Leptin is a hormone released from fat cells which tell the brain, essentially, two things: how much bodyfat you have, and how much you’re eating. Leptin basically ‘tells’ your brain what’s going on with your fat and energy stores. When you overfeed, leptin goes up; when you diet, leptin plummets.

Leptin inhibits fat storage in fat cells, promotes glycogen storage in muscle (and increases fat oxidation in muscle), plays a role in immune system function, is involved in fetal development during pregnancy, can kill fat cells permanently, is probably involved in bone growth, and a whole bunch of other things.

In response to falling leptin, appetite goes up, metabolic rate crashes, hormones go to hell, fat storage increases. In response to increasing leptin (to a degree), appetite goes down, metabolic rate goes up, hormone levels increase, the body tries to put a brake on fat storage and pushes calories to muscle for burning. Leptin was the partitioning hormone we’d been looking for.

So we (we at this point was myself and Elzi Volk) started looking for ways to raise leptin. Short of drug solutions, the easiest way is to overfeed for short periods of time (there are also nutrients like zinc, vitamin E and fish oils that play a role too).

Because, in the same way that leptin drops way faster than fat is lost, it rebounds way faster than fat is gained. So underfeed for a week and leptin drops by like 50%. Overfeed for a few days, and it rebounds by some percentage (depending on how much you overeat). The key is eating enough calories for long enough to rebound leptin (thus ‘telling’ your brain that it’s ok, to normalize metabolism) without putting all, or hopefully any, of the fat back on.
Of course, this is also helpful psychologically, prevents the real food binges from occurring, because the cheat days are now planned.

In one of the early leptin studies, this had actually sort of been demonstrated but the researchers were too dense to see what was going on. In that study, they dieted the hell out of a bunch of fat women for 4 weeks. Leptin and bodyfat both dropped. Then they refed them gradually for a week. Leptin came back up. But fat continued to be lost. To me, this was a profound observation, I don’t recall the researchers even really noticing it (I may be wrong: this may have been the study where the one guy said ‘maybe keeping leptin up on a diet is important’, well, duh!).

Now, fundamentally, there was really nothing that new about refeeds. Bodybuilders have been using cyclical diets (of one sort or another) for decades. In hindsight, I really feel that the carb-load was the reason that the Bodyopus diet worked, not the keto phase so much. It turns out that ketogenic diets per se aren’t really protein sparing in lean folks. But the carb-load was bumping leptin and keeping the body running better overall, metabolically speaking. That’s also on top of the psychological effects of being able to ‘eat anything on a diet’ every week.

I’d known since the early Bodyopus days that having someone eat at maintenance (or even a little bit higher, say 10% over) for a week to 10 days was frequently the best way to break a fat loss plateau. That it ‘reset metabolism’ or however you want to look at it. Even Dan’s old dieting scheme was 4 weeks diet, 2 weeks off, 4 weeks diet, 2 weeks off.

If nothing else, we could give a good physiological rationale behind refeeds (you’d be amazed how much the average dieter hates the idea of breaking their diet, and the reasoning of ‘it just works’ doesn’t get you very far).

.....ghrelin actually had far more important effects than just GH secretion; it was yet another hormone involved in overall energy and bodyweight balance. In both rats and humans, ghrelin injection stimulates hunger. In fact, ghrelin is the first chemical found to do so in humans (i.e. to stimulate hunger upon injection). In rats at least, chronically high ghrelin levels causes weight gain. It does it by increasing food intake but that’s only half of it; ghrelin also causes a decrease in metabolic rate and fat burning. Basically, ghrelin is predisposing the body towards fat gain by slowing metabolism and fat burning. Whether ghrelin has these secondary effects in humans is still being researched.

In animal studies, for example, high carb, low protein diets increase ghrelin, while higher fat diets tend to lower it. I have to wonder if this doesn’t explain some of the relative failure of the ‘standard’ ADA diet (high carb, low protein) compared to your typical bodybuilders diet (high protein): higher ghrelin = more hunger and maybe more negative metabolic effects. Or the general superiority of moderate fat diets over very low fat diets. I mean, if on top of all the effects on gastric emptying, blood glucose, insulin, etc. higher fat diets are keeping ghrelin levels lower overall, that can only be a benefit from the standpoint of the dieter.

When leptin is low, your body/brain thinks you’re starving to death. And levels of NPY/AGRP are going to go up driving appetite and slowing metabolic rate, ghrelin or not. Ghrelin is simply one of the short-term signals for energy intake (since it seems to be determined by actual nutrient intake into the gut) that is, part of the overall big picture. Without correcting the problem of low leptin (or leptin resistance), I’m simply not convinced that any of this will have any real effect.

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