By Lyle McDonald: www.bodyrecomposition.com

Over the many years I’ve been involved in the fat loss game, I’ve seen some weird stuff happen.  When I was in my 20’s and only thought I knew what I was talking about (as opposed to now when I’m simply usually sure I do), I had observed one of the things I’m going to talk about today but didn’t have any real clue why it happened.  With clients or whatever, the only answer I could give was “Because it does.” or “Magic!”.

Now, I have a bit more clue what’s going on, or at least what I think is going on so I’m going to share one of these with you (I’ll address others in future articles).  Today I want to talk about something that I like to call the LTDFLE,  an acronym that I genuinely hope you will use at every possible chance on forums to confuse people, and which will make sense shortly.

By Lyle McDonald: www.bodyrecomposition.com

A few weeks back I answered a question about Not Losing Fat at a 20% Deficit, What Should I Do? and among other things, one comment I made had to do with a water retention that often occurs during fat loss which can mask fat loss and make it appear as if the diet is not working.  I also mentioned specifically that I had written (with a straight-face no less) about whooshes in The Stubborn Fat Solution, along with a related phenomenon which I call squishy fat.

In any case, to expand on that issue, I’m going to excerpt the chapter section from The Stubborn Fat Solution dealing with both phenomena.  With that introduction, I give you (again, with a straight face)…

Ok, although this is one of those topics that truly could have endless posts made about it, most of what I wanted to cover regarding bodyweight regulation and such was covered in the posts on leptin.

However, as I mentioned in that series, leptin turns out to be far from the only hormone involved in this.

I already talked a little about insulin in that series but there are still more hormones of some importance. With more likely to be discovered as time goes on. Oxyntomodulin, GLP-1, PP and others are being discussed in recent reviews and further research will go towards determining what in the hell is actually going on.

Tangentially, this is one of the big problems in trying to find a true ’solution’ to the issue of weight loss and obesity: the human body has a number of overlapping, integrated and redundant pathways that all send signals to the brain. Fix one and something else eventually steps in to fill the role and cause problems.

In Bodyweight Regulation: Leptin Part 5, I explained that, while injectable leptin would be a true boon for dieters, it appears unlikely that it will ever reach commercial or clinical use.

This leaves us with other approaches (e.g. nutritional, supplements, training) to attempt to manipulate either leptin levels or signaling.

There are basically three places where dieters might impact leptin levels and/or activity in terms of fighting off the adaptations to dieting.

1. Production at the fat cell

2. Signaling in the brain

3. Transport into the brain

Summarizing what I’ve discussed so far:

1. Human bodyweight appears to be biologically regulated, that is it makes some attempt (that can be overcome by environment, of course) to maintain body fat within some range or level.

2. The system regulating body fat is assymetrical, for most people it defends against fat loss much more strongly than against weight gain.

3. For proper regulation, the body needs a way of ‘knowing’ two things: how much fat you’re carrying and how much you’re eating; a variety of hormones play a role here.

4. At least in terms of indicating the amount of body fat is present, the hormones leptin and insulin appear to play a major role. Leptin scales with subcutaneous body fat levels (higher in women), insulin scales with visceral fat levels (usually higher in men); there is some indication of a gender difference in response to the different hormones.

By Lyle McDonald: www.bodyrecomposition.com

Don’t worry, slowly, I’m getting to the point.

So when you are in an energy deficit and/or losing body fat, leptin levels drop.

Although I haven’t talked much about the role of exercise here I’d only note that whether or not the deficit comes from caloric restriction or exercise per se doesn’t appear to have much of an effect on how much leptin drops.

Basically, the body appears to be sensing ‘energy availability’ (defined as energy intake minus expenditure) and adjusting things based on that. I’d, of course, note that exercise still plays plenty of other crucial roles (including psychological, which I am getting back to slowly but surely) in terms of dieting and fat loss.

In any case, what happens now?

By Lyle McDonald: www.bodyrecomposition.com

Ok, so now that you know what leptin is and a little bit about what regulates leptin levels, I want to look at what leptin ‘does’ in the body. The short answer is a whole lot of things.

Here’s the long answer:

Like most hormones in the body, leptin has effects nearly everywhere in the body. In skeletal muscle, it’s involved in promoting fat oxidation, it impacts on fat cell metabolism directly, liver metabolism, is involved in immune system function (which may be why dieters get sick when they get very lean) and more recent research is implicating effects on brain function, neurogenesis, breathing and a whole host of other stuff.

By Lyle McDonald: www.bodyrecomposition.com

In the Bodyweight Regulation: Leptin Part 1, I talked primarily about leptin (and a bit about insulin,and a very little bit about the other hormones) and its discovery and how it may be the (or at least one of the) long-sought after hormones involved in regulating bodyweight. Today I want to take a quick look at what leptin is and how it’s regulated. Next time I’ll look at what leptin is doing (or not doing as the case may be).

Leptin is a protein hormone released primarily from fat cells although skeletal muscle, the gut and possibly the brain releases it too. But, in terms of overall quantity, fat cells are the primary place where leptin is synthesized and released.

By Lyle McDonald: www.bodyrecomposition.com

As I noted Set Points, Settling Points and Bodyweight Regulation Part 2, although I’ve been using bodyweight/body fat during this discussion, it’s probably more likely that it is body fat levels per se that are being regulated. Today you’ll see why and from here on out I’ll only talk about bodyfat regulation.

With early research (I’m talking the 1950’s) having established the existence of some type of setpoint (again, primarily in animal models), early researchers had to sort of guess what might be going on in terms of regulating body fat levels.

Essentially they postulated that the brain of the animal must be responding in some form or fashion to a hormone that scaled with body fat levels. They could only postulate what it was and it would take another 40 years before a major candidate would make itself known.

In Set Points, Settling Points and Bodyweight Regulation Part 1, I took a little bit of a look at the issue of bodyweight regulation and the concept of the set point, examining various bits of research supporting the existence of such a thing. At the end of that piece, I also mentioned that not all researchers believe in the concept of a set point, feeling instead that a settling point is a more accurate representation of what’s actually going on.

Recall from Part 1 that the set point idea basically says that the body will attempt to defend some body weight (or body fat) level (or perhaps range) by adjusting things such as metabolic rate, activity, hunger, etc. in response to changes in weight or fat.