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Background During pregnancy, a variety of factors can influence fetal growth and development. Intrauterine growth may impact on later life and health. Neonatal body composition may be a more sensitive marker for the intrauterine environment than established anthropometric parameters at birth. Methods To study neonatal body composition determined by air displacement plethysmography in healthy, term singletons as national reference data, and to establish factors impacting on neonatal body composition in this population. This prospective cross-sectional observational study included 271 healthy, full-term, singletons born between June 2014 and July 2015. Body composition was measured within 96 h of birth using air displacement plethysmography. Results Median (Q1, Q2) fat mass / total body mass (BF%) in German singletons was 10.8% (7.7–13.4) and fat free mass (FFM) 2843 g (2606–3099). Female infants had significantly increased BF% compared to male infants (11.2% (8.7–14.0) vs. 9.6% (7.2–12.1)). On multiple regression analysis, BF% and fat mass increased with female gender, maternal pre-pregnancy body mass index, non-smoking mother and parity, whereas FFM increased with male gender and increasing gestational age at birth. Gestational weight gain category, birth mode, and postnatal age at measurement were not associated with BF%, FFM or fat mass. Conclusions We generated BF% and FFM centiles for healthy, term, singletons born in Germany; these are similar to those found in other European countries. Infant body composition at birth was associated with modifiable (pre-pregnancy body mass index, smoking), and given factors (gender, gestational age at birth, parity).

BackgroundBehavioral and cognitive control are vital for healthy eating behavior. Patients with binge eating disorder (BED) suffer under recurrent binge eating episodes accompanied by subjective loss of control that results, among other factors, from increased impulsivity.MethodsIn the current study, we investigated the frontal network using functional near-infrared spectroscopy (fNIRS) during a food specific go/nogo task to assess response inhibition in 24 patients with BED (BMI range 22.6–59.7kg/m2) compared to 12 healthy controls (HC) (BMI range 20.9–27kg/m2). Patients with BED were invited to undergo fNIRS measurements before an impulsivity-focused cognitive behavioral group treatment, directly after this treatment and 3months afterwards. As this was a planned subgroup analysis of the randomized controlled IMPULS trial, patients with BED were randomized either to the treatment group (n=14) or to a control group (n=10). The treatment group received 8 weekly sessions of the IMPULS treatment.ResultsWe found a significant response inhibition effect (nogo minus go), in terms of an increased oxygenated hemoglobin response in the bilateral prefrontal cortex in both groups. The greatest response was observed when participants were instructed to go for healthy and withhold their response to unhealthy high caloric food cues. The healthy nogo condition failed to show a significant prefrontal inhibitory response, which was probably related to the task design, as the condition was considered more demanding. BED patients, especially those with higher trait impulsivity, showed a weaker activation of the prefrontal cortex during response inhibition, predominantly in the right hemisphere. Interestingly, three months after the treatment, patients of the treatment group increased their right prefrontal cortex activity during response inhibition. Likewise, increased prefrontal cortex activation correlated with decreased trait impulsivity after treatment.ConclusionsOur results suggest that patients with BED have limited resources to activate the prefrontal cortex when asked to inhibit a reaction onto food-specific stimuli. However, this effect could be partly driven by differences in BMI between the HC and BED group. Cognitive-behavioral therapy targeting impulsive eating behavior may improve prefrontal cortex recruitment during response inhibition.

Maternal nutrition in pregnancy has a key influence on optimum fetal health. Eating disorders (EDs) during pregnancy may have detrimental effects on fetal growth and the child's early development. There is limited knowledge concerning the eating behavior, dietary intake and derived nutritional biomarkers as well as the nutrient supplementation in women with EDs during pregnancy. We performed a systematic review according to the PRISMA statement to synthesize current evidence in this field. Of N = 1203 hits, 13 full-texts were included in the qualitative synthesis. While women with current Binge Eating Disorder (BED) showed higher energy and fat intakes during pregnancy, women with a lifetime Anorexia Nervosa (AN), Bulimia Nervosa (BN) or both (AN + BN) had similar patterns of nutrient intake and dietary supplement use as healthy women. There is evidence, that women with a history of EDs have a sufficient diet quality and are more likely to be vegetarian. Dieting and bingeing improved substantially with pregnancy. The highlighted differences in the consumption of coffee/caffeine and artificially sweetened beverages as well as the elevated prevalence of iron deficiency anemia in women with a past or active ED during pregnancy might have an important impact on fetal development.

Introduction: We have previously shown that fetuses of mothers with gestational diabetes mellitus (GDM) and insulin resistance exhibit a prolongation of fetal auditory event-related brain responses (fAER) compared to fetuses of normal glucose tolerant women during an oral glucose tolerance test (oGTT). This implies that maternal metabolism may program the developing fetal brain. We now asked whether a family history of type 2 diabetes without metabolic programing also impacts fetal brain activity. We therefore investigated brain activity in fetuses of normal glucose tolerant mothers with and without family history of type 2 diabetes (FHD+ and FHD-).Methods: A 75 g oGTT was performed in healthy pregnant women. Plasma glucose and insulin levels were measured after 0, 60, and 120 min. Each blood draw was preceded by fetal magnetoencephalographic (fMEG) recordings of fAER. From a group of 167 participants, a subsample of 52 metabolically healthy women, 37 with a negative, and 15 with a positive FHD (at least one first- or second-degree relative) was carefully selected based on the following inclusion criteria: inconspicuous pregnancy, no GDM, BMI 18.5-30 kg/m(2), no preterm birth and at least two fMEG with detectable fetal responses during oGTT.Results: An ANOVA showed a significant interaction between fMEG measurement time during the oGTT and FHD on fAER latency [F-(2) = 4.163, p = 0.018]. Fetuses of mothers with FHD+ had a prolonged fAER (273 +/- 113 ms) compared to fetuses of mothers with FHD- (219 +/- 69 ms) at 60 min during the oGTT [F-(1() )= 4.902, p = 0.032]. There were no significant differences in age, BMI before pregnancy, weight gain during pregnancy and gestational age between the groups. Maternal glucose levels and insulin sensitivity were also not significantly different.Discussion: In addition to the previously shown influence of maternal metabolism on fetal brain activity, maternal family history of diabetes (FHD) is also linked to fetal postprandial brain activity. This indicates that genetic and/or epigenetic factors modulate the postprandial brain response of the developing fetus.

Intrauterine growth restriction (IUGR), which is already known to be a risk factor for pathological intrauterine development, perinatal mortality, and morbidity, is now also assumed to cause both physical and cognitive alterations in later child development. In the current study, effects of IUGR on infantile brain function were investigated during the fetal period and in a follow-up developmental assessment during early childhood. During the fetal period, visual and auditory event-related responses (VER and AER) were recorded using fetal magnetoencephalography (fMEG). VER latencies were analyzed in 73 fetuses (14 IUGR fetuses) while AER latencies were analyzed in 66 fetuses (11 IUGR fetuses). Bayley Scales of Infant Development, Second Edition (BSID-II) were used to assess the developmental status of the infants at the age of 24 months. The Mental Development Index (MDI) was available from 66 children (8 IUGR fetuses) and the Psychomotor Development Index (PDI) from 63 children (7 IUGR fetuses). Latencies to visual stimulation were more delayed in IUGR than in small for gestational age (SGA) or appropriate for gestational age (AGA) fetuses, albeit not to any significant extent (p = 0.282). The MDI in former IUGR infants was significantly lower (p = 0.044) than in former SGA and AGA infants. However, IUGR had no impact on PDI (p = 0.213). These findings support the hypothesis that IUGR may constitute a risk factor for neurodevelopmental delay. Further investigation of the possible underlying mechanisms, as well as continued long-term developmental research, is therefore necessary.

Das Gehirn spielte in der Diabetesforschung lange keine Rolle, inzwischen ist es in den Fokus der Forscher gerückt. Denn Studien der vergangen Jahre belegen: Das Gehirn ist ein insulinsensitives Organ. So reagiert eine Reihe von Gehirngebieten auf Insulin – dazu zählen Areale, die für die Nahrungsaufnahme, den Stoffwechsel und das Gedächtnis wichtig sind. Vermutlich dämpft das Hormon im Gehirn den Hunger oder verstärkt die Sättigung nach dem Essen. Das Gehirninsulin verbessert auch die Wirkung des Hormons im übrigen Körper. Diese Arbeiten eröffnen neue Angriffspunkte in der Diabetestherapie. &nbsp