Adverse effects of parental smoking during pregnancy in urban and rural areas Risk of childhood leukemia associated with parental smoking and alcohol consumption prior to conception and during pregnancy: the cross-Canada childhood leukemia study Paternal Age and Congenital Malformations in Offspring in California, 1989–2002 Risk factors for astrocytic glioma and primitive neuroectodermal tumor of the brain in young children: a report from the Children's Cancer Group. Maternal and Paternal Smoking During Pregnancy and Risk of ADHD Symptoms in Offspring: Testing for Intrauterine Effects Maternal Smoking and Child Psychological Problems: Disentangling Causal and Noncausal Effects Parental, fetal, and infant risk factors for preschool overweight: the Generation R Study Parental age and risk of bipolar disorder in offspring Paternal age and sporadic neurofibromatosis 1: a case-control study and consideration of the methodologic issues. Parental Obesity and Risk of Autism Spectrum Disorder Advanced Maternal Age and Adverse Perinatal Outcome Parental smoking during pregnancy and cardiovascular structures and function in childhood: the Generation R Study. Parental smoking during pregnancy, early growth, and risk of obesity in preschool children: the Generation R Study. Early life risk factors for obesity in childhood: cohort study Risk factors for autism: perinatal factors, parental psychiatric history, and socioeconomic status. Prenatal exposure to parents' smoking and childhood cancer. Advancing paternal age and bipolar disorder. Effects of paternal and maternal lifestyle factors on pregnancy complications and perinatal outcome. A population-based birth-cohort study: the GECKO Drenthe cohort. Advanced paternal age and risk of fetal death: a cohort study. Advanced paternal age and mortality of offspring under 5 years of age: a register-based cohort study. Perinatal characteristics and retinoblastoma Parental Tobacco and Alcohol Use and Risk of Hepatoblastoma in Offspring: A Report from the Children's Oncology Group Parental smoking and alcohol consumption and risk of neuroblastoma. Passive smoking and behavioural problems in children: results from the LISAplus prospective birth cohort study. Advanced Paternal Age and Risk of Musculoskeletal Congenital Anomalies in Offspring. Paternal age and risk of schizophrenia in adult offspring. Parental Age at Birth and Risk of Hematological Malignancies in Older Adults. Paternal influences on birthweight Parental anthropometrics, early growth and the risk of overweight in pre-school children: the Generation R Study. Parental cigarette smoking and the risk of congenital heart septal defects. Increased paternal age in CHARGE association Prenatal exposure to tobacco smoke and childhood brain tumors: results from the United States West Coast childhood brain tumor study. Paternal age effect in Down's syndrome Prediction of obesity in children at 5 years: a cohort study.
Background Parental smoking during pregnancy is associated with lower birthweight and gestational age , as well as with the risks of low birthweight ( LBW ) and preterm birth . The present study aims to assess the association of  parental smoking during pregnancy with birth outcomes in urban and rural areas . Methods This was a secondary analysis of data collected in the Indonesia Family Life Survey , between 1993 and 2007 , the first national prospect i ve longitudinal cohort study in Indonesia . Retrospective data of parental smoking habits , socioeconomic status , pregnancy history and birth outcomes were collected from parents with children aged 0 to 5 years ( n = 3789 ) . We assessed the relationships between the amount of  parental smoking during pregnancy with birthweight ( LBW ) and with gestational age ( preterm birth ) . Results We found a significant reduction in birthweight to be associated with maternal smoking . Smoking ( except for paternal smoking ) was associated with a decrease in the gestational age and an increased risk of preterm birth . Different associations were found in urban area , infants born to smoking fathers and both smoking parents ( > 20 cigarettes/day for both cases ) had a significant reduction in birthweight and gestational age as well as an increased risk of LBW and preterm birth . Conclusions Residence was found to be an effect modifier of the relation between parental smoking during pregnancy , amount of parental smoking , and birth outcomes on their children . Smoking cessation/reduction and smoking intervention program should be advised and prioritized to the area that is more prone to the adverse birth outcomes Objective As part of a larger case – control study , the authors evaluated risk of  childhood leukemia  relative to parental self-reported smoking and alcohol consumption . Methods Children 0–14 years of age diagnosed with leukemia between 1990 and 1994 were ascertained through population -based sources at the time of diagnosis . For each participating case , an age , gender , and area-matched control was r and omly selected from provincial government health insurance rolls . Risk factor information was obtained through personal interviews with each child ’s parents . Conditional logistic regression models were used to examine risk of leukemia associated with parental smoking and drinking . Results Maternal alcohol consumption prior to conception ( OR = 1.37 , 95 % CI , 0.99–1.90 ) and during pregnancy ( OR = 1.39 , 95 % CI , 1.01–1.93 ) was associated with an excess risk of childhood leukemia , with a positive dose-response trend for increasing weekly consumption ( p < 0.05 ) . Similar results were observed for children diagnosed with acute lymphoblastic leukemia  ( ALL ) . Odds ratios for maternal cigarette smoking before and during pregnancy were consistently elevated above one , but not statistically significant . No relationship was observed with paternal drinking or smoking in the perinatal period . Conclusions Our study suggests that maternal alcohol drinking before or during pregnancy may contribute to an increased risk of childhood leukemia This study examined the association between  paternal age  and a wide range of structural birth defects . Data were drawn from The California Birth Defects Monitoring Program , a population -based active surveillance system for collecting information on infants and fetuses with defects born between 1989 and 2002 . The analysis included 46,114 cases with defects , plus a r and om sample of 36,838 non-malformed births . After adjustment for maternal age , risks of anomalies of the nervous system for 38 and 42 year-old fathers , as compared to 29 year-old fathers , were 1.05-fold [ 1.00 , 1.11 ] and 1.10-fold [ 1.02 , 1.18 ] higher , respectively . Similar results were observed for anomalies of the limbs , where 38 and 42 year-old fathers had a 1.06-fold [ 1.02 , 1.11 ] and 1.11-fold [ 1.05 , 1.18 ] higher risk , respectively . Risks of anomalies of the integument were 1.05-fold [ 1.00 , 1.09 ] and 1.10-fold [ 1.03 , 1.16 ] higher for 38 and 42 year olds , respectively . Young paternal age , i.e. , less than 29 years , was associated with an increased risk of amniotic b and s ( OR : 0.87 [ 0.78 , 0.97 ] ) , pyloric stenosis ( OR : 0.93 [ 0.90 , 0.96 ] ) and anomalies of the great veins ( OR : 0.93 [ 0.87 , 1.00 ] ) . In sum , both advanced and young paternal age was associated with select birth defects in California between 1989 and 2002 We conducted a matched case-control study to investigate risk factors for the two most common types of brain tumors in children , astrocytic glioma and primitive neuroectodermal tumor ( PNET ) . Since the study focused on gestational exposures , we restricted it to young children because these exposures would be expected to act early in life . Parents of 155 astrocytic glioma cases , 166 PNET cases , and controls identified by r and om digit dialing completed telephone interviews . Few associations occurred with the hypothesized risk factors , which were gestational exposure to alcohol , hair coloring products , farms , and substances containing N-nitroso compounds ( passive smoking , makeup , incense , new cars , pacifiers , baby bottles , beer ) . Of the products studied that contain N-nitroso compounds , only beer was associated with a significantly increased risk of either tumor type [ odds ratio ( OR ) for PNET = 4.0 ; 95 % confidence interval ( CI ) , 1.1 - 22.1 ; P = 0.04 ] . Elevated ORs for PNET were observed for farm residence of the mother during the pregnancy ( OR = 3.7 ; 95 % CI , 0.8 - 23.9 ; P = 0.06 ) and of the child for at least a year ( OR = 5.0 ; 95 % CI , 1.1 - 46.8 ; P = 0.04 ) . Significant associations with astrocytoma were observed for mother 's use of kerosene ( OR = 8.9 ; 95 % CI , 1.1 - 71.1 ; P = 0.04 ) and birth by Caesarean section ( OR = 1.8 ; 95 % CI , 1.1 - 3.2 ; P = 0.03 ) . History of miscarriage was associated with a lower risk of PNET ( OR = 0.5 ; 95 % CI , 0.3 - 0.9 ; P = 0.02 ) . ( ABSTRACT TRUNCATED AT 250 WORDS Maternal smoking during pregnancy is associated with  attention deficit hyperactivity disorder ( ADHD ) in offspring . It is assumed by many that this association is causal . Others suggest that observed associations are due to unmeasured genetic factors or other confounding factors . The authors compared risks of maternal smoking during pregnancy with those of paternal smoking during pregnancy . With a causal intrauterine effect , no independent association should be observed between paternal smoking and offspring ADHD . If the association is due to confounding factors , risks of offspring ADHD should be of similar magnitudes regardless of which parent smokes . This hypothesis was tested in 8,324 children from a well-characterized United Kingdom prospect i ve cohort study , the Avon Longitudinal Study of Parents and Children ( data from 1991–2000 ) . Associations between offspring ADHD and maternal  and paternal smoking during pregnancy were compared using regression analyses . Offspring ADHD symptoms were associated with exposure to both maternal and paternal smoking during pregnancy ( mothers : β = 0.25 , 95 % confidence interval : 0.18 , 0.32 ; fathers : β = 0.21 , 95 % confidence interval : 0.15 , 0.27 ) . When  paternal smoking  was examined in the absence of maternal smoking , associations remained and did not appear to be due to passive smoking exposure in utero . These findings suggest that associations between maternal smoking during pregnancy and child ADHD may be due to genetic or household-level confounding rather than to causal intrauterine effects OBJECTIVE : To explore associations of  maternal prenatal smoking and child psychological problems and determine the role of causal intrauterine mechanisms . PATIENTS AND METHODS :  Maternal smoking and child psychological problems were explored in 2 birth cohorts in Pelotas , Brazil ( n = 509 , r and om sub sample ) , and the Avon Longitudinal Study of Parents and Children ( ALSPAC ) in Britain ( n = 6735 ) . Four approaches for exploring causal mechanisms were applied : ( 1 ) cross- population comparisons between a high-income and a middle-income country ; ( 2 ) multiple adjustment for socioeconomic and parental psychological factors ; ( 3 ) maternal-paternal comparisons as a test of putative intrauterine effects ; and ( 4 ) search ing for specific effects on different behavioral subscales . RESULTS : Socioeconomic patterning of maternal prenatal smoking was stronger in the ALSPAC compared with the Pelotas cohort . Despite this difference in a key confounder , consistency in observed associations was found between these cohorts . In both cohorts , unadjusted maternal smoking was associated with greater offspring hyperactivity , conduct/externalizing problems , and peer problems but not with emotional/internalizing problems . After adjusting for confounders and paternal prenatal smoking , only the association with conduct/externalizing problems persisted in both cohorts ( conduct problems in the ALSPAC cohort , odds ratio [ OR ] : 1.24 [ 95 % confidence interval ( CI ) : 1.07–1.46 ] , P = .005 ; externalizing problems in the Pelotas cohort , OR : 1.82 [ 95 % CI : 1.19–2.78 ] , P = .005 ; ORs reflect ordinal odds ratios of maternal smokers having offspring with higher scores ) . Maternal smoking associations were stronger than paternal smoking associations , although statistical evidence that these associations differed was weak in 1 cohort . CONCLUSION : Evidence from 4 approaches suggests a possible intrauterine effect of maternal smoking on offspring conduct/externalizing problems Background : Overweight has its origins largely in early life . We aim ed to identify the most important parental , fetal , and infant risk factors of preschool overweight . Methods : In a prospect i ve cohort study , among 3,610 Caucasian preschool children , we assessed the associations of 34 putative parental , fetal , and infant factors with overweight risk . Results : Higher maternal BMI , paternal BMI , and birth weight were associated with higher risk of preschool overweight ( odds ratio ( OR ) : 1.23 , 95 % confidence interval ( CI ) : 1.10 , 1.39 ; OR : 1.35 , 95 % CI : 1.19 , 1.53 ; and OR : 2.71 , 95 % CI : 2.27 , 3.25 , respectively , per SD increase ) . The same model identified low household income ( OR : 1.74 , 95 % CI : 1.24 , 2.45 ) , being female ( OR : 1.55 , 95 % CI : 1.20 , 2.01 ) , and experiencing third-trimester accelerated growth ( OR : 1.73 , 95 % CI : 1.24 , 2.40 ) or postnatal accelerated growth ( OR : 6.39 , 95 % CI : 4.54 , 8.99 ) as risk factors for preschool overweight . Higher polyunsaturated fat intake at 14 mo was associated with a lower risk of preschool overweight ( OR : 0.77 , 95 % CI : 0.62 , 0.96 per SD ) . Conclusion : Parental anthropometrics and household income , fetal and infant accelerated growth , and infant dietary fat intake are the major risk factors for the development of preschool overweight . Further studies need to explore whether these risk factors could be potential targets for preventive interventions We investigated prospect ively documented parental age and bipolar disorder ( BD ) in a multi-ethnic birth cohort . The study was based on a nested case-control design from the Child Health and Development Study ( CHDS ) birth cohort from 1959 to 1966 . Potential cases with BD were ascertained by data base linkages between CHDS , Kaiser Permanente Medical Care Plan ( KPNC ) , and Alameda County Behavioral Health Care Services , and mailed question naires . Consensus diagnoses with the SCID for DSM-IV-TR were made . The total number of BD cases was 94 . Controls ( N=746 ) were selected from the birth cohort and matched on date of birth , sex , and KPNC membership or residence in Alameda County . For every 10-year increment of paternal age , there was no significant association with BD , adjusting for maternal age . There was also no significant association between maternal age , modeled in 10-year increments , and risk of BD after adjustment for paternal age and maternal race , although there was a suggestion for a protective relationship between increasing maternal age and BD with psychotic features . These findings suggest that if advanced paternal age is a risk factor for BD , the strength of the relationship is small Sporadic neurofibromatosis 1 ( NF1 ) occurs in the absence of a family history of the disease and usually results from a new mutation in the germ cell of one of the parents , most commonly the father . Older paternal age may increase the risk for a new germinal NF1 mutation , but the results of studies to address this question conflict . We investigated paternal age in sporadic NF1 by using a case-control study design . Patients who were seen at two specialty NF clinics in Houston , Texas , born between 1970 and 1992 and living in the Houston area and surrounding counties , were studied .  Birth certificates with information on the father were found for 89 cases . For each case , two birth certificates were chosen at r and om from the same year and county of birth . In this way , the control group of 178 individuals was formed . Fathers of patients with NF1 were 1.5 years older than fathers of control subjects at the birth of the child , but the difference was only of borderline statistical significance ( P = 0.07 ) . This paternal age difference was not changed by adjustment for socioeconomic status or maternal age . These and previous data are consistent with either a small paternal age effect in sporadic NF1 or a bias such as that result ing from the selection of cases and /or controls OBJECTIVES : The objective of the study was to investigate the associations among  maternal prepregnancy BMI , paternal BMI  , and the risk of autism spectrum disorders ( ASDs ) in children . METHODS : The study sample of 92 909 children was derived from the population -based , prospect i ve Norwegian Mother and Child Cohort Study . The age range was 4.0 through 13.1 ( mean 7.4 ) years . Relative risks of ASDs were estimated by odds ratios ( ORs ) and 95 % confidence intervals ( CIs ) from logistic regression models . RESULTS : At the end of follow-up on December 31 , 2012 , 419 children in the study sample had been diagnosed with ASDs : 162 with autistic disorder , 103 with Asperger disorder , and 154 with pervasive developmental disorder not otherwise specified . Maternal obesity ( BMI ≥30 ) was only weakly associated with ASD risk , whereas paternal obesity was associated with an increased risk of autistic disorder and Asperger disorder . The risk of autistic disorder was 0.27 % ( 25 of 9267 ) in children of obese fathers and 0.14 % ( 59 of 41 603 ) in children of fathers with normal weight ( BMI < 25 ) , generating an adjusted OR of 1.73 ( 95 % CI : 1.07–2.82 ) . For Asperger disorder , analyses were limited to children aged ≥7 years ( n = 50 116 ) . The risk was 0.38 % ( 18 of 4761 ) in children of obese fathers and 0.18 % ( 42 of 22 736 ) in children of normal-weight fathers , and the adjusted OR was 2.01 ( 95 % CI : 1.13–3.57 ) . No associations were found for pervasive developmental disorder not otherwise specified . CONCLUSIONS : Paternal obesity is an independent risk factor for  ASDs in children . The associations should be investigated further in genetic and epigenetic studies OBJECTIVE : The aim of this study was to investigate the influence of maternal age on perinatal and obstetric outcome in women aged 40–44 years and those 45 years or older and to estimate whether adverse outcome was related to intercurrent illness and pregnancy complications . METHODS : National prospect i ve ,  population  -based ,  cohort study in women aged 40–44 years and those 45 years or older and in a control group of women aged 20–29 years who delivered during the period 1987–2001 .  Adjusted odds ratios ( OR ) were calculated after adjustments for significant malformations , maternal pre-existing diseases , and smoking . Main outcome measures were perinatal mortality , intrauterine fetal death , neonatal death , preterm birth , and preeclampsia . RESULTS : During the 15-year period , there were 1,566,313 deliveries ( 876,361 women were 20–29 years of age , 31,662 were 40–44 years , and 1,205 were ≥ 45 years ) . Perinatal mortality was 1.4 % , 1.0 % , and 0.5 % in women 45 years or older , 40–44 , and 20–29 years , respectively . Adjusted OR for perinatal mortality was 2.4 ( 95 % confidence interval [ CI ] 1.5–4.0 ) in women aged 45 years or older , compared with 1.7 ( 95 % CI 1.5–1.9 ) in women 40–44 years . Adjusted OR for intrauterine fetal death was 3.8 ( 95 % CI 2.2–6.4 ) in women aged 45 years or older , compared with 2.1 ( 95 % CI 1.8–2.4 ) in women 40–44 years . Preterm birth , gestational diabetes , and preeclampsia were more common among women 40–44 years of age and those 45 years or older . Perinatal mortality was increased in women with intercurrent illness or pregnancy complications compared with women without these conditions , but there was no evidence that these factors became more important with increasing age . CONCLUSION : Perinatal mortality , intrauterine fetal death , and neonatal death increased with age . There was also an increase in intercurrent illnesses and pregnancy complications with increasing age , but this did not entirely explain the observed increase in perinatal mortality with age . LEVEL OF EVIDENCE : BACKGROUND Foetal smoke exposure might lead to foetal developmental adaptations that permanently affect the cardiovascular system . We assessed the associations of both maternal and paternal smoking during pregnancy with childhood cardiovascular structures and function . METHOD In a prospect i ve cohort study among 5565 children , we examined whether maternal and paternal smoking during pregnancy are associated with blood pressure , carotid-femoral pulse wave velocity and left cardiac structures and function in 6-year-old children . RESULTS As compared with children from non-smoking mothers , children from mothers who smoked more than 10 cigarettes per day had a higher diastolic blood pressure [ difference 1.43 mmHg ( 95 % confidence interval : 0.22 , 2.63 ) ] . Maternal smoking during pregnancy was not associated with systolic blood pressure , childhood carotid-femoral pulse wave velocity or left cardiac structures . Maternal smoking of 10 or more cigarettes per day was associated with a higher fractional shortening in childhood [ difference 1.01 % ( 95 % confidence interval : 0.18 , 1.84 ) ] . Among mothers who did not smoke during pregnancy , paternal smoking was associated with aortic root diameter but not with other cardiovascular outcomes . CONCLUSIONS Maternal smoking during pregnancy is associated with higher diastolic blood pressure and fractional shortening , although the effect estimates are small . The stronger effect estimates for maternal smoking compared with paternal smoking might suggest that direct intrauterine adaptive responses are involved as underlying mechanisms BACKGROUND Maternal smoking during pregnancy seems to be associated with obesity in offspring . Not much is known about the specific critical exposure periods or underlying mechanisms for this association . OBJECTIVE We assessed the associations of active maternal and paternal smoking during pregnancy with early growth characteristics and risks of overweight and obesity in preschool children . DESIGN This study was a population -based , prospect i ve cohort study from early fetal life until the age of 4 y in 5342 mothers and fathers and their children .  Growth characteristics [ head circumference , length , weight , and body mass index ( BMI ; in kg/m(2 ) ) ] and overweight and obesity were repeatedly measured at the ages of 1 , 2 , 3 , and 4 y. RESULTS In comparison with children from nonsmoking mothers , children from mothers who continued smoking during pregnancy had persistently smaller head circumferences and heights until the age of 4 y , whereas their weights were lower only until the age of 3 mo . This smaller length and normal to higher weight led to an increased BMI [ SD score difference : 0.11 ; 95 % CI : 0.02 , 0.20 ; P < 0.05 ) ] and an increased risk of obesity ( odds ratio : 1.61 ; 95 % CI : 1.03 , 2.53 ; P < 0.05 ) at the age of 4 y. In nonsmoking mothers , paternal smoking was not associated with postnatal growth characteristics or risk of obesity in offspring . Maternal smoking during pregnancy was associated with a higher BMI at the age of 4 y in children with a normal birth weight and in those who were small for gestational age at birth . CONCLUSION Our findings suggest that direct intrauterine exposure to smoke until late pregnancy leads to different height and weight growth adaptations and increased risks of overweight and obesity in preschool children Abstract Objective To identify risk factors in early life ( up to 3 years of age ) for obesity in children in the United Kingdom . Design Prospect i ve cohort study . Setting Avon longitudinal study of parents and children , United Kingdom . Participants 8234 children in cohort aged 7 years and a sub sample of 909 children ( children in focus ) with data on additional early growth related risk factors for obesity . Main outcome measures Obesity at age 7 years , defined as a body mass index 3 95th centile relative to reference data for the UK population in 1990 . Results Eight of 25 putative risk factors were associated with a risk of obesity in the final models : parental obesity ( both parents : adjusted odds ratio , 10.44 , 95 % confidence interval 5.11 to 21.32 ) , very early ( by 43 months ) body mass index or adiposity rebound ( 15.00 , 5.32 to 42.30 ) , more than eight hours spent watching television per week at age 3 years ( 1.55 , 1.13 to 2.12 ) , catch-up growth ( 2.60 , 1.09 to 6.16 ) , st and ard deviation score for weight at age 8 months ( 3.13 , 1.43 to 6.85 ) and 18 months ( 2.65 , 1.25 to 5.59 ) ; weight gain in first year ( 1.06 , 1.02 to 1.10 per 100 g increase ) ; birth weight , per 100 g ( 1.05 , 1.03 to 1.07 ) ; and short ( < 10.5 hours ) sleep duration at age 3 years ( 1.45 , 1.10 to 1.89 ) . Conclusion Eight factors in early life are associated with an increased risk of obesity in childhood Research suggests that heredity and early fetal development play a causal role in autism . This case-control study explored the association between perinatal factors , parental psychiatric history , socioeconomic status , and risk of autism . The study was nested within a cohort of all children born in Denmark after 1972 and at risk of being diagnosed with autism until December 1999 . Prospect ively recorded data were obtained from nationwide registries in Denmark . Cases totaled 698 children with a diagnosis of autism ; each case was individually matched by gender , birth year , and age to 25 controls . Analyses by conditional logistic regression produced risk ratios and 95 % confidence intervals . Adjusted analyses showed that the risk of autism was associated with breech presentation ( risk ratio ( RR ) = 1.63 , 95 % confidence interval ( CI ) : 1.18 , 2.26 ) , low Apgar score at 5 minutes ( RR = 1.89 , 95 % CI : 1.10 , 3.27 ) , gestational age at birth < 35 weeks ( RR = 2.45 , 95 % CI : 1.55 , 3.86 ) , and parental psychiatric history ( schizophrenia-like psychosis : RR = 3.44 , 95 % CI : 1.48 , 7.95 ; affective disorder : RR = 2.91 , 95 % CI : 1.65 , 5.14 ) . Analyses showed no statistically significant association between risk of autism and weight for gestational age , parity , number of antenatal visits , parental age , or socioeconomic status . Results suggest that prenatal environmental factors and parental psychopathology are associated with the risk of autism . These factors seem to act independently The relation between  parents ' tobacco smoking prior to birth and cancer in the offspring was investigated with the use of data from a case-control study . Incident cases included all children ( aged 0 - 14 years ) diagnosed in Denver , Colorado from 1976 to 1983 . Controls were selected through r and om digit dialing , and matched to cases on age , sex , and geographic area . Information on smoking by parents and other household members was obtained by personal interview for 223 cases and 196 controls . After adjustment for father 's education , mother 's smoking during the first trimester of pregnancy was associated with an increased risk for all cancers combined ( odds ratio ( OR ) = 1.3 , 95 % confidence interval ( CI ) 0.7 - 2.1 ) , acute lymphocytic leukemia ( OR = 1.9 , 95 % CI 0.9 - 4.1 ) , and lymphomas ( OR = 2.3 , 95 % CI 0.8 - 7.1 ) . Adjusting for father 's education , associations with father 's smoking in the absence of mother 's smoking were found for all cancers combined ( OR = 1.2 , 95 % CI 0.8 - 2.1 ) , acute lymphocytic leukemia ( OR = 1.4 , 95 % CI 0.6 - 3.1 ) , lymphomas ( OR = 1.6 , 95 % 0.5 - 5.4 ) , and brain cancer ( OR = 1.6 , 95 % CI 0.7 - 3.5 ) . In spite of imprecision result ing from small numbers of cases in diagnostic subgroups , these results are suggestive of a possible influence of parents ' smoking on childhood cancer CONTEXT Advancing paternal age has been reported as a risk factor for neurodevelopmental disorders . OBJECTIVES To determine whether advanced paternal age is associated with an increased risk of BPD  in the offspring and to assess if there was any difference in risk when analyzing patients with early-onset BPD separately . DESIGN A nationwide nested case-control study based on Swedish registers was performed . Risk for BPD in the offspring of older fathers was estimated using conditional logistic regression analysis controlling for potential confounding of parity , maternal age , socioeconomic status , and parental family history of psychotic disorders . SETTING Identification of 7,328,100 individuals and their biological parents by linking the nationwide Multigeneration Register and the Hospital Discharge Register . PARTICIPANTS A total of 13,428 patients with a BPD diagnosis on at least 2 separate hospital admissions was identified . Five healthy control subjects matched for sex and year of birth were r and omized to each case . Main Outcome Measure Bipolar disorder based on ICD codes at discharge from hospital treatment . RESULTS An association between paternal age and risk for BPD in the offspring of older men was noted . The risk increased with advancing paternal age . After controlling for parity , maternal age , socioeconomic status , and family history of psychotic disorders , the offspring of men 55 years and older were 1.37 ( 95 % confidence interval [ CI ] , 1.02 - 1.84 ) times more likely to be diagnosed as having BPD than the offspring of men aged 20 to 24 years . The maternal age effect was less pronounced . For early-onset ( < 20 years ) cases , the effect of paternal age was much stronger ( odds ratio , 2.63 ; 95 % CI , 1.19 - 5.81 ) , whereas no statistically significant maternal age effect was found . CONCLUSIONS Advanced paternal age is a risk factor for BPD in the offspring . The results are consistent with the hypothesis that advancing paternal age increases the risk for de novo mutations in susceptibility genes for neurodevelopmental disorders STUDY QUESTION Do paternal and maternal lifestyle factors influence the risk of hypertensive pregnancy complications , gestational diabetes mellitus ( GDM ) , spontaneous preterm birth and small-for-gestational-age ( SGA ) ? SUMMARY ANSWER Paternal lifestyle factors do not exert an independent effect on the investigated outcomes while maternal prepregnancy BMI and maternal smoking during pregnancy influence the risk of hypertensive pregnancy complications , GDM and SGA . WHAT IS KNOWN ALREADY Maternal lifestyle factors are associated with perinatal complications , but the impact of paternal lifestyle factors is unclear . STUDY DESIGN , SIZE , DURATION Data from the GECKO ( Groningen Expert Center for Kids with Obesity ) Drenthe cohort , a prospect i ve population -based birth-cohort of children born between April 2006 and April 2007 in a northern province of The Netherl and s , were analysed . The parents of 2958 children ( 62 % of those approached ) gave their consent to participate in the study and the data of 2264 ( 77 % ) couples were available for analysis . PARTICIPANTS / MATERIAL S , SETTING S , METHOD All pregnant women in the Dutch province of Drenthe with an expected date of delivery between April 2006 and April 2007 were invited to participate and included during the third trimester of their pregnancy or within 6 months after delivery . All consenting couples received extensive question naires including lifestyle , biological and socio-demographic-related questions covering the period of 6 months prior to conception . Outcome data were obtained from midwives and hospital registries . Univariable and multivariable logistic regression analyses were used to determine the impact of the lifestyle factors on the primary outcome measures . MAIN RESULTS AND THE ROLE OF CHANCE Of all 2264 women , 241 women ( 10.6 % ) developed a hypertensive pregnancy complication , 50 women ( 2.2 % ) developed GDM , 79 ( 3.5 % ) children were spontaneously delivered preterm and 155 children ( 6.8 % ) were SGA . All paternal and maternal lifestyle factors were positively correlated . Multivariable analysis showed that paternal lifestyle factors did not have an independent influence on the investigated outcomes . Of the maternal factors , prepregnancy BMI was independently associated with an increased risk of a hypertensive disorder during pregnancy ( odds ratio ( OR ) : 1.12 , 95 % CI 1.09 - 1.16 ) , a higher risk of GDM ( OR BMI > 23 kg/m(2 ) , per BMI unit : 1.13 , 95 % CI 1.08 - 1.18 ) and with a decreased risk of SGA ( OR per BMI point 0.94 , 95 % CI 0.90 - 0.99 ) . Maternal smoking during pregnancy was significantly associated with SGA ( OR 3.00 , 95 % CI 1.80 - 4.99 ) in multivariable analysis . LIMITATIONS , REASONS FOR CAUTION The retrospective nature of the question naire may have induced recall bias . Selection bias might have occurred , as ethnic minorities were less willing to co-operate in the GECKO Drenthe study . The possibility of misclassification bias regarding the primary outcome measures can not be ruled out . Inclusion bias might have occurred as not all question naires of the parents of the children participating in the GECKO Drenthe cohort were completed . WIDER IMPLICATION S OF THE FINDINGS Paternal lifestyle factors do not have an independent effect on the investigated adverse pregnancy outcomes . However , as paternal and maternal lifestyles are positively correlated , both partners should be involved in preconception counselling regarding the investigated outcome measures A possible detrimental paternal age effect on offspring health due to mutations of paternal origin should be reflected in an association between paternal age and fetal loss . The authors used data from a prospect i ve study of 23,821 pregnant women recruited consecutively to the Danish National Birth Cohort from 1997 to 1999 to assess the association between  paternal age and fetal death . Fathers of the pregnancies were identified by record linkage to population registers . The paternal age-related risks of fetal death and its components , early and late fetal loss , were estimated using survival analysis . Pregnancies fathered by a man aged 50 or more years ( n = 124 ) had almost twice the risk of ending in a fetal loss compared with pregnancies with younger fathers ( hazard ratio = 1.88 , 95 % confidence interval : 0.93 , 3.82 ) , after adjustment for maternal age , reproductive history , and maternal lifestyle during pregnancy . Various approaches to adjustment for potential residual confounding of the relation by maternal age did not affect the relative risk estimates . The paternal age-related risk of late fetal death was higher than the risk of early fetal death and started to increase from the age of 45 years . It should , however , be interpreted cautiously because of the restricted number of fetal deaths STUDY QUESTION Do children born to fathers of advanced age have an increased risk of dying before the age of 5 years ? SUMMARY ANSWER Children born to fathers aged 40 years or more have an increased risk of dying in early childhood due to an excess risk of fatal congenital anomalies , malignancies and external causes . WHAT IS KNOWN ALREADY Advanced paternal age has previously been associated with adverse reproductive outcomes and some long-term health problems in the offspring . This is possibly due to specific point mutations , a condition known to increase in the sperm with increasing paternal age . STUDY DESIGN , SIZE , DURATION A Danish population -based register study , design ed as a prospect i ve cohort study , of 1 575 521 live born children born from 1978 to 2004 . The age of the child ( in days ) was used as the underlying time and the children entered the cohort the day they were born and were followed until 31 December 2009 . The children were censored on date of turning 5 years , date of death or date of emigration , whichever occurred first . PARTICIPANTS / MATERIAL S , SETTING , METHODS Data from population -covering registers from Statistics Denmark including the Integrated Data base for Labour Market Research , the Medical Birth Registry and the Registry of Causes of Death was linked using the unique civil registry number . Hazard ratios ( HR ) with 95 % confidence intervals ( CI ) were used to estimate the risk of under-five mortality . The effect of paternal age was examined using restricted cubic splines and paternal age groups . MAIN RESULTS AND THE ROLE OF CHANCE Compared with children born to fathers aged 30 - 34 years , a statistically significant excess risk was found for children born to fathers aged 40 - 44 years [ HR : 1.10 ( 95 % CI : 1.00 - 1.21 ) ] and children born to fathers aged 45 + years [ HR : 1.16 ( 95 % CI : 1.02 - 1.32 ) ] . When only looking at 1 - 5 year olds , the relative risk ( HR ) among children born to fathers aged 40 - 44 years increased to 1.24 ( 95 % CI : 1.00 - 1.53 ) and the risk in the oldest paternal age group ( 45 + years ) rose to 1.65 ( 95 % CI : 1.24 - 2.18 ) . The results suggest that the elevated risk for children of fathers aged 40 years or more was primarily attributed to an elevated risk of dying from congenital malformations , malignancies and external causes . LIMITATIONS , REASONS FOR CAUTION Specific causes of death might be misclassified ; however , this is not likely to be dependent on paternal age . In some cases , the biological father may differ from the father registered . This misclassification is most likely non-differential . WIDER IMPLICATION S OF THE FINDINGS The excess risk of mortality among children born to older fathers is in accordance with the literature . The association needs further attention as it can provide valuable knowledge of the etiology of genetic diseases . Also , the association could become of greater importance in the future if the proportion of fathers aged 40 + years keeps growing . STUDY FUNDING /COMPETING INTEREST ( S ) None Purpose The etiology of retinoblastoma remains poorly understood . In the present study , we examined associations between perinatal factors and retinoblastoma risk in California children . Methods We identified 609 retinoblastoma cases ( 420 unilateral , 187 bilateral , and 2 with laterality unknown ) from California Cancer Registry records of diagnoses 1988–2007 among children < 6 years of age . We r and omly selected 209,051 controls from California birth rolls . The source of most study data was birth certificates .  Multivariable logistic regression was used to examine associations between retinoblastoma and perinatal characteristics . Results Bilateral retinoblastoma was associated with greater paternal age [ for fathers over 35 , crude odds ratio ( OR ) = 1.73 , 95 % confidence interval ( CI ) 1.20 , 2.47 ] and with twin births ( OR = 1.93 , 95 % CI 0.99 , 3.79 ) . Among unilateral cases , we observed an increased risk among children of US-born Hispanic mothers ( OR = 1.34 , 95 % CI 1.01 , 1.77 ) while a decreased risk was observed for infants born to mothers with less than 9 years of education ( OR = 0.70 , 95 % CI 0.49 , 1.00 ) , a group that consisted primarily of mothers born in Mexico . We observed that maternal infection in pregnancy with any STD ( OR = 3.59 , 95 % CI 1.58 , 8.15 ) was associated with bilateral retinoblastoma . Conclusions This study supports the findings of previous investigations reporting associations between parental age , HPV infection , and retinoblastoma Background : Hepatoblastoma is a rare pediatric liver tumor that has significantly increased in incidence over the last several decades . The International Agency for Research on Cancer ( IARC ) recently classified hepatoblastoma as a tobacco-related cancer . Parental alcohol use has shown no association . We examined associations between parental tobacco and alcohol use around the time of pregnancy and hepatoblastoma in a large case – control study . Methods : Maternal interviews were completed for 383 cases diagnosed in the United States during 2000–2008 . Controls ( n = 387 ) were identified through U.S. birth registries and frequency-matched to cases on birth weight , birth year , and region of residence . We used unconditional logistic regression to calculate ORs and 95 % confidence intervals ( CI ) for associations between parental smoking and maternal drinking and offspring hepatoblastoma . Results : We found no association between hepatoblastoma and maternal smoking at any time ( OR , 1.0 ; 95 % CI , 0.7–1.4 ) , within the year before pregnancy ( OR , 1.1 ; 95 % CI , 0.8–1.6 ) , early in pregnancy ( OR , 1.0 ; 95 % CI , 0.7–1.6 ) , or throughout pregnancy ( OR , 0.9 ; 95 % CI , 0.5–1.6 ) . We observed marginally positive associations between hepatoblastoma and paternal smoking in the year before pregnancy ( OR , 1.4 ; 95 % CI , 1.0–2.0 ) and during pregnancy ( OR , 1.4 ; 95 % CI , 0.9–2.0 ) . Maternal alcohol use was not associated with hepatoblastoma . Conclusion : Our results do not provide evidence for an etiologic relationship between maternal smoking or drinking and hepatoblastoma , and only weak evidence for an association for paternal smoking in the year before pregnancy . Impact : Our study provides limited support for hepatoblastoma as a tobacco-related cancer ; however , it remains wise to counsel prospect i ve parents on the merits of smoking cessation . Cancer Epidemiol Biomarkers Prev ; 22(10 ) ; 1837–43 . © 2013 AACR Previous studies and animal evidence have suggested a relationship between parental  tobacco or alcohol use and the  risk  of some  childhood cancers , including  neuroblastoma .  A case-control study was conducted to investigate the relationship between  parental tobacco smoking , alcohol consumption , and risk of neuroblastoma .  Cases were children diagnosed with neuroblastoma over the period 1992 - 1994 at Children 's Cancer Group and Pediatric Oncology Group institutions throughout the United States and Canada . One matched control was selected using r and om-digit dialing . Information on parental smoking and drinking history was obtained from 504 case and 504 control parents by telephone interview . Overall , there was no consistent pattern of association with parental smoking and alcohol consumption . For example , both maternal smoking and drinking during the period from 1 month before pregnancy through breastfeeding had adjusted odds ratios ( ORs ) of 1.1 [ 95 % confidence interval ( CI ) , 0.8 - 1.4 ] . There was no association with paternal smoking ( OR , 1.2 ; 95 % CI , 0.8 - 1.6 ) or paternal drinking 1 month before conception ( OR , 1.0 ; 95 % CI , 0.7 - 1.4 ) . There was no consistent increase in risk by the amount of smoking or drinking during any time period relative to pregnancy . There was no suggestion of an increased risk when only one parent smoked . Smoking or drinking among both parents did not jointly increase the risk of neuroblastoma in their offspring . The child 's age at diagnosis , stage , or MYCN oncogene amplification status did not material ly alter the OR estimates . It is concluded that the results from this study do not indicate any evidence for a relationship between neuroblastoma and parental tobacco or alcohol use OBJECTIVE To analyse the association between pre- and postnatal exposure to tobacco smoke and child behavioural problems  and to further investigate the influence of trimester-specific exposure to maternal smoking and the impact of paternal smoking at home on the same outcome . METHODS Data of 3097 German children recruited at birth for a population -based , prospect i ve study were used . Detailed information on children 's tobacco smoke exposure was collected by self-administered question naires at each follow-up . Behavioural outcomes were measured by the Strengths and Difficulties Question naire applied at 10-year follow-up . RESULTS Children exposed to environmental tobacco smoke at home showed increased risks of hyperactivity/inattention problems . Only smoking during the entire pregnancy increased the risk for conduct and hyperactivity/inattention problems ( proportional odds ratio (pOR)=1.58 , 95 % confidence interval (CI)=1.06 - 2.37 and pOR=1.67 , CI=1.03 - 2.72 ) . Pre- and postnatal exposure to paternal smoking was associated with hyperactivity/inattention problems in children of non-smoking mothers ( pOR=1.97 , CI=1.06 - 3.65 ) . Effect estimates were adjusted for study centre , sex , parental educational level , mother 's age at birth , having a single parent and time spent in front of a screen . CONCLUSIONS Not only maternal smoking during pregnancy but also paternal smoking at home should be considered as a risk for hyperactivity/inattention problems in children OBJECTIVE Previous research suggests that advanced paternal age increases the risk of musculoskeletal congenital anomalies ( CAs ) in offspring , but findings are inconsistent . This study aims to investigate the risk of musculoskeletal CAs according to paternal age at birth in an unselected population covering cohort of children . STUDY DESIGN A register-based prospect i ve study of 1,605,885 children born in Denmark , 1978 - 2004 , using information from record-linked health and administrative registers . The association between paternal age and overall musculoskeletal CAs , limb anomalies , craniosynostosis , skeletal dysplasias , syndromic musculoskeletal CAs , and other musculoskeletal CAs were investigated by multiple logistic regression analysis . RESULTS For overall musculoskeletal CAs , a slightly higher risk per 10-year increase in paternal age was found ( odds ratio [ OR ] = 1.06 [ 95 % CI : 1.01 - 1.11 ; where CI is confidence interval ] ) . A 26 % ( 95 % CI : 2 - 56 % ) excess risk was found for fathers aged 50 + years compared to fathers aged 30 - 34 years . For syndromic musculoskeletal CAs , excess risks were found for fathers aged 40 + years , compared to fathers aged 30 - 34 years ( 40 - 44 : OR = 1.38 [ 95 % CI : 1.01 - 1.88 ] , 45 - 49 : OR = 1.45 [ 95 % CI : 0.89 - 2.34 ] , 50 + : OR = 1.42 [ 95 % CI : 0.73 - 2.79 ] ) . The risks in all other subgroups of musculoskeletal CAs were increased for fathers aged 50 + years . CONCLUSIONS A slightly higher risk for overall musculoskeletal CAs in offspring was found with increasing paternal age , mainly due to an excess risk of syndromic musculoskeletal CAs for fathers aged 40 + years . While associations between paternal age 50 + years and increased risk of all subtypes of musculoskeletal CAs were indicated , advanced paternal age likely plays a minor role in the etiology of these anomalies OBJECTIVE The study examined the relation between paternal age at the time of birth and risk of schizophrenia in the adult offspring . METHOD Data from the birth cohort of the Prenatal Determinants of Schizophrenia study were used in this study . Virtually all members of this birth cohort had prospect i ve information about paternal age at the time of the offspring 's birth . Subjects with schizophrenia and other schizophrenia spectrum disorders ( N=71 ) among members of this birth cohort were previously ascertained . In separate analyses , paternal age was modeled as a continuous variable and as a categorical variable , and its relation with the risk of adult schizophrenia and other schizophrenia spectrum disorders and with the risk of schizophrenia separately were examined . RESULTS There was a marginally significant , monotonic association between advancing paternal age and risk of adult schizophrenia and schizophrenia spectrum disorders . The association held after the analysis controlled for the effects of maternal age and other potential confounders . Similar results were observed when only subjects with schizophrenia were included in the analysis . CONCLUSIONS Advanced paternal age at the time of birth of the offspring may be a risk factor for adult schizophrenia The proportion of parents aged ≥35 years at the birth of their child continues to increase , but long-term health consequences for these children are not fully understood . A recent prospect i ve study of 110,999 adult women showed an association between paternal-but not maternal-age at birth and sporadic hematological cancer risk . To further investigate this topic , we examined these associations in women and men in the American Cancer Society Cancer Prevention Study -II Nutrition Cohort . Among 138,003 Cancer Prevention Study -II participants , 2,532 incident hematological cancers were identified between 1992 and 2009 . Multivariable-adjusted hazard ratios and 95 % confidence intervals were computed by using Cox proportional hazards regression . There was no clear linear trend in the risk of hematological malignancies by either paternal or maternal age . However , there was a strong , positive association with paternal age among participants without siblings . In that group , the hazard ratio for fathers aged ≥35 years compared with < 25 years at birth was 1.63 ( 95 % confidence interval : 1.19 , 2.23 ) , and a linear dose-response association was suggested ( Pspline = 0.002).There were no differences by subtype of hematological cancer . Results of this study support the need for further research to better underst and the association between paternal age at birth and hematological malignancies Objective . To assess the influence of paternal size on birthweight after suitable control for maternal and fetal factors BACKGROUND There are limited data regarding the associations of both maternal and paternal anthropometrics with longitudinally measured post-natal growth measures in early childhood . OBJECTIVE To assess the associations of maternal and paternal anthropometrics with growth characteristics and the risk of overweight in pre-school children . STUDY DESIGN Population -based prospect i ve cohort study from early foetal life onwards in the Netherl and s. METHODS Maternal pre-pregnancy anthropometrics and gestational weight gain  , and paternal anthropometrics were related to foetal and post-natal growth measures and the risk of overweight until the age of 4 years . Analyses were based on 5674 mothers , fathers and their children . RESULTS Both pre-pregnancy maternal and paternal height , weight and body mass index were associated with corresponding foetal and post-natal anthropometric measures . Maternal body mass index had a significantly stronger effect on childhood body mass index than paternal body mass index . As compared to children from parents with normal body mass index , children from two obese parents had an increased risk of overweight at the age of 4 years ( odds ratio 6.52 ( 95 % confidence interval 3.44 , 12.38 ) . Maternal gestational weight gain was only among mothers with normal body mass index associated with body mass index and the risk of overweight in the children . CONCLUSION Maternal and paternal anthropometrics affect early growth in pre-school children differently . Gestational weight gain in mothers without overweight and obesity is related to the risk of overweight in early childhood UNLABELLED The objective of this study was to determine the association between parental cigarette smoking and the  risk of congenital heart septal defects in Kaunas infant population in 1995 - 2005 . MATERIAL AND METHODS An epidemiological case-control study was conducted . The study comprised 261 newborns with congenital heart septal defects ( cases ) and 1122 r and omly selected newborns without any defects ( controls ) , born in Kaunas city during 1995 - 2005 . Information on potential risk factors of newborns ' health was collected through an interview with parents using st and ardized question naires . Multivariate logistic regression analysis was used to assess the association between parental smoking and septal defects while controlling for possible confounders . RESULTS According to the vali date d registry , 371 newborns with congenital heart malformations were born in Kaunas city during 1995 - 2005 ; 70.3 % of cases had ventricular and /or atrial septal defects . After adjustment for possible confounding factors - maternal education , social status , marital status - a statistically significant relationship was observed between parental smoking and congenital heart septal defects . Parental , maternal , and paternal smoking was significantly associated with a 2.27-fold ( adjusted OR=2.27 ; 95 % CI , 1.49 - 3.46 ) , 2.2-fold ( adjusted OR=2.20 ; 95 % CI , 1.01 - 4.79 ) , and 1.45-fold ( adjusted OR=1.45 ; 95 % CI , 1.03 - 2.03 ) increased risk of defects if compared with nonsmoking parents . CONCLUSIONS According to the results of our study , parental smoking was significantly associated with an increased risk of congenital heart septal defects in infants The acronym CHARGE refers to a non‐r and om clustering of congenital malformations whose cause remains unknown . Here , we report on a series of 41 patients and find a significant increase in mean paternal age of birth of CHARGE patients ( 33.7±8 years ) compared with the control population ( 30.8±5 years ) . In contrast , maternal age was not statistically different in patients and controls . These data suggest the possible role of a dominant mutation or , less likely , a subtle chromosomal abnormality in CHARGE association Data from a large , population -based case-control study were analyzed to investigate the relationship between prenatal exposure to tobacco smoke and  childhood brain tumors ( CBTs ) . A total of 540 CBT patients , diagnosed between 1984 and 1991 , were identified from population -based tumor registries in 19 West Coast counties that included Seattle , WA ( 13 counties ) , San Francisco , CA ( 5 counties ) , and Los Angeles , CA ( 1 county ) . R and om digit dial was used to select 801 control subjects from the three geographical regions to obtain a case : control ratio of 1:2 in San Francisco and Seattle and 1:1 in Los Angeles . The data first were analyzed separately by geographical site and then were combined with adjustments made for gender , age at the time of diagnosis ( or reference date of control subjects ) , birth year of the index child , and maternal race . No association was found between the risk of CBTs and maternal or paternal smoking before pregnancy and there was no association between CBTs and maternal smoking during pregnancy [ odds ratio ( OR ) = 0.98 ; 95 % confidence interval ( CI ) = 0.72 - 1.3 ] . A slightly increased OR for CBTs was found for paternal smoking during pregnancy in the absence of maternal smoking ( OR = 1.2 ; 95 % CI = 0.90 - 1.5 ) and for maternal exposure to passive smoke from any source ( OR = 1.2 ; 95 % CI = 0.95 - 1.6 ) . The results of this analysis are consistent with results from several prior epidemiological studies that showed no significant association between CBTs and maternal smoking before or during pregnancy or maternal exposure to passive smoke during pregnancy Increasing incidence of Down 's syndrome with advancing paternal age for given maternal age has been demonstrated . Comparisons are made between an almost complete Down 's syndrome sample from the Copenhagen Metropolitan Area and a r and omly selected sample of births from the same area and the same time period . Men above 55 years have a significantly increased risk of getting children with Down 's syndrome OBJECTIVE To examine determinants of moderate and severe obesity in children at 5 years of age . METHODOLOGY A prospect i ve cohort of mothers were enrolled at first antenatal visit , and interviewed shortly after delivery , at 6 months and 5 years . Detailed health , psychological and social question naires were completed at each phase by mothers , and child health question naires at 6 months and 5 years . At 5 years 4062 children were assessed physically , the  Peabody Picture Vocabulary Test  administered and mothers completed a modified Child Behaviour Checklist .  Moderate obesity was defined as BMI between 85th and 94th percentiles inclusively , and severe obesity as a BMI greater than the 94th percentile . RESULTS Independent predictors of severe obesity at 5 years were birthweight , female gender , maternal BMI and paternal BMI . Moderate obesity at 5 years was predicted by birthweight , paternal BMI and sleeplessness at 6 months , while small for gestational age ( SGA ) status and feeding problems at 6 months were protective factors for moderate obesity . Obesity was not associated with problems of language comprehension or behaviour . CONCLUSIONS Findings of this study suggest that biological rather than psychosocial factors are the major determinants of obesity at 5 years
BACKGROUND Maternal factors , including increasing childbearing age and various life-style factors , are associated with poorer short- and long-term outcomes for children , whereas knowledge of paternal parameters is limited .
Recently , increasing paternal age has been associated with adverse obstetric outcomes , birth defects , autism spectrum disorders and schizophrenia in children .
OBJECTIVE AND RATIONALE The aim of this systematic review is to describe the influence of paternal factors on adverse short- and long-term child outcomes .