund University, Sweden.
    Stromberg, Bo
    Uppsala University, Sweden.
    Aden, Ulrika
    Karolinska Institute, Sweden.
    Kallen, Karin
    Lund University, Sweden.
    Neurodevelopmental Outcomes Among Extremely Preterm Infants 6.5 Years After Active Perinatal Care in Sweden2016In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 170, no 10, p. 954-963Article in journal (Refereed)
    Abstract [en]

    IMPORTANCE Active perinatal care increases the rate of survival of extremely preterm infants, but there are concerns that improved survival might increase the rate of disabled survivors. OBJECTIVE To determine the neurodevelopmental outcomes of a national cohort of children 6.5 years of age who had been born extremely preterm (amp;lt;27 weeks gestational age) in Sweden. DESIGN, SETTING, AND PARTICIPANTS Population-based prospective cohort study of consecutively born extremely preterm infants. All of these infants were born in Sweden during the period from April 1, 2004, to March 31, 2007. Of 707 live-born extremely preterm infants, 486 (68.7%) survived to 6.5 years of age. These children were assessed and compared with matched controls who had been born at term. Comparison estimates were adjusted for demographic differences. Assessments ended in February 2014, and analysis started thereafter. MAIN OUTCOMES AND MEASURES Cognitive ability was measured with the fourth edition of the Wechsler Intelligence Scale for Children (WISC-IV), and the mean (SD) scores of the children who had been born extremely preterm were compared with those of the controls. Clinical examinations and parental questionnaires were used for diagnosis of cerebral palsy, hearing and vision impairments, and cognition for the children who were not assessed with the WISC-IV. RESULTS Of 486 eligible infants who were born extremely preterm, 441 (90.7%) were assessed at 6.5 years of age (59 by medical record review only) alongside 371 controls. The adjusted mean (SD) full-scale WISC-IV score was 14.2 (95% CI, 12.1-16.3) points lower for children who had been born extremely preterm than for controls. Cognitive disability was moderate for 18.8% of extremely preterm children and 2.2% of controls (P amp;lt; .001), and it was severe for 11.1% of extremely preterm children and 0.3% of controls (P amp;lt; .001). Cerebral palsy was observed in 9.5% of extremely preterm children and 0.0% of controls (P amp;lt; .001), blindness was observed in 2.0% of extremely preterm children and 0.0% of controls (P amp;lt; .001), and hearing impairment was observed in 2.1% of extremely preterm children and 0.5% of controls (P = .07). Overall, 36.1%(95% CI, 31.7%-40.6%) of extremely preterm children had no disability, 30.4%(95% CI 26.3%-34.8%) had mild disability, 20.2%(95% CI, 16.6%-24.2%) had moderate disability, and 13.4%(95% CI, 10.5%-16.9%) had severe disability. For extremely preterm children, moderate or severe overall disability decreased with gestational age at birth (adjusted odds ratio per week, 0.65 [95% CI, 0.54-0.79]; P amp;lt; .001) and increased from 26.6% to 33.5%(P = .01) for children assessed both at 2.5 and 6.5 years. CONCLUSIONS AND RELEVANCE Of the 441 extremely preterm infants who had received active perinatal care, 293 (66.4%) had no or mild disability at 6.5 years; of the 371 controls, 11 (3.0%) had moderate or severe disability. Disability rates at 6.5 years increased relative to the rates at 2.5 years. Results are relevant for health care professionals and planners, and for clinicians counseling families facing extremely preterm births.

  • 23.
    Serenius, Fredrik
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics. Section for Pediatrics, Department of Women’s and Children’s Health, Uppsala University, Uppsala, Sweden.
    Ewald, Uwe
    Farooqi, Aijaz
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Fellman, Vineta
    Hafstrom, Maria
    Hellgren, Kerstin
    Marsal, Karel
    Ohlin, Andreas
    Olhager, Elisabeth
    Stjernqvist, Karin
    Stromberg, Bo
    Aden, Ulrika
    Kallen, Karin
    Neurodevelopmental Outcomes Among Extremely Preterm Infants 6.5 Years After Active Perinatal Care in Sweden2016In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 170, no 10, p. 954-963Article in journal (Refereed)
    Abstract [en]

    IMPORTANCE Active perinatal care increases the rate of survival of extremely preterm infants, but there are concerns that improved survival might increase the rate of disabled survivors. OBJECTIVE To determine the neurodevelopmental outcomes of a national cohort of children 6.5 years of age who had been born extremely preterm (<27 weeks' gestational age) in Sweden. DESIGN, SETTING, AND PARTICIPANTS Population-based prospective cohort study of consecutively born extremely preterm infants. All of these infants were born in Sweden during the period from April 1, 2004, to March 31, 2007. Of 707 live-born extremely preterm infants, 486 (68.7%) survived to 6.5 years of age. These children were assessed and compared with matched controls who had been born at term. Comparison estimates were adjusted for demographic differences. Assessments ended in February 2014, and analysis started thereafter. MAIN OUTCOMES AND MEASURES Cognitive ability was measured with the fourth edition of the Wechsler Intelligence Scale for Children (WISC-IV), and the mean (SD) scores of the children who had been born extremely preterm were compared with those of the controls. Clinical examinations and parental questionnaires were used for diagnosis of cerebral palsy, hearing and vision impairments, and cognition for the children who were not assessed with the WISC-IV. RESULTS Of 486 eligible infants who were born extremely preterm, 441 (90.7%) were assessed at 6.5 years of age (59 by medical record review only) alongside 371 controls. The adjusted mean (SD) full-scale WISC-IV score was 14.2 (95% CI, 12.1-16.3) points lower for children who had been born extremely preterm than for controls. Cognitive disability was moderate for 18.8% of extremely preterm children and 2.2% of controls (P < .001), and it was severe for 11.1% of extremely preterm children and 0.3% of controls (P < .001). Cerebral palsy was observed in 9.5% of extremely preterm children and 0.0% of controls (P < .001), blindness was observed in 2.0% of extremely preterm children and 0.0% of controls (P < .001), and hearing impairment was observed in 2.1% of extremely preterm children and 0.5% of controls (P = .07). Overall, 36.1%(95% CI, 31.7%-40.6%) of extremely preterm children had no disability, 30.4%(95% CI 26.3%-34.8%) had mild disability, 20.2%(95% CI, 16.6%-24.2%) had moderate disability, and 13.4%(95% CI, 10.5%-16.9%) had severe disability. For extremely preterm children, moderate or severe overall disability decreased with gestational age at birth (adjusted odds ratio per week, 0.65 [95% CI, 0.54-0.79]; P < .001) and increased from 26.6% to 33.5%(P = .01) for children assessed both at 2.5 and 6.5 years. CONCLUSIONS AND RELEVANCE Of the 441 extremely preterm infants who had received active perinatal care, 293 (66.4%) had no or mild disability at 6.5 years; of the 371 controls, 11 (3.0%) had moderate or severe disability. Disability rates at 6.5 years increased relative to the rates at 2.5 years. Results are relevant for health care professionals and planners, and for clinicians counseling families facing extremely preterm births.

  • 24.
    Serenius, Fredrik
    et al.
    Section for Pediatrics, Department of Women’s and Children’s Health, Uppsala University, Uppsala, Sweden; Department of Pediatrics, Institute of Clinical Sciences, Umeå University, Umeå, Sweden.
    Ewald, Uwe
    Section for Pediatrics, Department of Women’s and Children’s Health, Uppsala University, Uppsala, Sweden.
    Farooqi, Aijaz
    Department of Pediatrics, Institute of Clinical Sciences, Umeå University, Umeå, Sweden.
    Fellman, Vineta
    Department of Pediatrics, Clinical Sciences Lund, Lund University, Lund, Sweden.
    Hafström, Maria
    Department of Pediatrics, Institute of Clinical Sciences, The Queen Silvia Children’s Hospital, University of Gothenburg, Göteborg, Sweden; Department of Paediatrics, St Olavs Hospital Trondheim, Trondheim, Norway; Department of Laboratory Medicine, Children's and Women's Health, Norwegian University of Science and Technology, Trondheim, Norway.
    Hellgren, Kerstin
    Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
    Marsál, Karel
    Department of Obstetrics and Gynecology, Clinical Sciences Lund, Lund University, Lund, Sweden.
    Ohlin, Andreas
    Örebro University, School of Medical Sciences. Department of Pediatrics, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Olhager, Elisabeth
    Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
    Stjernqvist, Karin
    Department of Psychology, Lund University, Lund, Sweden.
    Strömberg, Bo
    Section for Pediatrics, Department of Women’s and Children’s Health, Uppsala University, Uppsala, Sweden.
    Ådén, Ulrika
    Department of Women’s and Children’s Health, Karolinska Institutet, Stockholm, Sweden.
    Källén, Karin
    Centre of Reproductive Epidemiology, Lund University, Lund, Sweden.
    Neurodevelopmental Outcomes Among Extremely Preterm Infants 6.5 Years After Active Perinatal Care in Sweden2016In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 170, no 10, p. 954-963Article in journal (Refereed)
    Abstract [en]

    IMPORTANCE: Active perinatal care increases the rate of survival of extremely preterm infants, but there are concerns that improved survival might increase the rate of disabled survivors.

    OBJECTIVE: To determine the neurodevelopmental outcomes of a national cohort of children 6.5 years of age who had been born extremely preterm (<27 weeks' gestational age) in Sweden.

    DESIGN, SETTING, AND PARTICIPANTS: Population-based prospective cohort study of consecutively born extremely preterm infants. All of these infants were born in Sweden during the period from April 1, 2004, to March 31, 2007. Of 707 live-born extremely preterm infants, 486 (68.7%) survived to 6.5 years of age. These children were assessed and compared with matched controls who had been born at term. Comparison estimates were adjusted for demographic differences. Assessments ended in February 2014, and analysis started thereafter.

    MAIN OUTCOMES AND MEASURES: Cognitive ability was measured with the fourth edition of the Wechsler Intelligence Scale for Children (WISC-IV), and the mean (SD) scores of the children who had been born extremely preterm were compared with those of the controls. Clinical examinations and parental questionnaires were used for diagnosis of cerebral palsy, hearing and vision impairments, and cognition for the children who were not assessed with the WISC-IV.

    RESULTS: Of 486 eligible infants who were born extremely preterm, 441 (90.7%) were assessed at 6.5 years of age (59 by medical record review only) alongside 371 controls. The adjusted mean (SD) full-scale WISC-IV score was 14.2 (95% CI, 12.1-16.3) points lower for children who had been born extremely preterm than for controls. Cognitive disability was moderate for 18.8% of extremely preterm children and 2.2% of controls (P < .001), and it was severe for 11.1% of extremely preterm children and 0.3% of controls (P < .001). Cerebral palsy was observed in 9.5% of extremely preterm children and 0.0% of controls (P < .001), blindness was observed in 2.0% of extremely preterm children and 0.0% of controls (P < .001), and hearing impairment was observed in 2.1% of extremely preterm children and 0.5% of controls (P = .07). Overall, 36.1%(95% CI, 31.7%-40.6%) of extremely preterm children had no disability, 30.4%(95% CI 26.3%-34.8%) had mild disability, 20.2%(95% CI, 16.6%-24.2%) had moderate disability, and 13.4%(95% CI, 10.5%-16.9%) had severe disability. For extremely preterm children, moderate or severe overall disability decreased with gestational age at birth (adjusted odds ratio per week, 0.65 [95% CI, 0.54-0.79]; P < .001) and increased from 26.6% to 33.5%(P = .01) for children assessed both at 2.5 and 6.5 years.

    CONCLUSIONS AND RELEVANCE: Of the 441 extremely preterm infants who had received active perinatal care, 293 (66.4%) had no or mild disability at 6.5 years; of the 371 controls, 11 (3.0%) had moderate or severe disability. Disability rates at 6.5 years increased relative to the rates at 2.5 years. Results are relevant for health care professionals and planners, and for clinicians counseling families facing extremely preterm births.

  • 25.
    Serenius, Fredrik
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, Pediatrics. Umea Univ, Inst Clin Sci, Dept Pediat, Umea, Sweden..
    Ewald, Uwe
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, Pediatrics.
    Farooqi, Aijaz
    Umea Univ, Inst Clin Sci, Dept Pediat, Umea, Sweden..
    Fellman, Vineta
    Lund Univ, Clin Sci Lund, Dept Pediat, Lund, Sweden..
    Hafström, Maria
    Univ Gothenburg, Queen Silvia Childrens Hosp, Inst Clin Sci, Dept Pediat, Gothenburg, Sweden.;St Olavs Hosp Trondheim, Dept Paediat, Trondheim, Norway.;Norwegian Univ Sci & Technol, Dept Lab Med Childrens & Womens Hlth, Trondheim, Norway..
    Hellgren, Kerstin
    Karolinska Inst, Dept Clin Neurosci, Stockholm, Sweden..
    Maršál, Karel
    Lund Univ, Clin Sci Lund, Dept Obstet & Gynecol, Lund, Sweden..
    Ohlin, Andreas
    Univ Orebro, Fac Med & Hlth, Dept Pediat, Orebro, Sweden..
    Olhager, Elisabeth
    Linkoping Univ, Dept Clin & Expt Med, Linkoping, Sweden..
    Stjernqvist, Karin
    Lund Univ, Dept Psychol, Lund, Sweden..
    Strömberg, Bo
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Women's and Children's Health, Pediatrics.
    Ådén, Ulrika
    Karolinska Inst, Dept Womens & Childrens Hlth, Stockholm, Sweden..
    Källén, Karin
    Lund Univ, Ctr Reprod Epidemiol, Lund, Sweden..
    Neurodevelopmental Outcomes Among Extremely Preterm Infants 6.5 Years After Active Perinatal Care in Sweden2016In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 170, no 10, p. 954-963Article in journal (Refereed)
    Abstract [en]

    IMPORTANCE Active perinatal care increases the rate of survival of extremely preterm infants, but there are concerns that improved survival might increase the rate of disabled survivors. OBJECTIVE To determine the neurodevelopmental outcomes of a national cohort of children 6.5 years of age who had been born extremely preterm (<27 weeks' gestational age) in Sweden. DESIGN, SETTING, AND PARTICIPANTS Population-based prospective cohort study of consecutively born extremely preterm infants. All of these infants were born in Sweden during the period from April 1, 2004, to March 31, 2007. Of 707 live-born extremely preterm infants, 486 (68.7%) survived to 6.5 years of age. These children were assessed and compared with matched controls who had been born at term. Comparison estimates were adjusted for demographic differences. Assessments ended in February 2014, and analysis started thereafter. MAIN OUTCOMES AND MEASURES Cognitive ability was measured with the fourth edition of the Wechsler Intelligence Scale for Children (WISC-IV), and the mean (SD) scores of the children who had been born extremely preterm were compared with those of the controls. Clinical examinations and parental questionnaires were used for diagnosis of cerebral palsy, hearing and vision impairments, and cognition for the children who were not assessed with the WISC-IV. RESULTS Of 486 eligible infants who were born extremely preterm, 441 (90.7%) were assessed at 6.5 years of age (59 by medical record review only) alongside 371 controls. The adjusted mean (SD) full-scale WISC-IV score was 14.2 (95% CI, 12.1-16.3) points lower for children who had been born extremely preterm than for controls. Cognitive disability was moderate for 18.8% of extremely preterm children and 2.2% of controls (P < .001), and it was severe for 11.1% of extremely preterm children and 0.3% of controls (P < .001). Cerebral palsy was observed in 9.5% of extremely preterm children and 0.0% of controls (P < .001), blindness was observed in 2.0% of extremely preterm children and 0.0% of controls (P < .001), and hearing impairment was observed in 2.1% of extremely preterm children and 0.5% of controls (P = .07). Overall, 36.1%(95% CI, 31.7%-40.6%) of extremely preterm children had no disability, 30.4%(95% CI 26.3%-34.8%) had mild disability, 20.2%(95% CI, 16.6%-24.2%) had moderate disability, and 13.4%(95% CI, 10.5%-16.9%) had severe disability. For extremely preterm children, moderate or severe overall disability decreased with gestational age at birth (adjusted odds ratio per week, 0.65 [95% CI, 0.54-0.79]; P < .001) and increased from 26.6% to 33.5%(P = .01) for children assessed both at 2.5 and 6.5 years. CONCLUSIONS AND RELEVANCE Of the 441 extremely preterm infants who had received active perinatal care, 293 (66.4%) had no or mild disability at 6.5 years; of the 371 controls, 11 (3.0%) had moderate or severe disability. Disability rates at 6.5 years increased relative to the rates at 2.5 years. Results are relevant for health care professionals and planners, and for clinicians counseling families facing extremely preterm births.

  • 26. Tiberio, Stacey S.
    et al.
    Kerr, David C.R.
    Capaldi, Deborah
    Pears, Katherine C.
    Kim, Hyoun K.
    Nowicka, Paulina
    Parental Monitoring of Children’s Media Consumption: The Long-term Influences on Body Mass Index in Children2014In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 168, no 15, p. 414-421Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: To examine the potential influences of maternal and paternal monitoring of child media exposure and children’s general activities on body mass index (BMI) in middle childhood.

    DESIGN, SETTING, AND PARTICIPANTS: A longitudinal study, taken from a subsample of the Three Generational Study, a predominantly white, Pacific Northwest community sample (overall participation rate, 89.6%), included assessments performed from June 1998 to September 2012. Analyses included 112 mothers, 103 fathers, and their 213 children (55.4% girls) at age 5, 7, and/or 9 years. Participation rates ranged from 66.7%to 72.0% of all eligible Three Generational Study children across the 3 assessments.

    EXPOSURES: Parents reported on their general monitoring of their children (whereabouts and activities), specific monitoring of child media exposure, children’s participation in sports and recreational activities, children’s media time (hours per week), annual income, and educational level. Parental BMI was recorded.

    MAIN OUTCOMES AND MEASURES: Predictions to level and change in child BMI z scores were tested.

    RESULTS: Linear mixed-effects modeling indicated that more maternal, but not paternal, monitoring of child media exposure predicted lower child BMI z scores at age 7 years (95%CI, −0.39 to −0.07) and less steeply increasing child BMI z scores from 5 to 9 years (95%CI, −0.11 to −0.01). These effects held when more general parental monitoring, and parent BMI, annual income, and educational level were controlled for. The significant negative effect of maternal media monitoring on children’s BMI z scores at age 7 years was marginally accounted for by the effect of child media time. The maternal media monitoring effect on children’s BMI z score slopes remained significant after adjustment for children’s media time and sports and recreational activity.

    CONCLUSIONS AND RELEVANCE These findings suggest that parental behaviors related to children’s media consumption may have long-term effects on children’s BMI in middle childhood. They underscore the importance of targeting parental media monitoring in efforts to prevent childhood obesity.

  • 27.
    Wernroth, Mona-Lisa
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular epidemiology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Svennblad, Bodil
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, UCR-Uppsala Clinical Research Center.
    Fall, Katja
    Orebro Univ, Sch Med Sci, Clin Epidemiol & Biostat, Orebro, Sweden..
    Fang, Fang
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden..
    Almqvist, Catarina
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden.;Karolinska Univ Hosp, Astrid Lindgren Childrens Hosp, Lung & Allergy Unit, Stockholm, Sweden..
    Fall, Tove
    Uppsala University, Science for Life Laboratory, SciLifeLab. Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Molecular epidemiology.
    Dog Exposure During the First Year of Life and Type 1 Diabetes in Childhood2017In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 171, no 7, p. 663-669Article in journal (Refereed)
    Abstract [en]

    IMPORTANCE The association between early exposure to animals and type 1 diabetes in childhood is not clear. OBJECTIVE To determine whether exposure to dogs during the first year of life is associated with the development of type 1 diabetes in childhood. DESIGN, SETTING, AND PARTICIPANTS A nationwide cohort study utilizing high-quality Swedish national demographic and health registers was conducted. A total of 840 593 children born in Sweden from January 1, 2001, to December 31, 2010, were evaluated. Type 1 diabetes was identified using diagnosis codes from hospitals and dispensed prescriptions of insulin. Cox proportional hazards regression models were used to assess the association between exposure to dogs and risk of type 1 diabetes in childhood. The possible association was further investigated by performing dose-response and breed group-specific analyses. The cohort was followed up until September 30, 2012. Data analysis was conducted from October 15, 2015, to February 8, 2017. EXPOSURES Having a parent who was registered as a dog owner during the child's first year of life. MAIN OUTCOMES AND MEASURES Childhood-onset type 1 diabetes. RESULTS Of the 840 593 children reviewed, 408 272 (48.6%) were girls; mean (SD) age at diagnosis of type 1 diabetes was 5.1 (2.6) years. Dog exposure was identified in 102 035 children (12.1%). Follow-up started at age 1 year, and the children were followed up for as long as 10.7 years (median, 5.5 years). During follow-up, 1999 children developed type 1 diabetes. No association was found between exposure to dogs (adjusted hazard ratio [HR], 1.00; 95% CI, 0.86-1.16) and type 1 diabetes in childhood. The size of the dog (adjusted HR per 10-cm increase in height, 0.96; 95% CI, 0.86-1.06) or number of dogs in the household (1 dog: adjusted HR, 1.07; 95% CI, 0.91-1.26; 2 dogs: 0.79; 95% CI, 0.54-1.15; >= 3 dogs: 0.50; 95% CI, 0.23-1.12; compared with nonexposed children) also was not associated with type 1 diabetes risk. An analysis of children whose parent had type 1 diabetes (210 events) yielded an adjusted HR of 0.71 (95% CI, 0.43-1.17) for dog exposure. CONCLUSIONS AND RELEVANCE In a nationwide study, no evidence supporting an association of register-derived measures of dog exposure with childhood type 1 diabetes was identified.

  • 28.
    Wernroth, Mona-Lisa
    et al.
    Department of Medical Sciences, Molecular Epidemiology and Science for Life Laboratory, Uppsala University, Uppsala, Sweden; Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden.
    Svennblad, Bodil
    Uppsala Clinical Research Center, Uppsala University, Uppsala, Sweden.
    Fall, Katja
    Örebro University, School of Medical Sciences.
    Fang, Fang
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Almqvist, Catarina
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Astrid Lindgren Children’s Hospital, Lung and Allergy Unit, Karolinska University Hospital, Stockholm, Sweden.
    Fall, Tove
    Department of Medical Sciences, Molecular Epidemiology and Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
    Dog Exposure During the First Year of Life and Type 1 Diabetes in Childhood2017In: JAMA pediatrics, ISSN 2168-6203, E-ISSN 2168-6211, Vol. 171, no 7, p. 663-669Article in journal (Refereed)
    Abstract [en]

    IMPORTANCE: The association between early exposure to animals and type 1 diabetes in childhood is not clear.

    OBJECTIVE: To determine whether exposure to dogs during the first year of life is associated with the development of type 1 diabetes in childhood.

    DESIGN, SETTING, AND PARTICIPANTS: A nationwide cohort study utilizing high-quality Swedish national demographic and health registers was conducted. A total of 840 593 children born in Sweden from January 1, 2001, to December 31, 2010, were evaluated. Type 1 diabetes was identified using diagnosis codes from hospitals and dispensed prescriptions of insulin. Cox proportional hazards regression models were used to assess the association between exposure to dogs and risk of type 1 diabetes in childhood. The possible association was further investigated by performing dose-response and breed group-specific analyses. The cohort was followed up until September 30, 2012. Data analysis was conducted from October 15, 2015, to February 8, 2017.

    EXPOSURES: Having a parent who was registered as a dog owner during the child's first year of life.

    MAIN OUTCOMES AND MEASURES: Childhood-onset type 1 diabetes.

    RESULTS: Of the 840 593 children reviewed, 408 272 (48.6%) were girls; mean (SD) age at diagnosis of type 1 diabetes was 5.1 (2.6) years. Dog exposure was identified in 102 035 children (12.1%). Follow-up started at age 1 year, and the children were followed up for as long as 10.7 years (median, 5.5 years). During follow-up, 1999 children developed type 1 diabetes. No association was found between exposure to dogs (adjusted hazard ratio [HR], 1.00; 95% CI, 0.86-1.16) and type 1 diabetes in childhood. The size of the dog (adjusted HR per 10-cm increase in height, 0.96; 95% CI, 0.86-1.06) or number of dogs in the household (1 dog: adjusted HR, 1.07; 95% CI, 0.91-1.26; 2 dogs: 0.79; 95% CI, 0.54-1.15; >= 3 dogs: 0.50; 95% CI, 0.23-1.12; compared with nonexposed children) also was not associated with type 1 diabetes risk. An analysis of children whose parent had type 1 diabetes (210 events) yielded an adjusted HR of 0.71 (95% CI, 0.43-1.17) for dog exposure.

    CONCLUSIONS AND RELEVANCE: In a nationwide study, no evidence supporting an association of register-derived measures of dog exposure with childhood type 1 diabetes was identified.

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