Prolonged, unrecognized cold stress may divert calories to produce heat, impairing growth. Neonates have a metabolic response to cooling that involves chemical (nonshivering) thermogenesis by sympathetic nerve discharge of norepinephrine in the brown fat. This specialized tissue of the neonate, located in the nape of the neck, between the scapulae, and around the kidneys and adrenals, responds by lipolysis followed by oxidation or re-esterification of the fatty acids that are released. These reactions produce heat locally, and a rich blood supply to the brown fat helps transfer this heat to the rest of the neonate’s body. This reaction increases the metabolic rate and O 2 consumption 2- to 3-fold. Thus, in neonates with respiratory insufficiency (eg, the preterm infant with respiratory distress syndrome), cold stress may also result in tissue hypoxia and neurologic damage. Activation of glycogen stores can cause transient hyperglycemia. Persistent hypothermia can result in hypoglycemia and metabolic acidosis and increases the risk of late-onset sepsis and mortality.