This view is supported by several lines of evidence in our early life stress model, including 1) persistent hypocortisolemia (Coplan et al., 1996) leading to reduced tissue catabolism for gluconeogenesis, 2) elevated concentrations of CSF CRF (Coplan et al., 1996), a stress neuropeptide with anorexogenic effects (Pelleymounter et al., 2000), 3) CRF inversely predicting the trophic signaling of GH in response to the GH secretagogue, clonidine (Coplan et al., 2000) and 4) insulin resistance and features of the metabolic syndrome (Kaufman et al., 2007). The gene discussed is CRH; the disease is metabolic syndrome.