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Polycystic ovary syndrome (PCOS) is a common endocrinopathy affecting women of reproductive age, with varying signs and symptoms. Its various manifestations will bring PCOS patients to healthcare providers from different backgrounds, for differing reasons. The metabolic, endocrine, and reproductive aspects of PCOS interact and intertwine, and all may be influenced by nutrition and alternative metabolic pathways. These have been highlighted by research in recent years, which will be reviewed in this chapter. Treatment of PCOS may be enhanced by this evolving knowledge, in all aspects of the syndrome, including short-term problems such as acne or infertility, and long-term problems such as obesity, diabetes mellitus, atherosclerosis, and even possibly breast cancer (Kaaks 1996).
Pathogenesis of PCOS and nutrition
Polycystic ovary syndrome is a syndrome whose appearance depends on a combination of genetic and environmental factors. Environmental/nutritional factors may come into play even before birth, as birthweight depends both on genetic factors and maternal nutrition and uteroplacental function (Armitage et al. 2004). A positive correlation has been found between birthweight and subsequent presentation of polycystic ovaries (Michelmore et al. 2001). Conversely, large population-based studies in the United Kingdom clearly correlated low birthweight to subsequent markers of metabolic syndrome (Godfrey and Barker 2000). Rapid early postnatal weight gain (possibly following maternal–uterine restraint) strongly predicts later childhood obesity and insulin resistance (Ong and Dunger 2004). It is becoming clear that nutrition in early life has an immense impact on adult health.
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