Optimal Diet For Increasing Lifespan

haidut

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Despite their many drawbacks due to being guided by wrong theories, some modern nutrition studies are starting to go in the right direction. This latest study looked at some important issues covered by both Peat and mainstream medicine. The issues are whether caloric restriction increases lifespan, if yes then by what mechanism, and what is the optimal diet for increasing lifespan as much as possible. Peat wrote that dietary restriction per se does NOT increase lifespan, but it is rather the restriction of PUFA that goes together with decreased caloric intake, which is responsible for the increased lifespan. This latest study uses the state-of-the-art Geometric Framework for nutrition (GF) to answer some questions that are of interest to both Peat and mainstream medicine.

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

I strongly recommend reading the study, but here is a summary just in case:

1) Dietary/caloric restriction itself does NOT increase lifespan. In fact, it has an opposite effect and makes the experimental animals overeat to compensate for the reduced caloric input. So, one point for Peat.

2) Percentage of dietary fat as a portion of total caloric input does not seem to decrease lifespan, but it does not increase it either. Since it had no effect on satiety, increasing fat as percentage of caloric input made the rodent fat over time since they kept eating until they satisfied their other macronutrient requirements (protein and carbs) regardless of how much fat they had already ingested. So, fat intake should be kept low if one wants to stay lean but otherwise has no effect on lifespan (in terms of quantity only; the study did NOT look at effects of type of fat).

3) Ratio of carbs:protein is what affected lifespan and higher ratios of carbs:protein is what led to almost 30% maximum lifespan increase COMBINED with increased oxidative metabolism and mitochondrial activity. So, a second point for Peat.

4) Increasing carbs:protein ratio did lead to symptoms of fatty liver and increased weight, but SURPRISINGLY these effects were protective and in old age the overweight and fatty liver phenotype mouse was also the healthiest and longest living. So, another point for Peat and many others studying the so-called "obesity paradox" pointing out that being lean (as measured by BMI) in old age is NOT good for you.

So, after reading all of this the question most people will ask is what is the "optimal" carbs:protein ratio for increasing lifespan? Based on the study above, the answer is that it depends if you want to increase the average of maximum lifespan. See attached screenshot with different macronutrient breakdown and its effect on average or maximum lifespan. Optimizing for both requirements, the carb:protein ratio should be as high as possible but making sure protein is about 15%-20% of daily caloric intake. For a 2,000 calorie diet this translates to 75g-100g of protein a day falling perfectly within Peat's recommendations that only very active (or sick) people would need 120g+ of protein a day and everybody else should be able to do fine with 80g-100g. Fat should be adjusted more or less based on taste and desire to lose weight or not. I have seen studies where about 50g of fat a day was deemed "optimal" from the perspective of staying lean but also ensuring nutrient absorption (fat-soluble vitamins) and steroid synthesis.
Combining all of the above, and assuming 2,000 calorie diet as benchmark, the "optimal" diet should contain 75g-100g of protein, 50g of fat (saturated of course) and 250g-300g of sugar. This translates to a carb:protein ratio of 2:1 to 4:1. Interestingly enough, if you look at past Peat interviews and email exchanges this is more or less the diet he has claimed to have been eating in terms of macronutrient breakdown. I saw references to his fat intake varying as needed (which also matches well with the study recommendations) but in general he said he stays around 50g of fat a day. He also said that protein is only safe when consumed with enough sugar and recommended a ratio of at least 2:1 in favor of carbs.

The only problem I have with the study is that they did not test for life extension properties of diets with varying amounts of PUFA (or PUFA deficient altogether). The oil used for all diets was soy oil. However, that is to be expected given that to most researchers this scenario is not interesting since PUFAs are assumed to be essential for health but neutral for lifespan unless the organism is deficient in them.

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?
 

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I think caloric restriction activates certain reactions to a constant estrogenic state which could mildly protect against sudden stresses. Resveratrol in particular mimicks this condition. Definitely not the rational approach to lifespan extension.
 

haidut

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Such_Saturation said:
I think caloric restriction activates certain reactions to a constant estrogenic state which could mildly protect against sudden stresses. Resveratrol in particular mimicks this condition. Definitely not the rational approach to lifespan extension.

I personally would not touch resveratrol. Aside from the fact that it is quite potent phytoestrogen and activates both ER-alpha and ER-beta, the clinical trials (human) were halted b/c it increased significantly the deaths in the treatment group. I think the trial was for kidney failure. The trials were funded by the company of the resveratrol guy Sinclair and GSK bought the company for $700mil. So, Sinclair is probably sipping his drink somewhere on the Bahamas while GSK is scratching its head how to get away form the resveratrol scam and what to do with the (useless) company they bought. Jusr search Google for "resveratrol scam Sinclair".

Anyways, any beneficial effects of resveratrol seems to depend on increasing NAD+.

http://precedings.nature.com/documents/4421/version/1

Exercise does that a lot more effectively - walking 1-2 miles a day would be a lot more effective for that purpose than taking resveratrol. On the other hand, there are studies showing resveratrol decreases NAD+, increases NADH and thus decreases the NAD/NADH ratio.

http://www.ncbi.nlm.nih.gov/pubmed/21706162

So, aside from what I ingest with a glass of wine or eating grapes I would personally stay away from resveratrol:):
 
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I wouldn't say otherwise. However the guys who eat 1200 calories per day and run ten miles need something to waste money on. The latest craze is ingesting Buckminsterfullerene, which gets permanently embedded into cell surfaces.
 

haidut

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Such_Saturation said:
I wouldn't say otherwise. However the guys who eat 1200 calories per day and run ten miles need something to waste money on. The latest craze is ingesting Buckminsterfullerene, which gets permanently embedded into cell surfaces.

There was a study several years ago showing the "Bucky Balls" doubled lifespan of rats, so that may be one reason people are gobbling it up. I wonder how long before PubMed starts showing ads on their page next to the studies. Kind of like Google, but for dietary supplements (or drugs).
 
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haidut said:
Such_Saturation said:
I wouldn't say otherwise. However the guys who eat 1200 calories per day and run ten miles need something to waste money on. The latest craze is ingesting Buckminsterfullerene, which gets permanently embedded into cell surfaces.

There was a study several years ago showing the "Bucky Balls" doubled lifespan of rats, so that may be one reason people are gobbling it up. I wonder how long before PubMed starts showing ads on their page next to the studies. Kind of like Google, but for dietary supplements (or drugs).

Don't give them ideas! We shall be remembered as "Generation Abstract" because that's all we read :mrgreen:
 
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haidut said:
Such_Saturation said:
I think caloric restriction activates certain reactions to a constant estrogenic state which could mildly protect against sudden stresses. Resveratrol in particular mimicks this condition. Definitely not the rational approach to lifespan extension.

I personally would not touch resveratrol.
The first article I ever read by Peat was his "Resveratrol is a Scam" article. The article was pirated on another website, without attribution, and so it was that when I searched google for the author of the article, it led me for the first time to raypeat.com. That was a good day for me.

h, I have the same issue as you do with the study, and that is that they are not breaking out the tryptophan/methionine from the protein, they are not separating the PUFAs from the fat, and for that matter, they are not separating the starches and fibers from the fruit sugars. So pretty much, the whole study seems flawed.

I do think there's a question as to whether limiting protein/fat does nothing more than limit tryptophan/methionine and PUFAs.

Also, there has been so much success with the ketogenic diet 85/10/5 (SFAs/protein/sugar). See Seyfreid et al. I think there's a chance one might say Peat could be "wrong" ONLY IF you were to read him (as you seem to?), advocating for some ratio of carbs/protein/fat. I think the evidence against glucose (or generic carbs) is pretty strong. I also think casein and cartilage are far superior proteins to all others.

But I do feel Peat need not be read as advocating ratios, and could also be read as saying that
1) certain drug-like foods are critically important: for example, coffee, salt, and thyroid.
2) eliminating tryptophan/methionine and PUFAs is also critically important.
3) Ratios of casein/cartilage, fructose and SFAs don't matter, as long as you don't deplete glycogen stores.

So, in one example, I've begun a test of having coconut/MCT oil/casein all day (with no fructose), and keeping small amounts of fructose only for bedtime. There is no reason I can see why "carbohydrates" are needed to digest casein, and MCTs won't do just as well.

You?
 
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visionofstrength said:
haidut said:
Such_Saturation said:
I think caloric restriction activates certain reactions to a constant estrogenic state which could mildly protect against sudden stresses. Resveratrol in particular mimicks this condition. Definitely not the rational approach to lifespan extension.

I personally would not touch resveratrol.
The first article I ever read by Peat was his "Resveratrol is a Scam" article. The article was pirated on another website, without attribution, and so it was that when I searched google for the author of the article, it led me for the first time to raypeat.com. That was a good day for me.

h, I have the same issue as you do with the study, and that is that they are not breaking out the tryptophan/methionine from the protein, they are not separating the PUFAs from the fat, and for that matter, they are not separating the starches and fibers from the fruit sugars. So pretty much, the whole study seems flawed.

I do think there's a question as to whether limiting protein/fat does nothing more than limit tryptophan/methionine and PUFAs.

Also, there has been so much success with the ketogenic diet 85/10/5 (SFAs/protein/sugar). See Seyfreid et al. I think there's a chance one might say Peat could be "wrong" ONLY IF you were to read him (as you seem to?), advocating for some ratio of carbs/protein/fat. I think the evidence against glucose (or generic carbs) is pretty strong. I also think casein and cartilage are far superior proteins to all others.

But I do feel Peat need not be read as advocating ratios, and could also be read as saying that
1) certain drug-like foods are critically important: for example, coffee, salt, and thyroid.
2) eliminating tryptophan/methionine and PUFAs is also critically important.
3) Ratios of casein/cartilage, fructose and SFAs don't matter, as long as you don't deplete glycogen stores.

So, in one example, I've begun a test of having coconut/MCT oil/casein all day (with no fructose), and keeping small amounts of fructose only for bedtime. There is no reason I can see why "carbohydrates" are needed to digest casein, and MCTs won't do just as well.

You?

There's a chance certain tissues cannot use ketones properly but of course this is hard to measure and lots of studies are old and short and hard to reach.
 
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S_S, Interesting! what tissue can't use ketones? some say:

red blood cells have no mitochondria

the liver has no thiophorase

Renal medulla has less oxidative capacity

Anything else?
 

kiran

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haidut said:
Such_Saturation said:
I wouldn't say otherwise. However the guys who eat 1200 calories per day and run ten miles need something to waste money on. The latest craze is ingesting Buckminsterfullerene, which gets permanently embedded into cell surfaces.

There was a study several years ago showing the "Bucky Balls" doubled lifespan of rats, so that may be one reason people are gobbling it up. I wonder how long before PubMed starts showing ads on their page next to the studies. Kind of like Google, but for dietary supplements (or drugs).

C60 has high electron affinity (2.66eV). I seem to recall asking RP about C60, he said there might be purity issues.

Ray Peat said:
Koch’s understanding of the oxidative apparatus of life, as a matter of electron balances, involved the idea that molecules with a low ionization potential, making them good electron donors, amines specifically, interfered with respiration, while quinones, with a high affinity for electrons, making them electron acceptors, activated respiration. The toxic effects of tryptophan derivatives, indoles, and other amines related to the behavior of their electrons. (Serotonin wasn’t known at the time Koch was doing his basic research.) Koch believed that similar electronic functions were responsible for the effects of viruses.
 
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kiran said:
haidut said:
Such_Saturation said:
I wouldn't say otherwise. However the guys who eat 1200 calories per day and run ten miles need something to waste money on. The latest craze is ingesting Buckminsterfullerene, which gets permanently embedded into cell surfaces.

There was a study several years ago showing the "Bucky Balls" doubled lifespan of rats, so that may be one reason people are gobbling it up. I wonder how long before PubMed starts showing ads on their page next to the studies. Kind of like Google, but for dietary supplements (or drugs).

C60 has high electron affinity (2.66eV). I seem to recall asking RP about C60, he said there might be purity issues.
I'd not looked into C60 fullerenes until seeing these posts, but now that I did a little, the anti-aging benefits look credible to me. If it works by uncoupling, as Koch's work seems to suggest, then there could be measurable thermogenesis from it.

The purity issue seems to have been resolved by mixing it with olive oil. And the price is right. Has anybody tried it?
 
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visionofstrength said:
The first article I ever read by Peat was his "Resveratrol is a Scam" article. The article was pirated on another website, without attribution, and so it was that when I searched google for the author of the article, it led me for the first time to raypeat.com. That was a good day for me.
Just noticed that the resveratrol article I first found is not on raypeat.com, it seems. Instead, it's posted here: http://doctorsaredangerous.com/articles ... l_scam.htm

At the time, I was learning about the ability of brown adipose tissue (BAT) to increase body temperature. This article was the first time I had seen Peat (or anyone else) explain the phenomenon in this way:
Ray Peat said:
The cells in each organ and tissue of the body are arranged in ways that allow them to make their contribution to the function of the organism, while receiving oxygen, glucose, and regulatory substances in the blood, and maintaining and renewing themselves. Except for the skin, their situation amid other cells assures that they will live in a high concentration of carbon dioxide.

There are proteins (uncoupling proteins, UCP) that cause the mitochondria to increase their consumption of oxygen without increasing their synthesis of ATP. The synthesis of ATP is usually thought of as the main reason for the consumption of oxygen, so the UCP have been assumed to exist to increase heat production. The formation of carbon dioxide is usually thought of as just an unavoidable consequence. UCP proteins, however, exist in situations in which heat production doesn’t seem appropriate (Borecký & Vercesi, 2005; Aguilera, et al., 2005; Gnanalingham, et al., 2005). For example, fasting or calorie restriction increases UCP, tending to cause tissues to consume energy more rapidly. Stress and hypoxia also can increase UCP, suggesting that these enzymes have protective functions.

Increasing the formation of carbon dioxide seems to me to be the essential function of the UCP. Thyroid hormone (T3) increases UCP, and UCP increases the formation of new mitochondria. Increased activity of the UCP is closely associated with increased lifespan. A decreased amount of T3 in tissues during aging corresponds to decreasing mitochondrial function.

Increased CO2 inhibits the formation of lactate, decreases the lipolytic effect of adrenaline, and the lowered energy charge produced by the UCP would prevent the diversion of glucose into other uses.
To me, it seems that if Peat is right about this, all aging or anti-aging mechanisms in animals, whether from diet or C60 fullerenes or living at altitude, can be explained in one general theory, which might be as simple as: the rate of aging is related to the mass of the body and the amount of CO2 in the tissues. What might such a formula be?

[spoil][tab=30]a = mco[sub]2[/sub] ?? What do you think?[/spoil]
:cool:

[Edit: I've split this thought to its own thread, so it's a little easier for visitors to find:
viewtopic.php?f=10&t=4641]
 

slayers

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When I was very lean and healthy.... I was eating around 2400 calories roughly 300g carbs, 170g protein and 40-50g fat.
 
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visionofstrength said:
S_S, Interesting! what tissue can't use ketones? some say:

red blood cells have no mitochondria

the liver has no thiophorase

Renal medulla has less oxidative capacity

Anything else?

These concern the brain. As you can see rat experiments are pretty much useless in this because our ketosis is so much better.

[http://www.ncbi.nlm.nih.gov/pubmed/15877199]
[http://www.ncbi.nlm.nih.gov/pubmed/451608]
[http://www.ncbi.nlm.nih.gov/pubmed/2937307]
 
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Such_Saturation said:
These concern the brain. As you can see rat experiments are pretty much useless in this because our ketosis is so much better.

[http://www.ncbi.nlm.nih.gov/pubmed/15877199]
[http://www.ncbi.nlm.nih.gov/pubmed/451608]
[http://www.ncbi.nlm.nih.gov/pubmed/2937307]
Thanks! I see what you mean, almost everything in rats, mice or rabbits.

Studies like this (using rats) lead me to think that high saturated fats like those in mother's milk are ideal foods, designed to transition from fetal high carbohydrate diets to neonatal high fat diets:
http://www.ncbi.nlm.nih.gov/pubmed/21209089
http://www.ncbi.nlm.nih.gov/pubmed/23689508

I see a survey done on glucose levels in neonatal infants here:
http://www.ncbi.nlm.nih.gov/pubmed/11446016

"Early and exclusive breastfeeding and the maintenance of normal body temperature are usually sufficient preventive measures in healthy infants."

My observation is my own adult brain energy and glucose levels seems also to be related to frequent feeding of high saturated fats and maintenance of body temperature (and I would add sufficient sleep and avoiding stressful exertion). Milk itself provides lactose sugars. So maybe we don't need to change much from newborns, who don't need fruit at all when we have abundant MCTs in mother's milk, and we are not stressed by cold or exertion.

For comparison, the ratios in breast milk (by weight) are:
"3%--5% fat, 0.8%--0.9% protein, 6.9%--7.2% carbohydrate calculated as lactose"
See http://www.ncbi.nlm.nih.gov/pubmed/392766

The percentages of calories might be roughly 60:5:35 (fat:protein:sugar).
 
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I like that thinking. Would pure fructose break ketosis?
 
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Such_Saturation said:
I like that thinking. Would pure fructose break ketosis?
Not sure, what do you think? Ketosis may not be well-defined, but suppose we say: Ketosis is the state in which glucose is relatively limited or lacking as a fuel and cells begin to use fat as a primary fuel source. Then Peat describes something similar like this:
Ray Peat said:
One of the points at which fatty acids suppress the use of glucose is at the point at which it is converted into fructose, in the process of glycolysis. When fructose is available, it can by-pass this barrier to the use of glucose, and continue to provide pyruvic acid for continuing oxidative metabolism, and if the mitochondria themselves aren't providing sufficient energy, it can leave the cell as lactate, allowing continuing glycolytic energy production. In the brain, this can sustain life in an emergency.
From that, it would seem fructose does something similar to ketones, and provides energy when glucose or glycolosis cannot - a good thing, right?

The ketosis proponents seem to think (FWIW) that it's insulin that breaks ketosis, but Peat thinks fructose does not spike insulin, so again, fructose and ketones should play nice together?
 
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Well it looks like the only way to achieve high levels of acetyl-coa is by burning fat which also doesn't make pyruvate which can recharge oxaloacetate (pulls acetyl-coa into citric acid cycle) directly. Still oxaloacetate seems a pretty protective substance and we want the citric acid cycle going anyway. I guess another way to make lots of acetyl-coa (to make ketones) are the ketogenic aminoacids. Or, thyroid.

<<The rate-limiting step in the manufacture of ketones in the liver is the transfer of fatty acids (acyl groups) from Coenzyme A to carnitine. Carnitine acyl transferase I is the relevant enzyme, often referred to as CAT-I. To a certain degree, increased levels of carnitine will drive this transfer, but the main factor that inhibits CAT-I is the level of malonyl CoA in the liver. High levels of malonyl CoA effectively turn off the enzyme.

Malonyl CoA is manufactured by another enzyme called Acetyl CoA carboxylase. Acetyl CoA carboxylase activity is in turn regulated by the amount of citric acid in the cell. The more the Krebs' cycle is whirling around (and citrate is being produced), the greater the activity of Acetyl CoA carboxylase, which in turn results in inhibition of ketoacid production. Turn off the supply of substrate into Krebs' cycle, and ketoacids are formed.>> [http://www.anaesthetist.com/icu/organs/endocr/dm/Findex.htm#dka.htm]

So low malonyl CoA will allow fats to enter mitochondria apparently.

Effects of thyroid state and fasting on the concentrations of CoA and malonyl-CoA in rat liver.
Thyroid Hormone Regulates Carnitine Palmitoyltransferase Iα Gene Expression through Elements in the Promoter and First Intron*

This guy [http://www.sciencedirect.com/science/article/pii/S0006291X09004306] makes the same reasoning as Ray Peat but wishes to conclude that fructose does not cause satiety, etc. Perhaps fructose is really helpful for coming out of hibernation and other high fat states.
 

narouz

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Such_Saturation said:
Well it looks like the only way to achieve high levels of acetyl-coa is by burning fat which also doesn't make pyruvate which can recharge oxaloacetate (pulls acetyl-coa into citric acid cycle) directly. Still oxaloacetate seems a pretty protective substance and we want the citric acid cycle going anyway. I guess another way to make lots of acetyl-coa (to make ketones) are the ketogenic aminoacids. Or, thyroid.

<<The rate-limiting step in the manufacture of ketones in the liver is the transfer of fatty acids (acyl groups) from Coenzyme A to carnitine. Carnitine acyl transferase I is the relevant enzyme, often referred to as CAT-I. To a certain degree, increased levels of carnitine will drive this transfer, but the main factor that inhibits CAT-I is the level of malonyl CoA in the liver. High levels of malonyl CoA effectively turn off the enzyme.

Malonyl CoA is manufactured by another enzyme called Acetyl CoA carboxylase. Acetyl CoA carboxylase activity is in turn regulated by the amount of citric acid in the cell. The more the Krebs' cycle is whirling around (and citrate is being produced), the greater the activity of Acetyl CoA carboxylase, which in turn results in inhibition of ketoacid production. Turn off the supply of substrate into Krebs' cycle, and ketoacids are formed.>> [http://www.anaesthetist.com/icu/organs/endocr/dm/Findex.htm#dka.htm]

So low malonyl CoA will allow fats to enter mitochondria apparently.

Effects of thyroid state and fasting on the concentrations of CoA and malonyl-CoA in rat liver.
Thyroid Hormone Regulates Carnitine Palmitoyltransferase Iα Gene Expression through Elements in the Promoter and First Intron*

This guy [http://www.sciencedirect.com/science/article/pii/S0006291X09004306] makes the same reasoning as Ray Peat but wishes to conclude that fructose does not cause satiety, etc. Perhaps fructose is really helpful for coming out of hibernation and other high fat states.

When you guys figure this out,
I'm counting on you to explain it to me in universal language. :D
 
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