Most of you have probably not yet heard of leptin, and, unless you follow the MFW newsgroup, even if you have heard it mentioned somewhere, you probably have no idea of its profound significance in the manipulation of body composition. You soon will.
I would expect that within a year, it will be everywhere in the bodybuilding world, and within two, it will be the topic of infomercials. It will be bigger than Atkins/ketogenic diets, and bigger than The Zone. When it comes to body composition, this is THE master hormone that controls almost all of the others. It is the reason that prolonged dieting causes fat loss to stop and the main reason overfeeding helps us gain muscle.
I would love to say "you heard it here first" but I must give credit where credit is due. Lyle McDonald discovered its supreme importance for bodybuilding in the summer of 2000. I had it on my "to do" list at the time because it kept popping up in any research I did on fat loss, but it was not a priority. Lyle, in a moment of ill-advised excuuberance over his discovery made a couple of posts on MFW mentioning it -- and, because I consider him to have the best combination of knowledge and mind in this field, it immediately moved to the top of my list. I believe he communicated his thoughts on its importance to Elzi Volk at the time, but she dismissed it somewhat for a period, so I think it is accurate to say I was the second person to really look into it.
With that aisde, let us get down to business. This will be the first part of a several part series -- probably at least 4 or 5 -- as this is a massively complicated subject. The present article will be a mere introduction, just to give you some idea of how important this hormone is and how widespread its actions are. In later articles we will delve much deeper into the subject -- from the hard-core, basic science, to the real-world ways in which we can manipulate leptin levels through alterations our diet and supplementation.
And, I promise the follow-up articles will not be delayed to the same extent that this third issue has been :)
Background
In 1953, Kennedy (1) proposed the existence of a centrally acting lipostatic negative feedback signal, produced by adipocytes, in proportion to triacylglycerol content, which regulated body stores via alterations in food intake and energy expenditure -- thus the adipostatic model of weight regulation (aka the "Set-point" theory) was born.
Strong evidence in favor of this idea came with the discovery of the mutation obese (ob) in mice, which led to early onset of obesity (2), and the subsequent use of parabiosis studies (shared blood supply between two organisms) in the late 60's and early 70's which found that overfeeding of one of the pair, led to decreased food intake in the other (3,4).
In 1994, the ob gene was cloned and found to code for a 16 kDa protein which was termed "Leptin" from the Greek "leptos", meaning "thin" (5,6). Leptin was the long-sought lipostatic signal and was anointed as the magic bullet that would vanquish obesity. However, this would not be the case, for reasons you will soon learn, and leptin quickly fell off the public map.
Though, it has remained out of the public eye, a huge amount of research has continued on the subject (and as usual, most of the researchers have shown a gross lack of understanding of leptin -- though of late a few do seem to be getting it, and a huge number of good reviews have been published in the last 2 years.) -- and, though there are numerous unanswered questions, there is enough data to formulate a pretty thorough understanding.
