Optimal Diet For Increasing Lifespan

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Filip1993 said:
@Visionofstrength Have you read Edwards blog? I know he was banned from here but I think you might like some of his stuff. http://edwardjedmonds.com

EDIT: Is it okey to post this here btw?
I have seen that, just recently. The citations alone were worth the price of admission, but like Charlie, he doesn't seem to monetize. I found his thinking about Peat interesting, if only because he describes it as so much of a work-in-progress. It seems like he at least thinks he disagrees with Peat, or will someday, when his work is done. That's sometimes the sign of a good student, probing and tweaking the teacher.

Had I been a member here when he was, I would have enjoyed rousing a defense of Peat, as I try to now whenever it seems Peat is tweaked, even by his students. I mean, not that it takes much to defend Peat. His work really just speaks for itself.

In just one example, if one wants to cite studies on harmful effects of fructose, then one needs to look for studies that use controls where unsaturated fats have been eliminated, since any putative harmful effects of fructose, like those of ethanol, may be caused (in Peat's view) by even small amounts of PUFAs.

But if (as I assume) a habit for name-calling was the offense that got him voted off by the 4 mods? then perhaps his own blog is a better forum.

Thanks for pointing to that, f. Appreciate it.
 
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narouz said:
When you guys figure this out,
I'm counting on you to explain it to me in universal language. :D
Basically, that's called, showing us your chops. S_S just showed more original thinking in those few lines than we are likely to see in a thousand academic papers. Really. Peat would be proud.

Thanks, S_S!

Here's a video that explains all these terms, and the acetyl coa that S_S is thinking about is shown about 5 minutes in...
[BBvideo 560,340:36l618br]https://www.youtube.com/watch?v=juM2ROSLWfw[/BBvideo]
 
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Better not be pork chops :mrgreen: This is what comes out:


I think taking T3 will make you burn fat but it could all turn into ATP or heat depending on conditions. I think interplay between hypothalamus, nerves attached to it, T3, T2, malonyl-CoA regulate this but it's not too easy.

3,5-Diiodo-L-thyronine powerfully reduces adiposity in rats by increasing the burning of fats
Hypothalamic AMPK and fatty acid metabolism mediate thyroid regulation of energy balance
Hypothalamic malonyl-CoA triggers mitochondrial biogenesis and oxidative gene expression in skeletal muscle: Role of PGC-1α
Conversion of T3 and rT3 to 3,3'-T2: pH dependency.

Thyroid hormones: igniting brown fat via the brain
 

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Filip1993

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"Now a high RQ is not always associated with weight gain, this is why RQ really should not be associated with the rate of metabolism. If you are into calorie counting, you can have a high RQ on a high carbohydrate diet without gaining weight. But DNL is going to be very active. You’ll be burning fat just as quickly as you make it. Your triglycerides will probably increase, but they might not if you are taking thyroid. which is going to enhance fatty acid oxidation." -Edward

Thoughts on this? Please move this post to another section or something if this is the wrong place for this type of discussion.
 
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Such_Saturation said:
S_S, can you help me to understand how you see the fructose pathways you're describing as they might fit into uncoupling? In your graphic, I see fructose entering into (what I think is) the "coupled" pathway, but can you suggest where you feel fructose might enter in any "uncoupled" pathway?*

The thing I'm trying to understand is uncoupling. I feel like that's the great unexplained phenomenon. And I think Peat points to uncoupling as the key metabolic process in his general theory of "anti-ageitivity".

From my own experiments, I've noticed that both cold-exposure and high-fat feeding raise my body temperature and cause me to exhale more CO2. This seems paradoxical, but it's been reported consistently, as a phenomenon linked to brown fat, known to be good at "uncoupling".
http://jeb.biologists.org/content/205/15/2275.full.pdf
I wonder if there's more to it that we could learn using the model of how brown fat does uncoupling?

[Edit: *either enter the "uncoupled" pathway, or perhaps promote it, delay it, or affect it in anyway?]
 

Filip1993

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@Visionofstrenght "In just one example, if one wants to cite studies on harmful effects of fructose, then one needs to look for studies that use controls where unsaturated fats have been eliminated, since any putative harmful effects of fructose, like those of ethanol, may be caused (in Peat's view) by even small amounts of PUFAs"- Vos

I totally agree with you. Dewitt wrote this over at peatarian: "There has been some evidence that fructose inhibits cellular respiration but I think this effect can be ascribed to the negative effects of PUFA consumption on fructose utilization."

Damn, so many quotes from me...
 
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Filip1993 said:
"Now a high RQ is not always associated with weight gain, this is why RQ really should not be associated with the rate of metabolism. If you are into calorie counting, you can have a high RQ on a high carbohydrate diet without gaining weight. But DNL is going to be very active. You’ll be burning fat just as quickly as you make it. Your triglycerides will probably increase, but they might not if you are taking thyroid. which is going to enhance fatty acid oxidation." -Edward

Thoughts on this? Please move this post to another section or something if this is the wrong place for this type of discussion.

I think thyroid can in some amount recouple respiration especially if a fasting state can shift from ATP production to thermogenesis which I guess would be desirable in hibernation. If an old guy is fermenting 99% then obviously his RQ will be high. Maybe we should use it in conjunction with respiratory rate for better information.
 
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visionofstrength said:
Such_Saturation said:
S_S, can you help me to understand how you see the fructose pathways you're describing as they might fit into uncoupling? In your graphic, I see fructose entering into (what I think is) the "coupled" pathway, but can you suggest where you feel fructose might enter in any "uncoupled" pathway?*

The thing I'm trying to understand is uncoupling. I feel like that's the great unexplained phenomenon. And I think Peat points to uncoupling as the key metabolic process in his general theory of "anti-ageitivity".

From my own experiments, I've noticed that both cold-exposure and high-fat feeding raise my body temperature and cause me to exhale more CO2. This seems paradoxical, but it's been reported consistently, as a phenomenon linked to brown fat, known to be good at "uncoupling".
http://jeb.biologists.org/content/205/15/2275.full.pdf
I wonder if there's more to it that we could learn using the model of how brown fat does uncoupling?

[Edit: *either enter the "uncoupled" pathway, or perhaps promote it, delay it, or affect it in anyway?]

Uncoupling is just the abatement of the field gradient in the mitochondrion to let hydrogen mix freely with oxygen to make water and heat. If the hypothalamus has a role in that decision, fructose might influence its decision differently than glucose for example.
 
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Filip1993 said:
"Now a high RQ is not always associated with weight gain, this is why RQ really should not be associated with the rate of metabolism. If you are into calorie counting, you can have a high RQ on a high carbohydrate diet without gaining weight. But DNL is going to be very active. You’ll be burning fat just as quickly as you make it. Your triglycerides will probably increase, but they might not if you are taking thyroid. which is going to enhance fatty acid oxidation." -Edward

Thoughts on this? Please move this post to another section or something if this is the wrong place for this type of discussion.

RQ = CO[sub]2 eliminated[/sub] / O[sub]2 consumed[/sub]

I've become an RQ skeptic, in the sense that I find that O[sub]2 consumed[/sub] is tied not to the caloric value of the food you've eaten, but instead, if it is directly measured, to one's overall state of health. So to illustrate, at the extreme, someone suffering from hypoxia will have a very poor O[sub]2 consumed[/sub], if it is directly measured, regardless of what food they've eaten, or not eaten.

[NB: I'm not disagreeing with the principle that calories are involved in combustion of food types, ex vivo. I'm just saying in vivo you can't assume that combustion of food types is the only variable, or even an important variable.]

Because I'm an RQ skeptic, I just use exhaled CO2 at rest for my experiments, and it seems to work fine. So to answer your question, I agree that "RQ really should not be associated with the rate of metabolism" but I think CO[sub]2 eliminated[/sub] at rest can be an adequate measure of metabolism, and perhaps even the best and most practical measure, and available to most of us for our own experimentation.
 
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Such_Saturation said:
Uncoupling is just the abatement of the field gradient in the mitochondrion to let hydrogen mix freely with oxygen to make water and heat. If the hypothalamus has a role in that decision, fructose might influence its decision differently than glucose for example.
I'm trying to understand Peat's mechanism for uncoupling, below. Does it seems to be the "structural temperature" of vicinal water/gel, and the ability of that water/gel to retain carbon dioxide? (and incidentally, this is a second, theoretical reason why I'm an RQ skeptic):

Ray Peat said:
A dangerously high level of ammonia in the blood (hyperammonemia) can be produced by exhaustive exercise, but also by hyperbaric oxygen (or a high concentration of oxygen), by high estrogen, and by hypothyroidism. It tends to be associated with an excess of lactic acid, probably because ammonia stimulates glycolysis. Excess oxygen, like hypothyroidism, is equivalent to "hyperventilation," in producing an abnormally low level of carbon dioxide in the blood. The Krebs cycle, during stress, is limited by the unavailability of carbon dioxide. These factors result in the waste of glucose, turning it into lactic acid, rather than carbon dioxide and energy. In these ways, the metabolism of fatigued muscle (or any cell under stress) is similar to tumor metabolism.

Hyperammonemia disturbs excitatory processes, and can cause seizures, as well as stupor, and is probably involved in mania and depression. Lithium happens to complex electronically with ammonia, and I think that accounts for some of its therapeutic effects, but carbon dioxide is the main physiological factor in the elimination of ammonia, since it combines with it to form urea. The changes in cell water in the excited/fatigued state represent an increase in the water's "structural temperature," and that would imply that less carbon dioxide could remain dissolved during excitation.

Eating sugar and using caffeine, which increases the oxidation of sugar (Yeo, et al., 2005), can reduce fatigue, both subjectively and objectively. Metabolically, they increase the production of carbon dioxide. Increasing sugar decreases the liberation and use of fatty acids, and by a variety of mechanisms, helps to lower the production of ammonia, lactate, and inflammatory cytokines. (Lactic acid, in combination with acidosis and free phospholipids, can interfere with efficient cell functions [Pacini and Kane, 1991; Boachie-Ansah, et al., 1992].) Free fatty acids release tryptophan from albumin, contributing to the formation of serotonin, which increases the sense of fatigue.

Aspirin and niacin help to prevent fatigue symptoms, and to prevent many of the harmful systemic oxidative after-effects. (Both are antilipolytic; aspirin uncouples mitochondria.)

Uncoupling of mitochondrial oxidative metabolism from ATP production helps to consume the sugar which otherwise would be diverted into lactic acid, and converts it into carbon dioxide instead. Mild hypoxia, as at high altitude, suppresses lactic acid production ("the lactate paradox"), and increases the amount of carbon dioxide in tissues.

Aspirin and thyroid (T3) increase uncoupling. A drug that used to be used for weight reduction, DNP, also uncouples mitochondrial metabolism, and, surprisingly, it has some of the beneficial effects of thyroid and aspirin. It stimulates the consumption of lactic acid and the formation of carbon dioxide.

The squirrel monkey, which on average weighs about 2 or 3 pounds as an adult, lives much longer than other mammals of its size, usually about 20 years, as long as 27. It has an extremely high rate of oxygen consumption. This is probably the result of natural uncoupling of the mitochondria, similar to that seen in long-lived mice. Mice with 17% higher resting oxygen consumption lived 36% longer than slow respiring mice of a related strain (Speakman, et al., 2004).

Living at a high altitude, people tend to eat more and stay leaner than when they live near sea level. Apparently, their mitochondria are relatively uncoupled, and they have more mitochondria, which would partly account for their lower production of lactic acid during muscular exertion. Increased thyroid activity, too, tends to increase mitochondrial mass, as well as their uncoupling.

In that light, he says sugar and coffee is an uncoupler, and so I presume he means the fructose component of sucrose is an uncoupler. But how does sugar/fructose affect the structural temperature of the vicinal water, leading to a greater concentration of CO2 -- and hence, in Peat's view, to uncoupling"?

I should add, for clarity, that medical textbooks may not help with any of this:

Ray Peat said:
Water in the body occupies three major compartments--blood vessels, extracellular matrix, and the moist cell substance itself--and its condition in each compartment is a little different, and subject to variation. There are no textbooks in use in the U.S. that treat intracellular water scientifically, and the result is that physicians are confused when they see patients with edema or with disturbances in blood volume. It rarely occurs to physicians to consider disturbances of water distribution in problems such as chronic fatigue, fibromyalgia, sleep disturbances, frequent urination, slow bladder emptying, anxiety, paresthesia, movement disorders, the tunnel syndromes, or even slowed thinking, but "intracellular fatigue" leading to over-hydration is probably the central problem in these, and many other degenerative and inflammatory problems.

The improvements in cell functions and water distribution that are inversely related to oxygen pressure, and directly related to carbon dioxide, won't be discussed in medical textbooks until they have given up the idea of membrane-regulated cells.
 
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I think CO2 is a good Lewis acid and insures sound cell structure and keeps oxygen pressure at bay. Uncoupling means any sugar not needed for ATP will become CO2 instead of lactic acid. In short he advocates for a tight coupling of cell sugar to mitochondrial sugar. What enters the cell should eventually enter the mitochondrion. This tendency is favoured by anything which promotes sugar burning by creating space for it in the mitochondria and making some amount of CO2 which is the key in that self-strengthening circuit.
 
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Such_Saturation said:
...Uncoupling means any sugar not needed for ATP will become CO2 instead of lactic acid. In short he advocates for a tight coupling of cell sugar to mitochondrial sugar. ... This tendency is favoured by anything which promotes sugar burning by creating space for it in the mitochondria and making some amount of CO2 which is the key in that self-strengthening circuit.
So in this light, would fructose be an "uncoupler" because if it's not needed for ATP it would be converted to CO2 instead of lactic acid? Or is it that it promotes sugar-burning of glucose to ATP? or both?

Just to tie it together with your earlier posts, can you help understand how high-fat/SFA/MCT feeding might be an uncoupler, in this light, as you've just described uncoupling?

Thanks!
 
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visionofstrength said:
Such_Saturation said:
...Uncoupling means any sugar not needed for ATP will become CO2 instead of lactic acid. In short he advocates for a tight coupling of cell sugar to mitochondrial sugar. ... This tendency is favoured by anything which promotes sugar burning by creating space for it in the mitochondria and making some amount of CO2 which is the key in that self-strengthening circuit.
So in this light, would fructose be an "uncoupler" because if it's not needed for ATP it would be converted to CO2 instead of lactic acid? Or is it that it promotes sugar-burning of glucose to ATP? or both?
These articles make a case for fructose as an uncoupler:
http://www.andrewkimblog.com/2013/01/ca ... ctive.html
http://www.andrewkimblog.com/2013/02/re ... uttal.html
 

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visionofstrength said:
RQ = CO[sub]2 eliminated[/sub] / O[sub]2 consumed[/sub]

I've become an RQ skeptic, in the sense that I find that O[sub]2 consumed[/sub] is tied not to the caloric value of the food you've eaten, but instead, if it is directly measured, to one's overall state of health. So to illustrate, at the extreme, someone suffering from hypoxia will have a very poor O[sub]2 consumed[/sub], if it is directly measured, regardless of what food they've eaten, or not eaten.

[NB: I'm not disagreeing with the principle that calories are involved in combustion of food types, ex vivo. I'm just saying in vivo you can't assume that combustion of food types is the only variable, or even an important variable.]

Because I'm an RQ skeptic, I just use exhaled CO2 at rest for my experiments, and it seems to work fine. So to answer your question, I agree that "RQ really should not be associated with the rate of metabolism" but I think CO[sub]2 eliminated[/sub] at rest can be an adequate measure of metabolism, and perhaps even the best and most practical measure, and available to most of us for our own experimentation.

I don't think you must confuse "rate of metabolism" with the composition thereof. Meaning, the more oxygen you consume / kg body mass generally means a higher metabolism. The type of fuel burned though is shown by the RQ ratio, ie glucose vs fat ratio. For the same amount of ATP produced, you need more O2 per molecule ATP if you burn mostly fat, ie metabolising at a low RQ ratio of say 0.7 . For the same amount of ATP produced one would expect a pure fat burner to breathe harder or more and the heart/CVD system to work harder/faster.
 

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haidut said:
http://www.eurekalert.org/pub_releases/ ... 022714.php
http://www.cell.com/cell-metabolism/ful ... %2900065-5

A related a human study (epidemiological) came to very similar conclusions with the added caveat that protein intake should increase in old age, which is also something that Peat recommends for maintaining muscle mass.

http://www.medicalnewstoday.com/articles/273533.php

Finally, protein intake at 45% of daily calories seems be bad for the kidneys.

http://www.medicalnewstoday.com/articles/271663.php

Thoughts?

Hi Haidut

These are realtively "old" studies measured in internet time these days :) and were extensively discussed in the media at the time and also by LC and HC proponents.

I have also looked at the data and was especially interested in the mice study. Here were my thoughts at the time :

All the Low Energy density diets did poorly, not only those Low Protein. Out of the 10 LEDD (Low Energy Density Diets), 3 was not even included in results because they "were discontinued due to weight loss (≥20%), rectal prolapse or failure to thrive". Of the remaining 7 LEDD, 6 were placed at the bottom of the results ito median and max life span. Only 1 of the LEDD placed a mere 5 positions higher and it contained the lowest amount of fat of all the LEDD. This one had the 2nd highest median life span of all though. So one conclusion can be that it is definitely not good for long term life span to eat LEDD and IF you do manage to survive on a LEDD, make sure it contains very little fat.

Of the MEDD, 2 also were not included for some of the same reasons of the LEDD. Although it took a bit longer for the mice to "fail to thrive", ie 23 weeks vs only 10 weeks on the LEDD . It is interesting that even Vit and mineral supplements did not prevent this and is confirmation of Ancel Keys's observation during his Great Starvation Experiment that it was adequate calories that helped the men regain weight and strength, and not supplements.

Of the 2 MEDD discontinued, it is insightfull that they were both very Low Protein. The only other very Low Protein MEDD that "survived" was Low FAT. In fact, this was the diet with the highest OVERALL Max life span. So again, a conclusion could be that if your diet is Low Protein, even with Medium Energy Density, make sure it's Low Fat.

So, of the starting 9 Low Protein diets, only 4 "survived", 3 in the HEDD category and 1 in the MEDD category. Of the 4 diets surviving, 2 were placed in the top 3 positions ito Max Life Span, both with the lowest Fat %.

Of the 3 High Protein (60%) starting diets, 2 of the 3 ( the MEDD and HEDD) finished just above the ALL the LEDD while the LEDD HP diets finished 2nd last overall.

So it seems HP is not healthy and LP is, at least looking at these data in mice for maximum life span.

What is further interesting is that out of the 3 starting High Carb (75%) diets the 2 surviving, ie not LEDD, but MEDD and HEDD, finished in position no 1 and 3 repectively . Something to chew on .
 
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SAFarmer said:
visionofstrength said:
RQ = CO[sub]2 eliminated[/sub] / O[sub]2 consumed[/sub]

I've become an RQ skeptic, in the sense that I find that O[sub]2 consumed[/sub] is tied not to the caloric value of the food you've eaten, but instead, if it is directly measured, to one's overall state of health. So to illustrate, at the extreme, someone suffering from hypoxia will have a very poor O[sub]2 consumed[/sub], if it is directly measured, regardless of what food they've eaten, or not eaten.

[NB: I'm not disagreeing with the principle that calories are involved in combustion of food types, ex vivo. I'm just saying in vivo you can't assume that combustion of food types is the only variable, or even an important variable.]

I don't think you must confuse "rate of metabolism" with the composition thereof. Meaning, the more oxygen you consume / kg body mass generally means a higher metabolism. The type of fuel burned though is shown by the RQ ratio, ie glucose vs fat ratio. For the same amount of ATP produced, you need more O2 per molecule ATP if you burn mostly fat, ie metabolising at a low RQ ratio of say 0.7 . For the same amount of ATP produced one would expect a pure fat burner to breathe harder or more and the heart/CVD system to work harder/faster.
What you state is the theory, I agree, of how it has been found to work ex vivo. However, when you do direct measurements of CO2 and O2 you find that the ex vivo results do not hold in vivo.

You can see this when directly measuring someone who is hypoxic. But you can also see it with the converse of hypoxia, uncoupling. Uncoupling produces large amounts of CO2 without any ATP -- it's uncoupled from ATP. When you directly measure CO2 and O2 in a person who has considerable uncoupling, your RQ calculation will not measure caloric consumption as it occurs ex vivo, it will measure uncoupling in vivo.

[Edit: Sorry, I didn't say this well, and wanted to come back and try to fix it...
Takeaway: Those who do studies based on RQ calculations can't measure the effects of hypoxia and uncoupling, and much of their work is likely unreliable, as it relates to caloric metabolism.Peat feels that RQ is a good measure of metabolism and that a higher ratio reflects either a more efficient production of ATP, or more uncoupling, or both.

This flies in the face of many nutritionists who advise their clients that a low RQ is a healthy sign, because it signals, they claim, burning or losing fat.

For more explanation about why uncoupling and the efficient production of ATP is healthy (hence a higher RQ), see the Weight Loss Miracle thread.
 

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visionofstrength said:
What you state is the theory, I agree, of how it has been found to work ex vivo. However, when you do direct measurements of CO2 and O2 you find that the ex vivo results do not hold in vivo.

You can see this when directly measuring someone who is hypoxic. But you can also see it with the converse of hypoxia, uncoupling. Uncoupling produces large amounts of CO2 without any ATP -- it's uncoupled from ATP. When you directly measure CO2 and O2 in a person who has considerable uncoupling, your RQ calculation will not measure caloric consumption as it occurs ex vivo, it will measure uncoupling in vivo.

Takeaway: Those who do studies based on RQ calculations can't measure the effects of hypoxia and uncoupling, and much of their work is likely unreliable, as it relates to caloric metabolism.
I think you are talking in circles here. Stay within the limits/definition of "rate of metabolism" vs RQ , which is 2 different things.

Before we discuss further I think you need to quote your references on which you base your theories on, ie specifically this quote,

When you directly measure CO2 and O2 in a person who has considerable uncoupling, your RQ calculation will not measure caloric consumption as it occurs ex vivo, it will measure uncoupling in vivo,

so I can try to get on your same page.
 
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SAFarmer said:
visionofstrength said:
What you state is the theory, I agree, of how it has been found to work ex vivo. However, when you do direct measurements of CO2 and O2 you find that the ex vivo results do not hold in vivo.

You can see this when directly measuring someone who is hypoxic. But you can also see it with the converse of hypoxia, uncoupling. Uncoupling produces large amounts of CO2 without any ATP -- it's uncoupled from ATP. When you directly measure CO2 and O2 in a person who has considerable uncoupling, your RQ calculation will not measure caloric consumption as it occurs ex vivo, it will measure uncoupling in vivo.

Takeaway: Those who do studies based on RQ calculations can't measure the effects of hypoxia and uncoupling, and much of their work is likely unreliable, as it relates to caloric metabolism.
I think you are talking in circles here. Stay within the limits/definition of "rate of metabolism" vs RQ , which is 2 different things.

Before we discuss further I think you need to quote your references on which you base your theories on, ie specifically this quote,

When you directly measure CO2 and O2 in a person who has considerable uncoupling, your RQ calculation will not measure caloric consumption as it occurs ex vivo, it will measure uncoupling in vivo,

so I can try to get on your same page.
I'm may be drawing a distinction perhaps between theory and practice.

In practice, you directly measure CO2 eliminated and O2 consumed, using devices that measure these things. RQ is the ratio of these two direct measurements.

In theory taught in university (or any theory even as summarized on wikipedia), RQ can be deduced without direct measurement. See for example this online calculator:
http://home.fuse.net/clymer/rq/

But these theoretical deductions, without direct measurement, are only true in theory, or ex vivo. They do not explain what you directly measure in practice, because in practice you are directly measuring the effects of hypoxia and uncoupling.

It's just something you observe when you do direct measurements, you find that RQ does not come out as the theory predicts, and then Peat's (and even Buteyko's) ideas about hypoxia and uncoupling help explain what you observe and directly measure.
 

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I wonder if an indirect calorimeter could help? :eek:
 
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Blossom said:
I wonder if an indirect calorimeter could help? :eek:
Yes, good example. Those directly measure CO2 and O2 but display the conventional "caloric" calculation, as described in the standard theory of RQ.

In my view, if Peat is right about hypoxia and uncoupling, the calorimeters are not calculating the "calories" the way they think, because the RQ standard theory ignores the effects of hypoxia or uncoupling (which don't follow the RQ standard theory about calories).
 

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