"Biggest Loser" Contestants Regained Weight. Peat Perspective

Koveras

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Wrong the goal of pharmaceutical companies is to make as much money possible. Even if that means selling drugs that don't work or to the point that they do biological damage for example DES and thalidomide.

I lost thirty pounds while taking Cynomel while increasing my food intake. Unless you have taken Cynomel (Grossman brand not including other brands) most people won't believe how well it works for fat loss. I won't say its a magic bullet for obesity, with diet changes it can definitely help fat loss and I think cure obesity.

Fat oxidation has nothing to do with weight loss. In fact, it can cause weight gain by inhibiting mitochondrial respiration and releasing free fatty acids into the blood stream. 2'4-dinitrophenol is a chemical that was use in 1930's for weight loss. It can cure type 2 diabetes and obesity. The studies on it are clear, it does this through uncoupling mitochondria which increases carbon dioxide. It decrease free fatty acids and increases the use of glucose. Bromocriptine has most of the same effects but though the increasing dopamine and decreasing prolactin and serotonin. People with type 2 diabetes are more likely to be obese or overweight. The mechanisms behind this are due to the Randle cycle.

Exactly - the goal is to make as much money as possible. This would be accomplished by "producing a drug that will cause weight loss in the absence of conscious lifestyle changes". It's not very profitable to give a drug that doesn't do all that much for weight loss on it's own but enhances the results of a diet that's well adhered to.

Glad to hear to of your positive experience and results, although context is everything, and thyroid hormone may be more beneficial for some causes of obesity than for others.

Fat oxidation has everything to do with weight loss. Fat doesn't magically disappear from your body. Lipolysis releases stored fats, which are then oxidized.

You mentioned "it does this through uncoupling mitochondria"

Uncoupled mitochondria = same amount of fuel produces less ATP

ie. If 1 glucose produced 32 ATP before, maybe when mitochondria are very strongly uncoupled 1 glucose only produces 16 ATP.

In this example this means if you need 2000 calories per day normally, and now you need twice the fuel to produce the same amount of ATP, you now need 4000 calories per day.

If you increased your calorie intake to 4000 calories per day with your new metabolism, you would maintain your weight, because you're eating as much as you're burning despite being strongly "uncoupled"

If you continue to eat 2000 calories like you did before, and you are now burning 4000, that means that you are going to need to burn about 2000 calories worth of body fat to serve your energy needs.

If even you started day 1 with hugely full glycogen reserves of 500 grams (~2000 calories worth), you might delay a good portion of fat oxidation until day 2, when even if you ate 2000 calories of sugar, that would all get burned rather then stored, and now all you're left with is fat to oxidize to meet your needs.

Also I stand corrected on my "thyroid hormone decreases fat oxidation" point - it would be more correct to say that thyroid hormone favours carbohydrate oxidation when carbohydrates are available, but that it also increases fat oxidation (and lipolysis and free fatty acid blood levels) in a calorie or carbohydrate restricted state.

Feel free to do a literature review to check the effect of thyroid hormone on fat oxidation and lipolysis.
 

Koveras

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Fat oxidation has nothing to do with weight loss. In fact, it can cause weight gain by inhibiting mitochondrial respiration and releasing free fatty acids into the blood stream. 2'4-dinitrophenol is a chemical that was use in 1930's for weight loss. It can cure type 2 diabetes and obesity. The studies on it are clear, it does this through uncoupling mitochondria which increases carbon dioxide. It decrease free fatty acids and increases the use of glucose. Bromocriptine has most of the same effects but though the increasing dopamine and decreasing prolactin and serotonin. People with type 2 diabetes are more likely to be obese or overweight. The mechanisms behind this are due to the Randle cycle.

Consistent with the above post, DNP also increases fat oxidation

http://www.ncbi.nlm.nih.gov/pubmed/10973929

"Synthesis of fatty acid (FA) in adipose tissue requires cooperation of mitochondrial and cytoplasmic enzymes. Mitochondria are required for the production of ATP and they also support the formation of acetyl-CoA and NADPH in cytoplasm. Since cellular levels of all these metabolites depend on the efficiency of mitochondrial energy conversion, mitochondrial proton leak via uncoupling proteins (UCPs) could modulate FA synthesis. In 3T3-L1 adipocytes, 2,4-dinitrophenol depressed the synthesis of FA 4-fold while increasing FA oxidation 1. 5-fold and the production of lactate 14-fold. Inhibition of FA synthesis in 3T3-L1 adipocytes was proportional to the decrease in mitochondrial membrane potential. FA synthesis from D-[U-(14)C] glucose was reduced up to fourfold by ectopic UCP1 in the white fat of transgenic aP2-Ucp1 mice, reflecting the magnitude of UCP1 expression in different fat depots and the reduction of adiposity. Transcript levels for lipogenic enzymes were lower in the white fat of the transgenic mice than in the control animals. Our results show that uncoupling of oxidative phosphorylation depresses FA synthesis in white fat. Reduction of adiposity via mitochondrial uncoupling in white fat not only reflects increased energy expenditure, but also decreased in situ lipogenesis."
 

Ledo

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Cron-OCD tells me that in order for me to maintain my current weight of 136 lbs. I can eat 1431 calories per day, of course if I lose the Last Dreaded Ten pounds that maintenance number will drop even lower.....maintenance will be somewhere around 1200 calories per day. Total Starvation.

I'm eating well over a thousand calories per day above and beyond what they say I should be eating.....that's way more than 25%.

Makes NO sense to me.
Cron would have to know your metabolic rate to provide that info
 

jaguar43

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Exactly - the goal is to make as much money as possible. This would be accomplished by "producing a drug that will cause weight loss in the absence of conscious lifestyle changes". It's not very profitable to give a drug that doesn't do all that much for weight loss on it's own but enhances the results of a diet that's well adhered to.

Glad to hear to of your positive experience and results, although context is everything, and thyroid hormone may be more beneficial for some causes of obesity than for others.

Fat oxidation has everything to do with weight loss. Fat doesn't magically disappear from your body. Lipolysis releases stored fats, which are then oxidized.

You mentioned "it does this through uncoupling mitochondria"

Uncoupled mitochondria = same amount of fuel produces less ATP

ie. If 1 glucose produced 32 ATP before, maybe when mitochondria are very strongly uncoupled 1 glucose only produces 16 ATP.

In this example this means if you need 2000 calories per day normally, and now you need twice the fuel to produce the same amount of ATP, you now need 4000 calories per day.

If you increased your calorie intake to 4000 calories per day with your new metabolism, you would maintain your weight, because you're eating as much as you're burning despite being strongly "uncoupled"

If you continue to eat 2000 calories like you did before, and you are now burning 4000, that means that you are going to need to burn about 2000 calories worth of body fat to serve your energy needs.

If even you started day 1 with hugely full glycogen reserves of 500 grams (~2000 calories worth), you might delay a good portion of fat oxidation until day 2, when even if you ate 2000 calories of sugar, that would all get burned rather then stored, and now all you're left with is fat to oxidize to meet your needs.

Also I stand corrected on my "thyroid hormone decreases fat oxidation" point - it would be more correct to say that thyroid hormone favours carbohydrate oxidation when carbohydrates are available, but that it also increases fat oxidation (and lipolysis and free fatty acid blood levels) in a calorie or carbohydrate restricted state.

Feel free to do a literature review to check the effect of thyroid hormone on fat oxidation and lipolysis.

If the pharmaceutical companies produce a drug that causes weight loss than everyone would take it. Ray Peat has said that pharmaceutical companies are interested in drugs that make the patient take them for the rest of their lives in his book generative energy.

Thyroid can increase adrenaline which could increase lipolysis and fatty acids. The difference, is the degree to which directional biochemical path way it's going. when a persons adrenaline rises due to inadequate energy. That situation is different when one increases thyroid production which leads to increases adrenaline which can happen if one takes too much thyroid too soon. Thyroid is still increasing metabolic rate and it is an uncoupler. You need to take these things into consideration.

Your comments on calories seem to be assuming that a calorie is just a calorie.Without taking into account the different food one is consuming. Eating 200o calories of a high fat diet is going to have different repercussions than someone eating 2000 calories of high carbohydrate diet.

The 32 ATP you are referring to doesn't necessarily reflect your basal metabolic rate or oxygen consumption. Plus that still wouldn't matter because uncoupling chemicals produce oxidation without producing ATP. Thyroid is an uncoupler so is aspirin.

Uncoupling--In cellular respiration, oxidation of "fuel" in the mitochondrion is coupled to the phosphorylation of ADP, forming ATP. Uncouplers are chemicals that allow oxidation to proceed without producing the usual amount of ATP. -Ray Peat

Prostate Cancer
 

jaguar43

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Consistent with the above post, DNP also increases fat oxidation

Decreased fatty acid synthesis due to mitochondrial uncoupling in adipose tissue. - PubMed - NCBI

"Synthesis of fatty acid (FA) in adipose tissue requires cooperation of mitochondrial and cytoplasmic enzymes. Mitochondria are required for the production of ATP and they also support the formation of acetyl-CoA and NADPH in cytoplasm. Since cellular levels of all these metabolites depend on the efficiency of mitochondrial energy conversion, mitochondrial proton leak via uncoupling proteins (UCPs) could modulate FA synthesis. In 3T3-L1 adipocytes, 2,4-dinitrophenol depressed the synthesis of FA 4-fold while increasing FA oxidation 1. 5-fold and the production of lactate 14-fold. Inhibition of FA synthesis in 3T3-L1 adipocytes was proportional to the decrease in mitochondrial membrane potential. FA synthesis from D-[U-(14)C] glucose was reduced up to fourfold by ectopic UCP1 in the white fat of transgenic aP2-Ucp1 mice, reflecting the magnitude of UCP1 expression in different fat depots and the reduction of adiposity. Transcript levels for lipogenic enzymes were lower in the white fat of the transgenic mice than in the control animals. Our results show that uncoupling of oxidative phosphorylation depresses FA synthesis in white fat. Reduction of adiposity via mitochondrial uncoupling in white fat not only reflects increased energy expenditure, but also decreased in situ lipogenesis."

But the last line states it decreases lipogenesis. To oxidized fat one has to release it which happens under lipogenesis. According to the line you bolded DNP is still depressing fat synthesis more that it's producing fat oxidation.

Even if it would increase fat oxidation, it doesn't produce diabetes or obesity. it goes in the other direction. Ray Peat has said that estrogen increases fat oxidation.

The shift away from fat oxidation under the influence of aspirin doesn't lead to an accumulation of free fatty acids in the circulation, since aspirin inhibits the release of fatty acids from both phospholipids and triglycerides. Estrogen has the opposite effects, increasing fat oxidation while increasing the level of circulating free fatty acids, since it activates lipolysis, as do several other stress-related hormones.

Aspirin, brain, and cancer

A lowered metabolic rate and energy production is a common feature of aging and most degenerative diseases. From the beginning of an animal's life, sugars are the primary source of energy, and with maturation and aging there is a shift toward replacing sugar oxidation with fat oxidation. Old people are able to metabolize fat at the same rate as younger people, but their overall metabolic rate is lower, because they are unable to oxidize sugar at the same high rate as young people. Fat people have a similar selectively reduced ability to oxidize sugar.

Glucose and sucrose for diabetes.

Estrogen and stress are both known to create some of the conditions of diabetes, while increasing fat oxidation and inhibiting glucose oxidation. Emotional stress, overwork, trauma, and infections have been known to initiate diabetes. Estrogen increases free fatty acids and decreases glycogen storage, and when birth control pills were becoming popular, some researchers warned that they might cause diabetes. But the food oil industry and the estrogen industry were satisfied with the medical doctrine that diabetes was caused by eating too much sugar.

The antagonism between fat and sugar that Randle described can involve the suppression of sugar oxidation when the concentration of fats in the bloodstream is increased by eating fatty food, or by releasing fats from the tissues by lipolysis, but it can also involve the suppression of fat oxidation by inhibiting the release of fatty acids from the tissues, when a sufficient amount of sugar is eaten.


Glucose and sucrose for diabetes.


Your whole argument isn't true. Unless you are saying that Ray Peat is wrong.
 
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Cron would have to know your metabolic rate to provide that info

I guess this is what they use according to My Profile page:

Basal Metabolic Rate ( BMR ): 1192 kcal
Mifflin St. Jeor Equation

I don't know what any of this means, but I'm trying to learn....
 

Tarmander

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This is an interesting thread. It is amazing how often I hear of someone having issues with their job, relationship, or whatnot and it coincides with some new diet they are trying.

I had no idea t3 was so good at weight loss. It's amazing how the t4 the docs prescribes seems to not get much press's for helping.
 
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Koveras

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If the pharmaceutical companies produce a drug that causes weight loss than everyone would take it. Ray Peat has said that pharmaceutical companies are interested in drugs that make the patient take them for the rest of their lives in his book generative energy.

Thyroid can increase adrenaline which could increase lipolysis and fatty acids. The difference, is the degree to which directional biochemical path way it's going. when a persons adrenaline rises due to inadequate energy. That situation is different when one increases thyroid production which leads to increases adrenaline which can happen if one takes too much thyroid too soon. Thyroid is still increasing metabolic rate and it is an uncoupler. You need to take these things into consideration.

Your comments on calories seem to be assuming that a calorie is just a calorie.Without taking into account the different food one is consuming. Eating 200o calories of a high fat diet is going to have different repercussions than someone eating 2000 calories of high carbohydrate diet.

The 32 ATP you are referring to doesn't necessarily reflect your basal metabolic rate or oxygen consumption. Plus that still wouldn't matter because uncoupling chemicals produce oxidation without producing ATP. Thyroid is an uncoupler so is aspirin.

Uncoupling--In cellular respiration, oxidation of "fuel" in the mitochondrion is coupled to the phosphorylation of ADP, forming ATP. Uncouplers are chemicals that allow oxidation to proceed without producing the usual amount of ATP. -Ray Peat

Prostate Cancer

I don't see how Ray's quote is different from what I'm saying - he says "allow oxidation to proceed without producing the usual amount of ATP". I said the same amount of fuel oxidized would produce less ATP...

The amount of ATP I mentioned produced from glucose doesn't necessarily reflect your BMR or oxygen consumption as you said, that is correct - not what I was saying

In another example... Let's say the act of flexing your bicep for a second takes 320 ATP (numbers not representative of reality here). In an normal "non-uncoupled" system we can say that might take 10 glucose producing 32 ATP each. Now let's strongly uncouple our mitochondria, allowing oxidation to proceed without producing the usual amount of ATP. Now some glucose is oxidized without producing usable energy (ATP). We're going to hypothetically say it now required double, or 20 glucose, to produce the same 320 ATP total for that bicep flexing. The amount of ATP required for the muscular contraction doesn't change, but the amount of fuel needed to produce that ATP does. You can extend the same analogy to energy that might be required for the functioning of an organ.

Now let's say our total metabolic rate (activity included) is 3000 calories before strong uncoupling. That means without uncoupling, running this individuals organs and their usual activity would take 750 grams of carbohydrates (at 4 calories per gram) if thats all they ate. Now if that individual were uncoupled to the extent in the example above (which in reality would probably kill someone from the hyperthermia) - those same activities and organs, requiring the same amount of ATP, now require double the fuel or 1500 grams or carbohydrates (6000 calories). So that is the relationship between fuel, activities, and metabolism.

Anyway, as is mentioned many times on this forum, increasing your metabolism from any substance whether it be caffeine, methylene blue, thyroid, or DNP can provoke stress reactions and involve the counter-regulatory stress hormones if administered without adequate carbohydrates.

All I am saying is that

-If you increase metabolism and increase calorie intake to match, weight loss will not happen.

-If you increase metabolism and keep you calorie intake at the same lower level as before, you will lose weight, partly through a reduced likelihood of fat storage from the food you're eating, and partly from filling in for some of the calories you're not eating with calories from your fat stores (through lipolysis and fat oxidation).

-It seems that eating for health and eating for fat loss are often confused. Many individuals report gaining weight on this forum and also report many health benefits to their diet. Having a deranged carbohydrate metabolism is an often invoked 'reason' for gaining weight on the peat diet. Probably that is involved, but it should not be a surprise that fat gain happens, or that fat loss doesn't happen, when you strongly suppress the release and burning of fat for energy (which is all likelihood a 'healthy' thing to do).
 

Koveras

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But the last line states it decreases lipogenesis. To oxidized fat one has to release it which happens under lipogenesis. According to the line you bolded DNP is still depressing fat synthesis more that it's producing fat oxidation.

You are confusing lipogenesis (the creation of new fat) and lipolysis (the breakdown of fat)
 
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I think what is truly and indisputably "frightening and amazing" is that the "expert on metabolism" from no other but NIH is surprised and amazed at these findings!!! It shows the absolute, stunning stupidity at the highest scientific levels in the premier research institute in the world!

:clap::clap::clap::clap::clap::clap::clap::clap::clap::clap::clap::clap::clap:
 

Koveras

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Even if it would increase fat oxidation, it doesn't produce diabetes or obesity. it goes in the other direction. Ray Peat has said that estrogen increases fat oxidation.

Probably because whether you are in a state of caloric deficit, maintenance, or excess is an extremely important variable in the development of diabetes or obesity. DNP would tend to put you in a deficit, even while you are oxidizing fat.

So you have one factor working for you, and one working against you. In this case the calorie deficit is a more relevant factor in health improvements then fat oxidation.

Have a metabolism of 3000 calories, increase it to 4500 calories with DNP, and eat 9000 calories and tell me that you will be free of weight gain and diabetes.
 

jaguar43

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I don't see how Ray's quote is different from what I'm saying - he says "allow oxidation to proceed without producing the usual amount of ATP". I said the same amount of fuel oxidized would produce less ATP...

It's not producing ATP. Uncouplers don't need produce ATP to produce oxidative metabolism. Thats the point.

The amount of ATP I mentioned produced from glucose doesn't necessarily reflect your BMR or oxygen consumption as you said, that is correct - not what I was saying

In another example... Let's say the act of flexing your bicep for a second takes 320 ATP (numbers not representative of reality here). In an normal "non-uncoupled" system we can say that might take 10 glucose producing 32 ATP each. Now let's strongly uncouple our mitochondria, allowing oxidation to proceed without producing the usual amount of ATP. Now some glucose is oxidized without producing usable energy (ATP). We're going to hypothetically say it now required double, or 20 glucose, to produce the same 320 ATP total for that bicep flexing. The amount of ATP required for the muscular contraction doesn't change, but the amount of fuel needed to produce that ATP does. You can extend the same analogy to energy that might be required for the functioning of an organ.


Now let's say our total metabolic rate (activity included) is 3000 calories before strong uncoupling. That means without uncoupling, running this individuals organs and their usual activity would take 750 grams of carbohydrates (at 4 calories per gram) if thats all they ate. Now if that individual were uncoupled to the extent in the example above (which in reality would probably kill someone from the hyperthermia) - those same activities and organs, requiring the same amount of ATP, now require double the fuel or 1500 grams or carbohydrates (6000 calories). So that is the relationship between fuel, activities, and metabolism.


You initially state that numbers don't represent reality and yet you continue with the "example". I think you are shaping your argument to control the outcome.

Anyway, as is mentioned many times on this forum, increasing your metabolism from any substance whether it be caffeine, methylene blue, thyroid, or DNP can provoke stress reactions and involve the counter-regulatory stress hormones if administered without adequate carbohydrates.

I agree with this statement.

All I am saying is that

-If you increase metabolism and increase calorie intake to match, weight loss will not happen.

Wrong, you have to increase calorie intake to match metabolism. Ray Peat has talked about how small dogs eat the same amount as a larger dog and the small dog doesn't get fat and lives longer than the larger dog. A child can eat and eat and never get fat. Why ?

-If you increase metabolism and keep you calorie intake at the same lower level as before, you will lose weight, partly through a reduced likelihood of fat storage from the food you're eating, and partly from filling in for some of the calories you're not eating with calories from your fat stores (through lipolysis and fat oxidation).

This is also wrong. Ray Peat has stated that estrogen increases fat oxidation and lipolysis. Does that mean estrogen makes you lose weight ?

It seems that eating for health and eating for fat loss are often confused. Many individuals report gaining weight on this forum and also report many health benefits to their diet. Having a deranged carbohydrate metabolism is an often invoked 'reason' for gaining weight on the peat diet. Probably that is involved, but it should not be a surprise that fat gain happens, or that fat loss doesn't happen, when you strongly suppress the release and burning of fat for energy (which is all likelihood a 'healthy' thing to do).

Individuals should listen to Ray Peat's recommendation and try to understand what he is saying. Ray Peat explicitly stated that one should increase metabolic rate to lose weight. Eating a different diet doesn't always change that.
 
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jaguar43

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You are confusing lipogenesis (the creation of new fat) and lipolysis (the breakdown of fat)

So your argument is that since the study said the DNP increases fat oxidation by 1.5 fold( however much that is) then it proves that fat oxidation leads to weight loss ? Did you not read my other post sharing Ray Peats view on fat oxidation ?
 

jaguar43

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Probably because whether you are in a state of caloric deficit, maintenance, or excess is an extremely important variable in the development of diabetes or obesity. DNP would tend to put you in a deficit, even while you are oxidizing fat.

So you have one factor working for you, and one working against you. In this case the calorie deficit is a more relevant factor in health improvements then fat oxidation.

Have a metabolism of 3000 calories, increase it to 4500 calories with DNP, and eat 9000 calories and tell me that you will be free of weight gain and diabetes.

Again, you are thinking in terms of calories in and out. It doesn't help your argument.

The idea of using bromocriptine for the treatment of type 2 diabetes came while studying the metabolism of migrating birds. It was noted that they developed seasonal changes in body fat stores and insulin sensitivity. In vertebrates, body fat stores and insulin action are controlled by the temporal interaction of circadian neuroendocrine oscillations. Many vertebrate species develop obesity and insulin resistance (IR) during hibernation, migration, and overwintering, when food availability is very low.

Bromocriptine in type 2 diabetes mellitus

That study states that birds developed obesity and insulin resistance BECAUSE low availability of food, overwintering and migration. Not the other way around.

During transition to this insulin-resistant state, the basal lipolytic activity increases, to spare glucose utilization by the peripheral tissues and fat oxidation becomes predominant. Hepatic glucose production and gluconeogenesis rise to supply glucose to the CNS during prolonged periods of winter food deprivation.This adaptation helps survival in times of seasonal famine. At the end of the season animals revert to the insulin-sensitive / glucose-tolerant phase and become lean.

This centrally acting antidiabetic agent has a novel mechanism of action and reduces plasma glucose, triglycerides, Free Fatty Acid (FFA) levels, and possibly cardiovascular events. The utility of bromocriptine in diabetes patients has been recognized, based on its activity in modulating central glucose and energy metabolism pathways

Bromocriptine in type 2 diabetes mellitus

The inability to properly use glucose through fat oxidation is central in developing obesity and type 2 diabetes. The calorie or fat oxidation ideology isn't true. It's based on years of marketing of low-carb diets and falsifying science and facts.
 
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Koveras

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It's not producing ATP. Uncouplers don't need produce ATP to produce oxidative metabolism. Thats the point.

Ray said "Uncouplers are chemicals that allow oxidation to proceed without producing the usual amount of ATP"

Ray did not say "Uncouplers are chemicals that allow oxidation to proceed without producing any amount of ATP"

You initially state that numbers don't represent reality and yet you continue with the "example". I think you are shaping your argument to control the outcome.

The numbers don't invalidate the argument or formula. Feel free to do further research on the ATP required for muscular contraction.

All I am saying is that

-If you increase metabolism and increase calorie intake to match, weight loss will not happen.
Wrong, you have to increase calorie intake to match metabolism. Ray Peat has talked about how small dogs eat the same amount as a larger dog and the small dog doesn't get fat and lives longer than the larger dog.

What Ray said "Many dog owners are aware that small dogs eat much more food in proportion to their size than big dogs do. And small dogs have a much greater life expectancy than big dogs, in some cases about twice as long "

Ray says that small dogs eat more in proportion their size to big dogs and are healthier.

What Ray doesn't say "Eat more then big dogs"

I'll use some more math here and avoid unrealistic numbers ;)

Big dog weighs 2X and eats 2Y food
Small dog weighs X and eats 1.5Y food

Small dog eats more in proportion to large dog. Small dog also eats less then large dog.

More to the point with the dogs -

Where does Ray say the small dogs are losing weight because of their fast metabolisms? He doesn't. Because they are maintaining their weight. They are eating an amount of calories that maintains their weight. This happens to be more food (relatively speaking) then a bigger dog with a slower metabolism.

Here's good definition of calorie maintenance

"As an example – If you are eating 50,000 calories a day and not gaining fat, congratulations you are still eating at maintenance. If you are eating 8 Calories a day and not losing body mass, congratulations you are also eating at maintenance. The amount of calories you consume does not determine if you are eating deficit, maintenance or surplus, the changes in your body does. Lack of a loss of body mass and absence of a gain of body fat defines eating at maintenance."
"
And here's one for eating at a calorie deficit.

"From my understanding, by definition this means an amount of food that results in loss of body mass. By this definition you cannot be in a deficit if you are not losing body mass. You can be eating less, a little, not much, like a bird, and not lose body mass since these are all subjective descriptions of an amount of food, but if you are eating less food than is needed to provide the energy you require to power your daily activities then a loss of mass must occur. This loss may be masked by fluctuations in bodyweight caused by water or the weight of the food in your digestive track (at least for a little while), but make no mistake, it is the loss of body mass that defines the deficit, not eating below an estimated amount of needed calories. The Loss of Mass is what defines a Deficit.

A child can eat and eat and never get fat. Why ?

I guess childhood obesity isn't a thing?

-If you increase metabolism and keep you calorie intake at the same lower level as before, you will lose weight, partly through a reduced likelihood of fat storage from the food you're eating, and partly from filling in for some of the calories you're not eating with calories from your fat stores (through lipolysis and fat oxidation).

This is also wrong. Ray Peat has stated that estrogen increases fat oxidation and lipolysis. Does that mean estrogen makes you lose weight ?

No, because as I mentioned fat oxidation and lipolysis doesn't happen it a vacuum. Whether it occurs in the context of your overall caloric intake and expenditure is important for fat loss.

Individuals should listen to Ray Peat's recommendation and try to understand what he is saying. Ray Peat explicitly stated that one should increase metabolic rate to lose weight. Eating a different diet doesn't always change that.

True, Ray suggests losing weight by increasing your metabolism, he suggests not starving yourself for improving your metabolism, and he also suggests that the healthiest/least harmful way to lose fat is very slowly

What Ray doesn't say "Increase your metabolism, and then keep increasing your food intake to the point where you don't lose weight". Amount of food / food calories is still important.

The inability to properly use glucose through fat oxidation is central in developing obesity and type 2 diabetes. The calorie or fat oxidation ideology isn't true. It's based on years of marketing of low-carb diets and falsifying science and facts.

How about this one?

Bromocriptine: a novel approach to the treatment of type 2 diabetes. - PubMed - NCBI


RESEARCH DESIGN AND METHODS:

There were 22 obese subjects with type 2 diabetes randomized to receive a quick-release formulation of bromocriptine (n = 15) or placebo (n = 7) in a 16-week double-blind study. Subjects were prescribed a weight-maintaining diet to exclude any effect of changes in body weight on the primary outcome measurements. Fasting plasma glucose concentration and HbA(1c) were measured at 2- to 4-week intervals during treatment. Body composition (underwater weighing), body fat distribution (magnetic resonance imaging), oral glucose tolerance (oral glucose tolerance test [OGTT]), insulin-mediated glucose disposal, and endogenous glucose production (2-step euglycemic insulin clamp, 40 and 160 mU x min(-1) x m(-2)) were measured before and after treatment.

RESULTS:
No changes in body weight or body composition occurred during the study in either placebo- or bromocriptine-treated subjects. Bromocriptine significantly reduced HbA(1c) (from 8.7 to 8.1%, P = 0.009) and fasting plasma glucose (from 190 to 172 mg/dl, P = 0.02) levels, whereas these variables increased during placebo treatment (from 8.5 to 9.1%, NS, and from 187 to 223 mg/dl, P = 0.02, respectively). The differences in HbA(1c) (delta = 1.2%, P = 0.01) and fasting glucose (delta = 54 mg/dl, P < 0.001) levels between the bromocriptine and placebo group at 16 weeks were highly significant. The mean plasma glucose concentration during OGTT was significantly reduced by bromocriptine (from 294 to 272 mg/dl, P = 0.005), whereas it increased in the placebo group. No change in glucose disposal occurred during the first step of the insulin clamp in either the bromocriptine- or placebo-treated group. During the second insulin clamp step, bromocriptine improved total glucose disposal from 6.8 to 8.4 mg x min(-1) kg(-1) fat-free mass (FFM) (P = 0.01) and nonoxidative glucose disposal from 3.3 to 4.3 mg min(-1) x kg(-1) FFM (P < 0.05), whereas both of these variables deteriorated significantly (P < or = 0.02) in the placebo group.

There you go, an improvement in glucose control with no change in body weight or body composition because the subjects ate at maintenance calories.

Dopamine is helpful for weight loss because it improves metabolism but also because it tends to increase the motivation for general physical activity and exercise.

Serotonin is not helpful for weight loss because it worsens metabolism and also because it tends to reduce activity

ie. These neurotransmitters improve the "calories out" side of the calories in - calories out equation.
 

jaguar43

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There you go, an improvement in glucose control with no change in body weight or body composition because the subjects ate at maintenance calories.

Dopamine is helpful for weight loss because it improves metabolism but also because it tends to increase the motivation for general physical activity and exercise.

Serotonin is not helpful for weight loss because it worsens metabolism and also because it tends to reduce activity

ie. These neurotransmitters improve the "calories out" side of the calories in - calories out equation.

How does the "motivation" theory of dopamine explain the migrating birds. Because the last time I checked birds don't diet.
 
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NathanK

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I had no idea t3 was so good at weight loss. It's amazing how the t4 the docs prescribes seems to not get much press's for helping.
It is well known that T3 burns indiscriminately both fat and muscle. I feel Haidut's, and others, posts are a bit out of context. Bodybuilders often take T3 in mega doses and balance the imminent massive loss of muscle by taking massive doses of anabolics. They dont just take 4mcg/hr T3 and shed the fat (tho that should help anyone hypothyroid).

It pains me to see respected poster Haidut say "the smart ones" take bromo or caber when they both can have very serious sides (which he has written about) and should be taken under medical supervision. Just sounds a little irresponsible to say it that way.

Im with the other poster who mentioned refeeds. Not EOD fasting, but once a week cutting calories by half. That would be a very safe and slow way of losing weight without destroying metabolism or causing excessive FFA dump (not any more than people are already doing with caffeine anyway)
 

jaguar43

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It is well known that T3 burns indiscriminately both fat and muscle. I feel Haidut's, and others, posts are a bit out of context. Bodybuilders often take T3 in mega doses and balance the imminent massive loss of muscle by taking massive doses of anabolics. They dont just take 4mcg/hr T3 and shed the fat (tho that should help anyone hypothyroid).

It pains me to see respected poster Haidut say "the smart ones" take bromo or caber when they both can have very serious sides (which he has written about) and should be taken under medical supervision. Just sounds a little irresponsible to say it that way.

Im with the other poster who mentioned refeeds. Not EOD fasting, but once a week cutting calories by half. That would be a very safe and slow way of losing weight without destroying metabolism or causing excessive FFA dump (not any more than people are already doing with caffeine anyway)

Haidut was referring to the biochemical mechanism of bromocriptine and cabergoline. One shouldn't take everything literal, he probably meant smart as in being bio-endocrine conscious. People who insisted that all one has to lower calories are ignoring the evidence.

Caffeine doesn't dump Free fatty acids into the bloodstream. You are mistaking caffeine with clenbuterol.

Its amazing how people just say whatever they think is right.
 
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It's very obvious that the Biggest Losers are just exactly that...these poor folks worked so incredibly hard and they thought they were regaining their lives, but in the end their extreme exercise routine coupled with poor nutrition and starvation levels of calories has resulted in major metabolic damage. Biggest Loser Indeed.

We see this over and over, entire industries are built off of this very concept....Nutri-System, Jenny Craig, Weight Watchers, HCG etc.

I'm pretty sure it will take years for these peeps to recover from the damage, a tough lesson for sure.

Permanent fat loss isn't simply CICO, the kinds of calories do matter......and RP is right, eradicating nutritional deficiencies, reducing stress, improving sleep and eating enough to raise metabolism is key.
 

jaguar43

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Ray said "Uncouplers are chemicals that allow oxidation to proceed without producing the usual amount of ATP"

Ray did not say "Uncouplers are chemicals that allow oxidation to proceed without producing any amount of ATP"



The numbers don't invalidate the argument or formula. Feel free to do further research on the ATP required for muscular contraction.




What Ray said "Many dog owners are aware that small dogs eat much more food in proportion to their size than big dogs do. And small dogs have a much greater life expectancy than big dogs, in some cases about twice as long "

Ray says that small dogs eat more in proportion their size to big dogs and are healthier.

What Ray doesn't say "Eat more then big dogs"

I'll use some more math here and avoid unrealistic numbers ;)

Big dog weighs 2X and eats 2Y food
Small dog weighs X and eats 1.5Y food

Small dog eats more in proportion to large dog. Small dog also eats less then large dog.

More to the point with the dogs -

Where does Ray say the small dogs are losing weight because of their fast metabolisms? He doesn't. Because they are maintaining their weight. They are eating an amount of calories that maintains their weight. This happens to be more food (relatively speaking) then a bigger dog with a slower metabolism.

Here's good definition of calorie maintenance

"As an example – If you are eating 50,000 calories a day and not gaining fat, congratulations you are still eating at maintenance. If you are eating 8 Calories a day and not losing body mass, congratulations you are also eating at maintenance. The amount of calories you consume does not determine if you are eating deficit, maintenance or surplus, the changes in your body does. Lack of a loss of body mass and absence of a gain of body fat defines eating at maintenance."
"
And here's one for eating at a calorie deficit.

"From my understanding, by definition this means an amount of food that results in loss of body mass. By this definition you cannot be in a deficit if you are not losing body mass. You can be eating less, a little, not much, like a bird, and not lose body mass since these are all subjective descriptions of an amount of food, but if you are eating less food than is needed to provide the energy you require to power your daily activities then a loss of mass must occur. This loss may be masked by fluctuations in bodyweight caused by water or the weight of the food in your digestive track (at least for a little while), but make no mistake, it is the loss of body mass that defines the deficit, not eating below an estimated amount of needed calories. The Loss of Mass is what defines a Deficit.



I guess childhood obesity isn't a thing?





No, because as I mentioned fat oxidation and lipolysis doesn't happen it a vacuum. Whether it occurs in the context of your overall caloric intake and expenditure is important for fat loss.



True, Ray suggests losing weight by increasing your metabolism, he suggests not starving yourself for improving your metabolism, and he also suggests that the healthiest/least harmful way to lose fat is very slowly

What Ray doesn't say "Increase your metabolism, and then keep increasing your food intake to the point where you don't lose weight". Amount of food / food calories is still important.



How about this one?

Bromocriptine: a novel approach to the treatment of type 2 diabetes. - PubMed - NCBI


RESEARCH DESIGN AND METHODS:

There were 22 obese subjects with type 2 diabetes randomized to receive a quick-release formulation of bromocriptine (n = 15) or placebo (n = 7) in a 16-week double-blind study. Subjects were prescribed a weight-maintaining diet to exclude any effect of changes in body weight on the primary outcome measurements. Fasting plasma glucose concentration and HbA(1c) were measured at 2- to 4-week intervals during treatment. Body composition (underwater weighing), body fat distribution (magnetic resonance imaging), oral glucose tolerance (oral glucose tolerance test [OGTT]), insulin-mediated glucose disposal, and endogenous glucose production (2-step euglycemic insulin clamp, 40 and 160 mU x min(-1) x m(-2)) were measured before and after treatment.

RESULTS:
No changes in body weight or body composition occurred during the study in either placebo- or bromocriptine-treated subjects. Bromocriptine significantly reduced HbA(1c) (from 8.7 to 8.1%, P = 0.009) and fasting plasma glucose (from 190 to 172 mg/dl, P = 0.02) levels, whereas these variables increased during placebo treatment (from 8.5 to 9.1%, NS, and from 187 to 223 mg/dl, P = 0.02, respectively). The differences in HbA(1c) (delta = 1.2%, P = 0.01) and fasting glucose (delta = 54 mg/dl, P < 0.001) levels between the bromocriptine and placebo group at 16 weeks were highly significant. The mean plasma glucose concentration during OGTT was significantly reduced by bromocriptine (from 294 to 272 mg/dl, P = 0.005), whereas it increased in the placebo group. No change in glucose disposal occurred during the first step of the insulin clamp in either the bromocriptine- or placebo-treated group. During the second insulin clamp step, bromocriptine improved total glucose disposal from 6.8 to 8.4 mg x min(-1) kg(-1) fat-free mass (FFM) (P = 0.01) and nonoxidative glucose disposal from 3.3 to 4.3 mg min(-1) x kg(-1) FFM (P < 0.05), whereas both of these variables deteriorated significantly (P < or = 0.02) in the placebo group.

There you go, an improvement in glucose control with no change in body weight or body composition because the subjects ate at maintenance calories.

Dopamine is helpful for weight loss because it improves metabolism but also because it tends to increase the motivation for general physical activity and exercise.

Serotonin is not helpful for weight loss because it worsens metabolism and also because it tends to reduce activity

ie. These neurotransmitters improve the "calories out" side of the calories in - calories out equation.

I never said that child obesity doesn't exist. I never said that chemicals that uncouple don't produce ATP ever. You are taking words out of context with a straw man argument.


But you still didn't answer the question, if Ray Peat believes estrogen cause fat oxidation. Why does the pill cause women weight gain ? You say it's important for fat reduction but I studies show that lipolysis actually cause diabetes and obesity through releasing free fatty acids into the bloodstream causing insulin resistance. Prolactin, glucocorticoids, and estrogen increase free fatty acids through fat oxidation. It is well known that prednisone and other glucocorticoids can cause diabetes and weight. The mechanism is very well known, and it lowers insulin sensitivity.

Again, I never said people need to stuff there faces with food. Ray Peat has said that one has to increase food intake when there metabolism goes up. He has also said in a recent interview that women who eat 50o calories still can't lose weight because thyroid is suppressed. But according to your argument they should be loosing weight ?

Plasma FFA levels are usually elevated in obesity because 1) the enlarged adipose tissue mass releases more FFA and 2) FFA clearance may be reduced (8). Moreover, once plasma FFA levels are elevated, they will inhibit insulin’s anti-lipolytic action, which will further increase the rate of FFA release into the circulation (9).

Obesity and Free Fatty Acids (FFA)


In the Randle cycle free fatty acids are competing with glucose. Lipolysis frees FFA from the tissue which increases them into the bloodstream.


There is a widespread acceptance in the literature that plasma nonesterified fatty acids (NEFA), also called free fatty acids (FFA), can mediate many adverse metabolic effects, most notably insulin resistance. Elevated NEFA concentrations in obesity are thought to arise from an increased adipose tissue mass. It is also argued that the process of fatty acid mobilization from adipose tissue, normally suppressed by insulin, itself becomes insulin resistant—thus, lipolysis is further increased, potentially leading to a vicious cycle.

Fatty Acids, Obesity, and Insulin Resistance: Time for a Reevaluation

It has been hypothesized that visceral adipose tissue lipolysis releases excess FFAs into the portal vein, exposing the liver to higher FFA concentrations........

We conclude that the contribution of visceral adipose tissue lipolysis to hepatic FFA delivery increases with increasing visceral fat in humans and that this effect is greater in women than in men......

Visceral adipocytes are more lipolytically active than subcutaneous adipocytes in vitro (8, 9), suggesting that the association between greater amounts of visceral fat and the metabolic complications of obesity may reflect excess FFAs originating from visceral adipose tissue lipolysis (6, 7). These FFAs are released directly into the portal vein, exposing the liver to more FFAs than would be predicted from systemic FFA availability data. Thus, enlarged visceral fat stores could increase the proportion of hepatic FFA delivery coming from visceral, as opposed to systemic, sources.


Splanchnic lipolysis in human obesity

lipolysis is central to lipid metabolism. Fat oxidation breaks down triglycerides and free fatty acids.
 
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