Current Opinion in Endocrinology, Diabetes & Obesity:
GROWTH AND DEVELOPMENT: Edited by Lynne L. Levitsky
Levitsky, Lynne L.
Division of Pediatric Endocrinology, Department of Pediatrics, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA
Correspondence to Lynne L. Levitsky, MD, Pediatric Endocrinology, Massachusetts General Hospital, 5th Floor, 175 Cambridge Street, Boston, MA 02114, USA. Tel: +1 617 726 5790; fax: +1 617 724 0581; e-mail: LLevitsky@partners.org
The reviews in this growth and development section of Current Opinion in Endocrinology and Diabetes are almost equally divided between those that focus on prenatal and neonatal issues and those that reflect the later effects of the environment and disease on development. The interplay between genetics and environment is brought home by the careful review of epigenetic factors and growth by Netchine and her group (pp. 30–38) in Paris. They review not only the complex nature of the closely associated imprinting loci for Beckwith–Wiedeman and Russell–Silver syndrome, but also the newly described general disorders of faulty imprinting, and the role of nutritional and environmental imprinting on later development. Mitchell and colleagues (pp. 39–44), who were among the pioneers in newborn screening for endocrine disorders like congenital hypothyroidism and congenital adrenal hyperplasia, update us on the difficulties of adequate screening for these conditions and the largely beneficial outcomes of early and effective treatment. An updated perspective on the long-running medical saga of neonatal hypoglycemia by Rozance (pp. 45–50) characterizes the continuing difficulties in determining which at-risk infants should be treated, how they should be managed, and the ill-defined, long-term outcomes of infants with transient hypoglycemia of nongenetic cause. Abrams and Tiosano (pp. 51–55) bridge the gap between vitamin D levels and metabolism in the fetus and associated chronic disorders, as well as the relationship between metabolism of vitamin D and calcium homeostasis. They point out that the ‘vitamin D bandwagon’ associating many common disorders with vitamin D deficiency in early life is largely unsubstantiated and that the availability of high-dose vitamin D preparations may actually increase the incidence of potentially dangerous hypercalcemia in some susceptible children with impaired catabolism of 1,25-dihydroxyvitamin D, as well as children who are overtreated with high-dose vitamin D.
Postinfancy nutritional environmental influences on growth and maturation are addressed by Darendeliler (pp. 56–63) who updates us on metabolic syndrome in the young, and Singhal and Misra (pp. 64–70) who eruditely bring us up-to-date about the endocrinology of starvation and its effects on bone and other tissues, using anorexia nervosa as a paradigm. Darendeliler (pp. 56–63) carefully reviews the recent attempts to codify a definition of metabolic syndrome in the young, pointing out that the prevalence of the disorder depends upon the definition chosen. He also reviews the biology of metabolic syndrome, updating us on the continuing paradox that epigenetic imprinting induced by both undernutrition and overnutrition during fetal life and infancy can program the individual as well as future generations to be insulin resistant, obese, and develop the signs of metabolic syndrome during childhood and adolescence. He reviews the role of adipokines such as adiponectin and resistin in the development of metabolic syndrome and insulin resistance, and leaves us with an international perspective on metabolic syndrome in Western and non-Western countries. Singhal and Misra (pp. 64–70) review the recent literature on the changes in many neuroendocrine axes induced by anorexia nervosa and focus specifically on the alterations in bone mineral density, and the potential endocrine/paracrine and neuroendocrine control of bone–fat relationship. The factors influencing the metabolic partitioning and body composition are examined in this model for severe acquired chronic undernutrition.
Finally, Chemaitilly and Hudson (pp. 71–76) review deleterious endocrine and metabolic late effects noted in the increasing numbers of survivors of childhood neoplasia who have been treated with chemotherapy and irradiation. They note that these well recognized effects of treatment on linear growth and body composition, including adiposity and bone mineral density, require careful follow-up and evaluation. Secondary thyroid neoplasia represents a significant risk, and reproductive health often suffers as a result of treatment of childhood malignancies. They introduce the recent studies that statistically assess the risk for these phenomena in terms of age at treatment, length of follow-up, and treatment modalities. These studies will prove useful in determining long-term follow-up in the still vulnerable survivors of childhood neoplasia.
These reviews as a group address the important aspects of the relationship between nature and nurture in the programming of child development and elucidate, referencing many recently published studies, that normal growth and development is dependent on a complex interplay between a functioning endocrine/paracrine system, carefully controlled epigenetic modification of the individual genome, and the external environment.
Conflicts of interest
L.L.L.: Novonordisk: Consultant Insulin; Novonordisk – PI(local) growth hormone registry; Eli Lilly PI (local) Growth hormone registry; and Pfizer PI (local) growth hormone study.