ABSTRACT: Objectives:To investigate whether age at menarche is related to maternal blood pressure in pregnancy and, if so, whether obesity and insulin resistance can modify the associations. Study Design:Analysis of data collected from 438 pregnant women from the longitudinal and prospective Cambridge Baby Growth Study. Main Outcome:Testing associations between questionnaire-derived age at menarche and blood pressure measurements in pregnancy collected from hospital notes, and investigating whether any associations were altered by maternal pre-pregnancy body mass index (BMI) and insulin resistance. Measures:Mean arterial blood pressure at four time points across pregnancy, age at menarche, (Homeostasis Model Assessment) insulin resistance around week 28 of pregnancy. Results:For each increased year in age at menarche there was a drop in mean arterial blood pressure (mmHg) of 0.6 at 11.9 weeks, 0.9 at 31.4 and 37.0 weeks, and 0.4 at 38.8 weeks (a maximal difference of over 7 mmHg across extremes of AAM). Each association was attenuated by both maternal pre-pregnancy BMI and insulin resistance. Conclusions:Age at menarche is negatively associated with future blood pressure in pregnancy, so those with the earliest age at menarche have the highest blood pressures. Either these associations may be mediated by links between age at menarche and obesity/insulin resistance, or there may be a confounder (e.g. systemic inflammation) that links age at menarche to each of them.
Project description:Age of puberty has declined substantially in developed settings and is now declining in the rest of the world with economic development. Early age of puberty is associated with non-communicable diseases in adulthood, and may be a long-term driver of population health with effects over generations. In a non-Western setting, we examined the association of maternal age of menarche with blood pressure in late childhood/adolescence.We used generalised estimating equations to estimate the adjusted association of maternal age of menarche with age-, sex- and height-adjusted blood pressure z-score from 10 to 16 years in Hong Kong's population-representative birth cohort, "Children of 1997" (n = 8327). We also assessed whether associations were mediated by body mass index (BMI) or pubertal stage.Earlier maternal age of menarche was associated with higher systolic blood pressure in adolescence [-0.02 z-score per year older maternal age of menarche, 95% confidence interval (CI) -0.04 to -0.003]. The association of maternal age of menarche with systolic blood pressure was mediated by adiposity and/or pubertal stage at 11 years. Maternal age of menarche was not associated with diastolic blood pressure.Earlier maternal age of puberty was associated with higher systolic blood pressure, largely mediated by adiposity, highlighting the importance of tackling childhood obesity as a public health priority in view of the secular trend of declining age of puberty.
Project description:OBJECTIVE:This study aimed to examine the associations of maternal early-pregnancy glucose and insulin concentrations with offspring cardiometabolic risk factors and fat distribution. METHODS:In a population-based prospective cohort study among 3,737 mothers and their children, random maternal glucose and insulin concentrations were measured at a median gestational age of 13.2 (95% range 10.5-17.1) weeks. Childhood fat, blood pressure, and blood concentrations of lipids, glucose, and insulin at the age of 10 years were measured. RESULTS:Higher maternal early-pregnancy glucose and insulin concentrations were associated with a higher risk of childhood overweight, and higher maternal early-pregnancy insulin concentrations were associated with an increased childhood risk of clustering of cardiometabolic risk factors (all P?<?0.05). These associations were explained by maternal prepregnancy BMI. Independent of maternal prepregnancy BMI, one SD score (SDS) higher maternal early-pregnancy glucose and insulin concentrations were associated with higher childhood glucose (0.08 SDS, 95% CI: 0.04-0.11) and insulin concentrations (0.07 SDS, 95% CI: 0.03-0.10), but not with childhood blood pressure, lipids, and fat measures. CONCLUSIONS:These results suggest that maternal early-pregnancy random glucose and insulin concentrations are associated with childhood glucose and insulin concentrations but not with other childhood cardiometabolic risk factors.
Project description:Associations have been reported between age at menarche and the later risk of gestational diabetes. However, it is not known whether these associations reflect differences in insulin sensitivity and/or pancreatic ?-cell function in pregnancy.We examined this question in women enrolled in the prospective Cambridge Baby Growth Study who recalled their age at menarche in questionnaires during pregnancy. Polynomial logistic and linear regression models were used to relate menarche timing to the risk of gestational diabetes, both unadjusted and adjusted for the Homeostasis Model Assessments of insulin resistance (HOMA IR) and pancreatic ?-cell function (HOMA B) at week 28 of pregnancy.Age at menarche showed a U-shaped association with gestational diabetes risk (linear term: p?=?9.5?×?10-4; quadratic term: p?=?1.0?×?10-3; n?=?889; overall model p?=?8.1?×?10-3). Age at menarche showed a negative linear association with insulin resistance (HOMA IR: ??=?-0.13, p?=?5.2?×?10-4, n?=?771), which explained the relationship between age at menarche and gestational diabetes risk (adjusted linear term going from p?=?0.03-0.08; adjusted quadratic term going from p?=?0.04-0.08; n?=?771). Age at menarche also showed a negative linear association with ?-cell function (HOMA B: ??=?-0.11, p?=?2.8?×?10-3, n?=?771) but this did not attenuate the relationship between age at menarche and gestational diabetes (adjusted linear term p?=?0.02; adjusted quadratic term p?=?0.03, n?=?771).These results suggest that the associations between age at menarche and risk of gestational diabetes and raised pregnancy glucose concentrations may be mediated by insulin resistance.
Project description:Maternal pre-pregnancy obesity may increase the risk of childhood obesity but it is unknown whether other metabolic factors in early pregnancy such as lipid profile and hypertension are associated with offspring cardiometabolic traits.Our objective was to investigate whether fasting lipid, glucose, and insulin levels during early pregnancy and maternal pre-pregnancy weight status, are associated with offspring adiposity measures, lipid levels and blood pressure at preschool age.The study included 618 mother-child pairs of the pregnancy cohort "Rhea" study in Crete, Greece. Pregnant women were recruited at the first prenatal visit (mean: 12 weeks, SD: 0.7). A subset of 348 women provided fasting serum samples for glucose and lipid measurements. Outcomes measures were body mass index, abdominal circumference, sum of skinfold thickness, and blood pressure measurements at 4 years of age. A subsample of 525 children provided non-fasting blood samples for lipid measurements.Pre-pregnancy overweight/obesity was associated with greater risk of offspring overweight/obesity (RR: 1.83, 95%CI: 1.19, 2.81), central adiposity (RR: 1.97, 95%CI: 1.11, 3.49), and greater fat mass by 5.10 mm (95%CI: 2.49, 7.71) at 4 years of age. These associations were more pronounced in girls. An increase of 40 mg/dl in fasting serum cholesterol levels in early pregnancy was associated with greater skinfold thickness by 3.30 mm (95%CI: 1.41, 5.20) at 4 years of age after adjusting for pre-pregnancy BMI and several other confounders. An increase of 10 mmHg in diastolic blood pressure in early pregnancy was associated with increased risk of offspring overweight/obesity (RR: 1.22, 95%CI: 1.03, 1.45), and greater skinfold thickness by 1.71 mm (95% CI: 0.57, 2.86) at 4 years of age.Metabolic dysregulation in early pregnancy may increase the risk of obesity at preschool age.
Project description:BACKGROUND: The influence of multiple maternal and pregnancy characteristics on offspring cardiometabolic traits at birth is not well understood and was evaluated in this study. METHODS AND FINDINGS: The Family Atherosclerosis Monitoring In earLY life (FAMILY) Study prospectively evaluated 11 cardiometabolic traits in 901 babies born to 857 mothers. The influence of maternal age, health (pre-pregnancy weight, blood pressure, glycemic status, lipids), health behaviors (diet, activity, smoking) and pregnancy characteristics (gestational age at birth, gestational weight gain and placental-fetal ratio) were examined. Greater gestational age influenced multiple newborn cardiometabolic traits including cord blood lipids, glucose and insulin, body fat and blood pressure. In a subset of 442 singleton mother/infant pairs, principal component analysis grouped 11 newborn cardiometabolic traits into 5 components (anthropometry/insulin, 2 lipid components, blood pressure and glycemia), accounting for 74% of the variance of the 11 outcome variables. Determinants of these components, corrected for sex and gestational age, were examined. Baby anthropometry/insulin was independently predicted by higher maternal pre-pregnancy weight (standardized estimate 0.30) and gestational weight gain (0.30; both p<0.0001) and was inversely related to smoking during pregnancy (-0.144; p?=?0.01) and maternal polyunsaturated to saturated fat intake (-0.135;p?=?0.01). Component 2 (HDL-C/Apo Apolipoprotein1) was inversely associated with maternal age. Component 3 (blood pressure) was not clustered with any other newborn cardiometabolic trait and no associations with maternal pregnancy characteristics were identified. Component 4 (triglycerides) was positively associated with maternal hypertension and triglycerides, and inversely associated with maternal HDL and age. Component 5 (glycemia) was inversely associated with placental/fetal ratio (-0.141; p?=?0.005). LDL-C was a bridging variable between the lipid factors and glycemia. CONCLUSIONS: Maternal health, health behaviours and placenta to fetal weight ratio are associated with newborn cardiometabolic traits over and above gestational age. Future investigations are needed to determine if these factors remain important determinants of cardiometabolic health throughout childhood.
Project description:OBJECTIVE:We aimed to test the fetal overnutrition hypothesis by comparing the associations of maternal and paternal adiposity (sum of skinfolds) with adiposity and cardiovascular risk factors in children. DESIGN:Children from a prospective birth cohort had anthropometry, fat percentage (bio-impedance), plasma glucose, insulin and lipid concentrations and blood pressure measured at 9.5 years of age. Detailed anthropometric measurements were recorded for mothers (at 3±2 weeks’ gestation) and fathers (5 years following the index pregnancy). SETTING:Holdsworth Memorial Hospital, Mysore, India. SUBJECTS:Children (n 504), born to mothers with normal glucose tolerance during pregnancy. RESULTS:Twenty-eight per cent of mothers and 38% of fathers were overweight/ obese (BMI?25.0 kg/m²), but only 4% of the children were overweight/obese (WHO age- and sex-specific BMI?18.2 kg/m²). The children’s adiposity (BMI, sum of skinfolds, fat percentage and waist circumference), fasting insulin concentration and insulin resistance increased with increasing maternal and paternal sum of skinfolds adjusted for the child’s sex, age and socio-economic status. Maternal and paternal effects were similar. The associations with fasting insulin and insulin resistance were attenuated after adjusting for the child’s current adiposity. CONCLUSIONS:In this population, both maternal and paternal adiposity equally predict adiposity and insulin resistance in the children. This suggests that shared family environment and lifestyle, or genetic/epigenetic factors, influence child adiposity. Our findings do not support the hypothesis that there is an intrauterine overnutrition effect of maternal adiposity in non-diabetic pregnancies, although we cannot rule out such an effect in cases of extreme maternal obesity, which is rare in our population.
Project description:AIMS:A growing body of evidence suggests that a higher maternal pre-pregnancy body mass index results in higher offspring's blood pressure, but there is inconsistency about the impact of father's body mass index. Furthermore, evidence is limited with regard to low and middle income countries. We aimed to determine the association between parental pre-pregnancy body mass index and offspring's blood pressure during the first year of life. METHODS:In 587 infants of the BReastfeeding Attitude and Volume Optimization (BRAVO) trial systolic and diastolic blood pressure were measured twice at the right leg in a supine position, using an automatic oscillometric device at day 7, month 1, 2, 4, 6, 9 and 12. Parental pre-pregnancy body mass index was based on self-reported weight and height. Linear mixed models were performed to investigate the associations between parental pre-pregnancy body mass index and offspring blood pressure patterns. RESULTS:Each unit increase in maternal body mass index was associated with 0.24 mmHg (95% confidence interval 0.05; 0.44) and 0.13 mmHg (0.01; 0.25) higher offspring's mean systolic and diastolic blood pressure, respectively, during the first year of life. A higher offspring blood pressure with increased maternal pre-pregnancy body mass index was seen at birth and remained higher during the first year of life. The association with systolic blood pressure remained similar after including birth size and offspring's weight and height over time. The association with diastolic blood pressure attenuated slightly to a non-significant result after including these variables. Paternal body mass index was not associated with offspring's blood pressure. CONCLUSION:Higher maternal pre-pregnancy body mass index, but not paternal pre-pregnancy body mass index, is associated with higher offspring blood pressure already from birth onwards.
Project description:We investigated the association between maternal anthropometric measurements in prepregnancy and at the end of pregnancy and their children's systolic (SBP) and diastolic (DBP) blood pressure at 11 years of age, in a prospective cohort study.All hospital births which took place in 1993 in the city of Pelotas-Brazil, were identified (5,249 live births). In 2004, the overall proportion of follow-up was 85% and we obtained arterial blood pressure measurements of 4,452 adolescents.Independent variables analyzed included maternal prepregnancy weight and body mass index (BMI) and maternal weight, and height at the end of pregnancy. Multiple linear regression analysis controlling for the following confounders were carried out: adolescent's skin color, family income at birth, smoking, alcohol intake during pregnancy, and gestational arterial hypertension. Mean SBP and DBP were 101.9 mmHg (SD 12.3) and 63.4 mmHg (SD 9.9), respectively. Maternal prepregnancy weight and BMI, and weight at the end of pregnancy were positively associated with both SBP and DBP in adolescent subjects of both sexes; maternal height was positively associated with SBP only among males.Adequate evaluation of maternal anthropometric characteristics during pregnancy may prevent high levels of blood pressure among adolescent children.
Project description:Animal and cross-sectional epidemiological studies suggest that prenatal lead exposure is related to delayed menarche, but this has not been confirmed in longitudinal studies. We analyzed this association among 200 girls from Mexico City who were followed since the first trimester of gestation. Maternal blood lead levels were analyzed once during each trimester of pregnancy, and daughters were asked about their first menstrual cycle at a visit between the ages of 9.8 and 18.1 years. We estimated hazard ratios (HRs) and 95% confidence intervals (CI) for probability of menarche over the follow-up period using interval-censored Cox models, comparing those with prenatal blood lead level ?5 µg/dl to those with prenatal blood lead <5 µg/dl. We also estimated HRs and 95% CI with conventional Cox regression models, which utilized the self-reported age at menarche. In adjusted analyses, we accounted for maternal age, maternal parity, maternal education, and prenatal calcium treatment status. Across trimesters, 36-47% of mothers had blood lead levels ?5 µg/dl. Using interval-censored models, we found that during the second trimester only, girls with ?5 µg/dl prenatal blood lead had a later age at menarche compared with girls with prenatal blood lead levels <5 µg/dl (confounder-adjusted HR=0.59, 95% CI 0.28-0.90; P=0.05). Associations were in a similar direction, although not statistically significant, in the conventional Cox regression models, potentially indicating measurement error in the self-recalled age at menarche. In summary, higher prenatal lead exposure during the second trimester could be related to later onset of sexual maturation.
Project description:OBJECTIVES:The long-term consequences of maternal physical activity during pregnancy for offspring cardiovascular health are unknown. We examined the association of maternal self-reported physical activity in pregnancy (18 weeks gestation) with offspring cardiovascular risk factors at age 15. DESIGN:Prospective cohort study. SETTING:The Avon Longitudinal Study of Parents and Children (ALSPAC). PARTICIPANTS:4665 maternal-offspring pairs (based on a sample with multiple imputation to deal with missing data) from the ALSPAC, a prospective cohort based in the South West of England with mothers recruited in pregnancy in 1991-1992. PRIMARY AND SECONDARY OUTCOME MEASURES:Offspring cardiovascular risk factors at age 15; body mass index (BMI), waist circumference, systolic blood pressure, diastolic blood pressure, glucose, insulin, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol and triglycerides. RESULTS:Greater maternal physical activity was associated with lower BMI, waist circumference, glucose and insulin in unadjusted analyses. The magnitude of associations was generally small with wide CIs, and most associations attenuated towards the null after adjusting for confounders. The strongest evidence of association after adjustment for confounders was for glucose, although the 95% CI for this association includes the null; a one SD greater physical activity during pregnancy was associated with a -0.013 mmol/L difference in offspring glucose levels (equivalent to approximately one-third of a SD; 95% CI -0.027 to 0.001 mmol/L). CONCLUSIONS:Our results suggest that maternal physical activity in pregnancy, measured at 18 weeks gestation, is unlikely to be an important determinant of later offspring cardiovascular health. There was some suggestion of association with offspring glucose, but given that all other associations (including insulin) were null after adjustment for confounders, this result should be interpreted with caution.