Metabolic Efficiency And Metabolic Rate - Doubt

[gilson dantas]

@Mittir @Blossom @narouz @burtlancast
I have been treating a prostate tumor based on the physiological and nutritional principles that I have learned on R Peat writings; and I think I'm evolving more or less well, although with some difficulty to adjust t3 supplementation;
If possible, I would like any of you help me to solve some questions, and in this way I can expand my understanding of R Peat´s physiological thinking; specifically on the concept of metabolic rate in health and disease:

1 - In few words, what is the difference between metabolic efficiency and the oxidative burning of glucose?
2 - If we have the stress of fasting, the metabolic rate drops? OK, but in the case of caloric restriction, the metabolic rate increases? Why? What is the mechanism? Maybe because there is less calories, then metabolic rate rises?
3 - I gained weight, 16 pounds, these months on a diet R Peat´s style. This is a expected effect of a phase of transitiondominated by cortisol going to a stage dominated by T3? I mean: I am not more dominated by cortisol but the thyroid does not already own hegemony in my metabolism? In this case we have a drop in metabolic rate? [Since, as I see every day, the temperature does not go beyond the 36 C? ]
4 - How to understand the claim of Kate Deering that if someone starts to primarily consume fats, the body will become more efficient, but the metabolic rate will fall? How it is possible?? I understand that the metabolic rate falls [to the Randle effect], OK; but I do not understand that the efficiency goes up.
5 - Changing of issue: who's that person Bukovsky? He calls himself peatarian, but I see he is essentially against R Peat! One question: based on what he says that people with lower metabolic rate and increased TSH die less? Where he took such a statement?
fraternally

Gilson Dantas

 

[Fearlessgolfer]

@Mittir @Blossom @narouz @burtlancast
I have been treating a prostate tumor based on the physiological and nutritional principles that I have learned on R Peat writings; and I think I'm evolving more or less well, although with some difficulty to adjust t3 supplementation;
If possible, I would like any of you help me to solve some questions, and in this way I can expand my understanding of R Peat´s physiological thinking; specifically on the concept of metabolic rate in health and disease:

1 - In few words, what is the difference between metabolic efficiency and the oxidative burning of glucose?
2 - If we have the stress of fasting, the metabolic rate drops? OK, but in the case of caloric restriction, the metabolic rate increases? Why? What is the mechanism? Maybe because there is less calories, then metabolic rate rises?
3 - I gained weight, 16 pounds, these months on a diet R Peat´s style. This is a expected effect of a phase of transitiondominated by cortisol going to a stage dominated by T3? I mean: I am not more dominated by cortisol but the thyroid does not already own hegemony in my metabolism? In this case we have a drop in metabolic rate? [Since, as I see every day, the temperature does not go beyond the 36 C? ]
4 - How to understand the claim of Kate Deering that if someone starts to primarily consume fats, the body will become more efficient, but the metabolic rate will fall? How it is possible?? I understand that the metabolic rate falls [to the Randle effect], OK; but I do not understand that the efficiency goes up.
5 - Changing of issue: who's that person Bukovsky? He calls himself peatarian, but I see he is essentially against R Peat! One question: based on what he says that people with lower metabolic rate and increased TSH die less? Where he took such a statement?
fraternally

Gilson Dantas

Good questions here, Gilson. Hope your prostate treatment is going well.

I've done leangains cutting (calorie restriction) and intermittent fasting, 24+ hour fasting, ketogenic diet with weekly reefed with carbs will all good results. I have gained 8 lbs so far going on a month eating RP'ish. What are your food choices and how much do you eat (Calories & Macros)?

Not sure any fasting or calorie restriction will increase metabolism.

Would like to know how your question #4 of Kate Deering's claim.

The whole time, I should have worked on my increasing metabolism. I believe my optimizing metabolism, many good things should fall in place for wellness.

Yesterday I read @haidut said he now eats more variety of foods while watching PUFAs. This is great news.

 

[Amazoniac]

Dear Gilson,

2. It's that quote that I sent you via PM: "I’ve occasionally mentioned that the typical calorie restricted diet increases the metabolic rate and decreases oxidative damage by reducing PUFA, cysteine, methionine, tryptophan, and iron, possibly some random toxins. In one of the big nurses studies, someone noticed that those who ate the most lived the longest, i.e., had the highest metabolic rate."

3. It can be (partly) water that's needed to repair, or the dairy fat that tends to be more directly fattening in comparison to small amounts of other fats that's adding up every day (especially in low metabolism), or eating much more than you need in attempt to keep stress low.

5. You know my opinion on him, I like the guy. It's a fine statement and it doesn't imply that you have to increase your TSH or lower your metabolism to live more; but it's a comparison that if you take the same person at old age, with greatly reduced capacity to generate energy despite eating and living decently, then it's probably slightly protective to slow things down a bit and it's likely that the person will live more (not so much about quality). In fact it's about not requiring that intervention, but when you do, then it can be beneficial.
He seems to be allergic to the word Peatarian, but it can be just an impression..

Eternally,
pboy

 

[raypeatclips]

5. It is nice people are challenging Peat's ideas but I don't think Bukowski always gets the right end of the stick. He uses this study to prove that high TSH is beneficial. I said this before last time it came up.

Mortality in a complete 4-year follow up of 85-year-old residents of Leiden, classified by serum level of thyrotropin and thyroxine. - PubMed - NCBI

"The study found 85 year olds and analysed their bloods and then derive a mortality rate in groupings based on their TSH level.

They managed to recruit 67 subjects with abnormally high TSH and recruited 491 subjects with normal to low TSH. They recruited over seven times more alive people with normal TSH, than high. But then deduct from the study that high TSH equal longer life? The obvious question is, are all the other high TSH subjects not in the study, not there because they are dead?"

 

[gilson dantas]

I ask again if any of you have a short answer about this [are very importante questions to me to undestand R Peat]:
1 - In few words, what is the difference between metabolic efficiency and the oxidative burning of glucose? They are different? In what way?
2 - If we have the stress of fasting, the metabolic rate drops? OK, but in the case of caloric restriction, the metabolic rate increases? Why? What is the mechanism? Maybe because there is less calories, then metabolic rate rises?
3 - How to understand the claim of Kate Deering that if someone starts to primarily consume fats, the body will become more efficient, but the metabolic rate will fall? How it is possible?? I understand that the metabolic rate falls [to the Randle effect], OK; but I do not understand that the efficiency goes up.
Perhaps @Mittir, perhaps @Blossom, @narouz perhaps someone else? [I already wrote to @haidut but there is no answer]
Thanks, Gilson

 

[gilson dantas]

Thanks @raypeatclips, you gave a good argument about bukowski [I really think he is wrong].

 

[haidut]

I ask again if any of you have a short answer about this [are very importante questions to me to undestand R Peat]:
1 - In few words, what is the difference between metabolic efficiency and the oxidative burning of glucose? They are different? In what way?
2 - If we have the stress of fasting, the metabolic rate drops? OK, but in the case of caloric restriction, the metabolic rate increases? Why? What is the mechanism? Maybe because there is less calories, then metabolic rate rises?
3 - How to understand the claim of Kate Deering that if someone starts to primarily consume fats, the body will become more efficient, but the metabolic rate will fall? How it is possible?? I understand that the metabolic rate falls [to the Randle effect], OK; but I do not understand that the efficiency goes up.
Perhaps @Mittir, perhaps @Blossom, @narouz perhaps someone else? [I already wrote to @haidut but there is no answer]
Thanks, Gilson

Metabolic efficiency is a term that means the exact opposite of what you think when it is used by doctors. Metabolic efficiency, medically speaking, means slow metabolism - i.e. you can subsist on very few calories. In general, you don't want that. Metabolic inefficiency, in medical circles (usually) means uncoupled metabolism - i.e. the one often seen in hyperthyroidism where calories are consumed very rapidly and the ratio of heat/ATP generated increases. So, the metabolism is less efficient in the sense that calories are "wasted" as heat and CO2 and less ATP is produced. Animals with uncoupled metabolism tend to live much longer.
These terms come from the second law of thermodynamics. If human beings are seen as internal combustion engines, efficient metabolism is one that produces as little heat as possible and inefficient is the one that produces as much heat as possible. So, in that sense, you want inefficient metabolism.
You can also have pathological metabolic inefficiency, such as in excessive glycolysis, where you truly waste calories but not because you burn them fast but because the metabolism is stuck in the first step (glycolysis) and cannot proceed further. In that state you produce a lot of lactate from the food you eat and not much ATP and even less heat.
I think to avoid confusion, the terms used should be complete respiration (oxidative metabolism) vs. incomplete respiration (fermentation). The complete respiration can be coupled or uncoupled. You definitely want complete respiration and moved a bit towards the uncoupled state.
Fasting depletes partially the PUFA inside the cell. So, for the first 2-3 days there may be increase in metabolism. That is why only intermittent fasting works, not chronic one. In chronic fasting you will start to break down muscle tissue, which contains amino acids that suppress the thyroid and there are other signals that tell your body you are in starvation mode so it will downregulate your thyroid synthesis to keep you from consuming youself in a period of food scarcity. Chronic fasting is most certainly not good as it will destroy your thymus, muscle mass, brain will atrophy, etc. Your resting metabolism (which is the strongest known predictor of health and longevity in humans) depends primarily on muscle mass, so obviously starving won't help you build any of that or even maintain it. All the people who run themselves to death or do other exhaustive exercises are artificially raising their metabolic rate through stress hormones like adrenaline and cortisol and in the process mimic a state of chronic fasting - i.e. destroy muscle mass, lower thyroid function, etc. It would be interesting to do a study to see if all the people who claim they are "addicted" to exercise are simply making a desperate attempt to raise their metabolism, and of course end up doing the exact opposite in the long run.

 

[lollipop]

Metabolic efficiency is a term that means the exact opposite of what you think then it is used by doctors. Metabolic efficiency, medically speaking, means slow metabolism - i.e. you can subsist on very few calories. In general, you don't want that. Metabolic inefficiency, in medical circles (usually) means uncoupled metabolism - i.e. the one often seen in hypothyroidism where calories are consumed very rapidly and the ratio of heat/ATP generated increases. So, the metabolism is less efficient in the sense that calories are "wasted" as heat and CO2 and less ATP is produced. Animals with uncoupled metabolism tend to live much longer.
You can also have pathological metabolic inefficiency, such as in excessive glycolysis, where you truly waste calories but not because you burn them fast but because the metabolism is stuck in the first step (glycolysis) and cannot proceed further. In that state you produce a lot of lactate from the food you eat and not much ATP and even less heat.
I think to avoid confusion, the terms used should be complete respiration (oxidative metabolism) vs. incomplete respiration (fermentation). The complete respiration can be coupled or uncoupled. You definitely want complete respiration and moved a bit towards the uncoupled state.
Fasting depletes partially the PUFA inside the cell. So, for the first 2-3 days there may be increase in metabolism. That is why only intermittent fasting works, not chronic one. In chronic fasting you will start to break down muscle tissue, which contains amino acids that suppress the thyroid and there are other signals that tell your body you are in starvation mode so it will downregulate your thyroid synthesis to keep you from consuming youself in a period of food scarcity. Chronic fasting is most certainly not good as it will destroy your thymus, muscle mass, brain will atrophy, etc. Your resting metabolism (which is the strongest known predictor of health and longevity in humans) depends primarily on muscle mass, so obviously starving won't help you build any of that or even maintain it. All the people who run themselves to death or do other exhaustive exercises are artificially raising their metabolic rate through stress hormones like adrenaline and cortisol and in the process mimic a state of chronic fasting - i.e. destroy muscle mass, lower thyroid function, etc. It would be interesting to do a study to see if all the people who claim they are "addicted" to exercise are simply making a desperate attempt to raise their metabolism, and of course end up doing the exact opposite in the long run.

Thank you @haidut. Great explanatory information.

 

[Amazoniac]

Regeneration and degeneration:
"Regenerative healing also requires freedom from substances that inhibit the digestion of the debris. The great decline in proteolytic autophagy that occurs with aging (Del Roso, et al., 2003) can be reduced by inhibiting the release of fatty acids. This effect is additive to the antiaging effects of calorie restriction, suggesting that it is largely the decrease of dietary fats that makes calorie restriction effective (Donati, et al., 2004, 2008)."

 

[lvysaur]

Metabolic inefficiency, in medical circles (usually) means uncoupled metabolism - i.e. the one often seen in hypothyroidism where calories are consumed very rapidly and the ratio of heat/ATP generated increases.

Did you mean to say hyperthyroidism?

 

[haidut]

Did you mean to say hyperthyroidism?

Yes, sorry about my typo. I fixed it.

 

[gilson dantas]

@haidut:

Fasting depletes partially the PUFA inside the cell. So, for the first 2-3 days there may be increase in metabolism.

--- This increase in metabolism have something to do with less or lower Randle effect?

 

[tyw]

Fasting depletes partially the PUFA inside the cell. So, for the first 2-3 days there may be increase in metabolism.

Not true, the increase in metabolism is on the order of 3-10% within 36-48 hours, and metabolic rate starts to drop after around 60 hours.

- Resting energy expenditure in short-term starvation is increased as a result of an increase in serum norepinephrine. - PubMed - NCBI
- Enhanced thermogenic response to epinephrine after 48-h starvation in humans. - PubMed - NCBI

This is entire explained by the extreme rise in catacholamines -- Resting energy expenditure in short-term starvation is increased as a result of an increase in serum norepinephrine .... +20% within a day, and basically more than doubling by the 4 day mark.

Short term fasting will not deplete PUFA in any meaningful way. Most of the fat that is being mobilised will be from adipose stores, which will then be put into circulation. This does not impact PUFA stores in the mitochondria of tissues that govern metabolic rate.

For PUFA depletion to have any effect, you need for example, to actually reduce the amount of PUFA on the inner and outer membrane on tissues governing energy production, like the liver.

In mice, you restrict their food intake, and endogenous fatty acid regulation systems take over, and MORE PUFA is produced in the liver -- Fasting enriches liver triacylglycerol with n-3 polyunsaturated fatty acids: implications for understanding the adipose–liver axis in serum docosahexaenoic acid regulation

This is unlikely to be the case with humans. But the point being made here is that with fasting that produces any amount of large energetic deficit, the body's endogenous systems will kick in, and try to regulate everything (and that includes how much PUFA should be stored). For a particular individual, whether this means "hang on to PUFA", or "Drop PUFA", or "do nothing", we do not know.

Intermittent fasting, if done in a eucaloric fashion, does not produce this sort of large energetic deficit; in most people who are not exercise strenously, a 16-hour fast will use maybe 50-80% of their liver glycogen, and muscle glycogen will barely be affected, and there is no reason at all for the body to want to adapt to a homeostatic imbalance.

The only cases where fasting does induce an acute energetic deficit is when either the diet is hypo-caloric in nature, or the user is also engaging in subsequent strenous exercise (usually timed during periods of fasting) -- in which case, there is the same sort of acute catacholamine release that we see in the above cited studies. Note that the "exercise" and "hypo-caloric" parts are the significant factors, and not the "fasting" part.

Metabolic efficiency is a term that means the exact opposite of what you think when it is used by doctors. Metabolic efficiency, medically speaking, means slow metabolism - i.e. you can subsist on very few calories. In general, you don't want that. Metabolic inefficiency, in medical circles (usually) means uncoupled metabolism - i.e. the one often seen in hyperthyroidism where calories are consumed very rapidly and the ratio of heat/ATP generated increases. So, the metabolism is less efficient in the sense that calories are "wasted" as heat and CO2 and less ATP is produced. Animals with uncoupled metabolism tend to live much longer.

These terms come from the second law of thermodynamics. If human beings are seen as internal combustion engines, efficient metabolism is one that produces as little heat as possible and inefficient is the one that produces as much heat as possible. So, in that sense, you want inefficient metabolism.
You can also have pathological metabolic inefficiency, such as in excessive glycolysis, where you truly waste calories but not because you burn them fast but because the metabolism is stuck in the first step (glycolysis) and cannot proceed further. In that state you produce a lot of lactate from the food you eat and not much ATP and even less heat.

Disagree entirely.

There are animals that have coupled metabolisms, and produce a lot of ROS, but yet live long due to ability to cleanup that ROS very effectively. Naked Mole Rats fall in this category.

Then there are animals that have coupled metabolisms, but very slow ones, and they live very long. Turtles fall in this category.

Then there are animals that have very low (relative) mitochondrial PUFA concentrations, the ability to alternate between coupled and uncoupled metabolism, and thus have very low ROS production rates even in the face of high metabolic rate. Long-lived Birds fall into this category.

All sets of these use different strategies to achieve long lives. We are not these animals, and this does not apply to us -- PUFA, Birds, and Genetics

Humans fall into the realm of "moderate-to-low miochondrial PUFA levels", "moderate metabolism", and "moderate-to-good ROS cleanup capacity". What this means, we have absolutely no clue, and to suggest that "more uncoupling is better" cannot be a statement made in certainty, and is disproved by populations like the okinawans, who have "better cleanup", and "more coupling" in order to produce less ROS over their lifetimes. As usual, the answer is that we have no clue what sort of metabolism is best to maximise a particular individual's longevity and health.

Then, I have discussed metabolic efficiency in detail in this thread -- Haidut's Summary Of PUFA

....

 

[haidut]

Not true, the increase in metabolism is on the order of 3-10% within 36-48 hours, and metabolic rate starts to drop after around 60 hours.

Isn't this what my statement said as well? namely, a person may see an increase in metabolism the first few days and then it drops. Also, the study with monkeys and PUFA depletion I posted I think showed that PUFA stores start to drop within the first day of fat-free diet, which I am equating with fasting here as both would mobilize fat stores.

Disagree entirely

Which part - the definition of efficient metabolism or the whether we should always have one? My explanation was focused mainly on why doctors, Peat and various other people seem to use the phrase "efficient metabolism" in so many different ways. Sometimes they use it to mean fast and other times slow metabolism. You point on whether fast metabolism is always desired is not contested - obviously there are times where you don't want fast metabolism and the organism has clear signals when it does not want it. For instance, intense exercise acutely lowers T3 and for a very good reason - if it didn't, that would lead to excessive muscle breakdown and maybe even overheating and shock. But, on average, the higher your resting metabolism the healthier you are and the longer you would/should live.
http://press.endocrine.org/doi/full/10.1210/jc.2004-0390

If caffeine and aspirin greatly increase maximum lifespan. You don't think that it is a coincidence that they also act like thyroid and raise the metabolic rate, right?
https://raypeatforum.com/community/threads/caffeine-extends-lifespan-in-animal-model-by-52.2114/
Aspirin Pro-Drug From Willow Bark Extends Yeast Lifespan By Almost 400%
Caffeine Has Same Effects On Metabolism As Dinitrophenol

I know, we are neither worms not flies, but the fact that caffeine and aspirin worked in such different animal models and achieved consistent results points to them having similar effects. What systemic effect, other than their pro-metabolic one, do you think could be responsible for these striking lifespan extension results?

 

[Drareg]

Isn't this what my statement said as well? :) namely, a person may see an increase in metabolism the first few days and then it drops. Also, the study with monkeys and PUFA depletion I posted I think showed that PUFA stores start to drop within the first day of fat-free diet, which I am equating with fasting here as both would mobilize fat stores.


Which part - the definition of efficient metabolism or the whether we should always have one? My explanation was focused mainly on why doctors, Peat and various other people seem to use the phrase "efficient metabolism" in so many different ways. Sometimes they use it to mean fast and other times slow metabolism. You point on whether fast metabolism is always desired is not contested - obviously there are times where you don't want fast metabolism and the organism has clear signals when it does not want it. For instance, intense exercise acutely lowers T3 and for a very good reason - if it didn't, that would lead to excessive muscle breakdown and maybe even overheating and shock. But, on average, the higher your resting metabolism the healthier you are and the longer you would/should live.
http://press.endocrine.org/doi/full/10.1210/jc.2004-0390

If caffeine and aspirin greatly increase maximum lifespan. You don't think that it is a coincidence that they also act like thyroid and raise the metabolic rate, right?
https://raypeatforum.com/community/threads/caffeine-extends-lifespan-in-animal-model-by-52.2114/
Aspirin Pro-Drug From Willow Bark Extends Yeast Lifespan By Almost 400%
Caffeine Has Same Effects On Metabolism As Dinitrophenol

I know, we are neither worms not flies, but the fact that caffeine and aspirin worked in such different animal models and achieved consistent results points to them having similar effects. What systemic effect, other than their pro-metabolic one, do you think could be responsible for these striking lifespan extension results?

How does this apply to those trying to use T3 as a recovery aid while maintaining training/excercise regimes? Also stressful work regimes? Athletes etc
People use T3 before workouts?
It seems a lot of people on here use T3 like this.

 

[tyw]

Isn't this what my statement said as well? :) namely, a person may see an increase in metabolism the first few days and then it drops. Also, the study with monkeys and PUFA depletion I posted I think showed that PUFA stores start to drop within the first day of fat-free diet, which I am equating with fasting here as both would mobilize fat stores.

No, we agree with the observed result. But the mechanism isn't "PUFA Depletion". It's the catecholamines.

We may see decrease in serum PUFAs during short term fasting, but that says nothing for mitochondrial membrane PUFAs. We must look at mitochondrial membrane PUFAs if we are to discuss anything to do with PUFA depletion in the context of metabolism, because it is precisely PUFAs in this locus that controls ECT kinetics.

- There is no evidence to show that PUFAs in the mitochondria of metabolic active tissue decreases over a single day of fasting.

- Observationally the body does not re-model mitochondrial PUFAs very quickly ... even in rats, which have very high PUFA flux, we're talking about a week of heavy PUFA restrict to see any change in mitochondrial PUFAs. In humans, we probably need to quadruple that figure (a month).

- The very significant increase in catecholamines is more than enough to explain the proportionate increase in metabolic rate.

PUFA is not a factor in this observation.

Which part - the definition of efficient metabolism or the whether we should always have one? My explanation was focused mainly on why doctors, Peat and various other people seem to use the phrase "efficient metabolism" in so many different ways. Sometimes they use it to mean fast and other times slow metabolism. You point on whether fast metabolism is always desired is not contested - obviously there are times where you don't want fast metabolism and the organism has clear signals when it does not want it. For instance, intense exercise acutely lowers T3 and for a very good reason - if it didn't, that would lead to excessive muscle breakdown and maybe even overheating and shock. But, on average, the higher your resting metabolism the healthier you are and the longer you would/should live.
http://press.endocrine.org/doi/full/10.1210/jc.2004-0390

If caffeine and aspirin greatly increase maximum lifespan. You don't think that it is a coincidence that they also act like thyroid and raise the metabolic rate, right?
Caffeine extends lifespan in animal model by 52%
Aspirin Pro-Drug From Willow Bark Extends Yeast Lifespan By Almost 400%
Caffeine Has Same Effects On Metabolism As Dinitrophenol

I know, we are neither worms not flies, but the fact that caffeine and aspirin worked in such different animal models and achieved consistent results points to them having similar effects. What systemic effect, other than their pro-metabolic one, do you think could be responsible for these striking lifespan extension results?

I will disagree with the statement -- "But, on average, the higher your resting metabolism the healthier you are and the longer you would/should live"

The study you quoted doesn't support this statement at all. All it showed was that people who:

- Already happened to live long
- Do not experience the same degree of Drop in Metabolic Rate relative to their youthful baseline

This is about protection against decline, and not about increase beyond baseline. Whatever that healthy baseline is, it certainly isn't referring to an artificially propped up metabolic rate.


And again, studying the lifespans of yeast, and or other animal lifespans, etc ... are only useful to elucidate very low level mechanics. Caffeine works on a level higher than the base level mechanics that are shared between such organisms. ie: We cannot extrapolate these results to humans at all.

Caffeine has not been proven to increase longevity in humans, and is likely not going to on the basis of increasing metabolic rate.

Aspirin works on so many different mechanics other than metabolic rate, that this is an unfair comparison. We will all agree that chronic low dose aspirin in Humans is likely not harmful, and very likely very helpful (and this is due to decades and decades of human use and research).

Okinawan centenarians are known to eat little and be in pseudo calorie restriction.

Thyroid seems to have nothing at all to do with longevity:
- http://press.endocrine.org/doi/10.1210/jcem.77.5.8077303?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed
- http://press.endocrine.org/doi/pdf/10.1210/jc.2009-2198
- Centenarians and supercentenarians: a black swan. Emerging social, medical and surgical problems

Some quotes:

In fact it has been showed an age-related decline of the TSH levels and a significant increase of the reverse T3 (rT3) concentrations in centenarians by comparison to old controls.

....

Why would higher levels of TSH be related to longevity? A possible explanation could be that the higher TSH in centenarians and their offspring represents a lower bioactivity of thyroid hormone, although the higher levels of FT4 in female offspring compared with controls in the study by Atzmon et al.(10) do not support this hypothesis.

However, even thyroid hormone levels within the normal range might be associated with thyroid hormone-related endpoints. This is illustrated by the observation that even in euthyroid subjects with normal TSH, FT4 is independently associated with atrial fibrillation, especially in the elderly (19). In addition, in ambulatory elderly men, a higher FT4 within the reference range is associated with lower physical performance, independent of age and illness (8). So these higher levels of TSH within the normal range could still represent a slightly lower bioactivity of thyroid hormone. A lower activity of thyroid hormone, and thus a lower basal metabolic rate, could possibly serve as an adaptive mechanism to prevent catabolism in the elderly​

The only valid conclusion there is that we have no clue whatsoever how the various Thyroid hormones interact with metabolism and otherwise to produce the long-lived phenotype in these people who are clearly living beyond 100 years old in good health ......


I am very clear in saying that I don't know what leads to longevity. But I can say for sure that there is enough conflicting data to say that maintenance of a high metabolic rate is not the key factor.

.......

 

[Orion]

I am very clear in saying that I don't know what leads to longevity. But I can say for sure that there is enough conflicting data to say that maintenance of a high metabolic rate is not the key factor.

RP mentioned in an interview that some people living at high altitude (Peru) were living to 150-180yrs old, tying among other things c02 levels to longevity. They would come down from high altitude to tour North America as 'freaks' in the early to mid 1900s, then die when returning home!

 

[Fearlessgolfer]

No, we agree with the observed result. But the mechanism isn't "PUFA Depletion". It's the catecholamines.

We may see decrease in serum PUFAs during short term fasting, but that says nothing for mitochondrial membrane PUFAs. We must look at mitochondrial membrane PUFAs if we are to discuss anything to do with PUFA depletion in the context of metabolism, because it is precisely PUFAs in this locus that controls ECT kinetics.

- There is no evidence to show that PUFAs in the mitochondria of metabolic active tissue decreases over a single day of fasting.

- Observationally the body does not re-model mitochondrial PUFAs very quickly ... even in rats, which have very high PUFA flux, we're talking about a week of heavy PUFA restrict to see any change in mitochondrial PUFAs. In humans, we probably need to quadruple that figure (a month).

- The very significant increase in catecholamines is more than enough to explain the proportionate increase in metabolic rate.

PUFA is not a factor in this observation.



I will disagree with the statement -- "But, on average, the higher your resting metabolism the healthier you are and the longer you would/should live"

The study you quoted doesn't support this statement at all. All it showed was that people who:

- Already happened to live long
- Do not experience the same degree of Drop in Metabolic Rate relative to their youthful baseline

This is about protection against decline, and not about increase beyond baseline. Whatever that healthy baseline is, it certainly isn't referring to an artificially propped up metabolic rate.


And again, studying the lifespans of yeast, and or other animal lifespans, etc ... are only useful to elucidate very low level mechanics. Caffeine works on a level higher than the base level mechanics that are shared between such organisms. ie: We cannot extrapolate these results to humans at all.

Caffeine has not been proven to increase longevity in humans, and is likely not going to on the basis of increasing metabolic rate.

Aspirin works on so many different mechanics other than metabolic rate, that this is an unfair comparison. We will all agree that chronic low dose aspirin in Humans is likely not harmful, and very likely very helpful (and this is due to decades and decades of human use and research).

Okinawan centenarians are known to eat little and be in pseudo calorie restriction.

Thyroid seems to have nothing at all to do with longevity:
- http://press.endocrine.org/doi/10.1210/jcem.77.5.8077303?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed
- http://press.endocrine.org/doi/pdf/10.1210/jc.2009-2198
- Centenarians and supercentenarians: a black swan. Emerging social, medical and surgical problems

Some quotes:

In fact it has been showed an age-related decline of the TSH levels and a significant increase of the reverse T3 (rT3) concentrations in centenarians by comparison to old controls.

....

Why would higher levels of TSH be related to longevity? A possible explanation could be that the higher TSH in centenarians and their offspring represents a lower bioactivity of thyroid hormone, although the higher levels of FT4 in female offspring compared with controls in the study by Atzmon et al.(10) do not support this hypothesis.

However, even thyroid hormone levels within the normal range might be associated with thyroid hormone-related endpoints. This is illustrated by the observation that even in euthyroid subjects with normal TSH, FT4 is independently associated with atrial fibrillation, especially in the elderly (19). In addition, in ambulatory elderly men, a higher FT4 within the reference range is associated with lower physical performance, independent of age and illness (8). So these higher levels of TSH within the normal range could still represent a slightly lower bioactivity of thyroid hormone. A lower activity of thyroid hormone, and thus a lower basal metabolic rate, could possibly serve as an adaptive mechanism to prevent catabolism in the elderly​

The only valid conclusion there is that we have no clue whatsoever how the various Thyroid hormones interact with metabolism and otherwise to produce the long-lived phenotype in these people who are clearly living beyond 100 years old in good health ......


I am very clear in saying that I don't know what leads to longevity. But I can say for sure that there is enough conflicting data to say that maintenance of a high metabolic rate is not the key factor.

.......

Wow!

"The only valid conclusion there is that we have no clue whatsoever how the various Thyroid hormones interact with metabolism and otherwise to produce the long-lived phenotype in these people who are clearly living beyond 100 years old in good health ......


I am very clear in saying that I don't know what leads to longevity. But I can say for sure that there is enough conflicting data to say that maintenance of a high metabolic rate is not the key factor."

How much of research is opinion based on? This is incredible statement @tyw

 

[haidut]

No, we agree with the observed result. But the mechanism isn't "PUFA Depletion". It's the catecholamines.

We may see decrease in serum PUFAs during short term fasting, but that says nothing for mitochondrial membrane PUFAs. We must look at mitochondrial membrane PUFAs if we are to discuss anything to do with PUFA depletion in the context of metabolism, because it is precisely PUFAs in this locus that controls ECT kinetics.

- There is no evidence to show that PUFAs in the mitochondria of metabolic active tissue decreases over a single day of fasting.

- Observationally the body does not re-model mitochondrial PUFAs very quickly ... even in rats, which have very high PUFA flux, we're talking about a week of heavy PUFA restrict to see any change in mitochondrial PUFAs. In humans, we probably need to quadruple that figure (a month).

- The very significant increase in catecholamines is more than enough to explain the proportionate increase in metabolic rate.

PUFA is not a factor in this observation.



I will disagree with the statement -- "But, on average, the higher your resting metabolism the healthier you are and the longer you would/should live"

The study you quoted doesn't support this statement at all. All it showed was that people who:

- Already happened to live long
- Do not experience the same degree of Drop in Metabolic Rate relative to their youthful baseline

This is about protection against decline, and not about increase beyond baseline. Whatever that healthy baseline is, it certainly isn't referring to an artificially propped up metabolic rate.


And again, studying the lifespans of yeast, and or other animal lifespans, etc ... are only useful to elucidate very low level mechanics. Caffeine works on a level higher than the base level mechanics that are shared between such organisms. ie: We cannot extrapolate these results to humans at all.

Caffeine has not been proven to increase longevity in humans, and is likely not going to on the basis of increasing metabolic rate.

Aspirin works on so many different mechanics other than metabolic rate, that this is an unfair comparison. We will all agree that chronic low dose aspirin in Humans is likely not harmful, and very likely very helpful (and this is due to decades and decades of human use and research).

Okinawan centenarians are known to eat little and be in pseudo calorie restriction.

Thyroid seems to have nothing at all to do with longevity:
- http://press.endocrine.org/doi/10.1210/jcem.77.5.8077303?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed
- http://press.endocrine.org/doi/pdf/10.1210/jc.2009-2198
- Centenarians and supercentenarians: a black swan. Emerging social, medical and surgical problems

Some quotes:

In fact it has been showed an age-related decline of the TSH levels and a significant increase of the reverse T3 (rT3) concentrations in centenarians by comparison to old controls.

....

Why would higher levels of TSH be related to longevity? A possible explanation could be that the higher TSH in centenarians and their offspring represents a lower bioactivity of thyroid hormone, although the higher levels of FT4 in female offspring compared with controls in the study by Atzmon et al.(10) do not support this hypothesis.

However, even thyroid hormone levels within the normal range might be associated with thyroid hormone-related endpoints. This is illustrated by the observation that even in euthyroid subjects with normal TSH, FT4 is independently associated with atrial fibrillation, especially in the elderly (19). In addition, in ambulatory elderly men, a higher FT4 within the reference range is associated with lower physical performance, independent of age and illness (8). So these higher levels of TSH within the normal range could still represent a slightly lower bioactivity of thyroid hormone. A lower activity of thyroid hormone, and thus a lower basal metabolic rate, could possibly serve as an adaptive mechanism to prevent catabolism in the elderly​

The only valid conclusion there is that we have no clue whatsoever how the various Thyroid hormones interact with metabolism and otherwise to produce the long-lived phenotype in these people who are clearly living beyond 100 years old in good health ......


I am very clear in saying that I don't know what leads to longevity. But I can say for sure that there is enough conflicting data to say that maintenance of a high metabolic rate is not the key factor.

.......

Sure, we don't know with certainty but don't you think we have enough evidence pointing in the same direction? Aspirin and caffeine may not be enough as examples but there are others that added up together to paint pretty much the same picture.
Pregnenolone Increases Maximum Lifespan By 60% (animal Model)
Inhibiting Serotonin During Protein Feeding Doubles Maximum Lifespan
Blocking Serotonin Extends Lifespan By 40%, Triples Youthspan
Serotonin Antagonists Extend Lifespan, SSRI Dramatically Shorten It
[INSERT HERE ALL THE STUDIES ON LIFESPAN EXTENSION BY RESTRICTING TYPROPHAN/METHIONINE/CYSTEINE]

So, I am not asking for a definitive answer as I know there is none currently. But when you have all of these chemicals extending maximum (and sometimes average) lifespan the question naturally arises - assuming they all work (and it is a big assumption until more is known) what is the common mechanism behind them. Is there a least common denominator of action so to speak? Well, there may be more than one but the one we do know about is that these all have the effect of increasing RMR. So, if you know of another plausible explanation (even though it may be speculative) please share it as I would like to follow up on it. My post is not so much about "hey these things work" as it about "IF these things work, what else other than metabolism can you suggest as a mechanism".
So, happy to hear your comments on that one.

 

[Drareg]

No, we agree with the observed result. But the mechanism isn't "PUFA Depletion". It's the catecholamines.

We may see decrease in serum PUFAs during short term fasting, but that says nothing for mitochondrial membrane PUFAs. We must look at mitochondrial membrane PUFAs if we are to discuss anything to do with PUFA depletion in the context of metabolism, because it is precisely PUFAs in this locus that controls ECT kinetics.

- There is no evidence to show that PUFAs in the mitochondria of metabolic active tissue decreases over a single day of fasting.

- Observationally the body does not re-model mitochondrial PUFAs very quickly ... even in rats, which have very high PUFA flux, we're talking about a week of heavy PUFA restrict to see any change in mitochondrial PUFAs. In humans, we probably need to quadruple that figure (a month).

- The very significant increase in catecholamines is more than enough to explain the proportionate increase in metabolic rate.

PUFA is not a factor in this observation.



I will disagree with the statement -- "But, on average, the higher your resting metabolism the healthier you are and the longer you would/should live"

The study you quoted doesn't support this statement at all. All it showed was that people who:

- Already happened to live long
- Do not experience the same degree of Drop in Metabolic Rate relative to their youthful baseline

This is about protection against decline, and not about increase beyond baseline. Whatever that healthy baseline is, it certainly isn't referring to an artificially propped up metabolic rate.


And again, studying the lifespans of yeast, and or other animal lifespans, etc ... are only useful to elucidate very low level mechanics. Caffeine works on a level higher than the base level mechanics that are shared between such organisms. ie: We cannot extrapolate these results to humans at all.

Caffeine has not been proven to increase longevity in humans, and is likely not going to on the basis of increasing metabolic rate.

Aspirin works on so many different mechanics other than metabolic rate, that this is an unfair comparison. We will all agree that chronic low dose aspirin in Humans is likely not harmful, and very likely very helpful (and this is due to decades and decades of human use and research).

Okinawan centenarians are known to eat little and be in pseudo calorie restriction.

Thyroid seems to have nothing at all to do with longevity:
- http://press.endocrine.org/doi/10.1210/jcem.77.5.8077303?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed
- http://press.endocrine.org/doi/pdf/10.1210/jc.2009-2198
- Centenarians and supercentenarians: a black swan. Emerging social, medical and surgical problems

Some quotes:

In fact it has been showed an age-related decline of the TSH levels and a significant increase of the reverse T3 (rT3) concentrations in centenarians by comparison to old controls.

....

Why would higher levels of TSH be related to longevity? A possible explanation could be that the higher TSH in centenarians and their offspring represents a lower bioactivity of thyroid hormone, although the higher levels of FT4 in female offspring compared with controls in the study by Atzmon et al.(10) do not support this hypothesis.

However, even thyroid hormone levels within the normal range might be associated with thyroid hormone-related endpoints. This is illustrated by the observation that even in euthyroid subjects with normal TSH, FT4 is independently associated with atrial fibrillation, especially in the elderly (19). In addition, in ambulatory elderly men, a higher FT4 within the reference range is associated with lower physical performance, independent of age and illness (8). So these higher levels of TSH within the normal range could still represent a slightly lower bioactivity of thyroid hormone. A lower activity of thyroid hormone, and thus a lower basal metabolic rate, could possibly serve as an adaptive mechanism to prevent catabolism in the elderly​

The only valid conclusion there is that we have no clue whatsoever how the various Thyroid hormones interact with metabolism and otherwise to produce the long-lived phenotype in these people who are clearly living beyond 100 years old in good health ......


I am very clear in saying that I don't know what leads to longevity. But I can say for sure that there is enough conflicting data to say that maintenance of a high metabolic rate is not the key factor.

.......

I think the centarians and thyroid is essentially a look at thyroid levels near the end of life,they are close to death regardless of being a centarian,they are winding down metabolically.
Could we not construe the study as high RT3 as pushing them closer to death.
Lower active thyroid hormone Its protective to a certain point ,beyond this point is dangerous as with RT3 having a protective effect to a certain point.
I think we would need a full thyroid work up from 80 years old and on to deduce anything from this.

See Mittirs post here on the okinawan diet and longevity,it's an interesting angle,Peat mentioned it before and other have also,the Japanese are notorious for lying about older people's age,some were dead already for 20 years as their children kept collecting their pension and pocketing it.
One example of pension fraud .Sogen Kato - Wikipedia

Mittirs post Epidemiological Evidence?