Yeah... they jump from whether starvation just depletes fat cells, or kills them, to whether you can stick to a "healthy regimen" long enough. Is that a healthy regimen of starvation?
If starvation or semi-starvation doesn't stick, or comes and goes, what do you get? Maybe a growth promoting stressor, in starvation. When you push muscles to their limits, when you challenge brain or bone, what happens? It grows, increases connectivity, becomes denser, makes the appropriate adaptations. What's the appropriate adaptation to a starvation challenge? Getting fatter, so the next bout of starvation will be less life-threatening?
A few years ago, Turtle posted another study in female mice, reducing their food intake to 95 percent of controls made the mice fatter. I always wished they'd had a control for the restricted arm of the study, where mice were restricted to 100 percent. I think all you can eat is probably less stressful than all you could have eaten, the control mice didn't have that much more food, but they had the option to eat much more if they'd wanted. If a wild mouse can only just barely get the amount it wants to eat--maybe that's a signal that even harder times might be coming, and it had better become metabolically stingy. Of course this works with chow, probably doesn't work with a Chinese food buffet.
In the Minnesota Starvation study, when the men regained their weight, lean mass didn't return to it's original levels until after the fat mass had surpassed its original levels.
http://www.ncbi.nlm.nih.gov/pubmed/19602538
Quote:
Adipose tissue plasticity during catch-up fat driven by thrifty metabolism: relevance for muscle-adipose glucose redistribution during catch-up growth.
Abstract
OBJECTIVE:
Catch-up growth, a risk factor for later type 2 diabetes, is characterized by hyperinsulinemia, accelerated body-fat recovery (catch-up fat), and enhanced glucose utilization in adipose tissue. Our objective was to characterize the determinants of enhanced glucose utilization in adipose tissue during catch-up fat.
RESEARCH DESIGN AND METHODS:
White adipose tissue morphometry, lipogenic capacity, fatty acid composition, insulin signaling, in vivo glucose homeostasis, and insulinemic response to glucose were assessed in a rat model of semistarvation-refeeding. This model is characterized by glucose redistribution from skeletal muscle to adipose tissue during catch-up fat that results solely from suppressed thermogenesis (i.e., without hyperphagia).
RESULTS:
Adipose tissue recovery during the dynamic phase of catch-up fat is accompanied by increased adipocyte number with smaller diameter, increased expression of genes for adipogenesis and de novo lipogenesis, increased fatty acid synthase activity, increased proportion of saturated fatty acids in triglyceride (storage) fraction but not in phospholipid (membrane) fraction, and no impairment in insulin signaling. Furthermore, it is shown that hyperinsulinemia and enhanced adipose tissue de novo lipogenesis occur concomitantly and are very early events in catch-up fat.
CONCLUSIONS:
These findings suggest that increased adipose tissue insulin stimulation and consequential increase in intracellular glucose flux play an important role in initiating catch-up fat. Once activated, the machinery for lipogenesis and adipogenesis contribute to sustain an increased insulin-stimulated glucose flux toward fat storage. Such adipose tissue plasticity could play an active role in the thrifty metabolism that underlies glucose redistribution from skeletal muscle to adipose tissue.
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Maybe a warning here for any form of weight-loss-however adipoctyes are depleted, whether by starvation or ketogenic diet, returning to a high carbohydrate diet might be risky--the weight loss might predispose to an increase not just in fat storage, but also an increase in adipocyte number. This might explain anecdotal evidence that a low carb diet doesn't always work as well the second or third time around. The role of insulin in fat storage doesn't change, but fat cell structure might.
Playing devil's advocate--by being low in protein, and very low in fat, it's possible that something like the potato hack or the Rice diet approaches this from another angle--they might provide nutrition with a low-anabolic potential, not just for muscle tissue, but for fat tissue as well, carbohydrate, protein and fat could all be individually rate limiting for cell proliferation.