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Growth, metabolism, genetics, and the environment - Alice was not a scientist.

DOI:10.1097/MED.0000000000000304 ‘It was much pleasanter at home,’ thought poor Alice, ‘when one wasn’t always growing larger and smaller, and being ordered about by mice and rabbits.’ Lewis Carroll, Alice in Wonderland, Chapter 4. Our understanding of growth during infancy and childhood has become more nuanced in recent years. We have long recognized that growth and eventual adult height are based upon a complex interaction between genetic capacity and environmental inputs, including chronic illness and nutritional factors. We are now developing a working understanding of the endocrine, genetic, and epigenetic mechanisms responsible for the effects of this interaction. Our observations are largely drawn from clinical research but many of our conclusions are indeed drawn from studies in ‘mice and rabbits’ as well as other experimental models. Some of the observations derived from animal models have been distinctly unsettling endocrinologists and others whose scientific home is that of hormones and their growth effects. The reviews in the Growth and Development section of Current Opinion this year all exemplify different aspects of the genetic and environmental interaction. The studies by Shoemaker and Jüppner (pp. 33–38), as well as by Bonfig (pp. 39–42) address growth and other manifestations of two rare genetic disorders, one maternally imprinted and the other autosomal recessive. Shoemaker and Jüppner (pp. 33–38) have reexamined a prototypic imprinting disorder, pseudohypoparathyroidism type Ia, and demonstrated that there are many features not previously recognized, which are directly associated with the biology of the disorder. They describe bone complications, including spinal stenosis related to reactive bone formation and ligamental ossification. Brachydactyly increases the risk of problems with fine motor function and handwriting and carpal tunnel syndrome is often seen. Sleep apnea is very common and may be related to direct biomechanical effects as well as altered Gsa expression in the central nervous system. Recurrent otitis media perhaps because of craniofacial abnormalities may increase the risk of early deafness and dental abnormalities, including enamel hypoplasia and delayed tooth eruption may