I have been asked on numerous occasions why I don't discuss leptin resistance, or even mention the fact that all science speculates that the more leptin you produce the less it works. First, I am not an expert. I am a motivated person who really appreciates explanation for why and how things works. If there isn't an answer I'm not afraid to work to find one that might make some sense of things. Second, the idea that there is leptin resistance is because scientists are still not quite sure why the body is doing what it's doing because there is still an incredible amount of research to be done, and leptin resistance is an easy way to explain that something changes from what we'd expect, which creates a point of diminishing returns. To make this easier to understand: leptin resistance = more doesn't function the same as less.
I see leptin from two angles:
1) Leptin within the endocrine system,
2) and leptin within fat cells for fueling purposes.
The science of leptin began in the brain, observing the function of hunger. When obese mice have elevated leptin levels they won't eat, even when they have an abundance of food available. The feeding behavior of mice is very predictable based on their hypothalamic (brain) leptin levels. Because the method of thought has been (and for most still is) to assume "calories in vs. calories out" all fat people, based on this concept, have to eat more than they expend in a day (which could total more than 4000 calories per day). Scientists have assumed fatter people must be hungry all the time and therefore must be eating, all the time. NOT TRUE. They first hypothesized the more fat a person had, the less leptin they have which is why they must eat all the time. Well, that turned out to be false. The more fat you have, the exponentially higher your leptin levels are.
In order to eat as many calories it requires to gain fat, they speculated there must be a problem with leptin that would force Americans to eat so much. They have to be hungry all the time, so there must be some resistance. Now this is where I have observed the opposite.
The more fat a person has the less hunger they have, and the less they eat relative to their expenditure. Per calorie burned they eat less then their leaner counter parts! (ready why skinny b*tches eat more) Mice may not eat when their leptin levels are elevated, but put a bunch of Americans in a room with food, and there is no discussion of hunger but instead, how good the food must taste, how deserving we are to eat it for whatever reason, and it's free! Eat up! Eating in our culture has NOTHING to do with hunger. NOTHING.
Here's what I've observed: the more fat a person has the less hunger they experience- whether they are on the protocol or not. More fat = less frequency of hunger. (read my blog on why breakfast isn't as important as we thought it was)
Where leptin resistance does make complete sense is within the endocrine system and team of organs that directly work for and against leptin. As fat cells multiply, and new fat cells are bigger and more explosive than the original fat cells, the amount of leptin a person is capable of producing grows at an accelerated rate. A serious problem occurs when corresponding organs can't grow in size and cannot create the correlated response at the same rate. For example, as fat accumulates and more and more leptin is produced, the pancreas is challenged to match the output of leptin with insulin. As fat cells get bigger, and continue to multiply, the pancreas hits a rate limit that can no longer match the output of leptin, unless the pancreas were to grow in size. There comes a point where it is impossible for the pancreas to excrete insulin at the level that fat is excreting leptin, because fat cells outweigh and outnumber what the pancreas is capable of. The only solution would be for the pancreas to grow in size (which is impossible) or to inject insulin to match the output of leptin from fat.
On the other hand, if leptin suppresses an organ, the more leptin you have the more suppressed the organ becomes. For example, leptin in the anterior pituitary suppresses the signal to the adrenals. The adrenals stimulate your fight-or-flight response and produce hormones that help you feel active, motivated, and excited. The more leptin you have the more suppressed the activation from the brain is to the adrenals. However, there is a point where the adrenals can't suppress any lower because those organs would die. My point is that each organ that corresponds to leptin has a limit and the more leptin you have there does come a point where that organ can no longer respond. This would be leptin resistance.
Lets discuss leptin and it's function in fat cells. Each fat cell produces over six hormones! Leptin has been the main focus of science because of it's influence on the entire endocrine system, and also because of it's control over fueling from fat cells and energy homeostasis. This is where I believe there is no leptin resistance. Why? Because fat cells can increase in size and can multiply and spread, so there is no limit with the function that leptin has within fat cells for fuel. The more leptin you have the more fuel is released.
There is no cap, no rate limit, no resistance. Otherwise, every obese person would be in continual starvation with severe hunger, have severe drops in blood glucose uncountable times daily, would have muscle wasting, and would have difficulty gaining fat. If there was leptin resistance in fat cells, there would be a limit to how much leptin is created, how much fuel is released, there would be a limit to how much fat is gained, and there would be a bell curve graph to fat's function as more fat is accumulated. This is NOT the case. The curve is an exponential curve, that shows only acceleration. As fat increases, leptin levels increase even more. If fat cells were "leptin resistant" there would be a point of deceleration within the function of fat and this is not the case.
If leptin resistance does not apply to the function within fat cells and energy fueling, then the body has the ability to adapt, to create more fat cells, and to and store more fuel, which would make sense based on the human body's need to survive chronic famine. I believe, based on what I've witnessed and observed through thousands of hCG protocols, fat metabolism doesn't have resistance to leptin which is why hunger is not resistant to leptin either. Hunger is in direct proportion to fueling and is communicated in response to maintain fueling balance. This is why I never force anyone to eat breakfast, meals, or pre-portioned food because hunger is a better assessment of fueling needs then anything else. The more fat you have the more fuel you get, the less frequent you experience hunger, and the less hormonal need you have for food. It is that simple.
So I speculate that corresponding organs that cannot grow in size to match fat's growth will absolutely have leptin resistance. Fat on the other hand, has no resistance to leptin due to the fact that as leptin increases so does fat cell count, and so does fat's fueling function.
I COULD BE WRONG, BUT IF I WAS- THE HCG PROTOCOL WOULD NOT MAKE SENSE.
I see leptin from two angles:
1) Leptin within the endocrine system,
2) and leptin within fat cells for fueling purposes.
The science of leptin began in the brain, observing the function of hunger. When obese mice have elevated leptin levels they won't eat, even when they have an abundance of food available. The feeding behavior of mice is very predictable based on their hypothalamic (brain) leptin levels. Because the method of thought has been (and for most still is) to assume "calories in vs. calories out" all fat people, based on this concept, have to eat more than they expend in a day (which could total more than 4000 calories per day). Scientists have assumed fatter people must be hungry all the time and therefore must be eating, all the time. NOT TRUE. They first hypothesized the more fat a person had, the less leptin they have which is why they must eat all the time. Well, that turned out to be false. The more fat you have, the exponentially higher your leptin levels are.
In order to eat as many calories it requires to gain fat, they speculated there must be a problem with leptin that would force Americans to eat so much. They have to be hungry all the time, so there must be some resistance. Now this is where I have observed the opposite.
The more fat a person has the less hunger they have, and the less they eat relative to their expenditure. Per calorie burned they eat less then their leaner counter parts! (ready why skinny b*tches eat more) Mice may not eat when their leptin levels are elevated, but put a bunch of Americans in a room with food, and there is no discussion of hunger but instead, how good the food must taste, how deserving we are to eat it for whatever reason, and it's free! Eat up! Eating in our culture has NOTHING to do with hunger. NOTHING.
Here's what I've observed: the more fat a person has the less hunger they experience- whether they are on the protocol or not. More fat = less frequency of hunger. (read my blog on why breakfast isn't as important as we thought it was)
Where leptin resistance does make complete sense is within the endocrine system and team of organs that directly work for and against leptin. As fat cells multiply, and new fat cells are bigger and more explosive than the original fat cells, the amount of leptin a person is capable of producing grows at an accelerated rate. A serious problem occurs when corresponding organs can't grow in size and cannot create the correlated response at the same rate. For example, as fat accumulates and more and more leptin is produced, the pancreas is challenged to match the output of leptin with insulin. As fat cells get bigger, and continue to multiply, the pancreas hits a rate limit that can no longer match the output of leptin, unless the pancreas were to grow in size. There comes a point where it is impossible for the pancreas to excrete insulin at the level that fat is excreting leptin, because fat cells outweigh and outnumber what the pancreas is capable of. The only solution would be for the pancreas to grow in size (which is impossible) or to inject insulin to match the output of leptin from fat.
On the other hand, if leptin suppresses an organ, the more leptin you have the more suppressed the organ becomes. For example, leptin in the anterior pituitary suppresses the signal to the adrenals. The adrenals stimulate your fight-or-flight response and produce hormones that help you feel active, motivated, and excited. The more leptin you have the more suppressed the activation from the brain is to the adrenals. However, there is a point where the adrenals can't suppress any lower because those organs would die. My point is that each organ that corresponds to leptin has a limit and the more leptin you have there does come a point where that organ can no longer respond. This would be leptin resistance.
Lets discuss leptin and it's function in fat cells. Each fat cell produces over six hormones! Leptin has been the main focus of science because of it's influence on the entire endocrine system, and also because of it's control over fueling from fat cells and energy homeostasis. This is where I believe there is no leptin resistance. Why? Because fat cells can increase in size and can multiply and spread, so there is no limit with the function that leptin has within fat cells for fuel. The more leptin you have the more fuel is released.
THE MORE LEPTIN YOU HAVE THE MORE FUEL IS RELEASED!
There is no cap, no rate limit, no resistance. Otherwise, every obese person would be in continual starvation with severe hunger, have severe drops in blood glucose uncountable times daily, would have muscle wasting, and would have difficulty gaining fat. If there was leptin resistance in fat cells, there would be a limit to how much leptin is created, how much fuel is released, there would be a limit to how much fat is gained, and there would be a bell curve graph to fat's function as more fat is accumulated. This is NOT the case. The curve is an exponential curve, that shows only acceleration. As fat increases, leptin levels increase even more. If fat cells were "leptin resistant" there would be a point of deceleration within the function of fat and this is not the case.
If leptin resistance does not apply to the function within fat cells and energy fueling, then the body has the ability to adapt, to create more fat cells, and to and store more fuel, which would make sense based on the human body's need to survive chronic famine. I believe, based on what I've witnessed and observed through thousands of hCG protocols, fat metabolism doesn't have resistance to leptin which is why hunger is not resistant to leptin either. Hunger is in direct proportion to fueling and is communicated in response to maintain fueling balance. This is why I never force anyone to eat breakfast, meals, or pre-portioned food because hunger is a better assessment of fueling needs then anything else. The more fat you have the more fuel you get, the less frequent you experience hunger, and the less hormonal need you have for food. It is that simple.
So I speculate that corresponding organs that cannot grow in size to match fat's growth will absolutely have leptin resistance. Fat on the other hand, has no resistance to leptin due to the fact that as leptin increases so does fat cell count, and so does fat's fueling function.
I COULD BE WRONG, BUT IF I WAS- THE HCG PROTOCOL WOULD NOT MAKE SENSE.
Robin,
ReplyDeleteWhen I'm on the HCG protocol, I feel so good. Almost as if the HCG acts as a antidepressent. I just finished P2, now on the 72 hours with the pellets and I'm not feeling as "happy, positive or energized" as when I was on them.
Would you recommend taking Leptin supplements to get these same feelings?
Gratefully,
Liz