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PubMed1988

Direct and maternal variances and covariances and maternal phenotypic effects on preweaning growth of beef cattle.

Birth weights (BW) and weaning weights (WW) of 4,423 non-creep-fed Hereford calves were used to estimate direct and maternal sources of variation and maternal phenotypic effects (fm). Seventeen different (co)variances among relatives were estimated through Henderson's Method III and restricted estimated maximum likelihood procedures. Direct and maternal (co)variances and fm were evaluated by multiple regression procedures. Estimates of h2 for BW and WW were .28 and .28 respectively, by the paternal half-sib procedure and .45 and .88, respectively, based on full-sibs. Repeatability estimates were .21 for BW and .30 for WW. Heritabilities based on regression of offspring on dam and offspring on sire were .45 and .21 for BW and .28 and .06 for WW, respectively. Negative correlations were found between solutions for additive genetic direct and additive maternal effects (rG). Estimates of rG ranged from -.86 to -1.05 for BW and from -.57 to -.79 for WW. Estimates of heritability for direct effects (h2o), for maternal effects (h2m) and for total additive genetic effects (h2T) were .16 to .27, .18 to .63 and -.02 to .05 for BW and .26 to .32, .27 to .67 and .10 to .20 for WW. Dominance affected both direct and maternal effects for BW and WW. Values of -.15 (BW) and -.25 (WW) were found for fm (path coefficient between the maternal phenotypes of dam and daughter). These results indicated that selection response would be decreased due to the negative genetic correlation between direct and maternal effects.

Analysis of Variance↗

PubMed1977

Craniomyeloschisis: a spontaneous mutation of the rat.

Craniomyeloschisis (proposed gene symbol cms) was a spontaneous mutation of the rat inherited as an autosomal recessive trait with complete penetrance. Homozygous offspring died at birth with failure of closure of the neural tube caudal to the midbrain. Neural crest derivatives were relatively normal. There were associated severe malformations of the axial skeleton including skull, vertebral column, and ribs. The pattern of malformations was quite uniform. Heterozygotes were anatomically normal. The mutation is extinct.

Abnormalities, Multiple↗

PubMed1992

Trends in rates of multiple vascular disruption defects, Atlanta, 1968-1989: is there evidence of a cocaine teratogenic epidemic?

Research suggests that, perhaps through mechanisms initiated by vasoconstriction and leading to vessel thrombosis or embolism, cocaine causes vascular disruption defects, and that frequent cocaine use during early pregnancy could disrupt multiple organ systems in the fetus. We hypothesized that if cocaine is an important cause of multiple vascular disruption defects, a rising prevalence of cocaine use by mothers during pregnancy should be accompanied by rising rates of these defects in their offspring. Using data from the Metropolitan Atlanta Congenital Defects Program, we identified all infants born in Atlanta from 1968 through 1989 who had nonsyndromic, provisional vascular disruption defects affecting more than one organ system: 61 infants (78%) had gastrointestinal and genitourinary defects, 7 (9%) had gastrointestinal and abdominal wall defects, 2 (3%) had gastrointestinal and limb reduction defects, 2 (3%) had limb reduction and abdominal wall defects, 2 (3%) had central nervous system and gastrointestinal defects, 2 (3%) had genitourinary and limb reduction defects, 1 (1%) had genitourinary and abdominal wall defects, and 1 (1%) had central nervous system and genitourinary defects. The prevalence of Atlanta infants with more than one vascular disruption defect is 0.13 per 1,000 live births. Chi-square analysis for trends showed no increase in prevalence during the study period. Our data are from one of the first population-based studies in which trends for defects potentially caused by maternal cocaine use are examined; the results of our study show no significant change in the prevalence of multiple vascular disruption defects over time.(ABSTRACT TRUNCATED AT 250 WORDS)

Abnormalities, Drug-Induced↗

PubMed1982

Offspring of teenage mothers: congenital malformations, low birth weights and other findings.

Teenage mothers were found to have congenitally malformed infants with a significantly higher frequency when compared to a published control population. Low birth weight and perinatal death were common among the infants of mothers 17 and younger. No chromosomal anomalies were found among the infants of this population, but this result does not unequivocally rule out an increased frequency of these disorders.

Abnormalities, Multiple↗

PubMed1992

Variation in maternal care and individual differences in play, exploration, and grooming of juvenile Norway rat offspring.

Individual differences in two different forms of maternal licking, time in nest and nursing, were measured during the first 2 weeks after birth. Two treatments were imposed to reduce maternal anogenital licking (AGL): peripheral zinc sulfate to interfere with reception of pup chemosignals, and dietary saline to reduce appetite for pup urine. Both treatments reduced AGL but did not affect other maternal licking. Zinc sulfate was more effective than saline during the first week, but was somewhat less selective as it also increased time in nest. Selected behavioral patterns were measured in male and female juveniles and related by multiple regression to the behavior of their mothers. Independent of the method of manipulation, maternal AGL was a significant predictor of play and open-field defecation males and of some forms of activity in the open field in both sexes. The relationships between other maternal variables and juvenile behavior were more modest. These data demonstrate that intervening in the sensory regulation of maternal behavior can produce predictable changes in stimulation provided by the dam, thereby providing a useful means for investigating the effects of protracted differences in early stimulation in otherwise normal developmental contexts.

Animals↗

PubMed1998

Maternal occupation in the leather industry and selected congenital malformations.

OBJECTIVES: Data from a hospital based case-control study were analysed to assess the relation between maternal occupation in the leather industry and several groups of congenital defects (nervous system, cardiac defects of closure, oral cleft, epispadia or hypospadia, and multiple anomalies). METHODS: Cases and controls were selected from eight public hospitals in Comunidad Valenciana, Spain, in 1993 and 1994. Cases were located from the hospital discharge records, including children born and diagnosed in some of the selected hospitals during their first year of life. Controls were selected from births without congenital defects in the same hospitals and dates of the cases (ratio 1:1). Both parents of selected children were interviewed (mainly by phone) and information about potential confounding variables and occupational history during the three years before the birth was collected in structured questionnaires. RESULTS: A total of 261 cases and the same number of controls were included in the study. Adjusted odds ratios (ORs) were estimated for maternal occupation in the leather industry in the period between three months before the conception and the birth of the child (n = 22), and each selected group of congenital malformations: nervous system defects (OR 1.02, 95% confidence interval (95% CI) 0.12 to 8.51), cardiac defects of closure (OR 1.78, 95% CI 0.44 to 7.17), oral clefts (OR 6.18, 95% CI 1.48 to 25.69), for epispadia or hypospadia (OR 4.05, 95% CI 0.77 to 21.44), and multiple anomalies (OR 3.14, 95% CI 0.82 to 12.00). CONCLUSION: These data are compatible with an increased risk for oral clefts in the offspring of women working in the leather industry. Some other categories of defect could have an increased risk as well, although for these our data cannot exclude random error as an explanation. Given these results and previous findings in similar studies, some precautionary recommendations regarding maternal exposure in leather industries, probably in relation to solvents, would be justified.

Case-Control Studies↗

PubMed2006

Offspring birthweight is not associated with paternal insulin resistance.

AIMS/HYPOTHESIS: Low birthweight is associated with insulin resistance and other insulin resistance-related phenotypes: diabetes, hypertension, and vascular disease in later life. The underlying mechanism is unclear. The foetal insulin hypothesis proposes that a single genetic predisposition to beta cell dysfunction/insulin resistance results in both reduced insulin-dependent foetal growth in utero, hence low birthweight, and predisposition to type 2 diabetes. The aim of this study was to test whether, as predicted by the foetal insulin hypothesis, there is an association between measures of paternal insulin resistance and offspring birthweight. SUBJECTS AND METHODS: The Exeter Family Study of Childhood Health (EFSOCH) is a community-based study within central Exeter (UK), established to test the foetal insulin hypothesis prospectively. Associations were tested between offspring birthweight and paternal insulin resistance, calculated by homeostasis model assessment analysis in 986 families using data relating to singleton, non-diabetic, UK white pregnancies. Ethics approval was given by the North and East Devon local ethics committee. RESULTS: Offspring birthweight was not significantly correlated with log paternal insulin resistance (r=0, p=0.91), log HDL cholesterol concentration (r=-0.02, p=0.47) or log triglyceride concentration (r=0, p=0.99) when corrected for paternal BMI and common confounders. Multiple linear regression analysis confirmed that paternal insulin resistance was not an independent predictor of offspring birthweight. CONCLUSIONS/INTERPRETATION: Results from a young, adult, non-diabetic population do not support the foetal insulin hypothesis as an explanation for the association of low birthweight with insulin resistance.

Adult↗

PubMed2005

Mitochondrial polymorphisms and susceptibility to type 2 diabetes-related traits in Finns.

Mitochondria play an integral role in ATP production in cells and are involved in glucose metabolism and insulin secretion, suggesting that variants in the mitochondrial genome may contribute to diabetes susceptibility. In a study of Finnish families ascertained for type 2 diabetes mellitus (T2DM), we genotyped single nucleotide polymorphisms (SNPs) based on phylogenetic networks. These SNPs defined eight major haplogroups and subdivided groups H and U, which are common in Finns. We evaluated association with both diabetes disease status and up to 14 diabetes-related traits for 762 cases, 402 non-diabetic controls, and 465 offspring of genotyped females. Haplogroup J showed a trend toward association with T2DM affected status (OR 1.69, P=0.056) that became slightly more significant after excluding cases with affected fathers (OR 1.77, P=0.045). We also genotyped non-haplogroup-tagging SNPs previously reported to show evidence for association with diabetes or related traits. Our data support previous evidence for association of T16189C with reduced ponderal index at birth and also show evidence for association with reduced birthweight but not with diabetes status. Given the multiple tests performed and the significance levels obtained, this study suggests that mitochondrial genome variants may play at most a modest role in glucose metabolism in the Finnish population. Furthermore, our data do not support a reported maternal inheritance pattern of T2DM but instead show a strong effect of recall bias.

Adenosine Triphosphate↗

PubMed2007

Nurses with dermal exposure to antineoplastic drugs: reproductive outcomes.

BACKGROUND: Nurses and other hospital workers are exposed to antineoplastic drugs during daily activities. Previous studies suggest that antineoplastic drugs at occupational exposure levels may be toxic to reproduction, but these studies are not consistent or conclusive. METHODS: Self-administered questionnaires were completed by 4393 exposed and nonexposed nurses employed between 1990 and 1997 (79% response). Questions were asked about pregnancy outcome, work-related exposures, and lifestyle. Exposure to antineoplastic drugs was estimated using task-based dermal exposure measurements and self-reported task frequencies. Time to pregnancy was modeled using survival analysis, and odds ratios (ORs) with 95% confidence intervals (CIs) were calculated for other reproductive outcomes using multiple logistic regression analysis. Associations were further explored by nonparametric regression modeling. RESULTS: Nurses highly exposed to antineoplastic drugs took longer to conceive than referent nurses (adjusted hazard ratio = 0.8; CI = 0.6-0.9). Exposure to antineoplastic drugs was associated with premature delivery (OR per unit increase in ln[exposure] = 1.08; CI = 1.00-1.17) and low birth weight (OR per unit increase in ln[exposure] = 1.11; 1.01-1.21). Penalized smoothed spline plots corroborated these log-linear relations. Spontaneous abortion, stillbirth, congenital anomalies, and sex of offspring appeared not to be related to exposure to antineoplastic drugs. CONCLUSION: Antineoplastic drugs may reduce fertility and increase poor neonatal outcomes among occupationally exposed oncology nurses.

Adult↗

PubMed2004

Effects of maternal nutrition on fetal and neonatal reproductive development and function.

Maternal undernutrition and, under certain circumstances overnutrition, before or during pregnancy or during early postnatal life can alter reproductive function of the offspring. Effects can be exerted at many stages of development, from prior to conception until after birth and may be expressed at the time of the nutritional insult or later. Since patterns of development differ between species, it is probably more appropriate to consider effects in relation to a stage of development rather than relative to the time of birth. Effects exerted at one stage of development may be expressed later, even if the nutritional influence is no longer present. The signals by which maternal nutrition affects the offspring must be related to maternal nutritional state and must have the capacity to reach the embryo, to be 'read' by it and to modify expression of selected genes. It is suggested that single nutrients and/or metabolites are unlikely to have direct impacts on the pattern of development of the reproductive system and it is postulated that multiple endocrine and metabolic signals are involved. Whilst it has been shown that many components of the hypothalamic-pituitary-gonadal system are modified by early life nutritional influences, understanding of the mechanisms through which these effects are exerted remains limited.

Animals↗

PubMed1998

Prediction factors in the determination of final height in subjects born small for gestational age.

The aim of this study was to identify factors predictive of individual final height (FH) in subjects born small for gestational age (SGA). All full-term singleton subjects born SGA (birth weight and/or length <3rd percentile) during the period 1971-1978, matched with appropriate birth weight for gestational age (AGA) subjects (birth weight between 25th and 75th percentile) were followed from birth to FH and evaluated before puberty at a mean age +/- SD of 6.1 +/- 0.7 y and after puberty at a mean age of 20.8 +/- 2.0 y (subjects born SGA, n = 213; born AGA, n = 272). When adjusted for target height, a significant deficit in final height (p < 0.0001) was found in SGA as compared with AGA subjects for both male subjects (-3.99 cm with 95% confidence interval from -5.6 to -2.4) and female subjects (-3.64 cm with 95% confidence interval from -5.0 to -2.3), with 13.6% of subjects in the SGA population presenting short final stature. In a multiple regression analysis, target height and studied group (SGA or AGA) were found to be the strongest predictors of individual FH (p < 0.0001, r2 = 0.35 for male subjects, p < 0.0001, r = 0.40 for female subjects). For SGA subjects and according to a multiple stepwise linear regression model, 31% of the variability of individual FH [SD score (SDS)] and 58% of the variability of individual height gain SDS could be explained at birth from mother's height, father's height, and birth length SDS. No other variables were found to be predictive such as sex, gestational age (from 37 to 42 wk), birth weight SDS, ponderal index at birth, or risk factors during pregnancy associated with intrauterine growth retardation such as pregnancy-induced hypertension, smoking, or a history of SGA in offspring. Although a significant increase of body mass index SDS was documented before and after puberty in SGA subjects, puberty was not found to have any influence on growth outcome.

Adult↗

PubMed2001

Alcohol and pregnancy: highlights from three decades of research.

The detrimental effects of alcohol on offspring have been alluded to for centuries, although only in the past few decades has the relationship between alcohol and birth defects been shown conclusively. This review article begins with a historical overview of the understanding of alcohol's effects on the offspring, followed by a description of the first clinical reports of fetal alcohol syndrome. The contribution of animal models is highlighted and some possible mechanisms of alcohol's teratogenicity are discussed. Challenges and opportunities for future research are offered.

Abnormalities, Multiple↗

PubMedDate not supplied

Prevention of developmental abnormalities with particular emphasis of primary prevention.

The Hungarian total (birth + fetal) prevalences of different developmental abnormalities offer a possibility to estimate the proportion of preventable development abnormalities. The effectiveness of primary, secondary and tertiary preventive methods are evaluated with a particular emphasis of primary prevention based on periconceptional folic acid or folic acid-containing multivitamin supplementation. The total prevalence of informative offspring with developmental abnormalities is 66.83 per 1,000 in Hungary and within this major DAs have 27.01 per 1,000 rate. The latter can be reduced by 26.6% by primary preventive methods due to mainly periconceptional folic acid/multivitamin supplementation. Secondary prevention particularly neonatal orthopedic screening is very effective for deformities such as congenital dislocation of the hip. Antenatal diagnoses followed by termination of pregnancy can avoid the birth of malformed newborn infants in 8.7% of DAs, however, this figure is 20 and 27% among major and multiple developmental abnormalities, respectively. Early surgical intervention can achieve a complete recovery in 33.5% of cases with developmental abnormalities. Thus there are two major conclusions: at present the major part of developmental abnormalities are preventable, however, different developmental abnormalities do not represent a single pathological category therefore there is no single strategy for their prevention.

Congenital Abnormalities↗

PubMed1990

Paternal occupational exposure to electromagnetic fields and neuroblastoma in offspring.

Investigators in Texas have reported an association between paternal employment in jobs linked with exposure to electromagnetic fields and risk of neuroblastoma in offspring. In an attempt to replicate this finding, the authors conducted a case-control study in Ohio. A total of 101 incident cases of neuroblastoma were identified through the Columbus (Ohio) Children's Hospital Tumor Registry. All cases were born sometime during the period 1942-1967. From a statewide roster of birth certificates, four controls were selected for each case, with individual matching on the case's year of birth, race, and sex, and the mother's county of residence at the time of the (index) child's birth. Multiple definitions were employed to infer the potential for paternal occupational exposure to electromagnetic fields from the industry/occupation statements on the birth certificates. Case-control comparisons revealed adjusted odds ratios ranging in magnitude from 0.5 to 1.9. For two of the exposure definitions employed--both of which are similar to one used by the Texas investigators--the corresponding odds ratios were modestly elevated (odds ratios = 1.6 and 1.9). Notably, the magnitude of these odds ratios is not inconsistent with the Texas findings, where the exposure definition referred to yielded an odds ratio of 2.1. Because the point estimates in this study are imprecise, and because the biologic plausibility of the association is uncertain, the results reported here must be interpreted cautiously. However, the apparent consistency between two independent studies suggests that future evaluation of the association is warranted.

Adolescent↗

PubMed2003

Transplacental carcinogenicity of inorganic arsenic in the drinking water: induction of hepatic, ovarian, pulmonary, and adrenal tumors in mice.

Arsenic is a known human carcinogen, but development of rodent models of inorganic arsenic carcinogenesis has been problematic. Since gestation is often a period of high sensitivity to chemical carcinogenesis, we performed a transplacental carcinogenicity study in mice using inorganic arsenic. Groups (n = 10) of pregnant C3H mice were given drinking water containing sodium arsenite (NaAsO(2)) at 0 (control), 42.5, and 85 ppm arsenite ad libitum from day 8 to 18 of gestation. These doses were well tolerated and body weights of the dams during gestation and of the offspring subsequent to birth were not reduced. Dams were allowed to give birth, and offspring were weaned at 4 weeks and then put into separate gender-based groups (n = 25) according to maternal exposure level. The offspring received no additional arsenic treatment. The study lasted 74 weeks in males and 90 weeks in females. A complete necropsy was performed on all mice and tissues were examined by light microscopy in a blind fashion. In male offspring, there was a marked increase in hepatocellular carcinoma incidence in a dose- related fashion (control, 12%; 42.5 ppm, 38%; 85 ppm, 61%) and in liver tumor multiplicity (tumors per liver; 5.6-fold over control at 85 ppm). In males, there was also a dose-related increase in adrenal tumor incidence and multiplicity. In female offspring, dose-related increases occurred in ovarian tumor incidence (control, 8%; 42.5 ppm, 26%; 85 ppm, 38%) and lung carcinoma incidence (control, 0%; 42.5 ppm, 4%; 85 ppm, 21%). Arsenic exposure also increased the incidence of proliferative lesions of the uterus and oviduct. These results demonstrate that oral inorganic arsenic exposure, as a single agent, can induce tumor formation in rodents and establishes inorganic arsenic as a complete transplacental carcinogen in mice. The development of this rodent model of inorganic arsenic carcinogenesis has important implications in defining the mechanism of action for this common environmental carcinogen.

Adrenal Gland Neoplasms↗

PubMed1998

Introduction to the special section: studying intergenerational continuity and the transfer of risk.

This special section, "Longitudinal Studies of Intergenerational Continuity and the Transfer of Psychosocial Risk," examines the continuity of behavior across generations and the processes whereby parental characteristics, history, and experiences may place offspring at risk for various social, psychological, and health problems. The 8 prospective longitudinal studies in this section were initiated during the childhood of the parental generation and followed these individuals over time to the formation of new families. Topics include prediction of aggression, difficult temperament, social withdrawal, smoking, low academic achievement and high school dropout, adolescent parenthood, problematic fertility and birth circumstances, spousal violence, and problematic parenting practices. Predictors of successful adaptation to high-risk backgrounds and environments are examined, with an emphasis on protective factors and multiple determinants of outcomes.

Adolescent↗

PubMed2003

Safety issues in assisted reproduction technology. From theory to reality--just what are the data telling us about ICSI offspring health and future fertility and should we be concerned?

Concerns about the effects of ICSI on offspring health and fertility include the rate of chromosomal anomalies, cystic fibrosis (CF) gene mutations associated with congenital bilateral absence of the vas deferens (CBAVD) and Y-chromosome microdeletions. The evidence in favour of screening for these in the presence of azoospermia or severe oligozoospermia is beyond debate. Concerns requiring further investigation include the effects of ICSI on imprinted genes and genes involved in DNA replication error repair. There is evidence of an increased risk of low birth weight, cerebral palsy and major birth defects following assisted reproductive technologies (ART), including ICSI, although the causes remain unknown. Given the large studies required to investigate these questions, particularly for rarer genetic conditions, we may simply have to accept that we may not know for many years if there are increased risks associated with ICSI. It would be prudent, however, to acknowledge this as a possibility and counsel patients accordingly. In terms of certainty of outcome and magnitude of impact the single most important health effect of ART for the offspring remains the iatrogenic multiple pregnancy rate. A reduction of iatrogenic multiples is the single most important and achievable means of preventing cerebral palsy currently available. Once achieved, the occurrence of rare genetic conditions will assume greater importance.

Child Welfare↗

PubMed1987

Inbreeding and prereproductive mortality in the Old Order Amish. II. Genealogic epidemiology of prereproductive mortality.

The effects of offspring and parental inbreeding on prereproductive mortality (death before age 20 years) in the historical population of the Lancaster County, Pennsylvania, Old Order Amish were investigated using the Amish genealogic registry, which contains information on 42,465 births dating to the time of the pioneer migrants in the 1700s. Inbreeding coefficients for offspring and parents were computed using the path method of tracing common ancestors in the multigenerational pedigrees. In this population, prereproductive mortality declined from about 15% in the late 1800s to about 5% after 1930. Offspring inbreeding was found to be an independent predictor of prereproductive mortality after multivariate adjustment for demographic risk factors for mortality. Moreover, the higher the coefficient, the higher the relative risk of prereproductive death, and the higher the risk of multiple deaths in the same sibship. There was no evidence of declining inbreeding effects over 10 generations of continuous inbreeding, nor of any significant parental inbreeding effects. Because of the high levels of inbreeding, it could be shown that inbreeding accounts for about 40% of all prereproductive deaths in the present population. Genetic load analysis showed an average of about 1.7 lethal equivalents and a mostly mutational load.

Adult↗