Maternal growth during adolescent pregnancy and its effects on pregnancy outcome have been a source of controversy. Maternal growth during pregnancy has been difficult to quantify because of the tendency of young and older women to "shrink" in stature with pregnancy. In the Camden Study, maternal growth during pregnancy was monitored with the Knee Height Measuring Device, which measures growth of the lower leg, a body segment less susceptible to "shrinkage." Attempts of other investigators to detect maternal growth during adolescent pregnancy are reviewed here. New data from the Camden Study, also presented, suggest that growing adolescents have infants that weigh less compared to nongrowing adolescents and mature controls (aged 19-29 years). Prior work had suggested that the effects of maternal growth on birth weight were confined to adolescent multiparas. However, with expanded enrollment it was found that infants of growing primiparas and multiparas were both affected. The hypothesis of the competition for nutrients between a still-growing gravida and her fetus is discussed.
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"Due to low intake of fresh vegetables, fruits and high-quality protein food, deficiencies of amino acids, vitamins and minerals in humans are fairly prevalent all over the world   . Maternal undernutrition often occurs during pregnancy because of the competition for nutrients between fetus and mother   , which may result in intrauterine growth restriction (IUGR), as well as high risk for perinatal maternal complications and neonatal death  . IUGR, which is defined as the impaired growth and development of the fetus or its organs , also increases the risk for the development of metabolic syndrome in adult life, including type 2 diabetes, cardiovascular disease, visceral obesity, hypertension, dyslipidemia, hyperglycemia and insulin resistance     . "
[Show abstract][Hide abstract] ABSTRACT: Recent findings from human and animal studies indicate that maternal undernutrition or overnutrition affects covalent modifications of the fetal genome and its associated histones that can be carried forward to subsequent generations. An adverse outcome of maternal malnutrition is the development of metabolic syndrome, which is defined as a cluster of disorders including obesity, hyperglycemia, hyperinsulinemia, hyperlipidemia, hypertension and insulin resistance. The transgenerational impacts of maternal nutrition are known as fetal programming, which is mediated by stable and heritable alterations of gene expression through covalent modifications of DNA and histones without changes in DNA sequences (namely, epigenetics). The underlying mechanisms include chromatin remodeling, DNA methylation (occurring at the 5'-position of cytosine residues within CpG dinucleotides), histone modifications (acetylation, methylation, phosphorylation, ubiquitination and sumoylation) and expression and activity of small noncoding RNAs. The enzymes catalyzing these reactions include S-adenosylmethionine-dependent DNA and protein methyltransferases, DNA demethylases, histone acetylase (lysine acetyltransferase), general control nonderepressible 5 (GCN5)-related N-acetyltransferase (a superfamily of acetyltransferase) and histone deacetylase. Amino acids (e.g., glycine, histidine, methionine and serine) and vitamins (B6, B12 and folate) play key roles in provision of methyl donors for DNA and protein methylation. Therefore, these nutrients and related metabolic pathways are of interest in dietary treatment of metabolic syndrome. Intervention strategies include targeting epigenetically disturbed metabolic pathways through dietary supplementation with nutrients (particularly functional amino acids and vitamins) to regulate one-carbon-unit metabolism, antioxidative reactions and gene expression, as well as protein methylation and acetylation. These mechanism-based approaches may effectively improve health and well-being of affected offspring.
The Journal of nutritional biochemistry 08/2015; DOI:10.1016/j.jnutbio.2015.08.003 · 3.79 Impact Factor
"Approximately 50% of adult weight and 15% of adult height is attained during adolescence (Rogal et al. 2000, Spear 2000). Due to chronic malnutrition in developing countries, age at menarche is delayed by about 3 years and growth continues until age 20 (Scholl et al. 1993, Riley et al. 1989). A World Health Organization analysis found that women with a pre-pregnancy weight of less than 45 kg and height of less than 145 cm were at increased risk of low birth weight and premature delivery (WHO 1995). "
[Show abstract][Hide abstract] ABSTRACT: The purpose of this study was to examine whether changes in the mid-upper arm circumference (MUAC) in pregnancy and early post-partum varied by maternal age. The MUAC of 3359 nulliparous pregnant women ≤25 years of age in rural Nepal was measured in early pregnancy and at 3 months post-delivery of a live-born infant. Regression was used to model the change in MUAC and prevalence of MUAC < 20 cm by maternal age, adjusted for confounders. A total of 5.2% of the pregnant women were under 16 years of age. The prevalence of MUAC measurements <20 cm was 11.3% in early pregnancy and did not differ by maternal age. The prevalence of low MUAC was 17.7% at post-partum, but those <16 years of age had a significantly higher prevalence of low post-partum MUAC [odds ratio: 2.47, 95% confidence interval (CI) 1.49, 4.10] compared with women 20-25 years of age, adjusted for maternal literacy, caste, meat consumption in early pregnancy and timing of measurements. All women reduced their MUAC from early pregnancy through post-partum. The adjusted loss of the MUAC among those under 16 years of age was 0.97 cm (95% CI: -1.33, -0.60), compared with 0.40 cm (95% CI: -0.70, -0.10) among women 20-25 years of age. In an energy-restricted environment, girls under 16 years contributed to a half centimetre more loss of MUAC than older women of the same parity. Such a loss of fat, muscle or both may put younger women and their breastfed offspring at greater risk of other adverse health and nutritional outcomes.
"In line with life history theory, the research conducted on the women of rural Gambia has found that younger age at first reproduction may be associated with shorter adult height (Allal, Sear, Prentice, & Mace, 2004; Sear, Allal, Mace, & McGregor, 2004). Furthermore, previous studies in epidemiology provide evidence that shorter adult height may also be related to earlier age at menarche (Georgiadis, 1997; Gigante, Horta, Lima, Barros, & Victora, 2006; Nettle, 2002; Okasha, McCarron, McEwen, & Smith, 2001; Onland-Moret et al., 2005) and that pregnancy in adolescent still-growing girls may impair their height gain (Gigante, Rasmussen, & Victora, 2005; Scholl & Hediger, 1993). In sum, the available data show associations compatible with the reproduction growth tradeoff in women. "
[Show abstract][Hide abstract] ABSTRACT: Women have been suggested to trade growth in height for reproduction, as an earlier age at menarche and first birth seem to be related to shorter adult stature. Although women likely accrue fitness benefits by maturing and starting reproduction at young age, short adult stature may be selected against by natural and sexual selection later in their life. We studied how age at menarche and first reproduction affected adult height and whether adult height in turn was related to lifetime reproductive success in Finnish women born 1946–1958. Our results show that a delay of 1 year in age at menarche and first reproduction was related to a 0.43-and 0.20-cm increase in adult height, respectively. The sex of the first-born offspring was not related to adult height. Moreover, women gained fitness benefits by starting reproduction early but not by growing tall. These findings among Finnish women are thus compatible with tradeoffs between reproduction and growth, by showing a compromised adult height at the cost of early age at menarche and first birth. However, in these women, natural selection favored those women who traded their stature for young motherhood.
Evolution and Human Behavior 05/2008; 29(3). DOI:10.1016/j.evolhumbehav.2007.11.009 · 3.13 Impact Factor