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• W2946935278 abstract "This review summarizes the impact of parental age on children's health outcomes beyond the perinatal period. In the last decades, delayed parenthood with both men and women has become a public health issue. For women, in particular, the size of this delay is substantial. For a few medical conditions, older parental age has a pronounced effect on child morbidity. For most other outcomes, a more modest effect is evident. Although these effects might be limited on an individual level, they have a substantial impact at the level of population health. This review summarizes the impact of parental age on children's health outcomes beyond the perinatal period. In the last decades, delayed parenthood with both men and women has become a public health issue. For women, in particular, the size of this delay is substantial. For a few medical conditions, older parental age has a pronounced effect on child morbidity. For most other outcomes, a more modest effect is evident. Although these effects might be limited on an individual level, they have a substantial impact at the level of population health. Discuss: You can discuss this article with its authors and other readers at https://www.fertstertdialog.com/users/16110-fertility-and-sterility/posts/48165-27786 Discuss: You can discuss this article with its authors and other readers at https://www.fertstertdialog.com/users/16110-fertility-and-sterility/posts/48165-27786 Delayed childbearing is a global phenomenon affecting both women and men. Since the 1970s, increased access to higher education, work outside the home, and improved contraception methods have led more women to delay childbearing, and assisted reproductive technologies have extended the reproductive span. Over the past several decades, the mean age of women giving birth for the first time has increased from the early 20s to the late 20s in Nordic countries (1National Institute for Health and Welfare. Nordic perinatal statistics 2014. Helsinki, Finland.Google Scholar), and the same pattern has been seen in the United States and worldwide (2Matthews T.J. Hamilton B.E. Delayed childbearing: more women are having their first child later in life.NCHS Data Brief. 2009; 21: 1-8Google Scholar). Men have followed a similar pattern, and paternal age has risen in parallel (3Khandwala Y.S. Zhang C.A. Lu Y. Eisenberg M.L. The age of fathers in the USA is rising: an analysis of 168 867 480 births from 1972 to 2015.Hum Reprod. 2017; 32: 2110-2116Google Scholar). In an analysis of over 168 million U.S. births, Khandwala et al. (3Khandwala Y.S. Zhang C.A. Lu Y. Eisenberg M.L. The age of fathers in the USA is rising: an analysis of 168 867 480 births from 1972 to 2015.Hum Reprod. 2017; 32: 2110-2116Google Scholar) found that the mean paternal age increased from 27.4 to 30.9 years over a 40-year period. This rise in age was observed among all races/ethnicities, for all levels of education, and across all geographic regions. The rise in paternal age was even more pronounced among college-educated men. A similar trend has been found in European countries such as Germany and the United Kingdom (4Kuhnert B. Nieschlag E. Reproductive functions of the ageing male.Hum Reprod Update. 2004; 10: 327-339Google Scholar, 5Bray I. Gunnell D. Davey Smith G. Advanced paternal age: how old is too old?.J Epidemiol Community Health. 2006; 60: 851-853Google Scholar). The association of older maternal age with adverse perinatal outcomes is well established (6Cnattingius S. Forman M.R. Berendes H.W. Isotalo L. Delayed childbearing and risk of adverse perinatal outcome: a population-based study.JAMA. 1992; 268: 886-890Google Scholar, 7Lawlor D.A. Mortensen L. Andersen A.M. Mechanisms underlying the associations of maternal age with adverse perinatal outcomes: a sibling study of 264 695 Danish women and their firstborn offspring.Int J Epidemiol. 2011; 40: 1205-1214Google Scholar), but less is known about the influence of the mother's age on the child's health outcomes and morbidity. The effect of father's age on perinatal outcomes and morbidity is even less studied, although a systematic review has been recently published (8Oldereid N.B. Wennerholm U.B. Pinborg A. Loft A. Laivuori H. Petzold M. et al.The effect of paternal factors on perinatal and paediatric outcomes: a systematic review and meta-analysis.Hum Reprod Update. 2018; 24: 320-389Google Scholar). The latter found serious health effects in child outcomes with increased paternal age, but the magnitude of these effects seemed modest. Our review summarizes the effects of parental age, both maternal and paternal, on health outcomes and morbidity in children, focusing on spontaneous conceptions and excluding the perinatal period. The following areas will be covered in this review: chromosomal aberrations, particular trisomy 21, birth defects, cancer, leukemia, Hodgkin/non-Hodgkin lymphoma, central nervous system (CNS) tumors, diabetes mellitus type 1, asthma, cerebral paresis (CP), neurodevelopment, autism/attention deficit hyperactivity disorder (ADHD), schizophrenia, bipolar disorders, and mental retardation. Risk estimates will be presented, and possible causal mechanisms (if known) will be elucidated. Further suggestions for improvement in or avoidance of adverse outcomes will be discussed. For maternal outcomes, we searched the PubMed and Cochrane databases up to October 5, 2018. For paternal outcomes, we used the search provided by a previous systematic review (8Oldereid N.B. Wennerholm U.B. Pinborg A. Loft A. Laivuori H. Petzold M. et al.The effect of paternal factors on perinatal and paediatric outcomes: a systematic review and meta-analysis.Hum Reprod Update. 2018; 24: 320-389Google Scholar) and added literature published up to October 5, 2018. The exposures were maternal and paternal age. The outcomes were chromosomal aberrations (trisomy 21, other chromosomal aberrations), birth defects (any birth defects, heart defects, orofacial cleft, gastroschisis, spina bifida, hypospadias, esophageal atresia), cancer, leukemia, Hodgkin/non-Hodgkin lymphoma, CNS tumors, diabetes mellitus type 1, asthma, cerebral paresis (CP), neurodevelopment, autism/ADHD, schizophrenia, bipolar disorders, and mental retardation. The terms used in the search were “Maternal Age”[Mesh] OR maternal age[ti] parental age[ti] “Paternal Age”[Mesh] OR paternal age[ti] “Congenital Abnormalities”[Mesh] OR congenital malformat*[tiab] OR congenital abnormal*[tiab] OR birth defect*[tiab] OR children[tiab] OR child[tiab] OR childhood[tiab] OR “Autism Spectrum Disorder”[Mesh] OR “Autistic Disorder”[Mesh] OR “Schizophrenia”[Mesh] OR autism[tiab] OR autistic[tiab] OR schizophrenia[tiab]. We added works from manually searching the references of the identified articles. The literature search was performed by a professional librarian (T. Svanberg) in collaboration with one of the authors (C.B.). All three authors (C.B., A.P., and U.B.W.) screened the abstracts and full papers. Original studies published in English were included. In cases of double publication, the most recent study was included. Studies with a control group and case series with more than 100 patients were included; for rare diseases, the studies with fewer cases were also included. Systematic reviews and narrative reviews were included as well. Studies published only as abstracts or case reports were excluded, and studies of paternal outcomes were mostly excluded if they were not adjusted for maternal age and vice versa. No formal grading of the quality of the articles was performed. The search strategy identified 6,355 articles, of which 85 were selected for inclusion in this review. Trisomy 21 (Down syndrome) occurs when trisomy or a translocation results in three instead of two copies of chromosome 21 or the specific area of chromosome 21 implicated in causing Down syndrome. It is the most common cause of congenital mental disability and is often associated with several birth defects, particularly in the cardiovascular system, as well as an increased risk of leukemia, diabetes, and thyroid diseases. The incidence, before screening, is estimated to around 1 in 800 live births, and it occurs without respect to race, geographical location, or socioeconomic condition. Prenatal diagnosis can allow for preparation for life with an affected child or for an offer to terminate the pregnancy. Down syndrome was first described by J.L. Down 1866 (9Down J.L. Observations on an ethnic classification of idiots. 1866.Ment Retard. 1995; 33: 54-56Google Scholar). Several years later, Penrose (10Penrose L.S. The relative effects of paternal and maternal age in mongolism.J Genet. 1933; 27: 219-224Google Scholar) demonstrated that maternal age was the key determining factor for Down syndrome. After the advent of karyotyping, the etiology of Down syndrome was identified as an extra chromosome 21 (11Jacobs P.A. Baikie A.G. Court Brown W.M. Strong J.A. The somatic chromosomes in mongolism.Lancet. 1959; 1: 710Google Scholar). Large cohort studies from the 1960s to 1970s before the widespread use of prenatal screening demonstrated a dramatic increase in the rate of Down syndrome by maternal age. These studies, originating from Sweden and the United States (12Hook E.B. Rates of chromosome abnormalities at different maternal ages.Obstet Gynecol. 1981; 58: 282-285Google Scholar, 13Hook E.B. Lindsjo A. Down syndrome in live births by single year maternal age interval in a Swedish study: comparison with results from a New York State study.Am J Hum Genet. 1978; 30: 19-27Google Scholar), presented incidence rates by 1-year interval of maternal age, starting from around 0.5 in 1,000 at the age of 20, 10 in 1,000 at the age of 40, and 100 in 1,000 in the upper 40s. A large U.S. study by Hook et al. (14Hook E.B. Cross P.K. Regal R.R. The frequency of 47,+21,47,+18, and 47,+13 at the uppermost extremes of maternal ages: results on 56,094 fetuses studied prenatally and comparisons with data on livebirths.Hum Genet. 1984; 68: 211-220Google Scholar), which included more than 56,000 fetuses without any known risk factor other than maternal age, demonstrated an even higher incidence at the most advanced maternal ages, with an exponential rise particularly after the age of 35 years. The mechanism behind the nondisjunction of chromosome 21 has been suggested to be a maternal age-dependent mechanism involving reduced recombination occurring during oocyte meiosis I. Two other chromosomal trisomies—47,+18 (Edwards syndrome) and 47,+13 (Patau syndrome)—follow the age same pattern but at a lower incidence level (12Hook E.B. Rates of chromosome abnormalities at different maternal ages.Obstet Gynecol. 1981; 58: 282-285Google Scholar, 14Hook E.B. Cross P.K. Regal R.R. The frequency of 47,+21,47,+18, and 47,+13 at the uppermost extremes of maternal ages: results on 56,094 fetuses studied prenatally and comparisons with data on livebirths.Hum Genet. 1984; 68: 211-220Google Scholar). Only 6% to 10% of all trisomy 21 cases are due to errors in spermatogenesis (15Sherman S.L. Freeman S.B. Allen E.G. Lamb N.E. Risk factors for nondisjunction of trisomy 21.Cytogenet Genome Res. 2005; 111: 273-280Google Scholar). Oldereid et al. (8Oldereid N.B. Wennerholm U.B. Pinborg A. Loft A. Laivuori H. Petzold M. et al.The effect of paternal factors on perinatal and paediatric outcomes: a systematic review and meta-analysis.Hum Reprod Update. 2018; 24: 320-389Google Scholar) summarized the studies in their meta-analysis of data from the Nordic countries (8Oldereid N.B. Wennerholm U.B. Pinborg A. Loft A. Laivuori H. Petzold M. et al.The effect of paternal factors on perinatal and paediatric outcomes: a systematic review and meta-analysis.Hum Reprod Update. 2018; 24: 320-389Google Scholar). A small but statistically significant increase was noted by high paternal age (≥40 years) (pooled estimate 1.13; 95% confidence interval [CI], 1.05–1.23). A large study from the EUROCAT working group (16Loane M. Dolk H. Morris J.K. Maternal age-specific risk of non-chromosomal anomalies.BJOG. 2009; 116: 1111-1119Google Scholar), which included nearly 39,000 children with birth defects from 15 European countries from 2000 to 2004, showed that the relative risk for various birth defects varied by maternal age. For gastroschisis, anencephaly, and nervous and digestive system defects in children, the risks were higher for young mothers (teenagers). Older mothers had a greater risk of children with encephalocele, esophageal atresia, and thanatophoric dwarfism. A U-shaped risk level was observed in two large U.S. studies (17Gill S.K. Broussard C. Devine O. Green R.F. Rasmussen S.A. Reefhuis J. Association between maternal age and birth defects of unknown etiology: United States, 1997–2007.Birth Defects Res A Clin Mol Teratol. 2012; 94: 1010-1018Google Scholar, 18Reefhuis J. Honein M.A. Maternal age and non-chromosomal birth defects, Atlanta—1968–2000: teenager or thirty-something, who is at risk?.Birth Defects Res A Clin Mol Teratol. 2004; 70: 572-579Google Scholar) that included 38,000 and 23,000 children with birth defects, respectively, and adding hypospadias and heart defects for the older group. The odds ratio (OR) varied between 1.5 and 7.0 for young women (<20 years), and 1.1 and 1.9 for older women (>35–40 years). The systematic review/meta-analysis by Oldereid et al. (8Oldereid N.B. Wennerholm U.B. Pinborg A. Loft A. Laivuori H. Petzold M. et al.The effect of paternal factors on perinatal and paediatric outcomes: a systematic review and meta-analysis.Hum Reprod Update. 2018; 24: 320-389Google Scholar) found a small but statistically significantly increased risk of any birth defect with higher paternal age (≥35 years) (pooled estimate 1.05; 95% CI, 1.02–1.07). A large study from the United States found a statistically significant association between maternal age and total heart defects and found higher rates for several individual congenital heart defects for mothers older than 35 years (adjusted prevalence ratio [aPR] 1.17; 95% CI, 1.05–1.31) (19Miller A. Riehle-Colarusso T. Siffel C. Frias J.L. Correa A. Maternal age and prevalence of isolated congenital heart defects in an urban area of the United States.Am J Med Genet A. 2011; 155a: 2137-2145Google Scholar), although a study from the United Kingdom could not confirm that result (20Best K.E. Rankin J. Is advanced maternal age a risk factor for congenital heart disease?.Birth Defects Res A Clin Mol Teratol. 2016; 106: 461-467Google Scholar). In the meta-analysis from Oldereid et al. (8Oldereid N.B. Wennerholm U.B. Pinborg A. Loft A. Laivuori H. Petzold M. et al.The effect of paternal factors on perinatal and paediatric outcomes: a systematic review and meta-analysis.Hum Reprod Update. 2018; 24: 320-389Google Scholar), no association was identified between paternal age and congenital heart defects. Several large, high-quality studies have investigated the association between parental age and orofacial clefts. A meta-analysis from 2012 (21Herkrath A.P. Herkrath F.J. Rebelo M.A. Vettore M.V. Parental age as a risk factor for non-syndromic oral clefts: a meta-analysis.J Dent. 2012; 40: 3-14Google Scholar) found both maternal and paternal age were associated with orofacial clefts, with higher rates in offspring occurring particularly after the parental age of 40. The effect of maternal age was summarized in a meta-analysis from 2002 (22Vieira A.R. Orioli I.M. Murray J.C. Maternal age and oral clefts: a reappraisal.Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2002; 94: 530-535Google Scholar), which found no association between maternal age and cleft lip or cleft palate. Later, large studies from Denmark (23Bille C. Skytthe A. Vach W. Knudsen L.B. Andersen A.M. Murray J.C. et al.Parent’s age and the risk of oral clefts.Epidemiology. 2005; 16: 311-316Google Scholar) and Norway (24Berg E. Lie R.T. Sivertsen A. Haaland O.A. Parental age and the risk of isolated cleft lip: a registry-based study.Ann Epidemiol. 2015; 25: 942-947.e1Google Scholar) found an association between older maternal age and orofacial clefts. However, in the Danish study the association between age and cleft palate disappeared after adjustment for paternal age, and both studies suggested that the increase in orofacial clefts with age was only apparent when the age of both parents was high. Paternal age was investigated in the recent systematic review and meta-analysis of Oldereid et al. (8Oldereid N.B. Wennerholm U.B. Pinborg A. Loft A. Laivuori H. Petzold M. et al.The effect of paternal factors on perinatal and paediatric outcomes: a systematic review and meta-analysis.Hum Reprod Update. 2018; 24: 320-389Google Scholar) who found a small but statistically significant increase in children's orofacial clefts for fathers older than 45 years (pooled estimate 1.14; 95% CI, 1.02–1.29). Gastroschisis is a congenital abdominal wall defect that results in intestines extruding into the amniotic space. It occurs very early in pregnancy, 3 to 5 weeks after conception. Globally there is an increasing incidence in gastroschisis, reaching a level of 4 to 5 per 10,000 live births (25Holland A.J. Walker K. Badawi N. Gastroschisis: an update.Pediatr Surg Int. 2010; 26: 871-878Google Scholar). A huge number of studies have been published that have investigated the association between maternal age and gastroschisis; a clear increase was found with young maternal age (18Reefhuis J. Honein M.A. Maternal age and non-chromosomal birth defects, Atlanta—1968–2000: teenager or thirty-something, who is at risk?.Birth Defects Res A Clin Mol Teratol. 2004; 70: 572-579Google Scholar, 26Baer R.J. Chambers C.D. Jones K.L. Shew S.B. MacKenzie T.C. Shaw G.M. et al.Maternal factors associated with the occurrence of gastroschisis.Am J Med Genet A. 2015; 167: 1534-1541Google Scholar, 27Kazaura M.R. Lie R.T. Irgens L.M. Didriksen A. Kapstad M. Egenaes J. et al.Increasing risk of gastroschisis in Norway: an age-period-cohort analysis.Am J Epidemiol. 2004; 159: 358-363Google Scholar). In a large study from the EUROCAT working group (16Loane M. Dolk H. Morris J.K. Maternal age-specific risk of non-chromosomal anomalies.BJOG. 2009; 116: 1111-1119Google Scholar) the relative risk of gastroschisis with mothers younger than 20 years was six times higher compared with mothers aged 25 to 29 years (adjusted relative risk [aRR] 6.32; 95% CI, 4.75–8.41). Two studies, from the United States and Canada (28Archer N.P. Langlois P.H. Suarez L. Brender J. Shanmugam R. Association of paternal age with prevalence of selected birth defects.Birth Defects Res A Clin Mol Teratol. 2007; 79: 27-34Google Scholar, 29Yang Q. Wen S.W. Leader A. Chen X.K. Lipson J. Walker M. Paternal age and birth defects: how strong is the association?.Hum Reprod. 2007; 22: 696-701Google Scholar), found a statistically significantly higher risk, up to 1.5 times, for gastroschisis in offspring when the father is a young man. This was confirmed in the meta-analysis by Oldereid et al. (8Oldereid N.B. Wennerholm U.B. Pinborg A. Loft A. Laivuori H. Petzold M. et al.The effect of paternal factors on perinatal and paediatric outcomes: a systematic review and meta-analysis.Hum Reprod Update. 2018; 24: 320-389Google Scholar) (pooled estimate 0.88; 95% CI, 0.78–1.00) (≥35 years). Although the risk increased with younger fathers, it was much less pronounced than it was for young mothers. Large studies, both from the United States (18Reefhuis J. Honein M.A. Maternal age and non-chromosomal birth defects, Atlanta—1968–2000: teenager or thirty-something, who is at risk?.Birth Defects Res A Clin Mol Teratol. 2004; 70: 572-579Google Scholar) and Europe (16Loane M. Dolk H. Morris J.K. Maternal age-specific risk of non-chromosomal anomalies.BJOG. 2009; 116: 1111-1119Google Scholar) have found an inverse association between maternal age and the risk for anencephaly, with teenage mothers showing the highest risks (relative risk [RR]/OR 1.7–1.8) compared with mothers age 25 to 29 years. A study combining data from the Norwegian registry and Russia confirmed these findings. Further, an inverse age association with spina bifida was found in in the Russian population (30Petrova J.G. Vaktskjold A. The incidence of neural tube defects in Norway and the Arkhangelskaja Oblast in Russia and the association with maternal age.Acta Obstet Gynecol Scand. 2009; 88: 667-672Google Scholar). The recent meta-analysis from Oldereid et al. (8Oldereid N.B. Wennerholm U.B. Pinborg A. Loft A. Laivuori H. Petzold M. et al.The effect of paternal factors on perinatal and paediatric outcomes: a systematic review and meta-analysis.Hum Reprod Update. 2018; 24: 320-389Google Scholar) found no association between spina bifida and paternal age. Hypospadias is one of the most common congenital birth defects, and its etiology is largely unknown. The prevalence of hypospadias shows large geographical variation, ranging from 2.0 to 43 in 10,000 births (31Bergman J.E. Loane M. Vrijheid M. Pierini A. Nijman R.J. Addor M.C. et al.Epidemiology of hypospadias in Europe: a registry-based study.World J Urol. 2015; 33: 2159-2167Google Scholar). The association between maternal age and hypospadias is controversial. In a large study from EUROCAT (31Bergman J.E. Loane M. Vrijheid M. Pierini A. Nijman R.J. Addor M.C. et al.Epidemiology of hypospadias in Europe: a registry-based study.World J Urol. 2015; 33: 2159-2167Google Scholar) that included 5.8 million births, the prevalence of hypospadias was 18.6 in 10,000 births, and no association with maternal age was identified. By contrast, two large studies from the United States (32Fisch H. Golden R.J. Libersen G.L. Hyun G.S. Madsen P. New M.I. et al.Maternal age as a risk factor for hypospadias.J Urol. 2001; 165: 934-936Google Scholar, 33Porter M.P. Faizan M.K. Grady R.W. Mueller B.A. Hypospadias in Washington state: maternal risk factors and prevalence trends.Pediatrics. 2005; 115: e495-e499Google Scholar) found a statistically significant association with advanced maternal age (>35 years) (OR 1.5–1.8). Few studies were identified that addressed a possible association between hypospadias and paternal age, and no clear results were found. Large studies from both the United States (17Gill S.K. Broussard C. Devine O. Green R.F. Rasmussen S.A. Reefhuis J. Association between maternal age and birth defects of unknown etiology: United States, 1997–2007.Birth Defects Res A Clin Mol Teratol. 2012; 94: 1010-1018Google Scholar) and Europe (16Loane M. Dolk H. Morris J.K. Maternal age-specific risk of non-chromosomal anomalies.BJOG. 2009; 116: 1111-1119Google Scholar) found a two to three times increased risk for mothers >35–40 years compared with younger women (adjusted OR [aOR] 2.9; 95% CI, 1.7–4.9; and aRR 2.10; 95% CI, 1.32–5.08, respectively). This finding was confirmed by a Swedish study (OR 3.04; 95% CI, 1.37–6.74) (34Oddsberg J. Jia C. Nilsson E. Ye W. Lagergren J. Influence of maternal parity, age, and ethnicity on risk of esophageal atresia in the infant in a population-based study.J Pediatr Surg. 2008; 43: 1660-1665Google Scholar). Increased maternal age is associated with an increase in chromosomal aberrations, in particular trisomy 21, and a slight increase is found with higher paternal ages. For birth defects, the most pronounced age effect is found for gastroschisis, where younger maternal age is associated with a substantial increase; this increase is also found for younger fathers, albeit to a lesser extent. Anencephaly also seems to be associated with young maternal age. The current literature suggests an association between high paternal age and orofacial clefts, but this increase seems to be small. No independent association appears to exist between maternal age and orofacial clefts. Esophageal atresia has been found to be associated with older mothers. Cancer is the leading cause of death from disease among children ages 0 to 14 years. It affects approximately 1 in 435 children under 15 years of age (35Howard S.C. Metzger M.L. Wilimas J.A. Quintana Y. Pui C.H. Robison L.L. et al.Childhood cancer epidemiology in low-income countries.Cancer. 2008; 112: 461-472Google Scholar). Older parental age has been associated with cancer in children, particularly leukemia and CNS tumors (36Johnson K.J. Carozza S.E. Chow E.J. Fox E.E. Horel S. McLaughlin C.C. et al.Parental age and risk of childhood cancer: a pooled analysis.Epidemiology. 2009; 20: 475-483Google Scholar, 37Yip B.H. Pawitan Y. Czene K. Parental age and risk of childhood cancers: a population-based cohort study from Sweden.Int J Epidemiol. 2006; 35: 1495-1503Google Scholar). Two large studies investigated the risk of any childhood cancer as well as different types of cancers (38Contreras Z.A. Hansen J. Ritz B. Olsen J. Yu F. Heck J.E. Parental age and childhood cancer risk: a Danish population-based registry study.Cancer Epidemiol. 2017; 49: 202-215Google Scholar, 39Wang R. Metayer C. Morimoto L. Wiemels J.L. Yang J. DeWan A.T. et al.Parental age and risk of pediatric cancer in the offspring: a population-based record-linkage study in California.Am J Epidemiol. 2017; 186: 843-856Google Scholar). The Danish study included 5,856 children with cancer diagnosed at ages younger than 16 years from 1968 to 2015 (38Contreras Z.A. Hansen J. Ritz B. Olsen J. Yu F. Heck J.E. Parental age and childhood cancer risk: a Danish population-based registry study.Cancer Epidemiol. 2017; 49: 202-215Google Scholar). The offspring of older mothers aged 35–39 and ≥40 years were at increased risk of any cancer (the reference group was 25 to 29 years). Per 5-year increase in age, an increase was noted when adjusted for paternal age (aOR 1.05; 95% CI, 1.01–1.09) (38Contreras Z.A. Hansen J. Ritz B. Olsen J. Yu F. Heck J.E. Parental age and childhood cancer risk: a Danish population-based registry study.Cancer Epidemiol. 2017; 49: 202-215Google Scholar). In a large population-based record-linkage study from the United States with 23,419 cases of cancer between 0 and 19 years of age and 87,593 controls, increasing maternal age was associated with a higher risk of childhood cancer (39Wang R. Metayer C. Morimoto L. Wiemels J.L. Yang J. DeWan A.T. et al.Parental age and risk of pediatric cancer in the offspring: a population-based record-linkage study in California.Am J Epidemiol. 2017; 186: 843-856Google Scholar). Compared with children born to mothers aged 20–24 years, those born to mothers in older age groups had a 13% to 36% higher risk of childhood cancer. Per 5-year increase in maternal age and after adjustment including paternal age, a statistically significant increase was noted (aOR 1.06; 95% CI, 1.04–1.09). In a systematic review and meta-analysis on paternal age and risk of cancer in offspring, higher paternal age was not associated with a risk of childhood cancer (8Oldereid N.B. Wennerholm U.B. Pinborg A. Loft A. Laivuori H. Petzold M. et al.The effect of paternal factors on perinatal and paediatric outcomes: a systematic review and meta-analysis.Hum Reprod Update. 2018; 24: 320-389Google Scholar). Further, a Danish study (38Contreras Z.A. Hansen J. Ritz B. Olsen J. Yu F. Heck J.E. Parental age and childhood cancer risk: a Danish population-based registry study.Cancer Epidemiol. 2017; 49: 202-215Google Scholar) found no association between paternal age and cancer. A U.S. study (39Wang R. Metayer C. Morimoto L. Wiemels J.L. Yang J. DeWan A.T. et al.Parental age and risk of pediatric cancer in the offspring: a population-based record-linkage study in California.Am J Epidemiol. 2017; 186: 843-856Google Scholar) found that compared with children born to fathers aged 20–24 years, those born to fathers in older age groups had a 5% to 15% higher risk of childhood cancer; per 5-year increase in paternal age and after adjustment including maternal age, a statistically significant increase was noted (aOR 1.03; 95% CI, 1.02–1.05). Acute lymphoblastic leukemia (ALL), the most common childhood cancer, accounts for 25% to 30% of all cancers in children younger than 15 years (40Steliarova-Foucher E. Colombet M. Ries L.A.G. Moreno F. Dolya A. Bray F. et al.International incidence of childhood cancer, 2001–10: a population-based registry study.Lancet Oncol. 2017; 18: 719-731Google Scholar). Childhood ALL is thought to be related to perinatal factors such as birth anthropometrics, early infections, and prelabor cesarean delivery. Furthermore, increased parental age has been suggested as a potential risk factor for childhood ALL (36Johnson K.J. Carozza S.E. Chow E.J. Fox E.E. Horel S. McLaughlin C.C. et al.Parental age and risk of childhood cancer: a pooled analysis.Epidemiology. 2009; 20: 475-483Google Scholar). A systematic review and meta-analysis from 2015 that included 69 case control studies and 8 cohort studies found an increased risk of ALL in the offspring of older mothers, when examining age both as a categorical (pooled RR 1.14; 95% CI 1.02–1.27 for <35 versus ≥35 years) and as a continuous variable (pooled RR 1.05; 95% CI, 1.01–1.10 per 5-year increments) (41Sergentanis T.N. Thomopoulos T.P. Gialamas S.P. Karalexi M.A. Biniaris-Georgallis S.I. Kontogeorgi E. et al.Risk for childhood leukemia associated with maternal and paternal age.Eur J Epidemiol. 2015; 30: 1229-1261Google Scholar). Three registry-based, record-linkage, nested case control studies from Denmark and the United States have reported on ALL and increasing maternal age (38Contreras Z.A. Hansen J. Ritz B. Olsen J. Yu F. Heck J.E. Parental age and childhood cancer risk: a Danish population-based registry study.Cancer Epidemiol. 2017; 49: 202-215Google Scholar, 39Wang R. Metayer C. Morimoto L. Wiemels J.L. Yang J. DeWan A.T. et al.Parental age and risk of pediatric cancer in the offspring: a population-based record-linkage study in California.Am J Epidemiol. 2017; 186: 843-856Google Scholar, 42Marcotte E.L. Druley T.E. Johnson K.J. Richardson M. v" @default.
• W2946935278 created "2019-06-07" @default.
• W2946935278 creator A5037649823 @default.
• W2946935278 creator A5048440817 @default.
• W2946935278 creator A5085234723 @default.
• W2946935278 date "2019-06-01" @default.
• W2946935278 modified "2023-09-26" @default.
• W2946935278 title "Parental age and child outcomes" @default.
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• W2946935278 doi "https://doi.org/10.1016/j.fertnstert.2019.04.026" @default.
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