Holly R. Hull

Longitudinal body composition of children born to mothers with normal weight, overweight, and obesity.

The longitudinal trajectories of body composition of children born to mothers with normal weight, overweight, and obesity have not been evaluated using precise body composition methods. This study investigated the relationship between maternal prepregnancy BMI and offspring body composition trajectories during the first 6 years of life.

An anthropometric model to estimate neonatal fat mass using air displacement plethysmography

BackgroundCurrent validated neonatal body composition methods are limited/impractical for use outside of a clinical setting because they are labor intensive, time consuming, and require expensive equipment. The purpose of this study was to develop an anthropometric model to estimate neonatal fat mass (kg) using an air displacement plethysmography (PEA POD® Infant Body Composition System) as the criterion.MethodsA total of 128 healthy term infants, 60 females and 68 males, from a multiethnic cohort were included in the analyses. Gender, race/ethnicity, gestational age, age (in days), anthropometric measurements of weight, length, abdominal circumference, skin-fold thicknesses (triceps, biceps, sub scapular, and thigh), and body composition by PEA POD® were collected within 1-3 days of birth. Backward stepwise linear regression was used to determine the model that best predicted neonatal fat mass.ResultsThe statistical model that best predicted neonatal fat mass (kg) was: -0.012 -0.064*gender + 0.024*day of measurement post-delivery -0.150*weight (kg) + 0.055*weight (kg)2 + 0.046*ethnicity + 0.020*sum of three skin-fold thicknesses (triceps, sub scapular, and thigh); R2 = 0.81, MSE = 0.08 kg.ConclusionsOur anthropometric model explained 81% of the variance in neonatal fat mass. Future studies with a greater variety of neonatal anthropometric measurements may provide equations that explain more of the variance.

Body fat differences by self-reported race/ethnicity in healthy term newborns.

Ethnic differences in total body fat (fat mass [FM]) have been reported in adults and children, but the timing of when these differences manifest and whether they are present at birth are unknown.

Relationship of circulating adipokines to body composition in pregnant women.

Circulating adipokines are associated with physiological and pathophysiological processes in both obesity and pregnancy. Obesity in pregnancy increases the risk of pregnancy complications and the majority of research uses body mass index (BMI) to assess fatness. Specific fat compartments are associated with obesity-induced health risks yet it is not known how abdominal fat mass in pregnancy is related to circulating adipokines. Plasma leptin, resistin, visfatin, and adiponectin were measured by immunoassay in healthy pregnant women of normal weight (BMI 18.5–24.9; n = 17) and overweight/obese pregnant women (BMI 25.0–40, n = 21) in the third trimester. Total body and abdominal subcutaneous and visceral fat mass were measured at 1–3 weeks postpartum. Overweight/obese women had greater total body fat (t = −6.210, P < 0.001) and abdominal subcutaneous fat (t = −5.072, P < 0.001) than normal-weight women while there was no difference in abdominal visceral fat. Overweight/obese women had higher leptin (66.3 ± 34.2 vs. 35.7 ± 19.3 ng/mL, P < 0.001) compared to normal-weight women. Leptin was associated with total body fat (r = 0.782, P < 0.001) and resistin was associated with abdominal visceral fat (r = 0.452, P = 0.045). No significant correlations were observed between adiponectin or visfatin and any measure of body composition. In pregnant women, resistin has the potential to be a circulating biomarker for visceral fat, an ectopic fat compartment. These observational data may provide insight for the pathophysiological roles of adipokines and the impact of visceral fat in pregnant women.

Maternal obesity influences the relationship between location of neonate fat mass and total fat mass

It is suggested that maternal obesity perpetuates offspring obesity to future generations.

Perioperative Immunonutrition Modulates Inflammatory Response after Radical Cystectomy: Results of a Pilot Randomized Controlled Clinical Trial

Purpose: Poor preoperative nutritional status is associated with a higher complication rate after radical cystectomy in patients with bladder cancer. Given the short interval between diagnosis and radical cystectomy, we compared the effect of short‐term specialized immunonutrition to that of a standard oral nutritional supplement on the acute inflammatory response and arginine status in patients treated with radical cystectomy. Materials and Methods: In this prospective, randomized study in 29 men 14 received specialized immunonutrition and 15 received oral nutritional supplement. Each group drank 3 cartons per day for 5 days before and 5 days after radical cystectomy. The Th1‐Th2 balance, plasma interleukin‐6 and plasma amino acids were measured at baseline, intraoperatively and on postoperative days 2, 14 and 30. Body composition was measured by dual energy x‐ray absorptiometry at baseline and on postoperative days 14 and 30. Differences in outcomes were assessed using the generalized linear mixed model. Results: In the specialized immunonutrition group there was a 54.3% average increase in the Th1‐Th2 balance according to the tumor necrosis factor‐&agr;‐to‐interleukin‐13 ratio from baseline to intraoperative day, representing a shift toward a Th1 response. In the oral nutritional supplement group the Th1‐Th2 balance decreased 4.8%. The change in the Th1‐Th2 balance between the specialized immunonutrition and oral nutritional supplement groups significantly differed (p <0.027). Plasma interleukin‐6 was 42.8% lower in the specialized immunonutrition group compared to the oral nutritional supplement group on postoperative day 2 (p = 0.020). In the specialized immunonutrition group plasma arginine was maintained from baseline to postoperative day 2 and yet the oral nutritional supplement group showed a 26.3% reduction from baseline to postoperative day 2 (p = 0.0003). The change in appendicular muscle loss between the groups was not statistically significant. Conclusions: Th1‐to‐Th2 ratios, peak interleukin‐6 levels and plasma arginine suggest that consuming specialized immunonutrition counteracts the disrupted T‐helper balance, lowers the inflammatory response and prevents arginine depletion due to radical cystectomy.

Abdominal visceral adiposity influences CD4+ T cell cytokine production in pregnancy

Women with pre-gravid obesity are at risk for pregnancy complications. While the macrophage response of obese pregnant women categorized by body mass index (BMI) has been documented, the relationship between the peripheral CD4(+) T cell cytokine profile and body fat compartments during pregnancy is unknown. In this study, third trimester peripheral CD4(+) T cell cytokine profiles were measured in healthy pregnant women [n=35; pre-pregnancy BMI: 18.5-40]. CD4(+) T cells were isolated from peripheral blood mononuclear cells and stimulated to examine their capacity to generate cytokines. Between 1 and 3weeks postpartum, total body fat was determined by dual-energy X-ray absorptiometry and abdominal subcutaneous and visceral fat masses were determined by magnetic resonance imaging. Pearsons correlation was performed to assess relationships between cytokines and fat mass. Results showed that greater abdominal visceral fat mass was associated with a decrease in stimulated CD4(+) T cell cytokine expression. IFN-gamma, TNF-alpha, IL-12p70, IL-10 and IL-17A were inversely related to visceral fat mass. Chemokines CCL3 and IL-8 and growth factors G-CSF and FLT-3L were also inversely correlated. Additionally, total body fat mass was inversely correlated with FGF-2 while abdominal subcutaneous fat mass and BMI were unrelated to any CD4(+) T cell cytokine. In conclusion, lower responsiveness of CD4(+) T cell cytokines associated with abdominal visceral fat mass is a novel finding late in gestation.

Intrauterine DHA exposure and child body composition at 5 y: exploratory analysis of a randomized controlled trial of prenatal DHA supplementation

Background Observational studies find associations between maternal docosahexaenoic acid (DHA) and greater fat-free mass and lower percentage of body fat, but randomized trials of prenatal DHA supplementation have not found significant intent-to-treat effects on childhood body composition. Objective This study sought to explore associations between intrauterine DHA exposure and body composition and size at 5 y in the offspring of women who participated in a randomized trial of prenatal DHA supplementation (corn and soybean oil placebo or 600 mg/d). Design At 5 y, body composition was measured by air displacement plethysmography in 154 offspring of women who had participated in the Kansas University DHA Outcomes Study and who had red blood cell (RBC) phospholipid (PL) fatty acids assessed at enrollment and delivery. We used linear regression models to analyze the relation among 3 indicators of intrauterine DHA exposure-1) intent-to-treat (placebo or DHA), 2) maternal RBC PL DHA status at delivery, and 3) change in maternal DHA (delivery minus enrollment)-and 6 outcomes of interest: 5-y fat mass, fat-free mass, percentage of body fat, height, weight, and body mass index z score. Results Change in maternal RBC PL DHA correlated with higher fat-free mass (r = 0.21, P = 0.0088); the association was unchanged after adjustment for maternal, perinatal, and childhood dietary factors. Intent-to-treat and DHA status at delivery showed positive trends with fat-free mass that were not statistically significant. There was no evidence relating intrauterine DHA exposure to any other body composition measure. Conclusions Change in maternal DHA status during pregnancy was related to higher offspring 5-y fat-free mass. The other 2 indicators of intrauterine exposure to DHA suggested a trend for higher offspring 5-y fat-free mass. Our findings agree with an earlier observational study from the United Kingdom. This trial was registered at clinicaltrials.gov as NCT00266825.