Originally Posted by teaser
There's that Minnesota starvation study again. Google "fat overshoot" and you see that study and the name Duloo. There was fat overshoot with the refeeding. Was there obesity? Did the men remain fat?
although binge-eating continued to be a problem for a few. Participants did not, after the end of the study, eat and eat until they were obese: in general, they regained their original weight plus about 10% in the rehabilitation phase, and their weight then gradually declined towards the pre-experiment levels during the the follow-up period.
Dulloo has suggested recovery of lean mass for the fat overshoot--fat mass recovered first, and the appetite didn't return to prestarvation levels until recovery of lean mass.
Binges are a slightly different issue, although obviously relevant. Rodent models of binge disorder often do not involve excess body fat.
Recovery of lean mass as the cause for fat overshoot? No.
Fuel partitioning. If more energy goes to fat tissue, less goes to lean tissue. However, fat tissue and lean tissue are made up of completely different stuff. So, it's not a question of fuel partitioning after a meal, but the content of the meal that determines beforehand where that energy will go once eaten. In other words, protein cannot convert to fat, nor can fat convert to protein, nor can carbs convert to protein, but carbs can convert to fat, and some amino acids can convert to glucose.
Suggesting lean tissue recovery as cause for fat overshoot is the same as suggesting protein converts to fat and fat converts to protein.
If we accept the premise that fat accumulates through lipoprotein lipase activation by insulin, which then esterifies fatty acids to triglycerides, driven by glucose metabolism resulting in production of glycerol, we could hypothesize that somehow dietary protein has the ability to convert to glucose (at least some amino acids) then stimulate insulin then convert this glucose to fat, but when protein is ingested, insulin is secreted, this insulin then dictates only one path for protein (for amino acids, more appropriately) to go - lean tissue. Insulin inhibits gluconeogenesis, inhibits proteolysis, stimulates protein synthesis. Insulin also stimulate LPL in fat tissue, which allows the hypothesis that dietary protein can lead to excess fat accumulation, but there's no new glucose, there's no new glycerol, there can't be fat accumulation.
This means that in order for excess fat accumulation and lean tissue recovery to occur simultaneously, there must be both dietary protein and dietary carbs. This then refutes any suggestion of causality from lean tissue recovery to fat overshoot. Instead, it's parallel effects by two distinct dietary agents.
Finally, excess fat accumulation doesn't occur during a meal, but in-between meals. During a meal, it's merely called storage. And in order for excess fat accumulation to occur in-between meals, insulin must remain higher than otherwise, this means dietary carbs. Neither can dietary fat nor dietary protein produce this. On the contrary, dietary fat has the unique ability to cause insulin to drop in-between meals, while dietary protein has a similar ability because it does not cause blood glucose to rise, but less so because it still stimulates insulin during a meal.
Apples and oranges? Let's see.
Are lean people more or less prone to growing fatter than fat people? Would a meal that makes a lean person fat, make a fat person fatter too? Would it make him fatter more or less easily? Are the mechanisms that make a lean person fat, the same mechanisms that make a fat person fatter?
This forum is dedicated to a low-carb diet, and to discussion about how a low-carb diet makes us leaner (support, science, media, recipes, journals, success stories, etc). We're fat. Does this same low-carb diet make lean people leaner too?
I prefer to see it as different points on the same spectrum.