An analysis of paternal age and 47,+21 in 35,000 new prenatal cytogenetic diagnosis data from the New York State Chromosome Registry: no significant effect

Summary In 35,680 fetuses of women who had prenatal cytogenetic diagnosis done upon amniotic fluid specimens obtained during 2nd trimester amniocentesis and in whom there was no increased cytogenetic risk except for age, there was no statistically significant evidence for an increase of 47,+21 at any paternal age after adjustment for maternal age. The ratio of observed-to-expected numbers in fathers less than 30 years old was 1.0 and in fathers 40 years or older was 0.9 when compared with numbers derived from maternal-age-specific rates in men 30–39 years old. The ratio was 1.1 for those younger than 34 years when compared with rates in fathers aged 34–39 years old. Only for men 55 years or older was there any, even suggestive, increase. The ratio was roughly 1.5 (9 observed to about 6 expected). This was not statistically significant, and moreover, the increase such as it was, was in men married to women 37–42 years old. Regression analyses using several additive parental age models introducing a parabolic function for paternal age, failed to reveal any paternal age contribution.     

A survey on maternal age and karyotype in Down's syndrome in Japan, 1947–1975

Summary Data on karyotype and maternal age of 1954 cases of Down's syndrome were analyzed to see if the rate of chromosome mutations leading to this abnormality has been enhanced during the last 20 years. Comparison of the data for patients born in 1947–1960 with those in 1961–1975 revealed little change with time in the proportions of cases due to different karyotypes, the overwhelming majority being of 21 trisomy type in both periods. However, there has been a remarkable decline in the mean maternal age from 33.1 years to 29.7 years as well as in the variance from 50.5 to 29.4. While the rate of decline in the variance was almost the same as that for all births occurring in the same periods, the decline in the mean maternal age was much greater for the patients than for all births, suggesting that the rate of nondisjunction might have increased in younger rather than in older mothers. However, when the risk of brearing a child with Down's syndrome for mothers aged 40–44 is taken as unity, no evidence was found for an increase with time in the relative risk for younger mothers. Moreover, results of surveys made in 1960 and thereafter in different parts of Japan indicate that the crude incidence rate of Down's syndrome at birth has been around 0.10%, giving no indication of an upward trend. These findings are discussed with reference to the serious environmental pollution, including possible genetic hazards, with which Japan has been faced since the 1960s.     

Implications of Advancing Paternal Age: Does It Affect Offspring School Performance?

Average paternal age is increasing in many high income countries, but the implications of this demographic shift for child health and welfare are poorly understood. There is equivocal evidence that children of older fathers are at increased risk of neurodevelopmental disorders and reduced IQ. We therefore report here on the relationship between paternal age and a composite indicator of scholastic achievement during adolescence, i.e. compulsory school leaving grades, among recent birth cohorts in Stockholm County where delayed paternity is notably common. We performed a record-linkage study comprising all individuals in Stockholm County who finished 9 years of compulsory school from 2000 through 2007 (n = 155,875). Data on school leaving grades and parental characteristics were retrieved from administrative and health service registers and analyzed using multiple linear regression. Advancing paternal age at birth was not associated with a decrease in school leaving grades in adolescent offspring. After adjustment for year of graduation, maternal age and parental education, country of birth and parental mental health service use, offspring of fathers aged 50 years or older had on average 0.3 (95% CI −3.8, 4.4) points higher grades than those of fathers aged 30–34 years. In conclusion, advancing paternal age is not associated with poorer school performance in adolescence. Adverse effects of delayed paternity on offspring cognitive function, if any, may be counterbalanced by other potential advantages for children born to older fathers.     

Association of paternal age with prevalence of selected birth defects

BACKGROUND: Unlike maternal age, the effect of paternal age on birth defect prevalence has not been well examined. We used cases from the Texas birth defect registry, born during 1996-2002, to evaluate the association of paternal age with the prevalence of selected structural birth defects. METHODS: Poisson regression was used to calculate prevalence ratios (PRs) and 95% confidence intervals (CIs) associated with paternal age for each birth defect, adjusting for maternal age, race/ethnicity, and parity. RESULTS: Relative to fathers ages 25-29 years, fathers 20-24 years of age were more likely to have offspring with gastroschisis (PR 1.47, 95% CI: 1.12-1.94), and fathers 40+ years old were less likely to have offspring with trisomy 13 (PR 0.40, 95% CI: 0.16-0.96). No association was seen between paternal age and prevalence of anencephaly and encephalocele. A selection bias was observed for the other birth defects in which cases of younger fathers were more often excluded from study. CONCLUSIONS: In studies of birth defect risk and paternal age, the source of information may affect the validity of findings.     

Increasing Maternal Age Is Associated with Taller Stature and Reduced Abdominal Fat in Their Children

Background

Maternal age at childbirth continues to increase worldwide. We aimed to assess whether increasing maternal age is associated with changes in childhood height, body composition, and metabolism.

Methods

277 healthy pre-pubertal children, born 37–41 weeks gestation were studied. Assessments included: height and weight corrected for parental measurements, DEXA-derived body composition, fasting lipids, glucose, insulin, and hormonal profiles. Subjects were separated according to maternal age at childbirth: <30, 30–35, and >35 years.

Results

Our cohort consisted of 126 girls and 151 boys, aged 7.4±2.2 years (range 3–10); maternal age at childbirth was 33.3±4.7 years (range 19–44). Children of mothers aged >35 and 30–35 years at childbirth were taller than children of mothers aged <30 years by 0.26 (p = 0.002) and 0.23 (p = 0.042) SDS, respectively. There was a reduction in childhood BMISDS with increasing maternal age at childbirth, and children of mothers aged >35 years at childbirth were 0.61 SDS slimmer than those of mothers <30 years (p = 0.049). Children of mothers aged 30–35 (p = 0.022) and >35 (p = 0.036) years at childbirth had abdominal adiposity reduced by 10% and 13%, respectively, compared to those in the <30 group. Children of mothers aged 30–35 years at childbirth displayed a 19% increase in IGF-I concentrations compared to offspring in <30 group (p = 0.042). Conversely, IGF-II concentrations were lower among the children born to mothers aged 30–35 (6.5%; p = 0.004) and >35 (8.1%; p = 0.005) compared to those of mothers aged <30 years. Girls of mothers aged 30–35 years at childbirth also displayed improved HOMA-IR insulin sensitivity (p = 0.010) compared to girls born to mothers aged <30 years.

Conclusions

Increasing maternal age at childbirth is associated with a more favourable phenotype (taller stature and reduced abdominal fat) in their children, as well as improved insulin sensitivity in girls.     

Retrospective audit of different antenatal screening policies for Down's syndrome in eight district general hospitals in one health region

ObjectiveTo compare the effectiveness of different screening policies for the antenatal detection of Down''s syndrome.DesignRetrospective six year survey.SettingMaternity units of eight districts.ParticipantsWomen who completed their pregnancies between 1 January 1994 and 31 December 1999 (155 501 deliveries).Results335 cases of Down''s syndrome were identified, 323 in continuing pregnancies or liveborn children. Of these, 171 were identified antenatally. Seven different screening policies were used, in three principal groups: serum screening offered to all mothers, maternal age with serum screening or nuchal translucency available to limited groups, and maternal age combined with anomaly scans. The districts that used serum screening detected 57%, those using maternal age plus serum or nuchal translucency screening 52%, and those using a maternal age of ⩾35 and anomaly scans detected 54%. The least successful district, which offered amniocentesis only to women aged over 37 years, detected only 31%. If amniocentesis had been offered from 35 years, as in all other districts, the detection rate would have risen to 54%. Across the region 15% (range 12-20%) of pregnant women were 35 years or more at delivery, and 58% (33-69%) of infants with Down''s syndrome were born to women in this age range.ConclusionsCurrent additional serum or nuchal translucency screening techniques for antenatal detection of Down''s syndrome are less advantageous than previously supposed. More pregnant women were aged over 35 than has been presumed in statistical models used in demonstration projects of serum screening and, as a result, the proportion of affected fetuses in this age group is much greater than predicted.

What is already known on this topic

Serum screening for Down''s syndrome has been presumed to be more effective than screening by maternal ageThere have been no controlled studies comparing serum screening with screening by maternal age, and its greater efficacy has been presumed from mathematical modelling, which assumed that only 5% of pregnant women were aged over 35 yearsThe modelling predicted that only 20-30% of cases of Down''s syndrome would arise in women aged over 35 and made no allowance for the effects of routine anomaly scanning

What this study adds

15% of pregnant women were aged over 35 years, more than double the 5-7% presumed in statistical models of screening58% of babies with Down''s syndrome were born to women aged 35 years or moreSerum screening and nuchal scanning did not achieve significantly higher antenatal detection rates of Down''s syndrome than the use of maternal age and routine anomaly scanning     

A reanalysis of the New York State prenatal diagnosis data on Down's syndrome and paternal age effects

Summary This paper reanalyzes the data from the Hook and Cross (1982) paper in this journal concerning the association between Down's syndrome and paternal age. The New York State (NYS) data are compared with a large European collaborative study by Ferguson-Smith and Yates (1984). The maternal-age-dependent risks in the NYS data were found to be significantly higher than in the European data. When the NYS data was divided into three groups by means of the paternal age, a marked two-peaked distribution was found. The maternal-age-dependent risk was high when the fathers were up to 33 years old, low when the fathers' ages were 34–39 years and high again when the fathers were at least 40 years old. The differences were significant. The results speak in favour of the existence of temporal, geographic, or environmental variations in the risk for de novo trisomy 21, as well as of a paternal age effect. The existence of a paternal age effect in at least some populations is confirmed. If the results of this paper are confirmed in other investigations, it will be necessary to revise present genetic counselling rules towards far more individually specified considerations.     

Effect of Paternal Age on Reproductive Outcomes of In Vitro Fertilization

Although the adverse effects of maternal aging on reproductive outcomes have been investigated widely, there is no consensus on the impact of paternal age. Therefore, we investigated the effect of paternal age on reproductive outcomes in a retrospective analysis of 9,991 in vitro fertilization (IVF) cycles performed at the Reproductive Medicine Center of the Third Affiliated Hospital of Guangzhou Medical University (China) between January 2007 and October 2013. Samples were grouped according to maternal age [<30 (3,327 cycles), 30–34 (4,587 cycles), and 35–38 (2,077 cycles)] and then subgrouped according to paternal age (<30, 30–32, 33–35, 36–38, 39–41, and ≥42). The groups did not differ in terms of fertilization rate, numbers of viable and high-quality embryos and miscarriage rate when controlling maternal age (P >0.05). Chi-squared analysis revealed that there were no differences in implantation and pregnancy rates among the different paternal age groups when maternal age was <30 and 35–38 years (P >0.05). However, implantation and pregnancy rates decreased with paternal age in the 31–34 y maternal age group (P <0.05). Our study indicates that paternal age has no impact on fertilization rate, embryo quality at the cleavage stage and miscarriage rate. For the 30–34 y maternal age group, the implantation rate decreased with increased paternal age, with the pregnancy rate in this group being significantly higher in the paternal <30 y and 30–32 y age groups, compared with those in the 36–38 y and 39–41 y groups.     

Paternal Age and Offspring Congenital Heart Defects: A National Cohort Study

Paternal age has been associated with offspring congenital heart defects (CHDs), which might be caused by increased mutations in the germ cell line because of cumulated cell replications. Empirical evidences, however, remain inconclusive. Furthermore, it is unknown whether all subtypes of CHDs are affected by paternal age. We aimed to explore the relationship between paternal age and the risk of offspring CHDs and its five common subtypes using national register data in Denmark. A total of 1 893 899 singletons born in Denmark from 1977 to 2008 were included in this national-based cohort study. Cox’s proportion hazards model with robust sandwich estimate option was used to estimate the hazards ratio (95% confidence interval) for the associations between paternal age and all CHDs, as well as subtypes of CHDs (patent ductus arteriosus (PDA), ventricular septal defect (VSD), atrial septal defect (ASD), tetralogy of fallot (TOF) and coarctation of the aorta (CoA)). We did not observe an overall association between paternal age and offspring CHDs. However, compared to the paternal age of 25–29 years, paternal age of older than 45 years was associated with a 69% increased risk of PDA (HR45+ = 1.69, 95%CI:1.17–2.43). We observed similar results when subanalyses were restricted to children born to mothers of 27–30 years old. After taking into consideration of maternal age, our data suggested that advanced paternal age was associated with an increased prevalence of one subtype of offspring congenital heart defects (CHDs), namely patent ductus arteriosus (PDA).     

Reexamination of paternal age effect in Down's syndrome

Summary The recent discovery that the extra chromosome in about 30% of cases of 47, trisomy 21 is of paternal origin has revived interest in the possibility of paternal age as a risk factor for a Down syndrome birth, independent of maternal age. Parental age distribution for 611 Down's syndrome 47,+21 cases was studied. The mean paternal age was 0.16 year greater than in the entire population of live births after controlling for maternal age. There was no evidence for a significant paternal age effect at the 0.05 level. For 242 of these Down's syndrome cases, control subjects were selected by rigidly matching in a systematic manner. Paternal age was the variable studied, with maternal age and time and place of birth controlled. There was no statistically significant association between paternal age and Down's syndrome. After adjustment for maternal age, these two studies were not consistent with an increase of paternal age in Down's syndrome.     

Parental age, parity and sex ratio in births in England and Wales, 1968-77

Variations in sex ratio with maternal age, paternal age, parity, and time are examined in data on all legitimate births in England and Wales, 1968-1977. Significant linear declines in sex ratio with both increasing parity and increasing paternal age, and a curvilinear relationship with maternal age are found. Results show that 1) before 1955 it seems likely that the sex ratio declined with an increase in maternal age, 2) between 1955 and 1968 there was an unexplained decline in the sex ratio of births to women aged 20-24 and an increase in that of births to women aged 30-34, and 3) there was no significant secular trend in sex ratio during the period 1968-1977. Using data provided by the Registrar General of England and Wales, a weighted multiple regression analysis is applied. Some possible explanations for the changes in sex ratios of births during the years studied are: 1) racial heterogeneity, 2) artificial insemination, 3) the pill, and 4) ovulation induction. Overall, some artifact or combination of artifacts has transformed the regression of sex ratio on maternal age from a monotonic decline to a cubic, or this hypothesis stands in need of modification.     

Can paternal preconceptional radiation account for the increase of leukaemia and non-Hodgkin's lymphoma in Seascale?

OBJECTIVE--To determine if the excess of leukaemia and non-Hodgkin''s lymphoma in Seascale is restricted to those born in the parish and whether it might be explained by the postulated relation with paternal preconceptional radiation. DESIGN--Comparison, separately for those born in the parish and those born elsewhere, of the numbers of these malignancies observed in Seascale with those expected on the basis of reference rates for England and Wales. Details of paternal radiation levels were sought for each case. SETTING--The parish of Seascale in west Cumbria. SUBJECTS--Residents of Seascale below age 25 years in the years 1951-91. MAIN OUTCOME MEASURES--The observed and expected numbers of cases of leukaemia and non-Hodgkin''s lymphoma within Seascale among those born there and among those born elsewhere. Also, the levels of any paternal preconceptional radiation associated with each case. RESULTS--A significant excess of leukaemia and non-Hodgkin''s lymphoma at ages 0-24 was found in Seascale in those who were born there (ratio of observed to expected cases 8.6 and 20.2 respectively; p < 0.01). This also applied to those not born there (7.2 and 16.5; p < 0.01), a group often regarded as not showing an excess. The estimates were then conservatively recalculated so as to overestimate the risks among those born in Seascale and underestimate them among those born elsewhere. On this basis the six cases in those born in Seascale compare with 0.38 expected (15.8; p < 0.001), of which two were associated with paternal preconceptional life-time levels of 100 mSv or greater and three others with levels of 90-99 mSv. Among those born elsewhere, there were five cases (expected 0.74; ratio 6.7, p < 0.01), of which only one was associated with a high level of such radiation. CONCLUSIONS--Paternal preconceptional radiation cannot be the sole cause of the excess in Seascale since it will not explain the excess among those born outside Seascale. It follows that, unless two causes are to be postulated, any single cause must be a factor other than paternal preconceptional radiation. On this basis, the association found among those born there, if not partly due to chance, may reflect an indirect relation with the true cause. The recent hypothesis about such paternal radiation has originated in a subgroup of the excess cases that have aroused concern.     

Paternal age and Down syndrome in British Columbia

Among Down syndrome cases born in 1964--1976 reported to the British Columbia Registry for Handicapped Children, the mean parental age was about half a year greater than in the entire population of live births after controlling for maternal age, a difference significant at the .05 level. After adjustment for maternal age, a regression analysis was consistent with an increase of 1.024-fold for each year of paternal age. Among Down syndrome cases in 1952--1963, however, for which ascertainment appears likely to be less complete, there was no evidence for a significant paternal age effect. The reasons for the variation between the two groups investigated here and the heterogeneity in results among studies of other populations are discussed.     

Paternal age and Down's syndrome genotypes diagnosed prenatally: No association in New York State data

Summary An investigation of a paternal age effect independent of maternal age was undertaken for 98 cases of Down's syndrome genotypes diagnosed prenatally compared to 10,329 fetuses with normal genotype diagnosed prenatally in data reported to the New York State Chromosome Registry. The mean of the difference (delta) in paternal age of cases compared to those with normal genotypes after controlling for maternal age, was slightly negative,-0.27 with a 95% confidence interval of-1.59 to +1.06. A regression analysis was also done in which the data were first fit to an equation of the type lny=(bx+c) and then to the equation ln y=(bx+dz+c) where y = rate of Down's syndrome, x = maternal age, z = paternal age, and b, d, and c are parameters. This also revealed no evidence for a paternal age effect. The value of d (the paternal age coefficient) was in fact slightly negative,-0.0058, with an asymptotic 95% confidence interval of-0.0379 to +0.0263. Lastly, multiple applications of the Mantel-Haenszel test considering various boundaries in paternal age also revealed no statistically significant evidence for a paternal age effect independent of maternal age. These results are at variance with claims of others elsewhere of a very strong paternal age effect detected in studies at prenatal diagnoses. Five different hypotheses are suggested which may account for discrepancies among studies to date in findings on paternal age effects for Down's syndrome: (i) there are temporal, geographic, or ethnic variations in paternal age effects, (ii) there is no paternal age effect and statistical fluctuation accounts for all trends to date; (iii) methologic artifacts have obscured a paternal age effect in some studies which did not find a positive outcome; (iv) methodologic artifacts are responsible for the positive results in some studies to date; (v) there is a rather weak paternal age effect independent of maternal age in most if not all populations, but because of statistical fluctuation the results are significant only in some data sets. The results of all data sets to date which we have been able to analyze by one year intervals are consistent with a mean delta of +0.04 to +0.48 and in the value of d (the paternal age coefficient) of +0.006 to +0.017, and it appears the fifth hypothesis cannot be excluded. Projections based on this assumption are presented.     

Paternal age and the occurrence of birth defects

The association between paternal age and the occurrence of birth defects was studied using data collected in Metropolitan Atlanta. Paternal-age information for babies born with defects was obtained from birth certificates, hospital records, and interviews with mothers; for babies born without defects, the information was obtained from birth certificates. Several statistical techniques were used to evaluate the paternal-age-birth-defects associations for 86 groups of defects. Logistic regression analysis that controlled for maternal age and race indicated that older fathers had a somewhat higher risk for having babies with defects, when all types of defects were combined; an equivalent association for older mothers was not found. Logistic regression analyses also indicated modestly higher risks for older fathers for having babies with ventricular septal defects and atrial septal defects and substantially higher risks for having babies with defects classified in the category chondrodystrophy (largely sporadic achondroplasia) and babies with situs inversus. An association between elevated paternal age and situs inversus has not been reported before; the magnitude of the estimated increased risk for situs inversus was about the same as that found in this study for chondrodystrophy.     

Risk for Asthma in Offspring of Asthmatic Mothers versus Fathers: A Meta-Analysis

Background

Many human epidemiologic studies demonstrate that maternal asthma confers greater risk of asthma to offspring than does paternal disease. However, a handful have shown the opposite. Given this disparity, a meta-analysis is necessary to determine the veracity and magnitude of the “maternal effect.”

Methodology/Principal Findings

We screened the medical literature from 1966 to 2009 and performed a meta-analysis to compare the effect of maternal asthma vs. paternal asthma on offspring asthma susceptibility. Aggregating data from 33 studies, the odds ratio for asthma in children of asthmatic mothers compared with non-asthmatic mothers was significantly increased at 3.04 (95% confidence interval: 2.59–3.56). The corresponding odds ratio for asthma in children of asthmatic fathers was increased at 2.44 (2.14–2.79). When comparing the odds ratios, maternal asthma conferred greater risk of disease than did paternal asthma (3.04 vs. 2.44, p = 0.037). When analyzing the studies in which asthma was diagnosed by a physician the odds ratios were attenuated and no significant differences were observed (2.85 vs. 2.48, N = 18, p = 0.37). Similarly, no significant differences were observed between maternal and paternal odds ratios when analyzing the studies in which the patient population was 5 years or older (3.15 vs. 2.60, p = 0.14). However, in all cases the trend remained the same, that maternal asthma was a greater risk factor for asthma than paternal.

Conclusions/Significance

The results show that maternal asthma increases offspring disease risk to a greater extent than paternal disease.     

Inverse relationship between age at onset of Huntington disease and paternal age suggests involvement of genetic imprinting.

It is well recognized that age at onset of Huntington disease (HD) is strongly influenced by the sex of the affected parent, and this has lead to suggestions that genetic imprinting or maternal specific factors may play a role in the expression of the disease. This study evaluated maternal and paternal ages, birth order, parental age at onset, and sex of the affected parent and grandparent in 1,764 patients in the National HD Roster by using linear-regression techniques which incorporated a weighted least-squares approach to accommodate the correlation among siblings. It was found that paternal age is negatively associated with age at onset of HD, particularly among subjects who inherit the mutant gene from grandfathers. Apparent associations between age at onset and birth order and between age at onset and maternal age were not significant after adjustment for paternal age. The paternal age effect is strongest among juvenile-onset cases and individuals with anticipation of greater than or equal to 10 years, although it is detectable across the entire age-at-onset distribution. The tendency for older fathers, including those not transmitting the HD gene, to have affected offspring with early-onset disease may be consistent with a gene imprinting mechanism involving DNA methylation. Because paternal age in unaffected fathers is also a significant determinant of age at onset, methylation in this context might involve HD modifier genes or the normal HD allele.     

Comparison of mathematical models for the maternal age dependence of Down's syndrome rates

Summary The maternal age dependence of Down's syndrome rates was analyzed by two mathematical models, a discontinuous (DS) slope model which fits different exponential equations to different parts of the 20–49 age interval and a CPE model which fits a function that is the sum of a constant and exponential term over this whole 20–49 range. The CPE model had been considered but rejected by Penrose, who preferred models postulating changes with age assuming either a power function X¹⁰, where X is age or a Poisson model in which accumulation of 17 events was the assumed threshold for the occurrence of Down's syndrome. However, subsequent analyses indicated that the two models preferred by Penrose did not fit recent data sets as well as the DS or CPE model. Here we report analyses of broadened power and Poisson models in which n (the postulated number of independent events) can vary. Five data sets are analyzed. For the power models the range of the optimal n is 11 to 13; for the Poisson it is 17 to 25. The DS, Poisson, and power models each give the best fit to one data set; the CPE, to two sets. No particular model is clearly preferable. It appears unlikely that, with a data set from any single available source, a specific etiologic hypothesis for the maternal age dependence of Down's syndrome can be clearly inferred by the use of these or similar regression models.     

Epidemiology of gastroschisis in metropolitan Atlanta, 1968 through 2000

BACKGROUND: An increase in the rate of gastroschisis has been documented by birth defects surveillance systems in the United States and in other countries. This study sought to evaluate historical trends in the rate of gastroschisis in Atlanta, Georgia, and to describe the epidemiology of gastroschisis over 33 years. METHODS: Gastroschisis cases were identified through the Metropolitan Atlanta Congenital Defects Program (MACDP) from 1968 through 2000. Poisson regression techniques were used to evaluate trends over time. Data on covariates were compared for three maternal age groups (< or =19, 20-24, and > or =25 years). RESULTS: From 1968 through 1975, the rate of gastroschisis was stable at 0.8 per 10,000 births. After 1975, the rate of gastroschisis was 2.3 per 10,000 births with no significant increase observed from 1976 through 2000. The rate of gastroschisis was six times higher among teenage mothers compared with mothers > or =25 years of age. Affected infants born to teenage mothers were less likely to be born to Black mothers compared to White mothers (rate ratio [RR], 0.4; 95% confidence interval [CI], 0.2-0.6). This was also true for mothers 20-24 years of age (RR, 0.5; 95% CI, 0.3-0.8) but not for mothers 25 years of age or older (RR, 1.6; 95% CI, 0.9-2.7). CONCLUSIONS: An increase in the rate of gastroschisis was observed in the mid-1970s, but no temporal trend has been observed since that time. In light of recent reports of an increasing prevalence of gastroschisis in the United States, continued monitoring of this birth defect is warranted.