Leptin got a lot of press in the mid-90's as obesity researchers thought that they had finally found the holy grail of obesity treatment. They hadn't of course but the discovery of leptin opened an exciting new chapter into obesity research, which had sort of stagnated. You can only study the benefits of fiber so many times.
Leptin is a hormone (a cytokine to be exact) that is released primarily from fat cells in more or less direct proportion to the amount of bodyfat a person has. No, it's not this exact and bodyfat patterns (i.e. male vs. female bodyfat patterns and visceral vs. subcutaneous bodyfat) and other factors can affect the relationship. Leptin is also made in placenta, is produced in the gut, and skeletal muscle produces a little bit. Some researchers even think that leptin is produced directly in the brain.
Women make roughly two to three times the leptin that men do, due to differences in total bodyfat levels (as well as differences in the proportion of subcutaneous versus visceral fat). Some research suggests that their fat cells are more active in making leptin as well, for what are assuredly hormonal reasons.
As well, women's brains may respond differently to changes in leptin. This may explain part of why women have a harder time dieting. In this vein, there is also data (in animals) suggesting a difference in how the brain responds to the hormones insulin and leptin with female brains responding more to leptin and men's brains more to insulin. The topic of another article perhaps.
In the early animal studies, leptin appeared to be playing a role primarily in controlling appetite. At first, researchers thought that was it's only role: to regulate appetite. Turns out leptin does that and so much more and they've found leptin receptors in just about every bodily tissue they've bothered to look at.
As well, because of the strikingly constant relationship between bodyfat percentage and leptin levels, researchers thought that leptin was mainly an indicator of bodyfat stores. That is, it 'told' the brain how much bodyfat you had, and controlled appetite by the signals that it sent. For several decades, the theory of a regulated bodyweight setpoint had existed and required a signal between fat cells and the brain; leptin seemed to fit the bill as that signal due to its extremely close relationship with bodyfat percentage. But leptin turns out to be far more than just an indicator of bodyfat percentage.
Leptin is also a marker of energy balance, decreasing when calories go down and increasing when calories go up but doing so out of proportion to fat loss. That is, when you under or overeat, leptin levels change by far more (in the short term) than you'd expect based on changes in fat mass. Within only a week of dieting, leptin levels can drop by 50% but you obviously haven't lost 50% of your bodyfat (wouldn't that be nice). After that, further drops in leptin tend to correlate with the true loss of bodyfat.
The same goes for overfeeding, mind you, which is the logic behind cyclical/refeeding based diets like the
Ultimate Diet 2.0. With 5 hours of overfeeding (and carbohydrates work better than fat), leptin can be increased. The longer the overfeeding period, the more leptin comes back up and this seems to help keep the diet from stalling out so much (many people experience what is popularly called a 'whoosh' and see a weight/bodyfat drop after they do a properly set up refeed). The trick is to find the length of time that lets you raise leptin without putting on appreciable bodyfat. This depends on a host of factors that I'll get to in a future article.
In essence, leptin not only tells your brain how much fat you are carrying, but also whether you're over or undereating. I should note that, in recent years, a whole slew of other compounds that feed into the same pathways in the brain have been found. This includes ghrelin, peptide YY, insulin, blood glucose levels and likely many others.
However, leptin's effects on metabolism tend to be more pronounced when it goes down then when it goes up. Originally, leptin was thought to be an 'anti-obesity' hormone. But it doesn't work very well in that regards. Rather, leptin exists as an anti-starvation hormone, causing metabolism to go down, appetite to go up, and a host of other adaptations when you undereat. I'll come back to this asymmetry in a future article (it's discussed at some length in the Bromocriptine booklet) as it also has some implications for why leptin didn't work very well in the original clinical research on obesity
Among it's other myriad effects (more are being discovered almost daily), leptin has a control in fat burning, glycogen storage and synthesis, appetite, metabolic rate, the levels of many hormones such as thyroid, growth hormone, testosterone and cortisol, and even plays a role in immune function (probably explaining part of why it's easier to get sick when you're dieting/very lean).
Leptin is also involved in reproductive function and a negative energy balance (which lowers leptin significantly) appears to be the major reason that females lose their menstrual cycle when they are dieting (bodyfat plays, at best, a secondary role). This makes sense, when you are starving to death is not a good time to get pregnant so the body shuts down that system; dropping leptin levels is a key signal.
One of the major roles for leptin is in controlling when or if puberty can start. Simply, until a sufficient amount of bodyfat is present, puberty won't occur. This explains two observations. The first is that of very lean athletes (especially females) such as gymnasts, figure skaters and ballet dancers. By keeping their bodyfat levels at extremely low levels, many delay puberty. Similarly, the age of puberty has decreased in recent years due to the increases of childhood obesity; by achieving the critical level of bodyfat earlier in life, puberty is occurring earlier.
Studies have shown that leptin deflects calories away from fat cells and towards muscle (partitioning at its finest) but only at a fairly high level (I'll come back to this). That is to say, the increase in leptin seen with increasing bodyfat appears to be an attempt by the body to limit further fat gains. At high concentrations (achievable by injection), it can actually cause fat cell death in lean rats. On and on it goes.
At least, it does all of these things in rats, there is still some debate over whether leptin has the all encompassing role in humans that it has in animals. As above, leptin is turning out to be part of a complicated puzzle including many hormones such as insulin, blood glucose, ghrelin, peptide YY and others that are being found by the day.
Now, some of you may be thinking 'But wait, didn't leptin more or less crap out when they tried it clinically for weight loss?" The answer is a conditional yes but explaining that will take at least one more article to explain. Which I'll run two weeks from now.
In any case, the point of all this is that your bodyfat percentage is one of, if not the, primary determinant in what happens when you diet or overfeed. And the effects of leptin (and other hormones related to fat mass) in the body is a key aspect of why (mind you, it's not the only reason, just a major one). Fatter individuals lose less lean body mass and more fat on a diet; they also gain less muscle and more fat when they gain weight. Leaner individuals tend to lose more muscle and less fat when they diet and gain more lean body mass and less fat when they gain weight. As I discuss in the article on the site, it's not quite as simple as this: dieted down individuals are not the same as naturally lean individuals in terms of how they partition calories.
Keeping leptin levels from dropping on a diet (and this is very different than raising them in already obese individuals, which I'll explain in a future article) would be expected to do impressive things. This, again, is the basis of cyclical dieting, refeeds and diet breaks. When your body starts fighting you (and dropping leptin is a big part of why it fights you), refeeding or taking a 10-14 day break from the diet can be a key to getting things moving again (this is discussed in more detail in the Guide to Flexible Dieting). Over the next series of articles, I'll not only explain why but give some guidelines for how to do it.
Layle McDonald (chyba sie nie obrazi?

)