Over recent months, the links between prenatal growth restraint and postnatal endocrinology and metabolism have been strengthened and their spectrum has been broadened. Recent progress has come from complementary angles, including the following: (1) Small for gestational age (SGA) and the human genetics of insulin-like growth factor (IGF)-I and its receptor: (a) IGF-I receptor mutations [1]; (b) single copy of IGF-I receptor gene [2]; (c) IGF-I gene polymorphisms [3]. (2) Adrenarche and polycystic ovary syndrome: (a) prenatal and postnatal weight gain: opposite effects on adrenarche in girls and boys [4]; (b) metformin therapy in low-birth-weight girls to prevent progression from precocious pubarche to polycystic ovary syndrome [5]. (3) Gynecological and pregnancy complications in women born SGA: (a) hypergonadotropinaemia and small uterus-ovaries [6]; (b) identification of low maternal birth weight as a risk factor for: (i) gestational diabetes, (ii) pregnancy-induced hypertension (with SGA offspring) [7, 8]. (4) Growth hormone (GH) therapy for short children born SGA: (a) efficacy of long-term, continuous GH therapy [9]; (b) normal puberty in short GH-treated SGA children [10]. Our knowledge of SGA and post-SGA endocrinology and metabolism continues to expand swiftly. Children born SGA may continue to experience SGA consequences or correlates, and SGA adults may confer intergenerational SGA risk. Given the dynamics of this research frontier, it is anticipated that multiple facets of GH therapy in short SGA children will regularly be challenged in the future. May those questions be welcomed and may their responses ultimately lead to optimal GH regimens that benefit not only SGA children themselves but also, in due course, their progeny.

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Van Pareren Y, Mulder P, Houdijk M, et al: Adult height after long-term, continuous growth hormone (GH) treatment in short children born small for gestational age: Results of a randomized, double-blind, dose-response GH trial. J Clin Endocrinol Metab 2003;88(8):3584–3590.
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