leptin fat stripper

[girlgerms]

Hunger hormone 'better fat stripper'
Wednesday Feb 27 00:02 AEDT
A hormone that suppresses hunger may be a more powerful weight loss tool than first thought, Australian scientists have discovered.

The hormone, called leptin, helps regulates appetite, controlling how much a person feels like eating and offering huge potential as a therapy to fight obesity.

However, since its discovery in the 1990s, scientists trialling injections of leptin have had weight loss success in rats but failed in humans.

Melbourne researchers have now discovered leptin plays a larger role in burning energy in the human body than was previously thought, opening up the potential of the appetite suppressant once again.




Leptin is produced by fat and acts on the brain to reduce appetite and increase energy use through a process called thermogenesis.

The scientists have discovered leptin not only triggers thermogenesis in a small number of fat cells, but that it also triggers the same response in muscle tissue, which makes up more than one third of body mass.

This finding, published in the journal Endocrinology, has significant repercussion for the development of weight loss strategies, said the researchers, Dr Belinda Henry and Professor Iain Clarke.

Drugs that mimic leptin could trick the body into weight loss by simply harnessing the body's natural process of thermogenesis, they say.

"Now that we have shown leptin increases energy utilisation in muscle tissue, the potential for the hormone to have a positive impact has been greatly magnified," Dr Henry said.

"We can now start to recreate and enhance this natural process for the purposes of assisting weight loss."

Prof Clarke said the challenge would be to trick the brain into triggering the response, as the hormone leptin is already higher in overweight people and the impact of the hormone is somehow reduced in the human body.


©AAP 2008

[M Levac]

The following is only Speculation, not based on facts.

I think leptin is inhibited by something that is involved in glycolysis. Just like lipolysis stops when too much insulin is present, leptin could be inhibited by insulin as well. Or, for leptin to have any effect, fat must already be burning in the cells. If glucose is the fuel used, leptin has no effect. If that is so, it won't matter how much leptin we inject, it won't affect weight loss in humans.

[ValerieL]

I think leptin is inhibited by something that is involved in glycolysis. Just like lipolysis stops when too much insulin is present, leptin could be inhibited by insulin as well. Or, for leptin to have any effect, fat must already be burning in the cells. If glucose is the fuel used, leptin has no effect. If that is so, it won't matter how much leptin we inject, it won't affect weight loss in humans.

More speculation.

Or do you have some evidentiary basis for this that you'd like to share?

[M Levac]

More speculation.

Or do you have some evidentiary basis for this that you'd like to share?

Yes, I was speculating. I thought I made it clear by starting my post with the word: Speculation. Allow me to make it even more clear.

[neverwhere]

Yes, I was speculating. I thought I made it clear by starting my post with the word: Speculation. Allow me to make it even more clear.

Your edit helped. I too thought you were saying the OP article was speculation, not your post.

[ValerieL]

Your edit clarified it. Originally it looked like it was damning the finding of the research as speculation.

[EMKAY 53]

Leptins are produced naturally in tomatoes....just thought I'd throw that in :P

[EMKAY 53]

Nevermind...that was lycopenes. Carry on....and disregard my ignorance.

[Squarecube]

Actually, I liked the speculation.

Fat people have plenty of fat cells. If their fat cells still produce leptin, then they make plenty of it

[M Levac]

Actually, I liked the speculation.

Fat people have plenty of fat cells. If their fat cells still produce leptin, then they make plenty of it

I was speculating that only the burning of fat results in the production of leptin. If indeed leptin is the agent that tells our brain to stop eating. The adipose tissue would then also need to burn fat for leptin to be released. Not just to contain fat. Adipose tissue stores fat as triglycerides. When fat is burned as fuel, it is burned as fatty acids, not as triglycerides. So the trigs contained within the adipose tissue would have no effect on leptin. Again, if my speculation has any value and if leptin is indeed the agent that tells our brain to stop eating.


The article says "Leptin is produced by fat" This is incorrect. Fat is not metabolically active. Thus, fat can't produce leptin. The only possibility here is that through the metabolism of fat (burning of fat or lipolysis), leptin is also produced. That is where I had the idea for my speculation.


The article also says obese people have high levels of leptin. So I don't know. Not enough information.

[M Levac]

I thought about it some more. The article doesn't make sense anymore. The body doesn't do something only to make sure something else is not done. For example, it doesn't release insulin only to tell us to not eat. It releases insulin to take care of glucose. As glucose is taken care of, less and less insulin is being released. The same should be true of leptin.

Leptin wouldn't be released constantly to remind us not to eat. Instead, it would be released constantly to remind us to eat. So that when we're satiated (sated?), leptin levels would go down. This mechanism would be consistent with obesity. As somebody grows fat, he also grows more hungry. If leptin does have something to do with hunger and if leptin levels are higher in obese people, then leptin is produced only to tell us to eat more. Not to tell us to not eat.

If leptin was released to tell us to not eat, it would have to be released continuously until the need to eat arises. This is not economical and goes against our body's tendency to maintain homeostasis.

[Groggy60]

My understanding, you need Leptin to burn fat. You need a low insulin amount to burn fat also.

Fat people on low carb loose weight more easily because they have Leptin. As the fat disappears, the Leptin goes down and fat loss become more difficult because you are not fat enough.

A nice catch-22, and perhaps a mechanism to prevent us from loosing too much weight. Maybe a clue that many weight goals are not realalistic.

Raising your insulin level will cause Leptin to be produced, thus carbing up becomes a way to loose fat when you are less fat. I did it with much success but it became very hard to do mentally after a while.

Lots of discussion on this a long time ago in the Tips formum.

[M Levac]

If leptin is the agent that tells us we're full, then eating fat is the most effective way to activate leptin since eating fat satiates us the most. Or would that be too much of a stretch of logic?

Reading further about leptin, I found this:

http://www.nature.com/ijo/journal/v26/n11/full/0802142a.html

Quote:

"Physiologically, obesity is a disorder of energy balance; excess energy is stored as fat whenever energy intake exceeds energy expenditure. Thus, the optimal treatment for obesity would be one that both suppresses food intake and increases energy expenditure. Energy intake and energy expenditure are closely regulated processes, as reflected in the relative stability of body weight in the presence of large daily fluctuations in energy intake.5 Complex interactions between hormone axes in the periphery are integral in maintaining homeostasis of a diverse range of functions. Feedback from these complex interactions is ultimately integrated at the level of the central nervous system (CNS) by a similarly complex array of neurotransmitter signals."


If we understand the quote, this means the study is based on the positive caloric balance hypothesis. As we know, the positive caloric balance hypothesis results in a psychological problem. Any conclusion from that study is thus flawed.

Further, any conclusion in the article linked to in the first post is equally flawed.

[M Levac]

From the same study I linked to:

Quote

"The diverse picture of where leptin is produced in the body indicates that the functions of the hormone may extend beyond the basic lipostatic model originally envisaged."

The way I see it: Don't mess with leptin. Yet.


I'm beginning to think that most of the studies on obesity are flawed. I think so because if I'm not mistaken, mice is a hibernating species. Humans are not. So, any observation we make of a species that hibernates can't translate to one that does not.

For example, as winter comes, mice are fat. We may be too. During winter, mice sleep it off. We don't. We continue to hunt fatty winter meat. We remain active while mice become essentially sedentary to conserve energy.

We assume that winter, at least for humans, is the scarcity environment. After careful consideration, it appears that it is instead the abundance environment.

[kneebrace]

We assume that winter, at least for humans, is the scarcity environment. After careful consideration, it appears that it is instead the abundance environment.

Martin, I get the impression you are suggesting that humans were somehow unique in facing constant food abundance? But other animals eat the same food as humans. And the critical point is that one of those 'other animals' is other humans. Nature is a competitive place. That's why evolution selects for those individuals that exploit their environmental niche most efficiently.

For humans that environmental niche was low predominantly low carb until very recently (the neolithic), so those individuals that used the available food source most efficiently were the ones who thrived. If the 'constant abundance' was being competed for, then it wasn't actually constant at all. And the individuals who were most able to store the excess of any low carb feast they were lucky or skilful enough to secure were most able to supply their nutritional needs until next time. Even if that time was spent making and developing tools, or having a cultural life with their peers.

It's easy to forget that if a food source becomes abundant, even briefly, the organisms that consume that food breed to take advantage of that abundance, and bingo, no more abundance. Because suddenly there are a lot more individuals (including individuals of your own species) competing for that resource.

Read up on the mechanism of evolution, Martin (apologies if you don't believe in evolution, each to their own :) ). Ongoing abundance (over millions of years) is impossible. It shouldn't come as any surprise that life on this planet has a palpable devotion to exchanging segments of DNA, so any short term food abundance is instantly exploited by more offspring.

Even contraception hasn't stopped humans fighting with each other and other species for available food resources. We have a natural affinity for having kids and providing for them as best we can, which inevitably means competing with other individuals doing exactly the same thing.

This notion that dietary fat makes you lean is incorrect in my view. The low carb diet that we evolved to eat satisfies appetite at a much lower calorie intake than higher carb, and optimizes health. On those points I assume we agree. But the notion that dietary fat metabolically makes you burn bodyfat is ridiculous. And quite apart from being incorrect, even suggesting it can only damage the credibility that a low carb approach to optimizing human health/bodycomp so richly deserves.

Stuart

[deirdra]

If leptin is the agent that tells us we're full, then eating fat is the most effective way to activate leptin since eating fat satiates us the most. Or would that be too much of a stretch of logic?That is my logic & the reason for my success! Eating plenty of fat keeps me satisfied and my urges for food are now like those of a ''normal'' person, not a binge-fanatic.

[M Levac]

(in reply to Kneebrace)

I can suggest anything I want concerning what happened 5 million years ago. So can you. That past is entirely open to discussion as far as I know. We have no proof of anything except a few bits here and there. Most of the information is merely hypothesis upon hypothesis.

Here's one I've been thinking of for a while now. It's entirely speculation but still it makes sense to me. For this hypothesis, we must first assume that the most adequate food for us humans is fat, especially saturated fat. Otherwise it just doesn't make sense.


The principles of abundance and scarcity.

In abundance, we waste
In greater abundance, we waste more

In scarcity, we save
In greater scarcity, we save more


What determines if we are in abundance or scarcity is insulin. What determines how much insulin we have is carbohydrates. So, when there's a lot of carbs available, it's a time of scarcity for us humans and we save as fast as we can. Come winter, it becomes a time of abundance of fatty winter meat and we waste as fast as we can.

It is so for us humans because we don't hibernate. If we did, we wouldn't have taken advantage of this winter time to use our most precious resource: Our brain. A good thing too for fatty winter meat is precisely what our brain needs to develop. Without fatty meat, our brain just doesn't develop properly and we can consider ourselves lucky to be able to lean anything in that case.


That we don't hibernate is a giant leap in our evolution. That we have adapted to eat mostly fatty winter meat is also a giant leap. Those two things combined are what made us what we are today. Without them, we might as well go back to our hole in the ground. We developed a bigger brain because of fatty winter meat and that allowed us to use our bigger brain to develop better tools to crack open bones and skulls to get at the fat marrow and brain. And so forth until this day.


Weston Price, in his observations of Native North Americans, describes their diet. He says that most of the muscle meat of the animals they hunt, they give to their dogs while they break the bones in pieces and splinters so that they could get to the marrow, the fattest part of the animal. I think perhaps even the most nutritious pound for pound. There is one hypothesis of our ancient past of millions of years ago that describes this exact method and also the tools invented for that purpose. Yet Weston Price describes this method as contemporary for those natives in his book published in 1939. As I see it, it's not a hypothesis anymore. And we are still fully adapted to this diet of fat marrow and brain.


Frequently, we see in studies and research how an experiment works in mice but not in humans. We see this in the case of fat metabolism. I think I have an idea about this. It's because mice are a species that hibernate, while humans are not. We have adapted to remain active during winter to take advantage of that time to eat fatty meat and as a direct result of this, we've developed a bigger brain. Mice, they're still very much like they were a few million years ago. Small, stupid and delicious.


As we stop eating carbs and start eating fat, we go into ketosis. We burn fat but we can also use ketones as fuel. As it happens, I think we don't use all the energy contained in fat when we burn it. Ketones, if I understand this correctly, are a by-product of fat metabolism. If we excrete ketones, it means we waste. We would continue to excrete and thus waste ketones until the fat on our bellies was completely gone. Then we would make full use of ketones as fuel and we would not waste anymore.


As we stop eating fat and start eating carbs, ketosis stops, lipolysis stops, glycolysis starts. We start burning glucose for fuel an we don't waste one bit of it. What we don't use, we store in adipose tissue. The rest, we all know.

So as we can see from my hypothesis, the principles of abundance and scarcity very much apply to us but differently than in species that hibernate.


Alas, we've come to a point where our ability to do has surpassed our ability to think. Now we eat carbs because there is an economic advantage. Not because it's better. As we eat more and more carbs, it affects our growth growth more and more. This disruption includes our brain. It certainly does not get bigger but I can't bet that it gets smaller. I can promise that it becomes defective. The more defective it becomes, the more stupid we become. In turn, our ability to think is diminished. Eventually, our ability to do will also diminish to a point where we won't even be able to produce the carbs that brought us here in the first place. Then, it's back to hunting which in turn will allow us to regain our ability to think and our ability to do.

At least, that' s how I see it for the most part. Anyway, it's much too many words only to explain why I think mice and men are different when it comes to lab results. Leptin? We don't know enough to start messing with it in humans. We already see that some lab results are wildly different in mice than humans.

[M Levac]

That is my logic & the reason for my success! Eating plenty of fat keeps me satisfied and my urges for food are now like those of a ''normal'' person, not a binge-fanatic.

That is also my logic. I eat as much fat as I'm able.

[M Levac]

Martin, I get the impression you are suggesting that humans were somehow unique in facing constant food abundance? But other animals eat the same food as humans. And the critical point is that one of those 'other animals' is other humans. Nature is a competitive place. That's why evolution selects for those individuals that exploit their environmental niche most efficiently.

For humans that environmental niche was low predominantly low carb until very recently (the neolithic), so those individuals that used the available food source most efficiently were the ones who thrived. If the 'constant abundance' was being competed for, then it wasn't actually constant at all. And the individuals who were most able to store the excess of any low carb feast they were lucky or skilful enough to secure were most able to supply their nutritional needs until next time. Even if that time was spent making and developing tools, or having a cultural life with their peers.

It's easy to forget that if a food source becomes abundant, even briefly, the organisms that consume that food breed to take advantage of that abundance, and bingo, no more abundance. Because suddenly there are a lot more individuals (including individuals of your own species) competing for that resource.

Read up on the mechanism of evolution, Martin (apologies if you don't believe in evolution, each to their own :) ). Ongoing abundance (over millions of years) is impossible. It shouldn't come as any surprise that life on this planet has a palpable devotion to exchanging segments of DNA, so any short term food abundance is instantly exploited by more offspring.

Even contraception hasn't stopped humans fighting with each other and other species for available food resources. We have a natural affinity for having kids and providing for them as best we can, which inevitably means competing with other individuals doing exactly the same thing.

This notion that dietary fat makes you lean is incorrect in my view. The low carb diet that we evolved to eat satisfies appetite at a much lower calorie intake than higher carb, and optimizes health. On those points I assume we agree. But the notion that dietary fat metabolically makes you burn bodyfat is ridiculous. And quite apart from being incorrect, even suggesting it can only damage the credibility that a low carb approach to optimizing human health/bodycomp so richly deserves.

Stuart


You wrote:

"And the individuals who were most able to store the excess of any low carb feast they were lucky or skilful enough to secure were most able to supply their nutritional needs until next time."

It seems you presume we can store fat. We can't. We don't have the mechanism for it. We can store carbs though and we've proven it time and time again. Yet when we eat fat, we lose the fat on our belly and can't seem to store any more of it either no matter how hard we try.


You wrote:

"...so those individuals that used the available food source most efficiently were the ones who thrived."

Thriving does not equate surviving. Also, it is not those who thrived that survived. It's the other way around. It's those who survived that thrived. As it happens, we survived, thus we thrived.


You wrote:

"It's easy to forget that if a food source becomes abundant, even briefly, the organisms that consume that food breed to take advantage of that abundance, and bingo, no more abundance. Because suddenly there are a lot more individuals (including individuals of your own species) competing for that resource."

The time of abundance for us is not when there's plenty of carbs since we don't tolerate carbs that well. The time of abundance is when there's a lot of fatty winter meat walking around. Or there's a lot of bones and skulls left over by other hunting predators. As it happens, there are few species that compete for marrow and brain.


Concerning eating fat to lose fat.

We've been over this. But I'll indulge just one last time for the hell of it.

As we eat fat we also use our stored fat. Thus, we must not simply count the fat that we eat when we count calories used. It's common to see very obese people lose upward of 5lbs per week of the fat on their bellies. That comes up to about 17500 calories. Divide that by 7 to get a good estimate of how many calories they use during the day and we get a whole lot more than just counting what they eat. But do they actually use it all? In my other reply to you, I explain that they don't. They waste a bit less than half of it through excretion. They waste both the fat on their bellies and the fat that they eat.


Some math

2000 calories of fat and protein eaten per day 14000/week
17500 of calories from stored fat
A total of 31500 calories/week 4500/day

That's a whole lot of calories used for somebody eating only 2000 calories a day. By the way, 2k calories a day is quite normal and not even close to starvation level. So it's all good there. But they waste about 40% of it through excretion of ketones so they don't use it all anyway.

4500 * 0.4 = 1800 calories of actual fuel used.

Make up your own mind.

Now can we get back to the subject without so much noise? Leptin it was.

[teaser]

Gina Kolata's "Rethinking Thin" has a chapter on leptin and weight loss. Leptin injection has been very successful, according to her, in at least one human subject. If someone's body doesn't produce enough leptin, and leptin is injected, the person's hypothalamus will actually "rewire" itself, and the obese girl she wrote about in her book actually became normal weight. The treatment is very expensive, and will only work in the leptin deficient.
A hormone that actually causes a part of the brain to remodel itself. Let's trust the drug companies with that.

[kneebrace]

(in reply to Kneebrace)

In abundance, we waste
In greater abundance, we waste more

In scarcity, we save
In greater scarcity, we save more


What determines if we are in abundance or scarcity is insulin. What determines how much insulin we have is carbohydrates. So, when there's a lot of carbs available, it's a time of scarcity for us humans and we save as fast as we can. Come winter, it becomes a time of abundance of fatty winter meat and we waste as fast as we can.

That is not how nature works Martin. In abundance we store, we grow or we breed, usually a combination of all three. Nothing is more certain in nature than that abundance never lasts. Competition and seasonal variation ensure that implacably. It's good to be ready. And abundance of fat doesn't affect insulin at all, at least as far as our current understanding of fat metabolism serves us. For most of our evolution, abundance was much more about fat than carbohydrate.


It is so for us humans because we don't hibernate. If we did, we wouldn't have taken advantage of this winter time to use our most precious resource: Our brain. A good thing too for fatty winter meat is precisely what our brain needs to develop. Without fatty meat, our brain just doesn't develop properly and we can consider ourselves lucky to be able to lean anything in that case.


Where did you get the idea that winter meat is fatty? Meat is fattiest at the end of spring/midsummer because the animals that contain it need it to last them over the food scarce winter. Vegetation doesn't grow well in winter.The longer winter lasts the more that fat resource is used up. In fact in winter when there were fewer (less fat) animals to hunt, human fat consumption probably decreased, because more of the animal would have been utilized. In summer plenty, the fattiest bits would definitely have been the first consumed and the rest given to the dogs.

That we don't hibernate is a giant leap in our evolution. That we have adapted to eat mostly fatty winter meat is also a giant leap. Those two things combined are what made us what we are today. Without them, we might as well go back to our hole in the ground. We developed a bigger brain because of fatty winter meat and that allowed us to use our bigger brain to develop better tools to crack open bones and skulls to get at the fat marrow and brain. And so forth until this day.


But as I pointed out, meat is fattiest and most abundant in the growing season, precisely because it has to last the animal through winter. We certaily had to develop bigger brains to last us through any food scarcity, including winter.


Weston Price, in his observations of Native North Americans, describes their diet. He says that most of the muscle meat of the animals they hunt, they give to their dogs while they break the bones in pieces and splinters so that they could get to the marrow, the fattest part of the animal. I think perhaps even the most nutritious pound for pound. There is one hypothesis of our ancient past of millions of years ago that describes this exact method and also the tools invented for that purpose. Yet Weston Price describes this method as contemporary for those natives in his book published in 1939. As I see it, it's not a hypothesis anymore. And we are still fully adapted to this diet of fat marrow and brain.


I couldn't agree more. But that doesn't change the fact that food of any kind, and fatty meat particularly is more scarce in winter. Geez, it was probably scarce some summers too, if the rains failed. Then, an individual's ability to store bodyfat and use dietary energy efficiently would have been even more important.




As we stop eating carbs and start eating fat, we go into ketosis. We burn fat but we can also use ketones as fuel. As it happens, I think we don't use all the energy contained in fat when we burn it. Ketones, if I understand this correctly, are a by-product of fat metabolism. If we excrete ketones, it means we waste. We would continue to excrete and thus waste ketones until the fat on our bellies was completely gone. Then we would make full use of ketones as fuel and we would not waste anymore.


The more fat we eat and the less carbohydrate, we go into deeper lipolysis, not ketosis necessarily. Traditionally living Inuit are only ever in very mild ketosis, despite spending their entire lives eating very little carbohydrate. The less carbohydrate you eat the more you use FFA's directly in cells without any need for the liver to churn out ketones. Ketosis is very inefficient, there is no question, which is why only people who have spent their entire lives on a high carb diet use it while they are adapting to FFA's. It is one reason why the longer you spend on a low carb diet, the less effective it is for bodyfat loss for the same calorie intake.

Human's evolved to follow a low carb diet. It is no wonder the stop gap machinery of ketosis ever becomes important. There was never any reason for FFA utilization to be able to become efficient quickly, because it always was. Not much carbohydrate around.

As we stop eating fat and start eating carbs, ketosis stops, lipolysis stops, glycolysis starts. We start burning glucose for fuel an we don't waste one bit of it. What we don't use, we store in adipose tissue. The rest, we all know.


Exactly, we start burning glucose for fuel and storing the fat. Martin you really need to reassess your understanding of abundance/scarcity.




Alas, we've come to a point where our ability to do has surpassed our ability to think. Now we eat carbs because there is an economic advantage. Not because it's better. As we eat more and more carbs, it affects our growth growth more and more. This disruption includes our brain. It certainly does not get bigger but I can't bet that it gets smaller. I can promise that it becomes defective. The more defective it becomes, the more stupid we become. In turn, our ability to think is diminished. Eventually, our ability to do will also diminish to a point where we won't even be able to produce the carbs that brought us here in the first place. Then, it's back to hunting which in turn will allow us to regain our ability to think and our ability to do.

Well this last paragraph really does demonstrate how kooky (IMHO) your ideas are Martin. We eat carbs because we evolved to find them delicious and they are easy energy. Throughout our evolution there never has been much of it around, so natural mechanisms for dealing with carbohydrate abundance never developed. Now our ingenuity has ensured constant carb availability and this species is paying a hefty metabolic price. Modern medicine ensures that even a lifetime of overeating food generally (remember, eating itself is inflammatory and degenerative, the less we do of it the better), and carbs specifically (we evolved to follow a low carb diet, so a lifetime of eating beyond our energy needs is going to be even more damaging when that excess is higher in carbs), will not prevent us breeding. So it's hardly likely to select for a return to 'hunting'.

The really good news is that on the low carb dietary approach that evolution equipped us to follow, it is much easier to consume only as much energy as you require, minimize the inevitable degenerative effect of eating, and burn the bodyfat you decide you would rather shed with the least hunger.

Which are extraordinarily good reasons for every human to eat low carb. So why do some low carb dreamers complicate the issue with this kind of wishful thinking?

Stuart

[M Levac]

Exactly, we start burning glucose for fuel and storing the fat. Martin you really need to reassess your understanding of abundance/scarcity.

Which are extraordinarily good reasons for every human to eat low carb. So why do some low carb dreamers complicate the issue with this kind of wishful thinking?

Stuart


We have no mechanism to store the fat we eat. The fat we store comes from lipogenesis. Lipogenesis is the process by which we convert glucose to fatty acids. You're the one who should really need to reassess your understanding of the subject.

You continue to imply that we should not use our own brain by pretending we are the one's wishing for something. It's obvious that you are responsible for much of the confusion in this very thread and many other threads too. If anybody is wishing for something, it's surely you. Don't blame others for your own actions.

[M Levac]

Gina Kolata's "Rethinking Thin" has a chapter on leptin and weight loss. Leptin injection has been very successful, according to her, in at least one human subject. If someone's body doesn't produce enough leptin, and leptin is injected, the person's hypothalamus will actually "rewire" itself, and the obese girl she wrote about in her book actually became normal weight. The treatment is very expensive, and will only work in the leptin deficient.
A hormone that actually causes a part of the brain to remodel itself. Let's trust the drug companies with that.

Enough is relative. Just like enough insulin is relative. We've been observing biological phenomenon under abnormal conditions for such a long time that we forget how our bodies work and when we eat fat we think "this is not normal, we shouldn't be in ketosis, it must be dangerous" and so forth. When all along eating fat was the normal thing to do and it is under those conditions that we should make our control group observations instead.

So when we say we have enough leptin, the normal amount may be much lower than what we see now with all the carbs we eat. Just like the amount of insulin is several orders of magnitude lower when we eat low carb and high fat. When it comes to hormones, a little goes a long way in a normal body. It's when the body is out of whack that things don't go as planned.

That girl with the leptin deficiency. Maybe she didn't have a deficiency after all. Maybe she was just very resistant to leptin just like we can become resistant to insulin. She wasn't strictly diabetic but she was suffering from some sort of diabetes. I bet this leptin deficiency can be fixed the same way we fix type II diabetes: By eating low carb and high fat.

[Thisbegins]

I was speculating that only the burning of fat results in the production of leptin. If indeed leptin is the agent that tells our brain to stop eating. The adipose tissue would then also need to burn fat for leptin to be released. Not just to contain fat. Adipose tissue stores fat as triglycerides. When fat is burned as fuel, it is burned as fatty acids, not as triglycerides. So the trigs contained within the adipose tissue would have no effect on leptin. Again, if my speculation has any value and if leptin is indeed the agent that tells our brain to stop eating.


The article says "Leptin is produced by fat" This is incorrect. Fat is not metabolically active. Thus, fat can't produce leptin. The only possibility here is that through the metabolism of fat (burning of fat or lipolysis), leptin is also produced. That is where I had the idea for my speculation.


The article also says obese people have high levels of leptin. So I don't know. Not enough information.
1) Leptin is produced by insulin acting on various body cells, mainly fat cells

2) Leptin is produced from body fat independently of insulin as well in a diurnal (day-night) pattern

(PS, and yes body fat is a very metabolically active if not influential tissue, leptin is just one of many hormones/cytokines it makes which profoundly influence metabolic and behavioral processes).

The obese have extremely high leptin levels. Leptin reflects fat storage trends, today (insulin) and yesterday (body fat). Leptin has nothing to do with weight loss, it is an antistarvation hormone.

[Thisbegins]

We have no mechanism to store the fat we eat. The fat we store comes from lipogenesis. Lipogenesis is the process by which we convert glucose to fatty acids. You're the one who should really need to reassess your understanding of the subject.

You continue to imply that we should not use our own brain by pretending we are the one's wishing for something. It's obvious that you are responsible for much of the confusion in this very thread and many other threads too. If anybody is wishing for something, it's surely you. Don't blame others for your own actions.
It's pretty easy to store fat on a 0 carb diet. When the mitochondria are hogged up by fatty acids, glucose tolerance goes to poop, which increases blood sugar (yes, you have sugar in your blood even if eating no carbs), which increases insulin, which stores the glut of fat you are eating.
Eat an extremely high energy diet with protein and zero carbs, I assure you that fat deposits will appear on your body. Unless you have type 1 diabetes. Metabolism will determine at what energy level fat deposits begin to appear, but I assure you they will, and it probably won't take all that many calories to get to that point (at least, a lot less than you think, as you seem to be under the impression it is impossible to build body fat in absence of carbohydrate which is completely silly, even if only utilizing a evolutionary logic perspective).


Of course, it is much more difficult to become fat while eating a zero carb diet, because carbs are much more effective at hogging up mitochondria and increasing insulin, not to mention the opiate addiction of sugar/insulin spike and all that jazz. But "more difficult' does not equal "impossible".

[Thisbegins]

Enough is relative. Just like enough insulin is relative. We've been observing biological phenomenon under abnormal conditions for such a long time that we forget how our bodies work and when we eat fat we think "this is not normal, we shouldn't be in ketosis, it must be dangerous" and so forth. When all along eating fat was the normal thing to do and it is under those conditions that we should make our control group observations instead.

So when we say we have enough leptin, the normal amount may be much lower than what we see now with all the carbs we eat. Just like the amount of insulin is several orders of magnitude lower when we eat low carb and high fat. When it comes to hormones, a little goes a long way in a normal body. It's when the body is out of whack that things don't go as planned.

That girl with the leptin deficiency. Maybe she didn't have a deficiency after all. Maybe she was just very resistant to leptin just like we can become resistant to insulin. She wasn't strictly diabetic but she was suffering from some sort of diabetes. I bet this leptin deficiency can be fixed the same way we fix type II diabetes: By eating low carb and high fat.
Leptin levels are easily measured, it is impossible to confuse leptin resistance with leptin deficiency. Especially considering leptin resistance would not have any clinically significant response to increasing leptin level to physiologically normal levels, whereas the leptin deficient person will have a complete metabolic 180 when given leptin to normal levels.

Leptin deficiency will cause diabetes as leptin is necessary for normal glucose tolerance (insulin sensitivity) and it also is necessary to metabolize protein properly (leptin deficiency breaks down protein and increases blood sugar at the same time). Her diabetes was secondary to her lack of leptin.

Leptin deficiency (homozygous) is extremely rare, but it does exist, and it is undeniable these people need exogenous leptin to live a normal healthy life. It's more common for leptin deficiency to be a result of lipodystrophy or strenuous exercise/massive weight loss.

[kneebrace]

We have no mechanism to store the fat we eat. The fat we store comes from lipogenesis. Lipogenesis is the process by which we convert glucose to fatty acids. You're the one who should really need to reassess your understanding of the subject.



Martin, this is incorrect. Even basal insulin is sufficient to drive both FFA's and triglycerides into adipocytes. Now you can bluster all you like that this is impossible. It is however well understood basic biochemistry. It just doesn't matter how much you want to believe your nonsense. Dietary fat can be and is stored by the human body even in the complete absence of carbohydrate. Otherwise those cultures who eat practically no carbohydrate would never have existed.

More carbohydrate just means that the carbohydrate will be burned and the food energy surplus to bodily requirements, both fat and any remaining carbohydrate, will be stored.

Don't forget, this doesn't change the fact that eating zero carbs makes it much more difficult to store dietary fat. But it is definitely not impossible.

Stuart

[dane]

Thanks to Kneebrace and Thisbegins for talking some sense in this thread! :clap:

[kneebrace]

You continue to imply that we should not use our own brain by pretending we are the one's wishing for something. It's obvious that you are responsible for much of the confusion in this very thread and many other threads too. If anybody is wishing for something, it's surely you. Don't blame others for your own actions.

Martin Martin. Whatever gave you that idea? How you use your brain is your business entirely. But if you continue to get all confused about basic biochemistry I will continue to do my level best to point out the confusion. Any less would be reprehensible. Low carb credibility is a very important issue to me.

And you do it no favours. It's that simple. Anybody who actually understands human biochemistry reading your posts can only hope that you are not indicative of the standard of debate. I'm so sorry you are offended, but the credibility of this forum (and low carb generally) simply demands that however damaging it is to your ego, the facts need to be kept in view.

Now there are plenty of threads I have participated in where there is indeed scope for disagreement. And time will tell who is correct. However this issue is beyond any disagreement. You may want to believe that ' Humans have no mechanism for storing dietary fat'. You obviously do earnestly believe this to be true. And I get the impression that you don't only believe that we don't store dietary fat in the absence of carbohydrate, which is definitely possible, but also a little more complicated. You also seem to believe that we don't even store dietary fat in the presence of carbohydrate, which is almost laughable.

So as annoying as it must be, you are simply mistaken. Not because I say so, but because there are actually certain fundamental biochemical processes that are not only very well understood , but are easily observable all around you. This may not suit your stiflingly narrow low carb blinkered vision. But perhaps it's time you removed the blinkers, instead of insisting that everyone else needs to blinker their vision also.

Stuart

[M Levac]

Leptin levels are easily measured, it is impossible to confuse leptin resistance with leptin deficiency. Especially considering leptin resistance would not have any clinically significant response to increasing leptin level to physiologically normal levels, whereas the leptin deficient person will have a complete metabolic 180 when given leptin to normal levels.

Leptin deficiency will cause diabetes as leptin is necessary for normal glucose tolerance (insulin sensitivity) and it also is necessary to metabolize protein properly (leptin deficiency breaks down protein and increases blood sugar at the same time). Her diabetes was secondary to her lack of leptin.

Leptin deficiency (homozygous) is extremely rare, but it does exist, and it is undeniable these people need exogenous leptin to live a normal healthy life. It's more common for leptin deficiency to be a result of lipodystrophy or strenuous exercise/massive weight loss.

I'm about there in my understanding of the subject as well. Still, not enough information.

[M Levac]

It's pretty easy to store fat on a 0 carb diet. When the mitochondria are hogged up by fatty acids, glucose tolerance goes to poop, which increases blood sugar (yes, you have sugar in your blood even if eating no carbs), which increases insulin, which stores the glut of fat you are eating.
Eat an extremely high energy diet with protein and zero carbs, I assure you that fat deposits will appear on your body. Unless you have type 1 diabetes. Metabolism will determine at what energy level fat deposits begin to appear, but I assure you they will, and it probably won't take all that many calories to get to that point (at least, a lot less than you think, as you seem to be under the impression it is impossible to build body fat in absence of carbohydrate which is completely silly, even if only utilizing a evolutionary logic perspective).


Of course, it is much more difficult to become fat while eating a zero carb diet, because carbs are much more effective at hogging up mitochondria and increasing insulin, not to mention the opiate addiction of sugar/insulin spike and all that jazz. But "more difficult' does not equal "impossible".

Pretty easy? Point to an example so that we can all see how easy it truly is. The example must be human, in good health and known. Once you are done, I'll point you to a few million examples of the contrary. All human, all in somewhat good health, mostly known at least to somebody else.


I can't believe a word you wrote. Not when you begin with "It's pretty easy to store fat on a 0 carb diet." This goes against everything we know about 0 carb diets. So your credibility starts below zero. The rest of what you wrote then suffers because of it. You assure me? With an immediate drop in credibility, any assurance you give me means nothing.

I would consider your words if you didn't go so overboard. I would consider your words if you provided supporting work or studies or research.


Your hypothesis breaks down. You wrote:

Quote: "...which increases insulin, which stores the glut of fat you are eating."

An increase in insulin results in a decrease in blood glucose which in turn results in an increase in glucagon which is somewhat the anti-insulin hormone. Glucagon inhibits lipogenesis and stimulates lipolysis. So whatever mysterious effect insulin could have on the fat in our veins, glucagon simply goes in and gives completely opposite orders. Then, it's just a matter of who has the loudest voice.


Further, digesting fat requires bile. We don't produce unlimited quantities of it. If I understand it correctly, without bile, we can't absorb the fat we eat and it goes through our digestive tract intact. So, there is a real limit to the amount of fat we can eat thus absorb regardless of the supposed potential for this fat to be stored.

[advantagec]

Leptin is produced by fat and acts on the brain to reduce appetite and increase energy use through a process called thermogenesis.

The scientists have discovered leptin not only triggers thermogenesis in a small number of fat cells, but that it also triggers the same response in muscle tissue, which makes up more than one third of body mass.

This finding, published in the journal Endocrinology, has significant repercussion for the development of weight loss strategies, said the researchers, Dr Belinda Henry and Professor Iain Clarke.

Drugs that mimic leptin could trick the body into weight loss by simply harnessing the body's natural process of thermogenesis, they say.

"Now that we have shown leptin increases energy utilisation in muscle tissue, the potential for the hormone to have a positive impact has been greatly magnified," Dr Henry said.

"We can now start to recreate and enhance this natural process for the purposes of assisting weight loss."


Leptin schmeptin. Who cares? I use ketones to curb my hunger thus avoiding injections and pills.

[M Levac]

Leptin is produced by fat and acts on the brain to reduce appetite and increase energy use through a process called thermogenesis.

The scientists have discovered leptin not only triggers thermogenesis in a small number of fat cells, but that it also triggers the same response in muscle tissue, which makes up more than one third of body mass.

This finding, published in the journal Endocrinology, has significant repercussion for the development of weight loss strategies, said the researchers, Dr Belinda Henry and Professor Iain Clarke.

Drugs that mimic leptin could trick the body into weight loss by simply harnessing the body's natural process of thermogenesis, they say.

"Now that we have shown leptin increases energy utilisation in muscle tissue, the potential for the hormone to have a positive impact has been greatly magnified," Dr Henry said.

"We can now start to recreate and enhance this natural process for the purposes of assisting weight loss."


Leptin schmeptin. Who cares? I use ketones to curb my hunger thus avoiding injections and pills.


I read one study on leptin. In it, it says leptin is metabolized by many more organs than just adipose tissue. This tells me that leptin responds to many more stimuli than just fat accumulation. So, even if we could affect fat accumulation by affecting leptin levels, it would certainly come with an unforeseen consequence. Maybe a bit like the ACCORD study even. The one where people died when their cholesterol dropped to normal levels using drugs.

Ketone Power!

[kneebrace]

Further, digesting fat requires bile. We don't produce unlimited quantities of it. If I understand it correctly, without bile, we can't absorb the fat we eat and it goes through our digestive tract intact. So, there is a real limit to the amount of fat we can eat thus absorb regardless of the supposed potential for this fat to be stored.

Martin, you do seem to be getting there. I detect a definite admission that it is indeed possible to store dietary fat as bodyfat in a zero carb environment. Now you seem to be saying that the amount of dietary fat you can store is limited by your gall bladders ability to produce bile.

Anyway, if you really want to understand the biochemistry of dietary lipid storage in the complete absence of carbs, just google 'Acylation Stimulating Protein'. When you've done some reading, come back and tell us wether you have changed your tune :) . Take your time. The human body is a complex machine. And it is very tempting to cling to low carb myths.

Stuart

[M Levac]

Martin, you do seem to be getting there. I detect a definite admission that it is indeed possible to store dietary fat as bodyfat in a zero carb environment. Now you seem to be saying that the amount of dietary fat you can store is limited by your gall bladders ability to produce bile.

Anyway, if you really want to understand the biochemistry of dietary lipid storage in the complete absence of carbs, just google 'Acylation Stimulating Protein'. When you've done some reading, come back and tell us wether you have changed your tune :) . Take your time. The human body is a complex machine. And it is very tempting to cling to low carb myths.

Stuart

I'm the one clinging to myths alright.

[kneebrace]

I'm the one clinging to myths alright.

Martin, ASP (Acylation Stimulating Protein). Please take the time to find out. What have you got to lose?

Stuart

[M Levac]

Martin, ASP (Acylation Stimulating Protein). Please take the time to find out. What have you got to lose?

Stuart

This is what I gather from my reading on ASP.

ASP stimulates triglycerides synthesis
ASP level is higher in obese persons
ASP level increases after food intake (one articles says specifically fat intake)

Yet I can't dismiss that I eat low carb and high fat and I'm still losing the fat on my belly as do several million other people. So, even if ASP does stimulate trig synthesis, it seems it doesn't do such a good job of it anyhow. Otherwise, we'd get fatter, not leaner. In other words, ASP is inconsequential.


I didn't have anything to lose. I just learned something new today. Have you?


After further reading.

ASP affects insulin secretion. But apparently, only when blood glucose levels were higher than normal. This suggests that for ASP to have any effect, something must increase blood glucose level above normal and thus insulin secretion above normal as well. In other words, without carbs and without insulin, ASP is useless.

[kneebrace]

I didn't have anything to lose. I just learned something new today. Have you?


After further reading.

ASP affects insulin secretion. But apparently, only when blood glucose levels were higher than normal. This suggests that for ASP to have any effect, something must increase blood glucose level above normal and thus insulin secretion above normal as well. In other words, without carbs and without insulin, ASP is useless.

Excellent, now we're getting somewhere. ASP definitely affects insulin secretion, but it's primary role in storing fat in the absence of carbs works independently of insulin. So when you eat carbs and fat together you get the double whammy dietary fat storage effect of the insulin (from the carbs) and the direct ASP effect.

Which is exactly what you see in the real world Martin. Eating fatty Carby food makes you store the dietary fat splendidly. Eating fat without the carbs, just less splendidly. And because fat is naturally satiating, you eat less calories in total, and you have your fat burning enzyme machinery up to speed, so between meals, you'll be much more likely to burn both the dietary fat, and hopefully some of the fat you've stored as well.

Also:

Yet I can't dismiss that I eat low carb and high fat and I'm still losing the fat on my belly as do several million other people. So, even if ASP does stimulate trig synthesis, it seems it doesn't do such a good job of it anyhow. Otherwise, we'd get fatter, not leaner. In other words, ASP is inconsequential.


No Martin, you are the first person to claim that eating dietary fat actively makes you burn existing bodyfat. A few people here have reported that deliberately eating heroic quantities of fat didn't result in bodyfat gain. I personally don't gain any bodyfat even if I over eat carby fatty food.

If you personally have found that you can eat fat and lose bodyfat I couldn't really give a toss. Good luck to you of course. But anecdotal reports are useless to anyone but the reporter. The point is whether it makes sense in terms of evolutionary logic and biochemically from our current understanding of how the human body works.

On neither of those grounds does losing bodyfat by eating more fat energy than you are burning make any sense.

The most telling factor in all this is that human beings have been storing excess fat calories for millions of years in a largely low carb environment for millions of years and burning them later when food became more scarce. Your sorry argument that 'hey food was always plentiful during our entire evolution, so we never had to store excess fat calories' is particularly tedious.

None of this changes the fact that restricting carb is the best way to optimize human health/bodycomp. In fact having spent our evolution eating low carb fare, it would be entirely surprising if it were otherwise.

Keep reading Martin, I've no doubt you'll eventually get there!

Stuart

[M Levac]

Kneebrace, conclusions come too quick for you.


Let's work with the same basis. In vitro and in vivo in lab studies, we observe:

ASP stimulates triglycerides synthesis
ASP level is higher in obese persons
ASP level increases after food intake (one articles says specifically fat intake)

This suggests triglycerides level would go up when we're obese and after we just ate or both. It also suggests we would grow fatter by eating dietary fat.


Real world observation below shows the opposite of lab observation above. As we cut the carbs and eat more fat, we see the following:

Triglycerides go down (in fact, it's the easiest thing we can do and they drop like a rock)
Adipocytes release their store of fat


This begs the question, where is ASP when you need it?


When we cut the fat and increase the carbs, we grow fatter. Based on what we know of ASP from lab observations, we can only scratch our heads and conclude ASP doesn't do its job when it's supposed to and works overtime when we expect it to go to bed instead.

ASP is required for adipocytes to retain triglycerides. In other studies, ASP deficiency inhibits the storage of triglycerides and only when injecting ASP will adipocytes recover their normal function. But here I speculate that ASP deficiency is not the cause but a symptom of some disorder that directly affects adipocytes since they are the ones responsible for ASP production in the first place.

[M Levac]

No Martin, you are the first person to claim that eating dietary fat actively makes you burn existing bodyfat. A few people here have reported that deliberately eating heroic quantities of fat didn't result in bodyfat gain. I personally don't gain any bodyfat even if I over eat carby fatty food.

If you personally have found that you can eat fat and lose bodyfat I couldn't really give a toss. Good luck to you of course. But anecdotal reports are useless to anyone but the reporter. The point is whether it makes sense in terms of evolutionary logic and biochemically from our current understanding of how the human body works.

On neither of those grounds does losing bodyfat by eating more fat energy than you are burning make any sense.

The most telling factor in all this is that human beings have been storing excess fat calories for millions of years in a largely low carb environment for millions of years and burning them later when food became more scarce. Your sorry argument that 'hey food was always plentiful during our entire evolution, so we never had to store excess fat calories' is particularly tedious.

None of this changes the fact that restricting carb is the best way to optimize human health/bodycomp. In fact having spent our evolution eating low carb fare, it would be entirely surprising if it were otherwise.

Keep reading Martin, I've no doubt you'll eventually get there!

Stuart


Study: "New" hepatic fat activates PPARalpha to maintain glucose, lipid, and cholesterol homeostasis. (2005)

http://www.ncbi.nlm.nih.gov/pubmed/16054078?ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum


Article: Eat Fat to Lose Fat (2005)

http://www.wired.com/medtech/health/news/2005/05/67473

Quote:

"We thought we would alter the levels of fats that circulate in blood," he said. "Instead we found you need to generate new fat to make a signal to burn fat in the liver."


I am hardly the first to come up with the idea. In fact, that's where I got the idea to eat more fat to lose more fat. It makes perfect sense to me.

[kneebrace]

[QUOTE]Kneebrace, conclusions come too quick for you.


Let's work with the same basis. In vitro and in vivo in lab studies, we observe:

ASP stimulates triglycerides synthesis
ASP level is higher in obese persons
ASP level increases after food intake (one articles says specifically fat intake)

This suggests triglycerides level would go up when we're obese and after we just ate or both. It also suggests we would grow fatter by eating dietary fat.


Real world observation below shows the opposite of lab observation above. As we cut the carbs and eat more fat, we see the following:

Triglycerides go down (in fact, it's the easiest thing we can do and they drop like a rock)
Adipocytes release their store of fat

Martin, triglycerides do go up after a fatty meal. What you are talking about is fasting triglycerides which do drop wonderfully the longer a carbohydrate restricted diet is followed. One of the reasons the triglycerides in your blood in the hours after a fatty meal are cleared from your blood so quickly (with or without the presence of dietary carbohydrate) is precisely because ASP produced by adipocytes allows them to be absorbed. They don't release their store of fat at all. They accept more. Where do you think the fat goes after it is absorbed into your blood following a fatty meal? Timbuctoo?

Real World observations are indeed useful, but you have to actually o-b-s-e-r-v-e, not just see what you want to see :)




When we cut the fat and increase the carbs, we grow fatter. Based on what we know of ASP from lab observations, we can only scratch our heads and conclude ASP doesn't do its job when it's supposed to and works overtime when we expect it to go to bed instead.

No we don't. We grow fatter when we eat an excess of calories. We grow fatter faster when we eat an excess of fatty carby calories. It is very difficult to grow fat quickly on carbs alone without also eating a lot of fat. Try it sometime. It is nevertheless difficult to lose already stored bodyfat on a high carb diet. But certainly not impossible. Determined low fat dieters do it by the millions every day. They are all miserable and constantly hungry, and I wouldn't recommend it to my worst enemy, but it can and does work. It is much easier to reduce calories enough to burn more energy than you are consuming on the low carb diet we evolved to follow (indeed most people seem to be able to do so without even trying, or even noticing that they are even reducing calorie intake)

ASP is required for adipocytes to retain triglycerides. In other studies, ASP deficiency inhibits the storage of triglycerides and only when injecting ASP will adipocytes recover their normal function. But here I speculate that ASP deficiency is not the cause but a symptom of some disorder that directly affects adipocytes since they are the ones responsible for ASP production in the first place.

Go for it Martin, speculate till you drop :) . You've already proved yourself to be an excellent metabolic mechanism speculator. It won't change ASP's role in storing dietary fat completely independently of carbohydrate in healthy humans (as evolution exquisitely designed us to do) one iota. You said it yourself anyway - 'healthy' adipocytes don't have a problem producing ASP, and try as you might to obfuscate, ASP is specifically designed to store dietary triglycerides independently of either insulin or dietary carbs.

Stuart

[vavcon]

I find these exchanges fascinating. I realize I'm being naieve, but to me, at least, the fact that low carb works! I'm still a little confused on the pro's and con's of lower fat / higher protien versus lower protien/higher fat. Any thoughts?
Thanks!
Chris

[M Levac]

[QUOTE=M Levac]Martin, triglycerides do go up after a fatty meal. What you are talking about is fasting triglycerides which do drop wonderfully the longer a carbohydrate restricted diet is followed. One of the reasons the triglycerides in your blood in the hours after a fatty meal are cleared from your blood so quickly (with or without the presence of dietary carbohydrate) is precisely because ASP produced by adipocytes allows them to be absorbed. They don't release their store of fat at all. They accept more. Where do you think the fat goes after it is absorbed into your blood following a fatty meal? Timbuctoo?

Real World observations are indeed useful, but you have to actually o-b-s-e-r-v-e, not just see what you want to see :)


No we don't. We grow fatter when we eat an excess of calories. We grow fatter faster when we eat an excess of fatty carby calories. It is very difficult to grow fat quickly on carbs alone without also eating a lot of fat. Try it sometime. It is nevertheless difficult to lose already stored bodyfat on a high carb diet. But certainly not impossible. Determined low fat dieters do it by the millions every day. They are all miserable and constantly hungry, and I wouldn't recommend it to my worst enemy, but it can and does work. It is much easier to reduce calories enough to burn more energy than you are consuming on the low carb diet we evolved to follow (indeed most people seem to be able to do so without even trying, or even noticing that they are even reducing calorie intake)



Do you mean to say that fasting triglycerides levels mean nothing? I'll ask my doctor and see what he says about that.

So triglycerides get taken care of at some point but they don't just vanish to wherever. OK. So does that mean the scale is lying and the mirror is lying and my pants are lying? It all makes sense when we look at ASP in the lab and see what it does. But when we look at everything together, it stops making sense. Then we must ask ourselves if ASP really did what we saw it do in the lab.

Regardless of what ASP is supposed to be doing, I can safely assume that fat is going to Timbuctoo. It's not staying here. Maybe it's converted to ketones and excreted in my urine and THEN goes to Timbuctoo. Just an idea I had.


There's the Positive Caloric Balance hypothesis again. As long as you stick to it, you can't understand the rest. We grow fat not because we eat more. Instead, we grow fat because we eat carbs, convert them to glucose, draw more insulin, drive lipogenesis, store that in adipocytes.

We grow fatter even in caloric deficit. It's only a matter of how insulin resistant we are. The more resistant we are, the easier it is to grow fatter. Until adipocytes become resistant themselves, then we become diabetic.

The mechanism known as Metabolic Syndrome.

Carbs convert to glucose. Glucose draws insulin. Insulin drives insulin resistance. Insulin resistance reduces glucose intake by cells. Hunger increases. We eat more. And round we go until we reach a point where we can't even use the glucose in our blood since our liver and muscle cells are so resistant to insulin. Yet we can still convert glucose to fatty acids and bind them to triglycerides and store them in adipocytes because they are still sensitive to insulin. So we grow fatter and more hungry and eventually become diabetic.

Gradually, we use less and less of the food we eat because we store more and more of it as insulin resistance progresses. So we eat more and more to compensate.

Further, the fatter we are, the easier it is to grow fat since ASP level is higher. At least, if we believe that ASP is doing its job properly. Which it isn't.

A bit like the smoker who smokes and his lungs become less efficient at taking in the smoke thus less nicotine so he smokes more for the same nicotine and it goes on like that until he can't even breathe anymore.

[kneebrace]

[QUOTE=kneebrace]
[QUOTE]

Do you mean to say that fasting triglycerides levels mean nothing? I'll ask my doctor and see what he says about that.

Of course they 'mean' something. You want low fasting tryglycerides. But fatty food raises blood triglycerides in the hours after eating it. Then those triglycerides are cleared into adipocytes and assuming you are in at least energy equilibrium, burnt over the time until your next (fatty, I assume) meal. I'm sure your Doctor can help you understand this.



So triglycerides get taken care of at some point but they don't just vanish to wherever. OK. So does that mean the scale is lying and the mirror is lying and my pants are lying? It all makes sense when we look at ASP in the lab and see what it does. But when we look at everything together, it stops making sense. Then we must ask ourselves if ASP really did what we saw it do in the lab.

Well, I can't really vouch for the honesty of either your scale, mirror, or pants Martin. But you may simply be overestimating your energy consumption. The simple fact is, if you are losing bodyfat, then you are consuming less energy than you are burning. Just because you are storing (some) of the dietary fat you are eating in the absence of carbohydrate, doesn't mean that at some stage during the interval leading up to your next meal you won't be burning some of it too. And if you are burning more than you are storing, you will be losing bodyfat.


Regardless of what ASP is supposed to be doing, I can safely assume that fat is going to Timbuctoo. It's not staying here. Maybe it's converted to ketones and excreted in my urine and THEN goes to Timbuctoo. Just an idea I had.

Yes a small percentage of it probably is (down the toilet, through your skin and breath, but believe me none to Timbuctoo) ketone loss. But this doesn't change the fact that you can and do store bodyfat in the complete absence of carbohydrate. Martin it just occured to me that you may simply not be considering this in NET terms. Just because you are storing dietary fat after a meal doesn't mean that you won't be burning it soon also. If you are storing more than you are burning, you'll gain weight, and vice versa.


There's the Positive Caloric Balance hypothesis again. As long as you stick to it, you can't understand the rest. We grow fat not because we eat more. Instead, we grow fat because we eat carbs, convert them to glucose, draw more insulin, drive lipogenesis, store that in adipocytes.

We grow fatter even in caloric deficit. It's only a matter of how insulin resistant we are. The more resistant we are, the easier it is to grow fatter. Until adipocytes become resistant themselves, then we become diabetic.

The mechanism known as Metabolic Syndrome.


Actually, try not to talk about 'caloric balance' It's a meaningless concept. What you need to consider is 'energy balance'. And we do indeed grow fat because we eat more than we burn. We grow fat much more quickly when we eat a lot of fatty carby food. As I said, it's almost impossible to grow fat by eating just carbs. Look around you Martin, you just won't see anyone growing fat by eating just carbohydrate. And don't forget your new understanding of how ASP stores fat in adipocytes even without insulin.

No we don't grow fatter in energy deficit. Insulin resistance just makes us grow fatter faster because it makes us constantly hungry so we eat more fatty carby food. And yes it is called Metabolic Syndrome, but it's got nothing to do with energy deficit.

Carbs convert to glucose. Glucose draws insulin. Insulin drives insulin resistance. Insulin resistance reduces glucose intake by cells. Hunger increases. We eat more. And round we go until we reach a point where we can't even use the glucose in our blood since our liver and muscle cells are so resistant to insulin. Yet we can still convert glucose to fatty acids and bind them to triglycerides and store them in adipocytes because they are still sensitive to insulin. So we grow fatter and more hungry and eventually become diabetic.

All true, but don't forget that all that excess insulin is making it even more likely that any dietary fat consumed is stored in adipocytes too. And fat is more energy dense than carbohydrate, so it makes a commensurately bigger dent on your waistline.


Further, the fatter we are, the easier it is to grow fat since ASP level is higher. At least, if we believe that ASP is doing its job properly. Which it isn't.


The function of ASP is to store dietary lipids in adipocytes independently of insulin. The only reason fatter people have more ASP is because they generally have more adipocytes. You still have to eat the energy surplus fat for the ASP to be able to work with. And if you are eating a lot of carby fatty food and/or are insulin resistant there'll be heaps of insulin to store any energy surplus, be it fat carbs or protein, so you won't even need the action of ASP.

Martin I can't stress enough how important it is for you to understand that insulin stores dietary fat in adipocytes even more efficiently than it stores carbs. Your Doctor can probably explain this to you far better than I. If you are eating high fat/carb, you'll get fat quickly and it will be very hard to lose it. If you eat fat without carbs, you can easily store it (ASP remember), but you can also easily burn stored fat as well, and because you are not as hungry you are much more likely to be in energy deficit and actually need to burn it to provide for your energy needs.

Anyway, I really do think you are starting to get it. Don't give up yet :)

Stuart

[M Levac]

ASP is contended to drive triglycerides synthesis and triglycerides storage.


Carbs drive serum triglycerides upward.
Dietary fats do the opposite.
If ASP has any effect, it does not show it up here.

Carbs drive triglycerides storage.
Dietary fats do the opposite.
Is ASP has any effect, it does not show it up here either.


So where does ASP show its purported effects?


I read the studies from my search on Google. The only one that produced a conclusive result is when they started with a full ASP deficiency then injected ASP. This conclusively shows that without ASP, we can't store fat. It shows nothing else. It does suggest that ASP is required for fat storage but that has not been demonstrated conclusively yet.

[kneebrace]

ASP is contended to drive triglycerides synthesis and triglycerides storage.


Carbs drive serum triglycerides upward.
Dietary fats do the opposite.
If ASP has any effect, it does not show it up here.

Carbs drive triglycerides storage.
Dietary fats do the opposite.
Is ASP has any effect, it does not show it up here either.


So where does ASP show its purported effects?

Carbs drive fasting serum triglycerides upward Martin. Dietary fats drive post (fatty) meal serum triglyceride upward. Both insulin and ASP independently clear that high post meal serum triglyceride level into adipocytes. If there is no carb elevated insulin, and baseline insulin is insufficient, ASP does the fat storage work. Insulin as well just gets it done a whole lot quicker.

Both protein and carbohydrate can be converted to fat and driven into adipocytes with insulin.

I'm curious, which part of 'ASP drives dietary fat storage independently of insulin' are you having trouble with?

Dietary fat is either burnt, stored or to some small extent excreted as unused ketones. Mike Eades did the Math a while ago on the limits to excretion of unburnt ketones in breath, urine skin. It was fairly insignifigant. The longer you spend low carbing the less your liver resorts to churning out ketones and the more efficient your body becomes at using FFA'a directly anyway.

Stuart

[M Levac]

I'm curious, which part of 'ASP drives dietary fat storage independently of insulin' are you having trouble with?



Yeah, I'm curious too. Which part of "I don't see ASP's effects on the scale, the mirror or my pants" are you having trouble with?

Perhaps you're the one who's not thinking in terms of NET effect.

[kneebrace]

Yeah, I'm curious too. Which part of "I don't see ASP's effects on the scale, the mirror or my pants" are you having trouble with?

Perhaps you're the one who's not thinking in terms of NET effect.

No Martin. that's the point, I am. Even if the Net effect is bodyfat loss, that usually does involve dietary fat storage, even in the complete absence of carbs.
And whether that Net effect is loss or gain will be wholly determined by whether you are consuming more energy than you are expending.

Even while you are admiring the effect of your net energy deficit in the mirror, ASP will be faithfully clearing high post fatty meal serum triglycerides into adipocytes expressly as millions of years of evolution designed it to do.

Stuart

[M Levac]

No Martin. that's the point, I am. Even if the Net effect is bodyfat loss, that usually does involve dietary fat storage, even in the complete absence of carbs.
And whether that Net effect is loss or gain will be wholly determined by whether you are consuming more energy than you are expending.

Even while you are admiring the effect of your net energy deficit in the mirror, ASP will be faithfully clearing high post fatty meal serum triglycerides into adipocytes expressly as millions of years of evolution designed it to do.

Stuart

Yeah, so...


Essentially, what you're saying, after all this debate on what ASP does, is that even if ASP stores fat, as it is designed to do from millions of years of evolution and natural selection, with all the available technology, with all the studies and knowledge on biochemistry and physiology, with all the human trials and other animal trials, we still can't put on fat when we cut carbs and eat mostly fat?

That was quite a bit of posturing for just a small tiny inconsequential detail that after all is said and done means zip in the grand scheme of things.


You win. :)

[kneebrace]

Yeah, so...


Essentially, what you're saying, after all this debate on what ASP does, is that even if ASP stores fat, as it is designed to do from millions of years of evolution and natural selection, with all the available technology, with all the studies and knowledge on biochemistry and physiology, with all the human trials and other animal trials, we still can't put on fat when we cut carbs and eat mostly fat?
.


You win. :)

On the contrary, you can indeed put on fat when you cut carbs and eat mostly fat, for those very reasons (ASP, evolution etc.). It's just much more difficult. I think, (correct me if I'm wrong) because you didn't understand the metabolic processes involved, you were arguing that it was impossible. Which is wrong.

It's not a matter of 'winning' Martin. I've never argued even for an instant that restricting carbohydrate wasn't the best way to optimize human health/bodycomp. It is important to understand why, of course.

And your persistent attempts to cloud the metabolic waters were regrettable and unnecessary. I do hope you've learnt something.

Stuart

[M Levac]

On the contrary, you can indeed put on fat when you cut carbs and eat mostly fat, for those very reasons (ASP, evolution etc.). It's just much more difficult. I think, (correct me if I'm wrong) because you didn't understand the metabolic processes involved, you were arguing that it was impossible. Which is wrong.

It's not a matter of 'winning' Martin. I've never argued even for an instant that restricting carbohydrate wasn't the best way to optimize human health/bodycomp. It is important to understand why, of course.

And your persistent attempts to cloud the metabolic waters were regrettable and unnecessary. I do hope you've learnt something.

Stuart

MY persistent attempts to cloud the metabolic waters?!?

You wrote and I quote:

"Actually, try not to talk about 'caloric balance' It's a meaningless concept. What you need to consider is 'energy balance'. And we do indeed grow fat because we eat more than we burn. We grow fat much more quickly when we eat a lot of fatty carby food. As I said, it's almost impossible to grow fat by eating just carbs. Look around you Martin, you just won't see anyone growing fat by eating just carbohydrate. And don't forget your new understanding of how ASP stores fat in adipocytes even without insulin."


Uh huh...

Calorie is a measure of energy. You state 'caloric balance' is a meaningless concept.

Then go right back to this meaningless concept by stating "What you need to consider is energy balance."

Then, as if it's not enough to confuse us with that, you write "And we do indeed grow fat because we eat more than we burn." Again the famous Positive Caloric Balance hypothesis that had already been proven flawed before the second World War.

And then you write "We grow fat much more quickly when we eat a lot of fatty carby food."

Then you contradict that previous statement "As I said, it's almost impossible to grow fat by eating just carbs. Look around you Martin, you just won't see anyone growing fat by eating just carbohydrate."

Then continue with the small tiny inconsequential detail that in the grand scheme of things makes no difference whatsoever "And don't forget your new understanding of how ASP stores fat in adipocytes even without insulin."



Who are you kidding?

[M Levac]

[QUOTE=M Levac][QUOTE=kneebrace]Of course they 'mean' something. You want low fasting tryglycerides. But fatty food raises blood triglycerides in the hours after eating it. Then those triglycerides are cleared into adipocytes and assuming you are in at least energy equilibrium, burnt over the time until your next (fatty, I assume) meal. I'm sure your Doctor can help you understand this.

Well, I can't really vouch for the honesty of either your scale, mirror, or pants Martin. But you may simply be overestimating your energy consumption. The simple fact is, if you are losing bodyfat, then you are consuming less energy than you are burning. Just because you are storing (some) of the dietary fat you are eating in the absence of carbohydrate, doesn't mean that at some stage during the interval leading up to your next meal you won't be burning some of it too. And if you are burning more than you are storing, you will be losing bodyfat.


Yes a small percentage of it probably is (down the toilet, through your skin and breath, but believe me none to Timbuctoo) ketone loss. But this doesn't change the fact that you can and do store bodyfat in the complete absence of carbohydrate. Martin it just occured to me that you may simply not be considering this in NET terms. Just because you are storing dietary fat after a meal doesn't mean that you won't be burning it soon also. If you are storing more than you are burning, you'll gain weight, and vice versa.

Actually, try not to talk about 'caloric balance' It's a meaningless concept. What you need to consider is 'energy balance'. And we do indeed grow fat because we eat more than we burn. We grow fat much more quickly when we eat a lot of fatty carby food. As I said, it's almost impossible to grow fat by eating just carbs. Look around you Martin, you just won't see anyone growing fat by eating just carbohydrate. And don't forget your new understanding of how ASP stores fat in adipocytes even without insulin.

No we don't grow fatter in energy deficit. Insulin resistance just makes us grow fatter faster because it makes us constantly hungry so we eat more fatty carby food. And yes it is called Metabolic Syndrome, but it's got nothing to do with energy deficit.

All true, but don't forget that all that excess insulin is making it even more likely that any dietary fat consumed is stored in adipocytes too. And fat is more energy dense than carbohydrate, so it makes a commensurately bigger dent on your waistline.

The function of ASP is to store dietary lipids in adipocytes independently of insulin. The only reason fatter people have more ASP is because they generally have more adipocytes. You still have to eat the energy surplus fat for the ASP to be able to work with. And if you are eating a lot of carby fatty food and/or are insulin resistant there'll be heaps of insulin to store any energy surplus, be it fat carbs or protein, so you won't even need the action of ASP.

Martin I can't stress enough how important it is for you to understand that insulin stores dietary fat in adipocytes even more efficiently than it stores carbs. Your Doctor can probably explain this to you far better than I. If you are eating high fat/carb, you'll get fat quickly and it will be very hard to lose it. If you eat fat without carbs, you can easily store it (ASP remember), but you can also easily burn stored fat as well, and because you are not as hungry you are much more likely to be in energy deficit and actually need to burn it to provide for your energy needs.

Anyway, I really do think you are starting to get it. Don't give up yet :)

Stuart


Quoting for archive purpose.

[Nancy LC]

Leptina: Fat Stripper

Watch her exotic dance on the pole and marvel at the size of her thighs! How do they make fish-nets that big?

[Beth1708]

Hi Martin,

(in reply to Kneebrace)

I can suggest anything I want concerning what happened 5 million years ago. So can you. That past is entirely open to discussion as far as I know. We have no proof of anything except a few bits here and there. Most of the information is merely hypothesis upon hypothesis.


There are some things that are know, for example, that humans evolved in Africa. In general, though, there are many gaps (to say the least) in what we know, I agree.


What determines if we are in abundance or scarcity is insulin. What determines how much insulin we have is carbohydrates. So, when there's a lot of carbs available, it's a time of scarcity for us humans and we save as fast as we can. Come winter, it becomes a time of abundance of fatty winter meat and we waste as fast as we can.


This makes, to me, a certain amount of sense.


That we don't hibernate is a giant leap in our evolution.

Come again? There are mammals that hibernate, but do humans descend from any of them? I would think that African mammals in general would not hibernate, because I doubt that the environment changes that much from summer to winter. You seem to be implying that some proto-human species did hibernate & I doubt there is any reason to think this is so.

Beth

[Beth1708]

Stuart said:


Then you contradict that previous statement "As I said, it's almost impossible to grow fat by eating just carbs. Look around you Martin, you just won't see anyone growing fat by eating just carbohydrate."


You won't ever see anyone grow fat (in the long run) eating just carbs, because they would die. The body needs both fat & protein to stay alive.

In the short run, aren't there pictures of starving kids with big bellies, where the big bellies (may not be fat) are a symptom of protein deficiency or something like that?

Beth

[M Levac]

Come again? There are mammals that hibernate, but do humans descend from any of them? I would think that African mammals in general would not hibernate, because I doubt that the environment changes that much from summer to winter. You seem to be implying that some proto-human species did hibernate & I doubt there is any reason to think this is so.

Beth

Yep. I went out with that one. I don't know that there is any reason to think so either but our ability to store excess nutrients is a hint in that direction. Would we have need of that ability otherwise?

[KarenJ]

But isn't it true that you need alpha glycerol phosphate to make the triglycerides in the first place? fewer carbs = less glucose = less glycerol = less alpha glycerol phosphate = fewer triglycerides.

[dane]

Leptina: Fat Stripper

Watch her exotic dance on the pole and marvel at the size of her thighs! How do they make fish-nets that big?
:lol: I was going to post similar--it's hard for my brain to take in the detail in this thread when it's focussed on a fat stripper. :p

[Beth1708]

Yep. I went out with that one. I don't know that there is any reason to think so either but our ability to store excess nutrients is a hint in that direction. Would we have need of that ability otherwise?

By storing excess nutrients, I think you mean adding lots of fat to the fat cells?

If Taubes is right that obesity means that fat is locked into the fat cells, and is not available to be burned, that suggests that becoming obese is not actually storing excess nutrients. For the fat to act as a nutrient, it must be available to be used, not just carried around like a overstuffed backpack with lead weights in locked pockets.

When you ask why we would have need for that ability, you are assuming there is an advantage to storing excess fat on the modern diet, rather than that human metabolism is adapted to a different nutritional environment and just doesn't work well on the one we have.

Beth

[M Levac]

By storing excess nutrients, I think you mean adding lots of fat to the fat cells?

If Taubes is right that obesity means that fat is locked into the fat cells, and is not available to be burned, that suggests that becoming obese is not actually storing excess nutrients. For the fat to act as a nutrient, it must be available to be used, not just carried around like a overstuffed backpack with lead weights in locked pockets.

When you ask why we would have need for that ability, you are assuming there is an advantage to storing excess fat on the modern diet, rather than that human metabolism is adapted to a different nutritional environment and just doesn't work well on the one we have.

Beth

That's what I'm thinking too. But I don't think we need the ability today. I mean we have the ability now which implies we have developed the need for it in our past. From our current ability combined with the implication that we developed it in the past, I speculated that we must have had need of it but then at some point it became less important i.e. hibernating at first but not later on. We would not have needed to be a mammal to be a hibernating species to acquire the ability. Genetics is built upon, not merely replaced. So, our genetics are built upon whatever we were in the ancient past.

I further speculate that considering the disparity between the regulation mechanisms we have for carbs storage versus those for fat utilization, the ability to store carbs and thus what is practically considered excess nutrients became superfluous and maybe even detrimental to our survival.

In my opinion, those who survived are those who were able to take advantage of the abundance of fatty winter meat and marrow and brain. Not those who had the ability to store carbs for winter or for any other purpose. This is a fundamental distinction in the reason for survival. Those who hibernated still do and continue to thrive but remain quite primitive today compared to us.

I thought all this up on the spot so don't take it too seriously.

[Wyvrn]

I suspect there were times in our evolution when there was plenty of low-carb calories to cause obesity (if you believe that calories cause obesity).

However an obese hominid is easy prey. There's your adaptive pressure for a biological anti-excess-fat storage mechanism.

And, we're still are fairly clueless about how those "excess" calories may be put to use when simple energy needs have been met. Mechanisms of calorie "wastage" are possibly not the whole story.