Hello again, and welcome to the Fat Loss Facts series. Every week the mysteries that surround our body’s stores of fat are uncovered, and with each passing week we become that much more knowledgable on this often confounding subject. With knowledge comes power, and that power can be used to obliterate any of the unwanted fat that you may have on your own body. Today we will continue our journey. If you’re ready, let’s begin.
To summarize our progress up to this point; Part 1 was focused on creating a caloric deficit, and the methods to use in order to accomplish that. Part 2 explained how to estimate the starting point of the diet regarding calories, in order to create a deficit. Part 3 was about the value of protein, and the method of calculating how much to include in the diet under the established caloric parameters, so that fat loss can begin. Part 4 dealt with essential fatty acids and other dietary fats, and how much we need to include in our diet plan. Part 5 was spent discussing how many carbohydrates are needed in our diet. Part 6 was about insulin sensitivity and resistance, and how that affects our macro nutrient needs. Part 7 offered a couple of different ways to structure the diet depending on insulin sensitivity/resistance. If you missed any of the articles please start the series at the beginning. Starting part way through defeats the purpose of this process. The point of this series is to educate so that you know what to do, and why. Short-cutting the learning process is not the way to be successful at anything, and fat loss is no exception.
There was a time before leptin was even known to the world of science, but something yet undiscovered was suspected to play the role that leptin does. Researchers in the 1950’s had established the existence of a set point in relation to body fat regulation, but were not clear on what caused it. They theorized that a hormone within our brain was reacting to the body fat levels of each individual, which created the set point that each person has regarding body fat regulation.
It wasn’t until 50 years later that a hormone that was to be called leptin was discovered in obese mice. Obese mice have been under study for decades now. Their characteristics are the same as those of obese humans. These shared values are a low resting metabolic rate, low levels of activity, a large appetite, and body fat that is gained easily. One particular mouse under study in the 50’s had a gene defect, and produced no leptin at all. When it was injected with the missing hormone, it lost weight rapidly.
This lead everyone to assume that in order to cure high levels of body fat, adding leptin to the mix was all that was necessary. A linear conclusion I must add, and like all conclusions that look at information in a vacuum, it turned out to be incorrect. The problem was that when they tested obese humans expecting to find low, or non-existent levels of leptin, they found the opposite. Most obese humans have very high levels of leptin, unlike the anomalous mouse that was under study. Even though there was a surplus of leptin, it was not sending the signal to the brain of these individuals to stop eating, and result in having body fat reduced as a result.
This brings us up to date, as the science community now believes that much like those insulin resistant individuals whose bodies over produce insulin in an attempt to overcome the resistance, the obese individual with high levels of leptin is believed to be experiencing the same issue; leptin resistance. Leptin resistance is caused by high blood triglyceride levels, and even by leptin itself. When levels in our body are consistently high, our brain ignores the signal. It’s like living next to the train tracks, or near an airport, after a while you no longer notice.
It is also currently being discussed if this theory is even accurate. Just because it is a sound theory, and is the case with insulin, does not mean that it is a definite when it comes to leptin. A leptin insufficiency theory is also under discussion. It is being theorized that even though there may be very high levels circulating within the body, there may be a lack of leptin in the brain. Regardless, the signal isn’t being sent or received in either case. It is likely to be a combination of high levels of leptin, and low sensitivity/insufficiency in the brain, in my uneducated opinion.
The relation to insulin goes a little further as well. There have been recent animal studies where directly injecting insulin into the brain of animals resulted in lower food intake, and body weight was reduced as a result. This leads me personally to draw the conclusion that most of what occurs hormonally within our bodies begins with a signal from our brain. The body and its actions are the catalyst, but it’s up to our brain to make the decision which move to make.
Another interesting tidbit I’ll include in this post is the role that gender plays in body fat regulation. Leptin seems to relate more so to subcutaneous body fat stores, which are generally (but not always) higher in women. Insulin on the other hand relates to visceral fat, which is generally higher in men. As this post is serving as an introduction to some of the more advanced methods, signalling, hormones, and eventually methods to enhance fat loss, this all will make a lot more sense later I assure you.
While this doesn’t directly add to the formula we have been working on, it’s an important hormone that interacts with both our body and brain to signal satiety, and other processes regarding our fat loss, as well as our body fat set point. This will be looked into further in the next fat loss article. Until then my friends,
This article was written and researched by Matt Taylor
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