This post from suppveristy clearly explains the problem better than I.
Adipocyte hyperplasia is THE problem why obesity is almost impossible to manage with dietary intervention. The below picture shows the leptin secretion of a fat cell in relation to its volume, the relationship in non-linear, small type I fat cells secrete 200 leptin, while larger type II fat cells secrete 7 times as much leptin, 1400.
Because of the negative feedback loop inherent to all adipocytes that their insulin sensitivity varies with their volume, you will find that adipocytes in the same region of the body are approximately of equal volume. Spreading your bodyfat out over many adipocytes will severely compromise your leptin output. This is why dieted down people have reduced energy expenditure because for a given bodyweight they are leptin insufficient.
Why do weight loss stalls happen? Because you have reached a point where you have reduced adipocyte volume enough to be in balance with 24hour insulin secretion. To continue weight loss some adipocyte apoptosis is probably necessary.
Now we know why overfeeding studies fail to generate the obesity phenotype, because the overfeeding may not be enough to produce the sufficient adipocyte hyperplasia. If during overfeeding all you do is increase adipocyte volume, these stuffed fat cells will become increasingly insulin resistant and leak FFA, increasing energy expenditure ( or increasing ectopic fat accumulation ) until their volume decreases enough to become insulin sensitive again to be in balance with 24hour insulin secretion.
Whats the cause of the obesity epidemic? I think its as simple as this......
Foods high in glycemic index + glycemic load -> explosive insulin secretion -> adipocyte multiplication!
No need to talk about "calories"!
Spreadbury's Carbohydrate density graph is a correct illustration of the "causes" of the problem, but I think he has the wrong hypothesis, it is not leptin resistance, Rice cake diet anyone?