The predominant model for a role of brown fat (BAT) is based upon the notion that an animal with a higher level of UCP1-BAT will burn off more calories than an animal with lower levels of BAT. Thus, we have the conclusions in the literature that elevated UCP/BAT levels reduce obesity based upon experiments in animals and in humans in which a negative correlation is observed between PET/BAT and obesity. The underlying assumption is that humans living at thermoneutrality in the absence of BAT have increased obesity. While there is some evidence for experiments in mice that such a behavior occurs, other evidence indicates that it is not always so, that is, Ucp1 KO mice at thermoneutrality are not always more susceptible to diet-induced obesity than wild-type mice. Accordingly, if you have the fatalistic view that humans are and will predominantly live at thermoneutrality, it is reasonable to pursue an anti-obesity strategy based upon increasing UCP1 levels. If you believe that a pharmaceutical approach will be essential to reduce obesity, than it is also reasonable to target drugs to cellular and molecular mechanisms that induce BAT levels and UCP1 expression. However, given that the molecular mechanisms for inducing Ucp1 and BAT are not specific, but participate broadly in the control of embryonic differentiation (and in cancer), then it behooves us to develop alternatives to taking drugs until such time as safe targets are developed. Much published evidence from studies of mice with reduced thermogenic capacity from inactivation of Ucp1 and other components of non-shivering thermogenesis shows the huge benefits from reducing the ambient temperature, even a few degrees below thermoneutrality. While inactivation of Ucp1 was unexpectedly and paradoxically found to augment the combustion of calories at reduced ambient temperature, the benefits for wild type mice are such that reduction of ambient temperature from 28 to 20°C reduced metabolic efficiency by half in mice fed a high fat diet. At lower temperatures the effects of the obesogenic environment are totally neutralized and the adiposity index of mice fed a standard low fat (11Kcal %) remains at a normal healthy level. An interesting aspect of the effects of the cool environment on body weight regulation is that they may be independent of UCP1/BAT, rather they are the response of systemic energy balance, which would include UCP1/BAT, but not be dependent on high levels of BAT. Thus, humans, with or without BAT, can benefit from the “cool” environment.