Both under- and over-nutrition in utero appear to produce permanent alterations in neural circuits that control appetite, in particular, relating to leptin (a hormone linked to satiety).58,59 Animal models suggest that infants born to mothers who experience malnutrition during pregnancy are born with lower levels of leptin, resulting in a more avid appetite – potentially with the purpose of promoting ‘catch-up’ growth.58,59 This, when combined with an obesogenic environment, can increase risk of obesity. The gene discussed is LEP; the disease is Obesity.