Evidence from previous studies suggests an association between prenatal exposure to famine and increased risk for depression. The aim of this study was to investigate whether prenatal exposure to the Dutch famine is associated with self-reported depression/anxiety and whether a potential association is mediated by the presence of cardio-metabolic disease. A total of 819 persons, born as term singletons around the 1944–1945 Dutch famine, filled out the Hospital Anxiety and Depression Scale (HADS) and were asked about their medical history. As indicators of cardio-metabolic disease we included type 2 diabetes (T2D), hypertension and coronary heart disease (CHD). In the total study population, exposure to famine during early gestation was associated with the presence of self-reported mild-to-severe anxiety. Evidence was found for several interactions between exposure in early gestation and sex. Subsequent analyses according to sex showed that men exposed to famine during early gestation scored higher on the HADS depression scale. Self-reported mild-to-severe anxiety symptoms were more prevalent among early exposed men. No such differences were found in women. T2D and hypertension were not correlated with any of the depression and anxiety measures. Adjusting for the presence of CHD did minimally attenuate the size of the reported associations. In conclusion, the present results do not match those previously reported in prenatally famine-exposed individuals. We found only weak evidence for an association between prenatal famine exposure and symptoms of depression and anxiety, which was shown exclusively in men exposed during early gestation.

The aim of this study was to compare physical growth from birth to 2 years of age of babies born to women with or without gestational diabetes mellitus (GDM), among the subjects of the 2004 Pelotas Birth Cohort. Mothers who gave birth in 2004 in any of the five maternity wards in the city of Pelotas, Southern Brazil, were interviewed shortly after delivery by trained interviewers, using tested, pre-coded questionnaires. GDM diagnosis was self-reported. Child weight, length and abdominal circumference were measured, and adjusted weight-for-age, height-for-age and weight-for-height Z-scores were calculated at birth, 3, 12 and 24 months. We studied 4239 children. Offspring of GDM mothers (OGDM; n = 125) had lower gestational age (GA; P = 0.004), greater weight (P = 0.002) and greater abdominal circumference (P < 0.001) at birth. Prevalence of large for GA (LGA) was threefold higher among OGDM (18.4% v. 6.8%). Mean weight-for-age (0.48 v. −0.07; P < 0.001) and weight-for-height (0.94 v. 0.51; P < 0.001) Z-scores were also higher among OGDM. During the first 3 months, there was an abrupt catch-down among OGDM babies, who remained lighter than non-GDM offspring until the 24th month. LGA OGDM were heavier than LGA offspring of non-GDM mothers at birth, but had caught down with babies born with adequate weight for GA to non-GDM by 3 months, and showed similar growth patterns from thereon. OGDM show different growth patterns when compared to offspring of non-GDM mothers, which may be part of a causal pathway or constitute a risk marker for future obesity, impaired glucose tolerance and diabetes mellitus.

The objectives of this study were to describe the prevalence of cigarette use and water pipe smoking in Jordanian university students and to analyze differences in determinants between cigarette smokers and non-smokers. A cross-sectional questionnaire was administered to a random sample of 400 students (18–24 years, 51% males). Smokers were compared with non-smokers on several smoking-related determinants. Data were analyzed using descriptive statistics, t-test, χ2 test and binary logistic regression analysis. The prevalence rates of cigarette use and water pipe smoking were 25.9% and 23.3%, respectively. Cigarette smokers differed significantly from non-smokers on almost all of the assessed determinants. The I-Change model explained 85% of the total variance of cigarette-smoking behavior. Cigarette smoking was determined by being male and older, having more depressive symptoms, having less Muslim identity, being more emancipated, perceiving more pros of smoking, having more modeling from peers and having lower self-efficacy. The popularity of cigarette use and water pipe smoking among Jordanian students necessitates health promotion interventions that motivate students not to engage in smoking behaviors by clearly outlining the outcomes of smoking and the healthier alternatives, how to cope with social influences and difficult situations in order to increase self-efficacy.

Experimental animal studies have shown that nicotine exposure during gestation alters the expression of fetal hypothalamic neuropeptides involved in the control of appetite. We aimed to determine whether the exposure to maternal smoking during gestation in humans is associated with an altered feeding behavior of the adult offspring. A longitudinal prospective cohort study was conducted including all births from Ribeirão Preto (São Paulo, Brazil) between 1978 and 1979. At 24 years of age, a representative random sample was re-evaluated and divided into groups exposed (n = 424) or not (n = 1586) to maternal smoking during gestation. Feeding behavior was analyzed using a food frequency questionnaire. Covariance analysis was used for continuous data and the χ2 test for categorical data. Results were adjusted for birth weight ratio, body mass index, gender, physical activity and smoking, as well as maternal and subjects’ schooling. Individuals exposed to maternal smoking during gestation ate more carbohydrates than proteins (as per the carbohydrate-to-protein ratio) than non-exposed individuals. There were no differences in the consumption of the macronutrients themselves. We propose that this adverse fetal life event programs the individual's physiology and metabolism persistently, leading to an altered feeding behavior that could contribute to the development of chronic diseases in the long term.

We investigated the effects of a postnatal fructose diet on the programmed hypertension and vascular and renal dysfunction in offspring from dams exposed to protein restriction. Pregnant Wistar rats were fed control and low-protein diets during the gestation and suckling periods. From the end of lactation, male offspring received standard chow or a 60% fructose diet: a control diet in the gestation and suckling periods and a control diet from the end of lactation, control-on-control (CC), 60% fructose diet-on-control (CF), control-on-low-protein diet (LPC) and 60% fructose diet-on-low-protein diet (LPF). The systolic blood pressure (SBP) was measured during treatment. At postnatal days 94–101, urinary 24 h nitrate/nitrite (NOx) content, protein levels of endothelial nitric oxide synthase (eNOS) and mRNA levels of endothelin-1 (ET-1), and NAD(P)H oxidase subunits in the aorta and kidney were examined. The SBP at postnatal days 97–101 increased in CF (137 ± 2 mmHg, P < 0.05), LPC (135 ± 1 mmHg, P < 0.05) and LPF (141 ± 2 mmHg, P < 0.05), compared with CC (124 ± 1 mmHg). The urinary NOx contents and eNOS phosphorylation in the aorta and kidney of CF, LPC and LPF decreased when compared with CC. In the aorta, the mRNA levels of NAD(P)H oxidase subunits p47phox in LPC and ET-1 in LPC and LPF increased. These results indicate that maternal protein restriction elevated the blood pressure, the downregulated nitric oxide production and eNOS phosphorylation, whereas the postnatal fructose diet made no significant difference to these alterations.

Maternal food restriction is known to cause developmental hypertension in offspring. We have previously shown that maternal high-protein diet can reverse fetal programming of hypertension and that branched-chain amino acid (BCAA) concentrations in maternal and fetal plasma were increased by maternal high-protein intake. Then, we hypothesized that isocaloric supplementation with BCAA to a maternal food restriction can reverse the adverse outcome. Pregnant rats were divided into four groups at 7.5 days postcoitum: normally nourished (NN) and 70% undernourished (UN) groups with and without BCAA supplementation (NN–standard diet (SD), NN–BCAA, UN–SD and UN–BCAA groups). Compared with pups in the NN groups, those in the UN–SD group had significantly increased systolic blood pressure (SBP) at 8 and 16 weeks of age (P < 0.05). However, the elevation of SBP was not observed in offspring in the UN–BCAA group. Offspring glomeruli number of the UN groups was significantly lower (P < 0.05) than that of the NN groups, independent of BCAA supplementation. Angiotensin II receptor type 2 (ATR2) mRNA and protein expression in the kidney was significantly augmented in the UN–BCAA group at 30 weeks of age. In conclusion, BCAA supplementation during maternal food restriction prevents developmental hypertension together with increased ATR2 expression in adult offspring kidney.

We have previously shown that neonatal high oxygen (O2) exposure in rats leads to hypertension and vascular dysfunction in adulthood. Pulse-wave velocity (PWV), an indirect measure of vascular biophysical properties (arterial stiffness or distensibility), is a sensitive marker of cardiovascular health. Its measurement in rats is mostly based on invasive hemodynamics measurements, prohibiting longitudinal studies particularly relevant in models of developmental programming of cardiovascular dysfunctions. With this study, we sought (1) to verify the feasibility and validity of measuring of aortic PWV in Sprague–Dawley rats by ultrasound; (2) to use the technique to compare aortic PWV in adult rats exposed to O2 as newborns (80% day 3–10 of life) v. controls; and (3) to develop an algorithm to calculate PWV in a non-invasive manner. We calculated aortic PWV using standard echocardiography and electrocardiogram, and validated the measures with PWV obtained by intraaortic catheters. Aortic full length was measured at sacrifice. PWV was significantly increased in O2 exposed (505 ± 18 cm/s) v. control animals (421 ± 17 cm/s, P < 0.01). With regard to weight, femur length and distance from the manubrium to the anal margin (MA length), the latter showed the best correlation (R = 0.84, P < 0.0001) with full aorta length derived from (L) = 0.339 × (MA length) + 4.281. The current data using echo-Doppler method demonstrated increased aortic stiffness in adult rats exposed to hyperoxia as newborns and suggests that non-invasive longitudinal studies of aortic PWV can be performed using the proposed algorithm for estimation of the full aorta length.

Feeding a low protein (LP) diet in rat pregnancy is associated with impaired cardiovascular health and function, possibly as a result of tissue remodelling. To assess whether cardiomyocytes retain differences induced by protein restriction, cells from neonatal rats exposed to control or LP diets in utero were cultured for a period of 10 days. At the end of this period, no differences in cell size, proliferation differentiation or metabolic function were noted. When treated with dexamethasone (0.1–10 μM) for 2 days, it was noted that insulin-stimulated glucose uptake was enhanced, but only in cells from LP rats. Increased glucocorticoid sensitivity of cardiomyocytes from LP rats could not be explained by differential expression of the glucocorticoid receptor or the glucose transporters, GLUT1 and GLUT4. The findings of the study suggest that sensitivity to endocrine signals may be permanently programmed by undernutrition through mechanisms that are preserved in vitro.