Increased neonatal fat mass, not lean body mass, is associated with maternal obesity

Sewell, M. F.; Huston-Presley, Larraine; Super, Dennis M.; Catalano, Patrick M.

doi:10.1016/j.ajog.2006.06.014

Cited by 361 publications

(245 citation statements)

References 12 publications

Supporting

Mentioning

221

Contrasting

Unclassified

Order By: Relevance

“…First, our data suggest that mothers who had higher adiposity levels established early in pregnancy, had babies of higher birth weight whom on average had a higher adiposity level as measured by skinfolds. Such a finding is consistent with other studies that showed that fatter mothers tend to have fatter babies; 8,42 however, the magnitude of effect of maternal obesity on neonatal skinfold measurements is quite modest (0.26 mm increase in SSF and 0.16 for TSF) and appears not to be a major factor associated with the variability in neonatal adiposity in this population of women who had early-pregnancy BMIs in the underweight-to-healthy categories. In addition, our findings showed that high maternal adiposity before and during pregnancy had a significant increased need for Caesarean sections.…”

Section: Discussionsupporting

confidence: 80%

“…5 However, birth weight alone may not be the most sensitive measure for determining fat deposits as it is determined by a number of factors that include internal organs, muscle, fat and fluids. 6 Although an increase in birth weight has been associated with maternal obesity and consequently macrosomic infants, 7,8 less is known about prenatal environmental determinants such as fat and lean mass that affect neonatal body composition.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Maternal and infant factors associated with neonatal adiposity: Results from the Tasmanian Infant Health Survey (TIHS)

et al. 2012

View full text Add to dashboard Cite

OBJECTIVE:To examine the maternal and neonatal factors associated with offspring adiposity and the role of birth and placental weight as potential mediators in such associations. DESIGN: The Tasmanian Infant Health Survey was a prospective cohort study conducted between 1988 and 1995 in Australia to investigate the cause of Sudden Infant Death Syndrome. This large infant cohort provides measurement of skinfolds on 7945 mothers and their offspring. SUBJECTS: Participants included singletons born X37 weeks gestation who were at high risk of sudden infant death syndrome identified through a composite score that included birth weight, maternal age, neonatal gender, season of birth, duration of second-stage labor and intention to breastfeed. MEASUREMENTS: Neonatal adiposity was assessed from skinfold measurements of the subscapular (SSF) and triceps folds (TSF) taken at birth. Maternal early-pregnancy body mass index (BMI) was calculated from self-reported height and weight. Neonatal data were extracted from birth records. Data relating to other environmental exposures were obtained from questionnaires administered when neonates were B4-days old. RESULTS: In multivariable models, higher maternal adiposity, increasing maternal age, gestation age, delivery by Caesarian section and female gender were associated with larger SSF independent of placental and birth weight (Po0.001). Maternal age and delivery by Caesarian section were significantly associated with larger TSF, whereas gestational age and male gender were associated with thinner TSF independent of placental and birth weight. Higher early-pregnancy BMI, maternal weight gain, maternal age, parity and gestational age were significantly associated with larger placental and birth weight. Smoking during pregnancy was associated with smaller birth weight but not with placental weight. CONCLUSION: In addition to birth weight, maternal adiposity and placental weight were important additional factors associated with neonatal adiposity.

show abstract

Section: Discussionsupporting

confidence: 80%

Section: Introductionmentioning

confidence: 99%

Maternal and infant factors associated with neonatal adiposity: Results from the Tasmanian Infant Health Survey (TIHS)

et al. 2012

View full text Add to dashboard Cite

show abstract

“…Although all people are exposed to some degree of stress, as one moves lower on the SES ladder, exposure to chronic, toxic stress increases (43). Both animal and human studies link greater stress experienced by the mother during pregnancy with slower offspring growth, impaired immune functioning, damage to brain structure and functioning, and a range of pediatric illnesses (31,33,(44)(45)(46).…”

Section: Causality and Its Discontentsmentioning

confidence: 99%

Rigor, vigor, and the study of health disparities

Adler

Bush²,

Pantell

2012

Proc. Natl. Acad. Sci. U.S.A.

104

View full text Add to dashboard Cite

Health disparities research spans multiple fields and methods and documents strong links between social disadvantage and poor health. Associations between socioeconomic status (SES) and health are often taken as evidence for the causal impact of SES on health, but alternative explanations, including the impact of health on SES, are plausible. Studies showing the influence of parents' SES on their children's health provide evidence for a causal pathway from SES to health, but have limitations. Health disparities researchers face tradeoffs between "rigor" and "vigor" in designing studies that demonstrate how social disadvantage becomes biologically embedded and results in poorer health. Rigorous designs aim to maximize precision in the measurement of SES and health outcomes through methods that provide the greatest control over temporal ordering and causal direction. To achieve precision, many studies use a single SES predictor and single disease. However, doing so oversimplifies the multifaceted, entwined nature of social disadvantage and may overestimate the impact of that one variable and underestimate the true impact of social disadvantage on health. In addition, SES effects on overall health and functioning are likely to be greater than effects on any one disease. Vigorous designs aim to capture this complexity and maximize ecological validity through more complete assessment of social disadvantage and health status, but may provide less-compelling evidence of causality. Newer approaches to both measurement and analysis may enable enhanced vigor as well as rigor. Incorporating both rigor and vigor into studies will provide a fuller understanding of the causes of health disparities.methodology | social determinants of health | cumulative risk G ood health and longevity are unequally distributed in populations. Although some unavoidable variations in health emanate from individual differences in vulnerability to disease, others are linked to membership in socially disadvantaged groups. The latter are unjust and have been the focus of considerable research and policy (1). Research on these health disparities has demonstrated consistent graded associations between various components of socioeconomic status (SES) and a wide range of health indicators; at each step up the social ladder, whether indexed by higher income, education, and/or occupational level, rates of morbidity and mortality decrease (2). The prevailing understanding of this relationship is that SES is a "fundamental cause" of health status (3), which operates through physical and/or psychosocial resources that are more readily available as SES increases, and hardships and adverse exposures that are more intense and frequent as SES decreases.Evidence for the SES-health gradient comes primarily from cross-sectional data linking contemporaneous measures of SES in adulthood with prevalence of disease, poor health, or mortality. Smaller literatures have established associations between socioeconomic conditions in childhood and childhood health, and betwe...

show abstract

“…The evidence includes studies in human cohorts, which have suggested that maternal obesity is a risk factor for development of childhood metabolic syndrome or obesity [9][10][11]. Children of obese mothers also have increased risk of higher BMI in adult life [12].…”

mentioning

confidence: 99%

Established diet-induced obesity in female rats leads to offspring hyperphagia, adiposity and insulin resistance

et al. 2009

View full text Add to dashboard Cite

Aims/hypothesis Accumulating evidence suggests that maternal obesity may increase the risk of metabolic disease in the offspring. We investigated the effects of established maternal diet-induced obesity on male and female offspring appetite, glucose homeostasis and body composition in rats. Methods Female Wistar rats were fed either a standard chow (3% fat, 7% sugar [wt/wt]) or a palatable obesogenic diet (11% fat, 43% sugar [wt/wt]) for 8 weeks before mating and throughout pregnancy and lactation. Male and female offspring of control and obese dams were weaned on to standard chow and assessed until 12 months of age. Results At mating, obese dams were heavier than control with associated hyperglycaemia and hyperinsulinaemia. Male and female offspring of obese dams were hyperphagic (p<0.0001) and heavier than control (p<0.0001) until 12 months of age. NEFA were raised at 2 months but not at 12 months. At 3 months, OGTT showed more pronounced alteration of glucose homeostasis in male than in female offspring of obese animals. Euglycaemic-hyperinsulinaemic clamps performed at 8 to 9 months in female and 10 to 11 months in male offspring revealed insulin resistance in male offspring of obese dams (p<0.05 compared with control). Body compositional analysis at 12 months also showed increased fat pad weights in male and female offspring of obese animals. Conclusions/interpretation Diet-induced obesity in female rats leads to a state of insulin resistance in male offspring, associated with development of obesity and increased adiposity. An increase in food intake may play a role.

show abstract

Increased neonatal fat mass, not lean body mass, is associated with maternal obesity

Cited by 361 publications

References 12 publications

Maternal and infant factors associated with neonatal adiposity: Results from the Tasmanian Infant Health Survey (TIHS)

Maternal and infant factors associated with neonatal adiposity: Results from the Tasmanian Infant Health Survey (TIHS)

Rigor, vigor, and the study of health disparities

Established diet-induced obesity in female rats leads to offspring hyperphagia, adiposity and insulin resistance

Contact Info

Product

Resources

About