differences between studies in the form of dietary loading (namely, chow-fed, high fat, or glucose-enriched), the common response was rapid weight gain, sympathetic nervous activation, and blood pressure elevation. 9–11 The contrast with hypothalamic forms of experimental obesity was striking in the directionally opposite changes in sympathetic nervous system activity. Drawing on these and other observations, in a highly influential review, Landsberg12 postulated that overeating initiates thermogenesis by stimulation of the sympathetic nervous system and that the sympathetic activation seen in experimental obesity represents an adaptive response to overeating, helping to stabilize body weight through stimulating thermogenesis. This is achieved, however, at the price of sympathetic nervous activation in the kidneys and vasculature secondarily elevating blood pressure. How well does this hypothesis conform to the findings in human obesity?