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PubMed2006

Maternal panic disorder and congenital abnormalities: a population-based case-control study.

BACKGROUND: Maternal panic disorder in pregnancy is the most common manifestation of anxiety disorders in Hungary. The association between panic disorder during pregnancy and structural birth defects, i.e., congenital abnormalities, was studied. METHODS: The prevalence of maternal panic disorder in cases with different congenital abnormalities was compared to that of matched controls in the population-based Hungarian Case-Control Surveillance System of Congenital Abnormalities. RESULTS: Of 22,843 cases with congenital abnormalities, 210 (0.9%) had mothers with panic disorder during pregnancy compared to 187 (0.5%) of 38,151 controls (adjusted prevalence odds ratio [POR] 1.6; 95% CI, 1.3-2.0). Specific groups of congenital abnormalities were also assessed versus controls. Cases with isolated cleft lip with or without cleft palate (CL/P) (adjusted POR, 3.4; 95% CI, 1.3-9.0) and multiple congenital abnormalities (adjusted POR, 3.0; 95% CI, 1.2-7.2) were more likely to have had mothers with panic disorder during the study pregnancy. Notably, among mothers with panic disorders, the associations were found only in offspring of untreated mothers. CONCLUSIONS: A higher rate of isolated CL/P and multiple congenital abnormalities may be caused by the direct biological effect of panic disorder or by the interaction of maternal panic disorder and lifestyle factors. Antipanic drug treatment seems to have a protective effect for isolated CL/P and multiple congenital abnormalities. Birth Defects Research (Part A), 2006.

Abnormalities, Multiple↗

PubMed1985

Clara cell adenomas of the mouse lung. Interaction with alveolar type 2 cells.

Multiple pulmonary adenomas were induced in the offspring of pregnant Swiss-Webster mice by transplacental exposure to ethylnitrosourea (ENU) on the 15th day of gestation. Development and growth of tumors were followed for up to a year after birth. Morphologic assessment indicated that the majority of adenomas were of Clara-cell origin and were relatively normal on the basis of structural features. Histochemical studies, utilizing nitroblue tetrazolium reductase activity as a marker for normal Clara cells demonstrated that the Clara-cell-derived tumors possessed nearly normal enzyme activity. Microscopic studies of the tumors and adjacent parenchyma revealed a unique Type 2 cell response to the presence of Clara-cell adenomas occurring in the alveoli beyond the margins of the tumor. Otherwise normal-appearing Type 2 cells, in a narrow zone around the Clara-cell tumors, accumulated large amounts of surfactantlike osmiophilic lamellar material within cytoplasmic vacuoles as early as 30 days after birth. These changes were clearly a Clara-cell-tumor-related response, and not seen in association with other non-Clara-cell adenomas of the same lung. Furthermore, the alterations occurred exclusively in Type 2 cells. The extent of Type 2 cell change was correlated with tumor size and age. Autoradiographic studies with tritiated choline showed marked incorporation of the labeled precursor by the altered Type 2 cells. By electron microscopy, these inclusions were membrane-limited and contained osmiophilic lamellar structures similar to lamellar bodies in normal Type 2 cells. Because these Clara cell adenomas may act as a concentrated focus of normal Clara cells, the alterations seen in Type 2 cells may reflect an amplification of a normal interaction between bronchiolar Clara cells and alveolar Type 2 cells in the centriacinar and juxtabronchiolar alveoli.

Adenoma↗

PubMed1978

Schwartz-Jampel syndrome. Clinical, electrophysiological and histopathological study of a severe variant.

This report describes a child, offspring of a first cousin marriage, with a severe and progressive disorder of bone and cartilage growth associated with a myotonia-like syndrome. Clinical manifestations of this disease began at birth with marked generalized muscle hypertrophy, stiffness, myotonia and multiple skeletal deformities. Successively severe dwarfism and mental retardation were observed. Neurophysiological studies showed continuous high frequently low voltage activity at rest and myotonic discharges which did not wax and wane. These abnormalities persisted after complete curarization. Muscle biopsy showed mild dystrophic changes. Polymeric glycosaminoglycans and degradation product excretion was normal. These findings are similar to those described in Schwartz-Jampel syndrome, but since the clinical picture was fully expressed at birth and was unusually severe, it is suggested that the patient's condition may have represented a severe variant of this syndrome.

Abnormalities, Multiple↗

PubMed1994

Prenatal dexamethasone exposure causes loss of neonatal hypoxia tolerance: cellular mechanisms.

Glucocorticoids promote lung cell differentiation and thus enhance surfactant synthesis in the management of neonatal respiratory distress syndrome. Because they also accelerate differentiation in other targets, glucocorticoids may compromise physiologic responses that operate through specialized fetal-neonatal mechanisms. The current study explores one such process, the capacity to maintain cardiac function during hypoxia, a critical function in light of the hypoxia associated with parturition and with neonatal respiratory distress. Pregnant rats were given 0.05, 0.2, or 0.8 mg/kg of dexamethasone on gestational d 17, 18, and 19, and the response to hypoxia was assessed in the offspring on the day after birth. Dexamethasone produced a dose-dependent impairment of survival during exposure to 5% O2 (5 kPa O2) for 120 min. ECG measurements showed that death in the dexamethasone-exposed animals was preceded by multiple arrhythmias and progressive atrioventricular conduction defects, terminating in cardiac arrest. Because maintenance of neonatal cardiac conduction during hypoxia depends on adrenergic mechanisms operating through adrenomedullary catecholamine release and actions at transiently expressed alpha 2-receptors in the immature myocardium, we examined these mechanisms in control and dexamethasone-exposed neonates. Dexamethasone caused cardiac alpha 2-receptors to disappear prematurely, an effect that was selective for this receptor population because no comparable changes were seen in alpha 1-receptors. Under normal circumstances, neonatal adrenomedullary responses to hypoxia operate in the absence of functional sympathoadrenal innervation, and cardiac-sympathetic innervation does not play a significant role; in a similar fashion, the dexamethasone-exposed animals did not display alterations in the functional state of sympathetic innervation of the adrenal medulla or heart at birth.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗

PubMed2006

Chronic hypertension as a risk factor for offspring to be born small for gestational age.

BACKGROUND: Chronic hypertension during pregnancy is associated with an increased risk for birth of small for gestational age offspring. The aim of this study was to determine whether the risk remains after consideration of maternal characteristics and superimposed pre-eclampsia. METHOD: A population-based cohort study based on the Swedish Medical Birth Register 1992-98 and comprising 560 188 women aged 15-44 years with singleton pregnancies including 2,754 women with chronic hypertension. The register contains data of maternal characteristics besides maternal and fetal complications. Multiple logistic regression analysis was used. Small for gestational age was defined as birth weight less than -2SD adjusted for gestational age and sex. RESULTS: Chronic hypertensive women have an independent risk for small for gestational age (OR 3.1; 95% CI 2.7-3.7) when controlling for confounding of maternal characteristics such as age, parity, BMI, smoking, and ethnic origin. After introducing superimposed pre-eclampsia in the model the risk remains but decreases (OR 2.4; 95% CI 2.1-2.9). CONCLUSION: Chronic hypertension is an independent risk factor for birth of small for gestational age offspring. Pre-eclampsia is a strong mediating factor.

Adolescent↗

PubMed1986

Effects of maternal smoking and caffeine habits on infantile apnea: a retrospective study.

To evaluate the relationship of antecedent maternal smoking and caffeine consumption habits on the occurrence of apnea in their offspring, rates for central and obstructive apnea were analyzed in a cohort of mother-infant pairs. The mothers of 298 infants with apnea responded to a questionnaire completed prior to a nine-hour polysomnogram performed as part of the patients' evaluations. Cigarette consumption estimates were computed on a 20-cigarette per pack basis, and caffeine intake, based on dietary sources (coffee, tea, chocolate, and colas), was summarized as milligrams of caffeine consumed per day. Rates of central and obstructive apnea of 6 to 10 seconds in duration were calculated. Multiple linear regression analysis determined that smokers tended to be younger and have lower birth weight infants who presented earlier with apnea than infants of nonsmokers. Increased rates of central apnea occurred in infants of smokers as compared with infants of nonsmokers. During pregnancy, a pack per day increase in maternal smoking habit was associated with a 1.88/h increase in central apneas in their offspring (P less than .01). Maternal smoking after delivery had a similar relationship. Obstructive apnea rates were similar in both groups. Both central and obstructive apnea rates associated positively with increasing maternal caffeine consumption. Smoking habits and caffeine ingestion were correlated (P less than .01). Infants with apnea have greater rates of central apnea when their mothers smoke during pregnancy. Therefore, a history of nicotine consumption should be included in the medical history of infants presenting with apnea.

Apnea↗

PubMed2006

Pre-conception energy balance and secondary sex ratio--partial support for the Trivers-Willard hypothesis in dairy cows.

According to the Trivers-Willard hypothesis, maternal condition at or around conception affects the secondary sex ratio in mammals. However, there are little or no data available on indicators of maternal condition in dairy cows on the sex of the resultant offspring. A total of 76,607 body condition score (BCS; scale of 1 to 5) records and 76,611 body weight (BW) records from 3,209 lactations across 1,172 cows were extracted from a research database collated from one research herd between 1986 and 2004, inclusive. Exclusion of multiple births and cows with no information before calving (e.g., nulliparous animals) resulted in 2,029 records with BCS and BW observations from the previous calving, and 2,002 and 1,872 lactations with BCS and BW observations at conception and midgestation, respectively. Change in BCS and BW between calving and conception and between conception and midgestation was calculated per lactation. Generalized estimating equations were used to model the logit of the probability of a male calf, in which cow was included as a repeated effect with a first-order autoregressive correlation structure assumed among records within cow. Of the BCS variables investigated, there was a linear relationship between the logit of the probability of a male calf and BCS change between calving and conception, the rate of BCS change over this period (BCS divided by days in milk), and BCS at the calving event immediately before conception. The birth of a bull calf was 1.85 times more likely in cows that lost no BCS from calving to conception compared with cows that lost one BCS unit from calving to conception. This increase in odds was equivalent to a 14% unit increase in the probability of a male calf (from 54 to 68%). The amount of BW lost between calving and conception and the rate of loss affected the sex of the resultant offspring. Less BW loss or greater BW gain between calving and conception was associated with greater likelihood of a male calf. Results suggested a positive effect of pre-conception BCS and BW change on secondary sex ratio, agreeing with the Trivers-Willard hypothesis that females in good physiological condition are more likely to produce male offspring.

Animal Feed↗

PubMed2004

Lack of prepubertal administration of ethinyl estradiol on susceptibility to multiple organ carcinogenesis in rats exposed to 7,12-dimethylbenz[a]anthracene and N-bis(2-hydroxypropyl)nitrosamine during adolescence.

Estrogen exposure during the adult period is widely known to promote tumor development in the female genital system, as well as in the mammary gland in experimental animals, but its carcinogenic potential with exposure at the prepubertal stage, for 6 weeks after birth, is not completely understood. In the present study, we therefore evaluated the modifying effects of prepubertal ethinyl estradiol (EE) treatment on susceptibility to multiple organ carcinogenesis with subsequent carcinogen exposure in F344 rats. Dams during the lactation period and their weaned offspring until postnatal-week 6 were fed diet containing 0, 0.2 or 1.0 ppm EE. The offsprings were then administered 7,12-dimethylbenz[a]anthracene (DMBA, 50mg/kg body weight) by gavage for mammary tumor induction in week 7 and given free access to drinking water containing N-bis (2-hydroxypropyl)nitrosamine (DHPN, 0.2%) for wide spectrum tumor induction in organs such as the thyroid, liver, lung and kidney from weeks 6-14. Male and female offspring were euthanized at weeks 27 and 36, respectively, for histopathological examination. While the incidence and multiplicity of mammary tumors showed a tendency for increase in females of the 0.2 and 1.0 ppm EE groups, this was without statistical significance. Furthermore, prepubertal EE exposure did not affect tumor induction in the thyroid, liver, lung, kidney, esophagus, ovary and lymphoid tissue in either sex. The present results thus indicate a lack of influence of estrogen early in life on carcinogenic susceptibility, although the possible impact on mammary carcinogenesis requires further examination.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed2003

Evaluation of the subfertile man.

Infertility affects 15 percent of couples, and 50 percent of male infertility is potentially correctable. Evaluation of the subfertile man requires a complete medical history, physical examination, and laboratory studies. The main purpose of the male evaluation is to identify and treat correctable causes of subfertility. In addition, many men seek an explanation for their condition, which can be discovered during their evaluation. Furthermore, the male fertility evaluation can uncover significant medical and genetic pathology that could affect the patient's health or that of his offspring. Although pregnancies can be achieved without any evaluation other than a semen analysis, this test alone is insufficient to adequately evaluate the male patient. Treatment of correctable male-factor pathology is cost effective, does not increase the risk of multiple births, and can spare the woman invasive procedures and potential complications associated with assisted reproductive technologies. Appropriate evaluation and treatment of the subfertile man are critical in delivering suitable care to the infertile couple.

Critical Pathways↗

PubMed1995

Impaired glucose tolerance in adolescent offspring of diabetic mothers. Relationship to fetal hyperinsulinism.

OBJECTIVE: To test the hypothesis that long-term postnatal development may be modified by metabolic experiences in utero. RESEARCH DESIGN AND METHODS: We enrolled offspring of women with pregestational diabetes (this included insulin-dependent diabetes mellitus [IDDM] and non-insulin-dependent diabetes mellitus [NIDDM]) and gestational diabetes in a prospective study from 1977 through 1983. Fetal beta-cell function was assessed by measurement of amniotic fluid insulin (AFI) at 32-38 weeks gestation. Postnatally, plasma glucose and insulin were measured yearly from 1.5 years of age after fasting and 2 h after 1.75 g/kg oral glucose. Control subjects had a single oral glucose challenge at 10-16 years. RESULTS: In offspring of diabetic mothers, the prevalence of impaired glucose tolerance (IGT) (2-h glucose concentration > 7.8 mmol/l) was: 1.2% at < 5 years, 5.4% at 5-9 years, and 19.3% at 10-16 years. The 88 offspring of diabetic mothers (12.3 +/- 1.7 years), when compared with 80 control subjects of the same age and pubertal stage, had higher 2-h glucose (6.8 +/- 1.4 vs. 5.7 +/- 0.9 mmol/l, P < 0.001) and insulin (660 +/- 720 vs. 455 +/- 285 pmol/l, P < 0.03) concentrations. The 17 subjects with IGT at > 10 years of age (9 boys and 8 girls) include one girl with NIDDM. IGT was not associated with the etiology of the mother's diabetes (gestational versus pregestational) or macrosomia at birth. IGT was found in only 3.7% (1 of 27) of adolescents whose AFI was normal ( < or = 100 pmol/l) and 33.3% (12 of 36) of those with elevated AFI (P < 0.001). Although most of the children with IGT are obese, AFI and obesity are independently associated with IGT by multiple logistic analysis. CONCLUSIONS: In confirmation of our original hypothesis, IGT in the offspring is a long-term complication of maternal diabetes. Excessive insulin secretion in utero, as assessed by AFI concentration, is a strong predictor of IGT in childhood.

Adolescent↗

PubMed1994

Prenatal alcohol exposure, birthweight, and measures of child size from birth to age 14 years.

OBJECTIVES: The purpose of the study was to examine the effect of prenatal alcohol exposure on offspring's weight, height, and head circumference from birth through 14 years of age. METHODS: This longitudinal prospective study examined a cohort of approximately 500 offspring (oversampled for heavier drinkers and stratified for smoking from a population of 1529 women in prenatal care at the 5th gestational month) at birth; 8 and 18 months; and 4, 7, and 14 years of age. Covariates were examined by means of multiple regression. Birth size measures were also examined as predictors of 7-year neurodevelopmental outcomes. RESULTS: Effects of alcohol were observed on weight, length, and head circumference at birth; these effects were not altered by adjustment for covariates including smoking. However, the birthweight effect is clearly transient: although alcohol effects remained observable at 8 months, they were not measurable thereafter through age 14 years. CONCLUSIONS: In this population-based sample, neither birthweight nor any later size measure was as useful an indicator of the enduring effects of prenatal alcohol exposure as were certain neurodevelopmental outcomes.

Adolescent↗

PubMed1993

Váradi syndrome (OFD VI) or Opitz trigonocephaly syndrome: overlapping manifestations in two cousins.

We report on 2 cousins, offspring of consanguineous matings, with multiple congenital anomalies. Square face, frontal bossing with metopic ridge, small anteverted nose, flat nasal bridge, slanted palpebral fissures, and epicanthal folds contributed to an unusual appearance. Multiple bucco-alveolar frenula and notched inferior alveolar ridges were present at birth and one had a notched uvula and submucous cleft of the hard palate. Both had congenital heart anomalies, micropenis, and cryptorchidism. Persistence of Müllerian structures was documented at necropsy in one patient. The surviving patient was mentally retarded and had unilateral central hexadactyly and partial agenesis of the corpus callosum. Bulimia and episodic hyperthermia were attributed to hypothalamic dysfunction. Results of unstimulated endocrine studies and gonadotropin releasing hormone (GnRH), and human chorionic gonadotropin (HCG) stimulation tests were normal. The manifestations of the 2 patients overlap those reported in the OFD VI and Opitz trigonocephaly syndromes.

Abnormalities, Multiple↗

PubMed2004

Reconstruction of parental microsatellite genotypes reveals female polyandry and philopatry in the lemon shark, Negaprion brevirostris.

Because sharks possess an unusual suite of reproductive characteristics, including internal fertilization, sperm storage, relatively low fecundity, and reproductive modes that range from oviparity to viviparity, they can provide important insight into the evolution of mating systems and sexual selection. Yet, to date, few studies have characterized behavioral and genetic mating systems in natural populations of sharks or other elasmobranchs. In this study, highly polymorphic microsatellite loci were used to examine breeding biology of a large coastal shark, the lemon shark, Negaprion brevirostris, at a tropical lagoon nursery. Over six years, 910 lemon sharks were sampled and genotyped. Young were assigned into sibling groups that were then used to reconstruct genotypes of unsampled adults. We assigned 707 of 735 young sharks to one of 45 female genotypes (96.2%), and 485 (66.0%) were assigned to a male genotype. Adult female sharks consistently returned to Bimini on a biennial cycle to give birth. Over 86% of litters had multiple sires. Such high levels of polyandry raise the possibility that polyandry evolved in viviparous sharks to reduce genetic incompatibilities between mother and embryos. We did not find a relationship between relatedness of mates and the number of offspring produced, indicating that inbreeding avoidance was probably not driving pre- or postcopulatory mate choice. Adult male sharks rarely sired more than one litter at Bimini and may mate over a broader geographic area.

Age Factors↗

PubMedDate not supplied

Achieving safe motherhood: applying a life course and multiple determinants perinatal health framework in public health.

Safe motherhood has begun to be identified as a priority for the health of American women. We argue that safe motherhood can be achieved through application of a life course and multiple determinants framework. This framework, with its focus on the preconception period, poses a dilemma in that it links together periods of life and domains of activities that have traditionally not been linked with maternal health. The interests of women and children have often been juxtaposed in the making of policy. Further, the domains of women's health, maternal and child health, and family planning have often clashed over policy priorities and funds. This framework shows that the research literature now links them inextricably to better health outcomes, albeit indirectly; there are no intervention studies that have demonstrated the empirical efficacy of this approach. Thus, although this framework creates a strong rationale for the linkages described, it also demands attention to a set of implementation strategies that will overcome existing barriers. Through a focus on one maternal factor, obesity, we discuss how a range of strategies grounded in the framework can be undertaken to address maternal morbidity and mortality. We then examine selected strategies at each level of the multiple determinants life course framework and emphasize how public policies and public and private sector professional practice can be reexamined to improve outcomes for women in all time periods and aspects of reproductive potential, which in turn might enhance outcomes for their offspring, both at birth and beyond. Our intent is to influence how policy makers, public health professionals, clinicians, and researchers approach safe motherhood.

Female↗

PubMed1984

Mental retardation and mother's hypertension during pregnancy.

A comparison of the history of hypertension in the mother during pregnancy was made between a group of 136 mentally retarded children and a randomly selected control group of 122 children. The cases and the controls were 9 or 10 years of age at the time of the survey. A number of potentially confounding factors were controlled for in a multiple logistic model. Maternal hypertension during pregnancy was associated with a relative risk of mental retardation in the offspring of 6.1 with 95% confidence interval of 1.3-28.9.

Birth Order↗

PubMed2003

IDDM2/insulin VNTR modifies risk conferred by IDDM1/HLA for development of Type 1 diabetes and associated autoimmunity.

AIM/HYPOTHESIS: Type 1 diabetes (T1D) is an autoimmune disease with multiple susceptibility genes. The aim of this study was to determine whether combining IDDM1/HLA and IDDM2/ insulin( INS) 5' variable number of tandem repeat locus (VNTR) genotypes improves T1D risk assessment. METHODS: Patients with T1D (n=488), control subjects (n=846), and offspring of parents with T1D (n=1122) were IDDM1 and IDDM2 genotyped. Offspring were followed for islet autoantibodies and T1D from birth until the age of 2 to 12 years. RESULTS: Compared to the I/I INS VNTR genotype, the I/III and III/III genotypes reduced T1D risk conferred by IDDM1/HLA in all HLA genotype categories of the case-control cohort by 1.6-fold to three-fold. The highest T1D risk was associated with INS VNTR class I/I plus HLA DR3/DR4-DQ8 (20.4% in patients, 0.6% in control subjects) or HLA DR4-DQ8/DR4-DQ8 (6.3% in patients, 0.2% in control subjects). In the offspring, HLA DR3/DR4-DQ8 and DR4-DQ8/DR4-DQ8 conferred increased risk for early development of islet autoantibodies (14.6% and 12.9% by age 2 years). Offspring with these high risk IDDM1 genotypes plus the INS VNTR class I/I genotype (n=71; 6.3%) had the highest risk of developing islet autoantibodies (21.8% by age 2 years vs 8.9% in offspring with high risk IDDM1 plus INS VNTR class I/III or III/III genotypes, p<0.05) and T1D (8.5% by age 6 years vs 4.3%). Offspring who developed autoantibodies to multiple antigens had increased frequencies of both high risk IDDM1 and IDDM2 genotypes (p<0.0001), whereas offspring who developed autoantibodies to GAD only had increased frequencies of high risk IDDM1 and protective IDDM2 genotypes, suggesting that IDDM2 influences the autoimmune target specificity. CONCLUSION/INTERPRETATION: Combining IDDM1 and IDDM2 genotyping identifies a minority of children with an increased T1D risk.

Autoantibodies↗

PubMed1997

The relationship between maternal birthweight and gestational age in twins and singletons and those of their offspring in Norway.

In order to elucidate whether maternal plurality affects offspring intrauterine growth, the relationship between birthweight and gestational age of twins and singletons and those of their first singleton liveborn children in Norway was studied using data from the Medical Birth Registry. The population-based sample consisted of 49,698 mother-offspring pairs (48,842 with singleton and 856 with twin-mothers). In bivariate analyses, no significant differences in mean birthweight and gestational age of offspring of twin and singleton mothers were found, although the mean birthweight and gestational age of the twin-mothers themselves were significantly lower than those of singletons (819 g and 14 days respectively). In multiple regression analysis, the expected birthweight of offspring was 230.3 g (95% CI: 193.2-267.4 g) higher when the mother was a twin than when the mother was a singleton, when controlling for non-standardised maternal birthweight. When adjusting for relative maternal birthweight (z-score), the association between maternal plurality and offspring birthweight was not statistically significant. The results suggest that being born as a twin has no substantial consequences on offspring growth in utero and show that mean differences in birthweight between twins and singletons should be standardised when both groups are included in multivariate studies.

Birth Weight↗

PubMed2003

Maternal gestational diabetes, birth weight, and adolescent obesity.

OBJECTIVE: Obesity increases risk of many adverse outcomes, but its early origins are obscure. Gestational diabetes mellitus (GDM) reflects a metabolically altered fetal environment associated with high birth weight, itself associated with later obesity. Previous studies of GDM and offspring obesity, however, have been few and conflicting. The objectives of this study were to examine associations of birth weight and GDM with adolescent body mass index (BMI) and to determine the extent to which the effect of GDM is explained by its influence on birth weight or by maternal adiposity. METHODS: We conducted a survey of 7981 girls and 6900 boys, 9 to 14 years of age, who are participants in the Growing Up Today Study, a US nationwide study of diet, activity, and growth. In 1996, participants reported height, weight, diet, activity, and other variables by self-administered mailed questionnaire. We linked these data with information reported by their mothers, participants in the Nurses' Health Study II, including GDM, height, current weight, and child's birth weight. We excluded births <34 weeks' gestation and mothers who had preexisting diabetes. We defined overweight as BMI (kg/m(2)) >95th percentile, and at risk for overweight as 85th to 95th percentile, for age and gender from US national data. RESULTS: Mean birth weight was 3.4 kg for girls and 3.6 kg for boys. Among the 465 subjects whose mothers had GDM, 17.1% were at risk for overweight and 9.7% were overweight in early adolescence. In the group without maternal diabetes, these estimates were 14.2% and 6.6%, respectively. In multiple logistic regression analysis, controlling for age, gender, and Tanner stage, the odds ratio for adolescent overweight for each 1-kg increment in birth weight was 1.4 (95% confidence interval: 1.2-1.6). Adjustment for physical activity, television watching, energy intake, breastfeeding duration, mother's BMI, and other maternal and family variables reduced the estimate to 1.3 (1.1-1.5). For offspring of mothers with GDM versus no diabetes, the odds ratio for adolescent overweight was 1.4 (1.1-2.0), which was unchanged after controlling for energy balance and socioeconomic factors. Adjustment for birth weight slightly attenuated the estimate (1.3; 0.9-1.9); adjustment for maternal BMI reduced the odds ratio to 1.2 (0.8-1.7). CONCLUSIONS: Higher birth weight predicted increased risk of overweight in adolescence. Having been born to a mother with GDM was also associated with increased adolescent overweight. However, the effect of GDM on offspring obesity seemed only partially explained by its influence on birth weight, and adjustment for mother's own BMI attenuated the GDM associations. Our results only modestly support a causal role of altered maternal-fetal glucose metabolism in the genesis of obesity in the offspring. Alternatively, GDM may program risk for a postnatal insult leading to obesity, or it may merely be a risk marker, not in the causal pathway.

Adolescent↗