Nutrition and the age of puberty
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Mechanisms underlying the early and late onset of puberty
Over the last hundred years, the age of puberty in the developed world has significantly decreased. Our project starts from the hypothesis that the onset (as well as the end) of the reproductive period are regulated by evolutionary mechanisms, which are underpinned by environmental signals during development. These signals include nutrition, maternal care and bonding. The work of our clinical and experimental collaborators, in humans and in rats, has shown that fetal adaptation to poor nutrition advances pubertal onset, highlighting the importance of prenatal and postnatal interactions in influencing reproductive strategies. New studies have suggested that poor maternal care and bonding can also impact on reproductive maturation. We draw on the knowledge of evolutionary biology and anthropology to build models and hypotheses tested in experimental research and in clinical studies.
Key publications:
Gluckman PD and Hanson MA. Evolution, development and timing of puberty. Trends in Endocrinology and Metabolism 2006; 17: 7-12.
Sloboda DM, Howie GJ, Pleasants A, Gluckman PD and Vickers MH. Pre- and postnatal nutritional histories influence reproductive maturation and ovarian function in the rat. PLoS One 2009; 4(8): e6744.
Nutrition and the age of puberty
Over the course of the twentieth century, the age of puberty in developed countries has decreased from 17 to 12.5 years. Following clinical studies that showed that girls small at birth but large at 8 years, reached menarche earlier, animal models were used to explore if low-calorie nutrition before birth and/or during lactation accelerated the age of sexual maturation. In the graph on the right we see results of a study conducted on rats undernourished (UN) or fed a control (Cont, C) or a high fat (HF) diet during pregnancy (P), lactation (L) and afterwards (following ‘+’ sign). The earliest onset of menarche was found in the group undernourished in pregnancy and lactation but fed a high fat diet afterwards.
Interestingly, the group which received a high fat diet through all stages also entered puberty early in comparison to controls, yet progesterone levels in the two groups were divergent: low in the UN and high in the HF group. This indicates that the lowering of the age of puberty takes place in two different evolutionary scenarios. In the first case, the offspring of undernourished dams matured early to hasten reproduction in expectation of a short lifespan in the predicted poor nutritional environment; in the second, the offspring of dams fed the high fat diet the goal might have ‘chosen’ to extend the length of the reproductive period. The former can be viewed as an attempt to maintain fitness in a difficult environment, the latter an opportunistic increase in fitness in response to a predicted abundance.
This graph is based on data published in Sloboda et al. Pre- and postnatal nutritional histories influence reproductive maturation and ovarian function in the rat. PLoS One 4(2009), e6744.
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