I guess we just disagree here. Alcohol can give a person some useful energy. Beyond a point though, it's just harmful. Best thing to do, once it's in the system, is burn it off. Some fat may be synthesized, but at that point, it really is more important to get the stuff out of the system than it is to use the energy produced efficiently. Protein--not quite like alcohol, but again, there's a limit to the rate of protein synthesis, so some gets wasted as energy, some is used to synthesize carbohydrate or fat. Carbohydrate--same thing, there's a limit to our glycogen storage, at a certain point, energy will be wasted--although in this case there's a more obvious purpose, some of the carbs being used up in the synthesis of fat, a more practical long-term energy storage.
Efficiency is important when something is scarce. Desert animals might need metabolic adaptations to spare water. In an animal that lives in the water--the same adaptations that work for a camel might be quite wasteful, optimizing for one situation is unlikely to be optimal for another.
I also doubt fat as an adaptation for insulation vs. the cold. If you look at the fattest mammals in the world, various arctic sea animals, most of them fast for long periods, some around half a year, some go through pregnancy and much of lactation during a fast--the insulation is at best secondary, they need the fat for those long fasts and to generate heat in those conditions.
One question here is how exactly the "brown" fat here is "wasting" energy. Are we talking about white adipocytes becoming brown and then becoming white again? That's some rapid cell differentiation and redifferentiation going on...
Beige adipocytes can interconvert between white and brown-like states and switch between energy storage versus expenditure. Here we report that beige adipocyte plasticity is important for feeding-associated changes in energy expenditure and is coordinated by the hypothalamus and the phosphatase TCPTP. A fasting-induced and glucocorticoid-mediated induction of TCPTP, inhibited insulin signaling in AgRP/NPY neurons, repressed the browning of white fat and decreased energy expenditure. Conversely feeding reduced hypothalamic TCPTP, to increase AgRP/NPY neuronal insulin signaling, white adipose tissue browning and energy expenditure. The feeding-induced repression of hypothalamic TCPTP was defective in obesity. Mice lacking TCPTP in AgRP/NPY neurons were resistant to diet-induced obesity and had increased beige fat activity and energy expenditure. The deletion of hypothalamic TCPTP in obesity restored feeding-induced browning and increased energy expenditure to promote weight loss. Our studies define a hypothalamic switch that coordinates energy expenditure with feeding for the maintenance of energy balance.
Okay, we're talking about "states." One way a cell can go into "energy wasting" mode as opposed to "storage" mode is by increasing fatty acid synthesis from glucose. If you're just looking at energy in/energy out, that looks pretty good, you lose about a quarter of the calories.
Of course fasting decreases metabolic rate, but calling that "energy storage" mode really is pretty loony.
Brown fat does seem to have a role to play in fatty acid synthesis;
Fatty acid synthesis in mouse brown adipose tissue. The influence of environmental temperature on the proportion of whole-body fatty acid synthesis in brown adipose tissue and the liver.
Fatty acid synthesis has been measured in vivo with 3H2O in mice acclimated at different environmental temperatures (33, 22, 4 degrees C), and the importance of brown adipose tissue and the liver to whole-body fatty acid synthesis at each temperature assessed. At 33 degrees C, when non-shivering thermogenesis is minimal, the rate of fatty acid synthesis in interscapular brown adipose tissue was lower than in the liver, but higher than in white adipose tissue and the carcass. At 4 degrees C, when non-shivering thermogenesis is maximal, the fatty acid synthesis rate in interscapular brown adipose tissue was many times greater than in any other tissue. High fatty acid synthesis rates were also found in other brown adipose tissue depots--subscapular, dorsocervical and axillary--of cold-acclimated mice. In mice maintained at 22 degrees C the rate of fatty acid synthesis was also higher in brown adipose tissue than in other tissues. Overall, the relative importance of brown adipose tissue as a site of fatty acid synthesis increased with lower environmental temperatures, while that of the liver decreased. It was calculated that brown adipose tissue in total accounted for approx. 5% of whole-body fatty acid synthesis at 33 degrees C, 10% at 22 degrees C and 30% at 4 degrees C. In contrast, hepatic synthesis amounted to 32% of whole-body fatty acid synthesis at 33 degrees C, 16% at 22 degrees C and only 11% at 4 degrees C. An estimate of the contribution that de novo synthesis makes to total fatty acid utilization by interscapular brown adipose tissue suggests that fatty acid synthesis and breakdown constitutes a significant heat-dissipating 'cycle' in brown adipose tissue of cold-acclimated mice. Such a cycle is not evident in suckling animals since fatty acid synthesis in brown adipose tissue is very low during early development.