Catch-up growth: an overview.

Normal growth in humans results from interactions between several mechanisms (genetic, nutritional, environmental, social and economic) that lead in concert to gain in weight and height. Many systemic diseases and environmental conditions do impair linear growth. When remission occurs, growth often resumes at a rate faster and beyond the normal rate for age. This phase of accelerated growth constitutes the "catch-up growth" phenomenon, which may be complete or incomplete depending upon the final height with reference preferably to the genetic target height. The exact mechanisms of catch-up growth remain unknown, but two hypotheses have been proposed: the neuroendocrine or sizostat hypothesis; and the growth plate hypothesis. Although no experimental data supports the former, it is most likely that the catch-up growth process involves both systemic and local (growth plate) factors, with the participation of a normally functioning GH-Thyroid-IGF-I axis. The Ob gene protein, leptin serves as an afferent signal in a negative feedback loop to regulate the size of adipose tissue mass (body weight). Experimental studies have demonstrated its links with the GH - Thyroid - IGF-I and growth plate axis. To resume normal growth or initiate catch-up growth, an undernourished child must regain up to 85% of weight for height. This may mean that a close relationship exists between mechanisms regulating weight and those regulating linear growth. More studies are needed to determine the links that probably exist between the chondrocyte, adipocyte, leptin, and GH - Thyroid - IGF-I axis on one side and the catch-up growth on the other.