Environmental adversity and reproductive development

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Sexual maturation and growth occur with a social and economic context that influence developmental trajectories. Developmental data suggest a strong relation between patterns of growth and development on the one hand, and reproduction on the other. This relation is entirely consistent with life history theory (see above), which suggests that assuming adequate current nutritional support conditions that imperil survival will accelerate the timing of sexual maturation. The fatal error of life history is that of the complete failure to reproduce resulting in the loss of the lineage. Thus evolutionary theory suggests that selection will favor mechanisms for reducing the risk for lineage extinction in environments that offer a high risk for mortality and uncertain resource availability (Chisholm and Burbank, 2001; Maynard Smith, 1982): "When the future is risky and uncertain the optimal reproductive strategy is to take whatever resources are available and quickly convert them into offspring" (Chisholm and Burbank, 2001, p. 207). Strong support for this prediction is found in the literature on the relation between birth weight (a proxy measure for fetal adversity, Matthews and Meaney, 2005) and female puberty in humans.

The complexity of the relation between nutrition and female sexual maturation is reflected in the fact that while there is a secular trend for earlier menarche, there is no such change in birth weight (Ellis, 2005). Malnutrition certainly delays sexual maturation and reproductive activity. Severe energy demands or malnutrition preclude reproduction. Nutrient deprivation in early life leads to more complex scenarios. Early periods of growth retardation followed by exposure to adequate nutritional resources are a formula for the acceleration of sexual maturation in females and such effects are apparent in studies on birth weight and age of menarche. In developed countries where energy resources are not rate limiting, low birth weight is reliably associated with an early age of menarche (Chisholm, 1993; Coall and Chisholm, 2003; Ellis, 2005). Importantly, as with other outcome measures associated with birth weight, this relation is continuous across birth weights and is not restricted to a unique sample of very low birth weight babies (Phillips, 1998). Thus, the more successful the growth of the fetus, the later the onset of puberty.

Low birth weight (birth weight that is less than expected for gestational age) followed by a postnatal period of adequate nutritional resources is commonly associated with a period of catch-up growth over the first 3 years of life. As predicted by Chisholm and Burbank (2001), it is precisely this population of children that show an advanced age of sexual maturation. This same population shows an increased risk for obesity and metabolic diseases (Barker et al., 1989, 2002; Gluckman and Hanson, 2004a; Hales and Barker, 2001; Phillips, 1998). Compared with controls (i.e., children born at weights that are average for gestational age) children showing low birth weight and postnatal catch-up growth reveal evidence for hyperinsulinemia, dyslipidemia, and increased body fat with reduced lean body mass. This condition is also associated with increased leptin levels (Ong et al., 1999; Pulzer et al., 2001). Increased insulin activity is thought to advance adrenarche by stimulating the activity of P450c17 that promotes adrenal androgen [dihydroepiandrosterone (DHEA)] synthesis and release. (Ibanez et al., 2000). The relation between low birth weight and early sexual maturation is also evident in prospective studies conducted with children well before the onset on even the earlier stages of pubertal development (Veening et al., 2004). Adrenarche reliably predicts the onset of endocrine events that culminate in pubarche (eruption of pubic hair) and ultimately sexual maturation in females. Thus, the age of adrenarche is significantly advanced in low birth weight girls that show postnatal catch-up growth (Ong et al., 2004). Interestingly, this condition likely derives from an effect of endocrine signals associated with nutrition and growth (leptin, insulin) on reproductive systems.

The relation between interuterine growth retardation, resulting in diminished birth weight, and an early onset of sexual maturation may seem somewhat counterintuitive. Note, however, that this relation is only apparent under conditions of adequate postnatal nutrition, and indeed is best reflected in those children that reveal postnatal catch-up growth. Interuterine growth retardation is a reliable consequence of materno-fetal function under conditions of environmental adversity. Indeed, increased activity of the maternal and/or fetal hypothalamic-pituitary-adrenal (HPA) axis is considered the proximal cause of interuterine growth retardation (Goland et al., 1993, 1995; Matthews and Meaney, 2005; Meaney et al., in press; Seckl, 1998). Thus, poverty is associated with a significantly increased risk for inter-uterine growth retardation (IUGR) and the major predictors of low birth weight, maternal protein deprivation, tobacco and alcohol consumption, and maternal stress/anxiety are related to

SES and each activates the HPA axis. Williams et al. (1997) found that lower SES is associated with a higher ratio of placental weight/fetal weight. Placental hypertrophy is considered a fetal adaptation to restricted maternal provisioning (bear in mind the placenta is largely of fetal origin). Predictably, there are increased chord levels of both corticotrophin-releasing factor (CRF) and cortisol in small babies compared with controls (Goland et al., 1993, 1995). Moreover, studies with both rodent and primate models reveal that the risk for IUGR associated with factors such as protein deprivation is directly mediated by maternal HPA activity (Langley-Evans, 1997; Seckl, 1998).

The relation between materno-fetal environmental adversity and IUGR is critical for the understanding of the adaptive nature of early menarche in low birth weight children. Life history theory suggests that when environmental conditions predict an increased risk for mortality, it is advantageous to utilize existing energy resources to accelerate reproduction (Worthman, 1999). The alternative associated with delayed sexual maturation is that death will occur prior to reproduction—lineage extinction. Evidence for the trade-off in life history strategies is apparent in the finding that girls that show early puberty are significantly shorter than their peers, and that this relation is evident even before the onset of puberty.

In a comparative analysis across 48 mammalian species, Promislow and Harvey (1990) found that high mortality rates predicted an early age of sexual maturity. Perhaps the ideal human study was that showing that children adopted from developing countries into affluent western families experienced earlier puberty than do children from either the country of origin or the host country (Mul et al. 2002). Thus, if energy resources permit, the ideal strategy under conditions of adversity in early development is to enhance the age of reproduction, even if, as in human populations, early reproduction is associated with increased health risks for the offspring (Coall and Chisholm, 2003). Worthman (1999) suggested that girls experiencing deprivation would react to an increase in resource availability by hastening reproduction, thus exploiting what might be a unique window of reproductive opportunity. Indeed, the relation between environmental adversity and early sexual maturation in human females is also revealed in studies of the influences of postnatal adversity.

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