			Home About us Contact

Maternal Obesity (maternal + obesity)

Distribution by Scientific Domains

Medical Sciences	78%
Life Sciences	21%

Selected Abstracts

Effects of Obesity on Pregnancy

JOURNAL OF OBSTETRIC, GYNECOLOGIC & NEONATAL NURSING, Issue 2 2008
Shelia A. Smith
ABSTRACT Objectives:, To examine physiologic and psychological outcomes associated with maternal obesity in pregnancy and patterns of pregnancy weight gain. To identify effective interventions for maternal obesity. Data sources and study selection:, Search of obesity and pregnancy research conducted over the past 10 years using CIHAHL, Medline ERIC, and PyscInfo databases. Studies including the following keywords were included in the review: obesity, weight gain, body image, pregnancy weight gain, pregnancy obesity complications, preeclampsia and gestational diabetes. Articles were included based on scientific merit and research outcomes. Data synthesis and conclusions:, Maternal obesity is a serious condition that significantly impacts not only mothers' health but also the health and future of their children. It is paramount that all levels of health care providers be aware of consequences of obesity and be knowledgeable of effective interventions. No effective long-term interventions have been demonstrated to prevent or control obesity during pregnancy. The paucity of published results of pregnancy and postpartum interventions to address weight gain in pregnancy suggests the need for more community and individualized based intervention studies, especially focusing on long-term effects. [source]

AMP-activated protein kinase signalling pathways are down regulated and skeletal muscle development impaired in fetuses of obese, over-nourished sheep

THE JOURNAL OF PHYSIOLOGY, Issue 10 2008
Mei J. Zhu
Maternal obesity and over-nutrition give rise to both obstetric problems and neonatal morbidity. The objective of this study was to evaluate effects of maternal obesity and over-nutrition on signalling of the AMP-activated protein kinase (AMPK) pathway in fetal skeletal muscle in an obese pregnant sheep model. Non-pregnant ewes were assigned to a control group (Con, fed 100% of NRC nutrient recommendations, n= 7) or obesogenic group (OB, fed 150% of National Research Council (NRC) recommendations, n= 7) diet from 60 days before to 75 days after conception (term 150 days) when fetal semitendinosus skeletal muscle (St) was sampled. OB mothers developed severe obesity accompanied by higher maternal and fetal plasma glucose and insulin levels. In fetal St, activity of phosphoinositide-3 kinase (PI3K) associated with insulin receptor substrate-1 (IRS-1) was attenuated (P < 0.05), in agreement with the increased phophorylation of IRS-1 at serine 1011. Phosphorylation of AMP-activated protein kinase (AMPK) at Thr 172, acetyl-CoA carboxylase at Ser 79, tuberous sclerosis 2 at Thr 1462 and eukaryotic translation initiation factor 4E-binding protein 1 at Thr 37/46 were reduced in OB compared to Con fetal St. No difference in energy status (AMP/ATP ratio) was observed. The expression of protein phosphatase 2C was increased in OB compared to Con fetal St. Plasma tumour necrosis factor , (TNF,) was increased in OB fetuses indicating an increased inflammatory state. Expression of peroxisome proliferator-activated receptor , (PPAR,) was higher in OB St, indicating enhanced adipogenesis. The glutathione: glutathione disulphide ratio was also lower, showing increased oxidative stress in OB fetal St. In summary, we have demonstrated decreased signalling of the AMPK system in skeletal muscle of fetuses of OB mothers, which may play a role in altered muscle development and development of insulin resistance in the offspring. [source]

Maternal obesity and pregnancy complications: A review

AUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 3 2008
Jonathan RAMACHENDERAN
Obesity in women of reproductive age is increasing at an unprecedented rate in western societies. Maternal obesity is associated with an unequivocal increase in maternal and fetal complications of pregnancy. Excessive maternal weight gain in pregnancy also appears to be an independent risk factor, regardless of prepregnancy weight. Few guidelines exist regarding appropriate weight gain in pregnancy in obese women. We review the association of maternal obesity with pregnancy complications. We also suggest that appropriate diet and lifestyle intervention can enable women with severe prepregnancy obesity to safely achieve quite strict targets for limited weight gain in pregnancy. [source]

Poor uterine contractility in obese women

BJOG : AN INTERNATIONAL JOURNAL OF OBSTETRICS & GYNAECOLOGY, Issue 3 2007
J Zhang
Objective, The aim of the study was to elucidate the reason for the high rate of caesarean section in obese women. We examined the following hypotheses: (1) obese women have a high incidence of complications related to poor uterine contractility,caesarean section for dysfunctional labour and postpartum haemorrhage. 2) The myometrium from obese women has less ability to contract in vitro. Design, First, a clinical retrospective analysis of data from 3913 completed singleton pregnancies was performed. Secondly, in a prospective study the force, frequency and intracellular [Ca2+] flux of spontaneously contracting myometrium were related to the maternal body mass index. Setting, Liverpool Women's Hospital and University of Liverpool. Population, The clinical study involved all women who delivered in one hospital in 2002. The in vitro study myometrial biopsies were obtained from 73 women who had elective caesarean section at term. Results, Maternal obesity carried significant risk of caesarean section in labour that was highest for delay in the first stage of labour (OR 3.54). The increased risk of caesarean section in obese women largely occurred in women with normal- and not with high-birthweight infants. Obese women delivering vaginally had increased risk of prolonged first stage of labour and excessive blood loss. Myometrium from obese women contracted with less force and frequency and had less [Ca2+] flux than that from normal-weight women. Conclusions, We suggest that these findings indicate that obesity may impair the ability of the uterus to contract in labour. [source]

Following in mother's footsteps?

DIABETIC MEDICINE, Issue 3 2010
Mother, cardiovascular disease 15 years after gestational diabetes, daughter risks for insulin resistance
Diabet. Med. 27, 257,265 (2010) Abstract Aims, To determine effects on mothers and daughters of gestational diabetes mellitus/gestational impaired glucose tolerance (GDM/GIGT) on their future metabolic and cardiovascular risks. Methods, Case mothers who had GDM/GIGT in pregnancy (cases; n = 90) and normoglycaemic control women (n = 99) and their daughters underwent lifestyle assessment and metabolic tests 15-years post-partum. Results, Prevalence of glucose intolerance (GI) in daughters was 1.1%. Maternal prevalence was 44.4% in cases compared to 13.1% in controls, with conversion best predicted by weight gain. Case daughters had higher insulin resistance (IR) and greater waist circumference (WC) (51.2%) relative to control daughters (36.4%, p < 0.05) made worse if case mothers became GI at follow-up (65%) (relative risk =1.8; 95% confidence interval 1.2,2.9). In multivariable linear regression analyses adjusting for daughters' birthweight, maternal obesity (> 30.0 kg/m2) at 15years and mothers' case-control status were strong predictors of daughters' WC (p < 0.01; P < 0.01, respectively). For daughters' body mass index (BMI) percentile and percentage of body fat, maternal obesity was a stronger predictor (p < 0.01; p < 0.001)) than mothers' case-control status (p < 0.01; P = 0.09). Conclusions, GDM/GIGT pregnancies led to increased conversion to GI in mothers, minimal in daughters. Case daughters have increased risk of central adiposity and insulin resistance, whereas maternal obesity strongly predicted daughters' BMI percentile and per cent of body fat. Controlling hyperglycaemia in pregnancy and family weight management may provide the key to preventing offspring obesity and glucose intolerance post GDM/GIGT. [source]

Effects of Obesity on Pregnancy

Does maternal smoking during pregnancy cause childhood overweight?

PAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 2 2003
Marius Widerøe
Summary The objective of this study was to examine a possible association between maternal smoking in pregnancy and childhood overweight. From a population-based cohort of 5722 women from Trondheim, Bergen (Norway) and Uppsala (Sweden) enrolled in early pregnancy during 1986,92, a random sample of 482 women was selected for participation. They were followed up throughout pregnancy, and their children from birth until 5 years of age. Data on maternal smoking and diet, socio-economic determinants and breast feeding were recorded prospectively. During pregnancy and childhood, anthropometric measures were also recorded. Maternal smoking status was based on reported number of cigarettes smoked in week 17 of pregnancy. Child overweight was defined by body mass index (BMI) and sum of skinfold thickness (SFT) , 85th percentile at 5 years of age. Children of mothers who smoked in pregnancy had increased risk of overweight at 5 years of age (RR 2.5, 95% CI 1.5, 4.2 for BMI; and RR 1.8, 95% CI 1.1, 3.0 for SFT). Adjusting for maternal diet, breast feeding, maternal obesity and socio-economic status did not suggest confounding. However, adjustment for birthweight increased the observed risk. A linear increase in BMI and SFT was observed with increasing number of cigarettes smoked. In conclusion, smoking during pregnancy may be a risk factor for development of childhood overweight. This study may support the hypothesis of ,fetal origin of adult disease', but the risk of overweight associated with smoking during pregnancy was independent of intrauterine growth retardation, and may thus be attributed to specific effects of cigarette smoke. [source]

Ultrasound screening for fetal aneuploidy using soft markers in the overweight and obese gravida,

PRENATAL DIAGNOSIS, Issue 9 2010
Lily J. Tsai
Abstract Objective To determine the completion rate of ultrasound surveys for aneuploidy markers by maternal body mass index (BMI). Methods A retrospective review of ultrasounds on midtrimester singleton pregnancies was performed. Subjects were grouped as normal, overweight (BMI 25,29.9 kg/m2), and obese: class I (30,34.9 kg/m2), class II (35,39.9 kg/m2), and class III (, 40 kg/m2). Examinations with visualization of at least seven of eight markers were considered complete. Results Of 14 353 ultrasounds reviewed, 5690 patients were eligible: 43% normal, 29% overweight, 27% obese. Completion rates differed significantly between groups (64% normal, 64% overweight, 61% class I, 55% class II, 47% class III, p < 0.001). The screen positive rates (,1 marker) differed significantly overall (16% normal, 13% overweight, 15% class I, 12% class II, 10% class III, p < 0.02), but not for complete examinations (p = 0.42). Conclusions Since completion rates for ultrasound aneuploidy screening are inversely related to maternal obesity, obese women are underscreened. Copyright © 2010 John Wiley & Sons, Ltd. [source]

AMP-activated protein kinase signalling pathways are down regulated and skeletal muscle development impaired in fetuses of obese, over-nourished sheep

Maternal periodontal disease and perinatal mortality

AUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 2 2009
Alexis SHUB
Background: Periodontal disease has been associated with increased perinatal mortality. Aims: To examine the association between maternal periodontal disease and perinatal mortality. Methods: We performed a retrospective and prospective matched case,control study of women with unexplained perinatal mortality at more than 20 weeks gestational age. Women were matched for socioeconomic status, smoking status and time since delivery. All women underwent a detailed periodontal examination and completed a questionnaire describing oral health symptoms. No intervention took place. Results: Fifty-three women who had experienced a perinatal death and 111 controls completed the study. Thirty-two women were recruited retrospectively and 21 women were recruited prospectively. Twenty-three (43.4%) women who had experienced a perinatal death and 27 (24.3%) controls had periodontal disease. There were no differences in oral health behaviours or symptoms between cases and controls. Perinatal death was associated with periodontal disease (odds ratio (OR) 2.34, 95% confidence interval (CI) 1.05, 5.47). Periodontal disease was more strongly associated with perinatal mortality due to extreme prematurity (OR 3.60, 95% CI 1.20, 12.04). Multivariate analysis showed this relationship to be consistent after inclusion of higher parity, country of birth, advanced maternal age and maternal obesity in the model (OR 4.56, 95% CI 1.25, 21.27). Conclusions: Maternal periodontal disease may contribute to perinatal mortality, especially that caused by extreme prematurity. [source]

Maternal obesity and pregnancy complications: A review

CARDIOVASCULAR AND METABOLIC EFFECTS OF OBESITY

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2008
Margaret J Morris
SUMMARY 1Obesity is an important risk factor for hypertension and its incidence is increasing around the world. 2The mechanisms underlying obesity-related hypertension include sympathetic activation, altered vascular responses, hormonal changes, enhanced inflammatory markers and structural changes. 3This review summarizes recent evidence of the underlying impact of obesity on blood pressure. A number of candidate mechanisms include increased sympathetic activity, activation of the renin-angiotensin system, altered vasoconstrictor or dilator responses and the attendant systemic inflammatory state. 4While adult lifestyle factors undoubtedly contribute to the incidence of obesity and its attendant hypertension, evidence suggests that the programming of obesity may occur following over-nutrition during development. A growing body of evidence links maternal obesity, offspring obesity and hypertension. 5Finally, epigenetic modification of genes relevant to hypertension may contribute to the development of hypertension following a suboptimal intrauterine environment. To date the cardiovascular effects of early nutritional changes have been largely investigated following maternal under-nutrition or protein restriction; further work is necessary to determine the impact of maternal obesity. [source]