Somatic growth in the first six months of life of infants exposed to maternal smoking in pregnancy

Background: Some studies suggest a relationship between maternal smoking during pregnancy and not only intrauterine fetal growth restriction or low birth weight, but also with changes in the postnatal growth and development. The objective of the present study was to investigate the effects of smoking during pregnancy on infants growth in the first 6 months of life compared with a control group and a group with idiopathic intrauterine growth restriction. Methods: Longitudinal observational study using a convenience sample of newborns divided into three groups: infants of smoking mothers (tobacco), with idiopathic intrauterine growth restriction (IUGR) and a control group. The sample was selected from two hospitals in Porto Alegre, located in southern Brazil, between 2011 and 2015. Newborns were evaluated at birth, 7 and 15 days, and in the first, third, and sixth month. Anthropometric measures were weight, length and head circumference. The growth indicators used were expressed as z-scores. The analyses were performed using the generalized estimating equation method. Results: The sample included 273 mother/newborn pairs: 86 tobacco group, 34 IUGR group, and 153 control group. In terms of weight at birth, all groups differed significantly (p < 0.001). The birth length of tobacco and control groups were similar, but the IUGR group was lower than both (p < 0.001). We found no differences in growth trajectory between tobacco and control group, but there were differences in the growth of the IUGR group when compared with the other groups. At 6 months of age, all groups had similar anthropometric measurements. Conclusion: Intrauterine growth restriction had major impact on the growth trajectory of the infants studied, regardless of other factors, such as smoking and diet

Maternal smoking during pregnancy and offspring overweight : is there a dose–response relationship? An individual patient data meta-analysis

We want to thank the funders of the individual studies: the UK Medical Research Council and the Wellcome Trust (Grant ref: 102215/2/13/2) and the University of Bristol, the Danish National Research Foundation, Pharmacy Foundation, the March of Dimes Birth Defects Foundation, the Augustinus Foundation, and the Health Foundation, the US NICHD (contracts no. 1-HD-4-2803 and no. 1-HD-1-3127, R01 HD HD034568), the NHMRC, the CNPq (Portuguese acronym for the National Research Council—grant 523474/96-2) and FAPESP (Portuguese acronym for the São Paulo State Research Council—grant 00/0908-7). We would like to thank the participating families of all studies for the use of data. For the ASPAC study, we want to thank the midwives for their help in recruiting families, and the whole ALSPAC team, which includes interviewers, computer and laboratory technicians, clerical workers, research scientists, volunteers, managers, receptionists, and nurses. This work was supported by the Deutschen Forschungsgesellschaft (German Research Foundation, DFG) [KR 1926/9-1, KU1443/4-1]. Dr. Gilman’s contribution was supported by the Intramural Research Program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development.Peer reviewedPostprin

The Barker hypothesis

The Barker hypothesis proposed that adverse nutrition in early life, including prenatally as measured by birth weight, increased susceptibility to the metabolic syndrome which includes obesity, diabetes, insulin insensitivity, hypertension, and hyperlipidemia and complications that include coronary heart disease and stroke. Periods of rapid postnatal growth associated with high-energy intake seem to be risk factors, along with a high-energy western diet. Theories proposing the mechanism of this association include the thrifty gene, bet-hedging, fetal predictive adaptive response, and drifty phenotype hypotheses. The cause of metabolic syndrome is likely to be multifactorial, with many nuclear DNA and cellular RNA sequences acting in concert with environmental influences. Epidemiological data in humans and experimental data indicate that transgenerational epigenetic inheritance is a possible mechanism where a history of starvation or deprivation during early life is seen in a grandparent and transgenerational effects are seen in their grandchildren. It remains to be seen whether this is mediated by heritable RNA sequences, or by acquired, possibly mosaic mutations in DNA coding for example for regulatory RNAs. Recent research has raised the possibility that the nature and quantity of gastrointestinal microorganisms (microbiota) can be modified by diet and conversely can modify an animal's metabolic program. As the microbiota is inherited largely from the mother, modification of her nutrition, health before and during pregnancy, and mode of delivery could influence the child's microbiota, introducing further potential avenues to improve the prevention, reduction of complications, and treatment of malnutrition and metabolic syndrome

Placental vascular defects in compromised pregnancies: effects of assisted reproductive technologies and other maternal stressors

Many factors negatively affect pregnancy establishment and subsequent fetal growth and development, including maternal factors such as nutritional stress, age, body mass index, and genetic background, and external factors including environmental stress, psychosocial stress, multiple fetuses, medical conditions (e.g., polycystic ovary syndrome), lifestyle choices (e.g., alcohol consumption, smoking), and assisted reproductive technologies. These same factors have similar consequences for placental growth and development, including vascular development. We and others have shown that placental vascular development begins very early in pregnancy and determines, to a large extent, placental function—that is, the magnitude of the increase in placental blood flow and thus nutrient transport to the fetus. During the peri-implantation period and also later in pregnancy, cloned (somatic cell nuclear transfer) embryos exhibit a variety of placental defects including reduced vascularization and altered expression of angiogenic factors. Although placental defects are less pronounced in pregnancies resulting from the transfer of in vitro fertilized embryos, we and others have recently demonstrated that vascularization, expression of angiogenic factors, sex steroid receptors, several epigenetic markers, and growth of utero-placental tissues all were altered during early pregnancy after transfer of embryos obtained through natural mating, in vitro fertilization, or other assisted reproductive techniques. These observations are in agreement with the recent reports that in humans even singleton pregnancies established with assisted reproductive techniques are at increased risk of preterm delivery and low birth weight, and seem especially relevant considering the rapidly expanding use of these techniques in humans and animals