"Biggest Loser" Contestants Regained Weight. Peat Perspective

haidut

Member
Forum Supporter
Joined
Mar 18, 2013
Messages
19,795
Location
USA / Europe
That's an excellent summing up @haidut . Do you know of any athletes directly that have used bromocriptine for fat loss? What was their experience like? I know Lyle MacDonald recommends its use, albeit in the context of calorie restriction.

I think some of the famous tennis players like Sharapova and the Williams sisters got burned a few times for testing positive for bromo. I think all dopaminergic drugs are on the official doping list, and as you can see it is for a good reason. IMO, something like caffeine and a substance that inhibits the stress response like pregnenolone or emodin would also be a viable way to lose weight without exercising yourself to sickness. Emodin is a powerful and selective 11b-HSD1 inhibitor and some Chinese athletes are already using it for effortless weight loss given its excellent track record in diabetes II and hypercortisolemia.
 

jaguar43

Member
Joined
Oct 10, 2012
Messages
1,310
Huh? I thought it was pretty well established that caffeine can cause a rise in FFAs.

Anything can increase FFA. Stress, driving, low-blood sugar, starvation. The question is to what degree is the FFA being produce and the biological context in which it's produced.

Increasing FFA from coffee( through adrenaline specifically) isn't the same thing as increasing FFA from taking birth control or Glucocorticoids. And increasing adrenaline through coffee isn't the same as increasing adrenaline due to low biological energy. Adrenaline and dopamine increase FFA in proportion to what is needed. But not to the extended that people get diabetes. Do you understand the difference ?

A diabetic doesn't metabolize glucose the same way a non-diabetic would.


Drinking coffee seems to be very protective against developing diabetes. Its niacin and magnesium are clearly important, but it is also a rich source of antioxidants, and it helps to maintain normal thyroid and progesterone production. Chocolate is probably protective too, and it is a good source of magnesium and antioxidants.

Glucose and sucrose for diabetes.


Mechanistically thinking is going to be the downfall of this forum.
 

Peater Piper

Member
Joined
Mar 18, 2016
Messages
817
I didn't think anyone was saying caffeine was bad, just that it increases FFAs. If they're being dumped from the liver and preferentially burned (since caffeine increases fat oxidation) then that's probably one of the mechanisms that makes it protective against diabetes. Coffee is something else besides caffeine.
 

Koveras

Member
Joined
Dec 17, 2015
Messages
720
Sure, you seem to be arguing with a straw man as well...

Implying that because I said "calories are important", that I mean "calories are the only thing that are important".

Again, energy balance is defined as "Calories In - Calories Out"

Calories In includes things like:
-Food intake
-Digestive efficiency (is the food you eat broken down and metabolized efficiently, metabolized further by bacteria, speed of transit optimal, etc)

Calories Out includes things like:
-Basal metabolic rate
-Energy expended through activity

And then you have some modifying factors like macronutrient ratios, nutrient timing, food composition, micronutrients, drugs, etc.

People that say CICO doesn't work, are typically saying that they had issues with eating less and exercising more, but those are only two aspects of the energy balance equation.

It's not overly useful to simplify things to the point of saying 'calories don't matter' or 'metabolism is the only thing that matters'.

If your goal is to be relatively lean rather than just taking yourself from obese to 'healthy overweight', it helps to understand as much as possible.

In regards to the birds, when it is time to migrate various hormonal signals work to decrease metabolism, so that they gain fat weight on the same or similar intake as before (the calorie out part of the equation has decreased). They then oxidize and lose a large amount of that stored fat during their long flights, despite very high stress hormones (calorie intake is low, and output from activity is high).

How does the "motivation" theory of dopamine explain the migrating birds

I mentioned motivation for physical activity (exercise,"NEPA",and "NEAT") as one facet of dopamine's relevance for weight loss - with another facet being improved metabolism.

Probably there a multitude of factors in the birds, and motivated activity may be less relevant for them in that sense, does not necessarily mean the case is so humans.

Putting desire on a budget: dopamine and energy expenditure, reconciling reward and resources. - PubMed - NCBI

"Accumulating evidence indicates integration of dopamine function with metabolic signals, highlighting a potential role for dopamine in energy balance, frequently construed as modulating reward in response to homeostatic state. Though its precise role remains controversial, the reward perspective of dopamine has dominated investigation of motivational disorders, including obesity. In the hypothesis outlined here, we suggest instead that the primary role of dopamine in behavior is to modulate activity to adapt behavioral energy expenditure to the prevailing environmental energy conditions, with the role of dopamine in reward and motivated behaviors derived from its primary role in energy balance. Dopamine has long been known to modulate activity, exemplified by psychostimulants that act via dopamine. More recently, there has been nascent investigation into the role of dopamine in modulating voluntary activity, with some investigators suggesting that dopamine may serve as a final common pathway that couples energy sensing to regulated voluntary energy expenditure. We suggest that interposed between input from both the internal and external world, dopamine modulates behavioral energy expenditure along two axes: a conserve-expend axis that regulates generalized activity and an explore-exploit axes that regulates the degree to which reward value biases the distribution of activity. In this view, increased dopamine does not promote consumption of tasty food. Instead increased dopamine promotes energy expenditure and exploration while decreased dopamine favors energy conservation and exploitation. This hypothesis provides a mechanistic interpretation to an apparent paradox: the well-established role of dopamine in food seeking and the findings that low dopaminergic functions are associated with obesity. Our hypothesis provides an alternative perspective on the role of dopamine in obesity and reinterprets the "reward deficiency hypothesis" as a perceived energy deficit. We propose that dopamine, by facilitating energy expenditure, should be protective against obesity. We suggest the apparent failure of this protective mechanism in Western societies with high prevalence of obesity arises as a consequence of sedentary lifestyles that thwart energy expenditure."

Low Dopamine D2 Receptor Increases Vulnerability to Obesity Via Reduced Physical Activity Not Increased Appetitive Motivation. - PubMed - NCBI

"BACKGROUND:
The dopamine D2 receptor (D2R) has received much attention in obesity studies. Data indicate that D2R is reduced in obesity and that the TaqA1 D2R variant may be more prevalent among obese persons. It is often suggested that reduced D2R generates a reward deficiency and altered appetitive motivation that induces compulsive eating and contributes to obesity. Although dopamine is known to regulate physical activity, it is often neglected in these studies, leaving open the question of whether reduced D2R contributes to obesity through alterations in energy expenditure and activity.
METHODS:
We generated a D2R knockdown (KD) mouse line and assessed both energy expenditure and appetitive motivation under conditions of diet-induced obesity.
RESULTS:
The KD mice did not gain more weight or show increased appetitive motivation compared with wild-type mice in a standard environment; however, in an enriched environment with voluntary exercise opportunities, KD mice exhibited dramatically lower activity and became more obese than wild-type mice, obtaining no protective benefit from exercise opportunities.
CONCLUSIONS:
These data suggest the primary contribution of altered D2R signaling to obesity lies in altered energy expenditure rather than the induction of compulsive overeating."

Non-exercise activity thermogenesis: the crouching tiger hidden dragon of societal weight gain. - PubMed - NCBI

"Non-exercise activity thermogenesis (NEAT) is the energy expenditure of all physical activities other than volitional sporting-like exercise. NEAT includes all the activities that render us vibrant, unique, and independent beings such as working, playing, and dancing. Because people of the same weight have markedly variable activity levels, it is not surprising that NEAT varies substantially between people by up to 2000 kcal per day. Evidence suggests that low NEAT may occur in obesity but in a very specific fashion. Obese individuals appear to exhibit an innate tendency to be seated for 2.5 hours per day more than sedentary lean counterparts. If obese individuals were to adopt the lean "NEAT-o-type," they could potentially expend an additional 350 kcal per day. Obesity was rare a century ago and the human genotype has not changed over that time. Thus, the obesity epidemic may reflect the emergence of a chair-enticing environment to which those with an innate tendency to sit, did so, and became obese. To reverse obesity, we need to develop individual strategies to promote standing and ambulating time by 2.5 hours per day and also re-engineer our work, school, and home environments to render active living the option of choice."

Role of nonexercise activity thermogenesis (NEAT) in obesity. - PubMed - NCBI

"Obesity develops when there is an imbalance between energy intake and energy expenditure, which can vary daily within and among individuals. High levels of energy intake and low levels of energy expenditure contribute to obesity, both together and independently. Energy expenditure from exercise associated with formal programs is encouraged for health and weight loss, but most individuals get very little formal exercise. Nonexercise activity thermogenesis (NEAT) is the cumulative energy expended through all other activities of daily living. It is highly variable among individuals; it is controlled by the environment and, possibly, neurobiologically. Mounting evidence suggests that NEAT is critical in determining a person's susceptibility to body fat deposition and is a major factor in human obesity. Recent research supported by the Minnesota Partnership for Biotechnology and Medical Genomics, a state-sponsored collaborative effort of the University of Minnesota and Mayo Clinic, is helping to define the complex brain regulation of NEAT and its role in obesity. This article reviews the evidence for NEAT and the impact of NEAT on obesity."

Role of nonexercise activity thermogenesis in resistance to fat gain in humans. - PubMed - NCBI

"Humans show considerable interindividual variation in susceptibility to weight gain in response to overeating. The physiological basis of this variation was investigated by measuring changes in energy storage and expenditure in 16 nonobese volunteers who were fed 1000 kilocalories per day in excess of weight-maintenance requirements for 8 weeks. Two-thirds of the increases in total daily energy expenditure was due to increased nonexercise activity thermogenesis (NEAT), which is associated with fidgeting, maintenance of posture, and other physical activities of daily life. Changes in NEAT accounted for the 10-fold differences in fat storage that occurred and directly predicted resistance to fat gain with overfeeding (correlation coefficient = 0.77, probability < 0.001). These results suggest that as humans overeat, activation of NEAT dissipates excess energy to preserve leanness and that failure to activate NEAT may result in ready fat gain."

It seems there is substantial evidence that a large part of dopamine's role in weight loss is occurring through increasing various forms of physical activity, or in other words "calories out". The improved glucose control from bromocriptine and other dopamine agonists is likely in large part from those individuals simply moving around and fidgeting more. The weight loss from bromocriptine can be countered easily by eating more (as was shown in a well designed study.

Finally in regards to fat oxidation, I said that it is a necessary part of losing fat. If whatever diet you're on is causing you to lose fat, then the fat that you previously had stored has very likely been released from fat cells through lipolysis and gone through oxidation on it's way out. In some circumstances, very slow fat loss can possibly occur without being run through the mitochondria. This would not be something that accounts for large amounts of fat loss from thyroid, DNP, or bromocriptine with diet.

Straw man #2 is implying that because I said fat oxidation occurs with weight loss, that anything that increases fat oxidation would cause weight loss.

Things can increase fat oxidation but not cause weight loss, due to the myriad of other factors involved. Even if estrogen did help with fat loss, it would not be desirable for looking leaner, due to edema, nor because of some of the other health implications.

One other factor then to consider is that almost all of the stress hormones such as cortisol, growth hormone, and estrogen can cause edema. Resolution of edema is one likely reason why improving metabolism with thyroid and diet could cause rapid weight loss (those old myxedema photos floating around here being one example).


To clarify my position

- Ray's approach to diet seems to be an optimal way to live long and healthy and for some individuals helps move them into a healthy BMI range (but is not ideal or the easiest for getting very lean - which probably isn't healthy anyway)

-Ray's approach also seems to make many individuals gain weight, and for these individuals, it is probably advisable to be conscious of calories/portions while they work to troubleshoot other issues that may be involved

-Many approaches to fat loss are more effective for fat loss than Ray's approach, in the short term. This does not make them healthy, advisable, or likely to be successful long term. Just because less obvious factors than food and exercise come more into play longer term, does not invalidate the importance of energy balance in anyone trying to achieve their ideal physique.
 
Last edited:

superhuman

Member
Joined
May 31, 2013
Messages
1,124
@haidut that is interesting. Do you know how the chinese and other athletes use emodin to lose weight? doses and frequency etc?
 
Joined
Jan 17, 2016
Messages
175
I think some of the famous tennis players like Sharapova and the Williams sisters got burned a few times for testing positive for bromo.

Technically it's Williams brothers.:shh:
 

haidut

Member
Forum Supporter
Joined
Mar 18, 2013
Messages
19,795
Location
USA / Europe
@haidut that is interesting. Do you know how the chinese and other athletes use emodin to lose weight? doses and frequency etc?

There is a lot of research in China with rhubarb and other emodin-containing herbs for weight loss, diabetes, performance improvement, etc. Here is a news piece on that.
Novel diabetes hope comes from Chinese herbs | (e) Science News

Given that emodin inhibits 11b-HSD1 in nanomolar concentrations, it looks like even small amounts would work but the in vivo animal studies used human equivalent doses of 300mg+ daily.
 

jaguar43

Member
Joined
Oct 10, 2012
Messages
1,310
Sure, you seem to be arguing with a straw man as well...

Implying that because I said "calories are important", that I mean "calories are the only thing that are important".

Again, energy balance is defined as "Calories In - Calories Out"

Calories In includes things like:
-Food intake
-Digestive efficiency (is the food you eat broken down and metabolized efficiently, metabolized further by bacteria, speed of transit optimal, etc)

Calories Out includes things like:
-Basal metabolic rate
-Energy expended through activity

And then you have some modifying factors like macronutrient ratios, nutrient timing, food composition, micronutrients, drugs, etc.

The question is how does one determined calorie intake ? How does one equate metabolic rate with the amount of calories they need ? Referring to the charts where they tell someone that they have to eat a certain amount of calories by how much they weigh is insufficient because it does not take into consideration the Basal Metabolic Rate. If two people weighed the same and one was given thyroid hormone and the other was not. How would one determine the amount of calories that they each need in accordance with metabolic rate ?

People that say CICO doesn't work, are typically saying that they had issues with eating less and exercising more, but those are only two aspects of the energy balance equation.

So what your saying to people who want to lose weight is, eat less worked out more ?

It's not overly useful to simplify things to the point of saying 'calories don't matter' or 'metabolism is the only thing that matters'.

If your goal is to be relatively lean rather than just taking yourself from obese to 'healthy overweight', it helps to understand as much as possible.

What is this "healthy overweight" that you are implying. You need to be specific on what you mean. Are you using BMI to definite what is considered overweight and not "overweight".


In regards to the birds, when it is time to migrate various hormonal signals work to decrease metabolism, so that they gain fat weight on the same or similar intake as before (the calorie out part of the equation has decreased). They then oxidize and lose a large amount of that stored fat during their long flights, despite very high stress hormones (calorie intake is low, and output from activity is high).

The study doesn't say that they lose fat on their long flights. They said that the birds become lean at the end of the season. Don't make things up.

Hepatic glucose production and gluconeogenesis rise to supply glucose to the CNS during prolonged periods of winter food deprivation.[5,6] 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.



I mentioned motivation for physical activity (exercise,"NEPA",and "NEAT") as one facet of dopamine's relevance for weight loss - with another facet being improved metabolism.

Probably there a multitude of factors in the birds, and motivated activity may be less relevant for them in that sense, does not necessarily mean the case is so humans.

Putting desire on a budget: dopamine and energy expenditure, reconciling reward and resources. - PubMed - NCBI

"Accumulating evidence indicates integration of dopamine function with metabolic signals, highlighting a potential role for dopamine in energy balance, frequently construed as modulating reward in response to homeostatic state. Though its precise role remains controversial, the reward perspective of dopamine has dominated investigation of motivational disorders, including obesity. In the hypothesis outlined here, we suggest instead that the primary role of dopamine in behavior is to modulate activity to adapt behavioral energy expenditure to the prevailing environmental energy conditions, with the role of dopamine in reward and motivated behaviors derived from its primary role in energy balance. Dopamine has long been known to modulate activity, exemplified by psychostimulants that act via dopamine. More recently, there has been nascent investigation into the role of dopamine in modulating voluntary activity, with some investigators suggesting that dopamine may serve as a final common pathway that couples energy sensing to regulated voluntary energy expenditure. We suggest that interposed between input from both the internal and external world, dopamine modulates behavioral energy expenditure along two axes: a conserve-expend axis that regulates generalized activity and an explore-exploit axes that regulates the degree to which reward value biases the distribution of activity. In this view, increased dopamine does not promote consumption of tasty food. Instead increased dopamine promotes energy expenditure and exploration while decreased dopamine favors energy conservation and exploitation. This hypothesis provides a mechanistic interpretation to an apparent paradox: the well-established role of dopamine in food seeking and the findings that low dopaminergic functions are associated with obesity. Our hypothesis provides an alternative perspective on the role of dopamine in obesity and reinterprets the "reward deficiency hypothesis" as a perceived energy deficit. We propose that dopamine, by facilitating energy expenditure, should be protective against obesity. We suggest the apparent failure of this protective mechanism in Western societies with high prevalence of obesity arises as a consequence of sedentary lifestyles that thwart energy expenditure."

Low Dopamine D2 Receptor Increases Vulnerability to Obesity Via Reduced Physical Activity Not Increased Appetitive Motivation. - PubMed - NCBI

"BACKGROUND:
The dopamine D2 receptor (D2R) has received much attention in obesity studies. Data indicate that D2R is reduced in obesity and that the TaqA1 D2R variant may be more prevalent among obese persons. It is often suggested that reduced D2R generates a reward deficiency and altered appetitive motivation that induces compulsive eating and contributes to obesity. Although dopamine is known to regulate physical activity, it is often neglected in these studies, leaving open the question of whether reduced D2R contributes to obesity through alterations in energy expenditure and activity.
METHODS:
We generated a D2R knockdown (KD) mouse line and assessed both energy expenditure and appetitive motivation under conditions of diet-induced obesity.
RESULTS:
The KD mice did not gain more weight or show increased appetitive motivation compared with wild-type mice in a standard environment; however, in an enriched environment with voluntary exercise opportunities, KD mice exhibited dramatically lower activity and became more obese than wild-type mice, obtaining no protective benefit from exercise opportunities.
CONCLUSIONS:
These data suggest the primary contribution of altered D2R signaling to obesity lies in altered energy expenditure rather than the induction of compulsive overeating."

Non-exercise activity thermogenesis: the crouching tiger hidden dragon of societal weight gain. - PubMed - NCBI

"Non-exercise activity thermogenesis (NEAT) is the energy expenditure of all physical activities other than volitional sporting-like exercise. NEAT includes all the activities that render us vibrant, unique, and independent beings such as working, playing, and dancing. Because people of the same weight have markedly variable activity levels, it is not surprising that NEAT varies substantially between people by up to 2000 kcal per day. Evidence suggests that low NEAT may occur in obesity but in a very specific fashion. Obese individuals appear to exhibit an innate tendency to be seated for 2.5 hours per day more than sedentary lean counterparts. If obese individuals were to adopt the lean "NEAT-o-type," they could potentially expend an additional 350 kcal per day. Obesity was rare a century ago and the human genotype has not changed over that time. Thus, the obesity epidemic may reflect the emergence of a chair-enticing environment to which those with an innate tendency to sit, did so, and became obese. To reverse obesity, we need to develop individual strategies to promote standing and ambulating time by 2.5 hours per day and also re-engineer our work, school, and home environments to render active living the option of choice."

Role of nonexercise activity thermogenesis (NEAT) in obesity. - PubMed - NCBI

"Obesity develops when there is an imbalance between energy intake and energy expenditure, which can vary daily within and among individuals. High levels of energy intake and low levels of energy expenditure contribute to obesity, both together and independently. Energy expenditure from exercise associated with formal programs is encouraged for health and weight loss, but most individuals get very little formal exercise. Nonexercise activity thermogenesis (NEAT) is the cumulative energy expended through all other activities of daily living. It is highly variable among individuals; it is controlled by the environment and, possibly, neurobiologically. Mounting evidence suggests that NEAT is critical in determining a person's susceptibility to body fat deposition and is a major factor in human obesity. Recent research supported by the Minnesota Partnership for Biotechnology and Medical Genomics, a state-sponsored collaborative effort of the University of Minnesota and Mayo Clinic, is helping to define the complex brain regulation of NEAT and its role in obesity. This article reviews the evidence for NEAT and the impact of NEAT on obesity."

Role of nonexercise activity thermogenesis in resistance to fat gain in humans. - PubMed - NCBI

"Humans show considerable interindividual variation in susceptibility to weight gain in response to overeating. The physiological basis of this variation was investigated by measuring changes in energy storage and expenditure in 16 nonobese volunteers who were fed 1000 kilocalories per day in excess of weight-maintenance requirements for 8 weeks. Two-thirds of the increases in total daily energy expenditure was due to increased nonexercise activity thermogenesis (NEAT), which is associated with fidgeting, maintenance of posture, and other physical activities of daily life. Changes in NEAT accounted for the 10-fold differences in fat storage that occurred and directly predicted resistance to fat gain with overfeeding (correlation coefficient = 0.77, probability < 0.001). These results suggest that as humans overeat, activation of NEAT dissipates excess energy to preserve leanness and that failure to activate NEAT may result in ready fat gain."

It seems there is substantial evidence that a large part of dopamine's role in weight loss is occurring through increasing various forms of physical activity, or in other words "calories out". The improved glucose control from bromocriptine and other dopamine agonists is likely in large part from those individuals simply moving around and fidgeting more. The weight loss from bromocriptine can be countered easily by eating more (as was shown in a well designed study.

Bromocriptines mechanism for weight loss or improving health ( which doesn't necessarily lead to weight loss). Is lowering free fatty acids, improving insulin sensitivity, Decreasing prolactin ( which is diabetogenic according to Ray Peat) lowering insulin. Dopamine is also a serotonin antagonist. Ray Peat has said that the dopamine agonist is really a serotonin antagonist. And serotonin involvement in weight gain is widely known.

To say that the weight loss effect by bromocriptine is due to increasing motivation by increasing dopamine isn't wrong on the surface. But it doesn't explain the weight loss effect of things like 2'4-dinitrophenol ? DNP increase dopamine and even if it did, it still wouldn't explain its mechanism.



Finally in regards to fat oxidation, I said that it is a necessary part of losing fat. If whatever diet you're on is causing you to lose fat, then the fat that you previously had stored has very likely been released from fat cells through lipolysis and gone through oxidation on it's way out. In some circumstances, very slow fat loss can possibly occur without being run through the mitochondria. This would not be something that accounts for large amounts of fat loss from thyroid, DNP, or bromocriptine with diet.

I have posted a few studies showing that lipolysis is actually a major factor in become a type 2 diabetic.By releasing free fatty acids into the blood stream it competes with glucose for the substrate. This is known as the Randle Cycle. Metabolic Syndrome is associated with the inability to oxidized glucose. Symptoms including in metabolic syndrome are obesity, fatigue, high blood pressure,elevated fasting glucose. Here is a quote from the bird migrating example from the bromocriptine study

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.


Straw man #2 is implying that because I said fat oxidation occurs with weight loss, that anything that increases fat oxidation would cause weight loss.

Things can increase fat oxidation but not cause weight loss, due to the myriad of other factors involved. Even if estrogen did help with fat loss, it would not be desirable for looking leaner, due to edema, nor because of some of the other health implications.

One other factor then to consider is that almost all of the stress hormones such as cortisol, growth hormone, and estrogen can cause edema. Resolution of edema is one likely reason why improving metabolism with thyroid and diet could cause rapid weight loss (those old myxedema photos floating around here being one example).

Well you did say

"Finally in regards to fat oxidation, I said that it is a necessary part of losing fat."-koveras

Fat oxidation is a biochemical process. If fat oxidation doesn't lead to weight loss in other forms then its most likely not to be the biochemical pathway that leads to weight loss to begin with. Mechanisms that cause weight loss in different chemicals like DNP, thyroid, bromocriptine interpenetrate. They all do more things in common regarding the biochemical and endocrinological metabolic pathways than other chemicals and hormones.

But it is a fact that estrogen causes weight gain. Just ask any women on birth control.


To clarify my position

- Ray's approach to diet seems to be an optimal way to live long and healthy and for some individuals helps move them into a healthy BMI range (but is not ideal or the easiest for getting very lean - which probably isn't healthy anyway)

-Ray's approach also seems to make many individuals gain weight, and for these individuals, it is probably advisable to be conscious of calories/portions while they work to troubleshoot other issues that may be involved

-Many approaches to fat loss are more effective for fat loss than Ray's approach, in the short term. This does not make them healthy, advisable, or likely to be successful long term. Just because less obvious factors than
food and exercise come more into play longer term, does not invalidate the importance of energy balance in anyone trying to achieve their ideal physique.

If people gain weight taking Ray Peats advice. It isn't because Ray Peat is wrong. He has written about that topic and he goes into depth in his articles of the biochemical and endocrinological mechanisms of obesity, diabetes, hypothyroidism ect.

Did it ever occur to you that people aren't taking the time to understand his work ? Or providing Feedback for themselves in regard to how they are reacting to different types of food, chemicals, hormones.


The dominant cultures are creating a spoiled-child attitude in more and more people, an unwillingness to make an effort to understand things, or to independently solve problems. The ‘professions,’ the media, and manipulators generally depend on people who don't care to think.

-Ray Peat
 

Koveras

Member
Joined
Dec 17, 2015
Messages
720
The study doesn't say that they lose fat on their long flights. They said that the birds become lean at the end of the season. Don't make things up.

The dominant cultures are creating a spoiled-child attitude in more and more people, an unwillingness to make an effort to understand things, or to independently solve problems. The ‘professions,’ the media, and manipulators generally depend on people who don't care to think.

-Ray Peat

Do you you fact check before accusing others of making things up and make an honest effort yourself to understand things?

Here is some evidence that just as I said before, since I took the time to research my statements, that while stress hormones and certain neurobiological changes cause birds to gain weight pre-migration, that they then lose fat during their long flights, with high stress hormones, and that having a certain amount of fat is actually protective from stress, and getting too lean greatly increases the susceptibility to negative effects of stress.

Protein loss during long-distance migratory flight in passerine birds: adaptation and constraint. - PubMed - NCBI

"During long-distance flights, birds catabolize not only fat but also protein. Because there is no storage form of protein, protein catabolism entails a structural or functional loss. In this study, we investigated which organs were most reduced in lean mass during different phases of fat store loss and whether protein loss can be regarded as adaptive or as a constraint. Body and organ composition were analysed both during the autumn migration over continental Europe (sample from Switzerland) and after a long-distance flight over the Sahara and the Mediterranean Sea in spring (sample from Ventotene, Italy) in four species of passerine bird: pied flycatcher Ficedula hypoleuca, willow warbler Phylloscopus trochilus, garden warbler Sylvia borin and barn swallow Hirundo rustica. Large variations in protein mass occurred when long non-stop flights were performed. After a long-distance flight, birds showed a marked increase in net protein loss when fat stores were nearing depletion (analogous to the late phase of endurance fasting when the rate of protein catabolism is increased). When fat reserves were above approximately 5-10 %, protein was derived from all organs, but particularly from the breast muscles. When fat stores diminished further and protein catabolism increased, the mass of the digestive organs was reduced fastest. When the decrease in breast muscle mass during flight was regarded in terms of potential flight performance, it appeared that the use of breast muscle protein with decreasing body mass can be regarded as adaptive as long as fat stores did not reach a critical level. Below approximately 5-10 % body fat, however, protein loss reduced flight performance. This demonstrates that the phase of fasting (the size of the remaining fat stores) is an important condition for understanding the occurrence and effects of protein loss during endurance flights."

Regulation of protein breakdown and adrenocortical response to stress in birds during migratory flight. - PubMed - NCBI

"During long-term fasting at rest, protein utilization is maintained at low levels until it increases at a threshold adiposity. This study examines 1) whether such a shift in energy substrate use also occurs during endurance exercise while fasting, 2) the role of corticosterone, and 3) the adrenocortical response to an acute stressor. Ten species of migrating birds caught after an endurance flight over at least 500 km were examined. Plasma uric acid and corticosterone levels were low in birds with fat stores >5% of body mass and high in birds with smaller fat stores. Corticosterone levels were very high in birds with no visible fat stores and emaciated breast muscles. Corticosterone levels increased with handling time only in birds with large fat stores. These findings suggest that 1) migrating birds with appreciable fat stores are not stressed by endurance flight, 2) a metabolic shift (increased protein breakdown), regulated by an endocrine shift (medium corticosterone levels), occurs at a threshold adiposity, as observed in birds at rest, 3) adrenocortical response to an acute stressor is inhibited after this shift, and 4) an adrenocortical response typical for an emergency situation (high corticosterone levels) is only reached when muscle protein is dangerously low."

Empirical evidence for differential organ reductions during trans-oceanic bird flight. - PubMed - NCBI

"Since the early 1960s it has been held that migrating birds deposit and use only fat as fuel during migratory flight, with the non-fat portion of the bodyremaining homeostatic. Recent evidence from field studies has shown large changes in organ sizes in fuelling birds, and theory on fuel use suggests protein may be a necessary fuel during flight. However, an absence of information on the body condition of migrants before and after a long flight has hampered understanding of the dynamics of organs during sustained flight. We studied body condition in a medium-sized shorebird, the great knot (Calidris tenuirostris), before and after a flight of 5400 km from Australia to China during northward migration. Not only did these birds show the expected large reduction in fat content after migration, there was also a decrease in lean tissue mass, with significant decreases in seven organs. The reduction in functional components is reflected in a lowering of the basal metabolic rate by 42% [corrected]. Recent flight models have tried to separate the 'flexible' part of the body from the constant portion. Our results suggest that apart from brains and lungs no organs are homeostatic during long-distance flight. Such organ reductions may be a crucial adaptation for long-distance flight in birds."

Relationships between nutrient storage and nutrient utilisation in long-term fasting birds and mammals

"Birds and mammals adapt to prolonged fasting by mobilising fat stores and minimising protein loss. This strategy ends with an increase in protein utilisation associated with behavioural changes promoting food foraging. We review here the relationships between adiposity and the pattern of fuel utilisation during fasting. First, animals with small initial fat stores are unable to spare body proteins. Second, moderate fat stores initiate protein conservation. Third, higher initial adiposities enable longer fasts by allowing a more efficient and prolonged phase of protein sparing; however, there is a limit to the lowering of protein utilization since proteins account for no less than 4% of energy expenditure. Lastly, accumulation of too much fat could be detrimental for survival to fasting, primarily because a lethal depletion of body proteins may be reached before foraging behaviour is stimulated by a critical depletion of fat stores. Birds are also able to adapt the level of fat and protein storage to the specific energy and nutrient needs of the subsequent periods of food deprivation. For example, King Penguin Aptenodytes patagonicus chicks buildup more lipids before their long winter fast than do adults before the shorter incubating fast, and adult penguins build up more protein reserves before the molting fast during which they use endogenous protein for feather synthesis."

What is this "healthy overweight" that you are implying. You need to be specific on what you mean. Are you using BMI to definite what is considered overweight and not "overweight".

Referring to what Haidut discusses from a Peat perspective here:

Scientists now think that being fat can protect your health
Overweight people have lower mortality
Being fat in middle age protects against dementia and AD
The Obesity "paradox" - Confirmed Once Again

Bromocriptines mechanism for weight loss or improving health ( which doesn't necessarily lead to weight loss). Is lowering free fatty acids, improving insulin sensitivity, Decreasing prolactin ( which is diabetogenic according to Ray Peat) lowering insulin. Dopamine is also a serotonin antagonist. Ray Peat has said that the dopamine agonist is really a serotonin antagonist. And serotonin involvement in weight gain is widely known.

To say that the weight loss effect by bromocriptine is due to increasing motivation by increasing dopamine isn't wrong on the surface. But it doesn't explain the weight loss effect of things like 2'4-dinitrophenol ? DNP increase dopamine and even if it did, it still wouldn't explain its mechanism.

Why are you lumping everything together?

-Bromocriptine works through dopamine, which largely works through increasing various forms of activity
-Dopamine is a serotonin antagonist, yes, and what does serotonin do? Makes people depressed and inactive
-DNP works through mitochondrial uncoupling, which strongly increases fat oxidation in the absence of sufficient carbohydrates

So what your saying to people who want to lose weight is, eat less worked out more ?

No, I think people should work to improve their health, happiness, and metabolism, exercise moderately, and if they are doing all those things and still gaining weight, maintaining weight, or they lost weight initially, weight loss has stalled, and they wish to continue losing weight ...they may want to consider eating less....
 
Last edited:

Tarmander

Member
Joined
Apr 30, 2015
Messages
3,753
This might be slightly off topic...but here goes. Women who have lost their period, and under eat, almost always have to cease doing exercise to regain said period. Doesn't matter how much refeeding they do, until they stop exercising, their period will not return.

In a similar vein, for people who have chronically dieted and exercised, I think gaining weight is a must for their health to be regained. You can mess around with vitamins and supplements in an attempt to regain lost sleep and energy, but from my experience reading other's logs and attempts, they just spin their wheels until they put on the weight that their body really wants to put on.

This kind of relates to set point theory. Your body has a specific amount of fat it wants and it will defend that point. I think people get mixed up with fat and muscle. Muscle you definitely have more control over; you work it and it'll grow. But fat is more about what your body wants(although pufa will almost assuredly raise your set point over time). Somehow people think that they should be able to manipulate this organ and fight it into what They want...
 

jaguar43

Member
Joined
Oct 10, 2012
Messages
1,310
Do you you fact check before accusing others of making things up and make an honest effort yourself to understand things?

Here is some evidence that just as I said before, since I took the time to research my statements, that while stress hormones and certain neurobiological changes cause birds to gain weight pre-migration, that they then lose fat during their long flights, with high stress hormones, and that having a certain amount of fat is actually protective from stress, and getting too lean greatly increases the susceptibleility to negative effects of stress.

At this point you are arguing semantics. I was taking about the information regarding the study. The study never said the birds got lean during their transitional stage during migration. You can posted hundreds of study saying one thing and it still doesn't address the question. Just like there are thousands of studies showing that estrogen is beneficial. That doesn't prove that it's beneficial. So here is the question:

Why Did the birds develop insulin resistance and obesity while hibernation, migration, overwintering and when food availability was low ? You say that eating less will lead to fat loss. But that is exactly the opposite of what happened.


Referring to what Haidut discusses from a Peat perspective here:

Scientists now think that being fat can protect your health
Overweight people have lower mortality
Being fat in middle age protects against dementia and AD
The Obesity "paradox" - Confirmed Once Again



Why are you lumping everything together?

-Bromocriptine works through dopamine, which largely works through increasing various forms of activity
-Dopamine is a serotonin antagonist, yes, and what does serotonin do? Makes people depressed and inactive
-DNP works through mitochondrial uncoupling, which strongly increases fat oxidation in the absence of sufficient carbohydrates

I meant, Not increase dopamine in the last sentence.

DNP lowers , insulin, triglyceride and improves glucose tolerance and cures type 2 diabetes like bromocriptine. They both do similar things like I said before.

Mild mitochondrial uncoupling in mice affects energy metabolism, redox balance and longevity. - PubMed - NCBI

Controlled-release mitochondrial protonophore reverses diabetes and steatohepatitis in rats. - PubMed - NCBI

No, I think people should work to improve their health, happiness, and metabolism, exercise moderately, and if they are doing all those things and still gaining weight, maintaining weight, or they lost weight initially, weight loss has stalled, and they wish to continue losing weight ...they may want to consider eating less....

Ray Peat suggest increasing metabolic rate to lose weight, which will be different for everyone and to different degrees. The weight lost by eating less is most likely to be muscle and tissue.
 

Koveras

Member
Joined
Dec 17, 2015
Messages
720
Commentary from Brad Pilon

"Let’s talk about that ‘Biggest Loser Study’ everyone is talking about…

But we’re going to save some time and cut right to the chase.

All this study showed me was that you can’t out metabolism a bad diet.

Why?

Let’s start at the beginning, when these people had a measured resting metabolic of over 2,600!!!

That is an enormous amount of calories being expended at rest.

As an example, my resting metabolic rate is around 1,700. My good friend John Barban, who is 2 inches taller than me and carries around 15-20 pounds of more lean muscle then me has a resting metabolic rate of 1,850.

These people had a resting metabolic rate of 2,600…. almost 1,000 calories higher than mine!!

They also had almost 50% body fat at a weight of well over 300 pounds.

This was their supposed baseline… but I just don’t see how any sane scientist could call these numbers ‘baseline’ or ‘normal’

To me, they are obviously elevated. A state of hypermetabolism - I don’t know how else to say it, but these people were not well and it showed in their resting metabolic rate measurements.

At the end of 30 weeks of competition, they had lost more than 100 pounds (averaging more than 4 pounds per week of loss!!!)

They also lost almost 25 pounds of Lean body mass!

And their metabolic rate was measured at right around 2,000 calories (still much, much higher than mine)

THEN 6 years later these people had gained back over 12 pounds of lean body mass and (unfortunately) almost 80 pounds of fat.

Their resting metabolic rate was STILL around 1,900.

Still higher than most people.

The bottom line is In 6 years they gained back much of their weight, in spite of having a high metabolism.

YES the researchers in this study did use equations to guess at a predicted metabolic rate that was almost 500 calories higher… That’s what all the hoopla is about

These people’s high metabolisms weren’t as high as the scientists think they should have been based on they predictions?!?!.

That’s what the media is latching on to.

But I see something much different… they gained a lot of weight despite having a metabolism that is MUCH HIGHER than the average person.

So yes, there is a relationship between your metabolic rate and your ability to lose weight and your ability to keep the weight off… but don’t let the media fool you, these people weren’t suffering from a metabolic rate of zero… they just had a metabolic rate lower than this particular group of scientists expected (mind you it was higher than other equations would have predicted).

…There was much more going on with their physiology then just their metabolic rates.

In fact the most interesting part of the study was the wild fluctuations in Leptin that occurred in these groups while they were losing weight. Just another piece of the puzzle… a puzzle that obviously includes many unmeasured lifestyle factors.

In the end I want you to know that you can lose weight despite what your metabolism is or isn’t, and maintaining that weight loss takes significant adaptations to your lifestyle… "
 

Brandon

Member
Joined
Jan 16, 2016
Messages
100
"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!"

You're bold....
 

haidut

Member
Forum Supporter
Joined
Mar 18, 2013
Messages
19,795
Location
USA / Europe
"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!"

You're bold....

Well, the words in quotation marks are from the actual article. So, when the officially recognized experts are surprised/scared at something that has been known for such a long time, the situation does not look good for us. Imagine what the run-of-the-mill doctor in his office knows then. Not much, would be my guess... And now imagine what you are being prescribed and how solid the science behind it is. Even scarier, right?
 

Koveras

Member
Joined
Dec 17, 2015
Messages
720
Leigh Peele on the Biggest Loser Article

"I like studies that control for variables as any good research enthusiast should. This 2008 study shows the decrease in RMR was pretty insignificant but the decrease in daily energy expenditure was much more notable. In general, we see in research what slows down more is not resting metabolic rate (RMR), but our activity levels. Could those contestants have ramped up their activity at the time of testing? We don’t know. It wasn’t controlled. To me, while it is an interesting free-living experiment to chew on, it is not the smoking gun which says an RMR decrease is the reason we have a hard time keeping weight off once it is lost or losing it in the first place."

Long-term persistence of adaptive thermogenesis in subjects who have maintained a reduced body weight
 

Brandon

Member
Joined
Jan 16, 2016
Messages
100
Well, the words in quotation marks are from the actual article. So, when the officially recognized experts are surprised/scared at something that has been known for such a long time, the situation does not look good for us. Imagine what the run-of-the-mill doctor in his office knows then. Not much, would be my guess... And now imagine what you are being prescribed and how solid the science behind it is. Even scarier, right?
Scarier than Chucky.
 

jaguar43

Member
Joined
Oct 10, 2012
Messages
1,310
Commentary from Brad Pilon

"Let’s talk about that ‘Biggest Loser Study’ everyone is talking about…

But we’re going to save some time and cut right to the chase.

All this study showed me was that you can’t out metabolism a bad diet.

Why?

Let’s start at the beginning, when these people had a measured resting metabolic of over 2,600!!!

That is an enormous amount of calories being expended at rest.

As an example, my resting metabolic rate is around 1,700. My good friend John Barban, who is 2 inches taller than me and carries around 15-20 pounds of more lean muscle then me has a resting metabolic rate of 1,850.

These people had a resting metabolic rate of 2,600…. almost 1,000 calories higher than mine!!

They also had almost 50% body fat at a weight of well over 300 pounds.

This was their supposed baseline… but I just don’t see how any sane scientist could call these numbers ‘baseline’ or ‘normal’

To me, they are obviously elevated. A state of hypermetabolism - I don’t know how else to say it, but these people were not well and it showed in their resting metabolic rate measurements.

At the end of 30 weeks of competition, they had lost more than 100 pounds (averaging more than 4 pounds per week of loss!!!)

They also lost almost 25 pounds of Lean body mass!

And their metabolic rate was measured at right around 2,000 calories (still much, much higher than mine)

THEN 6 years later these people had gained back over 12 pounds of lean body mass and (unfortunately) almost 80 pounds of fat.

Their resting metabolic rate was STILL around 1,900.

Still higher than most people.

The bottom line is In 6 years they gained back much of their weight, in spite of having a high metabolism.

YES the researchers in this study did use equations to guess at a predicted metabolic rate that was almost 500 calories higher… That’s what all the hoopla is about

These people’s high metabolisms weren’t as high as the scientists think they should have been based on they predictions?!?!.

That’s what the media is latching on to.

But I see something much different… they gained a lot of weight despite having a metabolism that is MUCH HIGHER than the average person.

So yes, there is a relationship between your metabolic rate and your ability to lose weight and your ability to keep the weight off… but don’t let the media fool you, these people weren’t suffering from a metabolic rate of zero… they just had a metabolic rate lower than this particular group of scientists expected (mind you it was higher than other equations would have predicted).

…There was much more going on with their physiology then just their metabolic rates.

In fact the most interesting part of the study was the wild fluctuations in Leptin that occurred in these groups while they were losing weight. Just another piece of the puzzle… a puzzle that obviously includes many unmeasured lifestyle factors.

In the end I want you to know that you can lose weight despite what your metabolism is or isn’t, and maintaining that weight loss takes significant adaptations to your lifestyle… "

The question is, how are you measuring "metabolic rate" ?

The Basal metabolic rate test ( basal metabolism test termed used by Broda Barnes ) was really the only effected way to measure the metabolic rate. But even that test had major flaws. If the patient came in stress or agitated the test read off the charts. The patient was advice to not eat breakfast and take their time coming to the hospital slowly, then wait thirty minutes. If they lived to far away they were hospitalized over night. On top of that the test was administrated by putting clips on one's nose and breathing through a tube which was already stress inducing.


Broda Barnes believe that this test wasn't very efficient. He stated that it was administered incorrectly at times. By not taking into account if the patient was in a hurry or relax enough to give a correct reading. In his book hypothyroidism he told a story of a young college student who did the test in a hurry. The results were reading hyperthyroidism and the doctor advise her to get a thyroidectomy ! Only the third time was correct and it read a below metabolic rate. If there are people who are administrating the BMT. I would still be suspicious of the results because of the room of error.

Again, here you are making the assumption that people who are actually obese are actually hypermetabolic. Here is your exact quote.

These people had a resting metabolic rate of 2,600…. almost 1,000 calories higher than mine!!

They also had almost 50% body fat at a weight of well over 300 pounds.

I am remind of a quote by Ray Peat in one of his articles.

If a person is eating only about 1800 calories per day, and has a steady and normal body weight, any “hyperthyroidism” is strictly metaphysical, or as they say, “clinical.”

Preventing and treating cancer with progesterone.



Lat point, you state

but don’t let the media fool you, these people weren’t suffering from a metabolic rate of zero… they just had a metabolic rate lower than this particular group of scientists expected (mind you it was higher than other equations would have predicted).

I would like to see that study. Unfortunately the media isn't making Ray Peats argument. It is making your argument. Selling treadmills, protein shakes /bars, gym memberships. Even the Biggest Loser is pretty much a public relations campaign to promote working out, eating less and be screamed at by a trainer.
 
Last edited:

NathanK

Member
Joined
May 30, 2015
Messages
684
Location
Austin, TX
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.
I stand by what I said. This is a delicate and complicated subject. There are a lot of people, smart included, that are looking for magic pills on this forum and elsewhere. No disrespect to H, but with great influence comes responsibility. It is what it is.

Caffeine absolutely increases FFA in excessive doses. There is zero debate about that. As far as excessive adipose increases FFA is speculative. I posted a study last year that shows the body modulates NEFA independent of adipose mass. I'd look to find it for you, but I just moved and dont have time to get into any thread context conflicts.
 
EMF Mitigation - Flush Niacin - Big 5 Minerals

Similar threads

Back
Top Bottom